Characterization of Immunologic Markers in Smoky Coal Users in a Rural Region of China with High Lung Cancer Incidence

Abstract

Introduction: Lung cancer rates among never smoking women in Xuanwei, China are among the highest in the world. Studies have attributed these high risks to residential combustion of smoky (bituminous) coal. Immunologic alterations can play a key role in carcinogenesis; however, the relationship between coal use and changes in the immune system is unclear. To investigate this relationship, we characterized levels of immunologic and inflammatory markers in individuals who used various types of solid fuels, electricity, and liquid petroleum gas for home heating and cooking. Methods: A cross-sectional study was conducted in non-smoking women from Xuanwei and neighboring Fuyuan. Personal fine particulate matter (PM2.5) and benzo[a]pyrene (BaP) levels in air were measured for 24-hrs prior to blood collection. Sixty-seven plasma immunologic markers were analyzed with Luminex bead-based assays. Women who consistently used smoky coal (n=75) were compared to users of electricity or liquid petroleum gas (controls, n = 48) by Wilcoxon rank sum test. Adjusted linear regression models were used to assess the exposure-response relationships of PM2.5 and BaP to marker levels among solid fuel users. Results: Levels of multiple markers were significantly altered in smoky coal users compared to controls. For example, median (interquartile range) levels of CCL13 were 76 pg/mL (59-103) among smoky coal users compared to 107 pg/mL (86-119) among controls (False Discovery Rate= 0.0004). CCL13 levels were significantly and inversely associated with both PM2.5 and BaP among solid fuel users. Conclusions: We observed differences in multiple immunologic markers between users of smoky coal and relatively clean fuels. These markers have a diverse range of functions; for example, CCL13 induces chemotaxis in monocytes, eosinophils, T lymphocytes, and basophils. Overall, these findings may provide insights into the underlying mechanism of smoky coal and lung cancer pathogenesis in this population.