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Federal Court of Australia |
COURT
IN THE FEDERAL COURT OF AUSTRALIACATCHWORDS
Trade Practices - cigarettes - advertisement in newspaper - statement that "there is little evidence and nothing which proves scientifically that cigarette smoke causes disease in non-smokers" - whether the statement made in trade or commerce - whether statement misleading or deceptive - evidence - meaning of - admissibility of scientific journals - whether passive smoking causes cancer - whether passive smoking causes respiratory disease - whether passive smoking causes asthma - meaning of asthma - meaning of scientific proof - epidemiological studies - whether capable of proving causal relationship - delay in bringing proceedings - discretion - injunction restraining further publication of advertisementTrade Practices Act 1974, s.52
HEARING
SYDNEYCounsel for the applicant: D.M.J. Bennett QC, N.F. Francey
Instructed by Cashman and Partners
Counsel for the respondent: B.S.J. O'Keefe QC, B.W. Walker
Instructed by Clayton Utz
ORDER
The applicant is to file and serve draft minutes of the orders it seeks within 14 days of this date.The respondent is to file and serve within 28 days of this date draft minutes of the orders it proposes the Court should make.
Reserve question of costs.
Matter to be relisted on a date to be fixed for argument on costs and for
settlement of minutes of orders.
NOTE: Settlement and entry of orders is dealt with in Order 36 of the Federal Court Rules.
DECISION
Introduction - the advertisement2. It shorteneth life(British Journal of Preventive and Social Medicine (1973), 27, 150).
3. It breedeth many diseases
4. It breedeth melancholy
5. It hurteth the mind
6. It is ill for the smokers issue."
2. Nearly four centuries after the Doctor of Physic wrote his letter the
debate about the alleged harmful effects of tobacco continues.
The applicant
claims that the respondent has engaged in conduct that is misleading or
deceptive or is likely to mislead or deceive
in contravention of s.52 of the
Trade Practices Act 1974 ("the Act"). The alleged contravention is claimed
to have occurred by reason of the publication of an advertisement on 1 July
1986 in several
newspapers distributed in Australia. It is not in issue that
the respondent caused the advertisement to be published. The advertisement
was in the following terms:
"A message from those who do ...3. It is the words of the third and fifth paragraphs which the applicant submits are misleading or deceptive or likely to mislead or deceive. The respondent concedes that the words of the fifth paragraph do not give an accurate description of the number of people involved in the study undertaken by the Institute of Cancer Research, and consents to an order restraining the repetition of those words. It resists the claims that the words of the third paragraph are misleading or deceptive or likely to mislead or deceive.
to those who don't
Some non-smokers are annoyed by cigarette smoke. This
is a reality that's been with us for a long time.
Lately, however, many non-smokers have been led to
believe that cigarette smoke in the air can actually cause
disease.
And yet there is little evidence and nothing which
proves scientifically that cigarette smoke causes disease in
non-smokers.
The London Times reported findings from the Institute of
Cancer Research in Surrey, England, published in this
month's edition of the `British Journal of Cancer,' that
`passive smoking' for life-long non-smokers carries no
significant increase in the risk of lung cancer, bronchitis
or heart disease (all allegedly associated with smoking).
The Institute's conclusions are based on a wealth of
statistical detail from a study involving 12,000 people.
In a study by a Vice-President of the American Cancer
Society in 1981 which involved 175,000 people, it was
reported that `passive smoking' had `very little, if any'
effect on lung cancer rates among non-smokers.
In the follow-up study published in 1985, no
statistically significant increase in risk was reported.
Researchers at the Harvard School of Public Health found
that a non-smoker would have to spend 100 hours straight in
the smokiest bar to `absorb' the equivalent of a single
filter tip cigarette.
Major reviews on `passive smoking' over the last few
years have concluded that 'passive smoking' cannot be shown
to be a health risk. The weight of evidence is summed up in
the remarks at the conclusion of the 1984 Vienna Health
Conference which was held in co-operation with the World
Health Organisation: `should law makers wish to take
legislative measures with regard to passive smoking, they
will, for the present, not be able to base their efforts on
a demonstrated health hazard from passive smoking.'
Often our own concerns about health can take an unproved
claim and magnify it out of all proportion; so what begins
as a misconception turns into a frightening myth.
Alright, cigarette smoke may be annoying to some
non-smokers, but how shall we deal with these problems?
Confrontation? Segregation? Legislation?
No.
We think annoyance is neither a government nor a medical
problem. It's a people problem. Smokers can help by being
more considerate and responsible. Non-smokers can help by
being more tolerant. And both groups can help by showing
more respect for each others rights and feelings.
Don't let intolerant minority pressure groups use you to
create divisions between Australians.
Authorised by John Dollisson,
Tobacco Institute, Gold Fields House, Sydney."
4. For ease of reference, I shall hereafter refer to the contents of para. 3
of the advertisement as "the statement".
The history of the litigation
5. On 25 July 1986 the applicant complained to the Trade Practices Commission of the respondent's conduct in publishing the advertisement. On 7 January 1987 the Commission informed the applicant that the respondent had undertaken to run a follow-up advertisement in a form which had been agreed with the Commission and which was accepted by it as a sufficient correction of the original advertisement and that, as a consequence, it considered the matter closed.
6. The follow-up advertisement was published in January 1987. It did not
refer to what was said in the third paragraph of the original
advertisement.
After referring to other parts of the original advertisement it concluded with
the following quotation from remarks
made by two scientists at the conclusion
of the 1984 Vienna Health Conference:
"A drawback in all epidemiological studies up to now7. The applicant was dissatisfied with the terms of the follow-up advertisement and asserted that it did not correct what it claimed to be the misleading and deceptive words of the original advertisement. The applicant sought from the respondent undertakings as to the content of future advertisements but the respondent refused to give them.
consists in the fact that they have been conducted without
sufficient quantification of the contamination from passive
smoking. Further epidemiological investigations, in which
the problem of registering the amount of passive
contamination will have to be dealt with more, are urgently
needed. New attempts at doing so have been indicated.
Since, due to the annoyance connected with passive smoking
and the possible hazard to high-risk groups, it also further
constitutes a controversial social problem, international
co-operation among the various scientific disciplines is the
order of the day. Should lawmakers wish to take legislative
measures with regard to passive smoking, they will, for the
present, not be able to base their efforts on a demonstrated
health hazard from passive smoking."
8. Thereupon the present proceedings were commenced. By its defence the respondent denies that it has engaged in conduct proscribed by s.52. Further, it relies upon the publication of the follow-up advertisement and an undertaking it has given to the Commission not to re-publish the original advertisement as justification for the Court refusing the relief claimed by the applicant. It also claims that the applicant has been guilty of laches, acquiescence and delay in bringing the proceedings.
9. The respondent applied to have the statement of claim struck out upon
grounds which are no longer material. The application was
refused. Leave to
appeal against the decision was granted, but the appeal was dismissed: (1988)
19 FCR 469.
Was the advertisement published "in trade or commerce"?
10. It was submitted on behalf of the respondent that in publishing the advertisement it did not engage in conduct in trade or commerce. It was argued that the advertisement should be read as a contribution to the public health debate as to the alleged effect of environmental tobacco smoke on the health of non-smokers and that it has only a tenuous connection with dealings between cigarette manufacturers and distributors on the one hand and smokers on the other. It was argued that conduct is not proscribed by s.52 if it is merely conduct in relation to trade or commerce, that s.52 applies only to conduct in trade or commerce, and that the most that can be said of the respondent's conduct in publishing the advertisement is that it was conduct of the former kind.
11. It was further submitted that there is a great range of plausible circumstances in which people may make statements calculated to affect the lives and pecuniary interests of others. Counsel postulated the example of a campaign in support of higher indirect taxation which, if heeded by government, might affect the price of goods and thus their market appeal. The legislature cannot have intended, so it was submitted, that such political or intellectual activities would constitute conduct in trade or commerce within the meaning of those words in s.52. Such conduct, so it was said, would plainly be conduct which may affect trade or commerce and thus, in one sense, be conduct in relation to trade or commerce but it would not be conduct within the purview of s.52 because it would not be conduct in trade or commerce.
12. As was pointed out in Concrete Constructions (NSW) Pty Ltd v. Nelson
[1990] HCA 17; (1990) 64 ALJR 293 at 295 by Mason C.J., Deane, Dawson and Gaudron JJ. the
words "trade or commerce" when used in the context of s.52 of the Trade
Practices Act are not terms of art but are terms of common knowledge of the
widest import. As their Honours there said, the real problem involved
in the
construction of s.52 arises from the requirement that the conduct to which the
section refers be "in" trade or commerce. Their Honours said:
"The phrase `in trade or commerce' in s.52 has a13. Cigarettes are articles of commerce and restrictions on their use by consumers may render them less attractive as such, resulting in adverse economic consequences for their manufacturers and distributors. No doubt the participation by a trading corporation in a debate on a matter of public or social controversy will often not be conduct in trade or commerce. But the publication of the advertisement in the present case should not be viewed in isolation. It was published by a trading corporation which, so it may be safely inferred, was concerned to ensure that the sale of cigarettes would not be adversely affected by a belief on the part of the public as to a possible causal link between cigarette smoke and disease in non-smokers. The existence of such a link, or of evidence suggesting it, could affect the sale of cigarettes in various ways, e.g. public pressure to restrict the smoking of cigarettes in places where non-smokers are present.
restrictive operation. It qualifies the prohibition against
engaging in conduct of the specified kind. As a matter of
language, a prohibition against engaging in conduct `in
trade or commerce' can be construed as encompassing conduct
in the course of the myriad of activities which are not, of
their nature, of a trading or commercial character but which
are undertaken in the course of, or as incidental to, the
carrying on of an overall trading or commercial business.
If the words `in trade or commerce' in s. 52 are construed
in that sense, the provisions of the section would extend,
for example, to a case where the misleading or deceptive
conduct was a failure by a driver to give the correct
handsignal when driving a truck in the course of a
corporation's haulage business. It would also extend to a
case, such as the present, where the alleged misleading or
deceptive conduct consisted of the giving of inaccurate
information by one employee to another in the course of
carrying on the building activities of a commercial builder.
Alternatively, the reference to conduct `in trade or
commerce' in s. 52 can be construed as referring only to
conduct which is itself an aspect or element of activities
or transactions which, of their nature, bear a trading or
commercial character. So construed, to borrow and adapt
words used by Dixon J. in a different context in Bank of NSW
v. The Commonwealth [1948] HCA 7; (1948) 76 CLR 1 at 381, the words `in
trade or commerce' refer to `the central conception' of
trade or commerce and not to the `immense field of
activities' in which corporations may engage in the course
of, or for the purposes of, carrying on some overall trading
or commercial business.
As a matter of mere language, the arguments favouring
and militating against these alternative constructions of s.
52 are fairly evenly balanced. The scope of the prohibition
imposed by s.52 is, however, governed not only by `the terms
in which it is created' but by `the context in which it is
found': see Yorke v Lucas [1985] HCA 65; (1985) 158 CLR 661 at 668; and,
generally, Bank of NSW v. The Commonwealth, at 285. In that
regard, it is of particular significance that the words
`trade' and `commerce' have `about them a chameleon-like
hue, readily adapting themselves to their surroundings':
O'Brien v. Smolonogov (1983) 53 ALR 107 at 113, quoting
Federal Commissioner of Taxation v. Whitfords Beach Pty Ltd
[1982] HCA 8; (1982) 150 CLR 355 at 378-379. Section 52(2) precludes
limiting the scope of s.52(1) by implication drawn from the
contents of other provisions of Pt V. Nonetheless, when the
section is read in the context provided by other features of
the Act, which is `An Act relating to certain Trade
Practices', the narrower (ie the second) of the alternative
constructions of the requirement `in trade or commerce' is
the preferable one. Indeed, in the context of Pt V of the
Act with its heading `Consumer Protection', it is plain that
s.52 was not intended to extend to all conduct, regardless
of its nature, in which a corporation might engage in the
course of, or for the purposes of, its overall trading or
commercial business. Put differently, the section was not
intended to impose, by a side-wind, an overlay of
Commonwealth law upon every field of legislative control
into which a corporation might stray for the purposes of, or
in connection with, carrying on its trading or commercial
activities. What the section is concerned with is the
conduct of a corporation towards persons, be they consumers
or not, with whom it (or those whose interests it represents
or is seeking to promote) has or may have dealings in the
course of those activities or transactions which, of their
nature, bear a trading or commercial character. Such
conduct includes, of course, promotional activities in
relation to, or for the purposes of, the supply of goods or
services to actual or potential consumers, be they
identified persons or merely an unidentifiable section of
the public."
14. The advertisement had the potential, and was no doubt intended, to protect the commercial interests of cigarette manufacturers and distributors. Accepting that conduct "in trade or commerce" is confined to conduct which is itself an aspect of activities which, of their nature, bear a commercial character I think the proper conclusion is that the publication of the advertisement was conduct "in trade or commerce". Advertising products for sale is an aspect or element of the selling of those products. The selling of the products is indisputably a trading or commercial activity. Advertising may serve a number of purposes. One purpose may be to refute criticism of the seller's products thus protecting the market for them. The advertisement published by the respondent was calculated to achieve such a purpose.
15. To borrow the words used by Dixon J. in Bank of New South Wales v The
Commonwealth [1948] HCA 7; (1948) 76 CLR 1 at 381 quoted in Concrete Constructions at 295,
the publication of the advertisement was an activity within "the central
conception"
of trade or commerce. In my opinion the publication of the
advertisement was conduct "in trade or commerce".
The Meaning of the Advertisement
(i) Context and class of readers.
16. The meaning that the words of the third paragraph of the advertisement convey to a reader is of central importance to the case. Much argument was directed to the meaning of the words "evidence", "proves scientifically" and "disease". In my opinion it would be wrong to ascribe a meaning to any of those words, or to the whole paragraph, in isolation from the context in which they are set. As Gibbs C.J. observed in Parkdale Custom Built Furniture Pty Ltd v. Puxu Pty Ltd [1982] HCA 44; (1982) 149 CLR 191 at 199, where the conduct complained of consists of words it would not be right to select some words only and to ignore others which provide the context which gives meaning to the particular words.
17. When considering whether readers would be misled or deceived by the words
complained of, regard must be had to the class of persons
likely to read the
advertisement. The advertisement is directed at the general reading public.
(ii) Meaning of "evidence"
18. It is plain that the reference to "evidence" is not a reference only to material that would be admissible in a court of law. Even in the argot of lawyers, "evidence" includes, in some contexts, hearsay material. The first meaning given for the word in the Macquarie Dictionary is "ground for belief". In para. 3 of the advertisement the word is used in the collocation of words "evidence" .... that cigarette smoke causes disease ...." In my opinion many readers would understand the word as referring to data or material which affords grounds for believing that cigarette smoke causes disease in non-smokers. Such material would, in my opinion, include the published results of studies and research work, including collection of data, undertaken by scientists of repute. Many such published results, in the form of articles which have appeared in learned scientific journals, were tendered as part of the applicant's case and I admitted them into evidence.
19. Articles of this kind were referred to during the course of the case as "primary articles" and it will be convenient to so describe them in these reasons. Some of the primary articles contained comments by the authors on the research work and opinions of others and objection was taken to the admissibility of such comments.
20. The applicant also tendered a number of reports issued by scientific organisations and professional bodies which have considered the question whether cigarette smoke adversely affects the health of non-smokers. These reports were referred to during the course of the trial as "major reviews" and I shall so describe them in these reasons. They included the following: a monograph on the evaluation of the carcinogenic risk of chemicals to humans issued by the International Agency for Research on Cancer, which is part of the World Health Organisation ("the IARC report"); a report of a working party on the effects of passive smoking on health adopted by the Australian National Health and Medical Research Council ("the NH and MRC report"); a report on environmental tobacco smoke by the National Research Council, which is the principal operating agency of the National Academy of Sciences of the United States of America ("the N.R.C. report"); a report made in 1986 by the Surgeon General of the United States of America on the health consequences of involuntary smoking ("the Surgeon General's report"); and the fourth report of the Independent Scientific Committee on Smoking and Health, being a committee appointed by the British Government and chaired by Sir Peter Froggatt ("the Froggatt report").
21. Mr O'Keefe QC, senior counsel for the respondent, submitted that the major reviews were not admissible as opinion evidence to show the state of science nor admissible as evidence of the existence, extent or quality of "evidence .... that cigarette smoke causes disease in non-smokers". He submitted that the passages in the major reviews upon which the applicant relies are based upon nothing more than the work and opinions of other scientists. He contended that the reviews were no more than hearsay out-of-court statements which could not be identified with any particular member or members of the committees responsible for their authorship. In his submission, the reference to "evidence" in the advertisement cannot reasonably be understood as referring to opinions expressed by scientists or a group of scientists on the original work of other scientists.
22. It was also argued that although the primary articles might be admissible to show what had appeared in the scientific literature, they were not admissible to prove the proposition that cigarette smoke causes disease in non-smokers.
23. I appreciate the force of these arguments, but it is necessary to keep firmly in mind that the question in the present case is whether the statement made in para. 3 of the advertisement is misleading or deceptive or likely to mislead or deceive. In my opinion, many readers of the advertisement would think that the reference to "evidence" is a reference to, inter alia, opinions of competent scientists whether based on their own research or on the published results of the research of others.
24. First, I think the opinions of competent experts on a matter falling within their field of expertise may afford grounds for belief as to that matter. Many readers (amongst whom would be included the educated as well as the uneducated and the adolescent as well as the mature) would understand such opinions to be evidence relevant to the question whether cigarette smoke causes disease in non-smokers. This understanding would be reinforced by a reading of the entire advertisement. Paragraph 3 is immediately followed by a number of paragraphs in which references are made to published findings and conclusions of scientists and groups of scientists. These references include a statement, in heavy type, that: "Major reviews on `passive smoking' over the last few years have concluded that passive smoking cannot be shown to be a health risk". This statement is in turn followed by a reference to the "weight of evidence" which is said to be ascertained from the summation of views of persons who had attended a Health Conference in Vienna. In my opinion readers of the advertisement would conclude that there is little in the form of published opinions of scientists or groups of scientists to support the proposition that cigarette smoke causes disease in non-smokers. Accordingly, I think the major reviews are admissible to show whether readers would be misled if they reached that conclusion.
25. My decision in this case would have been the same had I formed a different view as to the admissibility of the major reviews. This is not surprising, since the contents of the primary articles which I admitted into evidence constitute the great bulk of the material upon which the authors of the major reviews base their opinions.
26. It was submitted that a reader who held the belief that the opinion of a
scientist or a group of scientists was "evidence" would
not hold that belief
as a result of anything said in the advertisement, but rather as a result of
his own misconception: cf Puxu
at p 225. There would be something to be said
for this argument if the advertisement did not contain references to findings
and
conclusions of scientists. But the inclusion of those references in the
advertisement makes the argument unsustainable.
(iii) Meaning of "scientific proof"
27. It is necessary to consider what the phrase "nothing which proves scientifically" conveys to the reader of the advertisement. There was substantial consensus between witnesses that scientists themselves do not commonly use the term "scientific proof". Dr Leslie, a witness called by the respondent said: - "I do not think one ever talks about scientific proof".
28. Dr Armstrong, a witness called by the applicant, said that every scientist recognises that, at any particular point in time, his knowledge is imperfect and that with the advance of knowledge something which he presently thinks is proven may subsequently be proven to be wrong. He said that scientists accordingly resile from any belief in absolute proof and recognise that proof is relative to the existing state of knowledge. As another witness, Dr Le Souef, said: "The philosophical approach of science is that you cannot absolutely prove anything just as there is no absolute truth."
29. Nevertheless several witnesses gave what might be called working
definitions of scientific proof. Dr Armstrong said: "The
only real meaning
of scientific proof that I can contribute is that one has a sufficient
conviction about the certainty as to take
certain consequential actions."
The difficulty about this approach is that it gives a variable meaning to
scientific proof according
to the consequential action that may be called for.
Dr Armstrong himself recognised this. As he said (T.1478):
"... I do not believe that there exists any objective or30. I think an observation made by Dr Witorsch, who was called by the respondent, affords the best guide to a definition of scientific proof. He said, in effect, that scientifically a proposition is proved when the data in support of it is compelling. I do not think Dr Witorsch's approach differs much from that taken by one of the applicant's witnesses, Sir Richard Doll, who thought that scientific proof was proof beyond reasonable doubt or "convincing" scientific proof.
identifiable standard which equals scientific proof. It is
very much dependent upon the circumstances for which it is
used. In the case of public health measures I would say
that the necessary level of proof had been attained when it
was considered to be more likely than not that the
proposition was true. ... That is good enough when you are
dealing with matters pertaining to public health and
particularly, and again one would have to qualify this,
where the measure that you propose is one which involves the
removal of a hazard."
31. I think that in the context of the advertisement, the words "nothing
which proves scientifically that cigarette smoke causes
disease in
non-smokers" mean "nothing which affords compelling or convincing evidence
that cigarette smoke causes disease in non-smokers".
This is the meaning
which I think most readers would give to the words.
Admissibility of evidence to show that statements in advertisement continued
to be misleading after date of publication.
32. The advertisement appeared in newspapers on 1 July 1986. Proceedings
were not commenced in this Court until 11 June 1987. On
that date an
application was filed in which a claim was made for, inter alia, an order in
the following terms:
"1. An injunction restraining the Respondent, its servants33. In the statement of claim, which was also filed on 11 June 1987, after references to the publication of the advertisement and other preliminary matters the allegation is made in para. 6 that, contrary to the statements contained in the advertisement, it is not the case that there is little evidence and nothing which proves scientifically that cigarette smoke causes disease in non-smokers. There follows an allegation that "in the premises" in or about July 1986 the respondent engaged in conduct proscribed by s.52. Further allegations are then made that the applicant complained of the respondent's conduct to the Trade Practices Commission, that the Commission thereupon took certain action, and that consequent upon that action the respondent published a further advertisement in which it did nothing to correct the misleading conduct referred to earlier in the statement of claim. Thereafter allegations are made that the applicant sought an undertaking from the respondent "that it would not, in any future advertisement or promotional material, represent that there is little evidence and nothing which proves scientifically that cigarette smoke causes disease in non-smokers or any similar assertion". Allegations are then made that the respondent declined to provide the undertaking and in the final paragraph (para. 18) it is alleged that: "In the premises, the respondent has continued in trade or commerce to engage in conduct that is misleading, deceptive or is likely to mislead or deceive" in contravention of Section 52 of the Trade Practices Act".
and agents from, in trade or commerce, engaging in conduct
that is misleading or deceptive or is likely to mislead in
the following respects:
a. stating that there is little evidence and
nothing which proves scientifically that cigarette smoke
causes disease in non-smokers;"
34. By its defence the respondent admitted that the undertaking had been sought from it and that it had declined to give it.
35. At the commencement of the hearing senior counsel for the applicant submitted to the Court a document which, according to him, identified the issues which fell to be determined in the case. One of the issues was said to be whether the statement in para. 3 of the advertisement " ... is and would be true as from the date these proceedings are determined ..." Another issue was said to be whether the statement "was true when these proceedings were commenced in June 1987". In a similar document submitted to the Court by senior counsel for the respondent, one of the issues was said in effect, to be whether the respondent was proposing to re-publish the advertisement.
36. Relevantly for present purposes, s.80(1) of the Act provides that where the Court is satisfied that a person has engaged or is proposing to engage, in conduct that constitutes or would constitute a contravention of a provision of Part V of the Act (in which s.52 appears) it may grant an injunction in such terms as it determines to be appropriate.
37. Since no claim for damages was made in the application, I take the essential allegations to be that the respondent on 1 July 1986 engaged in conduct proscribed by s.52, that it had declined to undertake not to engage in similar conduct in the future, and that, accordingly, an injunction was sought pursuant to s.80(1) of the Act to restrain the respondent from engaging in similar conduct.
38. As I have observed, it is alleged in para. 6 that " ... it is not the case that there is little evidence ..." (emphasis added). Having regard to the use of the present tense, this is an allegation as to the state of the evidence at the date of the statement of claim, i.e. 11 June 1987.
39. However, it was argued on behalf of the respondent that the allegation in para 8 that "In the premises, the Respondent did in or about July 1986, in trade or commerce, engage in conduct that was misleading ..." confines the allegation in para. 6 to the state of affairs that existed on 1 July 1986. It was submitted that because the Court has power under s.80(4)(a) of the Act to grant an injunction restraining a person from engaging in conduct proscribed by s.52, whether or not it appears to the Court that the person intends to engage again in conduct of that kind, the statement of claim should be construed as if there is no allegation that the respondent is proposing to engage in a repetition of past conduct.
40. I do not think the respondent's construction of the statement of claim is correct. Having regard particularly to the relief claimed in the application, I think it is reasonably plain that what the applicant alleges is that by publishing the advertisement on 1 July 1986 the respondent engaged in conduct proscribed by s.52, that it subsequently did nothing to correct that conduct, that it had refused to give an undertaking not to engage in similar conduct in the future and that accordingly it had continued in trade or commerce to engage in the conduct complained of. It is true that it would have been preferable for para. 18 of the statement of claim to have been framed so as to allege that the respondent " has continued and threatens to continue" rather than "has continued". But I think that on a fair reading of para. 18 it contains an allegation that the conduct complained of has continued up to the date of the statement of claim.
41. I should add that since the grant of the relief sought in the application requires the exercise of the Court's discretion the applicant was entitled to call evidence to prove that the statement remained misleading and deceptive as at the date of trial to persuade the Court to exercise the discretion in its favour.
42. There was much pre-trial correspondence between the parties in which
particulars were sought and given of the allegations in
the statement of
claim. The respondent argues that this correspondence shows that the applicant
particularised its claim in a manner
different from the way I interpret the
allegations in the statement of claim. There is some imprecision in the
particulars given
by the applicants but, in my opinion, they do not limit the
issues as the respondent contends. Accordingly, the respondent's submission
that 1 July 1986 is the only relevant date for examining the correctness of
the statement in the advertisement should be rejected.
6. Nature of Passive Smoking
43. Passive smoking involves inhalation of tobacco smoke from two sources:
sidestream smoke and exhaled mainstream smoke. Sidestream
smoke is smoke that
is emitted directly from a burning cigarette, pipe or cigar. Mainstream smoke
is cigarette smoke which is drawn
through the tobacco into the smoker's mouth.
The term "environmental tobacco smoke" refers to the combination of sidestream
smoke
and the fraction of exhaled mainstream smoke not retained by the smoker.
In contrast with mainstream smoke, environmental tobacco
smoke is diluted into
a larger volume of air, and it ages prior to inhalation. Mainstream smoke,
sidestream smoke and environmental
tobacco smoke are sometimes referred to as
"MS", "SS" and "ETS" respectively.
Cancer
(i) Explanation of some epidemiological and other terms
44. In support of its case that the statement in para. 3 of the advertisement is misleading or deceptive or likely to mislead or deceive insofar as it relates to the disease of cancer, the applicant relied upon the evidence of a number of witnesses and the primary articles and major reviews to which I have referred. Before referring to the oral evidence it is convenient to set out some of the more important findings referred to in some of the primary articles. An understanding of the articles will be enhanced by a brief explanation of some of the terms used in the literature.
45. Epidemiology relies on statistical analysis of populations to estimate the incidence of disease amongst those exposed to particular agents. Results are usually reported in terms of odds ratios or relative risk ratios. These reflect the ratio between the frequency of, say, a disease in an exposed group and that in an unexposed group. A risk ratio of 1.0 means that the disease is no more frequent in the exposed group than in the unexposed group. In crude terms, a relative risk above 1.0 is said to be positive and one below 1.0 is said to be negative.
46. These results can be characterised as being statistically significant or not. Statistical significance is an expression of the relative confidence that a particular result is a true effect and not due merely to chance. The level of statistical significance conventionally used in the scientific literature is the 95% confidence level. If a result, or range of results, is statistically significant at the 95% confidence level then it means that the probability that those results are due merely to chance or random variation is 1 in 20 or less. The reader can be 95% sure that the true effect is the result as reported.
47. Often that result is reported as a range of values clustered around a single value called a point estimate. The point estimate is the best estimate of the relative risk, based on the available data. The two figures on either side of the point estimate (the upper and lower confidence limits) define the range of values which are also well supported by the data, at the chosen confidence level. This range is known as the confidence interval.
48. To take an example, an investigation of the association between exposure (to an agent) and outcome (disease), having opted for a confidence level of 95%, may produce a point estimate of 2.5, with upper and lower confidence limits of 3.5 and 1.5. This means that based on the raw data, the best estimate is that those exposed have a 2 times greater chance of experiencing the disease than those not exposed. Further, one can be 95% sure that the true relative risk is somewhere between 1.5 and 3.5.
49. If the interval between the upper and lower confidence limits is wide, then the point estimate is less reliable than if it is narrow. Wide confidence intervals usually indicate a small number of observations.
50. The final point to note is the relationship between confidence intervals and statistical significance. The relative risk of disease normally associated with pure chance is 1.0: no increased risk, no decreased risk. So, using say the 95% confidence level, if the value 1.0 lies between the reported upper and lower confidence levels, then the probability that the result is due to chance has not been satisfactorily excluded, at the 95% level. Whenever the confidence interval straddles 1.0 then the result is not statistically significant. Two further illustrations may assist. Assume a 95% confidence level. Study A reports a point estimate of 2.5, with a confidence interval of 1.5 to 3.5. Study B reports a point estimate of 2.5 with a confidence interval of 0.8 to 4.0. The results in study A are statistically significant, those in study B are not.
51. I set out hereunder brief descriptions of some of the technical terms
commonly found in the literature.
Case control study - a group who have a disease (the(ii) The primary articles
cases) are selected, and matched to a group who do not (the
controls). Researchers then investigate whether or not
individuals in each group were exposed to the agent of
interest, and those results are then compared. A disease
appears first and the investigation of exposure occurs
retrospectively.
Cohort study - a group (cohort) of individuals is
identified and then divided into those exposed and those who
are not. The cohort is followed for a number of years, and
the individuals who contract the disease are identified to
determine if there is any difference in incidence between
the groups. Accordingly, cohort studies are generally prospective.
Dose response relationship - a dose response
relationship occurs when the observed incidence of the
disease increases as the dose (or exposure to the relevant
agent) increases. Such a relationship increases the
likelihood that a statistical association in fact represents
a true association.
Trend test - a test of statistical significance
applied across a set of results to ascertain the probability
that such a sequence of results could have been obtained by chance.
Publication bias - due to social, academic and other
pressures, it may be that positive research results are
written up and/or accepted for publication more frequently
than are negative results. This can yield spurious results
in meta-analysis.
Misclassification - if subjects are incorrectly
classified then it may produce spurious results. The most
commonly cited example in this case is the possibility of
smokers claiming for a variety of social, medical and other
reasons that they are non-smokers. Because of the strong
association between active smoking and lung cancer, such
misclassification artificially inflates the risk of lung
cancer amongst non-smokers.
Confounding - this occurs when sources other than the
exposure of interest (e.g. environmental tobacco smoke)
operate to affect the outcome, and are not controlled for by
researchers. Examples may include work-place pollution,
diet, lifestyle, etc.
Data dredging - if within the one study, a number of
hypothesised associations are tested, then a high or low
result in one particular category might be expected to occur
by pure chance. If 20 hypotheses are tested, for example,
it would not be surprising to find that one of them is
statistically significant at the 95% confidence level. To
seize upon such isolated results is said to be data dredging.
Meta-analysis - this is a statistical technique used
to combine the results of individual epidemiological
studies, in order to derive a quantitative summarisation of
data relating to a particular area of investigation.
Mutagenic - a mutagenic substance is a chemical that
can induce change in the genetic material in a manner that
is thought to be fundamental to the initiation of cancer.
Histological diagnosis of cancer - this biological
technique involves obtaining a tissue sample from the
patient and examining it under a microscope. It is
considered the most reliable form of cancer diagnosis,
particularly for distinguishing between primary and
secondary cancers.
Cytological diagnosis of cancer - in the case of lung
cancer, cytology involves obtaining cells from the lungs
either by having the patient cough up cells in the sputum,
or washing cells from the lung by use of bronchoalveolar
lavage, or extraction with a specialised hollow needle under
X-ray control. For a variety of reasons cytological
diagnosis of cancer is not considered to be as comprehensive
or reliable as histologic diagnosis.
52. This study was published in the International Journal of Cancer in 1981.
The abstract of the article, as published, reads as follows:
"Fifty-one women with lung cancer and 163 other53. This was a case-control study, the cases being all of the female, caucasian patients registered as residents of Athens who were admitted to any of three large hospitals in Athens between September 1978 and June 1980 with a final diagnosis of lung cancer other than adenocarcinoma or alveolar carcinoma. Of the 51 cases identified, 14 were histologically and 19 cytologically confirmed. In 18 cases the diagnosis was based on clinical and radiological evidence. A table published as part of the study shows the distribution of non-smoking women with lung cancer and of non-smoking control women according to current smoking habits of their husbands. The published data showed a statistically significant association between the husband's smoking and the woman's lung cancer risk. A non-smoking woman whose husband was a regular smoker had a risk of developing lung cancer which was twice as high as that of a non-smoking woman married to a non-smoker.
hospital patients were interviewed regarding the smoking
habits of themselves and their husbands. Forty of the lung
cancer cases and 149 of the other patients were non-smokers.
Among the non-smoking women there was a statistically
significant difference between the cancer cases and the
other patients with respect to their husbands' smoking
habits. Estimates of the relative risk of lung cancer
associated with having a husband who smokes were 2.4 for a
smoker of less than one pack and 3.4 for women whose
husbands smoked more than one pack of cigarettes per day.
The limitations of the data are examined; it is evident
that further investigation of this issue is warranted."
54. The authors of the study stated that it had obvious limitations, most seriously that the numbers of cases was small but that nevertheless the association between passive smoking and lung cancer was unlikely to be due to chance. They drew attention to the fact that, according to their study, the relative risk associated with passive smoking, i.e. 2.4 for all categories of smokers combined, was only slightly lower than the figure of 2.9 associated with active smoking by the women themselves. The authors offer a possible explanation for this circumstance in the text of their study.
55. The study reported in the International Journal of Cancer in 1981 was continued and further results of it were published in The Lancet in September 1983. The authors reported that there were then twice as many cases and 50% more controls in the study, but that the results remained substantially the same. The 1983 study, as published, wrongly calculated the relative risks. The correct relative risks of lung cancer associated with having a husband who smoked were 1.9 for a smoker of less than one pack and 2.5 for women whose husbands smoked more than one pack of cigarettes per day. Professor Trichopoulos explained in oral evidence that the equivalent figures which appeared in the 1983 publication, i.e. 2.4 and 3.4, were typographical errors. The 1983 figures (1.9 and 2.5) relate to the total data collected in the whole of the study, not merely to the data collected since the publication of the first study.
56. The authors concluded their 1983 study with a reference to a table
including the abovementioned risk ratios of 1.9 and 2.5 and
stated:
"The table increases the credibility of the hypothesis(b) Hirayama - Non-smoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan
implicating passive smoking as a factor in lung cancer.
Given the small size in the relative risk and the many
potential sources of bias, no single study will be able to
provide convincing evidence for or against this hypothesis;
only the convergence of results from different studies in
different populations will permit a reasonably sound
conclusion. We consider the Athens study a step in this
direction."
57. In the British Medical Journal of January 1981 Professor Hirayama, Chief
of the Epidemiology Division of the National Cancer
Centre Research Institute,
Tokyo, published findings of a study undertaken in Japan. The abstract of the
findings as published in
the article is as follows:
"In a study in 29 health centre districts in Japan 91(c) Hirayama - Cancer Mortality in Non-smoking Women with Smoking Husbands Based on a Large-Scale Cohort Study in Japan
540 non-smoking wives aged 40 and above were followed up for
14 years (1966-79), and standardised mortality rates for
lung cancer were assessed according to the smoking habits of
their husbands. Wives of heavy smokers were found to have a
higher risk of developing lung cancer and a dose-response
relation was observed. The relation between the husband's
smoking and the wife's risk of developing lung cancer showed
a similar pattern when analysed by age and occupation of the
husband. The risk was particularly great in agricultural
families when the husbands were aged 40-59 at enrolment. The
husbands' smoking habit did not affect their wives' risk of
dying from other disease such as stomach cancer, cervical
cancer, and ischaemic heart disease. The risk of developing
emphysema and asthma seemed to be higher in non-smoking
wives of heavy smokers but the effect was not statistically
significant.
