Impacts of air pollutions on cardiovascular and cerebrovascular diseases through inflammation: a comprehensive analysis of one million Chinese and half million UK individuals
Lin Fei, Guohua Li, Yongbin Wang, Pingshuan Dong, Kan Yang, Hui Liu, Na Xie, Jingyu Liu, Hengwen Chen, Xiaomei Liu, Huan Li, Xuefang Li, Dongxu Li, Siyu Sun, Xiuli Wang, Yujing Sun, Jun Li, Guoan Zhao, Zhigang Chen, Jun Pu
Abstract
Epidemiological studies have found an association between air pollution and cardiovascular and cerebrovascular diseases (CACD) and its subtypes. However, there is a lack of individual-level data to explore the associations of air pollutants on CACD and its subtypes, the interaction among them, and the potential mechanism. This study employed a two-stage design, combining a time-stratified case-crossover study with a cohort study, analyzing data from one million individuals from China and half million from the UK. The study assessed the impact of air pollutants on CACD and its subtypes, while also examining the mediating effects of inflammation. Distributed lag non-linear models were used to analyze the lagged effects of pollutants, and mediation analysis was conducted to evaluate the role of inflammatory markers (SII, SIRI, AISI) in the relationship between air pollution and CACD. A total of 829,135 CSDs patients were recorded in this study. An interquartile range (IQR) increase in concentrations of PM2.5, PM10, NO2, SO2, CO, and O3 was associated with increases of 11.3% [95% confidence interval (CI) 9.5%-13.2%], 10.5% (95% CI 8.6%-12.3%), 3% (95% CI 1%-5%), 15.2% (95% CI 13.3%-17.1%), 15.5% (95% CI 11.6%-19.5%), and 2.8% (95% CI 2.2%-3.4%) in CSDs, respectively. A similar positive association was also observed for cardiovascular and ischemic heart diseases. A significant synergistic interaction between PM2.5 and NO2 and CO for CSDs. Approximately 64.75%, 21.13%, 32.2%, 2.31%, 43.7% and 43.7% of the effects of PM2.5, PM10, NO2, SO2, CO, and O3 on CSDs were significantly mediated by SII. This study provides robust evidence that short-term exposure to common air pollutants significantly increases the risk of CACD and its subtypes, with inflammation playing a crucial mediating role. The findings underscore the importance of coordinated air pollution control strategies and public health interventions to mitigate the cardiovascular risks associated with air pollution.