Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing, China.
Department of Occupational and Environmental Health, School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Environ Pollut. 2022 Jan 1;292(Pt A):118336. doi: 10.1016/j.envpol.2021.118336. Epub 2021 Oct 8.
Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date.
To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O), nitrogen dioxide (NO), sulfur dioxide (SO), carbon dioxide (CO) and major inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α.
A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021.
The meta-analysis included 38 studies conducted among 210,438 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 μg/m increase in short-term exposure to O, NO, and SO, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 μg/m increase in NO was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses found more apparent associations in studies with better study design, higher quality, and smaller sample size. Meanwhile, the associations also varied across studies conducted in different geographical regions.
Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting that a systemic inflammatory state is activated upon exposure. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.
研究表明，气态空气污染物通过炎症途径与多种健康影响有关。几种主要的炎症生物标志物，包括 C 反应蛋白（CRP）、纤维蛋白原、白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α），也被认为是心血管疾病的预测因子。然而，迄今为止，还没有关于评估气态空气污染物与这些典型炎症生物标志物之间关系的荟萃分析。
评估短期和长期暴露于环境臭氧（O）、二氧化氮（NO）、二氧化硫（SO）、二氧化碳（CO）与包括 CRP、纤维蛋白原、IL-6 和 TNF-α 在内的主要炎症生物标志物之间的总体关联。
对截至 2021 年 2 月 1 日PubMed、Web of Science、Scopus 和 EMBASE 数据库中的出版物进行荟萃分析。
荟萃分析包括 210438 名参与者的 38 项研究。一般来说，我们仅观察到短期暴露于气态空气污染物与炎症生物标志物之间存在显著的正相关关系。对于短期暴露于 O、NO 和 SO 的每增加 10μg/m，CRP 分别显著增加 1.05%（95%CI：0.09%，2.02%）、1.60%（95%CI：0.49%，2.72%）和 10.44%（95%CI：4.20%，17.05%）。同时，NO 每增加 10μg/m，TNF-α 也增加 4.85%（95%CI：1.10%，8.73%）。长期暴露于气态空气污染物与这些生物标志物无统计学关联，但研究数量相对较少。亚组分析发现，在设计更好、质量更高、样本量更小的研究中，相关性更为明显。同时，这些关联在不同地理区域进行的研究中也存在差异。
短期暴露于气态空气污染物与循环炎症生物标志物水平升高有关，表明暴露后会激活全身炎症状态。需要更多研究来验证长期暴露于气态空气污染物和炎症生物标志物之间的关联。
