Distributed Lag Analyses of Daily Hospital Admissions and Source-Apportioned Fine Particle Air Pollution

摘要

Background Past time-series studies of the health effects of fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM_2.5)] have used chemically nonspecific PM_2.5 mass. However, PM_2.5 is known to vary in chemical composition with source, and health impacts may vary accordingly. Objective We tested the association between source-specific daily PM_2.5 mass and hospital admissions in a time-series investigation that considered both single-lag and distributed-lag models. Methods Daily PM_2.5 speciation measurements collected in midtown Manhattan were analyzed via positive matrix factorization source apportionment. Daily and distributed-lag generalized linear models of Medicare respiratory and cardiovascular hospital admissions during 2001–2002 considered PM_2.5 mass and PM_2.5 from five sources: transported sulfate, residual oil, traffic, steel metal works, and soil. Results Source-related PM_2.5 (specifically steel and traffic) was significantly associated with hospital admissions but not with total PM_2.5 mass. Steel metal works–related PM_2.5 was associated with respiratory admissions for multiple-lag days, especially during the cleanup efforts at the World Trade Center. Traffic-related PM_2.5 was consistently associated with same-day cardiovascular admissions across disease-specific subcategories. PM_2.5 constituents associated with each source (e.g., elemental carbon with traffic) were likewise associated with admissions in a consistent manner. Mean effects of distributed-lag models were significantly greater than were maximum single-day effect models for both steel- and traffic-related PM_2.5. Conclusions Past analyses that have considered only PM_2.5 mass or only maximum single-day lag effects have likely underestimated PM_2.5 health effects by not considering source-specific and distributed-lag effects. Differing lag structures and disease specificity observed for steel-related versus traffic-related PM_2.5 raise the possibility of distinct mechanistic pathways of health effects for particles of differing chemical composition.