The husband's drinking habit seemed to have no effect on
any causes of death in their wives, including lung cancer.
These results indicate the possible importance of
passive or indirect smoking as one of the causal factors of
lung cancer. They also appear to explain the long-standing
riddle of why many women develop lung cancer although they
themselves are non-smokers. These results also cast doubt
on the practice of assessing the relative risk of developing
lung cancer in smokers by comparing them with non-smokers."
58. This article (which appeared in Preventive Medicine in 1984) reported
further conclusions reached by Professor Hirayama as a
result of further data
derived from his study referred to in the preceding article. The abstract of
this further study reads as
follows:
"Mortality of 91,540 non-smoking wives was studied59. Professor Hirayama made the following observation:
in relation to the smoking habits of their husbands by means
of a cohort study in Japan. During 16 years of follow-up,
200 deaths from lung cancer took place. The relative risks
of lung cancer in these non-smoking wives were 1.00, 1.36,
1.42, 1.58, and 1.91 when husbands were non-smokers,
ex-smokers, or daily smokers of 1-14, 15-19, or 20 or more
cigarettes daily, respectively. Corresponding relative risks
for stomach cancer were 1.00, 1.16, 1.00, 1.00, and 1.01
respectively. Specificity of association and internal
consistencies were observed. Among cancers of each site, a
similar tendency toward risk elevation in non-smoking wives
with smoking husbands was observed for nasal sinus cancer,
brain tumors, and cancer of all sites besides lung cancer.
In interpreting these results, the significance of proximity
in exposure to sidestream smoke in Japanese homes was
stressed."
"This study confirms the correlation between lung60. The reference to the American Cancer Society study is a reference to Garfinkel's study (infra).
cancer and spousal smoking reported previously. The
correlation is quite specific in terms of diseases. For
instance, no risk elevation at all was observed for stomach
cancer. A striking internal consistency of association was
also observed. The results were essentially similar when
observed in terms of age of husbands, age of wives,
occupation of husbands, and differing periods of
observation. The results are in line with a Greek study by
Trichopoulos and others and a U.S. study by Correa and
others (external consistency), although they are slightly at
variance with an American Cancer Society study in the United
States and a case-control study conducted by Kabat and
Wynder."
61. Professor Hirayama also observed:
"When the effects of passive smoking due to husbands'(d) Garfinkel - Time Trends in Lung Cancer Mortality Among non-smokers and a Note on Passive Smoking
smoking were compared with the effects of direct smoking in
women, the results clearly indicated that the effect of
passive smoking is less than one-fifth that of direct
smoking. ... In terms of attributable risk, however, the
effect of passive smoking on lung cancer in women is nearly
as important as that of direct smoking because the
population of intrahousehold passive smokers at risk is four
times greater ... than the population of active smokers...
Therefore, although the relative risk of indirect smoking is
much smaller than that of direct smoking, the absolute
excess deaths from lung cancer due to passive smoking may be
quite important because of the large size of the exposed
group - especially in countries such as Japan where the
majority (nearly 70%) of adult men smoke, but only a
minority (15% or less) of adult women smoke."
62. This article appeared in the Journal of the National Cancer Institute in June 1981.
63. The author concluded that compared to non-smoking women married to
non-smoking husbands, non-smokers married to smoking husbands
showed very
little, if any, increased risk of lung cancer. The study revealed a small
increased risk of lung cancer for non-smokers
married to smokers. The
increased risk was not statistically significant. The mortality ratios for
lung cancer in non-smoking women
were 1.27 when the husbands were daily
smokers of less than 20 cigarettes, and 1.10 when they smoked more than 20
cigarettes per
day. The data examined by Garfinkel led him to conclude that
"it seems doubtful that those non-smokers who had been heavily exposed
to
cigarette smoke from others in their lives could have had many more precursor
lesions for the development of lung cancer than
non-smokers not so exposed.
Therefore, there is evidence from these studies that passive smoking cannot
play more than a very small
role in the development of lung cancer."
(e) Chan and Fung - Lung Cancer in Non-smokers in Hong Kong
64. This study was carried out in Hong Kong and was published in 1982. The
relevant finding in the study is at variance with that
found in the Hirayama
1981 study. Whereas Hirayama found that the mortality from lung cancer of
non-smoking women exposed to their
husband's cigarette smoke was increased
twofold, that was not confirmed by this study. The authors acknowledge that
the group studied
by them was very small in comparison to the group studied by
Hirayama.
(f) Correa et al. - Passive Smoking and Lung Cancer
65. This study appeared in The Lancet in September 1983. Correa et al
undertook a case-control study involving 1338 lung cancer
patients and 1393
comparison subjects in Louisiana, USA. They found that non-smokers married
to heavy smokers had an increased
risk of lung cancer, as did subjects whose
mothers smoked. No association was found between lung cancer risk and
paternal smoking.
The authors said, inter alia,
"Spouse-smoking Effect66. The authors expressed their conclusion as follows:
Our data strengthen the contention that heavy smoking by
one member of the spouse pair increases the lung cancer risk
of the non-smoking partner. Heavy smoking by wives may
increase the risk of the light smoking husband but this
finding requires further analysis and confirmation in larger
series. Smoking by husbands did not affect the risk of lung
cancer in women who smoked (relative risk 1.03), a finding
that suggests that active smoking is so powerful that it
overshadows any possible additional effect from concomitant
passive exposure.
...
The effect of the smoking habits of the spouse on lung
cancer risk was first reported by Hirayama in a Japanese
cohort study. A cohort study in the United States reported a
positive but not significant increase in risk for
non-smoking women married to smoking husbands. A case-control
study of non-smoking women diagnosed as having lung cancer
in Greece reported relative risks of approximately 2.5 for
those married to moderate smokers and 3 for those married to
heavy smokers, with a significant linear trend. Our numbers
are small but we think that the similarity between our
findings and those of Trichopolous et al strengthens the
suspicion that passive smoking may contribute to lung cancer risk.
Parental Smoking Effect
As far as we know, ours is the first case-control
study of lung cancer reporting on parental smoking history.
Parents' smoking behaviour influences the smoking habits of
their offspring, but we found that the smoking behaviour of
the father does not influence the lung cancer risk of his
offspring, whereas the behaviour of the mother does. This
difference may reflect the closer and more prolonged contact
that infants and young children have with their mothers than
with their fathers."
"The differences between the effects of passive(g) Koo et al. - Active and passive smoking among female lung cancer patients and controls in Hong Kong
exposure to spouse and maternal smoking are puzzling.
Passive exposure to spouse smoking is mostly detected in
non-smokers and light smoking males; maternal passive
smoking effects are seen mostly in smokers. Passive smoking
from spouses is introduced in adult life and in smokers is
concurrent with their own active smoking. The magnitude of
such an effect may be low when compared with active
concomitant smoking and it may not be detectable when both
types of smoking are present.
Maternal smoking, on the other hand, exerts its
influences early in life and in the absence of active
smoking is probably insufficient to produce carcinogenic
effects. Our findings indicate that maternal smoking
results in a slight increase in lung cancer risk but do not
indicate whether the effect is due to enhanced active
smoking of the offspring or to enhanced susceptibility to
lung cancer induction after the challenge of active smoking
later in life."
67. This was a case control study carried out in Hong Kong and published in
1983. The study, in which the number of cases and controls
were fairly small,
did not reveal a positive association between lung cancer and passive smoking.
The authors observed:
"Thus, if passive smoking had contributed to the risk(h) Buffler et al. - The Causes of Lung Cancer in Texas
for never smokers, it could only have acted as a co-factor
in a multi-factorial aetiology. The controversial findings
of various researchers ... on the role of passive smoking in
lung cancer could well be due to a failure in identifying
other co-factors in the carcinogenesis."
(The reference to the "various researchers" is a
reference to the findings of Garfinkel, Hirayama and
Trichopoulos).
68. This study was published in 1984 in Lung Cancer: Causes and Prevention.
Amongst other results, the authors reported the following:
"The role of `passive smoking' in contributing to risk69. The authors noted that the "lack of a `passive smoking' effect when the confounding effect of smoking of individual study subjects is considered, is not consistent with early reports. Although subsequent reports are also not consistent with regard to this association, it may be that the study population available was not sufficiently large to detect a fairly low-level effect and that this association needs to be assessed in a considerably larger study population".
of lung cancer was examined .... In this analysis the crude
(or unadjusted) odds ratio are increased and significant for
both males and females, 1.4 and 2.1, respectively.
However, when the confounding effect of individual subject
smoking was controlled by stratifying the male and female
study groups into smokers (ever) and non-smokers (never) and
examining the adjusted odds ratios, there was no significant
increase in risk associated with passive smoking. In fact,
the odds ratio for non-smokers living with a regular smoker
were not increased for either males or females, 0.52 and
0.78, respectively. However, odds ratios for smokers living
with a regular smoker were increased, although not
significantly, 1.28 and 1.80 for males and females. The
overall odds ratios (adjusted) associated with passive
smoking were only slightly increased and not significant for
either males or females, 1.2 and 1.3, respectively. When
the possibility of a `passive smoking' effect was examined
among non-smokers by the number of years lived with a
regular smoker, there was very little difference in risk for
females who lived with a regular smoker for 0-32 years.
The odds ratios for males suggest an increase by (sic) are
based on smaller numbers than the analysis in females."
70. This article appeared in the Journal of the National Cancer Institute in
September 1985. The authors state, inter alia:
"In a previous paper, we pointed out that in any study71. The authors undertook a case-control study in four hospitals from 1971 to 1981. All cases and controls were confirmed by histologic review of slides, and non-smoking status and exposures were verified by interviews. It was found that odds ratios increased with increasing numbers of cigarettes smoked by the husband, particularly if the cigarettes were smoked at home. The odds ratio for women whose husbands smoked 20 or more cigarettes at home was 2.11. The authors' conclusions included the following:
of involuntary smoking and lung cancer, categorizing
non-smokers by the smoking habit of the spouse may lead to
error in classification of exposure. In the United States
particularly, there may be many women, married to
non-smokers, who are exposed to the smoke of others at work
or in other areas. Conversely, some individuals married to
smokers may suffer acute effects from inhaling smoke and
consciously avoid such exposure. A survey of 38,000 subjects
by Friedman et al. confirmed this hypothesis. About 40% of
women non-smokers and 50% of men non-smokers who were married
to non-smokers were exposed to the smoke of others for some
periods of time during a week, and 47% of non-smoking women
married to smokers reported that they were not exposed to
tobacco smoke at home. In the study reported here, we record
the smoking habit of husbands (total No. of cigarettes
smoked and No. smoked at home), as well as the number of
hours a day the subjects were exposed to the smoke of others
at home, at work, and in other areas.
Other causes for concern are establishment of the
microscopic diagnosis of primary lung cancer and
verification of the smoking history. In a study of the
histologic type of lung cancer in relation to asbestos
exposure, 49 of 774 men and women with a discharge diagnosis
of microscopically proved lung cancer were recorded as
non-smokers in the hospital chart. After review of hospital
records, histologic sections, and interviews, only 10 cases
remained who had died of primary lung cancer and who had
never smoked. One-half of the others had smoked at some
time and one-half the confirmed non-smokers had a primary
cancer other than that of the lung.
It is apparent, therefore, that more studies on
involuntary smoking are needed, with particular attention
given to obtaining microscopic proof of primary lung cancer
and more detailed information about exposures to cigarette
smoke."
"We found an elevated risk of lung cancer, ranging(k) Akiba et al. - Passive Smoking and Lung Cancer among Japanese Women.
from 13 to 31%, in women exposed to the smoke of others,
although the increase was not statistically significant.
The women who were married to smokers of 40 or more
cigarettes a day or who were exposed to the smoke of at
least 20 cigarettes a day at home showed a risk twice as
high as that of women not exposed at all. This result is
consistent with the dose-response risk of exposure to the
husband's smoke shown in some case-control studies (2, 3)."
(The references at the end of the above quotation
are references to Trichopoulos et al (supra) and Correa et
al (supra).
72. This article was published in the September 1986 issue of Cancer Research, but appears to have been first published prior to 1 July 1986 since it is referred to in the NH and MRC report which was adopted in June 1986.
73. The abstract of the article, as published, reads as follows:
"A case-control study conducted in Hiroshima and74. The study was made as part of a case-control investigation of lung cancer among atomic bomb survivors conducted primarily to evaluate the interactive roles of cigarette smoking and ionizing radiation. Data were collected on the smoking habits of the subjects' spouses and parents. The article reports the effect of exposure to such passive smoking, particularly on married women who had never smoked themselves.
Nagasaki, Japan, revealed a 50% increased risk of lung
cancer among non-smoking women whose husbands smoked. The
risks tended to increase with amount smoked by the husband,
being highest among women who worked outside the home and
whose husbands were heavy smokers, and to decrease with
cessation of exposure. The findings provide incentive for
further evaluation of the relationship between passive
smoking and cancer among non-smokers."
75. The study showed that there was an increase in lung cancer risk with increasing amounts smoked per day by the husband, with the odds ratio slightly exceeding 2 for women whose husbands were heavy smokers. The odds ratio of lung cancer among non-smoking women according to 'recency of exposure to their husbands' smoking were lower among women who had not been exposed within the last ten years than among women exposed within the last ten years.
76. All the results in this study were reported using 90% confidence intervals. The odds ratio for non-smoking females married to smoking husbands was 1.5, statistically significant at that level. For non-smoking husbands married to smoking wives the odds ratio was 1.8, not statistically significant at the 90% level.
77. The authors said:
"The results from this case-control study suggestThe Japanese study referred to by the authors is the Hirayama 1981 study, and the other studies to which they refer are the Trichopoulos et al 1981 study, the Correa et al 1983 study and the Garfinkel et al 1985 study.
that there may be a moderate excess in lung cancer risk
associated with passive smoking. The odds ratios for lung
cancer among non-smoking women tended to increase with
amount smoked by their husbands, a trend seen among
housewives as well as women who worked outside the home.
The highest odds ratios among non-smokers were for women who
worked in blue collar jobs whose husbands were heavy
smokers, women presumably with the highest exposure to
environmental tobacco smoke. There was little association
with parental smoking or with ex-passive smoking, suggesting
that cessation of exposure may lower risk.
The findings are generally consistent with results of a
national cohort study of mortality among Japanese women and
of several epidemiological investigations conducted
elsewhere in the world."
78. The authors admit to concerns about adequacy of data provided by surrogate respondents and reliability of diagnoses of lung cancer but also note some reassuring factors.
79. The authors summarise the views they formed as a result of their study as
follows:
"In summary, the results of this investigation(l) Lee et al. - Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases
suggest that exposure to environmental tobacco smoke may
increase the risk of lung cancer among non-smokers. The
findings, from one of the two areas of the world where the
possibility of a passive smoking hazard was first
postulated, add to an accumulating body of evidence on the
issue. While the total evidence is not definitive and not
all studies show significantly positive associations, the
results are suggestive enough to warrant further evaluation
in larger studies where passive smoking exposures can be
more fully quantified."
80. This study was published in the British Journal of Cancer in 1986. The
authors reported results based on 143 patients. They
made the following
observations:
"Overall the results showed no evidence of an effect(m) Humble et al. - Marriage to a Smoker and Lung Cancer Risk
of passive smoking on lung cancer incidence among lifelong
non-smokers. In male patients, relative risks were
increased for some of the indices but numbers of cases were
small and none of the differences approached statistical
significance. In females, where numbers of cases were
larger, such trends as existed tended to be negative ...
The relative risk in relation to the spouse smoking during
the whole of the marriage was estimated to be 0.80 for the
sexes combined, with 95% confidence limits of 0.43 to 1.50."
"In the present study no significant relationship of
passive smoking to lung cancer incidence in lifelong
non-smokers was seen, either in the analyses based on the
information collected in hospital or in subsequent inquiry
of the spouses or both. It must be pointed out, however,
that the number of lung cancer patients who had never smoked
was rather small so that, though our findings are consistent
with passive smoking having no effect on lung cancer risk at
all, they do not exclude the possibility of a small increase
in risk, ... "
81. This study appeared in the American Journal of Public Health in May 1987.
In the introduction to their study, the authors make
the following statement:
"In 1980 we began collecting data in a population-based82. The authors analysed the data according to two models. On the first model, among never smokers, cigarette smoking by a spouse, regardless of pipe or cigar use, was associated with a three-fold increased risk of lung cancer. (OR 3.2, 90% CI 1.5 - 7.2). For females only the odds ratio was 2.3 with CI 90% 0.9 - 6.6. For exposure to cigarettes only, the odds ratios were slightly lower (for all subjects 2.9 90% CI 1.3 - 6.7; for females only 1.8 90% CI 0.6 - 5.4.
case-control study designed to explain differing lung
cancer occurrence in Hispanic and non-Hispanic Whites in New
Mexico. The original study questionnaire included questions
on tobacco smoke exposure from spouse smoking and on
indirect exposure to asbestos through a spouse's job. This
report describes the risks associated with these exposures
in smokers and non-smokers in New Mexico."
83. Odds ratios from use of the second model tended to be lower.
84. No effect was detected for marriage to a smoker by a current or former cigarette smoker, according to either model.
85. Under the heading "Discussion", the authors made the following
observations:
"In the context of a population-based case-control86. In conclusion, the authors made the following comments:
study in New Mexico, we have examined the risk of lung
cancer associated with marriage to a cigarette smoker. The
results indicated increased risk from this exposure in never
smokers, but not in active smokers.
Methodologic limitations of the case-control
approach for studying the relation between involuntary
exposure to tobacco smoke and lung cancer must be
considered. Misclassification of both active and passive
exposure to cigarette smoke is of particular concern."
"The results of the present case-control study(n) Pershagen et al. - Passive Smoking and Lung Cancer in Swedish Women
complement those from other case-control studies and from
cohort studies, which showed increased lung cancer risks in
never smokers married to smokers. The magnitude of the
effect of marriage to a smoker in the present study, about a
the two-fold increase in risk ... is comparable to findings
by Hirayama and by Akiba, et al, in Japan, by Trichopoulos,
et al, in Greece, and by Correa, et al, and by Dalager, et
al, in the United States. A weak exposure-response relation
was present with duration of passive exposure, but not with
average number of cigarettes smoked daily by the spouse ...
In active smokers, we found that residence with a
smoker did not elevate lung cancer risk ... The lack of
association in active smokers is consistent with the
quantitative differences in the exposures of active and
passive smoking."
87. Although this article was received for publication in January 1986 it was
not published until 1987, when it appeared in the American
Journal of
Epidemiology. The abstract reads as follows:
"The relation between passive smoking and lung cancer88. The authors reported at p 20 that:
was examined by means of a case-control study in a cohort of
27,409 non-smoking Swedish women identified from
questionnaires mailed in 1961 and 1963. A total of 77
cases of primary carcinoma of the bronchus or lung were
found in a follow-up of the cohort through 1980. A new
questionnaire in 1984 provided information on smoking by
study subjects and their spouses as well as on potential
confounding factors. The study revealed a relative risk of
3.3, constituting a statistically significant increase (p
0.05) for squamous cell and small cell carcinomas in women
married to smokers and a positive dose-response relation.
No consistent effect could be seen for other histologic
types, indicating that passive smoking is related primarily
to those forms of lung cancer which show the highest
relative risks in smokers."
"Pooling the control groups produces a relative risk89. Under the heading "Discussion" the authors stated the following:
of 3.3 for squamous cell and small cell carcinomas (95 per
cent confidence interval (CI) = 1.1-11.4) associated with
marriage to a smoker. Within this group, the relative
risks were increased for both histologic types. The
relative risks for the other histologic types and for the
entire group are 0.8 (95 per cent CI = 0.4-1.5) and 1.2 (95
per cent CI = 0.7-2.1) respectively."
"The results of our study indicate that exposure to(iii) The major reviews
environmental tobacco smoke is related to an increased risk
of those histologic types of lung cancer which show the
highest relative risks in smokers. This is in general
agreement with the findings of Trichopoulos et al.,
Garfinkel et al, and Koo et al, although these authors
looked at somewhat different carcinoma types and/or used
other definitions of exposure."
(p 22)
90. I shall now refer to some of the more significant passages in the major
reviews.
(a) The Monograph on Tobacco Smoking issued by the International Agency for
Research on Cancer.
91. The International Agency for Research on Cancer ("IARC") is part of the World Health Organisation. This monograph ("the IARC report") represents the views and opinions of an IARC working group on the evaluation of the carcinogenic risk of chemicals to humans. The group met in Lyons from 12-20 February 1985. The report was published in June 1986. The report is part of a monograph programme the objective of which is to elaborate and publish in the form of monographs, critical reviews of data on, inter alia, carcinogenicity for chemicals to which humans are known to be exposed, to evaluate the data in terms of human risk with the help of international working groups of experts, and to indicate where additional research efforts are needed.
92. In the report the term "carcinogenic risk" is taken to mean the probability that exposure to the chemical will lead to cancer in humans. Inclusion of a chemical in the report does not imply that it is a carcinogen, only that the published data have been examined. The 28 members of the IARC working group were drawn from a variety of academic, medical research and other institutions in Europe, Asia, the Americas and Australia.
93. The manner in which IARC monographs are prepared is described in the report as follows. In advance of a meeting of a working group all relevant biological data concerning the substance under examination are collected by IARC. Six months before the meeting, articles containing relevant biological data are sent to experts, or are used by IARC staff, to prepare first drafts of the sections on biological effects. The complete drafts are then compiled by IARC staff and sent, prior to the meeting, to all participants in the working group for their comments. The working group meets to discuss and finalise the text of the monographs and to formulate the evaluations.
94. According to the report, the evidence for carcinogenicity from studies in
humans is assessed by the working group and judged
to fall into one of four
groups, defined as follows:
"(i) Sufficient evidence of carcinogenicity indicates95. The final evaluations of the IARC working group appear at the end of the report and include the following:
that there is a causal relationship between the exposure and
human cancer.
(ii) Limited evidence of carcinogenicity indicates that
a causal interpretation is credible, but that alternative
explanations, such as chance, bias or confounding, could not
adequately be excluded.
(iii) Inadequate evidence of carcinogenicity, which
applies to both positive and negative evidence, indicates
that one of two conditions prevailed:
(a) there are few pertinent data; or
(b) the available studies, whilst showing
evidence of association, do not exclude chance, bias or
confounding.
(iv) No evidence of carcinogenicity applies when
several adequate studies are available which do not show
evidence of carcinogenicity."
(p 24)
"There is sufficient evidence that tobacco smoke is96. Whilst the reference to tobacco smoke in this evaluation is not entirely free from ambiguity, in my opinion it is a reference to tobacco smoke from three sources, viz., mainstream smoke, sidestream smoke and smoke exhaled to the general atmosphere by smokers.
carcinogenic to humans."
(p 314)
97. The bulk of the report is concerned with the effects of tobacco smoke on
active smokers. In relation to passive smoking it contains
the following
observation:
"Several epidemiological studies have reported an increased98. In a section headed "Conclusions and Evaluations", the following appears:
risk of lung cancer in non-smoking spouses of smokers,
although some others have not. In some studies, the risk of
lung cancer in non-smokers increased in relation to the
extent of spouses' smoking. Each of the studies had to
contend with substantial difficulties in determination of
passive exposure to tobacco smoke and to other possible risk
factors for the various cancers studied. The resulting
errors could arguably have artefactually depressed or raised
estimated risks, and, as a consequence, each is compatible
either with an increase or with an absence of risk. As the
estimated relative risks are low, the acquisition of further
evidence bearing on the issue may require largescale
observational studies involving reliable measures of
exposure both in childhood and in adult life."
(p 308)
"Tobacco smoke affects not only people who smoke but also99. Some time prior to June 1986 the Australian National Health and Medical Research Council set up a working party on the effects of passive smoking on health. The Chairman was Dr A.J. McMichael who, at the time, was Senior Principal Research Scientist, CSIRO Division of Human Nutrition. The other members of the working party were:
people who are exposed to the combustion products of other
people's tobacco. The effects produced are not
necessarily the same, as the constituents of smoke vary
according to its source. Three main sources exist: (i)
mainstream smoke, (ii) sidestream smoke, and (iii) smoke
exhaled to the general atmosphere by smokers. Smokers are
exposed to all three to a greater extent than are
non-smokers. It follows that it is unlikely that any
effects will be produced in passive smokers that are not
produced to a greater extent in smokers and that types of
effects that are not seen in smokers will not be seen in
passive smokers. Examination of smoke from the different
sources shows that all three types contain chemicals that
are both carcinogenic and mutagenic. The amounts absorbed by
passive smokers are, however, small, and effects are
unlikely to be detectable unless exposure is substantial and
very large numbers of people are observed. The
observations on non-smokers that have been made so far are
compatible with either an increased risk from `passive'
smoking or an absence of risk. Knowledge of the nature of
sidestream and mainstream smoke, of the materials absorbed
during `passive' smoking, and of the quantitative
relationships between dose and effect that are commonly
observed from exposure to carcinogens, however, leads to the
conclusion that passive smoking gives rise to some risk of
cancer."
(p 314)
(b) The National Health and Medical Research Council report
on Effect of Passive Smoking on Health
Dr R. Antic, Director of Thoracic Medicine, Royal100. The report of the working party was adopted by the National Health and Medical Research Council in June 1986.
Adelaide Hospital,
Dr C. Baker, Acting Executive Director of the Public
Health Service of South
Australian Health Commission,
Professor L. Landau, of the Department of Child
Health at Princess Margaret Hospital for Children, Perth,
Professor S.R. Leeder, Head of the Department of
Community Medicine, Westmead Hospital, Westmead,
Dr J.D. Potter, Senior Research Scientist at the
CSIRO Division of Human Nutrition,
Dr A. Woodward, Lecturer in the Department of
Community Medicine, Royal Adelaide Hospital, and
Dr A.F. Dick, of the Health Care Committee of the
Commonwealth Department of Health.
101. Chapter 7 of the report deals with passive smoking and cancer. The
following quotations from the report do not include a number
of footnotes in
which reference is made to the published work of other scientists:
"7.1 Introduction102. The report makes the following observations:
Tobacco smoke contains approximately sixty known or
suspected carcinogenic chemicals, of which at least fifty
occur in the phase that contains particulate matter. The
carcinogenic activity of tobacco smoke appears to require
this particulate phase. Animal bioassays indicate that
sidestream tobacco tar is more carcinogenic per unit weight
than mainstream tar. For public health purposes, therefore,
it would be prudent to assume, at this stage of research
activity, that mainstream and sidestream smoke have similar
human carcinogenic potency.
There is no disagreement about the biological
plausibility of an association between passive smoking and
lung cancer. Active smoking is the major known cause of
lung cancer, and there is a well-established monotonic
increase in risk with increasing dose-rate. Further, no
`safe level' threshold dose appears to exist. Thus,
although the dose rate for passive smokers is, overall,
substantially lower than for active smokers, it is a
reasonable inference from the studies of active smokers that
passive smokers experience a real, albeit smaller, increase
in lung cancer risk. Nevertheless, it remains unknown how
active and passive smoking might differ in terms of actual
carcinogens delivered to the respiratory tract. Sidestream
smoke is qualitatively richer in many smoke constituents
than is mainstream smoke.
An equivalent argument exists in relation to the
plausibility of passive smoking as a cause of cancers of
other sites known to be related to active smoking.
7.2 Types of Epidemiological Evidence
There are two types of evidence by which to examine the
relationship of passive smoking to cancer risk.
First, with knowledge of the established cancer risks
of active smoking, and using the documented relationship
between individual smoking behaviour and various biological
indices of absorbed constituents of smoke (e.g. measures of
nicotine and cotinine in blood and urine, thiocyanate and
cotinine in saliva, and carboxyhaemoglobin in blood) to make
direct estimations of the extent of non-smokers' exposure to
smoke, it is possible to estimate the attendant risk of
cancer. This approach presumes that the particular
biological indices used are also indices of the carcinogenic
potential of the inhaled and absorbed smoke. As indicated in
Section 4, estimates based on biological measures indicate
that passive smoking in the workplace typically entails
exposures (for eight hours per day) equivalent to light
active smoking. Light smokers are at approximately five
times higher risk of lung cancer than non-smokers.
The second, and more usual, type of epidemiological
evidence depends upon observing empirical associations
between reported individual smoking habits and the
occurrence of cancer. Such observations are made in either
cohort (prospective) studies or case-control (retrospective)
studies.
During 1979-85, eleven epidemiological studies
examining the association between passive smoking and lung
cancer have been reported. Most show a positive association,
albeit substantially less strong than that between active
smoking and lung cancer. Among non-smokers, the relative
risk of lung cancer in passively exposed versus unexposed
persons varies from approximately 1.2 to 3.5. A
dose-response relationship is present in four of nine studies
that have reported such an analysis. One cohort study has
examined and reported the change in lung cancer risk
associated with cessation of exposure (i.e. spouse as
ex-smoker); a reduction in risk occurred.
During the same period, four epidemiological studies of
passive smoking and non-lung cancers have been reported.
Their findings have been less consistent than those
pertaining to lung cancer.
These variable results reflect not only the apparently
smaller effect of passive smoking upon cancer risk than that
of active smoking, but the associated small numbers of cases
available for study, and the deficiencies in the validity
and precision of measurement of individual exposure to
passive smoking. Not only might some of the individuals
included as non- smokers be ex-smokers, but the actual
determination of exposure dosage - from varied sources and
across time - is intrinsically difficult. Further, for the
25-50 per cent of women and the great majority of men in
Western populations who work outside the home, the spouse's
smoking habit is a poor quantitative index of passive
smoking exposure - particularly since the exposure
concentration is estimated to be four times higher at work
than in the home. Nevertheless, to the extent that exposure
misclassification applies equally to all combined groups of
study subjects, it may have led to underestimation of the
relative risk associated with passive smoking."
"The evidence that passive smoking causes lung cancer103. The report concludes with the following quotation from a report of the interdisciplinary working group of the International Agency for Research in Cancer:
is strongly suggestive. It is plausible, moderately
consistent, and demonstrates dose-response relationships.
However, intrinsic difficulties in accurately classifying
individual exposure, and insufficient numbers of study
subjects in many studies, preclude a conclusive
interpretation of these empirical data when considered in
isolation from other corroborative scientific evidence."
"`Knowledge of the nature of sidestream and mainstream104. Chapter 7 of the NH and MRC report is a statement of the findings of the working party. The Statement and Recommendations of the National Health and Medical Research Council itself are in Chapter 9 of the report, which reads, in part, as follows:
smoke, of the materials absorbed during "passive" smoking,
and of the quantitative relationships between dose and
effect that are commonly observed from exposure to
carcinogens, ... leads to the conclusion that passive
smoking gives rise to some risk of cancer'."
"Council notes that there is mounting epidemiological(c) The 1986 report of the United States Surgeon General
evidence that passive smoking may increase the risk of
occurrence of lung cancer. Despite limitations in the amount
of data available, and despite research difficulties in
making satisfactory estimations of individual exposure, a
consistent pattern of moderately increased risk of lung
cancer in passive smokers has emerged. In view of this
pattern, of the known and substantial increase in risk of
lung cancer in active smokers (and the lack of threshold
dose), and of the documented levels of bodily assimilation
of passively-inhaled smoke, it is therefore prudent public
health policy to infer an increased risk of lung cancer from
passive smoking."
105. In 1986 the United States Surgeon General issued a report entitled "The Health Consequences of Involuntary Smoking". The report was submitted to Congress on December 15, 1986. The report was prepared by the United States Department of Health and Human Services. The report lists the names of a number of individuals who prepared portions of the report. These persons held positions in American universities. Acknowledgment is also given in the report to the assistance of about fifty scientists and physicians. It will be convenient to refer to this report as the "Surgeon General's 1986 Report".
106. The content of the report reflects the contributions of over sixty
scientists representing a variety of disciplines. The care
with which the
report was apparently prepared appears from the Introduction:
"Upon receipt of the final manuscripts from the authors,107. The Introduction contains an overview of the report. After referring to the inhalation of tobacco smoke during active cigarette smoking as "the largest single preventable cause of death and disability for the U.S. population", the overview continues:
the Office and its consultants edited and consolidated the
individual manuscripts into appropriate chapters. These
draft chapters were subjected to an extensive outside peer
review ... whereby each was reviewed by up to seven experts.
Their comments were integrated and the entire volume was
assembled. This revised edition of the Report was
resubjected to review by 17 distinguished scientists outside
the Federal Government, both in this country and abroad.
Parallel to this review, the entire Report was also
submitted to various institutes and agencies within the U.S.
Public Health Service for review and comment."
"The magnitude of the disease risks for active smokers108. The second conclusion does not, of course, relate to lung cancer.
secondary to their `high dose' exposure to tobacco smoke
suggests that the `lower dose' exposure to tobacco smoke
received by involuntary smokers may also have risks.
Although the risks of involuntary smoking are smaller than
the risks of active smoking, the number of individuals
injured by involuntary smoking is large both in absolute
terms and in comparison with the number injured by some
other agents in the general environment that are regulated
to curtail their potential to cause human illness.
This Report reviews the evidence on the
characteristics of mainstream tobacco smoke and of
environmental tobacco smoke, on the levels of exposure to
environmental tobacco smoke that occur, and on the health
effects of involuntary exposure to tobacco smoke. The
composition of the tobacco smoke inhaled by active smokers
and by involuntary smokers is examined for similarities and
differences, and the concentrations to tobacco smoke
components that can be measured in a variety of settings are
explored, as is smoke deposition and absorption in the
respiratory tract. The studies that describe the risks of
environmental tobacco smoke exposure for humans are
carefully reviewed for their findings and their validity.
The evidence on the health effects of involuntary smoking is
reviewed for biologic plausibility, and compared with
extrapolations of the risks of active smoking to the lower
dose of exposure to tobacco smoke found in non-smokers. This
review leads to three major conclusions:
1. Involuntary smoking is a cause of disease, including
lung cancer, in healthy non-smokers.
2. The children of parents who smoke compared with the
children of non-smoking parents have an increased frequency
of respiratory infections, increased respiratory symptoms,
and slightly smaller rates of increase in lung function as
the lung matures.
3. The simple separation of smokers and non-smokers
within the same air space may reduce, but does not
eliminate, the exposure of non-smokers to environmental
tobacco smoke."
109. The following statements are made in the report in relation to lung
cancer:
"Exposure to environmental tobacco smoke has been110. After making extensive reference to the scientific literature as to the relationship between passive smoking and lung cancer the Surgeon General's Report adopts the following summary:
examined in numerous recent epidemiological studies as a
risk factor for lung cancer in non-smokers. These studies
have compared the risks for subjects exposed to ETS at home
or at work with the risks for people not reported to be
exposed in these environments. Because exposure to ETS is
an almost universal experience in the more developed
countries, these studies involve comparison of more exposed
and less exposed people rather than comparison of exposed
and unexposed people. Thus, the studies are inherently
conservative in assessing the consequences of exposure to
ETS. Interpretation of these studies must consider the
extent to which populations with different ETS exposures
have been identified, the gradient in ETS exposure from the
lower exposure to the higher exposure groups, and the
magnitude of the increased lung cancer risk that results
from the gradient in ETS exposure.
To date, questionnaires have been used to classify ETS
exposure. Quantification of exposure by questionnaire,
particularly lifetime exposure, is difficult and has not
been validated. However, spousal and parental smoking
status identify individuals with different levels of
exposure to ETS. Therefore, investigation has focused on the
children and non-smoking spouses of smokers, groups for whom
greater ETS exposure would be expected and for whom
increased nicotine absorption has been documented relative
to the children and non-smoking spouses of non-smokers.
