Household air pollution and epigenetic aging in Xuanwei, China

Abstract

Background: Household air pollution (HAP) from indoor combustion of solid fuel is a global health burden linked to lung cancer. In Xuanwei, China, lung cancer rate for nonsmoking women is among the highest in the world and largely attributed to high levels of polycyclic aromatic hydrocarbons (PAHs) that are produced from combustion of smoky (bituminous) coal used for cooking and heating. Epigenetic age acceleration (EAA), a DNA methylation-based biomarker of aging, has been shown to be highly correlated with biological processes underlying the susceptibility of age-related diseases. We aim to assess the association between HAP exposure and EAA.

Methods: We analyzed data from 106 never-smoking women from Xuanwei, China. Information on fuel type was collected using a questionnaire, and validated exposure models were used to predict levels of 43 HAP constituents. Exposure clusters were identified using hierarchical clustering. EAA was derived for five epigenetic clocks defined as the residuals resulting from regressing each clock on chronological age. We used generalized estimating equations to test associations between exposure clusters derived from predicted levels of HAP exposure, ambient 5-methylchrysene (5-MC), a PAH previously found to be associated with risk of lung cancer, and EAA, while accounting for repeated-measurements and confounders.

Results: We observed an increase in GrimAge EAA for clusters with 31 and 33 PAHs reflecting current (β = 0.77 y per standard deviation (SD) increase, 95 % CI:0.36,1.19) and childhood (β = 0.92 y per SD, 95 % CI:0.40,1.45) exposure, respectively. 5-MC (ng/m³-year) was found to be associated with GrimAge EAA for current (β = 0.15 y, 95 % CI:0.05,0.25) and childhood (β = 0.30 y, 95 % CI:0.13,0.47) exposure.

Conclusions: Our findings suggest that exposure to PAHs from indoor smoky coal combustion, particularly 5-MC, is associated with GrimAge EAA, a biomarker of mortality.

Keywords: 5-methylchrysene; Epigenetic age acceleration; Household air pollution; Lung cancer; Polycyclic aromatic hydrocarbons.

Figure 1.

Associations between clusters for current (A), childhood (B) and cumulative (C) exposures derived from imputed individual air pollutants and epigenetic accelerated aging. Estimates represent change in years of epigenetic accelerated aging due to increase in 1 standard deviation for each cluster and were derived using generalized estimating equations adjusting for age, county, body mass index, education, and socioeconomic status. Estimate values are available in Supplementary Table 2.

Figure 2.

Associations between current (A), childhood (B) and cumulative (C) exposure to 5-methylchrysene and epigenetic accelerated aging. Estimates represent change in years of epigenetic accelerated aging and were derived using generalized estimating equations adjusting for age, county, body mass index, education, and socioeconomic status. Estimate values are available in Supplementary Table 2.