Black carbon (BC) is a key component of atmospheric fine particulate matter (PM_2.5) and it tends to adsorb various pollutants (e.g., heavy metals and organics) during atmospheric transport. This adsorption leads to the complexity and uncertainty of the source and chemical composition of PM_2.5, making the toxicologic effects and health risks induced by PM2.5 difficult to determine. Here, we used carboxylated black carbon (c-BC) and c-BC-lead complexes (c-BC-Pb) to investigate the in vitro and in vivo toxic effects and inflammatory responses. The physicochemical properties of c-BC and c-BC-Pb complexes were characterized by the transmission electron microscope (TEM), X-ray photoelectron spectroscopy (XPS), dynamic light scattering (DLS), and in ductively coupled plasma–atomic emission spectra (ICP−AES). Cytotoxicity in vitro showed that the exposure of human bronchial epithelial cells (BEAS-2B) to low-dose c-BC-Pb particles significantly induced greater toxicity than that of c-BC, suggesting that lead (Pb) might play an important role in induced cytotoxicity after combined exposure to c-BC-Pb particles. The findings were further confirmed by the results in vivo, which indicated that c-BC-Pb particles significantly induced inflammation and lung injury. Based on the results of this experiment, the differences in toxicity can be attributed to the synergistic effect of Pb on the BC particles, which play a synergistic role in vitro and in vivo in the development of toxicity. The c-BC-Pb particles model used in this study may be helpful for the evaluation of cytotoxicity induced by different sources of BC particles or BC-heavy metal complexes and provide a new approach for understanding PM_2.5-induced toxicity and health risks.

黑炭（BC）是大气细颗粒物（PM _2.5）的关键成分，在大气运输过程中往往会吸附各种污染物（例如重金属和有机物）。这种吸附导致PM _2.5来源和化学成分的复杂性和不确定性，使得难以确定PM2.5引起的毒理作用和健康风险。在这里，我们使用了羧化黑碳（c-BC）和c-BC-铅络合物（c-BC-Pb）来研究体外和体内毒性作用和炎症反应。通过透射电子显微镜（TEM），X射线光电子能谱（XPS），动态光散射（DLS）和电感耦合等离子体-原子发射光谱表征了c-BC和c-BC-Pb配合物的理化性质。 （ICP-AES）。体外细胞毒性表明，人支气管上皮细胞（BEAS-2B）暴露于低剂量c-BC-Pb颗粒比c-BC具有更大的毒性，表明铅（Pb）可能在其中起重要作用。联合暴露于c-BC-Pb颗粒后可诱导细胞毒性。体内结果进一步证实了这一发现，这表明c-BC-Pb颗粒显着诱导了炎症和肺损伤。根据本实验的结果，毒性的差异可归因于Pb对BC颗粒的协同作用，在体内和体外的毒性发展中起着协同作用。本研究中使用的c-BC-Pb颗粒模型可能有助于评估不同来源的BC颗粒或BC重金属络合物诱导的细胞毒性，并为理解PM _2.5诱导的毒性和健康风险提供一种新方法。