Abstract

The cytotoxicity of PM2.5 (fine particulate) derived from varying fuels burning in different microenvironments remains unclear. In this study, the toxicity of PM2.5 collected from northern China in the winter on human cervical carcinoma (HeLa) cells was determined. The PM2.5 from chunk coal (CC) combustion caused greater apoptosis (22.47%) than firewood (FW) burning (5.32%), while the effects on cell viability showed contrary patterns between FW (stimulation: 132.38%) and CC (inhibition: 87.05%). Furthermore, all the samples induced significant oxidative stress and inflammatory responses in cells. Intriguingly, PM2.5 samples collected from FW burning upregulated the expression genes involved in pathways in cancer, whereas those from CC burning downregulated the levels. Accordingly, the health risks of different samples were assessed through a probabilistic model. The risk level of samples of CC burning from the living room (CC/L) was 0.752, followed by CC from the bedroom (CC/B, 0.736), and then CC from the kitchen (CC/K, 0.562), FW without a chimney (FW‐C, 0.451), and FW with a chimney (FW+C, 0.446). Meanwhile, the survival curves established by gene expression indicated that PM2.5 from FW might be positively correlated with cancer progression. This pilot investigation demonstrated that CC combustion in the living room posed the highest health risk, and improved cookstoves (with a chimney) markedly reduced the risk. This pilot study presents a novel model for assessing health risks associated with air pollution using the toxicology method and real‐time PM2.5 quantification.

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