全身炎症
炎症
疾病
空气污染
期限(时间)
道路交通
暴露评估
环境卫生
环境科学
医学
空气污染物
免疫学
病理
生物
工程类
生态学
运输工程
物理
量子力学
作者
Sara Allaouat,Tarja Yli‐Tuomi,Pekka Tiittanen,Jaakko Kukkonen,Leena Kangas,Santtu Mikkonen,Tiia Ngandu,Pekka Jousilahti,Taina Siponen,Tanja Zeller,Timo Lanki
标识
DOI:10.1016/j.envres.2024.119846
摘要
Air pollution and traffic noise are detrimental to cardiovascular health. However, the effects of different sources of these exposures on cardiovascular biomarkers remain unclear. We explored the associations of long-term exposure to source-specific air pollution (vehicular exhausts and residential woodsmoke) at low concentrations and road-traffic noise with systemic inflammation and cardiovascular disease biomarkers. Modeled outdoor exposure to fine particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) from vehicular exhausts and residential woodsmoke, nitrogen dioxide (NO2) from road traffic, and road-traffic noise were linked to the home addresses of the participants (Finnish residents aged 25–74) in the FINRISK study 1997–2012. The participants were located in the cities of Helsinki, Vantaa, and the region of Turku, Finland. The outcomes were high-sensitivity C-reactive protein (CRP), a biomarker for systemic inflammation, and cardiovascular disease biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin I. We performed cross-sectional analyses with linear and additive models and adjusted for potential confounders. We found no association between PM2.5 from vehicular exhausts (% CRP difference for 1 μg/m3 increase in PM2.5: −0.9, 95% confidence interval, CI: −7.2, 5.8), or from residential woodsmoke (% difference: −8.1, 95% CI: −21.7, 7.9) and CRP (N = 4147). Road-traffic noise >70 dB tended to be positively associated with CRP (% CRP difference versus noise reference category of ≤45 dB: 18.3, 95% CI: −0.5, 40.6), but the association lacked significance and robustness (N = 7142). Otherwise, we found no association between road-traffic noise and CRP, nor between NO2 from road traffic and NT-proBNP (N = 1907) or troponin I (N = 1951). Long-term exposures to source-specific, fairly low-level air pollution from vehicular exhausts and residential woodsmoke, or road-traffic noise were not associated with systemic inflammation and cardiovascular disease biomarkers in this urban area.
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