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

Author:

Xu Jia1,Zhang Nan1,Fu Yucong2,Zhang Yujuan3,Li Penghui4,Han Jinbao5,Gao Shuang6,Wang Xinhua1,Geng Chunmei1,Yang Wen1,Zhang Liwen2,Han Bin1,Bai Zhipeng1

Affiliation:

1. Chinese Research Academy of Environmental Sciences

2. Tianjin Medical University

3. The Second Hospital of Tianjin Medical University

4. Tianjin University of Technology

5. Hebei University

6. Tianjin Normal University

Abstract

Abstract Environmental exposure to atmospheric polycyclic aromatic hydrocarbons (PAHs) can disturb the immune response. However, the evidence on adverse health effects caused by exposing to PAHs emitted from various sources among different vulnerable subpopulation is limited. In this study, we aimed to evaluate whether exposure to source-specific PAHs could increase the level of systemic inflammation in older adults. The present study included 101 community-dwelling older adults and collected filter samples personal exposure to PM2.5 during the winter of 2011 in Tianjin, China. We collected blood samples after the PM2.5 sample collection, and analyzed PM2.5 bound PAHs and serum inflammatory cytokines (interleukin (IL)1β, IL6, and tumor necrosis factor alpha) levels. The Positive Matrix Factorization model was applied to distinguish PAHs sources. We used a linear regression model to assess the relative effects of source-specific PM2.5 bound PAHs on the levels of measured inflammatory cytokines. The key finding lies on that after controlling for confounders, the levels of systemic inflammation were adversely affected by exposing to most PAHs sources, especially the biomass burning or diesel vehicle emission. An interquartile range (IQR) increase in the concentration of PAHs originated from biomass burning could significantly increase the level of IL1β (16.3%, 95% confidence interval [CI]: 0.7%, 29.8%) and IL6 (13.0%, 95% CI: 0.3%, 27.3%), and an IQR increase in PAHs contributed by diesel vehicle emission was significantly associated with the increase of IL6 levels (12.7%, 95% CI: 0.1%, 26.9%). The stratified analysis revealed that non-smokers were more susceptible to the PAHs emitted from biomass burning and diesel emission. In summary, exposure to PAHs from certain specific sources of PAHs may significantly enhance systemic inflammation in the elderly. These findings highlight the importance of considering exposure sources in epidemiological studies and that of controlling exposures to organic materials from specific sources.

Publisher

Research Square Platform LLC

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