Personal exposure PM samples aid in determining the sources and chemical composition of real-world exposures, particularly in settings with household air pollution. However, their use in toxicological research is limited, despite uncertainty regarding health effects in these settings and evidence of differential toxicity among PM2.5 sources and components. This study used women’s PM2.5 exposure samples collected using personal exposure monitoring in rural villages in three Chinese provinces (Beijing, Shanxi, and Sichuan) during summer and winter. Water-soluble organic carbon, ions, elements, and organic tracers (e.g. levoglucosan and polycyclic aromatic hydrocarbons [PAHs]) were quantified in water and organic PM2.5 extracts. Human lung epithelial cells (A549) were exposed to the extracts. Cell death, reactive oxygen species (ROS), and gene expression were measured. Biomass burning contributions were higher in Sichuan samples than in Beijing or Shanxi. Some PM characteristics (total PAHs and coal combustion source contributions) and biological effects of organic extract exposures (cell death, ROS, and cytokine gene expression) shared a common trend of higher levels and effects in winter than in summer for Shanxi and Beijing but no seasonal differences in Sichuan. Modulation of phase I/AhR-related genes (cyp1a1 and cyp1b1) and phase II/oxidative stress-related genes (HO-1, SOD1/2, NQO-1, and catalase) was either low or insignificant, without clear trends between samples. No significant cell death or ROS production was observed for water extract treatments among all sites and seasons, even at possible higher concentrations tested. These results support organic components, particularly PAHs, as essential drivers of biological effects, which is consistent with some other evidence from ambient PM2.5.