Household coal combustion, indoor air pollutants, and circulating immunologic/inflammatory markers in rural China

ABSTRACT

The study aim was to investigate whether household bituminous (“smoky”) coal use and personal exposure to combustion emissions were associated with immunologic/inflammatory marker levels. A cross-sectional study of healthy never-smoking women from rural Xuanwei and Fuyuan, China was conducted, which included 80 smoky coal and 14 anthracite (“smokeless”) coal users. Personal exposure to fine particulate matter (PM_2.5) and benzo[a]pyrene (BaP) was assessed using portable devices, while 67 circulating plasma immunologic/inflammatory markers were measured using multiplex bead-based assays. Multivariable linear regression models were employed to estimate associations between smoky coal versus smokeless coal use, indoor air pollutants, and immunologic/inflammatory markers. Six markers were altered among smoky coal users compared to smokeless coal, including significantly decreased interferon-inducible T-cell alpha chemoattractant (CXCL11/I-TAC), and increased serum amyloid P component (SAP). CXCL11/I-TAC was previously found to be reduced in workers exposed to high levels of diesel engine exhaust, which exhibits similar constituents as coal combustion emissions. Further, there was evidence that elevated PM_2.5 and BaP exposure was associated with significantly diminished levels of the serum amyloid A (SAA); however, the false discovery rates (FDRs) were >0.2 after accounting for multiple comparisons. Inflammatory processes may thus mediate the carcinogenic effects attributed to smoky coal emissions.

KEYWORDS:

• Smoky coal
• combustion
• indoor air pollution
• immunologic inflammatory markers

Acknowledgments

We extend our deepest appreciation to Chin-San Liu, Wen-Ling Cheng, and the late Robert S. Chapman for their support. This study was supported by intramural funding from the National Cancer Institute.

Declaration of Interest Statement

We declare no conflicts of interest.

Supplementry Material

Supplemental data for this article can be accessed on the publisher’s website.

Statement of Author Contributions

Jason Y.Y. Wong conducted statistical analysis and composed the manuscript. Bryan A. Bassig, Wei Hu, Wei Jie Seow, and Bu-Tian Ji conducted analysis and edited the manuscript. Meredith S. Shiels and Allan Hildesheim provided extensive consultation on immunologic/inflammatory markers and edited the manuscript. Wei Hu managed the study data. George S. Downward and Roel Vermeulen conducted the air pollution exposure assessment and edited the manuscript. Yunchao Huang, Kaiyun Yang, Jihua Li, Jun He, and Ying Chen provided medical/clinical expertise on lung cancer, recruited study participants, and edited the manuscript. Qing Lan and Nathaniel Rothman designed and supervised all aspects of the study.

Additional information

Funding

This work was supported by the National Cancer Institute [Intramural]