Cardiopulmonary Mortality and Fine Particulate Air Pollution by Species and Source in a National U.S. Cohort
Zachari A. Pond, Carlos Hernández, P. J. Adams, Spyros Ν. Pandis, George R. Garcia, Allen L. Robinson, Julian Marshall, Richard T. Burnett, Ksakousti Skyllakou, Pablo Garcia Rivera, Eleni Karnezi, Carver J. Coleman, C. Arden Pope
Abstract
The purpose of this study was to estimate cardiopulmonary mortality associations for long-term exposure to PM2.5 species and sources (i.e., components) within the U.S. National Health Interview Survey cohort. Exposures were estimated through a chemical transport model for six species (i.e., elemental carbon (EC), primary organic aerosols (POA), secondary organic aerosols (SOA), sulfate (SO4), ammonium (NH4), nitrate (NO3)) and five sources of PM2.5 (i.e., vehicles, electricity-generating units (EGU), non-EGU industrial sources, biogenic sources (bio), “other” sources). In single-pollutant models, we found positive, significant (p < 0.05) mortality associations for all components, except POA. After adjusting for remaining PM2.5 (total PM2.5 minus component), we found significant mortality associations for EC (hazard ratio (HR) = 1.36; 95% CI [1.12, 1.64]), SOA (HR = 1.11; 95% CI [1.05, 1.17]), and vehicle sources (HR = 1.06; 95% CI [1.03, 1.10]). HRs for EC, SOA, and vehicle sources were significantly larger in comparison to those for remaining PM2.5 (per unit μg/m3). Our findings suggest that cardiopulmonary mortality associations vary by species and source, with evidence that EC, SOA, and vehicle sources are important contributors to the PM2.5 mortality relationship. With further validation, these findings could facilitate targeted pollution regulations that more efficiently reduce air pollution mortality.