Of the epidemiologic studies reviewed in this Report
that have examined the question of involuntary smoking's
association with lung cancer, most (11 of 13) have shown a
positive association with exposure, and in 6 the association
reached statistical significance. Given the difficulty in
identifying groups with differing ETS exposures, the
low-dose range of exposure examined, and the small numbers of
subjects in some series, it is not surprising that some
studies have found no association and that in others the
association did not reach a conventional level of
statistical significance. The question is not whether
cigarette smoke can cause lung cancer; that question has
been answered unequivocally by examining the evidence for
active smoking. The question is, rather, can tobacco smoke
at a lower dose and through a different mode of exposure
cause lung cancer in non-smokers? The answer must be sought
in the coherence and trends of the epidemiologic evidence
available on this low- dose exposure to a known human
carcinogen. In general, those studies with larger
population sizes, more carefully validated diagnosis of lung
cancer, and more careful assessment of ETS exposure status
have shown statistically significant associations. A number
of these studies have demonstrated a dose-response
relationship between the level of ETS exposure and lung
cancer risk. By using data on nicotine absorption by the
non-smoker, the non-smoker's risk of developing lung cancer
observed in human epidemiologic studies can be compared with
the level of risk expected from an extrapolation of the
dose-response data for the active smoker. This
extrapolation yields estimates of an expected lung cancer
risk that approximate the observed lung cancer risk in
epidemiologic studies of involuntary smoking.
Cigarette smoke is well established as a human
carcinogen. The chemical composition of ETS is
qualitatively similar to mainstream smoke and sidestream
smoke and also acts as a carcinogen in bioassay systems. For
many non-smokers, the quantitative exposure to ETS is large
enough to expect an increased risk of lung cancer to occur,
and epidemiologic studies have demonstrated an increased
lung cancer risk with involuntary smoking. In examining a
low-dose exposure to a known carcinogen, it is rare to have
such an abundance of evidence on which to make a judgment,
and given this abundance of evidence, a clear judgment can
now be made: exposure to ETS is a cause of lung cancer.
The data presented in this Report establish that a
substantial number of the lung cancer deaths that occur
among non-smokers can be attributed to involuntary smoking.
However, better data on the extent and variability of ETS
exposure are needed to estimate the number of deaths with
confidence."
"Previous Reports of the Surgeon General have reviewed111. After detailed reference to the epidemiological studies referred to in the report, the summary concludes:
the data establishing active cigarette smoking as the major
cause of lung cancer. The absence of a threshold for
respiratory carcinogenesis in active smoking, the presence
of the same carcinogens in mainstream smoke and sidestream
smoke, the demonstrated uptake of tobacco smoke constituents
by involuntary smokers, and the demonstration of an
increased lung cancer risk in some populations with
exposures to ETS leads to the conclusion that involuntary
smoking is a cause of lung cancer."
"The epidemiological evidence that involuntary smoking
can significantly increase the risk of lung cancer in
non-smokers is compelling when considered as an examination
of low-dose exposure to a known carcinogen (i.e., tobacco
smoke). Eleven of the thirteen epidemiological studies to
date show a modest (10 to 300 percent) elevation of the risk
of lung cancer among non-smokers exposed to involuntary
smoking; in six studies positive associations were
statistically significant. The studies showing no or non
significantly positive findings were generally the weakest
in terms of sample size (Gillis et al. 1984; Chan and Fung
1982; Koo et al. 1984; Kabat and Wynder 1984; Wu et al.
1985; Lee et al. 1986), study design (Kabat and Wynder 1984;
Lee et al. 1986), or quality of data (Chan and Fung 1982)."
"The magnitude of risk associated with involuntary112. The following statements appear in the report:
smoking exposure is uncertain. Relative risks ranging from
2 to 3 were generally reported for the highest level of
exposure based on the spouses' smoking habits, but since
sample sizes in most studies are not large, the point
estimates of effect are unstable, and confidence limits are
broad and generally overlap from one study to another. An
index of involuntary smoking based on the smoking habits of
the spouse is a simplistic and convenient measure. There is
no reason to believe, however, that the excess risk
associated with involuntary smoking is restricted to
exposure from spouses. non-smokers married to smokers are
likely to be more tolerant of ETS exposure and to experience
more exposure to environmental tobacco smoke (Wald and
Ritchie 1984). Higher risk estimates for involuntary smoking
have been obtained in studies restricted to squamous cell
and small cell carcinomas of the lung.
Although involuntary smoking can be established as a
cause of lung cancer, important questions related to this
exposure require further research. More accurate estimates
for the assessment of exposure in the home, workplace, and
other environments are needed. Studies of sufficiently large
populations should also be performed. New data from such
studies should yield more certain risk estimates and
describe the magnitude of the lung cancer risk in
non-smokers."
"The appropriate framework for an examination of the(d) The National Research Council report on Environmental Tobacco Smoke 1986
lung cancer risk from involuntary smoking is that of a
low-dose exposure to a known human carcinogen. Over 30 years of
research have conclusively established cigarette smoke as a
carcinogen. This Report presents evidence that the chemical
composition of sidestream smoke is qualitatively similar to
the mainstream smoke inhaled by the active smoker, and that
both mainstream and sidestream smoke act as carcinogens in
bioassay systems. Data related to environmental levels of
tobacco smoke constituents and from measures of nicotine
absorption in non-smokers suggest that non-smokers are exposed
to levels of environmental tobacco smoke that would be
expected to generate a lung cancer risk; epidemiological
studies of populations exposed to ETS have documented an
increased risk for lung cancer in those non-smokers with
increased exposure.
It is rare to have such detailed exposure data or human
epidemiologic studies on disease occurrence when attempting
to evaluate the risk of low-dose exposure to an agent with
established toxicity at higher levels of exposure. The
relative abundance of data reviewed in this Report, their
cohesiveness, and their biologic plausibility allow a
judgment that involuntary smoking can cause lung cancer in
non-smokers. Although the number of lung cancers due to
involuntary smoking is smaller than that due to active
smoking, it still represents a number sufficiently large to
generate substantial public health concern.
It is certain that a substantial proportion of the lung
cancers that occur in non-smokers are due to ETS exposure;
however, more complete data on the dose and variability of
smoke exposure in the non-smoking U.S. population will be
needed before a quantitative estimate of the number of such
cancers can be made."
113. The National Research Council is the principal operating agency of the National Academy of Sciences of the United States of America. It was requested by the United States Department of Health and Human Services to evaluate methods for assessing exposure to environmental tobacco smoke and to review the literature on the health consequences of such exposure. The Council responded to this request by appointing eleven scientists to serve on a committee. The committee's charge was to review the then existing scientific literature and to identify the then current state of knowledge with respect to known facts and areas of uncertainty. (Ex D3,p.v). The committee membership represented the disciplines of toxicology, biochemistry, atmospheric science, epidemiology, bio-statistics and pulmonary physiology. For the most part, the members of the committee were drawn from American universities (including Harvard, Yale and Johns Hopkins), but its members also included Professor Nicholas Wald, Professor of Environmental and Preventative Medicine at St Bartholomew's Hospital, London, as well as Olav Axelson of the University Hospital, Linkoping, Sweden. According to its report, the committee conducted a public hearing on scientific studies relevant to its charge and reviewed the published scientific literature and received testimony from professional societies; medical, industry, consumer and public interest groups, academic scientists; and other involved in the generation and interpretation of scientific evidence on the health consequences of exposure to cigarette smoking. The public hearing was held on January 29, 1986. The report is undated but was first printed in November 1986. I think it is a reasonable inference that the material upon which the report was based was available to the scientific community as at July 1986. It will be convenient to refer to this report as "the NRC report".
114. With respect to lung cancer the report (pp 10-11) makes the following
statement:
"Considering the evidence as a whole, exposure to115. Chapter 12 of the report is entitled "Exposure to Environmental Tobacco Smoke and Lung Cancer". After observing that the risk of lung cancer in cigarette smokers is directly related to the number of cigarettes smoked and that, among smokers, an increase in exposure leads to an increase in risk, the authors state that passive smoking would, therefore, be expected to cause some increase in risk of lung cancer in active smokers, as well as in any other persons in whom the appropriate tissues are exposed. They continue:
ETS increases the incidence of lung cancer in non-smokers.
Estimates of the magnitude of the increased risk vary.
Among studies of various populations in Europe, Asia and
North America, the risk of lung cancer is roughly 30% higher
for non-smoking spouses of smokers than it is for non-smoking
spouses of non-smokers. There is consistency among the
studies in that all of the studies individually include the
30% increased risk within the 95% confidence intervals.
Patterns and extent of exposure may vary in different
communities and countries. Based on presently available
epidemiologic data, the estimate of the increased risk from
the American studies is lower than the average for all the
studies, though not significantly so. These estimates are
almost exclusively derived from the comparison of persons
identified as exposed, or unexposed, on the basis of their
spouse's smoking habits.
Certain errors in the reporting of smoking habits have
probably contributed to the risks observed in the
epidemiologic studies. Misclassification of current or
exsmokers as non-smokers would tend to produce an observed
relative risk that is larger than the true risk. The effect
was studied in detail using estimates of the extent of the
errors involved and judged to contribute only a portion of
the excess risk. Underestimation of the increased risk
might also be introduced because the supposedly unexposed
population had some exposure to ETS, although they were
classified as unexposed in the studies. Taking both types
of errors into account produces an estimate of the excess
lung cancer risk for non-smokers married to smokers compared
with completely unexposed individuals that is similar to the
relative risk observed in the epidemiologic studies
considered.
Since carcinogenic agents contained in ETS are inhaled
by non-smokers, in the absence of a threshold for
carcinogenic effects, an increased risk of lung cancer due
to ETS exposure is biologically plausible."
"The studies reviewed in this chapter have attempted116. After a detailed examination of the scientific literature on the subject and a consideration of bias and misclassification factors which may have affected some or all of the studies reported in the literature, the following summary is made:
to address the questions of whether an increase in risk of
lung cancer does occur in non-smokers exposed to ETS and
whether the dose-response relationship is similar to that in
smokers. In part, this depends on whether there is a
threshold dose of cigarette smoke exposure below which there
is no increase in risk. Biological theory and current
evidence on low-dose exposure to carcinogens do not provide
evidence for such a threshold, and it is generally thought
that one is unlikely (Office of Science and Technology
Policy, 1985). If there is no threshold, it follows that
exposure to tobacco smoke at low concentrations, such as
that experienced by non-smokers exposed to ETS, will cause an
increased risk of lung cancer. The risk, of course, will be
expected to be very much smaller than that associated with
active smoking because of the much lower exposure of the
bronchial epithelium to tobacco smoke."
"The weight of evidence derived from epidemiologic(e) The Froggatt Committee report 1988
studies shows an association between ETS exposure of
non-smokers and lung cancer that, taken as a whole, is
unlikely to be due to chance or systematic bias. The
observed estimate of increased risk is 34%, largely for
spouses of smokers compared with spouses of non-smokers. One
must consider the alternative explanations that this excess
either reflects bias inherent in most of the studies or that
it represents a causal effect. Misclassification can have
contributed to the result to some extent. Computations of
the effect of two sources of misclassification were
presented. Computations taking into account the possible
effects of misclassified exsmokers and the tendency for
spouses to have similar smoking habits placed the best
estimate of increased risk of lung cancer at about 25% in
persons exposed to ETS at a level typical of that
experienced by non-smokers married to smokers compared with
those married to non-smokers. Another computation using
information from cotinine levels observed in non-smokers and
taking into account the effect of making comparisons with a
reference population that is truly unexposed leads to an
estimated increased risk of about one-third when exposed
spouses were compared with a truly unexposed population.
The finding of such an increased risk is biologically
plausible, because non-smokers inhale other people's smoke
and, as a result, absorb smoke components containing
carcinogens.
What is Known
1. A summary estimate from epidemiologic studies
places the increased risk of lung cancer in non-smokers
married to smokers compared with non-smokers married to
non-smokers at about 34%. Assuming linearity at low-to-
average doses and a constant proportionality of nicotine and
carcinogens in mainstream smoke and ETS, extrapolation from
studies of active smokers using relative urinary cotinine
places the risk at about 10%.
2. To some extent, misclassification (bias) may have
contributed to the results reported in the epidemiologic
literature. However, bias is not likely to account for all
of the increased risk. The best estimate, allowing for
reasonable misclassification, is that the adjusted risk of
lung cancer is increased about 25% (i.e., RR = 1.25) in
non-smokers married to smokers compared with non-smokers
married to non-smokers. When one allows for exposure to
non-smokers who report themselves as unexposed, the adjusted
increased risk is at least 24%. The adjusted increased
risk to a group of non-smokers married to non-smokers is at
least 8% (i.e., RR = 1.08) compared with truly unexposed
subjects. This excess risk may come about from exposures in
the workplace or other public places."
117. This report was made in January 1988 by the Independent Scientific Committee on Smoking and Health to the Secretary of State for Social Services (UK). According to the Committee's Report its responsibility is "to advise ... on scientific aspects of matters concerning smoking and health ...".
118. Chapter 3 of the report addresses questions related to the effect of
exposure to ETS. In the following quotations from the
report I have omitted
footnotes which contain references to scientific literature:
"64. Nicotine is virtually unique to tobacco and(iv) Oral evidence
might be considered therefore as an index of ETS. Its
uptake by non-smokers, as measured by its metabolites,
indicates that some passive smokers may receive a dose
equivalent to that received by smokers who smoke a small
number of cigarettes. However, since sidestream and
mainstream smoke differ in composition such measurements
cannot be extrapolated to the whole range of potentially
harmful constituents of the smoke. For example, when
dimethylnitrosamine rather than nicotine is used as a
marker, the estimation of the uptake of tobacco smoke
produces a greater equivalence. Recent work has also pointed
to the role that ETS can play in enhancing concentrations of
radon daughter products indoors. For these, and other
reasons it is unwise to express ETS uptake in terms of an
equivalent number of cigarettes actively smoked despite its
undoubted convenience, a point made in our interim report in
March 1987.
65. The mutagenicity of particulate material sampled
from indoor and outdoor air has been studied using bacterial
systems and smoking was found to be an important factor with
its predominant effect on enzyme mediated mutagenesis, the
number of revertants increasing with the number of
cigarettes smoked.
66. Attempts have been made to evaluate relative risk
by means of epidemiological studies, not surprising given
the hypothesis of a zero threshold and that non-smokers
absorb some of the carcinogenic agents produced in smoking,
though the exact proportion is unknown. The commonest
method is to investigate lung cancer incidence among
non-smoking wives of husbands who are, or are not, smokers.
Studies of adequate size with documented smoking histories
of cases and spouses are few and our review has therefore
covered surveys from many countries.
67. In our Third Report we concluded (para 35) that the
reported association between passive smoking and lung cancer
was speculative. Since then a number of new studies have
been reported. The majority of reports conclude that passive
smoking is associated with an increased risk of lung cancer
in non-smokers. A minority conclude from their own data that
any effect of passive smoking on the risk of lung cancer or
other smoking-related disease in a non-smoker is negligible
and that the increased risk noted in other studies is
largely an artefact.
68. The published studies have been scrutinized by
various groups of researchers to determine whether
collectively they present a reasonably consistent picture
from which the existence and magnitude of the relative risk
might be assessed. The major problem is the extent to which
individuals with lung cancer were misclassified as
non-smokers when they were in fact smokers or ex-smokers. After
making allowances for such misclassifications, and other
artifacts, and then recalculating relative risks in each
study, most of the scientific groups conclude that while
none of the studies can on its own be accepted as
unequivocal the findings overall are consistent with there
being a small increase in the risk of lung cancer from
exposure to environmental tobacco smoke, in the range 10 per
cent-30 per cent, though some other workers have however
argued for a much lower relative risk, or no increased risk
at all. The Committee, studying the same data, agrees with
the former interpretation and so upholds the view expressed
in its interim statement.
69. It is helpful to state exactly what is meant by a
10% to 30% increased risk. It means that people who have
never smoked but who have been exposed to environmental
tobacco smoke through most of their lives have a 10% to 30%
higher risk of lung cancer than non-smokers not so exposed.
If the risk in the latter group is, say, 10 per 100,000 per
year (based on rates in non-smokers in the 35+ age range)
the risk in the exposed group would be 11 to 13 per 100,000
per year. Thus there might be 1 to 3 extra lung cancer
cases a year per 100,000 non-smokers regularly exposed to
ETS. Since there are no firm data on the numbers of people
who fall into that category, no more than a rough estimate
of the actual number of lung cancer deaths arising in this
way could be made. It might however amount to several
hundred out of the current annual total of about 40,000 lung
cancer deaths in the United Kingdom, a small but not
negligible proportion. In view of this conclusion we
recommend that -
FURTHER PUBLICITY SHOULD BE GIVEN TO THE RISK OF LUNG
CANCER ARISING FROM EXPOSURE TO OTHER PEOPLE'S TOBACCO
SMOKE"
119. I shall now refer to some of the oral evidence as to the alleged
association between passive smoking and cancer.
(a) Professor Stewart
120. Professor Bernard Stewart is Associate Professor in the School of Paediatrics at the University of New South Wales, and is the Principal Research Fellow in the Children's Leukaemia and Cancer Research Unit at the Prince of Wales Children's Hospital. He is a bio-chemist with specialist experience in the field of carcinogenesis. For a number of years he was the senior Research Fellow in Carcinogenesis of the New South Wales State Cancer Council.
121. Professor Stewart has had a great deal of experience in the study of the carcinogenic qualities of tobacco smoke. He expressed the opinion that there was no doubt whatever that cigarette smoke had been shown "to the point of absolute certainty" to be carcinogenic for humans (T. 433). In his opinion, exposure for a short time to a high concentration of tobacco smoke is less dangerous to humans than exposure to a low concentration of smoke over a long period of time. The reason for this is that if exposure occurs over a long period of time the likelihood of malignancy is increased because cells tend to be pushed towards transformation or alteration i.e. to become cancerous, rather than being killed outright. According to Professor Stewart, there is no safe level of exposure to carcinogenic substances, whereas the same cannot be said of toxic substances. A chemical is carcinogenic if it has the capacity to cause normal cells to become malignant. Toxic chemicals are those which kill normal cells (T. 396). Carcinogenic chemicals may also have a toxic effect.
122. Professor Stewart explained his view that there is no safe level of
exposure to carcinogens, as distinct from toxins, in the
following words:
"For the vast majority of toxins, for the vast majority123. It is apparent from statements made in the written material which I admitted into evidence that Professor Stewart's view that there is no safe level of exposure to a carcinogen is shared by many distinguished scientists.
of chemicals that adversely (affect) us as people, the
adversity that the chemicals produce is related to the dose.
If the dose is large then obviously the toxic chemical will
cause death - or large enough. As the dose is reduced so
the extent of pathology produced by that chemical is reduced
and if the dose is reduced and reduced there comes a point
where there is no discernible toxic effect at all. So that,
for argument's sake, in respect of caustic soda. Although
caustic soda is toxic, it will be possible to take a
solution of caustic soda and dilute and dilute it until it
was so diluted as to be consumed without causing any
clinical injury to the oesophagus. Now that concept is
(basic) to public health insofar as when measures to protect
the community from toxins are taken, the concept of a safe
level of exposure is crucial. That concept can be clearly
distinguished from the same basis when one approaches
carcinogenic hazards because carcinogenicity is not so
related to dose. At two levels because the theory of
carcinogenesis says that a single cell to be modified and
give rise to a tumour in theory such a single modification
could produce a lethal response. If you poison a cell in
the oesophagus with caustic soda the death of one cell could
not possibly cause the death of the whole person but if you
produce a single malignant cell then in theory that cell can
grow into a tumour and produce the death of the individual.
So that is a conceptual basis for the idea that there is no
safe dose for a known carcinogen. The other aspect of that
concept is based on the investigation of that whole area.
That is in addition to the conceptual basis of that idea, no
safe dose, there is a body of experimental evidence
pertaining to either people or experimental animals that
have been exposed to lower and lower levels of carcinogen by
one reason or another and all of that data taken as a whole
has failed to indicate a safe level of exposure for the
carcinogen under review. So it is a (basic) tenet of
carcinogenesis that there is no safe level of exposure, a
principle that lies at the very heart of all other areas of
toxicology."
(T.397-8)
124. It was put to Professor Stewart in cross-examination that if his view is correct, one molecule of a carcinogen could cause cancer. Whilst he agreed that, in theory, this was correct, he said that the one molecule example was a trivialisation of the significance of minimal exposure to carcinogens. I think this is correct, particularly in the context of the present case. The reference to cigarette smoke in the statement in para. 3 of the advertisement is quite general. It would extend, for example, to cigarette smoke inhaled by a non-smoker working for many years beside and in close proximity to a heavy smoker. If it be true that environmental tobacco smoke contains carcinogenic chemicals, it would be quite unrealistic to regard such a non-smoker as being exposed to the risk of inhaling only one molecule of a carcinogen.
125. Professor Stewart drew support for his opinions from the findings contained in some of the primary articles and also the findings in the IARC report. He conceded in one part of his evidence (T.521) that the available epidemiological evidence does not allow a judgment to be made on causality between lung cancer and exposure to environmental tobacco smoke. However, in the light of all his evidence, I did not understand this concession to be a concession that it has not been proved that cigarette smoke causes lung cancer in non-smokers. The concession he made was limited to the effect of the available epidemiological evidence, if considered in isolation from other evidence. It is plain from his evidence that he is firmly of the opinion that there is a considerable volume of evidence that cigarette smoke causes disease in non-smokers (T. 522). He thinks that exposure to tobacco smoke is an established carcinogenic hazard. According to him, this conclusion can be reached wholly on the basis of laboratory evidence without reference to the epidemiological studies. However, he thinks both types of evidence should be considered together. He said: "Complementarity of laboratory and epidemiological evidence, in respect of the carcinogenic hazard associated with exposure to environmental smoke is unequivocal. In view of these considerations, denial that evidence for a carcinogenic hazard from passive smoking has not been established, is absurd" (see annexure E to his affidavit).
126. A consideration of the whole of Professor Stewart's evidence leads me to
conclude that he is of the opinion that a causal link
has been established
between passive smoking and lung cancer in non-smokers, but that further
epidemiological evidence would add
weight to his opinion. In his affidavit he
said:
"In my opinion, understanding of the causation of lung127. Professor Stewart said that undiluted sidestream smoke is characterised by significantly higher concentrations of many of the toxic and carcinogenic compounds found in mainstream smoke. According to him, a comparison of the chemical composition of smoke inhaled by active smokers with that inhaled by involuntary smokers suggests that the toxic and carcinogenic effects would be qualitatively similar. He said that since carcinogenic agents in environmental tobacco smoke are inhaled by non-smokers, in the absence of a threshold for carcinogenic effects, an increased risk of lung cancer due to environmental tobacco smoke is anticipated.
cancer in cigarette smokers, taken together with knowledge
of the nature of sidestream and mainstream tobacco smoke, of
the materials absorbed during passive smoking and of the
quantitative relationships between dose and effect that are
commonly observed after exposure to carcinogens, leads to
the reasonable presumption that passive smoking does carry
some risk for lung and other cancers. In respect of lung
cancer, this presumption is now confirmed by a variety of
epidemiological and experimental evidence which are mutually
supportive. Knowledge of the causal relationship between
passive smoking and lung cancer is now sufficient as to
warrant measures to limit human exposure to this risk factor
as a necessary and practicable public health measure to
reduce the burden of lung cancer in the community."
128. Professor Stewart conceded that active smokers are exposed to greater quantities of tobacco smoke constituents than involuntary smokers. However, he is of the view that exposures to respirable suspended particulates are higher for non-smokers exposed to environmental tobacco smoke than for non-smokers who are not so exposed.
129. It was put to Professor Stewart in cross-examination that the proposition that there is no safe dose for a carcinogen was a public health principle and that public health principles depend upon dictates of caution whereas scientific proof of a proposition depends on demonstration of its correctness (T. 491-2). The Professor agreed, but I do not think his agreement is tantamount to an admission that there is not scientific proof that there is no safe dose for a carcinogen. He specifically disagreed with the proposition put to him (T. 494) that the concept that there was no threshold for carcinogens was not universally accepted. He said he knew of no experimental studies that had satisfactorily demonstrated that there was any such threshold (T. 494).
130. Professor Stewart said there was no qualitative distinction as to
carcinogens between the composition of mainstream smoke and
sidestream smoke
because both contained polycyclic hydro carbons and both contained nitroso
compounds or that group of nitroso compounds
called nitrosamines (T.416).
However, under cross-examination Professor Stewart conceded that it has not
been scientifically proven
that nitroso compounds cause cancer in humans
(T.485). He said he believed there was a split within the scientific
community on
that issue. In his opinion nitroso compounds "would be
appropriately characterized as a group 2A compound, that is they probably
cause cancer in humans but it is not proven" (T. 485). Later, Professor
Stewart elaborated:
"... whether nitroso compounds cause cancer in humans.131. I refer elsewhere to the contents of the IARC report and it is instructive to compare Professor Stewart's opinions with the conclusions reached in it. At p 314 of the report, after reference is made to the three main sources of tobacco smoke i.e. mainstream smoke, sidestream smoke, and smoke exhaled to the general atmosphere by smokers, it is said:
Now, that statement is by definition concerned with the
causation of cancer in humans and can only be resolved by
reference to epidemiology studies in humans. The animal
data are suggestive but not definitive and the reason I
appear to equivocate on it is that the generally appropriate
generalization is certainly that nitroso compounds probably
cause cancer in humans or nitroso compounds almost certainly
cause cancer in humans but my studies on rats and mice or on
rats are not relevant to the definitive determination that
nitroso compounds cause cancer in humans. They only provide
evidence consistent with such a proposition or even evidence
that was strongly suggestive or almost leaving no room for
doubt but they are not finally definitive ..."
(T.519-520).
"Examination of smoke from the different sources shows132. The report then makes the evaluation that:
that all three types contain chemicals that are both
carcinogenic and mutagenic. The amounts absorbed by passive
smokers are, however, small, and effects are unlikely to be
detectable unless exposure is substantial and very large
numbers of people are observed. The observations on
non-smokers that have been made so far are compatible with
either an increased risk from `passive' smoking or an
absence of risk. Knowledge of the nature of sidestream and
mainstream smoke, of the materials absorbed during `passive'
smoking, and of the quantitative relationships between dose
and effect that are commonly observed from exposure to
carcinogens, however, leads to the conclusion that passive
smoking gives rise to some risk of cancer."
"There is sufficient evidence that tobacco smoke is133. Reference to p 24 of the report shows that the expression "sufficient evidence" of carcinogenicity indicates that there is a causal relationship between the exposure and human cancer. Thus Professor Stewart's opinions seem not to differ from those expressed in the report.
carcinogenic to humans."
134. Professor Anthony McMichael is Professor of Occupational and Environmental Health in the Department of Community Medicine at the University of Adelaide. He was the Chairman of the working party which produced the NH and MRC report. Prior to taking up his present appointment he was Senior Principal Research Scientist with the Commonwealth Scientific Industrial and Research Organisation. He was at one time Assistant Professor in the Department of Epidemiology in the University of North Carolina, U.S.A.
135. Professor McMichael is of the opinion that it is not true to say that there is little evidence that cigarette smoke causes disease in non-smokers. In his opinion, there is a considerable volume of evidence that cigarette smoke causes disease in non-smokers and the evidence is sufficient to constitute scientific proof that it does so.
136. Professor McMichael took a very active part in the preparation of the chapter in the NH and MRC report dealing with cancer. It is plain from his evidence that he shares the view expressed in the report. Indeed, with respect to the statement made on p 33 of the report that: "The evidence that passive smoking causes lung cancer is strongly suggestive" the Professor said that this was an understatement of the view which he himself held at the time.
137. The respondent sought to diminish the weight which should be given to Professor McMichael's evidence by showing that he had altered a draft report prepared for the consideration of the working party. I do not think it was shown that he did anything untoward in the handling of the draft report. Certainly he was responsible for the making of some alterations, but I am quite satisfied there was nothing improper in what he did. The members of the working party were all persons with high qualifications and great experience. I think it is reasonable to assume that they did not concur with Professor McMichael's views unless they shared his opinions as expressed in the final report.
138. Counsel for the respondent criticised Professor McMichael for showing a copy of the draft NH and MRC report to a body known as ASH, an acronym for Action on Smoking and Health. However, I can see nothing wrong with what he did in this regard. It is true that the draft was, at the time, a confidential document but as he pointed out there were many groups concerned with public health who knew of its existence, or at least knew that work was being done on the report. There is nothing to suggest that if the respondent had asked to see a copy of the draft report it would not have been shown it.
139. Professor McMichael's opinions have firmed since the publication in July 1986 of the NH and MRC report. He said (T. 969) that as at January 1987 his view was "a little firmer that there was a causal relationship demonstrated between passive smoking and lung cancer." It is apparent from his evidence that one reason why his opinion had firmed was the publication in late 1986 of an article by Professor Wald and others published in the British Medical Journal. Reference to this article, and to Professor Wald's evidence in respect of it, is made elsewhere in these reasons. Professor McMichael said he agreed with the conclusions in Wald's article.
140. It would not be right, however, to treat Professor McMichael's evidence
as being merely an adoption and recapitulation of the
views expressed by Wald
and other writers of published scientific work. He made it plain that
although he had regard to the views
of others, he had arrived at his own
opinions. Thus he said:
"I do not depend centrally on Wald because Wald has141. Professor McMichael's views are perhaps best captured in the following statements he made towards the conclusion of his evidence. The statements were made in the context of drawing a comparison between the evidence showing a link between the consumption of alcohol and breast cancer and the evidence showing a link between passive smoking and lung cancer. Although the statement is lengthy, I set it out in full because it encapsulates the gist of the arguments relied upon by the applicant on the question whether passive smoking causes lung cancer. He said (T. 1413-4):
done simply quantitatively in a way that I consider to be
correct and appropriate the sort of thing that otherwise one
has done, one does mentally or qualitatively in appraising
the full set of results available."
(T. 1347)
"With respect to ... tobacco smoke in human cancer, ...142. Professor McMichael expressed the opinion that, qualitatively, environmental tobacco smoke and mainsteam smoke have much the same chemical constituency (T. 928). He accepted that there were important quantitative differences, one of which was that at the point of origin the concentration of a number of chemicals is actually greater in sidestream smoke than it is in mainstream smoke. He said these chemicals include several chemicals which are carcinogenic.
I would summarize the evidence in relation to active smoking
and here we are talking not about 5, 10 or 20 or even
hundreds of studies, but in totality thousands of human and
animal experimental studies as showing very consistent and
strong increases in risk of human cancer, particularly,
cancer of the lung in epidemiological research - that is
work spread now over three or four decades. An enormous
range of corroborative evidence from animal experiments with
tobacco smoke being encountered in different modes, either
by inhalation or painting on the skin. A lot of work on
the mutational capacity of cigarette smoke. Studies on the
induction of genetic mutations in mammalian cells and in
bacterial cells. With respect to the evidence on
environmental tobacco smoke we have first up the
epidemiological evidence, ... that is studies specifically
of the risk of lung cancer in life-long non-smokers exposed
to environmental tobacco smoke, so we have that direct
empirical evidence, although we have noted that the number
of studies is not great. It is moving towards a total of
around 20 now and if we were looking at those just on their
own, and if they had arisen out of the blue, as it were, as
has been the case for alcohol and breast cancer or
methylxanthenes and breast cancer, that had arisen recently
out of the blue, not against a background of all of this
other corroborative scientific work and all of this other
biological knowledge and theory, then we would be more
cautious in drawing a causal inference. But because there
is the overwhelming evidence from the studies of active
smoking because we have from the toxicologists and chemists
the evidence of the qualitative identity in terms of
chemical constituents present, of active and passive smoke
... we would reasonably infer that that exposure has a
capacity to produce cancers. ... we have a range of
metabolic epidemiological studies in which it has been
demonstrated that humans exposed to environmental tobacco
smoke, whether at home, at work or in some other context,
public transport and so, by measuring levels of cotinine in
blood, urine, saliva and so on, it has been clearly
established that non-trivial amounts of exposure are
incurred by those individuals and that that is in some
quantitative proportion to the types of exposures that might
be estimated by direct environmental observation or by
asking individuals, how much does your husband smoke and how
much is it at work, etcetera. So we ... not only ... have
those initial upfront studies from epidemiologists about
environmental tobacco smoke in lung cancer, but we have this
extraordinarily rich large and deep spectrum of scientific
research, some of it bearing directly on environmental
tobacco smoke, much of it bearing on active tobacco smoke
which provides the sort of corroboration that in my judgment
allows one to draw a reasonable inference of causality from
the sort of evidence that has now accrued in relation to
environmental tobacco smoke."
143. Professor McMichael also shares the views of other witnesses in the case, and a view expressed in much of the literature, that there is no apparent threshold for carcinogens, i.e. no apparent safe dose or level of exposure below which there is no increase in the risk of lung cancer from tobacco smoke (T.937).
144. The respondent sought to diminish the quality of some of the epidemiological studies referred to by Professor McMichael because the diagnosis of cancer in some of them depended upon cytological rather than histological examination. A histological examination involves taking a small piece of the tissue of the tumour of interest and examining it microscopically so as to form a judgment about its histology. Cytological examination involves taking specimen cells from the tumour and examining them microscopically. Professor McMichael accepted that histological examination provides a surer guide to a correct diagnosis than cytological examination, and that both are more reliable than diagnoses recorded on death certificates. There was no disagreement between the witnesses on this matter. However, in my opinion, the respondent's witnesses tended to place far too much emphasis on the absence of histological examination in some of the surveys.
145. Professor McMichael, in common with other witnesses, was cross examined
at length as to much of the detail in the epidemiological
studies relied upon
by the applicant. It is impracticable to traverse in these reasons all of the
ground covered in the cross examination.
In his cross examination of the
applicant's witnesses, Mr O'Keefe Q.C. was able to identify many aspects of
the studies upon which
they could be criticised. He was also able to show
that, within some of the studies, there were apparent inconsistencies. But
Professor McMichael would not accept that the studies could therefore be
discarded. He said repeatedly that what was of importance
from an
epidemiological point of view was consistency in epidemiological studies. As
he said:
"It is always very important to look for consistency of146. This approach is also reflected in his appreciation of the importance of statistical significance. Lack of statistical significance in data derived from a study was regarded on the respondent's side as of almost crucial importance. However, Professor McMichael's opinion is that it is inappropriate to regard statistical significance as the sole criterion of the value of an epidemiological study. He regards statistical significance as only one aid to judgment in deciding how much weight should be attached to a study.
findings across studies. There is a sort of hybrid vigour,
if you like, or robustness that derives from making similar
observations in different population settings and using
different study designs."
(T.923)
147. In Professor McMichael's opinion, the value of an epidemiological study cannot be ascertained by measuring it against set criteria. He said (T. 1238) that whilst there are recognised and important criteria for the drawing of judgments about causal inference, they are not and should not be seen as pre-requisites to the drawing of such judgments. In his opinion, the drawing of causal inferences can quite reasonably proceed, and often does, in the presence of some only of the well recognised criteria.
148. Professor McMichael's view that it is the totality of all the evidence
which is of importance can be seen from his view as to
when a causal inference
can be drawn. He said:
"(I) think we have to be aware again that we are149. Professor McMichael said that taking into account the totality of the scientific evidence he was satisfied that, as at mid-1986, there was sufficient evidence to allow the drawing of an inference of causality between exposure to passive smoking and the occurrence of lung cancer in humans. (T. 1269). The above references to his evidence barely scratch the surface of it. I have not attempted to deal with the detailed evidence he gave, much of it in the course of cross examination, about the epidemiological studies referred to in the primary articles. Indeed, it would be almost impossible to capture in these reasons the intricacies of that evidence. However, I should observe that I formed the opinion that Professor McMichael is highly skilled in the field of cancer epidemiology and that his opinions are entitled to great respect.
talking about a continuum that moves from uncertainty to
certainty in the drawing of these causal inferences, and
that is not really a binary option that you either do or do
not know that there is a causal relationship. It is very
much a question of the accrual of evidence and the level of
certainty that applies."
