Investigators in the Inner-City Asthma Study are listed in the Appendix. We thank the participants for making their homes available to us for 2-week periods. We also thank our excellent staff for performing the many tasks involved in a multiyear, multicity field study.

In this article we present results from a 2-year comprehensive exposure assessment study that examined the particulate matter (PM) exposures and health effects in 108 individuals with and without chronic obstructive pulmonary disease (COPD), coronary heart disease (CHD), and asthma. The average personal exposures to PM with aerodynamic diameters < 2.5 µm (PM 2.5 ) were similar to the average outdoor PM 2.5 concentrations but significantly higher than the average indoor concentrations. Personal PM 2.5 exposures in our study groups were lower than those reported in other panel studies of susceptible populations. Indoor and outdoor PM 2.5 , PM 10 (PM with aerodynamic diameters < 10 µm), and the ratio of PM 2.5 to PM 10 were significantly higher during the heating season. The increase in outdoor PM 10 in winter was primarily due to an increase in the PM 2.5 fraction. A similar seasonal variation was found for personal PM 2.5 . The high-risk subjects in our study engaged in an equal amount of dust-generating activities compared with the healthy elderly subjects. The children in the study experienced the highest indoor PM 2.5 and PM 10 concentrations. Personal PM 2.5 exposures varied by study group, with elderly healthy and CHD subjects having the lowest exposures and asthmatic children having the highest exposures. Within study groups, the PM 2.5 exposure varied depending on residence because of different particle infiltration efficiencies. Although we found a wide range of longitudinal correlations between central-site and personal PM 2.5 measurements, the longitudinal r is closely related to the particle infiltration efficiency. PM 2.5 exposures among the COPD and CHD subjects can be predicted with relatively good power with a microenvironmental model composed of three microenvironments. The prediction power is the lowest for the asthmatic children.

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We used real-time breath measurement technology to investigate the suitability of some volatile organic compounds (VOCs) as breath biomarkers for active and passive smoking and to measure actual exposures and resulting breath concentrations for persons exposed to tobacco smoke. Experiments were conducted with five smoker/nonsmoker pairs. The target VOCs included benzene, 1,3-butadiene, and the cigarette smoke biomarker 2,5-dimethylfuran. This study includes what we believe to be the first measurements of 1,3-butadiene in smokers' and nonsmokers' breath. The 1,3-butadiene and 2,5-dimethylfuran peak levels in the smokers' breath were similar (360 and 376 microg/m(3), respectively); the average benzene peak level was 522 microg/m(3). We found higher peak values of the target chemicals and shorter residence times in the body than previously reported, probably because of the improved time resolution made possible by the continuous breath measurement method. The real-time breath analyzer also showed the presence of the chemicals after exposure in the breath of the nonsmokers, but at greatly reduced levels. Single breath samples collected in evacuated canisters and analyzed independently with gas chromatography/mass spectrometry confirmed the presence of the target compounds in the postexposure breath of the nonsmokers but indicated that there was some contamination of the breath analyzer measurements. This was likely caused by desorption of organics from condensed tar in the analyzer tubing and on the quartz fiber filter used to remove particles. We used the decay data from the smokers to estimate residence times for the target chemicals. A two-compartment exponential model generally gave a better fit to the experimental decay data from the smokers than a single-compartment model. Residence times for benzene, 1,3-butadiene, and 2,5-dimethylfuran ranged from 0.5 (1,3-butadiene) to 0.9 min (benzene) for tau1 and were essentially constant (14 min) for tau2. These findings will be useful in models of environmental tobacco smoke exposure and risk.

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