Associations of Exposure to Fine Particulate Matter Mass and Constituents with Systemic Inflammation: A Cross-Sectional Study of Urban Older Adults in China

Systemic inflammation is a key mechanism in the development of cardiovascular diseases induced by exposure to fine particles (particles with aerodynamic diameter <= 2.5 mu m [PM2.5]). However, little is known about the effects of chemical constituents of PM2.5 on systemic inflammation. In this cross-sectional study, filter samples of personal exposure to PM2.5 were collected from community-dwelling older adults in Tianjin, China, and the chemical constituents of PM2.5 were analyzed. Blood samples were collected immediately after the PM2.5 sample collection. Seventeen cytokines were measured as targets. A linear regression model was applied to estimate the relative effects of PM2.5 and its chemical constituents on the measured cytokines. A positive matrix factorization model was employed to distinguish the sources of PM2.5. The calculated source contributions were used to estimate their effects on cytokines. After adjusting for other covariates, higher PM2.5-bound copper was significantly associated with increased levels of interleukin (IL)1 beta, IL6, IL10, and IL17 levels. Source analysis showed that an increase in PM2.5 concentration that originated from tire/brake wear and cooking emissions was significantly associated with enhanced levels of IL1 beta, IL6, tumor necrosis factor alpha (TNF alpha), and IL17. In summary, personal exposure to some PM2.5 constituents and specific sources could increase systemic inflammation in older adults. These findings may explain the cardiopulmonary effects of specific particulate chemical constituents of urban air pollution.

Automated summary

This study found that personal exposure to certain PM2.5 constituents and specific sources may increase systemic inflammation in older adults. These findings help explain the cardiopulmonary effects of specific particulate chemical constituents of urban air pollution.