The quest for the smoking gun

Around one-third of the global population relies on solid fuels like coal, wood, and plant residue for cooking and heating, the household air pollution (HAP) resulted from which has contributed to 3.2 million premature deaths globally in 2020. The neighboring counties of Xuanwei and Fuyuan in Yunnan Province, China, have among the highest lung cancer mortality rates, linked to the use of smoky (bituminous) coal, the users of which experienced 100-fold risk of lung cancer compared to those using smokeless (anthracite) coal. Lung cancer risk varied by geologic sources of smoky coal, which may be resulted from coal composition and associated exposures. Stove improvements have been shown to reduce lung cancer risk by up to 50% through decreased HAP exposure. However, most research focused on 24 h weighted exposures, which may not capture high-exposure scenarios like cooking. Additionally, while pollutants including PM2.5 and Benzo[a]pyrene are studied, toxic pollutants like methylated and oxygenated PAHs remain underexplored. For instance, recent findings suggested that 5-methylchrysene might be particularly relevant for lung cancer risk. In addition, the biological mechanisms linking coal emissions to lung cancer remain unclear, with limited evidence pointing to inflammatory and metabolic responses. This research aims to: 1. Examine exposures during stove use. 2. Expand the PAH exposure profile to include substituted PAHs. 3. Characterize changes in the human plasma metabolome from smoky coal emissions. 4. Assess the immunotoxicity of HAP from smoky and smokeless coal. Through a series of water boiling tests, we reveal that smoky coal produces significantly higher particle concentrations across all size ranges than smokeless coal. Nearly all emitted particle mass falls within the PM2.5 fraction (98%), with 75% in PM1 and 46% in PM0.3. Stove ventilation significantly reduced particle concentrations (13.5 vs. 1.3 mg/m3) and nearly doubles the coal-burning rate, highlighting its effectiveness in mitigating pollution exposure. PAH measurements from stove use indicate significantly higher levels of carcinogens in smoky coal emissions. Concentrations of 5-methylchrysene, Benzo[a]pyrene, and other PAHs were markedly higher in smoky coal samples than in smokeless coal samples. Models show exposure variations depending on the coal source, with fuel type playing a larger role in PAH concentrations than stove type. In addition, PAH concentrations during cooking activities were up to 100 times higher than 24-hour weighted exposures, indicating that cooking significantly contributes to PAH exposure. Through high-resolution metabolomics of plasma samples from Xuanwei and Fuyuan, we identified metabolites and metabolic pathways associated with HAP exposure, many of which mirrored those found in studies of ambient air pollution, suggesting shared biological effects. Immunotoxicity assessments using lung cell models showed epithelial barrier damage and transient inflammatory responses but little difference between smoky and smokeless coal samples, indicating that other mechanisms contribute to the lung cancer risk disparity. Overall, smoky coal use results in higher air pollutant concentrations, highlighting the need for clean fuel transitions and improved stoves to mitigate health risks. Global efforts must continue to promote access to cleaner cooking technologies to protect public health and the environment.