Respiratory disease continues to be a major public health problem. Chronic obstructive lung disease, chronic bronchitis and asthma continue to produce considerable morbidity and mortality. Environmental factors have long been recognized as important in the causation of these diseases. For example, there has been recent recognition that particulate air pollution may be accounting for excess morbidity and mortality, a problem with enormous regulatory significance, however, little is known about the nature of the particles people breathe. Investigators are only beginning to understand the true relationships of indoor and outdoor pollution with the various forms of respiratory disease. The SCEHSC offers a wide range of approaches to determining the acute and chronic respiratory effects of pollutants on a clinical or epidemiologic scale and Center investigators have published significant papers on this topic during 1999.

From the Children's Health Study, the two-part papers by Peters et al. (1999), reporting initial cross-sectional analyses, indicated that both symptoms and low lung function were associated more consistently with NO2, fine particulate matter, or airborne strong acid (all highly correlated with one another) than with O3. Further cross-sectional analysis in the paper by McConnell et al. (1999) indicated that chronic phlegm and bronchitis were more prevalent in asthmatics from areas with high PM or NO2 , although asthma prevalence was not associated with any measured pollutant. Subsequent longitudinal analyses, reported in the paper by Gauderman et al. (in press), associated PM/NO2/acid, but not O3, with reduced lung function growth rates. A separate daily time-series analysis of hospital admissions and air pollution in metropolitan Los Angeles, reported in the paper by Linn et al. (in press), associated asthma admissions with PM, NO2 , or CO, but not with O3. Thus, a broad range of new epidemiologic evidence from the Center points toward "primary" pollutants, rather than secondary photochemical oxidants, as the principal source of health risk in Southern California air. Other Center research relates to improving individual exposure assessment such as looking at proximity to roadways where exposure to primary pollutants occurs. The paper from Dr. Glen Cass and colleagues (Miguel, et al. 1999) shows that allergenic material in road dust becomes airborne from vehicular traffic. The mechanistic models described by Dr. Frank Gilliland (Gilliland et al, 1999) are very likely to reveal genetic polymorphisms associated with susceptibility to these pollutant effects. His preliminary data are already showing asthma risks associated with certain polymorphisms. The paper by Gong et al. (in press) demonstrates that it is feasible to expose volunteers to concentrated Southern California ambient PM and test a wide range of health responses; this approach will allow a range of realistic yet controlled exposure-effect studies which potentially can link the broader epidemiologic findings with the mechanism-oriented laboratory research. These examples demonstrate how the Center’s structure and mechanisms for collaboration facilitate complex, interdisciplinary research.