BACKGROUND: Several epidemiological studies have reported that long-term exposure to fine particulate matter (PM2.5) is associated with higher mortality. Evidence regarding contributions of PM2.5 constituents is inconclusive.
OBJECTIVES: We assembled a dataset of 12.5 million Medicare enrollees (≥65 yrs) to determine which PM2.5 constituents are: 1) associated with mortality controlling for previous-year PM2.5 total mass (main effect); and 2) elevated in locations exhibiting stronger associations between previous-year PM2.5 and mortality (effect modification).
METHODS: For 518 PM2.5 monitoring locations (Eastern US, 2000-2006), we calculated monthly mortality rates, monthly long-term (previous 1-year average) PM2.5, and 7-year averages (2000-2006) of major PM2.5 constituents [elemental carbon (EC), organic carbon matter (OCM), sulfate (SO4(=)), silicon (Si), nitrate (NO3(-)), and sodium (Na)] and community-level variables. We applied a Bayesian hierarchical model to estimate location-specific mortality rates associated with previous-year PM2.5 (model level 1) and identify constituents that contributed to the spatial variability of mortality, and constituents that modified associations between previous-year PM2.5 and mortality (model level 2), controlling for community-level confounders.
RESULTS: One standard deviation (SD) increases in 7-year average EC, Si, and NO3(-) concentrations were associated with 1.3% [95% posterior interval (PI): 0.3, 2.2], 1.4% (95% PI: 0.6, 2.4), and 1.2% (95% PI: 0.4, 2.1) increases in monthly mortality, controlling for previous-year PM2.5. Associations between previous-year PM2.5 and mortality were stronger in combination with 1-SD increases in SO4(=) and Na.
CONCLUSIONS: Long-term exposures to PM2.5 and several constituents were associated with mortality in the elderly population of the Eastern US. Moreover, some constituents increased the association between long-term exposure to PM2.5 and mortality. These results provide new evidence that chemical composition can partly explain the differential toxicity of PM2.5.