Tobacco and Public Health - TCSC Indonesia

566
TOBACCO AND CARDIOVASCULAR DISEASE
system, the convincing argument regarding the biological plausibility of passive smoking
as a cause of CVD means that the case in regard to active smoking must be even
more compelling. Significantly, the identification of a number of different mechanisms
via which tobacco smoke could harm the arterial tree makes it very difficult to modify
cigarettes to make them ‘safer’ in regard to the risk of CVD in smokers.
Passive smoking and arterial disease
The evidence that passive smoking increased the incidence of severe respiratory infections
in infants and young children (Colley et al. 1974; Harlap and Davies 1974) was
not seriously challenged when it emerged. This is probably because it was known by
the 1970s that active smoking caused COPD (Fletcher and Peto 1976) and was associated
with increased mortality from pneumonia in adults (Doll and Peto 1976), it was
obvious that children of this age could be heavily exposed if their parents smoked
around them, and the implications for policy were limited because the majority of that
exposure occurred in private homes, a domain that most communities are loathe to
regulate. However, the tobacco industry having been alerted in 1978 to the threat to its
well-being posed by the issue of passive smoking (Roper Organization 1978), the publication,
in 1981, of evidence (Hirayama 1981; Trichopoulos et al. 1981) that passive
smoking was associated with lung cancer in adults was accompanied by very considerable
controversy. The possible contribution of passive smoking to IHD, first identified
epidemiologically in 1985 (Garland et al. 1985), has proved even more contentious
because it appears to be similar in magnitude to the effect of passive smoking on the
risk of lung cancer, whereas the multiplying effect of active smoking on the risk of lung
cancer is at least five times its effect on IHD.
The National Heart Foundation of Australia was one of the first health organizations
to react to the paper from Garland et al. (1985), publishing a pamphlet on passive
smoking and heart disease entitled, “So you think you’re a non-smoker” (National
Heart Foundation of Australia 1985) in the same year. More systematic reviews of the
scientific evidence on passive smoking generally were published by the Surgeon-
General in the United States in 1986 (United States Department of Health and Human
Services 1986) and the National Health and Medical Research Council (NHMRC) in
Australia in 1987 (National Health and Medical Research Council 1987), but neither
body was persuaded at that time that passive smoking caused CVD. When the NHMRC
visited the question of passive smoking again (1997), many more epidemiological and
laboratory reports on the issue of CVD had been published, leading that body to a conclusion
that the evidence for a causal relationship was ‘strongly suggestive’. In Britain,
the Scientific Committee on Tobacco and Health was unambiguous in its report published
in 1998 that passive smoking is a cause of IHD (Department of Health 1998),
and Law et al.,working in the same country, had been persuaded by the evidence available
in the preceding year (1997), as had the California Environmental Protection
Agency (Office of Environmental Health Hazard Assessment 1997).