Department of Biostatistics, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan 250012, Shandong, China; Healthcare Big Data Research Institute, Cheeloo College of Medicine, Shandong University, Jinan 250012, Shandong, China.
Department of Pharmacy, Shandong Public Health Clinical Center, Jinan 250100, Shandong, China.
Sci Total Environ. 2022 Nov 1;845:157165. doi: 10.1016/j.scitotenv.2022.157165. Epub 2022 Jul 14.
Epidemiological evidence for the association between air pollutants exposure and venous thromboembolism (VTE) remains controversial. In this study, a total of 389,659 participants from the UK Biobank who were free of VTE in 2010 were included, and the annual mean concentrations of air pollutants near where participants lived were collected. During a median follow-up period of 8.25 years, 4986 VTEs were determined from the hospital admission records. The Cox proportional hazard model was used to examine the association between air pollutants and VTE. We firstly investigated the associations between air pollutants concentration and VTE and found only NO2 and NO increased VTE risk (P < 0.05). We further calculated the product of air pollutant concentrations and outdoor time to measure personal daily cumulative exposure and found that the hazard rates (HRs) of VTE for a 50-μg/m∗day increase in daily cumulative exposure to PM10, PM2.5, PM2.5-10, NO, and NO2 were 1.08 (1.05-1.12), 1.16 (1.09-1.24), 1.23 (1.11-1.37), 1.04 (1.01-1.06), and 1.05 (1.03-1.08), respectively. To measure joint exposure to various air pollutants and its effect on VTE, we created a weighted air pollutants exposure score (APES) and found a dose-response relationship between APES and VTE risk (P < 0.001 for trend). Compared with participants in the lowest quintile of APES, the HRs of VTE were 1.19 (1.08-1.30) for those within the highest quintile groups. Furthermore, we also found the effect of air pollutants on VTE was statistically significant only in individuals with low-middle VTE genetic risk score (GRS) (P < 0.05), but not in the high VTE GRS groups (P > 0.05). Our findings suggest that exposure to various air pollutants including PM2.5, PM2.5-10, PM10, NO, and NO2, either individually or jointly, were associated with an increased risk of VTE in a dose-response pattern. Our study highlights the importance of a comprehensive assessment of various air pollutants in VTE prevention.
关于空气污染暴露与静脉血栓栓塞症（VTE）之间的关联，流行病学证据仍存在争议。在这项研究中，共纳入了来自英国生物库的 389659 名 2010 年无 VTE 的参与者，收集了他们居住地点附近的空气污染物年平均浓度。在中位随访 8.25 年期间，根据住院记录确定了 4986 例 VTE。使用 Cox 比例风险模型来研究空气污染物与 VTE 之间的关联。我们首先研究了空气污染物浓度与 VTE 之间的关联，发现只有 NO2 和 NO 增加了 VTE 风险（P<0.05）。我们进一步计算了空气污染物浓度与户外活动时间的乘积，以衡量个人每日累积暴露量，发现 PM10、PM2.5、PM2.5-10、NO 和 NO2 的每日累积暴露量每增加 50μg/m∗day，VTE 的危险比（HR）分别为 1.08（1.05-1.12）、1.16（1.09-1.24）、1.23（1.11-1.37）、1.04（1.01-1.06）和 1.05（1.03-1.08）。为了衡量各种空气污染物的联合暴露及其对 VTE 的影响，我们创建了一个加权空气污染物暴露评分（APES），并发现 APES 与 VTE 风险之间存在剂量-反应关系（趋势 P<0.001）。与 APES 最低五分位组的参与者相比，APES 最高五分位组的 VTE 的 HR 为 1.19（1.08-1.30）。此外，我们还发现，只有在 VTE 遗传风险评分（GRS）处于中低水平的个体中，空气污染物对 VTE 的影响才有统计学意义（P<0.05），而在 VTE GRS 较高的组中则无统计学意义（P>0.05）。我们的研究结果表明，单独或联合暴露于 PM2.5、PM2.5-10、PM10、NO 和 NO2 等各种空气污染物与 VTE 风险呈剂量-反应关系增加有关。我们的研究强调了在 VTE 预防中全面评估各种空气污染物的重要性。
