Absence of a Causal Link between Elemental Carbon Exposure and Short-Term Respiratory Toxicity in Human-Derived Organoids and Cellular Models

Black carbon or elemental carbon (EC) in the atmosphere plays an ambiguous role in acute respiratory toxic effects. Here, we evaluate the contribution of EC to the short-term toxicity (including cytotoxicity and oxidative stress potency) of fine particulate matter (PM2.5) on the human respiratory tract using in vitro airway organoids and cell lines. The toxic potency of EC per unit mass, including char and soot, is more than 2 orders of magnitude lower than that of polycyclic aromatic hydrocarbons (PAHs), which are coemitted from incomplete combustion. EC contributes approximately 1 order of magnitude less to PM2.5 toxicity than PAHs, despite its positive associations with PM2.5-induced toxic potency (p < 0.0001). Furthermore, PAHs contribute 71.9 ± 12.2% and 61.9 ± 32.8% of the overall toxic potency of PM2.5 emitted from typical incomplete burning of solid and liquid fuels, respectively, while the PM2.5 toxicity significantly correlates with PAHs content (r = 0.94, p = 0.002). Hence, EC is not a cause of inducing acute toxicity, likely attributed to coemitted PAHs. These findings provide causal evidence for understanding the respiratory health risks associated with exposure to PM2.5 and further benefit to establishing efficient air pollution control policies.