Australian Federation of Consumer Organisations Inc v Tobacco Institute of Australia Ltd

Re: AUSTRALIAN FEDERATION OF CONSUMER ORGANISATIONS INC.
And: THE TOBACCO INSTITUTE OF AUSTRALIA LIMITED
No. G 253 of 1987
FED No. 9
Trade Practices
(1991) 13 ATPR 41-079/98 ALR 670
27 FCR 149

COURT

IN THE FEDERAL COURT OF AUSTRALIA

NEW SOUTH WALES DISTRICT REGISTRY
GENERAL DIVISION
Morling J.(1)

CATCHWORDS

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 advertisement

Trade Practices Act 1974, s.52

HEARING

SYDNEY

#DATE 7:2:1991

Counsel 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.

JUDGE1

Introduction - the advertisement

In a letter written in 1606 by a Doctor of Physic to a Gentleman it was asserted that tobacco was:

"1. Not safe for youth

2. It shorteneth life

3. It breedeth many diseases

4. It breedeth melancholy

5. It hurteth the mind

6. It is ill for the smokers issue."

(British Journal of Preventive and Social Medicine (1973), 27, 150).

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 ...

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."

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.
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
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.
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 now 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."

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.
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.
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"?
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.
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.
As was pointed out in Concrete Constructions (NSW) Pty Ltd v. Nelson (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 a 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) 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) 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) 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."

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.
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.
To borrow the words used by Dixon J. in Bank of New South Wales v The Commonwealth (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.
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) 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.
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"
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.
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.
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").

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.
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.
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.
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.
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.
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"
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".
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."
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 or 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."

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.
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.
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 servants 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;"

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".
By its defence the respondent admitted that the undertaking had been sought from it and that it had declined to give it.
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.
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.
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.
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.
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.
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.
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.
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
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
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.
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.
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.
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.
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.
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.
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.
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 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.

(ii) The primary articles

(a) Trichopoulos et al. - Lung Cancer and Passive Smoking

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 other 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."

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.
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.
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.
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 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."

(b) Hirayama - Non-smoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan

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 91 540 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."

(c) Hirayama - Cancer Mortality in Non-smoking Women with Smoking Husbands Based on a Large-Scale Cohort Study in Japan

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 studied 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."

Professor Hirayama made the following observation:

"This study confirms the correlation between lung 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."

The reference to the American Cancer Society study is a reference to Garfinkel's study (infra).
Professor Hirayama also observed:

"When the effects of passive smoking due to husbands' 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."

(d) Garfinkel - Time Trends in Lung Cancer Mortality Among non-smokers and a Note on Passive Smoking

This article appeared in the Journal of the National Cancer Institute in June 1981.
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
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
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 Effect

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 authors expressed their conclusion as follows:

"The differences between the effects of passive 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."

(g) Koo et al. - Active and passive smoking among female lung cancer patients and controls in Hong Kong

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 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).

(h) Buffler et al. - The Causes of Lung Cancer in Texas

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 risk 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."

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".
(j) Garfinkel et al. - Involuntary smoking and lung cancer: A case-control study.
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 study 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."

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:

"We found an elevated risk of lung cancer, ranging 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).

(k) Akiba et al. - Passive Smoking and Lung Cancer among Japanese Women.

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.
The abstract of the article, as published, reads as follows:

"A case-control study conducted in Hiroshima and 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."

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.
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.
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.
The authors said:

"The results from this case-control study suggest 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."

The 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.

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.
The authors summarise the views they formed as a result of their study as follows:

"In summary, the results of this investigation 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."

(l) Lee et al. - Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases

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 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, ... "

(m) Humble et al. - Marriage to a Smoker and Lung Cancer Risk

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-based 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."

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.
Odds ratios from use of the second model tended to be lower.
No effect was detected for marriage to a smoker by a current or former cigarette smoker, according to either model.
Under the heading "Discussion", the authors made the following observations:

"In the context of a population-based case-control 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."

In conclusion, the authors made the following comments:

"The results of the present case-control study 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."

(n) Pershagen et al. - Passive Smoking and Lung Cancer in Swedish Women

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 cancer 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."

The authors reported at p 20 that:

"Pooling the control groups produces a relative risk 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."

Under the heading "Discussion" the authors stated the following:

"The results of our study indicate that exposure to 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)

(iii) The major reviews

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.
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.
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.
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.
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 indicates 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)

The final evaluations of the IARC working group appear at the end of the report and include the following:

"There is sufficient evidence that tobacco smoke is carcinogenic to humans."

(p 314)

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.
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 increased 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)

In a section headed "Conclusions and Evaluations", the following appears:

"Tobacco smoke affects not only people who smoke but also 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

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:

Dr R. Antic, Director of Thoracic Medicine, Royal 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.

The report of the working party was adopted by the National Health and Medical Research Council in June 1986.
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 Introduction

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.

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.
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
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 to 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."

He later said (T.990):

"... there are perhaps 20 to 30 per cent of the population

(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."

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.
(c) Dr Le Souef
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
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.
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.
I gained the impression that Professor Witorsch's experience in this field is much less than Dr Breslin's.
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
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.
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.
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.
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.
Professor Huber's evidence included the following (T.3735):

"Do you hold any opinion as to whether it is wise for an 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. ..."

Further, at T.3737:

"(E)xposure to environmental tobacco smoke can in some 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."

(iii) Conclusion on Asthma

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.
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.
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.
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 degree of disability or functional impairment, or discomfort, which is inconsistent with the notion of health." (T.749)

This 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:

"A condition of the body, or of some part or organ of the body, in which its functions are disturbed or deranged."

The Macquarie Dictionary, revised edition, gives as the primary meaning of "disease":

"A morbid condition of the body, or of some organ or part; illness; sickness; ailment."

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.
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.
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.
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.
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.
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
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.
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
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.
The abstract published with the study reads as follows:

"To ascertain risk factors for persistent middle-ear 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."

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.
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 Confidence Control Subjects Interval (N=76)

Household

Cigarette

smokers

0 38 (50.0) 45 (59.2) 1.10 ...

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

Household

Cigarette use

No. packs per day

None 38(50.0) 45 (59.2) 1.0 ...

01.-09 11 (14.5) 7 (9.2) 1.9 0.7-5.3

1.0 - 1.9 13 (17.1) 14 (18.4) 1.1 0.5-2.6

2.0 - 2.9 7 (9.2) 8 (10.5) 1.0 0.3-3.1

s 3.0 7 (9.2) 2 (2.6) 4.1 0.919.2

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).
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. 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."

(b) Black - The Aetiology of Glue Ear - A Case-Control Study

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.
The abstract published with the study reads as follows:

"A case-control study was carried out to investigate many of 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) ...."

The author stated:

"A significant association was found (RR 1.64; P <0.05) 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)

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.
The respondent led no expert evidence directly on the issue of otitis media and environmental tobacco smoke.
(iii) The major reviews
The authors of the N.R.C. report state (at p 274):

"Household exposure to ETS is linked with increased rates of 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."

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:

"These studies are consistent in their demonstration of 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."

(iv) Conclusion

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.
In contrast, the respondent offered no detailed expert evidence on this question.
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?
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.
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.
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) 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.
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) 2 FCR 82 at p 88 the Court said:

"Many statements, for example, promises, predictions and 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."

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.
(12) Laches, Acquiescence and Delay
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.
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
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.
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
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.
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.
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.

[1991] FCA 9

07 FEBRUARY 1991