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Long-Term Exposure to Source-Specific Fine Particles and Mortality─A Pooled Analysis of 14 European Cohorts within the ELAPSE Project.

Jie ChenGerard HoekKees de HooghSophia RodopoulouZorana J AndersenTom BellanderJørgen BrandtDaniela FechtFrancesco ForastiereJohn GulliverOle HertelBarbara HoffmannUlla Arthur HvidtfeldtW M Monique VerschurenKarl-Heinz JöckelJeanette T JørgensenKlea KatsouyanniMatthias KetzelDiego Yacamán MéndezKarin LeanderShuo LiuPetter LjungmanElodie FaurePatrik K E MagnussonGabriele NagelGöran PershagenAnnette PetersOle Raaschou-NielsenDebora RizzutoEvangelia SamoliYvonne T van der SchouwSara SchrammGianluca SeveriMassimo StafoggiaMaciej StrakMette SørensenAnne TjønnelandGudrun WeinmayrKathrin WolfEmanuel ZittBert BrunekreefGeorge D Thurston
Published in: Environmental science & technology (2022)
We assessed mortality risks associated with source-specific fine particles (PM 2.5 ) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM 2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM 2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 μg/m 3 increase) across five identified sources. On a 1 μg/m 3 basis, the residual oil-related PM 2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM 2.5 mass, suggesting that past estimates using the generic PM 2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.
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