Does Nonsteroidal Anti-inflammatory Drug Use Modify All-Cause and Cause-Specific Mortality Associated with PM2.5 and Its Components? A Nationally Representative Cohort Study (2007-2017)

Wanzhou Wang; Chao Yang; Fulin Wang; Jinwei Wang; Feifei Zhang; Pengfei Li; Luxia Zhang

doi:10.1021/envhealth.4c00133

Does Nonsteroidal Anti-inflammatory Drug Use Modify All-Cause and Cause-Specific Mortality Associated with PM_2.5 and Its Components? A Nationally Representative Cohort Study (2007-2017)

Environ Health (Wash). 2024 Oct 22;3(1):14-25. doi: 10.1021/envhealth.4c00133. eCollection 2025 Jan 17.

Authors

Wanzhou Wang^{1

2

3}, Chao Yang^{3

4

5

6}, Fulin Wang^{1

2}, Jinwei Wang^{3

7}, Feifei Zhang^{1

2}, Pengfei Li⁵, Luxia Zhang^{1

2

3

4

5

6}

Affiliations

¹ Institute of Medical Technology, Peking University Health Science Center, Beijing 100191, China.
² National Institute of Health Data Science at Peking University, Beijing 100191, China.
³ Renal Division, Department of Medicine, Peking University First Hospital, Peking University Institute of Nephrology, Beijing 100034, China.
⁴ Research Units of Diagnosis and Treatment of Immune-Mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing 100034, China.
⁵ Advanced Institute of Information Technology, Peking University, Hangzhou 311215, China.
⁶ Digital Intelligence Medicine Center, Peking University First Hospital, Beijing 100034, China.
⁷ Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Peking University, Ministry of Education of the People's Republic of China, Beijing 100034, China.

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 (NH₄ ⁺), nitrate (NO₃ ^-), organic matter (OM), and sulfate (SO₄ ^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 SO₄ ^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/m³), 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.