(T. 1253)
150. Dr Bruce Armstrong is Commissioner of Health for the State of Western Australia. Prior to that appointment he was Director of the National Health and Medical Research Council's Research Unit in Epidemiology and Preventative Medicine and Professor of Epidemiology and Cancer Research at the University of Western Australia.
151. Dr Armstrong is of the opinion that it is not true to say that there is little evidence that cigarette smoke causes disease in non-smokers. He thinks there is considerable scientific evidence that cigarette smoke causes disease in non-smokers and that the evidence is sufficient to prove this relationship on the balance of probabilities. In his opinion sidestream smoke is a rich source of toxic substances and contains a variety of known or suspected chemical carcinogens in amounts as much as thirty times higher than in mainstream smoke. (Annexure E to his affidavit). He is of the view that there is no theoretical or empirical reason to postulate a low-dose threshold for tobacco smoke carcinogenesis. He holds the opinion that the products of tobacco combustion are readily measurable and that their inhalation and absorption in the human body is demonstrable by the measurement of cotinine in the urine of non-smokers.
152. Dr Armstrong adheres to the view he expressed in an article which he
published in 1987. In that article he said:
"Knowledge derived from studies of `active' smokers,153. I did not understand there to be any material difference between Dr Armstrong's views on matters relevant to this case as at 1 July 1986 and as at the date he gave his evidence.
evidence of exposure to tobacco smoke carcinogens through
passive smoking and the results of studies of passive
smokers themselves are concordant in suggesting that passive
smoking gives rise to a small increase in the risk of lung
cancer in non-smokers. The actual degree of increase in
risk must, for the present, be considered as somewhat
uncertain. Estimates of carcinogen exposure through
passive smoking suggest that it may be as low as 14 per
cent; studies of lung cancer itself suggest that it lies
between 24 per cent and 61 per cent. Similar or perhaps
greater absolute increases in risk of lung cancer due to
passive smoking would be likely in current and ex-smokers
but probably undetectable epidemiologically because of the
associated high incidence of lung cancer due to active smoking."
154. Dr Armstrong made a calculation in the article of the impact of the increased risk of lung cancer occasioned by passive smoking. Extrapolating from annual cancer mortality rates in the United States of America, he estimated that as at 1983 there were 60 deaths annually in Australia due to passive smoking. The estimate was higher making a different set of assumptions.
155. Dr Armstrong was asked his opinion as to the value which could be attached to an epidemiological study which disclosed only a low relative risk. He accepted that it is often stated in epidemiology that relative risks of 1.5 or below are difficult to interpret. However, he said that regard must be had to the "totality of the evidence on the subject." This includes evidence, if it exists, of a trend towards increasing risk of lung cancer with increasing passive exposure to tobacco smoking. He thinks such evidence is disclosed in the Trichopoulos and Hirayama studies. Other evidence to which regard must be had is evidence of biological plausibility. In his opinion there is an inherent biological plausibility of an association between passive smoking and lung cancer. He thinks that where evidence of this kind is available, a low relative risk is not particularly important.
156. He was prepared to agree that, notwithstanding his opinion to the contrary, another epidemiologist could properly have held the view as at the date of publication of the advertisement that the evidence associating environmental tobacco smoke with lung cancer was equivocal. But I do not take this to be a concession that his view was not correct. Concessions of a somewhat similar kind were made by other witnesses called by the applicant. I do not think concessions of this nature are of much significance. If an opinion is erroneous, the fact that it is honestly or "properly" held does not give it validity or diminish the strength of the evidence upon which a contrary opinion is based. If that evidence establishes the correctness of the contrary opinion, then the statement of the erroneous opinion may mislead or deceive a person to whom it is made.
157. Of course, it might be argued that if one scientist may properly hold a certain view on a matter, the correctness of the contrary view cannot be proved scientifically. I do not find this argument persuasive insofar as it is sought to be relied upon in the present case. The respondent failed to call one witness whose special expertise is in epidemiology and of whom it could be said that he "properly" held views contrary to those expressed by the distinguished epidemiologists called by the applicant. It is a fair assumption, I think, that such a witness would have been called by the respondent had he been available. In these circumstances, the concession made by Dr Armstrong and others was little more than an admission of the theoretical possibility that another epidemiologist may hold contrary views, rather than a concession that any competent epidemiologist does in fact hold contrary views.
158. Dr Armstrong was cross-examined at length as to the alleged deficiencies in the Hirayama and Trichopoulos studies. It is fair to say that he recognised that these and other epidemiological studies relied upon by the applicant had their limitations. But his recognition of these limitations did not cause him to alter his opinion that the totality of the evidence demonstrates a causal relationship between passive smoking and cancer.
159. Dr Armstrong did not agree with the proposition that an epidemiological study is not worthy of consideration unless it demonstrates a statistically significant association (T.1463). He agreed that if one is considering a single epidemiological study then the statistical significance of the data revealed by it is of great importance but he thought this was not the case if one is considering consistency among studies.
160. He acknowledged (T.1633) that a number of criticisms had been made of
the Hirayama studies and he conceded that, to an extent,
some of them were
valid. He was exhaustively cross-examined as to the limitations of the
Hirayama and other epidemiological studies
and acknowledged (T.1657) that the
cross examiner had been able to raise what he described as "issues of doubt
and uncertainty" in
some of those studies. But he maintained his opinion
that on the balance of probabilities it was correct to say that environmental
tobacco smoke causes lung cancer (T.1657).
(d) Professor Trichopoulos
161. Professor Trichopoulos is Professor of Epidemiology at the Harvard School of Public Health. He was formerly Professor and Director in the Department of Hygiene and Epidemiology at the University of Athens Medical School. He has served as a consultant or adviser to the World Health Organisation on, inter alia, cancer aetiology and prevention, health statistics, and epidemiology of various diseases and conditions. He has also served as a member of the Panel of Social Medicine and Epidemiology of the European Economic Community and of the Community's Special Working Group on Epidemiology and Bio-statistics. He is the author or co-author of a large number of publications including one of the primary articles referred to above.
162. Professor Trichopoulos responded to some of the criticisms (see infra) made by Professor Tweedie of his study. One of Professor Tweedie's criticisms was that the study excluded patients with adenocarcinomas and alveolar carcinomas. His answer was that these cell types are less associated with lung cancer in active smokers and this justified their exclusion in a study of passive smokers. He also thought that Professor Tweedie's criticism of the use of controls from a hospital for orthopaedic disorders was not justified because there was no warrant for an assumption that the wives of orthopaedic patients smoked less than others.
163. He also disputed that bias would have played a significant role in the results of the data collected. He claimed that at the time the study was undertaken, the doctor who conducted the interviews did not believe that passive smoking caused lung cancer and there was no public awareness of a potential link between passive smoking and lung cancer such as might have affected the answers given by patients. He accepted that in only a minority of the cases was there histological confirmation of the diagnosis of lung cancer, but he claimed that cytological diagnoses were available for two-thirds of the patients, and that such diagnoses were scientifically acceptable. He did not accept that any potential misclassification on the basis of smoking status would have changed the results of the study.
164. Professor Trichopoulos accepted that a critic can always point to weaknesses in a specific study, but he said that: "in epidemiology, you don't take a specific study in isolation and expect it to provide final answers on every aspect of the question." He admitted that in one important respect the result of his study had been incorrectly published in The Lancet, the journal in which it appeared. However, he said this was a typographical error and was corrected in the subsequent issue of the journal. I accept Professor Trichopoulos' evidence on this point. In the Professor's opinion, what is important about the risk ratios reported in his study is that they are statistically significant and that bias and confounding factors are reasonably excluded.
165. In spite of lengthy cross-examination of Professor Trichopoulos to show that he was not free from bias on the question in issue, I did not form an unfavourable impression of him in that regard. It is true that he had great difficulty in confining his answers to matters directly relevant to the questions asked of him. But I am confident that Professor Trichopoulos has great experience in the field of epidemiology and is also a man of professional integrity whose judgments are not affected by bias.
166. Professor Trichopoulos was criticised for not producing documents showing the data upon which his study was based. I think he might have made more effort than he did to produce these documents. However, the documents he was asked to produce were not in his custody. They were in the possession of the University of Athens. The documents were brought into existence about ten years ago. Whilst it might have been wise for him to have written to the University requesting it to make the documents available to him so that he could produce them to the respondent, he was under no obligation to do so. Moreover, I do not find it hard to believe that he thought that the request made of him was unreasonable because the class of documents he was asked to produce was very wide. It is, I think, highly unlikely that the professor and his co-authors of the study would have failed to have correctly analysed the data available to them.
167. Professor Trichopoulos agreed that his study had limitations but said that these were no different from those which he recognised himself in the text of his published article. He did not claim that his study, of itself, provided convincing evidence of a causal link between passive smoking and lung cancer. He agreed that only the convergence of results from different studies in different populations permits a reasonably sound conclusion to be drawn in that regard (T.4146-7).
168. Professor Trichopoulos' evidence was limited because of a ruling I gave
as to the matters upon which he could be examined in
chief. The ruling was
occasioned by the fact that he was not called in the applicant's case in chief
but only in reply.
(e) Professor Janerich
169. Professor Dwight Janerich is Professor of Epidemiology and Director of the Cancer Epidemiology Program and Cancer Prevention Research Unit at Yale University School of Medicine in New Haven, Connecticut. He is a past president of the American College of Epidemiology and has served on the Board of Directors of the College since 1979.
170. Professor Janerich was called to give evidence in respect of an unpublished thesis by Dr Luis Varela which was tendered by the respondent as part of its case. Dr Varela is now deceased. From 1982 to 1984 Professor Janerich was Director of the Division of Community Health and Epidemiology for the New York State Department of Health, where he was responsible for the design of the empirical study on which Dr Varela's thesis was based.
171. The professor explained in some detail how the data analysed by Dr Varela was collected. I do not think any good purpose would be served by a detailed account of the way in which the study was designed or the data collected. It is sufficient to say that the study appears to have been well conducted.
172. Senior counsel for the respondent claimed, in effect, that it was not possible for him to cross examine Dr Janerich because of the absence of the raw data upon which Dr Varela's thesis was based. I do not think that was the case. Dr Varela's thesis was tendered by the respondent. It is reasonable to assume it would not have been tendered if doubts were entertained as to its validity.
173. There were two classes of documents which counsel claimed he needed in order to cross examine Professor Janerich. They were the form of questionnaire which was used in the collection of the data, and the completed questionnaires. Professor Janerich said that the copy of the questionnaire which was annexed to Dr Varela's thesis included all the questions which were relevant to the passive smoking issue. Dr Varela himself must have thought that this was the case because he referred to only that part of the questionnaire in the appendix to his study.
174. I am not persuaded that the documents, if produced, would have thrown any further light on Dr Varela's thesis or Professor Janerich's comments upon it. It was not Dr Varela who administered the questionnaires. This was done by interviewers employed by the New York Department of Health. Dr Varela used data collected by the interviewers. If the questionnaires had been produced, there would have been no means of checking them to ascertain whether the answers recorded by the interviewers were correct. It is reasonable to assume that the answers were correctly recorded. I think it must be assumed that the interviewers accurately recorded the answers communicated to them. There is no reason to think that the interviewers were biased, dishonest or incompetent.
175. Professor Janerich said that he basically agreed with the conclusions
reached by Dr Varela in his thesis. Dr Varela concluded
that the data he
analyzed did not show a statistically significant association between spousal
smoking and lung cancer, but Professor
Janerich thought there were possible
explanations why this was so. He said that the evidence referred to in Dr
Varela's thesis
showed a positive effect and was, in his opinion, further
evidence that environmental tobacco smoke can cause lung cancer. He said:
"The New York study is population-based and from a large176. In the light of Professor Janerich's evidence, which was virtually unchallenged, I do not think Dr Varela's thesis adds weight to the respondent's case.
catchment area, which provides important assurances for the
case-control design. The study was designed to be
representative of this catchment area, and we did everything
we could to achieve that representiveness as the study was
conducted. In my opinion, the positive finding from this
study in respect of exposure to household smoking and the
inability to detect a positive finding with other measures
of exposure in no way detracts from the positive findings of
earlier studies."
177. Sir Richard Doll was formerly Regius Professor of Medicine in the University of Oxford. He holds honorary degrees of Doctor of Science from Harvard, London, Oxford and other universities. He has an enviable reputation as an epidemiologist. Indeed, I think it is fair to say that many of the distinguished epidemiologists who were called in evidence regard him as something of an icon in the field of epidemiology. His academic and professional distinctions are too numerous to relate. Although he vacated his Chair at Oxford in 1979, he has maintained a close and active interest in epidemiology. He was the Director of the Imperial Cancer Research Fund's Cancer Epidemiology and Clinical Trials Unit between 1978 and 1983 and between 1987 and 1989. He is currently a member of the World Health Organisation Commission on Health and Environment. He is a former member of the Council of the Royal Society and in 1986 was awarded its Royal Medal. He was the first Warden of Green College, Oxford, which was established in 1979 as a post-graduate college with a special interest in clinical medicine. His researches include studies of the health effects of smoking, ionizing radiation, and of the causes of lung cancer.
178. Sir Richard Doll explained the nature of epidemiological research. He
said that the results obtained from such research record
only associations (or
the absence of associations) and, as such, may be explained in several
different ways. He said that if similar
associations can be produced
experimentally in animals in a laboratory, it is easy to conclude that they
imply causation in humans.
But in the absence of such evidence interpretation
of the human evidence may be difficult. However, he made it plain that, in his
opinion, epidemiological evidence alone may be sufficient to establish that a
factor is a cause of a disease. He said (T.3886):
"It is perfectly possible to draw a conclusion about179. Sir Richard Doll gave persuasive reasons supporting his opinion. He said such conclusions have been reached in the past despite the fact that intensive laboratory investigation has failed to demonstrate a similar effect in animals. He gave as an example a conclusion which he and Professor Bradford Hill reached in 1950 that smoking is an important factor in the cause of carcinoma of the lung. That conclusion was reached despite the fact that tobacco smoke had not, at that time, been recognised to be carcinogenic in animal experiments.
causation in the absence of laboratory support. It is much
more difficult and one has to require somewhat different
conditions and you need a lot more thought and a lot of
weight will be attached to the conclusion. Therefore, you
have considerable responsibility in deciding upon the basis
of epidemiological evidence alone that a factor is a cause
of disease. But it can be done and has been done frequently
in the past ..."
180. The evidence which was led from Sir Richard Doll was limited because he was called only in reply. I ruled that counsel for the applicant was not entitled to lead evidence from him as to the weight which could be attached to the data referred to in the primary articles.
181. Sir Richard was cross-examined for the purpose of demonstrating the extremely cautious approach he took when seeking to ascertain whether there was proof that chemically treated oils imported into Spain as industrial oil and sold as pure olive oil were the cause of a toxic syndrome that affected many thousands of people in Spain in the summer of 1981. But I do not think I should infer from the cautious approach taken by Sir Richard in the Spanish oil disaster that he would not be satisfied that the epidemiological evidence demonstrates a causal link between passive smoking and lung cancer. Consistent with my ruling as to the evidence which could be given by Sir Richard, it was not possible for counsel for the applicant to ask his opinion on that matter. But counsel for the respondent could have sought Sir Richard's opinion on it. It should not be assumed that Sir Richard's view would have been adverse to the apllicant when his view could have been elicited by the respondent, but was not.
182. Sir Richard Doll was co-author with Professor Peto of an editorial which appeared in the British Journal of Cancer in 1986, in which it is stated: "Exposure to ambient smoke must be assumed to cause some lung cancers in non- smokers, as they inhale the same chemicals as smokers, and it is now generally accepted that a safe threshold is unlikely to exist for most carcinogens." This statement suggests that Sir Richard regards the biological plausibility of a link between passive smoking and lung cancer as an important adjunct to the epidemiological studies. That element of biological plausibility was absent in the Spanish oil case.
183. It is true that in the same editorial, having referred to reports in a number of epidemiological studies of increased lung cancer risks in the non-smoking spouses of smokers, Sir Richard Doll and Professor Peto refer to those reports as "equivocal evidence". But as I read the article, this is a reference to the reported estimates of risk, not to the presence of carcinogens in tobacco smoke and the absence of a safe threshold for them. In a letter to the British Journal of Cancer written after the publication of the editorial, Doll and Peto, referring to their previous editorial, said that in it - "we concluded that the evidence that passive smoking confers an appreciable risk, although inconclusive, is suggestive enough to justify concern." I think it is apparent from a reading of both the letter and the editorial that the authors are firmly of the view that non-smokers are exposed to an appreciable risk from passive smoking. The evidence which they regard as being equivocal and inconclusive relates to the quantification of the risk, not its existence.
184. With reference to the concept of relative risk, Sir Richard Doll was
asked whether he would agree that when a relative risk
is 1.5 or below, one's
confidence in causality is very much less than if it is above that number. He
agreed with this proposition
"in the absence of very strong other evidence"
(T.3934). He said he did not accept that a risk ratio of 2 or less was
necessarily
evidence of a weak association (T.3951).
(g) Professor Wald
185. Professor Nicholas Wald is Professor and Head of the Department of Environmental and Preventive Medicine at St Bartholomew's Hospital Medical College in the University of London. He was previously Deputy Director of the Imperial Cancer Research Fund Cancer Epidemiology and Clinical Trials Unit in the University of Oxford. He is the author and co-author of a large number of publications, many of them related to research into the effects of tobacco smoking. He is a member of the United Kingdom Independent Scientific Committee on Smoking and Health, and has sat on various committees concerned with tobacco and health, including the United States National Academy of Science Committee on Passive Smoking, and the World Health Organization International Agency for Research on Cancer's Working Group on Tobacco. He was the Chairman of the United Kingdom Medical Research Council's Smoking Review Committee. He was also a member of the British Government's Committee on Carcinogenicity of Chemicals in Food, Consumer Products and the Environment.
186. Professor Wald was called by the applicant to give evidence of a statistical technique sometimes described as meta-analysis. It is a statistical technique employed to combine the results of individual epidemiological studies in order to derive a quantitative summarisation of data relating to a particular area of investigation.
187. Professor Wald was the co-author of an article ("the Wald article") which appeared in the British Medical Journal in November 1986 in which a meta-analysis is made of many of the epidemiological studies tendered in evidence. His co-authors were a highly qualified research assistant with expertise in computer programming, a lecturer in medical statistics and a senior lecturer in cancer research who was a mathematician and epidemiologist. In his oral evidence the professor adhered to the views expressed in the article.
188. In meta-analysis information from several individual studies is pooled. Professor Wald said that the technique has a special value in situations where there are many studies each of which, on its own, may be too small to be expected to show an effect if there is one. There are a number of different statistical techniques for performing a meta-analysis. A somewhat similar approach to that taken in the Wald article was taken by the National Research Council in its report.
189. The meta-analysis in the Wald article was carried out in order to ascertain whether there is an overall association between exposure to environmental tobacco smoke and lung cancer. Professor Wald and his co-authors included only studies in which exposure was assessed by whether the subject lived with a smoker. This was done because the view was taken that such individuals were likely to be more heavily exposed to environmental tobacco smoke than non-smokers living with non-smokers. They excluded three epidemiological studies from the analysis for reasons which the professor gave. However, two of the excluded studies were consistent with the overall result achieved and the third also reported a positive effect.
190. Professor Wald recognised that the value of an epidemiological study may
be diminished by any one of a number of errors. Of
these, misclassification
bias appears to me to be the most significant and, since it is a matter of
considerable importance in the
case, I set out in some detail what he said
about it. He said in his statement of evidence:
"13. Examining the epidemiological evidence as aThe meta-analysis carried out in the Wald article showed that there was a highly significant 35% increase in the risk of lung cancer among non-smokers living with smokers compared with non-smokers living with non-smokers. The relative risk of 1.35 was statistically significant at the 95% confidence interval. The authors of the study recognised that misclassification of some smokers as non-smokers had probably exaggerated the estimated increase in risk. Adjustment for this error reduced their estimated relative risk to 1.30. However, as people who live with non-smokers may still be exposed to other people's smoke they revised this estimate again to allow for the fact that a truly unexposed reference group was not used. The increase in risk among non-smokers living with smokers compared with the completely unexposed group was thus estimated by them as 53%, i.e. a relative risk of 1.53.
whole, particularly that relating to lung cancer among
non-smokers who live with smokers compared with non-smokers who
do not, there is clear evidence of an association between
passive smoking and lung cancer. There are only two
explanations for this association; it either represents a
direct and causal effect of exposure to environmental
tobacco smoke, or it may be due to systematic error (i.e.
bias) or both explanations may in part apply. After
careful consideration of all the potential sources of bias
it can be concluded that only one source of bias must have,
to some extent, exaggerated the magnitude of the observed
association; this has become known as the misclassification
bias. This bias will tend to introduce a spurious
association between passive smoking and lung cancer. It
arises from the combination of three effects. Firstly, some
people who say that they are not smokers are in fact
smokers, or have smoked in the past. Secondly, smokers
tend to live with smokers. Thirdly, smoking is an important
cause of lung cancer. It follows that in a group of
reported non- smokers there will be some who, by virtue of
having in fact smoked, will have a higher risk of lung
cancer and also will be more likely to live with a smoker
than would be the case if they were genuinely non-smokers.
This will tend to produce an artefactual association between
passive smoking and lung cancer among self-described non-smokers.
14. It is possible to estimate the magnitude of each of
the effects that contribute to the bias, namely the
proportion of misclassified smokers, the relative risk of
lung cancer in those misclassified and the extent to which
smokers live with smokers. With this information, together
with estimates of the prevalence of smoking, one can
estimate the magnitude of the bias. This reveals that the
bias is very unlikely to explain the observed association
between passive smoking and lung cancer. In my opinion, the
observed association could only be completely explained in
this way if unreasonably high estimates of the magnitude of
the effects that contribute to the bias were used.
15. The validity of the misclassification bias depends
on the close association between active smoking and lung
cancer, an association that is accepted by scientists as
being causal. Invoking the bias accepts this link between
active smoking and lung cancer as well as the need to revise
the observed relative risk between passive smoking and lung
cancer to allow for the bias. It is illogical to accept it
for one purpose but not for the other. It illustrates the
importance of considering the evidence on lung cancer in
relation to active and passive smoking together, recognizing
the qualitative similarities in the two exposures and the
expectation that a little of what causes a large increase in
risk will still cause an increase in risk, albeit to a
smaller extent. It also demonstrates how it is necessary
when judging whether the association between passive smoking
and lung cancer is causal to have an informed view on this
issue with respect to active smoking and lung cancer. To
hold a view on the former without holding one on the latter
is logically untenable."
191. I have already referred to the fact that the National Research Council carried out a somewhat similar exercise. In the NRC report the relative risk of "exposed" non-smokers compared with truly "unexposed" non-smokers is stated to be 1.42.
192. The authors of the Wald article stated their conclusions in the
following terms:
"We conclude that breathing other people's tobacco smoke193. The authors estimated that about a third of the cases of lung cancer in non-smokers who lived with smokers, and about a quarter of the cases in non-smokers in general, may be attributed to exposure to environmental tobacco smoke.
does cause lung cancer, and our conclusion rests on several
observations. Firstly, carcinogens in tobacco smoke are
released into the air. Secondly, tobacco smoke is breathed
into the lungs by non-smokers. Thirdly, the general view
is that exposure to carcinogens does not have a threshold
below which there is no effect. Fourthly, people known to
have an increased exposure to environmental tobacco smoke
seem to have an excess risk of lung cancer, which is not
explained satisfactorily by bias. Fifthly, the magnitude
of the excess seems reasonable in view of the extent of
exposure and, sixthly, there is a dose response relation
between the extent of exposure and risk. In view of all
these observations, we could not have concluded otherwise."
194. Professor Tweedie (a witness called the respondent) identified potential sources of bias in most, if not all, of the epidemiological studies upon which the Wald meta-analysis is based. Professor Wald agreed that it is always possible that any epidemiological study may be affected by bias, but he did not think that this potentiality affected the validity of the exercise which he and his co-authors carried out. He said that the real issue is not whether there is a potentiality for bias. Rather, it is whether there is error of such character and magnitude that it has systematically disordered the results of the study in such a way as to lead to an association between passive smoking and lung cancer that would not otherwise have been observed. He said this had not been shown to have been the case. In particular, he did not think that Professor Tweedie's criticisms of the Hirayama and Trichopoulos studies showed them to be so flawed as to warrant their exclusion from the meta-analysis exercise. The voluminous evidence on this issue (and many other issues) is impossible to summarise in these reasons. However, I find Professor Wald's evidence on this matter most persuasive and I do not think that his meta- analysis was shown to be seriously flawed. As I have observed, the result of it is not greatly different from a similar exercise carried out by the National Research Council.
195. Dr Layard, another witness called by the respondent, expressed the opinion that the epidemiological studies upon which the Wald article is based lack consistency. Professor Wald holds a different view. In his opinion the undoubted variation in the point estimates in the studies is consistent with the sort of random variation that one would expect from a number of studies.
196. Dr Layard thinks that the utility of meta-analysis is very limited and that studies cannot be combined in a meta-analysis if the results in any of them may be due to bias or confounding. Professor Wald agreed that any epidemiological study which is so flawed as to make it uninformative should not be used as evidence, whether alone or in combination with other studies, in making a meta-analysis. However, he thinks that a study that is sufficiently sound to be considered as evidence on its own is eligible for inclusion in a meta-analysis. He agreed that a flawed study cannot be improved by inclusion in a meta-analysis. But he thinks that a sound study, albeit too small to show an effect on its own, can be used with other studies to show an effect. He agreed that meta-analysis cannot overcome bias, but said it can be used to overcome random error from small numbers in small studies.
197. Professor Wald was careful to point out that the risk ratio derived from a meta-analysis is a "summary estimate" of a given effect. That is to say, it is not the measure of the effect which will be applicable in all situations surveyed in all the epidemiological studies upon which the meta-analysis is based. In some social groups, exposure to environmental tobacco smoke may be more intense than in others and in these one would expect the effect of exposure to be greater. He illustrated his view by the observation that since room sizes in Japan are smaller on average than in the United States, exposure to environmental tobacco smoke in Japan is greater than in the United States. Hence one would expect that the relative risk estimate would be greater in the Japanese studies than in the American studies. But he thought that differences of this kind were no reason to conclude that the two sets of data cannot be combined to obtain an overall summary effect or to ascertain the overall level of statistical significance.
198. On a separate matter, Professor Wald said that cotinine is a reasonably sensitive measure of exposure to passive smoke and that it has many advantages in that respect over other markers (T.4352). He accepted that estimates of doses of tobacco smoke based upon cotinine measurements need to be considered cautiously (T.4404). He agreed that mainstream and environmental tobacco smoke differ in some respects, but thought that their similarities are more striking than their differences (T.4404).
199. On another separate matter, Professor Wald expressed the opinion that Dr Varela's thesis, which formed part of the respondent's case, lent some weight to the conclusion that passive smoking causes lung cancer. He accepted that the data analysed by Dr Varela are consistent both with no association between lung cancer and exposure to environmental tobacco smoke in the home and with the positive association reported in both his meta-analysis and the NRC report. However, he drew attention to Dr Varela's examination of the association between exposure to environmental tobacco smoke as measured by the total number of smokers in the household expressed in terms of the number of person-years of passive smoke exposure. This examination showed a statistically significant association between such exposure and lung cancer. These apparently inconsistent results suggested to him that in some studies spousal smoking alone may be a poor way of categorising a person's exposure to environmental tobacco smoke.
200. As is apparent from the statement of the conclusions in the Wald article, Professor Wald's opinion that passive smoking is a cause of lung cancer is by no means based only on the statistically significant association he and his co-authors found between lung cancer and passive smoking. I think the difference between his views and those of the other epidemiologists called by the applicant, and the views of witnesses called by the respondent is explained by the broader approach taken by the former group of witnesses.
201. Professor Wald and the other witnesses called by the applicant tended to regard the separate items of scientific material (e.g. epidemiological studies, the "no threshold" for carcinogens theory, the presence of carcinogens in environmental tobacco smoke, and cotinine levels in non-smokers) as constituent parts of a mosaic, each piece itself representing some evidence that environmental tobacco smoke causes cancer in non-smokers. On the other hand, the respondent's witnesses tended to evaluate each piece of evidence in isolation. I think therein lies the explanation for much of the collision of opinion between the witnesses for the parties.
202. Professor Wald sees the epidemiologist as one of a team, the members of
which collaborate in reaching a judgment. He said (T.4251):
"I am an epidemiologist. I am not a mathematician or a203. I was left with the impression that Professor Tweedie and Dr Layard do not take the same approach to their discipline, which is the science of statistics. I am inclined to think that they tended to work within their own discipline and that, accordingly, they tended to take a narrower approach when considering whether the whole of the available data warranted a conclusion as to a causal link between passive smoking and lung cancer.
statistician, but epidemiologists by nature of their work
collaborate closely with biologists, scientists, clinicians,
statisticians and work together with them as a team, and in
much of the work I do their components are performed by
colleagues and the responsibility for the different
components will vary depending on the different skills. In
computing the mathematical calculations that are involved in
some of these analyses I rely heavily on statistical
colleagues as do many - in fact all my epidemiological
colleagues, Richard Doll, Prof. Trichopoulos and others.
But at the end of the day I have to satisfy myself that what
has been performed by my colleagues is sound and is a
correct reflection of the scientific position and have to
accept the responsibility for it, but I cannot say that I do
every component bit of calculation. Indeed nor do they.
They rely very much on other contributions in order to reach
their judgments."
204. I have already observed that Professor Wald was a member of the National
Research Council's Committee on Passive Smoking which
produced the NRC report.
He prepared the first draft of Chapter 12 of the report, which deals with
exposure to environmental tobacco
smoke and lung cancer. He said that his
draft was worked on by others and also sent informally to scientific referees.
Before the
report was published it was sent to independent experts to judge
whether it was in a satisfactory form. He said that he agreed
with the
general conclusions in the document as finally settled, and that he still
adhered to the views expressed in it (T.4362).
(h) Dr Layard
205. Dr Maxwell Layard is a partner in a firm of consulting statisticians based in California. He was formerly an Assistant Professor of Mathematics at the University of California. From 1973 to 1979 he was a statistician in the Mathematical Statistical and Applied Mathematics Section of the National Cancer Institute. From 1979 to 1983 he was Senior Biostatistician at the United States Veterans' Administration clinical trials centre in California where he was involved in the planning and management of medical trials and served as technical adviser to the centre on statistical and clinical trials methodology. He has served as a referee for papers submitted to several medical and statistical journals.
206. Dr Layard holds the opinion that the statement:
"There is little evidence and nothing which proves207. Dr Layard reviewed the same studies as were considered by the applicant's witnesses, and which are referred to in the primary articles. In his opinion they do not establish a convincing statistical association between environmental tobacco smoke exposure and lung cancer. He analysed the published data and formed the opinion that, collectively, they failed to satisfy the accepted criteria for epidemiological evidence which would enable them, if corroborated by other evidence, to support an inference of causation.
scientifically that cigarette smoke causes disease in
non-smokers" accurately summarises the epidemiological evidence
available in July 1986 regarding environmental tobacco smoke
and cancer. He is also of the opinion that the statement
accurately summarises the epidemiological evidence available
at the time he gave his evidence. His opinions are based
on his review of the published reports of studies of
environmental tobacco smoke and the incidence of cancer.
208. Dr Layard's opinion as to the matters which must be proved to
demonstrate a causal association between an exposure and a health
effect and
his acknowledgment that the discipline of the statistician does not extend to
all those matters appears in the following
passage in his evidence:
"In assessing whether epidemiologic evidence reflects a209. It is plain from this passage that Dr Layard places greater emphasis on statistical significance than do the applicant's witnesses. Also his view that epidemiological evidence must be corroborated by other types of evidence before a causal inference can be drawn is not shared by many epidemiologists including Sir Richard Doll.
causal association between an exposure and a health effect,
it is first necessary to consider whether the data
demonstrates a statistically significant association, that
is, an association which is unlikely to be due to chance.
If a statistically significant association has been
demonstrated, it is then necessary to assess the validity
and weight of the evidence in the light of criteria, such as
strength and consistency of association, which refer to the
epidemiologic studies themselves. However, even after these
criteria have been considered, epidemiologic evidence must
be corroborated by other types of evidence before it is
appropriate to draw a causal inference. The biologic
plausibility of an observed association between exposure and
health effect must be considered. Considerations of
biologic plausibility involve such matters as knowledge of
disease mechanisms, coherence with known facts about the
natural history of the disease in question, and toxicologic
experiments with animals which avoid problems of confounding
and bias typically seen in epidemiologic studies. However,
these considerations are outside the scope of my expertise,
and I confine my comments in this statement to the
interpretation of data from the relevant epidemiologic
studies of ETS and cancer."
210. In Dr Layard's opinion, only the Trichopoulos and Hirayama studies reveal statistically significant associations and those studies are open to serious criticism. He thinks the studies as a whole do not establish a statistically significant association between exposure to environmental tobacco smoke and lung cancer. He acknowledged that the National Research Council had carried out a meta-analysis of all the studies (except that of Wu et al) which he had considered and that its meta-analysis produced a combined relative risk of 1.34 which was statistically significant. But he disputed that it was appropriate to combine the results of studies in this way.
211. He said that the meta-analysis carried out by the National Research Council might be flawed because of publication bias in the literature. I recognise, as did the applicant's witnesses, that publication bias may occur in a given situation but I think it is quite unlikely to have occurred in the publication of studies dealing with the health effects, if any, of passive smoking. If studies had been produced by competent epidemiologists negativing any association between passive smoking and disease it is likely that, for the reasons given by Professor Wald (T.4236-7 and Ex. SS, pp 8-9) they would have found a publisher.
212. Dr Layard is also of the opinion that meta-analysis should not be used unless the several studies in the analysis are reasonably comparable with respect to demographic and social characteristics of the study populations, disease diagnosis and other factors. He thinks the studies display substantial diversity in these and other areas and that most of them are not methodologically sound or free from potential biases and confounding factors which might have distorted their results. He pointed to the fact that some of the studies show quite small associations and may have been the result of bias and confounding factors to the extent that they were not simply due to chance.
213. Dr Layard is very firm in his opinion that if a statistically significant association is not demonstrated by the data then it cannot be used as evidence in a process of drawing a causal inference.
214. As with the evidence of other witnesses, it is not possible in these
reasons to give more than a summary of Dr Layard's evidence.
He made the
point that the relative risks revealed by most of the studies are, for the
most part, fairly weak. This point is
well made in the following table which
forms part of his evidence: Stud Sex Number of
Cases Relative Risk
Exposed GroupRelative Risks
M 5 1.00Buffler et al., 1984 F 33 0.80
M 5 0.51Gillis et al., 1984
M 8 1.31Garfinkel et al., 1985 F 92 1.12
.../Relative Risks Above 2
215. Dr Layard regards a relative risk of less than 2 as weak. There is a degree of disagreement between the epidemiologists as to what constitutes a weak association, but I think there would be general agreement that a relative risk below 1.5 is weak.
216. It is important to note the different approach taken by the statisticians (called by the respondent) and the epidemiologists (called by the applicant) to low relative risks revealed in the studies under consideration in the present case. The statisticians, as exemplified by Dr Layard, regard low relative risks as evidence only of a weak association. On the other hand, the epidemiologists, as exemplified by Professor Wald, took into account the strong association between active smoking and lung cancer and regarded the relative risks disclosed in the studies as evidence of a strong association at a low dose (Wald T.4227). It is plain that the epidemiologists' interpretation of the data revealed in the studies is affected by their belief that there is a strong association between cigarette smoke and cancer in active smokers.
217. Dr Layard referred to inconsistencies in some of the results in the studies, the absence in many of them of dose response relationships and the possibility of various types of bias having given rise to apparent associations that might have been spurious. Moreover, he questioned the soundness of the methodology upon which the studies were based. He said that they were all open to criticism for flaws in their design and execution.
