Source differences in the components and cytotoxicity of PM2.5 from automobile exhaust, coal combustion, and biomass burning contributing to urban aerosol toxicity
Authors: Luo Xiao-San , Huang Weijie , Shen Guofeng , Pang Yuting , Tang Mingwei , Li Weijun , Zhao Zhen , Li Hanhan , Wei Yaqian , Xie Longjiao , Mehmood Tariq 
Published: January 2024

Abstract. Although air quality guidelines generally use the atmospheric concentration of fine particulate matter (PM2.5) as a metric for air pollution evaluation and management, the fact cannot be ignored that different particle toxicities are unequal and significantly related to their sources and chemical compositions. Therefore, judging the most harmful source and identifying the toxic component would be helpful for optimizing air quality standards and prioritizing targeted PM2.5 control strategies to protect public health more effectively. Since the combustions of fuels, including oil, coal, and biomass, are the main anthropogenic sources of environmental PM2.5, their discrepant contributions to health risks of mixed ambient aerosol pollution dominated by the respective emission intensity and unequal toxicity of chemical components need to be identified. In order to quantify the differences between these combustion primary emissions, 10 types of PM2.5 from each typical source group, i.e., vehicle exhaust, coal combustion, and plant biomass (domestic biofuel) burning, were collected for comparative study with toxicological mechanisms. In total, 30 types of individual combustion samples were intercompared with representative urban ambient air PM2.5 samples, whose chemical characteristics and biological effects were investigated by component analysis (carbon, metals, soluble ions) and in vitro toxicity assays (cell viability, oxidative stress, inflammatory response) of human lung adenocarcinoma epithelial cells (A549). Carbonaceous fractions were plenteous in automobile exhaust and biomass burning, while heavy metals were more plentiful in PM2.5 from coal combustion and automobile exhaust. The overall ranking of mass-normalized cytotoxicity for source-specific PM2.5 was automobile exhaust > coal combustion > domestic plant biomass burning > ambient urban air, possibly with differential toxicity triggers, and showed that the carbonaceous fractions (organic carbon, OC; elemental carbon, EC) and redox-active transition metals (V, Ni, Cr) assisted by water-soluble ions (Ca2+, Mg2+, F−, Cl−) might play important roles in inducing cellular reactive organic species (ROS) production, causing oxidative stress and inflammation, resulting in cell injury and apoptosis, and thus damaging human health. Coupled with the source apportionment results of typical urban ambient air PM2.5 in eastern China, reducing toxic PM2.5 from these anthropogenic combustions will be greatly beneficial to public health. In addition to the air pollution control measures that have been implemented, like strengthening the vehicle emission standards, switching energy from coal to gas and electricity, and controlling the open incineration of agricultural straws, further methods could be considered, especially by preferentially reducing the diesel exhaust, lessening the coal combustion by replacement with low-ash clean coals, and depressing the rural crop straw biomass burning emissions.