Tobacco and Public Health - TCSC Indonesia

306
PASSIVE SMOKING AND HEALTH
relatively quickly with cessation. Active cigarette smoking is considered to: (1) increase
the risk of cardiovascular disease by promoting atherosclerosis; (2) increase the
tendency to thrombosis; (3) cause spasm of the coronary arteries; (4) increase the likelihood
of cardiac arrhythmias; and (5) decrease the oxygen-carrying capacity of the
blood (US Department of Health and Human Services 1990). Glantz and Parmley
(1991) summarized the pathophysiologic mechanisms by which passive smoking
might increase the risk of heart disease. It is biologically plausible that passive smoking
could also be associated with increased risk for CHD through the same mechanisms
considered relevant for active smoking, although the lower exposures to smoke components
of the passive smoker have raised questions regarding the relevance of the
mechanisms cited for active smoking.
Epidemiologic data first raised concern that passive smoking may increase risk for
CHD with the 1985 report of Garland et al. (1985), based on a cohort study in southern
California. There are now more than 20 studies on the association between environmental
tobacco smoke and cardiovascular disease. These studies assessed both fatal
and nonfatal cardiovascular heart disease outcomes, and most used self-administered
questionnaires to assess secondhand smoke exposure. They cover a wide range of populations,
both geographically and racially. While many of the studies were conducted
within the United States, studies were also conducted in Europe (Scotland, Italy, and
the United Kingdom), Asia (Japan and China), South America (Argentina), and the
South Pacific (Australia and New Zealand). The majority of the studies measured the
effect of secondhand smoke exposure due to spousal smoking; however, some studies
also assessed exposures from smoking by other household members or occurring at
work or in transit. Only one study included measurement of exposure biomarkers.
While the risk estimates for secondhand smoke and CHD outcomes vary in these studies,
they range from null to modestly significant increases in risk, with the risk for fatal
outcomes generally higher and more significant. In their 1997 meta-analysis, Law et al.
(1997) estimated the excess risk from secondhand smoke exposure as 30 per cent
(95 per cent CI: 22 per cent, 38 per cent) at age 65 years. The findings were similar in a
meta-analysis of 18 studies reported by He et al. (1999). The overall increase in risk
associated with passive exposure was 25 per cent and the risk increased with duration
and level of smoking. The California Environmental Protection Agency (National
Cancer Institute 1999) recently concluded that there is an overall excess risk of 30 per
cent for CHD due to exposure from secondhand smoke. The American Heart
Association’s Council on Cardiopulmonary and Critical Care has also concluded that
environmental tobacco smoke both increases the risk of heart disease and is ‘a major
preventable cause of cardiovascular disease and death’ (Taylor et al. 1992). This conclusion
was echoed in 1998 by the Scientific Committee on Tobacco and Health in the
United Kingdom (Scientific Committee on Tobacco and Health & HSMO 1998).
Respiratory symptoms and illnesses in adults. Only a few cross-sectional investigations
provide information on the association between respiratory symptoms in nonsmokers