Abstract
Several studies reported that nonsteroidal anti-inflammatory drug (NSAID) use could alleviate subclinical effects of short-term exposure to fine particulate matter (PM(2.5)). However, whether chronic NSAID use could mitigate the long-term effects of PM(2.5) and its components on population mortality has been unknown. Based on a national representative survey of 47,086 adults (2007-2010) with follow-up information on the primary cause of death (until 2017), we investigated the long-term associations of PM(2.5) and its major components, including black carbon (BC), ammonium (NH(4) (+)), nitrate (NO(3) (-)), organic matter (OM), and sulfate (SO(4) (2-)), with all-cause and cause-specific mortality using the Cox proportional hazards model. We also evaluated the effect modification by NSAID use (including broad NSAIDs, aspirin, or ibuprofen) on the associations using interaction models. Long-term exposures to PM(2.5) and its components were associated with increased risks of all-cause and cause-specific mortality, where BC, OM, and SO(4) (2-) showed stronger associations. Ibuprofen use could mitigate the associations of PM(2.5) and its components with mortality risks, while no significant modifying effects of aspirin were observed. For instance, along with per interquartile range increment in PM(2.5) concentration (34.8 μg/m(3)), the hazard ratios (HRs) of all-cause mortality were 1.21 (95% CI: 1.19, 1.22) and 1.10 (95% CI: 1.01, 1.19) in nonibuprofen and ibuprofen use groups (P for interaction = 0.026), respectively. Cause-specific analyses indicated that ibuprofen use could mainly mitigate risks of cardiovascular disease (CVD) especially ischemic heart disease (IHD) mortality attributable to PM(2.5) components. Stratified analyses found more apparent mitigating effects of ibuprofen use among participants without chronic diseases, participants ≤50 years, female participants, rural residents, and those with lower education levels. Our findings suggested potential implications in reducing population mortality caused by long-term exposures to PM(2.5) and its components through personalized interventions.