PM2.5 chemical constituents and chronic obstructive pulmonary disease mortality risk: The Pearl River Cohort study.

Abstract

Chronic obstructive pulmonary disease (COPD) imposes a major burden on global health, yet evidence on the prolonged health effects of individual PM2.5 constituents remains limited. Previous research has primarily employed traditional models, which may struggle to capture the complex correlations among the PM2.5 components and be less effective in confounding adjustment. We conducted a prospective cohort study involving 182,009 participants from the Pearl River Cohort (2013-2015) followed through 2020, applying inverse probability-weighted marginal structural Cox models and quantile g-computation (QGC) to assess the associations of individual PM2.5 components and their mixtures with COPD mortality, followed by stratified analyses for effect modification. Over 1.18 million person-years of follow-up, 422 COPD deaths were documented. Long-term exposure to ammonium (NH4+), black carbon (BC), nitrate (NO3-), organic matter (OM) and chloride (Cl-) was associated with higher COPD mortality, with HRs (95% CI) of 2.75 (1.86-4.05), 2.41 (1.64-3.55), 1.86 (1.45-2.39), 1.85 (1.33-2.57) and 1.45 (1.15-1.82), respectively. Mixture analysis showed that each one-quartile increase in the PM2.5 component mixture was associated with a 39% (29%-50%) higher risk of COPD mortality, primarily driven by OM, Cl-, and NO3- (weights = 0.34, 0.34, 0.32). Stratified analyses indicated greater associations among older adults, suggesting increased susceptibility in this group. Our findings underscore the potential contribution of individual PM2.5 constituents and their mixtures in COPD mortality, while suggesting actionable source-control priorities and coordinated precursor-reduction strategies, as well as population-specific prevention approaches.