218. I think that Dr Layard was hypercritical in his approach to the studies. They all were carried out by apparently highly competent researchers. Scientists of high repute do not share Dr Layard's jaundiced view of them. Not only the applicant's witnesses but also the many highly skilled authors of the reports produced by the United States Surgeon General, the National Research Council, and the National Health and Medical Research Council failed to perceive in the reports many of the defects which Dr Layard found in them. In making this observation I do not overlook some the highly relevant matters referred to by Dr Layard, e.g. internal inconsistencies in the Hirayama study.
219. A good deal of Dr Layard's practice is work undertaken on behalf of law firms who represent tobacco companies. Such work accounts for approximately 80% of his practice. The work includes the statistical analysis of published data relating to environmental tobacco smoke and health effects, and the presentation of papers which he has written at the request of law firms acting on behalf of tobacco companies. Plainly he has a very close association with the tobacco industry and depends upon it for most of his income. Not unnaturally, these matters were relied upon by counsel for the applicant as justifying the Court in taking a cautious approach to his evidence. I do not think that Dr Layard expressed opinions which he does not hold, but I do think his hypercritical approach to the epidemiological studies may not be disassociated with his close connection with the tobacco industry.
220. I think that even if all the epidemiological studies had been methodologically sound, free from bias of all kinds, free from confounding factors, and had consistently revealed statistically significant relative risks, Dr Layard would not have accepted them as proof that passive smoking is a cause of disease. When asked whether epidemiological studies had demonstrated a causal relationship between active smoking and disease he said that - "it would be more accurate to say that epidemiologic studies suggested the possibility of a casual relationship." (T.2631).
221. Dr Layard concluded his proof of evidence with the statment that it is
his opinion that little evidence and no scientific proof
exists as of the
present time that cigarette smoke causes cancer in non-smokers. He agreed with
counsel for the applicant that in
expressing this opinion he did not have
regard to the evidence that exists in relation to biological plausibility
because that is
not an area within his area of expertise (T.2650).
(j) Professor Tweedie
222. Professor Richard Tweedie is Dean, Information and Computing Sciences, at Bond University in the State of Queensland. He was formerly Associate Professor in the Department of Mathematics at the University of Western Australia and a Principal Research Scientist with the Division of Mathematics and Statistics in the Commonwealth Scientific Industrial Research Organisation.
223. Professor Tweedie's evidence fell into three broad categories. First,
he gave an explanation of what he considered to be the
requirements of
scientific proof, particularly from the basis of statistical reasoning.
Secondly, he made a detailed analysis of
and comments upon the epidemiological
studies referred to in the primary articles. Thirdly, he stated his conclusion
as to the effect
of the evidence after a consideration of those studies. His
conclusion was expressed in the following terms:
"Scientific proof requires consistent, significant results in224. In his written proof of evidence the professor did not express any opinion on the question whether or not it was correct to say that there is little evidence that cigarette smoke causes disease in non-smokers. At the conclusion of his evidence in chief he was asked his opinion on that matter and he said that he believed the statement to be accurate (T.2444). He made it plain in cross-examination that he had considered only the question of lung cancer, and not any other disease. He also conceded that in considering the accuracy of the statment in the advertisement he had considered only whether or not there was any scientific proof to be found in the epidemiological studies. As this is a matter of some importance I set out some of his evidence with respect to it:
repeated studies designed to test the hypothesis in question.
Virtually the whole case for an association between lung cancer
in women and exposure to ETS rests on the data from the study
by Trichopoulos et al, and that study is seriously flawed.
"I cannot detect any scientific proof, in the papers I have read,
of an increased risk in lung cancer from an association with
exposure to ETS."
"You did not direct your attention to other data that may be226. The impression I gained from the professor's evidence was that he had really concerned himself only with whether there was scientific proof, as distinct from little evidence, whether cigarette smoke causes disease in non-smokers.
obtained, for example, biological data of exposure of animals to
tobacco smoke? --I have read one or two papers on that subject but
in terms of the effect on lung cancer in humans I did not read
that as evidence.
"You did not direct your attention to other data that may be
obtained, for example, biological data of exposure of animals
to tobacco smoke? --I have read one or two papers on that subject
but in terms of the effect on lung cancer in humans I did not read
that as evidence.
And you paid no regard to the biochemical analysis of tobacco smoke
as between what is described as mainstream smoke, that is the smoke
drawn from the filter and environmental tobacco smoke that is side
stream smoke from the burning tip of the cigarette and exhaled
mainstream smoke?--That is not correct. I actually did read two or
three papers on that subject but as far as determining whether
that is relevant to the effect on human beings I do not believe
it can do other than add to the biological plausibility argument
which is part of scientific proof as opposed to whether or not
it does in fact cause harm.
But your limited reading of that material, was that able to assist
you in relation to the biological plausibility or did you not consider
that aspect?--I do not believe I am expert at considering that. It
certainly did not sway me to make a statement saying there is no
biological plausibility.
I am sorry, say that again? It did not?--It did not lead me to make
a statement saying there is no biological plausibility.
Thank you?--But I do not believe that is something I am expert in.
And I take it that nor did you examine the epidemiological data in
relation to direct smoking and lung cancer?--I have not read any
studies on that except insofar as some of the studies on exposure
to ETS have some small amount of active smoking data in them.
But to the extent that that data exists, would you agree with me
that it may assist another person to form some view as to the
biological plausibility of some of the hypotheses that are
being examined in the epidemiological data you examine?--It would
certainly seem to me to be a relative (sic) factor in deciding on
the biological plausibility - - -
And in that context, considering the phrase, there is little
evidence and nothing that proves scientifically that cigarette smoke
causes disease in non-smokers, you did not attempt to assess
whether or not there was little evidence or more than little
evidence, rather, you focused on the question of whether you could
detect any scientific proof. Is that correct?--I focused on the
question of whether I could detect any scientific proof in the
question of lung cancer, yes, that is correct."
(T.2445-6)
227. Professor Tweedie made it clear that he thought that, on his approach,
statistical significance was essential to scientific
proof. That this is so
appears from the following passages in his evidence (T.2383):
"HIS HONOUR: As I understand your approach and I do understand it I228. It is apparent that Professor Tweedie's approach to the question of scientific proof is fundamentally different from that taken by the epidemiologists called in the applicant's case. In the first place, statistical significance to them is a guide to thought, rather than a prerequisite of proof. And in the second place, they take into account non-statistical considerations such as biological plausibility and reliance upon trends shown in epidemiological studies, even though the trends be observed in non-statistical results.
think, you say that statistical significance is essential to
scientific proof?--I believe absolutely that it is, yes.
If you are looking - I mean, once you resort to statistical analysis
or epidemiological analysis you say that you have not got
scientific proof unless your conclusion is based on statistically
significant results; is that right?--I believe that very firmly,
I think."
229. The different approach of the epidemiologist and the statistician can be seen in some evidence which Professor Tweedie gave as to the Hirayama study. He agreed that Hirayama found an odds ratio of 2.23 in respect of persons aged between 40 and 59 years who were married to smokers of 20 or more cigarettes per day, and that this result was statistically significant. However, since it was only one of a relatively small number of statistically significant results found by Hirayama amongst a greater number of non-statistical results, Professor Tweedie thought it might be the result of data-dredging. He thought that the result may show a true association between passive smoking and lung cancer, but the result had not been shown to be incompatible with chance. When he was asked whether he had gone through the various studies to ascertain whether the statistically significant results appeared generally to be in the cases where there had been a high level of smoking by the husband he said he had not done any analysis to check whether this was so. Similarly, when it was suggested that the statistically significant results in the studies also tended to be in older age groups he said he had not done an analysis to check that. He was thus unable to agree with the proposition that the statistically significant results accorded with biological plausibility of the development of lung cancer in that the disease is dose-related and is marked by a long latency period. Indeed, when cross examined on this matter, senior counsel for the respondent objected to the questions on the ground that the professor eschewed any medical knowledge when giving his evidence in chief (T.2464)
230. Thus it will be seen that Professor Tweedie did not look for additional factors which the epidemiologists thought were of great importance in deciding whether there was a casual relationship between passive smoking and lung cancer.
231. It would be impossible in these reasons to capture the enormous detail of the criticisms made by Professor Tweedie of the studies referred to in the primary articles. The fact that I do not attempt to do so is no indication that I think that the studies are above criticism. But in general, I think he was over-critical of the methodology in most of the studies and gave more weight to potential flaws in them than was warranted.
232. In respect of the Hirayama study he thought it should be treated as hypothesis-generating and therefore unable to be used to prove or disprove the hypothesis itself. This is a criticism of the study which Professor McMichael regarded as unwarranted because of the existence of the hypothesis, which had been formed prior to the study being undertaken, as to the effect of mainstream smoke on smokers.
233. Professor Tweedie questioned the representativeness of the date in the Hirayama study. However, the relevance of this criticism was discussed by Professors McMichael and Wald (T.1322 and T.4302-3) and discounted. A similar attitude is taken in the Surgeon General's report (p 75).
234. The possibility of misclassification because death certificates were used by Hirayama as an indication of lung cancer was stressed by Professor Tweedie. But as it pointed out by some commentators, there is no reason to believe that error in recording the causes of death of wives was influenced by the smoking habits of their husbands, and if any misclassification of this kind took place it was likely to be random.
235. Professor Tweedie also expressed concern as to the reliability of the Hirayama study because of the possibility of misclassification of smokers as non-smokers. He noted that when the study was carried out smoking by women was neither common nor accepted in Japanese society, and he thought many smoking women may have desribed themselves as non-smokers. However, as the Surgeon General points out in his report, there is some assurance of the reliability of the smoking data provided by the Japanese women in the Hirayama case from results obtained from other studies. This is not to say, of course, that no misclassification occurred. But the professor seemed to me to take an excessively cautious approach on this matter, as with some other matters.
236. Professor Tweedie also pointed out that in the Hirayama study the smoking habit of the subject's husband was used as the indicator of exposure and that this is not necessarily an adequate measure of exposure. I agree that classifying non-smokers women upon the basis only of their husbands' smoking habits gives an imprecise measure of exposure. Obviously most non-smoking women will be exposed to passive smoke other than that generated by their husbands' smoking. Nevertheless, the classification based on the smoking habits of husbands seems to me to be a reasonable, if inexact, basis of classification.
237. Professor Tweedie also thought there were many potential confounding factors in the Hirayama study which had been unaccounted for. Some of these were occupation, diet, medical care, family history, lifestyle and home environment. It may be almost impossible to totally exclude the possibility of some of these being potential confounding factors but this is not to say that the study does not have a value when taken in conjunction with other studies.
238. I have already referred to Professor Tweedie's criticism of the statistically significant result found in respect of the 40 to 59 years age group where the husband smoked more than 20 cigarettes per day. He said it was data-dredging to use this admittedly statistically significant result. However, Dr Layard did not take the same view on this matter. (T.2658-9)
239. Professor Tweedie thought the Trichopoulos study afforded some support for an association between lung cancer and exposure to environmental tobacco smoke. He accepted that it was not hypothesis-generating and that some of the results were statistically significant. However, he thought that the study was so flawed as to render it incapable of providing data concerning an association between lung cancer and exposure to environmental tobacco smoke to which strong scientific credence can be given. He accepted that there was "some level of scientific credence in the study" (T.2521).
240. Professor Tweedie's criticisms of the Trichopoulos study were put to Professor Trichopoulos when he gave evidence and I shall not repeat them or his answers to them. As Professor Trichopoulos acknowledged in his published article, his study had obvious limitations, in particular, that the numbers of cases were small.
241. The study by Garfinkel was said by Professor Tweedie to be flawed particularly by possible misclassification and the measurement of environmental tobacco smoke. The criticisms of this study are noted in the Surgeon General's report where it is observed that the misclassification which may have occurred could have led to an underestimate of the effect of passive smoking.
242. As I have observed it was not asserted by the applicant's witnesses that some of the criticisms levelled at the studies by Professor Tweedie did not have some justification. There is therefore little point in seeking to identify all those criticisms. However, even if all the studies had been free from the criticisms made of them by Professor Tweedie, he still would have been persuaded that they proved a casual link between passive smoking and lung cancer.
243. Professor Tweedie carried out combined analyses for both the case
control studies and for the cohort studies. The overall result
for the cohort
studies was significant at the 5% level, whilst the overall result for the
case control studies was marginally insignificant
at that level. He pointed
out the Trichopoulos study dominated the case control analysis, and the
Hirayama study the cohort study
analysis. When those studies were omitted, the
results obtained were not statistically significant. However, I cannot see
any justification
for omitting them, nor did Professor Wald (Ex. SS, p 11).
(k) Professor Witorsch
244. Professor Phillip Witorsch is a physician and is currently Clinical Professor of Medicine, Adjunct Professor of Physiology, and Director, Section of Environmental Medicine and Toxicology in the Department of Medicine at the George Washington University School of Medicine and Health Sciences. He is also medical director at the Center for Environmental Health and Human Toxicology at the George Washington University Hospital. He is a Fellow of the American College of Physicians and of the American College of Chest Physicians and has served as an adviser and consultant to a number of Federal agencies in the United States, as well as to a number of industry and private groups, including the Tobacco Institute of the United States and the Tobacco Institute of Australia. Since 1985 he has been involved in the evaluation of data relating to a number of aspects of environmental tobacco smoke as a paid consultant to the Tobacco Institute of the United States of America.
245. He is the author of many articles which have been published in medical and scientific journals. Most of his time is now spent in clinical practice, medical teaching and scientific research.
246. Professor Witorsch is of the opinion that the statement made in para. 3 of the advertisement is an accurate characterisation of the evidence concerning environmental tobacco smoke that existed as at July 1986 and that it is still accurate when measured against the evidence that currently exists. He gave evidence as to the alleged association between passive smoking and lung cancer, respiratory disease in adult non-smokers, respiratory disease and respiratory function in children and cardiovascular disease. I shall consider in this section of my reasons only that part of his evidence as relates to the alleged association between passive smoking and lung cancer.
247. Professor Witorsch did not claim to have any special expertise in research into the causes of lung cancer. He said he was not an epidemiologist but that he did have some expertise in the field. (T.3114).
248. He is of the opinion that quantitative and qualitative differences between mainstream and environmental tobacco smoke are such that one cannot reach menaingful conclusions regarding passive smoking and disease by extrapolating from experimental and epidemiological data relative to active smoking. He said that inhalation exposure patterns differ between active smokers and non-smokers exposed to environmental tobacco smoke in that active smoking involves intermittent high dose exposure through the mouth with the constituents being inhaled deeply and retained in the lungs, whereas passive smoking involves low dose explosure in which tobacco constituents are not necessary deeply inhaled. He said that such differences in inhalation patterns may explain why only about 11% of the particulate portion of environment tobacco smoke is retained by respiratory tract, while retention of maintstream smoke particulates ranges from 50-80%.
249. In his opinion results of epidemiological studies can suggest an association which, when taken together with other appropriate evidence, may provide support for the formation of a judgment as to a casual relationship between an exposure and a disease outcome. But he thinks they cannot, by themselves, prove that such a relationship exists. Consistent with this opinion, he holds the opinion that it has not been proved scientifically that maintstream smoke causes lung cancer in active smokers.
250. Professor Witorsch referred to the possibility of epidemiological studies being affected by matters such as bias and misclassification. He thinks that since there is an acknowledged tendency for smokers to marry smokers, some of the subjects in the studies who were considered to be non-smokers may actually have been current or ex-smokers, and that such misclassification could have resulted in artificial increases in the risk ratios reported. He said that some of the epidemiological studies concerning environmental tobacco smoke and the incidence of lung cancer suggest an association between the two, whilst others do not.
251. He commented on individual studies, pointing out that many of them gave results which were not statistically significant. He is of the view that all of the epidemiological studies have methodological and other problems that made it difficult to reach meaningful conclusions regarding the hypothesised association between environmental tobacco smoke exposure and increased incidence of lung cancer.
252. He thinks the studies were affected, in particular, by problems of inadequate verification of exposure to environmental tobacco smoke and inadequate validation of the smoking status or classification of the study subjects. In his opinion an acceptable biological or environmental marker of environmental tobacco smoke exposure is desirable in an epidemiological study so as to be sure that the exposed group is indeed exposed. He thinks that reliance upon questionnaires lead to a higher probability of exposure misclassification.
253. I have no doubt that acceptable biological or environmental markers would reduce the incidence of misclassification, but that is not to say that in their absence responses to questionnaires do not provide a sufficiently sound basis for classification.
254. Professor Witorsch made criticisms of the studies similar to those made by Professor Tweedie. For the most part, he referred to criticisms of the studies made by other persons and adopted them. This is understandable in view of the fact that he did not claim to be a specialist epidemiologist.
255. He questioned the meta-analysis exercises carried out by Professor Wald and the National Research Council because he thought they are based on a number of questionable assumptions, particularly the assumption that spousal smoking is a valid and reliable surrogate index for environmental tobacco smoke exposure.
256. Professor Witorsch made no mention in his proof of evidence of some
matters which epidemiologists think are of great importance
in reaching a
conclusion whether there is a casual association between passivie smoking and
lung cancer, e.g. whether environmental
tobacco smoke contains carcinogenic
substances and whether there is no safe dose for carcinogens. In his opinion,
the question whether
exposure to environmental tobacco smoke is associated
with an increased risk of lung cancer remains unresolved.
(l) Professor Huber
257. Professor Gary Huber has been Professor of Medicine in the Department of Medicine at the University of Texas Health Center since 1985. He has been associated with research, teaching, diagnosis and treatment in the field of pulmonary medicine since 1962. He has been interested in and associated with research into smoking, tobacco smoke and health since 1972 when be became Director of the Smoking and Health Research Program at the Harvard Medical School, Boston. This program was initiated jointly by the Harvard Medical School and by the major cigarette manufacturers in the United States, with the intent of developing a multi-disciplinary evaluation of the potential health effects of tobacco smoke.
258. Professor Huber is of the view that the statement made in the advertisement accurately describes the state of the evidence both as at July 1986 and at the present time. He thinks a major difficulty in studying the health effects of environmental tobacco smoke on non-smokers is that non-smokers are exposed to a mixture which is both qualitatively and quantitatively different from that to which active smokers are exposed. He also thinks it is not scientifically appropriate, in the present state of knowledge, to transpose theories concerned with active smoking and health into the field of health issues related to environmental tobacco smoke.
259. Professor Huber said that although different researchers have reported different levels of nicotine in the atmosphere of places in which smoking occurs, all of the levels reported are low and the majority of reported data indicates that, overall, tobacco smoke contributes very little to indoor environmental pollution. This is a judgment which appears to me to be inconsistent with common experience of some indoor environments.
260. He said that the constituent chemical components in environmental tobacco smoke include benzo(a)pyrene and other constituents which are found in minute quantites in mainstream smoke and in even smaller quantities in environmental tobacco smoke. These are hydrocarbons and can, when applied at high concentrations in condensate form, produce tumours. In his opinion, it has not been demonstrated and it is highly improbable that they present a risk of cancer in humans in the concentrations at which they are found in environmental tobacco smoke.
261. Professor Huber's evidence related mostly to relationships between environmental tobacco smoke and cardiovascular diseases, acute pulmonary effects, chronic pulmonary effects in adults and children, and asthma. He did not claim to have any special expertise in cancer epidemiology.
262. He agreed (T.3724) that there are chemicals, such as vinyl chloride, exist both in mainstream smoke and sidestream smoke and that vinyl chloride had been shown to be carcinogenic in humans. He would not agree, however, that a passive smoker who inhales environmental tobacco smoke may inhale smoke which contains vinyl chloride. He said that some things cannot be detected in environmental tobacco smoke that can be measured in sidestream smoke. He does not know whether vinyl chloride had been detected in environmental tobacco smoke or not. He agreed that it was possible that a small child being nursed by a woman smoking a cigarette might inhale a molecule of vinyl chloride.
263. When asked whether it is generally accepted that a safe threshold is
unlikely to exist for most carcinogens, Professor Huber
said that he did not
know the exact answer to the question. When pressed with the exact answer to
the question. When pressed with
the question: "Do you agree that it is
unlikely that there is a threshold of low dose exposure to carcinogens below
which there is
no increase in risk?", he answered: "I would think that there
would be a threshold below which the risk is so small that it could
not be
measured." He agreed in cross-examination that in an article which was
published in January 1990 and of which he was the
co-author the following
statements appeared:
"As summarized by the Surgeon General there is little disagreement264. With respect to the last mentioned passage he said he had since expanded his reading signicantly and that, at the time he wrote the article, it was the best information he had. He also said that if he were to write the paper again, he would write it differently. I am bound to say that I found some of his answers unsatisfactory, as he did not persuade me that any significant body of scientific material had come to his notice since the paper was written.
that active smoking is associated with an increased risk for the
development of lung cancer, with a causal and probable does
response relationship between tobacco smoking and the
development of lung cancer."
"Furthermore there does not seem to be any safe threshold for an
absolute lower limit of tobacco smoking and the occurrence of lung
cancer."
"Depending on the extent of exposure the non-smoker may be exposed
to clearly quantitatively lesser amounts of smoke but for some
components qualitative exposure of the non smoker may differ little
from the active smoker."
265. Dr Huber claimed that the abovementioned statements had been taken out
of context, and in this respect the following excerpt
from his evidence is
relevant:
"MR FRANCEY: You complain, doctor, that two sentences I read to you266. I did not find Professor Huber a satisfactory witness in all respects. I thought, with all respect to him, that he was sometimes evasive in his answers. That this is so appears, I think, from the following passage in his evidence:
about threshold and similarity of the quality of smoke that non-smokers
are exposed to and smokers are exposed to were taken out of
context. Can I ask you this then, that in writing that article by
way of summary in relation to lung cancer you were of the view last
year that some of the existing data show a positive assocation
between passive smoking and lung cancer, although these data do not
always necessarily meet strict criteria of causality in this
association but considering the large number of persons exposed
to passive smoking, even the most minimal potential association
for the development of lung cancer in non smokers cannot,
however, be ignord?--I would agree with that.
And you would agree with it now?--Yes."
"HIS HONOUR: ... In your opinion, does active smoking cause267. I think Professor Huber is excessively cautious in drawing conclusions from available data. Of all the witnesses called by the respondent, I found him the least impressive.
cancer in some smokers?--In a susceptible group within the
smoking population.
No, leaving that aside. If I just ... asked you the question
whether in you opinion, does active smoking cause lung cancer in
some active smokers, what would your answer be?--My answer would be
the same. My answer would that there are associations and that
there are a variety of complex aspects to that question. I am not
trying to evade the question. I am trying to say it is a very
complex issue and that people who smoke develop lung cancer.
Would this be your answer and do not assent to it if it is not
right, would your answer be there is a strong, perhaps very strong
association between active smoking and the incidence of lung
cancer ... (but) I cannot say that there is a casual relationship
between the two?--There certainly is a strong association. I agree
with that. I do not understand the nature of the potential casual
relationship. I do not know that it is in tobacco smoke that might
cause cancer in humans. I know that there are 40 or 50 carcinogens
there that cause tumours in animals. I do not know which, if any of
those might be responsible for the induction of cancer in humans. I
do not know the mechanism by which that occurs. So I am left with a
strong association between cigarette smoking and the development
of cancer in some individuals and that is a strong association and
the mechanisms and the details of which have defied science to
this point. Does that answer your question?"
268. Dr Sven Malmfors is an independent consultant in toxicology and risk assessment. He resides in Sweden. He was, for a time, an Assistant Professor in the Department of Histology at the Karolinska Institute in Stockholm. Between 1972 and 1980 he was the head of the toxicology laboratory of a large pharmeceutical company. He left that position in 1980 to go into private practice as an independent consultant. He was worked part-time in the teaching of toxicology and the training of graduates in the science of toxicology. He is a past President of the Swedish Society of Toxicology.
269. In his capacity as a consultant, Dr Malmfors has spoken at seminars on behalf of the tobacco industry. Such seminars have been concerned with exposure to environmental tobacco smoke.
270. Dr Malmfors is of the opinion that the statement made in the advertisement was accurate at the time it was published and is still accurate. He said that a toxicological evaluation to determine the toxicity of a given chemical to humans requires the accumulation of data which may come from experimentation of epidemiology. Such experimentation may involve testing a biological system under artifical conditions in a laboratory, or experiments with animals or humans. He said if there are no experimental data other than epidemiological data, this is usually not sufficient from a toxicological point of view to establish a cause/effect relationship.
271. He draw attention to what he said were the qualitative and quantitative differences between mainstream and environmental tobacco smoke. He said unless particular chemicals, either alone or in the same combination, can be shown to be present in both mainstream and environmental tobacco smoke, it is not scientifically proper to extrapolate from mainstream smoke components to environmental tobacco smoke components or to use the former to found a reasoning process based on analogy. He thinks that data derived from experiments concerning the effect of mainstream smoke on animals is not relevant to the question whether passive smoking causes cancer in humans. The results of such experiments cannot, in his opinion, be extrapolated to exposure to environmental tobacco smoke.
272. It seems to me that Dr Malmfors' requirements for the establishment of
scientific truth are almost unattainable. Some idea
of the degree of proof
which he would require before being persuaded of a scientifically proved
cause/effect relationship between
environmental tobacco smoke and lung cancer
may be gained from the opinons which he expressed as to the proof (or absence
of it)
of a cause/effect relationship between active smoking and lung cancer.
His evidence included the following:
"HIS HONOUR: Would you agree that tobacco smoke contains several273. He said (T.2259) was unable to point to any evidence that showed there was a safe dose for any of the carcinogenic substances in tobacco smoke. He agreed that epidemiological studies have reported an association between active smoking and the incidence of lung cancer in smokers but he said, quite positively, that he did not accept that direct smoking causes lung cancer. He conceded that it was possible that there may be important toxicological data obtained from research in connection with active smoking that might throw light on the effect of environmental tobacco smoke, but that he had not studied it. I am bound to say that I found this concession surprising coming from a scientist of his calibre who is so closely interested in the effects of environmental tobacco smoke that he addresses seminars on the subject on behalf of the tobacco industry. I think it reflects a very narrow scientific approach and a reluctance to consider all available date which might contribute to an understanding of the effects, if any, of passive smoking.
agents which are cancer initiating and mutagenic?--Depends on under
which circumstances. There are chemicals in mainstream smoke which
under certain conditions initiate tumours and that is true.
Well under conditions which obtain when a human inhales the smoke?--No,
consider those conditions different from those conditions where there
are proof of (carcinogenicity) for those ...
I am not talking about ETS. I am talking about the active smoker?--Yes.
Is the smoke which he inhales, smoke which contains several agents
which are cancer initiating and mutagenic?--Yes, but the problem
is that they are not cancer inducing and mutagenic everywhere under
every condition. There are certain conditions which have to be
fulfilled before that, in effect, can occur.
Is it not your belief that those conditions are very often fulfilled
and that that leads to what is said to be an increased incidence of
lung cancer in active smokers?--I do not know which those conditions
are so I cannot comment on that."
(T.2270)
274. Professor John Clayton is Professor Emeritus of Pharmacology and Toxicology at the University of Arizona. He held the positions of Professor of Pharmacology and Toxicology and Professor of Microbiology and Medical Immunology at the University from 1974 to 1989.
275. He thinks that in order to evaluate a hypothesis as to whether or not environmental tobacco smoke causes chronic disease such as lung cancer in humans, scientists must consider two major types of data: epidemiological and toxicological. In his opinion, epidemiology alone is not sufficient to establish a cause and effect relationship. He thinks that well designed and well conducted animal experiments are required in addition to epidemiological data before it can be scientifically concluded that a particular agent causes a specific chronic disease. He knows of no animal inhalation experiments investigating the effects of environmental tobacco smoke as at 1 July 1986. In the absence of such studies he thinks there was no pertinent toxicological evidence at that time and that therefore, it had not been provided scientifically that environmental tobacco smoke caused chronic disease in non-smokers.
276. Professor Clayton said that there had been two animal experiments since July 1986 in which attempts had been made to measure the effects of environmental tobacco smoke on hamsters. One experiment revealed pulmonary changes in the hamsters, but of a kind which could have been expected to occur under similar exposure to other agents, e.g. dust. The investigators who carried out the other experiment reported that overall there was no marked increase in tumour incidence in animals exposed to either mainstream smoke or sidestream smoke over the normal lifespan of a hamster.
277. With reference to three studies referred to by Professor Stewart in his evidence, (Harris et al, Bernfeld et al and Dalbey et al) Professor Clayton said they were all studies concerned to simulate active smoking by exposure of mice, rates or hamsters to mainstream smoke, not environmental tobacco smoke. In any event, he thought there were other problems about the experiments, including that the concentrations of smoke used were very high and quite different from human exposure to environmental tobacco smoke. As to the theory that one molecule of a suspected carcinogen may initiate a carcinogenic process, the professor said there was no way to prove or disprove this theory.
278. Professor Clayton is of the opinion that toxicology has not provided any proof that mainstream smoke causes lung cancer in active smokers. As he said: "The toxicologist would say there is no demonstration that cigarette smoke inhalation causes lung cancer in humans." (T.2941). He accepted that some substances found in tobacco smoke, e.g. vinyl chloride and napthylamine are listed in the IARC report (Appendix Z at pp 389-94) as being chemicals in respect of which there is sufficient evidence that they are carcinogenic to both animals and humans. But as I understood his evidence, he was not prepared to concede that this was indeed the case.
279. The respondent tendered as part of its case Chapter 4 of the 1982 report of the United States Surgeon General on the health consequences of smoking in which the statement is prominently made that - "Cigarette smoking is the major single cause of cancer mortality in the United States."
280. Professor Clayton's views do not rest easily with this statement.
(o) Mr Leslie
281. Mr George Leslie is an independent toxicologist and pharmacologist. Between 1974 and 1987 he was head of the Toxicology and Pathology Department of Smith Kline and French where he worked on many projects of a toxicological nature. He has been a full time consultant in toxicology since 1987. He has lectured to students at a number of academic institutions, including London University and is an examiner of the candidates for the degree of Doctor of Philosophy in Pharmacology and Toxicology at the University of Wales. He has written many scientific papers.
282. Mr Leslie expressed the opinion that the statment made in the
advertisement was accurate as at 1986 with respect to possible
health effects
on the embryo or foetus in a woman exposed to environmental tobacco smoke. I
have had regard to Mr Leslie said in
his evidence regarding matters such as
the nature of scientific proof and the distinction between proof of an
association and proof
of a cause and effect relationship. The bulk of Mr
Leslie's evidence relates to matters other than the association, if any,
between
passive smoking and cancer in non-smokers and I shall not refer to it
in the present context.
(p) Professor Warren
283. Professor Warren is Professor of Pathology at the University of New
South Wales and has impressive qualifications as a pathologist.
He described
the histologic, cytologic and clinical techniques for diagnosing cancer of the
lung and some of the limitations of these
techniques. His evidence was
essentially non-controversial. The limitations of which he spoke were
recognised by the applicant's
witnesses. I do not think they diminish the
weight which I should give to their evidence and to the findings referred to
in the
primary articles.
(v) Comments on the epidemiological evidence
284. The respondent's witnesses, particularly Professor Tweedie and Dr Layard, criticised the methodology and quality of all the epidemiological studies upon which the applicant's witnesses relied. To a greater or lesser extent, the studies were said to be flawed because of a number of factors. These factors included reliability of the diagnoses of lung cancer, the adquacy of data provided by surrogate respondents, the representativeness of data, possible sources of bias and misclassification, the unreliability of using spousal smoking habits as an indicator of exposure to environmental tobacco smoke, and failure to account for confounding factors.
285. I think it is fair to say that the applicant's witnesses conceded, to a
limited extent, that the results in some of the studies
may have been affected
by some of these factors, albeit not to the extent of making them unreliable.
In their opinion, it was the
pattern which emerged from the studies which was
important. This opinion is reflected in Chapter 7 of the NHandMRC report
where
the following statement is made:
"In reviewing the literature on passive smoking and lung cancer, it286. I have referred above to statements to the same effect by some of the applicant's witnesses.
is important to include an overall assessment of the directionality
and coherence of the findings from the various individual studies.
Given the methodological impediments to making a conclusive finding
in any one epidemiological study, then it is important to examine
the pattern of findings. If, despite limitations and flaws in
individual studies, substantial consistency emerges - as is the case
for the reported evidence on passive smoking and lung cancer - then
the prudent public health response must be to infer that a real
effect is likely."
287. Counsel for the respondent submitted that Dr McMichael had, in effect, conceded that there was no demonstrated casual link between passive smoking and lung cancer in a paper he submitted to the National Health and Medical Research Council Carcinogenic Substances Committee in March 1983 (Ex.104). In that report, after a detailed discussion of the studies by Hirayama, Trichopoulos (1981 study only) and Garfinkel (1981 study only), he said that while the available epidemiological evidence suggested that passive smoking may increase the risk of lung cancer, the limitations in data and study design did not then allow a judgment on causality. But this paper was produced at a very early stage in the on-going investigation into the possible health hazard from passive smoking.
288. The intrinsic difficulties in appraising epidemiological studies of passive smoking and health are recognised in the scientific literature. Many of the limitations and criticisms of the studies referred to in the primary articles are dealt with in considerable detail in Chapter 2 of the Surgeon General's report. The Surgeon General's comments appear to me to be valid and I adopt them as part of these reasons. No useful purpose would be served by repeating them.
289. However, there are a few general comments I should make about the epidemiological evidence. In the first place, I think that more reliance can be placed upon non-statistically significant results than the respondent's witnesses were prepared to concede. I agree with Sir Richard Doll's view that statistical significance is "a guide to thought" rather than an absolute standard. If a positive relative risk is statistically insignificant because, say, the lower confidence limit is marginally below 1, I do not think that it should be rejected from consideration for that reason alone. In such a situation, lack of statistical significance calls for the exercise of caution in evaluating the study, but that is not to say it disqualifies the study from consideration.
290. On a related matter, I think that non-statistically significant data, which considered in isolation from other data, may be of little value i n forming an epidemiological judgment, may well be valuable aids to judgment if they form part of a pattern of positive findings.
291. I agree that spousal smoking is an imprecise measure of total exposure to passive smoke because it accounts for only one of what may be many possible sources of tobacco smoke exposure. But with all its imprecision, it seems to me to afford a reasonable basis for measuring exposure.
292. The applicant's and the respondent's witnesses were generally agreed
that what are known as the Bradford Hill criteria are standard
criteria for
evaluating epidemiological studies. However, the respondent's witnesses
placed more store on the observance of all
the criteria than did the
applicant's witnesses. For instance, Dr McMichael thought the criteria should
be applied only subject
to a caveat. He said (T.1238):
"Well, it is a general caveat that, whilst those are well-recognised293. It is this approach which appears to me to explain the differing views of the applicant's and the respondent's witnesses as to the evidentiary value of the studies referred to in the primary articles. I prefer the approach taken by the applicant's witnesses to that taken by the respondent's witnesses.
as useful and often important criteria in the drawing of judgments
about causal inference, they are not and should not be seen as
pre-requisites. In other words the drawing of causal inferences
can quite reasonably proceed and often does in the presence of
just several of those criteria."
294. As to misclassification, I take the view that although the risk of it occurring is always present, the respondent's witnesses have tended to exaggerate its significance and not to have regard to the fact it is often random in its distribution.
295. I think the respondent's witnesses tended to underestimate the
biological plausibility of a casual link between passive smoking
and lung
cancer. I agree with Professor Trichopoulos' evidence that:
"It is one thing to find strong statistical significance which comes296. Without wishing to derogate from the expertise of Professor Tweedie and Dr Layard as statisticians, I think their assessment of the value of the studies referred to in the primary articles tended to be over-technical. I have formed the opinion that the evaluations of the studies by the epidemiologists called by the applicant are to be preferred to the evaluations of them made by Professor Tweedie and Dr Layard.
out of the blue and it is quite different to find statistical significance
(in) something which is suspected on the (basis) of biological
grounds ..."
