Exposure to ambient fine particulate matter (PM2.5) triggers inflammatory responses that contribute to adverse health effects like cardiovascular disease, particularly in vulnerable populations. However, as a complex mixture of various chemical constituents in PM2.5-including carbonaceous fractions, inorganic ions, organic acids, and metal elements-the relative toxicity of PM2.5 depends on its specific components. In this longitudinal panel study conducted in Beijing during winter 2016 and summer 2017, we investigated how total PM2.5 and specific PM2.5 chemical components affect respiratory and systemic inflammation in elderly adults, with special attention to hypertension as a susceptibility modifier. Associations between PM2.5 and inflammatory biomarkers were evaluated using mixed-effects models, initially conducted on the entire population and subsequently stratified by hypertension status. The contributions of individual components were further assessed using weighted quantile sum (WQS) regression. Results showed that acute PM2.5 exposure significantly increased fractional exhaled nitric oxide (FeNO, 5.03 % per interquartile range increase) and systemic inflammation biomarkers. Hypertensive individuals showed distinct response patterns: weaker respiratory but stronger systemic inflammation, including elevated monocytes (0.92 % per interquartile range increase) absent in normotensive participants. Component-specific analyses identified water-soluble metals (e.g., water-soluble Bi, Ca, Ba, Fe, Sr) as major contributors to respiratory inflammation, while systemic inflammation was driven by broader metal species, including both soluble and insoluble forms. Overall, these findings underscore the critical yet understudied role of water-soluble metals within PM2.5, particularly highlighting hypertensive populations as more susceptible to component-specific systemic inflammatory responses.
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