Tobacco and Public Health - TCSC Indonesia

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PASSIVE SMOKING AND HEALTH
This difference in findings may reflect the focus of the cohort studies on the first two
years of life, the peak age of risk for middle ear disease. The case–control studies, on the
other hand, have been directed at older children who are not at lower risk for otitis
media. Exposure to secondhand smoke has been most consistently associated with
recurrent otitis media and not with incident or single episodes of otitis media. In their
1997 meta-analysis, Cook and Strachan (1997) found a pooled odds ratio of 1.48
(95 per cent CI: 1.08, 2.04) for recurrent otitis media if either parent smoked, 1.38
(95 per cent CI: 1.23, 1.55) for middle-ear effusions, and 1.21 (95 per cent CI: 0.95,
1.53) for outpatient or inpatient care for chronic otitis media or ‘glue ear.’
The US Surgeon General’s Office (US Department of Health and Human Services
1986), the National Research Council (National Research Council 1986), and the
US Environmental Protection Agency (1992) have all reviewed the literature on
secondhand smoke and otitis media and have concluded that there is an association
between secondhand smoke exposure and otitis media in children. The evidence
to date supports a causal relation, as noted by the WHO consultation
(WHO 1999).
Health effects of involuntary smoking on adults
Lung cancer. In 1981, reports were published from Japan (Hirayama 1981a) and from
Greece (Trichopoulos et al. 1981) that indicated increased lung cancer risk in nonsmoking
women married to cigarette smokers. Subsequently, this still-controversial
association has been examined in many investigations conducted in the United States
and other countries around the world, including a substantial number of studies
in Asia. The association of involuntary smoking with lung cancer derives biologic
plausibility from the presence of carcinogens in sidestream smoke and the lack of a documented
threshold dose for respiratory carcinogenesis in active smokers (US Department
of Health and Human Services 1982; IARC 1986). Moreover, genotoxic activity, the ability
to damage DNA, has been demonstrated for many components of secondhand smoke
(Claxton et al. 1989; Lofroth 1989; Weiss 1989). Experimental exposure of nonsmokers
to secondhand smoke leads to their excreting 4-(methylnitrosamino)-1-(3-pyridyl)-
1-butanol (NNAL), a tobacco-specific carcinogen, in their urine. Nonsmokers exposed
to secondhand smoke in their homes also excrete higher levels of this carcinogen
(Anderson et al. 2001). Nonsmokers, including children, exposed to secondhand
smoke also have increased concentrations of adducts of tobacco-related carcinogens,
that is detectable binding of the carcinogens to DNA of white blood cells, for example
(Maclure et al. 1989; Crawford et al. 1994).
The early report by Hirayama (1981a) was based on a prospective cohort study of
91 540 nonsmoking women in Japan. Standardized mortality ratios for lung cancer
increased significantly with the amount smoked by the husbands. The findings could
not be explained by confounding factors and were unchanged when follow-up of the
study group was extended (Hirayama 1984). On the basis of the same cohort, Hirayama