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Introduction 1. We have been asked by the Scientific Committee on Tobacco and Health (SCOTH) to review a submission from the Tobacco Manufacturers Association (TMA) comprising a meta-analysis of epidemiological data and supporting references, and a separate meta-analysis paper prepared by Dr A Hackshaw and Professor N Wald (a member of SCOTH). The data provided by the TMA comprised three volumes of reviews and references originally received by the SCOTH secretariat in 1994, and updated in February 1995. A key part of the TMA submission was a meta-analysis of epidemiological studies prepared by Mr P N Lee which was updated in December 1996. The TMA recently submitted 3 additional supplements dated January 1997 dealing with; misclassification bias, dose response (with and without exposed groups), and use of cotinine as a biomarker for exposure to ETS. We considered all of the submitted information at two meetings in 1997. A further meta-analysis report prepared by an ad-hoc European Working Group was also considered. We have also considered additional published literature on the formation and composition of ETS, the results obtained in animal experiments involving exposure to surrogates of ETS, and information regarding investigations to evaluate the potential genotoxicity and biological interactions of ETS in humans published up to June 1997. 2. Smoking tobacco is the predominant cause of lung cancer with approximately 90% of lung cancer deaths in Western populations attributable to cigarette usage. A lower percentage of lung cancer deaths may be attributed to tobacco smoking in developing non-Westernised populations. A number of epidemiological assessments undertaken by national regulatory agencies have reported a small but statistically significantly elevated relative risk for lung cancer in passive smokers of between 1.1 to 1.3 , whereas other reviewers concluded that the observed association is due to uncontrolled confounding and biases in these analyses. However, since many individuals within the population are exposed to ETS, it is important to resolve the scientific issues particularly as only a small increase in risk would be associated with many hundreds of deaths due to lung cancer per year. 3. Regarding the structure of our review, it was agreed to consider firstly the nature and composition of ETS followed by information on exposure and uptake of genotoxic components (eg adduct studies) with particular reference to the lung as the target organ. Finally to critically review the submitted epidemiological meta-analyses. All of the available information has been evaluated in accordance with our guidelines and also with regard to the criteria proposed by Sir Austin Bradford-Hill. These latter criteria, which are listed below, are generally regarded as being valuable in the consideration as to whether or not an association between an outcome (in this case lung cancer) and a putative risk factor (passive smoking) is causal. A specific reference to each of these criteria in respect of passive smoking and lung cancer has been included in our discussion. Bradford-Hill criteria
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