From a scientific standpoint, the story of exposure to secondhand smoke has been purposely muddled by pro-smoking advocates. These pro-smoking critics try to poke holes in the previous epidemiological research studies linking smoke exposure to long-term adverse health effects, such as cancer and heart disease.
What the pro-smoking critics seem to forget is that the health effects of most of the pollutants that make up secondhand smoke – such as fine particles, carbon monoxide, benzene, PAHs – already are well-known and documented in environmental science.
The pro-smoking critics also tend to ignore various acute, but still significant, health effects caused by the toxic pollution in secondhand smoke, such as an increased severity of asthma, respiratory infection, and simple irritation of the eyes or throat.
Prior to the enactment by cities, counties, and states of recent environmental laws designed to protect public health, the adverse effects of these pollutants already were documented and their effects were well-understood.
As we have seen, the enormous mass of pollutants generated by a single cigarette causes persons close to a smoker or living in the same house to be exposed to pollutant concentrations that are many times higher than those permitted outdoors under existing environmental laws. Any reasonable person must ask, "Does it make sense to set uniform national standards under the Clean Air Act for the maximum pollutant concentrations allowed in the ambient air, while at the same time exposing children and adults in homes, automobiles, and restaurants to pollutant levels many times higher than these standards?"
The potency of the cigarette in violating clean air standards has been greatly underestimated by pro-smoking advocates. This fact needs needs greater attention and understanding by the public. The potency of the cigarette as a generator of high concentrations of toxic pollutants that can cause cancer and other long and short-term health effects argues strongly for restricting smoking in public places as a matter of prudent public policy.
aromatic hydrocarbons [PAHs], and metals), or both on the cardiovascular system (see Figure 3-1 for summary). Those studies have yielded sufficient evidence to support an inference that acute exposure to secondhand smoke induces endothelial dysfunction, increases thrombosis, causes inflammation, and potentially affects plaque stability adversely. Those effects appear at concentrations expected to be experienced by people exposed to secondhand smoke.
Data from animal studies also support a dose–response relationship between secondhand-smoke exposure and cardiovascular effects (see Chapter 3). The relationship is consistent with the understanding of the pathophysiology of coronary heart disease and the effects of secondhand smoke on humans, including chamber studies. The association comports with known associations between PM, a major constituent of secondhand smoke, and coronary heart disease.
Overall, the pathophysiologic data indicate that it is biologically plausible for secondhand-smoke exposure to have cardiovascular effects, such as effects that lead to cardiovascular disease and acute myocardial infarction (MI). The exact mechanisms by which such effects occur, however, remain to be elucidated.
Characteristics of smoking bans can heavily influence their consequences. Interpretation of the results of epidemiologic studies that involve smoking bans must account for information on the bans and their enforcement.
Secondhand smoke should have been measured before and after implementation of a ban, and locations with and without bans should have been compared. Studies that include self-reported assessments of exposure to secondhand smoke cannot necessarily be compared with each other unless the survey instruments (such as interviews) were similar.
The comparability of the time and length of followup of the studies should be assessed. For example, the impact of a ban in one area may differ from the impact of a ban in another solely because the observation times were different and other activities may have occurred during the same periods. In comparing studies, it may be impossible to separate contextual factors associated with ban legislation—such as public comment periods, information announcing the ban, and notices about the impending changes—from the impact of the ban itself. The committee therefore included such contextual factors in drawing conclusions about the effects of a ban.
Interpretation needs to consider the timeframes in the epidemiologic evidence, for example, the time from onset of a smoking ban to the mea-