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

Abstract

Systemic inflammation is a key mechanism in the development of cardiovascular diseases induced by exposure to fine particles (particles with aerodynamic diameter ≤2.5 μm [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)­1β, 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 IL1β, IL6, tumor necrosis factor alpha (TNFα), 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.

Effect of Short- to Long-Term Exposure to Ambient Particulate Matter on Cognitive Function in a Cohort of Middle-Aged and Older Adults: KoGES

“…Discussions of the potential mechanisms that may explain our findings are warranted. One explanation is that metals and various compounds present in ambient PMs enter the circulatory system and trigger systemic inflammation and oxidative stress, which further exhibit harmful effects on cognitive function [ 62 , 63 ]. Ambient PM consists of various types of metals, such as aluminum, lead, arsenic, mercury, iron, copper, nickel, chromium, cadmium, manganese, and zinc, and some of these levels exceed the limits of the WHO or the respective country’s air quality standards [ 64 , 65 ].…”

Personal exposure to source-specific particulate polycyclic aromatic hydrocarbons and systemic inflammation: A cross-sectional study of urban-dwelling older adults in China

“…Several studies investigated the associations between systemic in ammation and PM constituents or sources [18][19][20][21][22]. In these studies, exposure to constituents from vehicle emission (e.g., organic carbon and elemental carbon from tailpipe emission, Cu/Zn from non-tailpipe emission) were found to enhance the levels of in ammatory cytokines.…”

FGF10 mediates protective anti-oxidative effects in particulate matter-induced lung injury through Nrf2 and NF-κB signaling

“…As a chemical mixture of solid particles and liquid droplets, PM mainly consists of exhaust particles from vehicles and those released as a result of the incomplete combustion of coal. Due to their aerodynamics characteristics in the context of a functional lung, PM deposits in the bronchial and alveolar epithelium ( 2 ). The deposition of PM in the pulmonary epithelium inevitably leads to premature epithelial senescence and secretion of pro-inflammatory cytokines, which closely relates to the oxidative stress and lays the foundation for the pathological characteristics associated with PM-induced lung injury ( 3 ).…”