The critical role of chemical and biological composition and sources in PM2.5 toxicity in Chinese megacities

Abstract

Fine particulate matter (PM2.5) has become a significant public health concern in China, where rapid urbanization and industrialization have led to severe air pollution. While previous studies have primarily focused on PM2.5 mass concentration and chemical composition, limited attention has been given to the specific chemical and biological components responsible for its toxicity, as well as the emission sources contributing to the toxicity. This study addresses these gaps by conducting an integrated assessment of PM2.5 in two Chinese megacities, Nanjing and Guangzhou, across six sites representing different land-use types. Through comprehensive chemical and biological characterization, in vitro toxicological assays, and source apportionment, this study quantifies the component- and source-specific contributions to PM2.5-induced toxicity. First, it investigates PM2.5 concentration, chemical composition, and metal-induced and PAH-induced health risks in six sampling sites in Nanjing and Guangzhou from June 2019 to May 2020, along with long-term trends from 2013 to 2020. During 2019–2020, PM2.5 levels mostly exceeded the World Health Organization (WHO) 24 h guideline (25 μg m⁻³), especially in autumn and winter. Urban and suburban-industrial sites in Nanjing exhibited higher PM2.5 concentrations than the rural site, while spatial differences of three sites in Guangzhou were less distinct. Chemical composition varied regionally: PM2.5 in Nanjing was dominated by water-soluble ions (WSI), while Guangzhou showed higher levels of carbonaceous matter. Despite the low mass concentration, trace metals posed considerable carcinogenic risk (CR), with Cr being the dominant contributor while Mn accounting for most non-carcinogenic risk (NCR). PAHs concentration was significantly higher in Nanjing, particularly at the suburban-industrial site, and was primarily from pyrogenic sources. Over the 7-year period from 2013 to 2020, both cities experienced significant reductions in PM2.5 and metal-induced health risks, reflecting the effectiveness of air pollution control policies, though risks from certain metals persisted. Second, the investigation shifts focus to biological components, specifically endotoxins and bacterial communities. PM2.5-bound endotoxins concentration in Guangzhou was nearly double those in Nanjing and varied significantly within Guangzhou, with urban sites exhibiting the highest levels. As an important toxic biological component, endotoxins were more abundant on cleaner days, indicating that PM2.5 mass does not adequately represent toxicity. Bacterial load was similar between cities, but the diversity was higher in Guangzhou. Gram-negative bacteria dominated compared to Gram-positive bacteria, and were positively associated with endotoxins levels, indicating their involvement in PM2.5-induced toxicity. In addition, there are associations between chemical and biological components in PM2.5. The concentrations of endotoxins were positively correlated with Al, Mg²⁺, and Ca²⁺, likely due to shared sources such as dust. Most Gram-negative bacteria also showed positive correlations with WSI, which may provide nutrients for bacteria and enhance their attachment. Following these findings, this study further evaluates the toxicological effects of PM2.5 using in vitro assays with BEAS-2B cells, focusing on intracellular oxidative stress as a toxicity endpoint. Endotoxins, trace metals, and PAHs together accounted for 35.9 - 56.9% of PM2.5-induced oxidative stress, despite contributing a small share (1.01-2.23%) to total PM2.5 mass. Metals (31.6-46.7%), particularly Fe and Mn, were the largest contributors, followed by endotoxins (4.24-12.2%) and PAHs (0.0218-0.135%). The toxic contribution of these components far exceeded their mass contributions, emphasizing the need for component-specific toxicity assessments. Source apportionment revealed that mass and toxicity were driven by different sources. In Nanjing, secondary aerosols and combustion dominated PM2.5 mass, but fugitive dust and combustion contributed more to toxicity. In Guangzhou, vehicle emissions were the dominant source of PM2.5 mass in the urban site, and combustion dominated in the semirural-industrial and suburban sites. In contrast, the major contributors to PM2.5-induced toxicity in Guangzhou were vehicle emissions, industrial emissions, combustion, and biological emissions. Notably, biological emissions contributed significantly to both PM2.5 mass and PM2.5-induced toxicity across six sites. In conclusion, this study provides an integrated assessment of PM2.5 chemical and biological composition, toxicity, and sources in two megacities in China. The findings highlight that PM2.5-induced toxicity were primarily driven by specific toxic components, particularly trace metals, endotoxins, and PAHs, rather than total mass. Moreover, emission sources contributing most to mass are not always those driving toxicity, highlighting the need for more targeted control strategies. Importantly, biological components such as endotoxins were shown to have a significant and previously underestimated role in PM2.5-induced toxicity. The integration of chemical, biological, and toxicological evidence presented in this study offers new insights for air quality regulation and public health protection.