(T.4030)
297. It emerged from time to time in the evidence that a statistician if less likely to find evidence of proof in an epidemiological study than is an epidemiologist. Because of Dr Layard's close association with the tobacco industry, it seems highly unlikely that he is unaware of the epidemiological studies as to the existence of a causal link between active smoking and lung cancer. As I have already noted, Chapter 4 of the 1982 report of the Surgeon General (which was tendered by the respondent) contains a most positive statement that active smoking causes cancer in smokers. Yet when Dr Layard was asked whether he had formed an opinion on the question whether a causal relationship had been established between active smoking and any form of disease, he said (T.2720) that he had not formed an opinion on that subject. When pressed why that was so he said: "I can only say that I do not feel that my knowledge of biological matters is sufficient for me to arrive at an informed conclusion on that subject."
298. I also think that Dr Witorsch and Professor Huber took an over-technical
approach to the epidemiological evidence and were hypercritical
of it.
(iv) Is there more than a little evidence that cigarette smoke causes cancer
in non-smokers?
299. In my opinion, the applicant has established that, in relation to the disease of cancer, it was misleading and deceptive to state on 1 July 1986 that there was then little evidence that cigarette smoke causes disease in non-smokers. So far from there then being little evidence that cigarette smoke caused lung cancer in non-smokers, there was much evidence to that effect. That was the situation, even if only the data referred to in the primary articles is regarded as evidence for the purposes of the advertisement. Measuring that evidence by any standard, it cannot be fairly described as "little".
300. Unaided by the opinions of the experts who were called, I would have concluded that it cannot be described as "little". The opinions of the experts called in the applicant's case confirm my conclusion. I much prefer the opinions of the applicant's witnesses on this matter. The evidence of a link between passive smoking and lung cancer comes from epidemiological studies supported by strong biological plausibility. The epidemioligists called by the applicant were most impressive witnesses. Their opinions are shared by many other distinguished epidemiologists who took part in the compilation of the major reviews.
301. The respondent did not call one witness whose primary expertise was in the field of epidemiology. I do not overlook the fact that Professor Tweedie and Dr Layard are experienced statisticians. Nor is it a matter of judging, as best I can, which opinions are entitled to the most weight. I have no hesitation in preferring the opinions expressed by the applicant's witnesses.
302. I have reached the conclusion that the opinions of the experts called by the applicant are to be preferred to the opinions expressed by the experts called by the respondent. I think the applicant's witnesses had more experience in some matters upon which they disagreed with the respondent's witnesses. In particular, on questions concerning the carcinogenic qualities of tobacco smoke and the existence or otherwise of a safe level of exposure to carcinogens I found the evidence of Professor Steward very persuasive and I prefer it to the respondent's evidence on the same matters.
303. As I have noted, the applicant's witnesses said that the statement that there is little evidence that cigarette smoke causes cancer in non-smokers is incorrect. I did not understand the respondent's counsel to submit that evidence of this kind was inadmissible. However, it was submitted that the statements by the applicant's witnesses as to their own opinions on the question whether cigarette smoke causes disease in non-smokers is not evidence in the sense in which that word is used in the advertisement. It was submitted that any probative value attaching to the findings referred to in the primary articles was not increased by the applicant's experts expressing their concurrence with them. I think there is some substance in this submission, but I do not think it advances the respondent's case. The experts were entitled to explain the contents of the primary articles and to depose as to the strengths and weaknesses of the studies referred to in them. If, after examination of a primary article, it is seen to disclose some evidence of a casual relationship between passive smoking and lung cancer it is hardly necessary for an expert to express his opinion that it does so.
304. Of course, if it is relevant to have regard to the state of the evidence after 1 July 1986 and to major reviews as well as primary articles, the applicant's case becomes even stronger. As I have said earlier in these reasons, I think that the applicant is not confined to the state of the evidence as at 1 July 1986 and I also think that the major reviews are "evidence" as that word is used in the advertisement.
305. On the question of the relevance of articles published after 1 July 1986, I should make special reference to the Wald article on meta-analysis. Although the article was published after 1 July 1986, the studies which Professor Wald and his co-authors analysed were all published before that date. The meta-analysis which they carried out could as easily have been carried out on 1 July 1986. What the article did was to show the strength of the evidence as it existed at 1 July 1986, not as at the date of publication of the article. Hence, I think regard can be had to the article for the purpose of assessing whether it was misleading or deceptive to say, as at 1 July 1986, that the evidence which then existed was "little".
306. Since I am of the opinion that on no view of the meaning of the word "little" can the evidence that passive smoking causes disease in non-smokers be so described, there is no need to attach a precise meaning to the word. The essential message which the advertisement, as a whole, attempts to convey to the reader is that cigarette smoke may be annoying to some non-smokers but that (as stated in the penultimate paragraph) "... annoyance is neither a governmental nor a medical problem". In substance, what the reader is told is that inhalation of cigarette smoke by non-smokers may be annoying to them but it is not a health problem. Having regard to the totality of the advertisement, the reference to "little evidence" seems to be a reference to evidence which is so inconsequential as not to support a reasonable apprehension that passive smoking may give rise to a medical or health problem.
307. It was submitted on behalf of the respondent that the evidence called by the applicant was not evidence that cigarette smoke causes disease in non-smokers. The evidence, so it was submitted, was no more than evidence of an association between cigarette smoke and disease. I am unable to accept that evidence of an association between passive smoking and lung cancer cannot be regarded as some evidence of a casual relationship between the two.
308. Nor do I accept the respondent's related submission that epidemiological
evidence alone cannot establish a cause and effect
relationship. The
submission would be valid only if the standard of proof required to establish
such a relationship is set at a
virtually unattainable level.
(vii) Is there scientific proof that cigarette smoke causes cancer in
non-smokers?
309. I have not so far considered whether the statement is erroneous in so far as it asserts that there is nothing which proves scientifically that cigarette smoke causes disease in non-smokers. As I have observed, I think that in the context of the advertisement the words "nothing which proves scientifically that cigarette smoke causes disease in non-smokers". Reading the statement in this way, I have come to the conclusion that it is erroneous.
310. The conclusion that cigarette smoke causes lung cancer in non-smokers
cannot be drawn from any one epidemiological study or
piece of evidence. But
I think it can be drawn from the totality of the available data and by valid
reasoning from it. A summary
of the reasons which lead me to this conclusion
is contained in the statement with which Professor Wald concluded his proof of
evidence.
I agree with what he there said, which was as follows:
"In our 1986 paper we concluded that breathing other people's311. It is obvious that Professor Wald's views that environmental tobacco smoke contains substances which are carcinogenic to humans and that there is no threshold level of exposure to carcinogens below which they cannot and do not cause cancer in humans, form an important part in his overall reasoning.
smoke was a cause of lung cancer and our conclusion rested on several
sources of evidence, not only the statistically significant
association between lung cancer and exposure to environmental
tobacco smoke. It also rested on other evidence, including the fact
that carcinogens in tobacco smoke are released into the air and that
tobacco smoke is breathed into the lungs by non-smokers. Non-smokers
who are exposed to environmental tobacco smoke absorb tobacco
products into their blood and tissues, and their urine contains
chemicals that are mutagenic, that is chemicals that can induce
change in the genetic material in a manner that is thought to be
fundamental to the initiation of cancer. It is known that active
smoking causes lung cancer, a strong effect in which the risk of
lung cancer is some 14 times that in non-smokers. It is the accepted
scientific view that exposure to carcinogens does not have a threshold
below which there is no effect and therefore one would expect that
non-smokers who inhale environmental tobacco smoke would have at
least some increased risk of lung cancer. The conclusion that the
excess risk is of the order of 30-50% is plausible in the light of
the much higher risk of lung cancer due to active smoking. Given
all the evidence I believe that the conclusion that breathing
other people's smoke is a cause of lung cancer is scientifically
sound."
(Ex.SS, pp 15-16)
312. The expert witnesses called by the applicant all accepted the validity of these views. They are also shared by numerous distinguished authors of many of the primary articles and major reviews. Those few scientists (and they mostly have a professional association with the tobacco industry) who do not share their views claim that their validity has not been established. They do not go so far as to assert that the conclusions are invalid.
313. Once it is accepted:
(a) that passive smoking involves inhalation of environmental tobacco smoke
which contains carcinogens;
(b) that there is no safe threshold level of exposure to carcinogens:
(c) that some of the studies referred to in the primary articles show a
statistically significant association between spousal smoking
and lung cancer;
and
(d) that meta-analysis of the results in such studies discloses a
statistically significant (adjusted) risk ratio of about 1.53 (Wald
et al) or
1.42 (NRC report) for non-smokers living with smokers compared with
non-smokers not exposed to environmental tobacco smoke;
then my conclusion must be that there is compelling scientific evidence that
cigarette smoke causes lung cancer in non-smokers. Although
not based upon
the findings made by the authors of the major reviews, my conclusion is
consistent with those findings.
314. Counsel for the repondent submitted that such a conclusion cannot be drawn because some of the applicant's witnesses conceded that other scientists may hold a contrary view. I do not accept this submission. I did not understand any of the applicant's witnesses to concede that their opinions were or might be incorrect merely because some hypothetical scientist may hold a contrary opinion.
315. Moreover, the views held by other scientists may be formed upon the
basis even that compelling evidence that passive smoking
causes lung cancer
does not establish proof for the purpose of the statement in the
advertisement. Indeed, I have formed the view
that the opinions of the
respondent's witnesses are difficult to justify except on this basis. An
extract from the evidence of Dr
Leslie (T.3470-1) illustrates this point:
"HIS HONOUR: ... assuming over a period of 50 years in every country316. It was also submitted that there are statements in the NH and MRC report which virtually concede the absence of scientific proof of a causal link between passive smoking and lung cancer. Reference was made particularly to the following statement made on p 33 of the report:
of the world an odds ratio of 10 had been established in
respect of smokers who smoked two packets of cigarettes a day
in relation to risk of cancer but no toxicology or other studies
had been undertaken, all you had was there was a stream of
consistent statistically significant results of that kind. That
would be, what, no evidence that cigarette smoke caused cancer
in smokers?
WITNESS: Well, it would be no direct evidence. it would be - - -
HIS HONOUR: It would point to a relationship?
WITNESS: It would make you put the odds against it of there being
a causal link as something astronomic but it still would not be
proof."
"The evidence that passive smoking causes lung cancer is stronglyDr McMichael said that the above passage under-stated the view of many scientists, including himself. More importantly, the passage on p 33 is followed by a reference to conclusions contained in the IARC report. After referring to the statement in that report that: "The observations on non-smokers that have been made so far are compatible with either an increased risk from passive smoking or an absence of risk" Dr McMichael and his colleagues conclude the chapter in the NH and MRC report on passive smoking and cancer with the following statement, with which they apparently agree, in the IARC report:
suggestive. It is plausible, moderately consistent, and demonstrates
dose-response relationships. However, intrinsic difficulties in
accurately classifying individual exposure, and insufficient numbers
of study subjects in many studies, preclude a conclusive
interpretation of these empirical data when considered in isolation
from other corroborative scientific evidence."
"Knowledge of the nature of sidestream and mainstream smoke, of the317. It is to be noted that this passage in the IARC report is followed by the following statement:
materials absorbed during 'passive' smoking, and of the
quantitative relationships between dose and effect that are
commonly observed from exposure to carcinogens, however, leads to
the conclusion that passive smoking gives rise to some risk of
cancer."
"There is sufficient evidence that tobacco smoke is carcinogenicAs I have already observed, I regard the reference to "tobacco smoke" as a reference to all kinds of tobacco smoke, including environmental tobacco smoke. In IARC's lexicon, "sufficient evidence" of carcinogenicity indicates that there is a casual relationship between the exposure and human cancer - vide p 24 of the IARC report.
to humans."
318. As I understand what is said in these statements in the NH and MRC and IARC reports, the authors of them accept that the epidemiological studies which had been made prior to the making of the reports, taken in isolation from other scientific evidence, did not demonstrate that passive smoking causes lung cancer. But they appear to conclude that a consideration of the totality of all the scientific evidence leads to the conclusion that passive smoking gives rise to some risk of cancer, i.e that some people will suffer from cancer as a result of their passive smoking.
319. Reliance was also placed by the respondent upon some statements made in
Chapter 9 of the NH and MRC report, in particular the
following passage:
"Council notes that there is mounting epidemiological evidenceIt was argued that the language used in the latter part of the above statement indicated that the authors of it were not persuaded that there was a proven link between passive smoking and lung cancer. It should be noted that Chapter 9 of the report was not written by the members of the working party, who were the authors of the chapter on passive smoking and cancer. Chapter 9 is the work of the National Health and Medical Research Council itself. Dr McMichael said that the function of the Council is to advise the Australian Government on matters of public health policy and this no doubt explains the language used by the Council. I do not think the language used by the Council should be taken as qualifying the views of the authors of Chapter 7 of the report.
that passive smoking may increase the risk of occurrence of lung
cancer. Despite limitations in the amount of data available,
and despite research difficulties in making satisfactory
estimations of individual exposure, a consistent pattern of
moderately increased risk of lung cancer in passive smokers has
emerged. In view of this pattern, of the known and substantial
increase in risk of lung cancer in active smokers (and the lack
of a threshold dose), and of the documented levels of bodily
assimilation of passively-inhaled smoke, it is therefore prudent
public health policy to infer an increased risk of lung cancer from
passive smoking."
320. It was also submitted on behalf of the respondent that the authors of
the NRC report did not reach a firm conclusion that passive
smoking is a cause
of lung cancer. I do not think this is the case. The National Research
Council reached the conclusion that the
relative risk of cancer incurred by
"exposed" non-smokers compared with a truly unexposed non-smoker was 1.42.
(This figure compares
with Professor Wald's calculated equivalent relative
risk of 1.53). The authors of the report then make the following statement (p
242):
"We can say, therefore, that while the epidemiologic studies show321. This statement is made on the basis of the epidemiological studies alone. When regard is had to the generally accepted view that exposure to carcinogens does not have a threshold below which there is no effect, the findings in the NRC report do not stand in the way of the conclusion which I have reached that there is compelling scientific evidence that passive smoking does indeed cause lung cancer.
a consistent and, in total, a highly significant association between
lung cancer and ETS exposure of non-smokers, the excess might, in
principle, possibly be explained by bias. However, detailed
consideration of the nature and extent of the bias shows that given some
reasonable assumptions the bias would be insufficient to explains
the whole effect. In fact, there are some types of bias that lead
to underestimates of the effect. It must be concluded, therefore,
that some, if not all, of the effect reported in spouse studies is
causal."
322. It follows from what I have written that the statement: "Yet there is
little evidence and nothing proves scientifically that
cigarette smoke causes
disease in non-smokers" was erroneous when it was first made on 1 July 1986
and remains so.
8. Repiratory Disease Young in Children
323. It is apparent from a consideration of the primary articles, the major reviews, and the oral evidence given by the applicant's and the respondent's witnesses that the applicant's case that cigarette smoke causes respiratory disease in non-smokers is at its strongest with respect to respiratory disease in children under the age of 12 months. For that reason I think it is unnecessary for the purpose of deciding the issues which arise in the present case to examine in detail the evidence as to the association between passive smoking and respiratory effects and pulmonary function in older children or in adults. If the applicant cannot, in respect of this part of its case, succeed in respect of children in the first year of life, it cannot succeed at all. I therefore do not propose to refer in any detail to the evidence as to the effect of passive smoking on older children or adults.
324. Before referring to the oral evidence in this part of the case I shall
set out some of the statements made in the primary articles
and the major
reviews upon which the applicant places reliance.
(i) The primary articles
(a) Harlap and Davies - Infant admissions to hospital and maternal
smoking.
325. This article appeared in The Lancet in 1974. The authors of the article
were from the Department of Medical Ecology at the
Hebrew University,
Jerusalem. The following summary of the study appears in the article:
"Admissions to hospital during the first year of life326. There was a study population of 10,672. At the time of the interviews, 9.2% of the mothers were smokers and 7.4% had given up smoking earlier. The admission rate (per 100 infants) for bronchitis and pneumonia was 9.5 for children of non-smokers and 13.1 for children of smokers. The equivalent figures for admissions for upper respiratory tract infections were 4.8 and 5.3 respectively, but these last-mentioned figures were not statistically significant. The article contains a table giving admission rates (per 100 infants) by diagnosis in relation to maternal smoking and the number of cigarettes smoked daily. The table is as follows:
were recorded in a prospective study of 10,672 infants whose
mothers' smoking habits were known. Infants with major
congenital malformations, and those dying before their first
birthday, were excluded. The infants of mothers who smoked
had significantly more admissions for bronchitis or
pneumonia, especially in the winter, and more injuries.
They were also admitted more frequently, though not
significantly so, for upper-respiratory-tract infections,
gastroenteritis, childhood infectious diseases, and other
diagnoses. The excess of bronchitis and pneumonia in the
group exposed to smoke increased with increasing number of
cigarettes smoked by the mother. It occurred within
subgroups of birth-weight, social class and birth order. It
was seen mainly in infants aged 6-9 months, while at older
and younger ages there was no significant effect of maternal
smoking. The findings support the hypothesis that
atmospheric pollution with tobacco smoke endangers the
health of non-smokers."
Non-smokers SmokersDiagnosis (8900) (786) Total
Never smoked Former smokers Cigarettes per day
1-10 11-20 21+ (10,672)Bronchitis 9.6 7.8 10.8 16.2 31.7 9.8
(747) (149) (60)
15.5 15.1 16.4 17.3 23.3 15.6Total
25.1 22.9 27.2 33.5 55.0 25.4Differences among three categories of smokers: for bronchitis and pneumonia, P <0.001, for other diagnoses, not significant.
327. The authors included the following observations in their study:
"Infants born to smokers were in hospital for an average of328. In their discussion of the findings, the authors state:
384 days per 100 infants before their first birthday, 151 of
them for bronchitis or pneumonia. These rates were 334 and
114, respectively, for the infants of non-smokers. However,
there were no significant differences between the groups,
exposed or not exposed to smoke, in average duration of each
type of admission episode.
Admissions for bronchitis or pneumonia increased in
frequency with increasing number of cigarettes smoked by the
mother (table II). There were no significant increases for
any of the other diagnoses measured separately. Infants of
mothers who had given up smoking had fewer admissions than
those whose mothers had never smoked. This difference,
which can be explained by the higher standard-of-living of
those who gave up smoking, is not, however, statistically
significant for any single diagnostic category. Infants
born to former smokers spent fewer days in hospital in the
first year of life (231 per 100 infants, 79 of them for
bronchitis or pneumonia), and their admission episodes
tended to be shorter for each diagnosis.
Women who smoke gave birth to smaller infants, and
birth-weight is an important predictor of admission to
hospital in West Jerusalem. Admissions for bronchitis or
pneumonia are more frequent in infants who are smaller or
larger than average at birth; while for other diagnoses,
increasing birth- weight predicts a decreasing probability
of going to hospital. Table III shows that the excess of
admissions for bronchitis or pneumonia in the passively
smoking infants could not be wholly attributed to lower
birth-weights, rates being higher than in the infants of
non-smokers for all three birth-weight groups."
...
"The excess risk associated with maternal smoking was
not uniform throughout the first year of life ... In the
first 5 months of life there were no significant differences
between infants born to smokers or non-smokers in rates of
admissions for bronchitis or pneumonia. Between the ages
of 6 and 9 months, on the other hand, there were greatly
increased rates of lower respiratory disease in the group
exposed to smoke, both in the summer and in the winter.
Toward the first birthday, differences between the two
groups again disappeared."
"This study relies on information on maternal smoking(b) Colley et al. - Influence of passive smoking and parental phlegm on pneumonia and bronchitis in early childhood.
which was collected antenatally. It is not known how
closely smoking in early pregnancy or mid-pregnancy
correlates with habits after the birth and in the baby's
first year, but it seems reasonable to assume that for most
mothers, smoking characteristics would have remained the
same. However there would inevitably have been some smoking
mothers who subsequently gave up the habit, and others,
especially former smokers, who took it up later. As a
result, this study tends to underestimate true differences
between infants of smokers and non-smokers, rather than the
opposite."
329. The authors were from the Department of Medical Statistics and Epidemiology at the London School of Hygiene and Tropical Medicine and from the Department of Community Medicine at St Thomas's Hospital Medical School, London.
330. This article appeared in The Lancet in November 1974. The following
summary of the study appears in the article:
"The incidence of pneumonia and bronchitis has been331. This study was conducted in Harrow, north-west of London, between 1963 and 1969 and involved all families living in six of the wards of the borough of Harrow who had an infant born in the period from July 1, 1963 to June 30, 1965. 2205 families were included in the study. After exclusions for some cases, such as multiple births, there were 2149 infants eligible for study. It was a longitudinal study conducted over five years. The authors describe the methodology of their study in considerable detail. Some of the results of the study are stated to be as follows:
studied in 2205 infants over the first five years of life.
In the same period their parents' smoking habits and
respiratory symptoms were recorded annually. The incidence
of pneumonia and bronchitis in the first year of life was
associated with parents' smoking habits; incidence was
lowest where both parents were non-smokers, highest where
both smoked, and lay between these two levels where only one
parent smoked. Over the age of one year the association was
not consistent. When parents' respiratory symptoms were
also studied a close association was found with the
incidence of pneumonia and bronchitis in the child; this
was independent of parents' smoking habits and was an almost
consistent finding throughout the first five years of life.
In the first year of life exposure to cigarette smoke
generated when parents smoked doubled the risk for the
infant of an attack of pneumonia or bronchitis."
"The annual incidence per 100 children of pneumonia andYear of Both non-smokers One smoker Both smokers Both ex-smokers All
bronchitis is given in table II by parents' smoking habit.
Parents have been classified into one of four groups: (1)
both parents non-smokers; (2) one parent smoker, the other
non-smoker; (3) both parents smokers; (4) both parents
ex-smokers, or one an ex-smoker, or parents who changed their
smoking habits during the study. The incidence of pneumonia
and bronchitis in the infant shows a gradient by parents'
smoking habit in the first year of life. Incidence is lowest
in infants with both parents non-smokers, highest where both
parents smoke, and lies between these values where one
parent smokes. This is a statistically significant gradient
(P <0.0005). In subsequent years there is no such clear
gradient.
In table III parents have been classified both by their
smoking habits and by their response to the question `Did
you usually bring up any phlegm from your chest first thing
in the morning in the last winter?' In all categories
except one, the incidence within a smoking category is
higher among children where one or both parents have winter
morning phlegm than in children whose parents are both free
of this symptom. Some of the incidence-rates in the
children - in particular those whose parents are both
non-smokers and who have winter morning phlegm - are based upon
small numbers and therefore may not be wholly reliable. On
the other hand, the incidence-rates in children where
neither parent has symptoms, whether they smoke or not, are
based upon substantial numbers. In them in the first year
of life a consistent gradient is seen in the incidence of
pneumonia and bronchitis in the children in relation to the
parents' smoking habits. The rates are lowest in children
of non-smoking parents and highest where both parents smoke.
In children over the age of a year there is, however, no
consistent gradient.
Exposure of the child to cigarette smoke may be more
precisely estimated from the total daily cigarette
consumption of both parents. In table IV the incidence of
pneumonia and bronchitis is given for parent pairs smoking
between them 1-14, 15-24, and 25 or more cigarettes per day,
by the presence of winter morning phlegm. A clear gradient
of increasing incidence is seen in the first year of life
that is independent of the presence of winter morning phlegm
and is of the same size as that in table III. In the
second year and thereafter the pattern is not consistent and
thus does not suggest an effect of exposure to tobacco smoke
at ages over one year."
Tables II, III and IV are reproduced below:
TABLE II - PNEUMONIA AND BRONCHITIS BY PARENTS' SMOKING HABITS
Annual incidence per 100 children (absolute numbers in parentheses)
of pneumonia and bronchitis
or smoking habit11.5
changed
1 7.8 11.4 17.6 9.2
TABLE III - PNEUMONIA AND BRONCHITIS IN THE FIRST FIVE YEARS OF LIFE BYYear of Both One smoker Both smokers Both ex-smokers All follow-up non-smokers or an ex-smoker
PARENTS' SMOKING HABIT AND MORNING PHLEGM
Annual incidence per 100 children (absolute numbers in parentheses)
of pneumonia and bronchitis
or smoking habitO/B
changed
N O/B N O/B N O/B N O/B N
DAY BY PARENTS AND WINTER MORNING PHLEGMYear of Both non-smokers One or both smokers* of following number of follow-up cigarette per day:
Annual incidence per 100 children (absolute numbers in
parentheses) of pneumonia and bronchitis
1-14 15-24 25 and over* Excluding parent pairs where one or both are ex-smokers or changed smoking habit. N = neither with winter morning phlegm. O/B = one or both with winter morning phlegm.
N O/B N O/B N O/B N O/B
1 7.6 10.3 10.4 15.1 11.1 14.5 15.2 23.2
(343) (29) (269) (53) (171) (76) (323) (138)
2 8.1 8.3 5.2 16.4 8.6 14.5 9.7 9.8
(322) (36) (231) (55) (151) (62) (269) (164)
3 6.9 8.1 11.2 8.6 8.2 9.5 8.6 11.2
(305) (37) (206) (58) (146) (42) (243) (161)
4 8.0 11.1 5.5 13.3 7.4 11.5 9.1 10.3
(287) (36) (163) (45) (136) (52) (243) (126)
5 6.7 14.7 6.3 11.4 4.4 7.6 4.1 10.6
(285) (34) (144) (44) (133) (53) (218) (142)
332. The authors also state:
"The infants of mothers who smoke in pregnancy are, on333. In the discussion of their paper, the authors observe:
average, lighter than those of mothers who do not smoke.
As infants of low birth-weight are more likely to suffer
respiratory illness than normal-weight infants, it is
possible that the gradients in respiratory disease observed
in the first year of life, and in particular the effects of
passive smoking, may be due, indirectly, to maternal smoking
during pregnancy. In this study, birth-weight, as
expected, shows a gradient by parents' initial smoking
habit, and to a lesser extent by winter morning phlegm.
Thus parents who smoke have lighter infants than parents who
do not smoke. The gradients in the incidence of pneumonia
and bronchitis with parental smoking, and with winter
morning phlegm, might therefore be partly attributable to
differences in birth-weight. However, within different
birth-weight categories the gradients for pneumonia and
bronchitis with parents' smoking habits persist. Thus
differences in birth-weight cannot account for the higher
risk of pneumonia and bronchitis in the first year of life
in children exposed to the cigarette smoke generated when
their parents smoke at home."
"Passive smoking by the infant, after differences in(c) Leeder et al. - Influence of family factors on the incidence of lower respiratory illness during the first year of life.
birth-weight and parental respiratory symptoms have been
allowed for, increases the risk to the infant of pneumonia
and bronchitis in the first year of life. When both parents
smoke, this risk is almost double that of infants with
non-smoking parents. The findings confirm and extend those of
Harlap and Davies. These workers did not, however, have
information on fathers' smoking habits, nor did they take
account of parents' respiratory symptoms.
A picture has thus emerged of a serious risk to infants
in the first year of life from exposure to their parents'
cigarette smoke. In contrast, between one and five years of
age, there does not appear to be any important effect of
passive smoking in increasing the risk of pneumonia and
bronchitis. Colley, in 6-14-year-olds also found no
association between passive smoking and the prevalence of
chronic cough.
The estimates of children's exposure to cigarette smoke
in this study are crude, being based either on whether
parents were smokers or not, or on their total daily
cigarette consumption. The smoke exposure of the children
may have been overestimated, since parents - in particular
the father - will smoke outside the home, or at times when
the infant is not present. The effects on the child may
thus have resulted from exposure to levels of cigarette
smoke less than those suggested by our study."
334. This article was published in 1976 in the British Journal of Preventive
and Social Medicine. The authors were from the Department
of Community
Medicine at St Thomas's Hospital, Medical School, London and the Department of
Community Health at Bristol. The following
summary of the study appears in
the article:
"In a study of a cohort of over 2000 children born335. The authors reported some of their findings in the following terms:
between 1963 and 1965, the incidence of bronchitis and
pneumonia during their first year of life was found to be
associated with several family factors. The most important
determinant of respiratory illness in these infants was an
attack of bronchitis or pneumonia in a sibling. The age of
these siblings, and their number, also contributed to this
incidence. Parental respiratory symptoms, including
persistent cough and phlegm, and asthma or wheezing, as well
as parental smoking habits had lesser but nevertheless
important effects. Parental smoking, however, stands out
from all other factors as the one most amenable to change in
seeking to prevent bronchitis and pneumonia in infants."
"During the first year of life, the incidence ofANNUAL INCIDENCE PER 100 INFANTS OF BRONCHITIS OR PNEUMONIA
bronchitis and pneumonia varied according to several family
factors. These illnesses occurred much more commonly in
infants born to families which had several other children
already, and in those families where the parents had
respiratory disability or were smokers.
Children whose parents both had a history of asthma-wheeze
had an incidence of bronchitis or pneumonia of 26.9%
which was three times greater than that found in children of
parents without such a history (9.4%) (Table III). The
effect of parental smoking was not so great. The incidence
of bronchitis or pneumonia in children of non-smoking
parents was 7.2% compared with 17.7% when both parents
smoked. When both smoking habits and asthma-wheeze were
examined for combined effects on the incidence of bronchitis
or pneumonia in the children, these contrasts widened. For
example, the incidence of bronchitis or pneumonia was 6.7%
in infants whose parents neither smoked nor had suffered
from asthma-wheeze; this contrasted with an incidence of
39.3% when both parents smoked and had a history of
asthma-wheeze."
TABLE III
IN THE FIRST YEAR OF LIFEParental asthma-wheeze One 8.9 18.0 22.3 7.4 15.6
BY PARENTAL HISTORY OF ASTHMA-WHEEZE AND SMOKING HABIT
Parental Smoking Habit
Neither One Both Habit Total
Changed
Neither 6.7 9.6 13.7 8.7 9.4
(451) (502) (314) (241) (1508)
(101) (178) (139) (81) (499)Populations in parentheses * Total excludes 27 infants with missing first year data and an additional 48 with missing initial and first year data on parent pairs.
Both 14.3 13.6 39.3 30.0 26.9
(7) (22) (28) (10)(67)
Total 7.2 11.8 17.7 9.0 11.5
(559) (702) (481) (332) (2074)*
336. This article appeared in the British Medical Journal in 1978. The
authors were from the University of Newcastle upon Tyne.
The contents of the
article are of only marginal significance for present purposes. In the
study, 35 children known to have had
respiratory syncytial virus bronchiolitis
in infancy were examined at the age of 8 and their respiratory function
tested. The results
were compared with those in 35 controls matched for age,
sex, and social class. The authors concluded, inter alia, that the parents
of the children who had had bronchiolitis smoked significantly more cigarettes
during the infant's first year of life than those
of the control children.
(e) Rantakallio - Relationship of maternal smoking to morbidity and
mortality of the child up to the age of five.
337. The author of this article which was published in 1978 was from the
Department of Paediatrics and the Department of Public Health,
University of
Oulu, Finland. The abstract of the article as published reads as follows:
"The effect of maternal smoking during pregnancy on the338. Table 6 in the article refers to the incidence of diseases during the first 5 years among the children of the smokers and the controls in the study. With respect to this table the authors state:
morbidity and mortality of the child up to the age of five
was studied in 12 068 births. The children of the smokers
were compared with those of controls of similar age, parity,
marital status and place of residence. Perinatal mortality
was no higher among the smokers, but postneonatal mortality
from 28 days to 5 years was almost significantly (p <0.05)
higher. The children of the smokers were highly
significantly (p <0.001) more often hospitalized in
pediatric departments, the difference being clearest below
the age of one. The average duration of hospital admissions
was longer among the children of the smokers, and similarly
the numbers of visits to the doctor and hospital admissions
to any hospital under the age of one were more frequent
among the children of the smokers. Respiratory diseases
caused highly significantly more hospitalizations among
these children."
"Table 6 presents the frequency of all disease groups(f) Fergusson et al. - Parental smoking and respiratory illness in infancy
diagnosed in children's departments per thousand live births
among the children of smokers and of their controls. If
the child had been in hospital more than once for the same
disease it was counted only once. Respiratory and skin
diseases were more frequent among the smokers than among the
controls, the difference being statistically highly
significant .... Among the respiratory diseases the ratio
of the incidence among the smokers to that of the controls
was 2.2 in pneumonia, 1.8 in bronchitis, and 1.5 in others
such as acute nasopharyngitis, sinusitis etc. ...
Under the age of one year the difference in the
diseases was in general greater between the heavy smokers
and their controls than between the light smokers and their
controls, but this was no longer true for the age from one
to five.
When the main causes of hospitalization in pediatric
departments per thousand live births was calculated for both
groups a statistically highly significant difference (p
<0.001) was found only in the case of respiratory diseases,
and an almost significant difference (p <0.05) in the case
of skin diseases. The more frequent hospitalization of the
children of smokers because of respiratory diseases was
clearest below the age of one, but also existed at the age
of one to five, the difference between the smokers and
controls at that age being almost significant (p <0.05).
Again the children of the heavy smokers were more affected
than those of the light smokers under the age of one, but
not at the age of one to five."
339. The authors of this article which was published in 1980 were from the Department of Paediatrics, Christchurch Hospital, New Zealand.
340. The data for the study were collected during the third stage of a study known as the Christchurch Child Development Study. In the project a cohort of infants was studied at birth, at four months and at one year.
341. The summary of their article reads as follows:
"The relationship between parental smoking and342. In their discussion of their paper, the authors make the following statements:
respiratory illness in a birth cohort of 1180 one-year-old
children was examined. Maternal smoking was associated with
an increased incidence of lower respiratory illness but
there was no statistically significant association between
paternal smoking and lower respiratory illness. While
children of mothers who smoked suffered more lower
respiratory illnesses, their overall risk of respiratory
infection was similar to that for children of non-smoking
mothers. The association between maternal smoking and
infantile lower respiratory illness persisted when the
child's social background, perinatal history, and postnatal
diet were taken into account. The findings favour the view
that prolonged exposure to cigarette smoke predisposes
infants to develop lower respiratory symptoms when they
contract a respiratory infection."
"Previous studies have considered the effects of(g) Fergusson et al. - Parental smoking and lower respiratory illness in the first three years of life.
parental smoking on lower respiratory illness only. The
findings reported here show that there is a complicated
relationship between parental smoking and all respiratory
illness. Overall, the children of mothers who smoke do not
have a greater risk of respiratory illness but they do have
a greater risk of suffering respiratory illness affecting
the lower respiratory tract. This finding suggests that
the effect of maternal smoking is to irritate the infantile
lung and thus facilitate the spread of infection to the
lower respiratory tract.
In addition, previous research has examined the
relationship between parental smoking and medical
consultation for lower respiratory illness. Since medical
consultations probably provide a biased sample of infant
illness, there is the possibility that the apparent
association between parental smoking and infant lower
respiratory illness could have arisen from some bias in
consulting practices. The results reported here show that
this is unlikely to be the case: an association between
maternal smoking and infantile lower respiratory illness has
been shown to exist both for illness needing medical
treatment and for maternal reports of lower respiratory
symptoms, irrespective of whether these symptoms were
treated by a medical practitioner.
Finally, the range of social and perinatal factors
controlled in this study is greater than that considered in
previous studies of the topic. On the basis of the
findings reported here, it may be concluded that the
association between maternal smoking and infantile lower
respiratory illness cannot be explained by the confounding
effects of such factors as adverse perinatal history,
depressed social background, or bottle feeding.
There now appears to be sufficient evidence to support
the view that people in regular and prolonged contact with
infants should not smoke, or if they must, they should not
do so in the presence of infants."
343. The authors of this study (save for one additional co-author) were also
the authors of the previous study. The article was
published in 1981. The
following summary of the study appears in the article:
"The relationships between parental smoking and the344. Table 2 of the report is as follows:
rates of lower respiratory illness during the first three
years of life were examined for a birth cohort of 1265 New
Zealand children. Lower respiratory illness varied
significantly with maternal smoking for the first year;
there was equivocal evidence of a relationship between
maternal smoking and lower respiratory illness in the second
year; and by the third year the relationship had clearly
disappeared. Paternal smoking had no significant effect on
rates of lower respiratory illness at any time.
