title: Distributed lag analyses of daily hospital admissions and source-apportioned fine particle air pollution.
abstract: BACKGROUND
  Past time-series studies of the health effects of fine particulate matter [aerodynamic diameter ≤ 2.5 µm (PM2.5)] have used chemically nonspecific PM2.5 mass. However, PM2.5 is known to vary in chemical composition with source, and health impacts may vary accordingly.
  
  
  OBJECTIVE
  We tested the association between source-specific daily PM2.5 mass and hospital admissions in a time-series investigation that considered both single-lag and distributed-lag models.
  
  
  METHODS
  Daily PM2.5 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 PM2.5 mass and PM2.5 from five sources: transported sulfate, residual oil, traffic, steel metal works, and soil.
  
  
  RESULTS
  Source-related PM2.5 (specifically steel and traffic) was significantly associated with hospital admissions but not with total PM2.5 mass. Steel metal works-related PM2.5 was associated with respiratory admissions for multiple-lag days, especially during the cleanup efforts at the World Trade Center. Traffic-related PM2.5 was consistently associated with same-day cardiovascular admissions across disease-specific subcategories. PM2.5 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 PM2.5.
  
  
  CONCLUSIONS
  Past analyses that have considered only PM2.5 mass or only maximum single-day lag effects have likely underestimated PM2.5 health effects by not considering source-specific and distributed-lag effects. Differing lag structures and disease specificity observed for steel-related versus traffic-related PM2.5 raise the possibility of distinct mechanistic pathways of health effects for particles of differing chemical composition.
authors.affiliation: New York University, School of Medicine, Department of Environmental Medicine, Tuxedo, New York 10987, USA. rl461@nyu.edu
authors.forename: Ramona
authors.initials: R
authors.lastname: Lall
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Ito
authors.forename: George D
authors.initials: GD
authors.lastname: Thurston
mesh_terms: D000368:Aged; D000393:Air Pollutants / Q000032:analysis*; D000397:Air Pollution / Q000706:statistics & numerical data*; D002318:Cardiovascular Diseases / Q000453:epidemiology; D004781:Environmental Exposure / Q000032:analysis / Q000706:statistics & numerical data; D006760:Hospitalization / Q000706:statistics & numerical data*; D006801:Humans; D008956:Models, Chemical; D052638:Particulate Matter / Q000032:analysis*; D012140:Respiratory Tract Diseases / Q000453:epidemiology
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter