<p>Exposure to fine particulate matter (PM<sub>2.5</sub>) is a leading global health risk factor. Effective mitigation demands a multidimensional understanding that integrates chemical, source and region-level differences in PM<sub>2.5</sub> toxicities relevant to human health. We present a standardized <i>in vitro</i> cellular assay dataset characterizing PM<sub>2.5</sub> toxic potencies across emission sources, chemical constituents and atmospheric environments. Real-world PM<sub>2.5</sub> samples from 23 major anthropogenic sources, covering industrial, transportation and residential sectors, were evaluated for cytotoxicity and oxidative stress potency, identifying key sources driving PM<sub>2.5</sub>-induced health risks. Toxic potency-adjusted concentrations of bioactive PM<sub>2.5</sub> components, including polycyclic aromatic hydrocarbons, elemental carbon, metals, and non-metal species, were quantified to attribute overall PM<sub>2.5</sub> toxicity to specific chemicals. Furthermore, the toxic potencies of ambient PM<sub>2.5</sub> collected from selected urban and rural areas in China were identified, enabling the development of evaluation metrics for quantifying regional inequalities in PM<sub>2.5</sub> health risks. This dataset establishes a universal toxicity benchmark for standardized comparisons of PM<sub>2.5</sub> health impacts, providing a valuable resource for exposure assessment, source prioritization, and air quality risk evaluation.</p>

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A Unified Cellular Toxic Potency Dataset of PM2.5 across Chemicals, Emission Sources, and Regions in China

  • Xiu Chen,
  • Di Wu,
  • Qing Li

摘要

Exposure to fine particulate matter (PM2.5) is a leading global health risk factor. Effective mitigation demands a multidimensional understanding that integrates chemical, source and region-level differences in PM2.5 toxicities relevant to human health. We present a standardized in vitro cellular assay dataset characterizing PM2.5 toxic potencies across emission sources, chemical constituents and atmospheric environments. Real-world PM2.5 samples from 23 major anthropogenic sources, covering industrial, transportation and residential sectors, were evaluated for cytotoxicity and oxidative stress potency, identifying key sources driving PM2.5-induced health risks. Toxic potency-adjusted concentrations of bioactive PM2.5 components, including polycyclic aromatic hydrocarbons, elemental carbon, metals, and non-metal species, were quantified to attribute overall PM2.5 toxicity to specific chemicals. Furthermore, the toxic potencies of ambient PM2.5 collected from selected urban and rural areas in China were identified, enabling the development of evaluation metrics for quantifying regional inequalities in PM2.5 health risks. This dataset establishes a universal toxicity benchmark for standardized comparisons of PM2.5 health impacts, providing a valuable resource for exposure assessment, source prioritization, and air quality risk evaluation.