Allaouat Sara, Yli-Tuomi Tarja, Tiittanen Pekka, Kukkonen Jaakko, Kangas Leena, Mikkonen Santtu, Ngandu Tiia, Jousilahti Pekka, Siponen Taina, Zeller Tanja, Lanki Timo
Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland; Lifestyles and Living Environments Unit, Department of Public Health, Finnish Institute for Health and Welfare, Kuopio, Finland.
Lifestyles and Living Environments Unit, Department of Public Health, Finnish Institute for Health and Welfare, Kuopio, Finland.
Environ Res. 2024 Dec 1;262(Pt 1):119846. doi: 10.1016/j.envres.2024.119846. Epub 2024 Aug 24.
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; PM) from vehicular exhausts and residential woodsmoke, nitrogen dioxide (NO) 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 PM from vehicular exhausts (% CRP difference for 1 μg/m increase in PM: -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 NO 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.
空气污染和交通噪音对心血管健康有害。然而，这些暴露的不同来源对心血管生物标志物的影响仍不明确。我们探讨了长期低浓度暴露于特定来源的空气污染（汽车尾气和住宅木柴烟雾）以及道路交通噪音与全身炎症和心血管疾病生物标志物之间的关联。
在1997 - 2012年的芬兰全国 FINRISK 研究中，将模拟的室外暴露于汽车尾气和住宅木柴烟雾中的细颗粒物（空气动力学直径≤2.5μm；PM）、道路交通产生的二氧化氮（NO）以及道路交通噪音与参与者（年龄在25 - 74岁的芬兰居民）的家庭住址相关联。参与者位于芬兰的赫尔辛基市、万塔市和图尔库地区。研究结果包括全身炎症的生物标志物高敏C反应蛋白（CRP）以及心血管疾病生物标志物N末端B型利钠肽原（NT - proBNP）和肌钙蛋白I。我们使用线性和加法模型进行横断面分析，并对潜在的混杂因素进行了调整。
我们发现，汽车尾气中的PM（PM每增加1μg/m³时CRP的差异百分比：-0.9，95%置信区间，CI：-7.2，5.8）或住宅木柴烟雾中的PM（差异百分比：-8.1，95%CI：-21.7，7.9）与CRP之间无关联（N = 4147）。道路交通噪音>70dB与CRP呈正相关趋势（与噪音参考类别≤45dB相比，CRP差异百分比：18.3，95%CI：-0.5，40.6），但该关联缺乏显著性和稳健性（N = 7142）。此外，我们发现道路交通噪音与CRP之间、道路交通产生的NO与NT - proBNP（N = 1907）或肌钙蛋白I（N = 1951）之间均无关联。
在该城市地区，长期暴露于汽车尾气和住宅木柴烟雾中特定来源的、相当低水平的空气污染或道路交通噪音与全身炎症和心血管疾病生物标志物无关。
