摘要：Asthma is a respiratory disease whose prevalence has been increasing since the mid 1970s and that affects more than 14.6 million residents of the United States. Environmental triggers of asthma include air pollutants that are respiratory irritants. Air toxics emitted into the ambient air are listed in the 1990 Clean Air Act Amendments as hazardous air pollutants (HAPs) if they can adversely affect human health, including the respiratory tract. HAPs include particulate and gaseous-phase pollutants, individual organic compounds and metals, and mixtures. Associations between asthma exacerbation and both particles and indoor volatile organic compounds (VOCs), often referred to as indoor air quality, have been reported. Studies conducted in the United States, Canada, and Europe over the past two decades have shown that most people living in the developed countries spend the majority of their time indoors and that the air concentrations of many air toxics or HAPs are higher indoors than in the ambient air in urban, suburban, and rural settings. Elevated indoor air concentrations result from emissions of air toxics from consumer products, household furnishings, and personal activities. The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to oversample homes in close proximity to ambient sources, excluding residences where smokers lived, to determine the contribution of ambient emissions to air toxics exposure. The ratios of indoor to outdoor air concentrations of some VOCs in homes measured during RIOPA were much greater than one, and for most other VOCs that had indoor-to-outdoor ratios close to unity in the majority of homes, elevated ratios were found in the paired samples with the highest concentration. Thus, although ambient emissions contribute to exposure of some air toxics indoors as well as outdoors, this was not true for all of the air toxics and especially for the higher end of exposures to most volatile organic air toxics examined. It is therefore critical, when evaluating potential effects of air toxics on asthma or other adverse health end points, to determine where the exposure occurs and the source contributions for each air toxic and target population separately and not to rely solely on ambient air concentration measurements.
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