Several occupational and residential settings can expose both normal and sensitive human subjects to odors and irritants. These settings include intensive agricultural operations housing swine and poultry, cigarette-smoke-filled bars, landfills and manufacturing processes. The literature suggests that adverse sensory reactions to strong odors and irritants may lead to the release of catecholamines and stress hormones. Physiological and biochemical measurements related to cardiovascular risk, e.g., blood pressure, heart rate, high-density lipoprotein (HDL) cholesterol level and serum triglyceride level, may be altered as a result of exposure to odor and irritant-induced release of catecholamines. Further work in the form of field studies and chamber exposure protocols is required to determine whether the physiological and biochemical changes observed to date represent an increase in cardiovascular risk, or are reversible changes within the normal homeostatic range.
Ten healthy male and 10 healthy female, "never-smoking " subjects (ages 21-50) participated in a 5-day environmental room study to determine if an acute exposure to a high level of fresh diluted sidestream smoke (FDSS) would alter pulmonary function. On Monday, Tuesday, Thursday and Friday, the twenty subjects sat in an environmenta l room for 7.33 hours and were exposed to ltered and humidi ed air. On Wednesday, the twenty subjects were exposed in an environmenta l room for 7.33 hours to an average respirable suspended particle (RSP) concentration of 179 micrograms per m 3 of FDSS generated by machine smoking Kentucky 1R4F reference cigarettes. This level of FDSS is 3.3 times the 95th percentile concentration of workplace environmental tobacco smoke exposure levels previously measured in the US. FVC and FEV 1 decreased approximatel y 1.6% ( p < 0.05) in both males and females after exposure. Similarly, PEF decreased approximately 1.3% ( p < 0.03) following exposure. The observed decrease in pulmonary function was consistent with a "stress" related norepinephrine-induce d alteration in blood ow leading to transient bronchoconstriction . Alternatively, a cholinergic re ex due to activation of bronchopulmonar y C bers may have also played a role in the transient bronchoconstriction . These small exposure-related decrement s in pulmonary function were reversible.Keywords. Environmental tobacco smoke; pulmonary function. INTRODUCTIONEnvironmental tobacco smoke (ETS) is the aged, diluted mixture of exhaled mainstream smoke and sidestream smoke. Mainstream smoke is the smoke directly inhaled through the back of the cigarette, and sidestream smoke is generated from the lit end of the cigarette. At least 18 epidemiology studies and 7 acute exposure studies have addressed the relationship between exposure to environmental tobacco smoke (ETS) in nonsmokers and pulmonary function measurements (20). Also, the USEPA (25) and California EPA (6) have issued reports containing sections on ETS and respiratory effects. Although no de nitive result has emerged, Carey et al (5) studied 1,623 British adults for 7 years and found a small de cit in lung function in adult nonsmokers exposed to ETS, consistent with their previous meta-analytic estimate of a 2.7% decrease. Similarly, Eisner et al (9) showed a small improvement in pulmonary function in a cohort of bartenders following a reduction in ETS exposure.Given the sensitivity of modern measurement and data analysis methods for detecting small physiological and biochemical changes in humans, the categorization of a change as "clinically signi cant" should be thoughtfully considered. Perspective on the clinical signi cance of a measured change in exposed nonsmokers can be attained by considering the reproducibility, magnitude, directionality, potential for reversibility, and possibility of adaptation. Proper consideration of these factors can allow the results of a series of carefully controlled studies to suggest whether a change is likely to be a negative health effect, a ...
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