Application of logistic regression showed that for
the first year rates of lower respiratory illness were
approximately linearly related to maternal smoking:
increases of five cigarettes a day resulted in an increase
of 2.5 to 3.5 incidents of lower respiratory illness per 100
children at risk. Statistical control for maternal age,
education, family size, and family living standards showed
that the relationship between maternal smoking and rates of
lower respiratory illness was not significantly influenced
by these factors."
Paternal BRONCHITIS/PNEUMONIA LOWER RESPIRATORY SYMPTOMS(cigs/day) 0 1-10 11+ 0 1-10 11+
smoking Maternal smoking (cigs.day) Maternal smoking (cigs.day)
0 7.0 12.8 13.4 37.6 47.4 50.9(112)
(588) (78) (112) (588) (78)
1-10 4.6 14.0 11.1 37.9 53.5 33.32ND YEAR 2ND YEAR 2ND YEAR 2ND YEAR 2ND YEAR 2ND YEAR 2ND YEAR
(66) (43) (18) (66) (43) (18)
11+ 8.8 12.7 19.7 42.4 43.6 53.1
(125) (55) (81) (125) (55) (81)
0 9.1 20.7 13.2 43.8 54.0 50.93RD YEAR 3RD YEAR 3RD YEAR 3RD YEAR 3RD YEAR 3RD YEAR 3RD YEAR
(584) (87) (114) (585) (87) (116)
1-10 7.9 3.3 12.0 44.7 51.6 36.0
(76) (30) (25) (76) (31) (25)
11+ 11.1 15.9 11.9 55.6 52.2 50.8
(108) (44) (67) (108) (48) (67)
0 8.9 5.5 12.1 37.4 39.7 45.3345. In their discussion of their work the authors observe:
(605) (73) (116) (605) (73) (117)
1-10 11.8 8.7 8.0 41.6 21.7 36.0
(76) (23) (25) (77) (23) (25)
11+ 10.2 13.5 6.1 36.1 40.5 41.5
(108) (37) (65) (108) (37) (65)
"In confirmation of the findings of Colley et al the(h) Ekwo et al. - Relationship of parental smoking and gas cooking to respiratory disease in children.
correlation between parental smoking and childhood lower
respiratory illness appeared to be most marked for the first
year of life and showed a steady decline with increasing
age. At one year, clear differences between the offspring
of smokers and non-smokers were evident; at two years the
evidence was equivocal; and by three years an association
between maternal smoking and infant lower respiratory
illness was clearly absent. However, these findings are
not entirely consistent with reports which have shown
greater rates of respiratory problems (morning cough and
breathlessness) among children of school age with smoking
parents. One hypothesis which satisfies the available data
is that the effect of parental smoking on childhood lower
respiratory illness and symptoms is two-fold. During early
life, and particularly the first year, prolonged contact
with cigarette smoke would appear to precipitate or
exacerbate lower respiratory illness in children; this
effect is relatively short-lived and disappears at the age
of about 2. However, prolonged exposure to cigarette smoke
over a period of years may have a compound interest effect
in compromising the respiratory function of children, with
the result that by the time middle childhood is reached,
children of smokers have a greater rate of lower respiratory
illness or symptoms."
346. The authors of this article, which was published in 1983, are from the University of Iowa Medical School.
347. The authors found that the risk of hospitalisation for respiratory
illness in children before age 2 years was increased when
at least one of the
parents smoked. The authors concluded that, based on the findings of their
report and from previously published
findings, "one is led to conclude that
parental smoking is associated with a risk of certain respiratory illnesses
and symptoms among
children living in the same environment."
(j) Schenker et al. - Risk factors for childhood respiratory disease.
The effect of host factors and home environmental exposures.
348. The authors of this article which was published in 1983 were from the Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston and the Department of Medicine, University of New Mexico School of Medicine.
349. Many of the findings of this study relate to matters of no present
concern. However, the authors concluded that chest illness
before two years
of age showed a significant positive linear trend with the number of parental
smokers.
(k) Ware et al. - Passive smoking, gas cooking, and respiratory health of
children living in six cities.
350. The authors of this study which was published in 1984 were from the
Harvard School of Public Health, the Harvard Medical School
and Brigham and
Women's Hospital, Boston. Part of the summary which appears in the article is
as follows:
"As part of a longitudinal study of the respiratory351. The authors explain the methodology of their study in considerable detail and make the following observations on their analyses of the data collected:
health effects of indoor and outdoor air pollutants,
pulmonary function, respiratory illness history, and symptom
history were recorded at 2 successive annual examinations of
10,106 white children living in 6 cities in the United
States. Parental education, illness history, and smoking
habits also were recorded, along with the fuel used for
cooking in the child's home. Maternal cigarette smoking was
associated with increases of 20 to 35% in the rates of 8
respiratory illnesses and symptoms investigated, and
paternal smoking was associated with smaller but still
substantial increases. Illness and symptom rates were
linearly related to the number of cigarettes smoked by the
child's mother. Illness rates were higher for children of
current smokers than for children of ex-smokers. The
associations between maternal smoking status and childhood
respiratory illnesses and symptoms were reduced but not
eliminated by adjustment for parental illness history.
Levels of forced expiratory volume in one second (FEV1) were
significantly lower for children of current smokers than for
children of non-smokers at both examinations and highest for
children of ex-smokers. Levels of forced vital capacity
(FVC) were lower for children of non-smokers than for
children of current smokers at both examinations, but the
difference was statistically significant only at the first
examination. Both the increase in mean FVC and the
decrease in mean FEV1 among children of current smokers were
linearly related to daily cigarette consumption. ... These
results provide strong support for a causal effect of
sidestream cigarette smoke on increased respiratory illness
and reduced FEV1 values in preadolescent children."
"These analyses show a consistent association between352. Current maternal cigarette smoking was associated with a 20 to 35% increase in the risk of all respiratory illnesses and symptoms in the past year. A history of either parent smoking was associated with a similar increase in the reported prevalence of early childhood respiratory illness. Each of these respiratory health indexes is linearly related to the current amount of cigarette smoking by either both parents or the mother alone. In all of these analyses, the association between impaired health and passive smoke exposure was stronger with maternal than with paternal or total parental smoking. Children of ex-smokers had respiratory illness and symptom frequencies that were typically between those of non-smoking and currently smoking mothers. This was true for recent illness and symptom experience, as well as for early childhood illnesses. These findings are consistent, at least in part, with the hypothesis that exposure to cigarette smoke increases the risk of contemporaneous respiratory illness."
parental cigarette smoking and increased respiratory illness
during childhood. Of the children in this sample, 43% had
mothers who were current smokers (table 4), 59% had fathers
who were current smokers, and 68% had at least one parent
who was a current smoker. Thus, effects of sidestream
cigarette smoke of the size observed in this study would
represent a substantial public health burden.
353. After referring to the stronger association with maternal rather than
paternal smoking for respiratory illness in childhood,
the authors state:
"The somewhat stronger association of respiratory(l) Pedreira et al. - Involuntary smoking and incidence of respiratory illness during the first year of life
illness with maternal than with paternal smoking habits need
not imply any special risk associated with maternal smoking.
A more plausible interpretation is that the risk factor is
exposure to sidestream cigarette smoke, and that children
are more likely to be with their mothers than with their
fathers at the times smoking occurs."
354. The authors of this article were from the Department of Paediatrics at
the George Washington University School of Medicine,
Washington, DC. The
article was published in 1985. The following summary of the study appears in
the article:
"A prospective study of 1,144 infants and their families(m) Chen et al. - Influence of passive smoking on admissions for respiratory illness in early childhood
was performed. Smoking and family histories were evaluated
with respect to the incidence of lower respiratory disease
during the first year of life. It was found that (1)
tracheitis and bronchitis occurred significantly more
frequently in infants exposed to cigarette smoke in the
home, (2) maternal smoking imposed greater risks upon the
infant than paternal smoking, (3) occurrence of neither
tracheitis nor bronchitis showed a consistent relationship
to the number of cigarettes smoked, (4) a family history
that was positive for respiratory illness (chronic cough or
bronchitis) significantly influenced the incidence of
bronchitis, (5) too few cases of laryngitis and pneumonia
were seen to warrant any opinions regarding the adverse
influence of either smoking or a family history that was
positive for respiratory illness, and (6) occurrence of
bronchiolitis was not affected by the presence of a smoker
nor influenced by a family history that was positive for
respiratory illness. It is concluded that passive smoking
is dangerous to the health of infants and that infants born
to families with a history that is positive for respiratory
illness (chronic cough or bronchitis) are at risk of
developing bronchitis."
355. The authors of this article were from the Department of Epidemiology, School of Public Health, Shanghai Medical University, Shanghai. The article was first published on 2 August 1986 in the British Medical Journal, but was accepted for publication in April 1986.
356. The following summary of the study appears in the article:
"An association was sought between passive smoking and357. These data suggest that exposure to household cigarette smoke of children in early life increases the risk of severe respiratory illness."
in-patient admissions for respiratory illness in 1058
children born between 1 June and 31 December 1981 and living
in the neighbourhoods of Nan-Jing Western Road and Yan-An
Western Road in Jing-An District, Shanghai. The admission
rate for first episodes of respiratory illness was
positively correlated with the total daily cigarette
consumption of family members during the children's first 18
months of life. The relative risk of developing a first
episode of respiratory illness was 1.80 for children living
in families including people who smoked 10 or more
cigarettes a day compared with those living in non-smoking
families. Multiple logistic regression analysis showed that
the effect of passive smoking on inpatient admission for
respiratory illness was independent of the child's birth
weight, type of feeding, father's education, size of the
home, and chronic respiratory disease among adults in the
family. The adjusted odds ratios compared with the
non-smoking group were 1.17 in families smoking 1-9 cigarettes
daily and 1.89 in families smoking 10 or more cigarettes
daily.
358. The authors of this article, which was received for publication on 27 February 1987, were from the Department of Child Health at the University of Bristol and the Departments of Paediatrics and Community Medicine at St Mary's Hospital Medical School, London.
359. The following summary of the study appears in the article:
"In a national study of 12 743 children maternal, but(ii) The major reviews
not paternal, smoking was confirmed as having a significant
influence on the reported incidence of bronchitis and
admission to hospital for lower respiratory tract illness
during the first five years of life. Reported rates of
admissions to hospital for lower respiratory tract diseases
were found to be as high in children born to mothers who
stopped smoking during pregnancy as in those whose mothers
smoked continuously both during and after pregnancy. Rates
of admissions to hospital for lower respiratory tract
diseases in children whose mothers started smoking only
postnatally were no higher than in those whose mothers
remained non-smokers. Postnatal smoking seemed to exert a
significant influence on the reported incidence of
bronchitis, but less than smoking during pregnancy.
These findings suggest that maternal smoking influences
the incidence of respiratory illnesses in children mainly
through a congenital effect, and only to a lesser extent
through passive exposure after birth."
360. The Surgeon General examined a number of studies, based on a variety of
different designs, examining the effects of involuntary
smoking on the acute
respiratory illness experience of children. Most of the studies contained in
the primary articles are considered
by the Surgeon General. He summarises his
assessment of these studies as follows (p 44):
"In summary, the results of these studies show excess acute361. The Surgeon General's Report contains a table (Table I) in which the studies are summarised. Although the table contains some references which are elliptical, I set it out so as to show the material upon which the Surgeon General based his conclusions.
respiratory illness in the children of parents who smoke,
particularly in children under 2 years of age. This
pattern is evident in studies conducted with different
methodologies and in different locales. The increased risk
of hospitalization for severe bronchitis or pneumonia
associated with parental smoking ranges from 20 to 40
percent during the first year of life. Young children
appear to represent a more susceptible population for the
adverse effects of involuntary smoking than older children
or adults. The time-activity patterns of infants, which
generally place them in proximity to their mothers, may lead
to particularly high exposures to environmental tobacco
smoke if the mother smokes."
(TABLE 1 OMITTED)362. The Surgeon General also examined studies as to the association between parental cigarette smoking and prevalence of chronic cough, chronic phlegm and persistent wheeze in children. His conclusion was as follows (p 48):
"In summary, children whose parents smoke had a 30 to 80(b) The National Research Council report
percent excess prevalence of chronic cough or phlegm
compared with children of non-smoking parents. For wheezing,
the increase in risk varied from none to over sixfold among
the studies reviewed. Many studies showed an exposure-related
increase in the percentage of children with reported
chronic symptoms as the number of parental smokers in the
home increased. Misclassification as non-smokers of children
who are actively smoking could bias the results of these
studies. Adolescent smokers may be reluctant to accurately
report their smoking habits, and more objective measures of
exposure may not help to distinguish active experimentation
with cigarettes from involuntary exposure to smoke (Tager
1986). Although misclassification of children who are
actively smoking as non-smokers must be considered, many
studies showing a positive association between parental
smoking and symptoms in children, including children at ages
before significant experimentation with cigarettes is
prevalent. In addition, many studies (Bland et al. 1978;
Weiss et al. 1980; Charlton 1984; Schenker et al. 1983;
Dodge 1982; Burchfiel et al. 1986) found significant
effects of parental smoking after considering active smoking
by the children."
363. At p 9 of this report the following appears:
"Respiratory symptoms, such as wheezing, coughing, and364. In the body of the report particular attention is given to the possibility of under-reporting of active smoking on the part of children, recall bias leading to over-reporting of symptoms by parents, and the confounding variables of infections in parents. All three of these may lead to an over-estimation of symptom prevalences among children of smokers. However, after considering studies that have compared children of parents who smoke with children of parents who do not smoke and after referring to a finding that adjustment for parental symptoms or respiratory illness decreases the strength of the apparent association between exposure to environmental tobacco smoke and respiratory symptoms, but does not eliminate it, the authors state:
sputum production, are increased in children of smoking
parents. These symptoms are more common in children of
smokers than children of non-smokers. The largest studies
place the increased risk of 20 to 80%, depending on the
symptom being assessed and number of smokers in the
household. Also, respiratory infections manifested as
pneumonia and bronchitis are significantly increased in
infants of smoking parents. Some studies have reported
that infants of smoking parents are hospitalized for
respiratory infections more frequently than children of
non-smokers. Among children aged under 1 year, studies are
remarkably consistent in showing an increased risk of
respiratory infections among children living in homes where
parents smoke. There is a dose-response relationship that
relates more to maternal smoking than paternal smoking. The
association persists after allowing for possible confounding
factors such as occupational data, respiratory illness in
the parents, and birthweight. The mechanisms of the
increased risk may either be a direct effect of ETS or due
to a higher risk of cross-infection in such homes.
Regardless of the mechanism, the exposure of small children
to smoking in the home appears to put them at risk of
respiratory illness."
"This finding leads to the reasonable conclusion that the(c) The National Health and Medical Research Council report.
exposures typical of ETS are sufficient to cause respiratory
symptoms in some children. The increases in frequency of
cough were 20 to 50%, and as high as 90%, when there were
smoking parents. The increases in frequency of wheezing
were more variable, which may indicate the difficulty in
assessing this symptom. Furthermore, there appears to be a
dose-response relationship between exposure and the
likelihood of the child's developing respiratory symptoms or
a respiratory illness."
365. The following are extracts from chapter 5 of this report, which deals
with Passive Smoking and Child Health. I have omitted
references to some of
the footnotes in the text of the report:
"Several adverse health effects resulting from passive366. The summary of the chapter in the report on Passive Smoking and Child Health is expressed in the following terms:
smoking during childhood have been demonstrated. Children
who receive a heavy passive exposure to cigarette smoke have
more symptoms and disability from respiratory tract
infection than other children. Although many controlled
studies have shown this increased prevalence of respiratory
symptoms in children of smoking mothers, this observation is
not universal.
The best longitudinal cohort studies, adjusted for
confounding variables, document that there is approximately
twice the incidence of respiratory symptoms and disability
due to respiratory disease in smokers' children in the first
year of life, compared to children of non-smokers. In fact,
no study negates this observation in the first year of life.
However, the relationship is less certain at later ages."
"Smoking during pregnancy has a clear detrimental effect on(iii) Oral evidence
the fetus. A consistent association of passive smoking with
respiratory morbidity in children has been reported in a
number of studies, based on different populations, using
different study designs with a variety of outcome measures.
There is strong evidence to suggest that maternal smoking is
associated with increased lower respiratory symptoms in the
first year of life. Associations of passive smoking with
respiratory symptoms, reduced lung function, or asthma
symptoms in later childhood have been suggested, but the
changes are small. Additional longitudinal studies will be
required to determine whether these changes are clinically
significant.
Smoking and non-smoking families differ in various respects
and, although such differences have been recorded and
adjusted for in many studies, it remains possible that some
of the apparent effect of passive smoking arises from other
environmental or behavioural confounding factors that have
not been adequately controlled. Further, it is not known
whether young children respond more to these irritants, nor
whether observed effects of passive smoking reflect
predominantly a small effect in large numbers or a larger
effect in a susceptible subgroup.
Passive smoking does appear to have some detrimental effect
on health at most ages from conception to adolescence. A
dose-response relationship with increasing maternal smoking
rate found in a number of studies makes a causal link
between passive smoking in infancy and respiratory illness,
abnormal lung function in childhood, increased asthmatic
symptoms and impaired growth seem likely. Further
longitudinal studies should help clarify these
observations."
367. Professor Louis Landau is a respiratory physician. He has been Professor of Child Health in the University of Western Australia since 1984. He was at one time Principal Research Fellow at the Royal Children's Research Foundation, Melbourne and is a former Head of the Professorial Department of Thoracic Medicine at the Royal Children's Hospital, Melbourne. The professor's clinical work is concerned exclusively with children with respiratory disorders. He has had considerable experience in clinical work.
368. In the course of his clinical experience over the past 15 years Professor Landau has examined and treated numerous non-smoking patients whose conditions and diseases were, in his view, directly or indirectly attributable to exposure to passive smoking. He is of the opinion that there is evidence which proves scientifically that cigarette smoke causes disease in non-smokers.
369. Professor Landau is of the opinion that tobacco smoke can harm children because of the effect of, inter alia, passively inhaled smoke. He said that measurements of continine in the secretions of children exposed to environmental tobacco smoke indicate significant intake of compounds which could exert a detrimental effect on their health. He said that although there is some variability in the measurements, there is a consistency of some effect and a dose-response to environmental tobacco smoke.
370. According to the professor, children who receive a heavy exposure to cigarette smoke have more symptoms and disabilities from respiratory illness than others. He believes that the best studies, adjusted for confounding variables, document at least double the incidence of respiratory symptoms in the first year of life. In his opinion, cigarette smoke may also have an adverse effect on the health of children with pre-existing lung disease. He said that a dose-response relationship and the presence of high levels of cotinine in secretions from the children exposed to passive smoking make a causal link between passive smoking and, inter alia, respiratory disease seem very likely.
371. Professor Landau was the principal author of Chapter 5 of the NH and MRC report. He said that his views, as I have summarised them above, were held by him as at July 1986.
372. He gained particular support for his opinions from the primary articles by Harlap and Davies, and by Fergusson et al. However, he referred to many other primary articles in his evidence, and drew support from them.
373. As will be seen when I refer to the evidence of Dr Witorsch as to the relationship between passive smoking and respiratory disease in children, there does not appear to be much difference between his and Professor Landau's views as to the effect of passive smoking on children in the first year of life.
374. Professor Landau was cross-examined as to his views, but, in my opinion, they were not shown to be in any way erroneous. He was asked very little about the effect of passive smoking on children under the age of one year. He was cross examined at some length as to the reasons why the first draft of part of the NH and MRC report had been altered. This part did not relate to respiratory symptoms in children in the first year of life. In any event, the professor's explanation of the making of the alteration leaves me in no doubt that it was properly made.
375. Professor Landau was cross examined at some length about the Harlap and Davies study. He agreed (T.2136) that it pointed to the need for more and more detailed studies on the subject. However, he said the study gave information which needed to be confirmed and which was subsequently confirmed, by other studies.
376. Professor Landau limited his assertion that there was scientific proof
that passive smoking causes disease to the causation
of respiratory disease in
children under the age of 12 months. But he said (T.2060):
"I think once we get beyond the first year of life the(b) Dr Le Soeuf
associations are strong, consistent, but it would be harder
to use the definition of scientific proof in them ..."
377. Dr Peter Le Soeuf is Director of the Department of Respiratory Medicine at Princess Margaret Hospital for Children, Perth. He has had extensive experience in paediatrics. He was formerly a Research Fellow in the Respiratory Physiology Department of the Hospital for Sick Children, Toronto, Canada. He has been a Fellow in Paediatric Respiratory Medicine at the Royal Children's Hospital, Melbourne. He has held his present position for the last six years during which time he has been a Senior Lecturer in the Department of Paediatrics at the University of Western Australia. He is the co-author of a large number of learned articles mostly related to respiratory functions in children.
378. Dr Le Soeuf is of the opinion that there is very strong scientific evidence that the passive inhalation of cigarette smoke causes disease in young children. He bases his opinion on his professional and clinical experience as a paediatrician and upon his reading of the scientific literature. He said that in the course of his clinical experience and in his capacity as a consultant respiratory physician, he has examined and treated 40 young children whose condition or disease was in his view directly or indirectly attributable to exposure to passive smoking. He said there is an abundance of pathological, clinical and epidemiological evidence suggesting that passive smoking is an important and significant cause of respiratory illness in infants and young children.
379. In Dr Le Soeuf's opinion, the strongest evidence of a causal
relationship between passive smoking and respiratory disease is
found in
studies of infants in the first year of life. He thinks that the studies of
children in this age group had detected a relationship
between parental
smoking and respiratory problems. He said that a significant relationship
between passive smoking and respiratory
disease or impaired lung function in
children beyond the age of infancy had also been found, but such relationship
has not been found
in every study involving older children. He summarised his
view as follows:
"In summary, there is a great deal of data from many(Annexure "E" to his affidavit)
different sources implicating passive smoking as a cause of
respiratory disease in children. The strongest data is in
the first year of life; every study in this age group has
found that respiratory problems and passive smoking are
significantly related. Overall, the data are so strong that
in my opinion the possibility that passive smoking is not
related to respiratory illness in young children is now
excessively remote."
380. Dr Le Soeuf said that as a consultant paediatric respiratory physician he has seen many children, mostly asthmatic children over five or six years of age, who report that cigarette smoke exacerbates their respiratory symptoms, and that accordingly they move away from smokers. He said that more than half the children he sees are unable to recognise the effect on them of smoke and are likely to remain in the vicinity of smokers. It is his opinion that there are several infants under his care who have required hospitalisation due to their parents' cigarette smoke.
381. Dr Le Soeuf has great experience in the treatment of children. He estimated that he sees about 500 each year. He agreed that his statement that he had treated 40 young children whose condition was directly or indirectly attributable to exposure to passive smoking was an assessment based on his general experience, rather than on case histories of particular patients.
382. Dr Le Soeuf was cross examined at length as to the reliability of some
of the studies upon which he placed reliance, particularly
that of Harlap and
Davies. But I do not think that it was shown that the studies were
unreliable. Nor do I think that the cross
examination of him showed that his
opinion as to the effect of passive smoking on very young children was
unsound.
(c) Dr Nolan
383. Dr Terence Nolan is Senior Lecturer in the Department of Paediatrics at the University of Melbourne. Amongst his other qualifications, he holds the Degree of Doctor of Philosophy from the Department of Epidemiology and Bio-statistics at McGill University. Dr Nolan lectures in Theoretical and Applied Epidemiology to students who are pursuing the Degree of Master of Science in Epidemiology.
384. According to Dr Nolan, the epidemiological evidence of adverse health effects due to passive cigarette smoking on infants and children is considerable. In his opinion, in most cases the available evidence, apart from being abundant, is consistent, plausible and "temporally appropriate", i.e. one can be sure that exposure has preceded the onset of disease.
385. In his opinion, passive exposure to cigarette smoke increases the risk of respiratory illnesses, such as pneumonia, bronchiolitis, bronchitis, tracheitis and laryngitis in infancy and early childhood, at least during the first two years of life.
386. Dr Nolan is of the opinion that the findings referred to in the primary articles cannot reasonably be explained by bias in investigational methods, nor attributed to chance, nor reasonably explained by other factors.
387. Dr Nolan said that the opinions which he now holds were also held by him
as at July 1986. Dr Nolan made particular reference
to the studies by
Colley, Fergusson et al., Harlap and Davies, Pedreira and Rantakallio. Cross
examination did not, in my opinion,
reveal any important deficiencies in these
studies or show that Dr Nolan was not justified in placing reliance upon them.
I formed
the opinion that Dr Nolan was particularly skilled in his specialist
field.
(d) Professor Phelan
388. Professor Peter Phelan has been Professor and Chairman, Department of Paediatrics, Melbourne University since 1983. He has been Chief Thoracic Physician at the Royal Children's Hospital, Melbourne since 1983. He has had a great deal of experience extending over many years in the treatment of children. For some years he was a Research Fellow in the Clinical Research Unit at the Royal Children's Hospital Research Foundation. He has been a visiting Professor in the Institute of Child Health at the University of London and an Honorary Consultant Physician at the Hospital for Sick Children, Great Ormond Street, London.
389. Professor Phelan said that there are many studies that indicate that the incidence of lower respiratory tract infection in children, particularly in the first one or two years of life, is increased amongst those exposed to cigarette smoke. Maternal smoking seems to have a much stronger effect than paternal smoking.
390. He said that evidence of an association between parental cigarette
smoking, particularly domestic exposure, and respiratory
illness in children
is overwhelming. When challenged on this statement, he said that:
".... I think it is the volume - the consistency of the391. He also said that it was his view that there is "extremely strong overwhelming evidence that there is an association between parental smoking and various types of respiratory illness in children" (T.1669).
studies that I have referred to, and in many of them the
very large numbers that together, in the view of experienced
epidemiologists, say the evidence is overwhelming."
(T.1668)
392. He was cross examined about this statement and his evidence included the
following (T.1670-71):
"Now, by `overwhelming' do you mean to suggest to his Honour394. In his opinion, it would be extremely difficult for someone who stood back and objectively looked at the evidence to come to any conclusion but that there is an association between exposure to cigarette smoke in a domestic environment and respiratory illness in children (T.1669).
that competent, well-informed, and reputable
epidemiologists, expert in this area, namely, childhood
respiratory disease and exposure to cigarette smoke could
not consistently with those quality (sic) hold the view that
it was less than overwhelming?---I cannot speak for every
reputable epidemiologist with interest in this area. All I
could say, I would find it very difficult to perceive how
someone who has studied the subject could come to a
different conclusion. But I cannot say that someone may
not."
(The word "quality" in the above question is, I think,
wrongly attributed in the transcript to the cross examiner.
The reference should be to "studies").
"Are you intending to suggest to his Honour perhaps that it
is beyond debate so far as you are concerned?---Certainly,
as far as I am concerned, it is beyond debate.
For how long has it been beyond debate so far as you are
concerned?---I think the studies became available from the
mid-70s onwards, and certainly by the early '80s, and
definitely by the mid-80s I believed it was a subject beyond
debate, as far as I personally am concerned.
What are the mid '80s? 1983 to 1988? 1987?---1984, 1985.
So, by 1984 or thereabouts, you tell his Honour, you
regarded the question of an association between childhood
respiratory illness and exposure to cigarette smoke as being
beyond debate. Is that correct?---I believed at that stage
that the evidence was very convincing.
And when I refer to `debate' I am, of course, referring to
debate amongst honest, competent, relevantly expert
scientists. Do you understand that?---I understand what
you are saying and - - -
Is that what you are saying, that by 1984, in your opinion,
this question was beyond such debate?---I believed, with my
recall of what evidence was available - and I would have to
go back and check precise dates - but by the mid 1980s as I
used (sic), that evidence was extremely convincing. Now, I
cannot say that there would not be people who wish to take
the opposite view. There are always in this world people
who may wish to take an opposite view. But it certainly
was a consensus of the people with whom I came in contact in
the field of paediatric respiratory disease believed that
evidence was convincing.
Now, you have referred to people who will always take an
opposite view. Do you mean by that to suggest to his
Honour that people who disagree with your view are ornery
persons who would disagree for the sake of disagreeing ---
?Not necessarily.
Do you agree that there - it is true to say that, as at 1
July 1986, it was open to reputable, competent,
well-informed epidemiologists and medical scientists, expert in
the area of respiratory disease in children and exposure to
cigarette smoke, to believe that there was, in fact, little
evidence of an association?---I would not agree with that
statement."
395. Professor Phelan referred, as did the other witnesses in the applicant's case, to the many epidemiological studies tendered in evidence. I do not think any useful purpose would be served by further reference to them in these reasons. He noted some criticisms which could be made of some of the studies and took account of them. I much prefer his assessment of them to those made by the respondent's witnesses. He described the Fergusson et al. study as "a very well undertaken epidemiological study" (T.1009-10). He was extensively cross examined as to this study but I do not think his evaluation of it was shown to be wrong.
396. Professor Phelan was asked to explain how the views expressed in
evidence could be reconciled with views he had expressed in
a recent edition
of a textbook of which he was co-author. In the book the following passage
appears:
"Uncertainty remains as to the reasons for the relationshipProfessor Phelan said that he and his co-authors were too careful in writing that passage and that if he was writing it again he would have written it differently. The book was first published in 1975 and the second edition appeared in 1982. Professor Phelan said that, in retrospect, he thought that the section of the book from which the above quotation is taken should have been re-written.
between parental smoking, parental winter phlegm and
childhood respiratory illness. It is possible that the
relationship is due to a similar genetic background. The
presence of parental phlegm could increase the risk of
cross-infection. Passive inhalation of tobacco smoke itself
may be a cause of respiratory damage. Whatever the
mechanism, parental cigarette smoking is a major risk factor
for lower respiratory infection in infants and children."
397. I do not think the weight of Professor Phelan's evidence was lessened by
the reference to the quotation from the book first
written in 1975. For the
purpose of this case, I am most concerned with his views as to the effect of
respiratory illness in children
in the first year or so of life. I do not
think the statement in the third edition of his book, which refers to
childhood respiratory
illness in general, diminishes the weight of his
evidence on the matter with which I am mostly concerned.
(e) Professor Witorsch
398. I have referred elsewhere to Professor Witorsch's qualifications and experience. The bulk of Professor Witorsch's clinical experience and academic research has been in the field of adult pulmonary disease (T.3102).
399. Professor Witorsch said that an important assumption underlying the epidemiological studies into the possible association between environmental tobacco exposure and respiratory function in children is that parental smoking is an adequate and reliable surrogate for direct measurement of exposure to environmental tobacco smoke of the children whose respiratory condition is being examined. He agreed that a number of the studies reported an association between parental (usually maternal) smoking and an increased frequency of respiratory symptoms and/or illness in infants and children below the age of 2 years. He said that while individual studies suffered from various methodologic and other problems, the overall data nevertheless showed an association between maternal smoking and respiratory symptoms and/or illness in this age group of children. However, he thought there were no studies that establish any association between these findings and the development of respiratory disease or dysfunction in later life.
400. Professor Witorsch made some criticisms of the studies tendered by the applicant (especially one by Professor Landau and Dr Le Soeuf) and drew attention to the possibility of confounding factors. However, it is fairly clear from his evidence that whilst he has reservations as to the effect of passive smoking on children over the age of 12 months, he accepts that in their first year of life children of smoking mothers are more likely to have respiratory problems than children of non-smoking mothers. (T.3085). He also said that he did not see any substantial difference in the evidence on this matter between 1986 and the present time (T.3086).
401. He thought that socio-economic factors may account, at least in part, for the increased frequency of respiratory symptoms and illness in young children associated with maternal smoking. Parental smoking is higher in lower income groups and is also positively correlated with a number of socio-economic related variables that can adversely affect childhood respiratory health, e.g. diet, housing, living density, ventilation, personal hygiene and other health habits, cooking and heating practices. He thought that in the studies associating parental smoking with respiratory health in young children adjustments for socio-economic status were either not performed or the complexities of them were not adequately taken into consideration. In this respect he pointed to the findings in the Harlap and Davies study that while there was an increased incidence of respiratory illness, there were also increased hospitalisations due to poisoning and injury in infants of smoking parents. This suggested to Professor Witorsch that the association reported in that study, and perhaps some of the other studies, may have been indicative of general parental neglect.
402. I do not think the socio-economic factors to which the professor
referred would have been likely to have so substantially affected
the results
of the study showing the effect of passive smoking on very young infants as to
render those results unreliable.
(f) Professor Huber
403. I have referred to Professor Huber's experience and qualifications elsewhere in these reasons. He does not appear to have had any special qualifications or experience in relation to respiratory disease in young children.
404. The professor commented upon many of the primary articles dealing with the association between environmental tobacco smoke and pulmonary functions. So far as they related to children, he said that the published results were neither uniform nor consistent and were difficult to interpret. In his proof of evidence he said little as to the effect of passive smoking on very young children, or as to the studies of such children. He made no mention of the Harlap and Davies study. With respect to the study by Fergusson et al, he thought that it did not define the precise nature of the outcomes which were being investigated. He said that in that study a child was defined as displaying symptoms of lower respiratory illness if he had received medical attention for bronchitis/pneumonia or if his mother reported "chesty colds or wheeze". He thought this definition lacked reliability and that, in any event, wheeze is usually not associated with lowers respiratory tract illness. He also thought that the reliability of the index used to define bronchitis or pneumonia was unreliable.
405. I do not agree with these criticisms of the Fergusson et al report, which were not made by other witnesses. The authors of the Fergusson et al. report were paediatricians and might be expected to have defined with reasonable precision the nature of the outcomes they were investigating. In his analysis of the studies, the Surgeon General makes no mention of the criticisms raised by Professor Huber.
406. Professor Huber said (Ex. 60, p 44) there is an approximately equal number of studies which report no significant association between parental smoking and respiratory illness in children, and cited a large number of articles in support of this argument. The two studies of which he made particular mention, viz. a study conducted in Holland by Kerrebijn et al. and published in 1977 and a study by Schilling et al. carried out in the United States and published in 1977, related to respiratory symptoms in school-age children. The subjects of the Schilling study were aged seven years or more and the children studied in the Kerrebijn study were attending school.
407. I have read all the studies referred to by Professor Huber and I do not think they provide data which is inconsistent with the findings by Harlap and Davies and by Fergusson et al. Professor Huber did not refer to any clinical experience which he had in treating very young children.
408. Upon examination, some of the studies referred to by Professor Huber,
but not elaborated upon in oral evidence, do not support
his opinions. For
instance, in a study by Bouhuys the statement is made that:
"Children of smoking parents may suffer unduly from409. The studies referred to in the above quotation are ones which were not made by Bouhuys but it is plain that he adopts them. At the time of writing the paper, Bouhuys was Professor of Medicine and Epidemiology at Yale University Lung Research Center.
respiratory disease. For example, infants of mothers who
smoke have significantly more attacks of bronchitis and
pneumonia than infants of non-smoking mothers. Also,
children of smoking parents who may or may not have symptoms
themselves have more bronchitis and pneumonia during their
first year of life than children of non-smoking parents.
However, this was not true during four subsequent years of
follow-up. But even older children may have an increased
incidence of acute respiratory disease in homes where
cigarettes are smoked. These studies have led to the
conclusion that passive smoking (inhaling other people's
smoke) is injurious to health."
410. The Bouhuys study was concerned with children between the ages of 7 and 18. It is true that Bouhuys concluded that exposure to low levels of smoke produced by cigarette smokers does not result in chronic respiratory symptoms among children and adults. However, it is plain that this conclusion does not relate to children in the first year or two of life.
411. Another study referred to by Dr Huber was that by Gardner et al. This was a relatively small study of 131 infants. The authors found that the infants of parents who smoked were not at greater risk for viral infection or respiratory illness, the only exception to this being a significant relationship between pneumonia and parental smoking, especially in mothers at home. The authors state that their observations are in contrast with those of Harlap and Davies and Leeder. It was a much smaller study than the Harlap and Davies and Fergusson studies. Most of the studies referred to by Professor Huber seem to me to have very little, if any, relevance to a consideration of the effects of passive smoking on children in the first year or two of life.
