title: Ischemic Heart Disease Incidence in Relation to Fine versus Total Particulate Matter Exposure in a U.S. Aluminum Industry Cohort.
abstract: Ischemic heart disease (IHD) has been linked to exposures to airborne particles with an aerodynamic diameter <2.5 μm (PM2.5) in the ambient environment and in occupational settings. Routine industrial exposure monitoring, however, has traditionally focused on total particulate matter (TPM). To assess potential benefits of PM2.5 monitoring, we compared the exposure-response relationships between both PM2.5 and TPM and incidence of IHD in a cohort of active aluminum industry workers. To account for the presence of time varying confounding by health status we applied marginal structural Cox models in a cohort followed with medical claims data for IHD incidence from 1998 to 2012. Analyses were stratified by work process into smelters (n = 6,579) and fabrication (n = 7,432). Binary exposure was defined by the 10th-percentile cut-off from the respective TPM and PM2.5 exposure distributions for each work process. Hazard Ratios (HR) comparing always exposed above the exposure cut-off to always exposed below the cut-off were higher for PM2.5, with HRs of 1.70 (95% confidence interval (CI): 1.11-2.60) and 1.48 (95% CI: 1.02-2.13) in smelters and fabrication, respectively. For TPM, the HRs were 1.25 (95% CI: 0.89-1.77) and 1.25 (95% CI: 0.88-1.77) for smelters and fabrication respectively. Although TPM and PM2.5 were highly correlated in this work environment, results indicate that, consistent with biologic plausibility, PM2.5 is a stronger predictor of IHD risk than TPM. Cardiovascular risk management in the aluminum industry, and other similar work environments, could be better guided by exposure surveillance programs monitoring PM2.5.
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: Andreas M
authors.initials: AM
authors.lastname: Neophytou
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Noth
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: Sa
authors.initials: S
authors.lastname: Liu
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: Sadie
authors.initials: S
authors.lastname: Costello
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: S Katharine
authors.initials: SK
authors.lastname: Hammond
authors.affiliation: Division of General Medical Disciplines, School of Medicine, Stanford University, Stanford, California, United States of America.
authors.forename: Mark R
authors.initials: MR
authors.lastname: Cullen
authors.affiliation: Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
authors.forename: Ellen A
authors.initials: EA
authors.lastname: Eisen
mesh_terms: D000535:Aluminum; D015331:Cohort Studies; D006801:Humans; D007221:Industry; D017202:Myocardial Ischemia / Q000139:chemically induced*; D016273:Occupational Exposure; D052638:Particulate Matter / Q000633:toxicity*; D014481:United States
chemical_list: D052638:Particulate Matter; D000535:Aluminum