Faculty Bibliography

Although the association between exposure to ambient fine particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and human mortality is well established, the most responsible particle types/sources are not yet certain. In May 2003, the U.S. Environmental Protection Agency's Particulate Matter Centers Program sponsored the Workshop on the Source Apportionment of PM Health Effects. The goal was to evaluate the consistency of the various source apportionment methods in assessing source contributions to daily PM2.5 mass-mortality associations. Seven research institutions, using varying methods, participated in the estimation of source apportionments of PM2.5 mass samples collected in Washington, DC, and Phoenix, Arizona, USA. Apportionments were evaluated for their respective associations with mortality using Poisson regressions, allowing a comparative assessment of the extent to which variations in the apportionments contributed to variability in the source-specific mortality results. The various research groups generally identified the same major source types, each with similar elemental makeups. Intergroup correlation analyses indicated that soil-, sulfate-, residual oil-, and salt-associated mass were most unambiguously identified by various methods, whereas vegetative burning and traffic were less consistent. Aggregate source-specific mortality relative risk (RR) estimate confidence intervals overlapped each other, but the sulfate-related PM2.5 component was most consistently significant across analyses in these cities. Analyses indicated that source types were a significant predictor of RR, whereas apportionment group differences were not. Variations in the source apportionments added only some 15% to the mortality regression uncertainties. These results provide supportive evidence that existing PM2.5 source apportionment methods can be used to derive reliable insights into the source components that contribute to PM2.5 health effects

BACKGROUND: The assessment of air pollution exposure using only community average concentrations may lead to measurement error that lowers estimates of the health burden attributable to poor air quality. To test this hypothesis, we modeled the association between air pollution and mortality using small-area exposure measures in Los Angeles, California. METHODS: Data on 22,905 subjects were extracted from the American Cancer Society cohort for the period 1982-2000 (5,856 deaths). Pollution exposures were interpolated from 23 fine particle (PM2.5) and 42 ozone (O3) fixed-site monitors. Proximity to expressways was tested as a measure of traffic pollution. We assessed associations in standard and spatial multilevel Cox regression models. RESULTS: After controlling for 44 individual covariates, all-cause mortality had a relative risk (RR) of 1.17 (95% confidence interval=1.05-1.30) for an increase of 10 mug/m PM2.5 and a RR of 1.11 (0.99-1.25) with maximal control for both individual and contextual confounders. The RRs for mortality resulting from ischemic heart disease and lung cancer deaths were elevated, in the range of 1.24-1.6, depending on the model used. These PM results were robust to adjustments for O3 and expressway exposure. CONCLUSION: Our results suggest the chronic health effects associated with within-city gradients in exposure to PM2.5 may be even larger than previously reported across metropolitan areas. We observed effects nearly 3 times greater than in models relying on comparisons between communities. We also found specificity in cause of death, with PM2.5 associated more strongly with ischemic heart disease than with cardiopulmonary or all-cause mortality.