412. I formed the opinion that Professor Huber sees difficulties and
limitations in studies which are not perceived by competent
researchers and
specialists in the field.
(iv) Does cigarette smoke cause respiratory disease in young children?
413. In my opinion the only conclusion open on the evidence is that the statement that there was little evidence and nothing which proves scientifically that cigarette smoke causes disease in non-smokers, was demonstrably false in 1986 insofar as it applied to respiratory disease in children in the first year of life. The statement remains false to this day. In my view the falsity of the statement is demonstrated whatever meaning one gives to the terms "little evidence" and "scientific proof". I share the opinion expressed by Professor Phelan that the evidence, establishing a causal relationship between passive smoking and respiratory disease in very young children is overwhelming. The evidence is of such strength that it constitutes scientific proof.
414. The evidence is of two kinds, epidemiological and clinical. I cannot help observing that none of the witnesses called by the respondent were specialist paediatricians or epidemiologists. On the other hand, the applicant's witnesses included specialists in both fields. I think that the respondent would have called specialists in these fields, of whom there must be many in this country and overseas, had they been able to give evidence favourable to the respondent's case.
415. I was greatly impressed by the applicant's witnesses and prefer to accept their opinions whenever they are in conflict with the opinions expressed by the respondent's witnesses.
416. As I have observed, the applicant tendered many primary articles and
called much oral evidence in support of its claim that
passive smoking causes
respiratory disease and loss of lung function in older children and adults. I
make no finding one way or
the other on this part of the applicant's case,
since it is unnecessary to do so for the purposes of deciding whether the
advertisement
is misleading or deceptive. To have dealt adequately with the
evidence on this issue would have greatly expanded these already lengthy
reasons.
(9) Asthma
417. It is part of the applicant's case that the statement in para. 3 of the
advertisement is misleading or deceptive in so far as
it applies to the
disease of asthma. In order to evaluate this part of the case it is necessary
to make brief mention of the nature
and symptoms of the disease.
(i) Meaning of "asthma"
418. Dr Breslin, to whose evidence I shall subsequently refer in greater
detail, said that the standard definition of asthma is "paroxysmal
generalised
airways obstruction which varies spontaneously or as a result of treatment"
(T.569). He explained the disease in the
following terms (T.569-70):
"Now, basically what asthma is; it is a narrowing of the419. Having said that the airways vary from a centimetre in width at the trachea down to the width of a thread of cotton, Dr Breslin said (T.571):
airways. The lungs are composed of two parts the breathing
tubes that take air down into the spongy tissue or the lungs
and the spongy tissue itself which is the lung substance.
And asthma is a disease of the airways and not of the lung
tissue.
I liken it - the lung structure to say an inverted tree
where you have got the trunk of the tree representing the
trachea, the branches of the tree representing the remaining
tubes that conduct air and the leaves of the tree being that
part of the lung tissue where gas exchange takes place,
oxygen is taken up by the body, carbon dioxide given off.
The trunk of the tree is the trachea, the various branches
are the bronchi, that gets smaller and smaller and smaller
and smaller as they go out towards the leaves or alveoli and
basically asthma is a disease of the conducting airways. It
is not a disease of the leaves or alveoli. The basic
abnormality in asthma is that out of the blue and from time
to time in some patients and all the time in others the
airways narrow down and then later on open up either
spontaneously or as a result of treatment. Some people
when a door slams leap out of their chair, some people cry
easily, some people blush easily, asthmatics' airways narrow
down easily. The reason they narrow down easily is because
they are twitchy or hypersensitive. So one of the basic
abnormalities in asthma is that the airways are twitchy.
... The airways are twitchy but having twitchy airways alone
does not mean you have got asthma because there are normal
people wandering around the community, probably some people
in this room, who have twitchy airways but do not have
asthma. In order to have asthma, the disease asthma, you
need what I originally referred to in the definition and
that is paroxysmal generalized airways obstruction. In
addition to the twitchiness you, as it were, need the door
to slam and have you leap out of the chair as it were ..."
"And these airways in asthmatics narrow down because they420. Dr Breslin's description of asthma was not challenged in cross-examination and I did not understand the respondent's witnesses t o disagree with it.
are twitchy and they narrow down to a variety of stimuli.
So when a person has, firstly, twitchy airways and secondly,
episodes of wheeze, chest tightness, shortness of breath and
measurable objective changes of their lung function, then we
call them asthmatic, they have the disease asthma. Having
the twitchy airways in itself is not a disease because a lot
of people without disease have that."
421. Dr Antony Breslin is a consultant thoracic physician. Since 1973 he has been the Senior Specialist in Charge (Chest Diseases) at the Repatriation General Hospital, Concord. He has for many years been a lecturer at the University of Sydney. He is a former chairman of the Thoracic Society of Australia (New South Wales) Branch and a member of the Court of Clinical Examiners, Royal Australasian College of Physicians. Dr Breslin has been specialising in respiratory disease and, in particular, asthma, for about 20 years.
422. Dr Breslin said that unless a person has attacks of asthma he does not
have the disease of asthma (T.650). It was put to him
in cross examination
that there is a distinction between the disease of asthma and attacks of
asthma but he refused to accept this
distinction. He supported his refusal
by drawing a comparison between asthma and epilepsy. He said:
"You can have the propensity to epilepsy but if you do not423. In his practice as a respiratory physician Dr Breslin sees a large number of patients of all ages suffering from bronchial asthma. A very large proportion of these patients indicate to him that passive smoking is harmful to their asthma and produces a deterioration in their asthmatic condition.
have fits you do not have epilepsy. You can have the
propensity to attacks but if you do not have attacks you do
not have asthma."
424. In order to confirm whether the views of his patients could be supported
objectively, Dr Breslin undertook a small study of
asthmatic patients and
exposed them to cigarette smoke. This study was carried out in 1984 and the
results of it were published,
in abbreviated form, in the Medical Journal of
Australia in February 1985. The abstract of the study as published reads as
follows:
"A study of the effect of passive smoking on patients with425. Dr Breslin said that his clinical experience since he carried out his study in 1984 has served to confirm even more forcibly his opinion that passive smoking is a medical hazard. He said he was convinced that there is a large volume of evidence confirming that passive smoking "is a frequent and very troublesome trigger for bronchial asthma in many patients".
asthma is presented. Six patients were exposed for one hour
to the air in a room in which tobacco smoke was produced
mechanically over that period. The effects on symptoms,
lung function and airways sensitivity to inhaled histamine
were then measured and compared with the same patient's
responses during a control day when they inhaled smoke-free
air. All six patients developed chest tightness and
symptoms similar to an attack of asthma. The findings of
respiratory and sensitivity tests suggest: (i) that
passive smoking may trigger asthma attacks in subjects who
suffer from asthma and (ii) that the airways of such
subjects show increased histamine reactivity four hours
after the passive smoke exposure."
426. Dr Breslin said that about 20% of children under the age of 20 and about 10% of the total Australian population have asthma. His practice is to initially ask his patients what sort of things they have noticed trigger their asthma and then he subsequently asks them directly whether other things, which he nominates, trigger it. Thirty to thirty-five per cent of patients volunteer that cigarette smoke appears to have an effect on their asthma. When patients are specifically asked whether cigarette smoke has an effect on their asthma, the percentage of patients who respond positively rises to the order of 50 or 60% (T.582).
427. Dr Breslin supported his opinion by reference to articles which had
appeared in learned scientific journals. One such article
by Dahms et al. was
published in November 1981. The authors concluded that:
"The results of this initial investigation indicate that428. There is some inconsistency among the studies referred to by Dr Breslin. One reason for the inconsistencies, as is observed in the NRC report at p 215, is the small sample sizes in the various studies. Further, as is noted in the report, the persons surveyed were not unaware of the presence of environmental tobacco smoke and therefore the authors could not exclude the possibility that pulmonary function changes could have been emotionally related to cigarette smoke exposure, especially in those patients who reported previous histories of adverse response to exposure to environmental tobacco smoke.
patients with bronchial asthma do respond adversely when
actively exposed to environmental tobacco smoke."
429. In the Surgeon General's 1986 report the statement is made that biases in observation and in the selection of subjects and the subjects' own expectations may have accounted for the divergent results. However, there is nothing in the major reviews to refute Dr Breslin's evidence that cigarette smoke causes attacks of asthma in some asthmatics.
430. Dr Breslin also referred to a study carried out by Kauffmann et al. the results of which were published in the American Review of Respiratory Diseases in 1986. He said the study showed that there was a statistically significant worsening of airways obstruction in asthmatic women as a result of exposure to cigarette smoke. Also, the study demonstrated that the greater the exposure to passive smoke, the worse was the effect on the asthma of the women.
431. Dr Breslin also referred to a study carried out by Murray et al., the
results of which were published in July 1986. The authors
summarised their
findings as follows:
"The effect of parental smoking was assessed in 94432. FEV refers to forced expiratory volume. Thus FEV 1 represents the amount of air that a person can get out of his lungs in a forced manoeuvre from full inspiration in the first second. FVC means forced vital capacity, that is, the total amount of air that one can expel in one forced manoeuvre. Normally FEV 1 should be greater than 80% of the FVC. That is to say, normally if a person takes a full deep breath and then exhales rapidly and to completion he should be able to exhale more than 80% of the air in the first second. It is a characteristic of asthmatics that the ratio of their FEV 1 to their FVC during an attack of asthma is less than 80%.
consecutively observed children, aged 7 to 17 years, who had
a history of asthmatic wheezing. The 24 children whose
mothers smoked, when they were compared with children whose
mothers did not smoke, had 47% more symptoms, a 13% lower
mean FEV percent, a 23% lower mean FEF, and fourfold greater
responsiveness to aerosolized histamine. A dose response
was evident. There was a highly significant correlation
between the results of the tests and the number of
cigarettes the mother smoked while she was in the house.
The differences between the children of smoking and
non-smoking mothers were greater in older than in younger
subjects. The smoking habits of the father were not
correlated with the severity of the child's asthma."
433. Murray et al. made the following observation on their study:
"The evidence suggests that it is airborne cigarette smoke434. In contrast to the smoking habits of the mother, those of the father had no significant correlation with the severity of the child's asthma. These findings agree with those in more recently published large epidemiologic studies. Several factors may account for this apparent paradox. One is our finding that the father, compared with the mother, smokes significantly fewer cigarettes when he is at home. Another is the possibility that the mother, more frequently than the father, is in the same room as the child when she smokes a cigarette. A third possibility is that the number of cigarettes smoked in the house are more accurately reported for the mother than for the father. The mother was usually the person who gave the information. Whatever the reason, the father's smoke did not appear to influence the child's asthma significantly. When we examined the effect of maternal and paternal smoking together, therefore, we found it to be less clear than when we examined the result of maternal smoking alone. This observation may explain the lack of effect of parental smoking on wheezing and spirometric values reported in some epidemiologic studies.
that causes the adverse effect. Not only is there a strong
association between maternal smoking and severity of the
child's asthma, but there is also evidence of a dose
response. We found a significant correlation between all
indicators of asthma severity and the logarithm of the
number of cigarettes the mother smoked while she was in the
home. There was also evidence that length of exposure had
an effect. The older children, who had presumably been
exposed to cigarette smoke for more years than the younger
ones, were more severely affected. This finding is similar
to that of Tager et al. They reported that the normal rate
of increase in FEV1 during adolescent growth is slowed in
children whose mothers smoked. Further evidence, that it is
passively inhaled smoke that is responsible for the changes,
is the effect observed when the mother stops smoking. Vedal
et al. report that children whose mothers are current
smokers do but children whose mothers are ex-smokers do not
have significant differences in pulmonary function from
those whose mothers are non-smokers.
....435. Dr Breslin also supported his opinion by reference to a study by O'Connell and Logan published in 1971. The summary of the findings in this study is as follows:
Our findings indicate that maternal smoking aggravates
asthma in children, the effect being clinically important as
well as statistically significant."
"The relationship between childhood asthma and parental436. As part of their study, O'Connell and Logan noted the effect of the cessation of parental smoking. They identified 37 children whose parents' smoking had a significantly adverse effect on their asthma. Of these 37 families, 35 were followed up six months to two years later. Among them, 20 had succeeded in stopping the children's exposure to smoke and improvement had been obtained in 18 of the children. Smoke exposure had continued in 15 of the families and improvement had occurred in only 4 of those families. The improvement in these four cases was attributed to the elimination of contact with other factors. The authors noted that in general where smoke exposure was a significant factor in asthma, its elimination was followed by improvement and with continuance of exposure improvement did not occur.
smoking was studied in 400 cases. The incidence of parental
smoking was about the same in asthmatic children's homes as
in those of controls. Tobacco smoke aggravated the asthma
in 50% of all the asthmatic children and in 67% of those
whose parents smoked. Exposure to tobacco smoke was
considered a significant factor in 10%. Elimination was
usually followed by clinical improvement."
437. O'Connell and Logan observed:
"From this study we assume that nearly two of every three438. Dr Breslin acknowledged that this study had the weakness of being retrospective. The authors carried out their study by examination of clinical files and records of 400 asthmatic children who were treated for their asthma in 1969, 1970 and early 1971.
children seen in the offices of Midwestern paediatricians
come from homes in which one or both parents smoke and that,
among asthmatic children from such homes, this daily air
pollution aggravates the asthma at least occasionally in
67%."
439. Dr Breslin referred in his evidence to a study by Shepherd. This study was not confined to persons suffering only from asthma. It included sufferers from chronic bronchitis and pulmonary emphysema. Dr Breslin described this as a "critical fault" in the study. The study considered 14 volunteer asthmatic subjects who were exposed to environmental tobacco smoke in a room. All the subjects developed some symptoms but there were only very slight changes in respiratory function tests. Four of the fourteen who gave a positive pre-test history of their asthma being worsened by exposure to passive smoking showed small changes in their FEV1, but the others did not. Dr Breslin thought it was hard to attach any significance to the study (T.602- 3).
440. Dr Breslin also referred to a study by Wiedemann et al. undertaken in 1983 but published in February 1986. The authors studied the acute effects of one hour of passive cigarette smoking on the lung function and airway activity of 9 young asthmatic volunteers. At the time of the study, the subjects were asymptomatic and had normal or nearly normal lung function. Passive smoking produced no change in their expiratory flow rate. The authors concluded that passive smoking presented no acute respiratory risk to young asymptomatic asthmatic patients. Dr Breslin observed of this study that it was made of subjects whom he described as "extremely mild asthmatics", none of whom was receiving any treatment. He drew a distinction between such persons and the type of persons referred to in the other studies.
441. Dr Breslin maintained that a person is an asthmatic if he gets attacks
of asthma. He described asthma as a "recurrent condition"
(T.623). His
clinical experience in treating asthmatic children was not challenged, nor was
his evidence as to the percentage of
his patients who informed him that
tobacco smoke appears to have an effect on their asthma.
(b) Professor Phelan
442. Professor Phelan said that passive exposure to cigarette smoke seems to
have a significant effect on asthmatic symptoms, and
that cessation of smoking
by parents leads to an improvement in asthmatic symptoms. As to the general
nature of asthma, the professor
said (T.989-90):
"I like to think of asthma as an inherited predisposition to443. He later said (T.990):
the development of the condition or disease called asthma.
It clearly is an inherited predisposition in the airways.
Then various trigger factors can lead to narrowing in those
airways that results in the symptoms of asthma and to be
(sic) asthma is a disease causing symptoms that interfere
with the patient's normal activities - cough, wheeze and
breathlessness. Between those overt symptoms there may be
some degree of airways narrowing persisting but it may not
be of sufficient degree to affect their day to day
activities and that term may then be called subclinical
asthma or - the propensity to asthma in children, we do not
have adequate data to say `Is there changes present all the
time in the child who has, say, three or four episodes of
asthma a year.' To obtain that information would require to
take pieces of the lining of the airways and that is
ethically unacceptable in children. I think there is much
evidence to suggest that three quarters of children probably
have normal airways between their episodes and those
episodes then are triggered by various factors."
"... there are perhaps 20 to 30 per cent of the population444. As well as referring to some of the epidemiological studies referred to by Dr Breslin, Professor Phelan referred to a study by Horwood et al. published in 1985. This was a study carried out in New Zealand in which no evidence was found to suggest that parental smoking played a significant role in the development of asthma in children up to the age of six years. Professor Phelan said that the number of children studied was small, there being only four girls with asthma from families in which both parents smoked. Nevertheless, he thought the study, particularly in respect of boys, showed a trend, i.e. when both parents smoked there was more asthma amongst the boys than when neither parent or only one parent smoked. The same trend was not apparent amongst girls.
(who) with appropriate trigger factors may develop allergic
manifestations. It may be hay fever, it may be skin weals.
Most of the time they are free of all symptoms but when they
are exposed to a particular trigger factor, it may be a
grass pollen, it may be an animal hair, they will develop
symptoms of that condition. Now, they have allergic
disease when they have those symptoms but when they are free
of the symptoms I find it hard to call - say they have
allergic disease as disease relates to something that is
impairing bodily function."
445. Dr Le Souef said that as a consultant paediatric respiratory physician
he has seen many children, mostly asthmatic individuals
over five or six years
of age, who report that cigarette smoke exacerbates their respiratory
symptoms. These children usually add
that they seek cleaner air by moving away
from smokers. However, more than half the children he sees are younger than
this and
are unable to recognise and report such associations. He said that
these younger children were then more likely to remain in the
vicinity of
smokers, particularly infants who are held by a smoker or are too young to be
mobile. It is his opinion that there are
several infants under his care who
have required hospitalisation due to their parents' cigarette smoke.
(d) Professor Witorsch
446. Professor Witorsch drew a distinction between asthma and an attack of asthma. He thought that "one is really a subdivision or a part of the other" (T.3093). He said that environmental tobacco smoke does not cause the disease of asthma but that it may produce or exacerbate symptoms in some asthmatics.
447. It seems to me that the difference between Professor Witorsch and Dr Breslin on the question of asthma is really one of semantics. They appear to agree that environmental tobacco smoke produces symptoms of asthma in some persons. But Professor Witorsch regards smoke as causing attacks of asthma, whereas Dr Breslin regards it as causing asthma.
448. I gained the impression that Professor Witorsch's experience in this field is much less than Dr Breslin's.
449. Professor Witorsch conceded that some individuals with asthma may have
attacks that are precipitated by environmental tobacco
smoke (T.3092). He
also agreed that when some asthmatic patients are asked what causes them to
have acute attacks of asthma they
include environmental tobacco smoke amongst
the causes (T.3099). He also agreed that the word "disease" can be taken to
refer
to, inter alia, acute disease and latent disease. I think it is
difficult to say that an attack of asthma sustained by a person
who suffers
from an underlying condition of asthma does not constitute an episode of a
latent disease.
(e) Professor Huber
450. I have referred elsewhere to Professor Huber's qualifications. Although they are extensive in the field of respiratory disease, he does not appear to have had any specialist experience in the field of asthma.
451. He is of the opinion that there is no reliable evidence that inhalation of environmental tobacco smoke causes asthma. He agreed that exposure to such smoke may provoke a reaction within the airways in some individuals who are already asthmatic. But he thought even that was uncertain. He thinks that when such reactions appear to occur it is unclear whether they are caused by an irritating effect of smoke on the airways or are psychological in origin. He said that even the sight of tobacco smoke may produce a reaction in some asthmatics. He thinks there is no evidence clearly indicating that a true allergic reaction occurs as a result of the inhalation of environmental tobacco smoke.
452. Professor Huber thinks that because psychological factors are known to produce bronchospasm in asthmatics, it is quite possible that the decrease in pulmonary function noted in some asthmatics in some of the studies can be related to the psychological factors associated with the experimental design used in the studies.
453. Professor Huber made no comment on Dr Breslin's evidence, based on his clinical experience, as to the proportion of his patients who identify tobacco smoke as being associated with attacks of asthma.
454. Professor Huber's evidence included the following (T.3735):
"Do you hold any opinion as to whether it is wise for an455. Further, at T.3737:
asthmatic child to be kept for any period of time in a
smoking environment, smoky (sic) meaning environmental
tobacco smoke environment?---I would not recommend that they
be in a smoking environment.
Why would that be?---Because some of these children will
react to the irritating effects of a smoking environment and
have an exacerbation of their asthma. ..."
"(E)xposure to environmental tobacco smoke can in some(iii) Conclusion on Asthma
persons who are sensitive to it convert them from being
someone with underlying asthma in respect of which they feel
no symptoms to a person experiencing an acute attack of
asthma in which they are constantly aware of symptoms?---
Yes."
456. There is overwhelming evidence, which is really not disputed by the respondent, that passive smoking causes some people to experience attacks of asthma. It is unnecessary to have regard to any of the epidemiological studies to prove that this is the case. However, the majority of the studies support the opinions expressed by the applicant's witnesses. As I have shown, the respondent's witnesses themselves virtually concede that cigarette smoke may trigger attacks of asthma.
457. On the other hand, the applicant has not shown that cigarette smoke of itself causes what might be described as the underlying condition of asthma.
458. The real question on this part of the case is whether one should characterise an attack of asthma as "disease" for the purposes of the statement made in para. 3 of the advertisement.
459. Dr Nolan, was asked what was his understanding of the word "disease".
He said that, broadly speaking, disease could be considered
to be anything
that is an unhealthy process. He said:
"... in general I guess the term `disease' implies a degreeThis seems to me to be a reasonably workable definition of the term, and coincides broadly with the ordinary meaning of the word and also with the meaning which I think would be attached to it by the reader of the advertisement. In the context of the advertisement, the most apposite meaning of the word as given in the Shorter Oxford English Dictionary is:
of disability or functional impairment, or discomfort, which
is inconsistent with the notion of health."
(T.749)
"A condition of the body, or of some part or organ of the460. The Macquarie Dictionary, revised edition, gives as the primary meaning of "disease":
body, in which its functions are disturbed or deranged."
"A morbid condition of the body, or of some organ or part;461. It seems to me that an attack of asthma fits easily within the dictionary definitions quoted above. Wheezing, which is one of the main symptoms of asthma, is plainly a condition of the body in which its functions are disturbed, often to a serious degree. I would think many lay persons would not distinguish between asthma and an attack of asthma. Those who did would, I think, regard the underlying condition of asthma referred to in some of the evidence as a latent disease and an attack of asthma as an acute manifestation of the disease. If such persons were told that there is little evidence and nothing which proves scientifically that cigarette smoke causes disease in non-smokers they may well be misled or deceived into believing that there is little evidence and nothing which proves scientifically that cigarette smoke causes attacks of asthma in non-smokers.
illness; sickness; ailment."
462. The likelihood of this happening is increased because, in its totality, the advertisement is directed at allaying the concerns of people that cigarette smoke may affect the health of non-smokers. Thus, people who are prone to asthma attacks could reasonably gain the impression from the statement made in para. 3 that they are not at risk of suffering attacks of asthma by reason of being exposed to cigarette smoke.
463. I accept Dr Breslin's evidence as to the nature and characteristics of asthma and of asthma attacks. I think there is much common sense in his approach that a person does not have asthma when he is not having an attack of asthma.
464. In my opinion the applicant's witnesses (particularly Dr Breslin) have a great deal more experience with asthma than the respondent's witnesses. Where there are differences in the opinions of the experts in this field, the opinions of the applicant's experts are to be preferred.
465. The evidence that cigarette smoke causes attacks of asthma is so overwhelming that I cannot accept that the draftsman of the advertisement held an opinion to the contrary. No rational basis exists for the holding of an opinion that there is little evidence and nothing which proves scientifically that cigarette smoke causes attacks of asthma. It was not suggested, nor could it have been, that any scientist could properly hold such an opinion.
466. I am satisfied that the applicant has established that the statement
made in para. 3 of the advertisement is misleading and
deceptive in so far as
it applies to the disease of asthma. This is so whether the relevant date be
regarded as 1 July 1986 or
at any date thereafter.
(10) Otitis Media
(i) Nature of the disease
467. The disease of chronic secretory otitis media is also known as middle ear effusion and "glue ear". It occurs when cells in the middle ear secrete abnormal amounts of a gluey substance which is then trapped in the middle ear. The resulting blockage can cause temporary deafness in children, and may require surgery to ventilate and drain the middle ear. According to Dr Nolan the result of the disease process is deafness in children which in turn has been shown to interfere with child development and learning. He said it is quite a significant disability for a child to have. It may be prolonged but it is not a permanent effect on the nerve cells of the auditory nerve. The effect of the disease is to impede transmission of sound waves into the middle ear and then to the auditory nerve.
468. Dr Nolan thinks that it is probable that involuntary exposure to
cigarette smoke causes chronic secretory otitis media.
(ii) Primary Articles
(a) Kraemer et al. - Risk Factors for Persistent Middle-Ear effusions.
Otitis Media, Catarrh, Cigarette Smoke Exposure and Atopy
469. The authors of this article came from the Children's Orthopedic Hospital and Medical Centre and the University of Washington School of Medicine, Seattle. It was published in the Journal of the American Medical Association in 1983.
470. The abstract published with the study reads as follows:
"To ascertain risk factors for persistent middle-ear471. Table I on p 1023 of the study sets out the relative risk of persistent middle-ear effusions according to the different variables about which information was obtained during interview. These variables included racial background, family size, frequency of catarrh, atopic disease, frequency of suppurative otitis media and household exposure to cigarette smoke.
effusions (PMEE), we interviewed the parents of two groups
of children. The first consisted of 76 children with PMEE
who were admitted to the hospital for tympanostomy-tube
insertion. The second, a control group, consisted of 76
children admitted for other types of surgery, who were
matched for age, sex, season, and surgical ward. Nearly all
(97%) of the children admitted for insertion of tympanostomy
tubes had one or more episodes of suppurative otitis media.
Only 59% of the control children had previous ear
infections. Frequent ear infections sharply increased the
risk for persistent effusions. Catarrh, household
cigarette smoke exposure, and atopy also occurred more
frequently in children with PMEE. The risk for middle-ear
effusions was greatest when these three factors were all
present. The avoidance of daily exposure to domestic tobacco
smoke and, if atopic, of specific allergens should be
included in the medical treatment of children with PMEE."
472. An extract from the table dealing with household cigarette exposure is
set out below:
Characteristic No. (%) of PMEE No. (%) of Relative 95%
Cases (N=76) Surgical Risk ConfidenceHousehold
Control Subjects Interval
(N=76)
0 38 (50.0) 45 (59.2) 1.10 ...Household
1 19 (25.0) 23 (30.3) 1.10 0.5-2.1
s2 19 (25.0) 8 (10.5) 2.8 1.1-7.0
473. This extract shows that a statistically significant relative risk of 2.8 was found for cases where there were 2 or more cigarette smokers in the household, but no increase in risk was found where there was one household smoker. It also shows that when exposure was measured by packs per day a linear dose response relationship was not apparent and no subgroup result was statistically significant. However when household cigarette use equalled or exceeded 3 packs per day, the relative risk of persistent middle-ear effusion was reported as 4.1 (95% C.I. 0.9 -19.2).
474. A later table in the study shows the combined effects of nasal
congestion, cigarette smoke exposure, and atopy. The authors
reported that:
"(N)asal congestion alone elevated the risk nearly fourfold.(b) Black - The Aetiology of Glue Ear - A Case-Control Study
When cigarette smoke exposure or atopy was added to nasal
congestion, the risk increased. Children with all three
factors were more than six times as likely to manifest
PMEE."
475. The author of this study was from the Department of Community Medicine and General Practice at Oxford University. The article was published in the International Journal of Pediatric Otorhinolaryngology in 1985.
476. The abstract published with the study reads as follows:
"A case-control study was carried out to investigate many ofThe author stated:
the proposed causes of glue ear in childhood. One hundred
and fifty cases with two matched controls were found to be
remarkably similar in nearly all medical and social aspects
of their past and present lives, thus providing no support
for many of the currently held views on the aetiology of
glue ear. Of the 5 factors which were found to increase the
risk of a child undergoing surgery for glue ear, only one of
these is thought to be related to the development of the
condition, rather than to the chances of its detection.
This factor was parental smoking (RR 1.64) ...."
"A significant association was found (RR 1.64; P <0.05)477. The statistically significant result of 1.64 emerged after original insignificant results were subjected to further (matched pair) analysis. It was suggested to Professor Landau in cross-examination that this was a weak association and that the author was attempting to use two reported weak associations to argue for a strong association. Professor Landau said that the conclusion of a strong association was based on the consistent findings. However, he agreed that the Black study (and also Kraemer's) showed no more than that cigarette smoke was a risk factor for glue ear.
between glue ear and the smoking habits of all household
members throughout the subject's life. This analysis
assumes a constant level of exposure to smoke throughout the
subject's life. Further study would be required to
determine whether or not the risk of smoke is associated
with any particular stage of childhood."
(p 131)
478. The respondent led no expert evidence directly on the issue of otitis
media and environmental tobacco smoke.
(iii) The major reviews
479. The authors of the N.R.C. report state (at p 274):
"Household exposure to ETS is linked with increased rates of480. The authors of the Surgeon General's report after referring to five studies (Black, Kraemer et al, Pukander, Said et al (1978) (Ex E333) and Iverson et al (1985) (Ex E192)) conclude:
chronic ear infections and middle-ear effusions in young
children. For children with nasal allergies and recurrent
otitis media, ETS exposure may synergistically increase
their risk of persistent middle-ear effusions."
"These studies are consistent in their demonstration of(iv) Conclusion
excess chronic middle ear effusions, a sign of chronic ear
disease, in children exposed to parental cigarette smoke.
Potential confounding factors for middle ear effusions
should be examined carefully in future studies. The long-term
implications of the excess middle ear problems deserve
further study."
481. The number of studies which have examined the association between otitis media and passive smoking is limited and there are some questions as to the consistency of data and the methodology of the studies. Nevertheless the studies by Black and Kraemer offer substantial support for the hypothesis that exposure to environmental tobacco smoke causes recurrent otitis media in children. Dr Nolan and Professor Landau are both distinguished medical researchers and their views are entitled to respect. The studies on which they rely were produced or published by institutions of international standing.
482. In contrast, the respondent offered no detailed expert evidence on this question.
483. I am not satisfied there is scientific proof of a causal association
between passive smoking and otitis media, mainly because
of the cautious note
of Professor Landau's answers in cross-examination. Nevertheless, I am
persuaded on the strength of the oral
evidence and the primary articles that
there was, in 1986, more than a little evidence that passive smoking causes
recurrent otitis
media in children.
(11) Does the advertisement state fact or opinion?
484. It was submitted on behalf of the respondent that the statement in the advertisement would be understood by the reader as being no more than an expression of opinion and that s.52 of the Act does not operate to restrict publication of opinions on scientific issues.
485. The statement made in the advertisement is not expressed to be an opinion. It is an assertion of the state of the evidence on the question whether cigarette smoke causes disease in non-smokers.
486. The statement must be read in the context of the whole of the advertisement. The paragraphs which immediately follow para. 3 contain statements which support the view that what is said in para. 3 itself is a reference to the state of the evidence, as distinct from the expression of an opinion, as to the existence of a causal link between cigarette smoke and disease in non-smokers. The references to the work of the Institute of Cancer Research, the American Cancer Society and the Harvard School of Public Health are calculated to cause the reader to believe that the published views of those bodies represent the state of the evidence as to a link between cigarette smoke and disease in non-smokers. The reference to major reviews is calculated to induce the same belief in the reader. That is to say, what the reader is told in para. 3 is not that some innominate person or body holds an opinion as to the relationship between cigarette smoke and disease in non- smokers, rather he is told what the state of the evidence is on the subject. In my opinion most readers would read the advertisement in that way. To put the matter at the very lowest, and to borrow words used by Deane J in Tillmanns Butcheries Pty Limited v Australasian Meat Industry Employees' Union [1979] FCA 84; (1979) 42 FLR 331 at 346, there is a real or not remote chance or possibility regardless of whether it is less or more than 50% that readers would understand the statement in para. 3 in that way.
487. In any event, I find it impossible to believe that a person who, on 1
July 1986 or at any time subsequently, acquainted himself
with the available
evidence as to the relationship between cigarette smoke and disease in
non-smokers could conclude that it was
"little". The evidence in the primary
articles alone is such as to deny a rational basis for the use of the phrase
"little evidence",
even if it be treated as a statement of opinion. In Global
Sportsman Pty Limited v Mirror Newspapers Pty Limited [1984] FCA 180; (1984) 2 FCR 82 at p 88
the Court said:
"Many statements, for example, promises, predictions and488. Had there been persuasive material which existed as at 1 July 1986 which cast serious doubt upon the evidence called by the applicant in respect of all the diseases the position may well have been different. In that case there would have been room for an argument that there was a basis for the making of the statement in the advertisement, whether that statement be regarded as one of fact or one of opinion. But that is not the case.
opinions, do involve the state of mind of the maker of the
statement at the time when the statement is made.
Precisely the same principles control the operation of
s.52(1) with respect to the making of such statements. A
statement which involves the state of mind of the maker
ordinarily conveys the meaning (expressly or by implication)
that the maker of the statement had a particular state of
mind when the statement was made and, commonly at least,
that there was basis for that statement of mind. If the
meaning contained in or conveyed by the statement is false
in that or in any other respect, the making of the statement
will have contravened s.52(1) of the Act. Compare Lyons v
Kern Konstructions (Townsville) Pty Limited (1983) 47 ALR
114."
489. Although this defence was pleaded, it was not developed at any length by counsel for the respondent. The advertisement appeared on 1 July 1986 and on 25 July 1986 the applicant complained to the Trade Practices Commission. It was reasonable for the applicant to await the outcome of its complaint to the Commission before commencing its own proceedings. It was not until the early part of 1987 that it became apparent to the applicant that the respondent was not prepared to fully retract the statements made in the advertisement. The application in this Court was filed on 11 June 1987.
490. In these circumstances, I think there is no substance in the defence
based on laches, acquiescence and delay. The delay in
commencing the
proceedings was not great, nor was the respondent prejudiced by such delay as
occurred.
(13) Discretion
491. There is no reason why in the exercise of the Court's discretion the applicant should be refused relief to which it is otherwise entitled. On the contrary, there is a strong public interest in the respondent being prevented from making the statement that there is little evidence and nothing which proves that cigarette smoke causes disease in non-smokers. Active smokers are likely to be misled or deceived by the statement into believing that their smoking does not prejudice the health of non-smokers, particularly small children. Non-smokers are likely to be deceived or misled by the statement into believing that cigarette smoke does not affect their own health or the health of their children. These are serious matters.
492. In the early stages of the litigation the respondent made an open offer
of settlement which was rejected by the applicant.
It was made plain by
counsel for the respondent that the rejection would be relied upon on the
question of costs should the respondent
lose the proceedings. However, I did
not understand counsel for the respondent to argue in final address that the
rejection of the
offer of settlement was relevant to the question of
discretion. Whilst I have some difficulty in seeing how the rejection of the
offer of settlement could affect the exercise of my discretion to grant
relief, I am prepared to reconsider the question should the
respondent wish to
put any further submission on that matter.
(14) Relief
493. The applicant seeks not only injunctive relief but also an order that the respondent publish a correcting advertisement. It is entitled to injunctive relief in appropriate terms, but I do not think I should make an order that the respondent publish an advertisement correcting what was said in the advertisements published on 1 July 1986 and in January 1987.
494. So much time has passed since the advertisements were published that it is unrealistic to think that members of the public who might read a correcting advertisement would have any clear recollection of what was said in the original advertisement. I think the fact that the respondent will be enjoined from making the offending statement in the future is sufficient vindication of the interests of the applicant and of the general public.
495. I direct the applicant to file and serve draft minutes of the orders it seeks within fourteen days of this date. I direct the respondent to file and serve within twenty eight days of this date draft minutes of orders it proposes that the Court should make. I reserve the question of costs. The matter is to be relisted on a date to be fixed for argument on question of costs and for settlement of minutes of orders.
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