The effects of active smoking on exercise tolerance, blood pressure, and the risk of developing cardiovascular disease have been reviewed elsehwere (U.S. Public Health Service, 1983). This chapter discusses studies of ETS exposure to nonsmokers and subsequent possible cardiovascular effects. The constituents that are thought to have the greatest effect on the cardiovascular system are carbon monoxide (CO) and nicotine. The possibility exists that the mechanisms, as well as the magnitude of the effects, for acute and chronic cardiovascular effects may be different for exposure to whole smoke and to ETS.
Administration of nicotine at level similar to those induced by active cigarette smoking is shortly followed by increases in heart rate and blood pressure (U.S. Public Health Service, 1983). Platelet aggregation has been shown to be increased in in vitro studies. CO rapidly combines with hemoglobin in the blood to form carboxyhemoglobin (COHb), thereby leading to some degree of tissue hypoxia. CO combines with muscle myoglobin, which is followed by some muscle hypoxia. The level of exposure of the nonsmoker to these cigarette smoke constituents, however, is less than that of the active smoker, and the effects are expected to be less.
Table 14–1 reviews some of the increases in COHb levels as seen in both experimental and observational studies. The levels of