Abstract:
Studies investigating the relationship between ambient air pollutants and liver function are scarce. Our objective was to examine the associations of acute exposure to PM2.5 and O3 with levels of hepatic enzymes in people living with HIV/AIDS (PWHA). Our study involved 163 PWHA, who were evaluated for serum hepatic enzymes up to four times within a year. We extracted daily average concentrations of PM2.5, PM2.5 components, and O3 for each participant, based on their residential address, using the Tracking of Air Pollution in China database. Linear mixed-effect models were utilized to assess the associations of acute exposure to PM2.5 and O3 with hepatic enzymes. Weighted quantile sum regression models were employed to identify the major constituents of PM2.5 that affect hepatic enzymes. The percent change of aspartate aminotransferase (AST) concentration was positively correlated with a 10 µg/m3 increase in PM2.5, ranging from 1.92 (95% CI: 3.13 to 4.38) to 6.09 (95% CI: 9.25 to 12.38), with the largest effect observed at lag06. Additionally, acute O3 exposure was related to increased levels of alanine aminotransferase (ALT), AST, and alkaline phosphatase (ALP) concentrations. Co-exposure to high levels of PM2.5 and O3 had an antagonistic effect on the elevation of AST. Further analysis revealed that SO42- and BC were major contributors to elevated AST concentration due to PM2.5 constituents. A stronger association was found between O3 exposure and ALT concentration in female PWHA. Our study found that short-term exposure to PM2.5 and O3 was associated with increased levels of hepatic enzymes, indicating that PM2.5 and O3 exposure may contribute to hepatocellular injury in PWHA. Our study also found that PWHA may be more vulnerable to air pollution than the general population. These findings highlight the relationship between air pollutants and liver function in PWHA, providing a scientific basis for the implementation of measures to protect susceptible populations from the adverse effects of air pollution. A reduction in the burning of fossil fuels and reduced exposure to air pollutants may be effective hazard reduction approaches.
摘要:
调查环境空气污染物与肝功能之间关系的研究很少。我们的目的是研究HIV/AIDS(PWHA)患者急性暴露于PM2.5和O3与肝酶水平的关系。我们的研究涉及163个PWHA,一年内对他们的血清肝酶进行了四次评估。我们提取了PM2.5的日平均浓度,PM2.5成分,和每个参与者的O3,根据他们的住址,使用中国空气污染跟踪数据库。线性混合效应模型用于评估急性暴露于PM2.5和O3与肝酶的关联。采用加权分位数和回归模型来识别影响肝酶的PM2.5的主要成分。天冬氨酸氨基转移酶(AST)浓度的百分比变化与PM2.5的10µg/m3增加呈正相关,范围为1.92(95%CI:3.13至4.38)至6.09(95%CI:9.25至12.38),在lag06观察到最大的效果。此外,急性O3暴露与丙氨酸氨基转移酶(ALT)水平升高有关,AST,和碱性磷酸酶(ALP)浓度。共同暴露于高水平的PM2.5和O3对AST的升高具有拮抗作用。进一步分析显示,由于PM2.5成分,SO42-和BC是AST浓度升高的主要原因。在女性PWHA中,O3暴露与ALT浓度之间存在更强的关联。我们的研究发现,短期暴露于PM2.5和O3与肝酶水平升高有关,表明PM2.5和O3暴露可能导致PWHA肝细胞损伤。我们的研究还发现,PWHA可能比普通人群更容易受到空气污染的影响。这些发现强调了空气污染物与PWHA肝功能之间的关系,为实施保护易感人群免受空气污染不利影响的措施提供科学依据。减少化石燃料的燃烧和减少对空气污染物的暴露可能是有效的减少危害的方法。