Outdoor ambient
air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of
asthma. However, the complexity of
pollutant mixtures and etiologic heterogeneity of
asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with
asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g.,
metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause
occupational asthma, only
formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific
volatile organic compounds (VOCs) identified in association with
occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric
asthma. In addition, experimental evidence indicates that airborne
polycyclic aromatic hydrocarbon (PAH) exposures linked to
diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on
asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or
asthma with exposures to ambient
air pollutant mixtures with PAH components, including black
smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco
smoke. Other particle-phase and gaseous co-
pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both
asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria
air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on
biological mechanisms, particularly
irritant and immunological pathways to
asthma onset and exacerbation.