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

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 (PM_2.5) 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 PM_2.5 toxicity than PAHs, despite its positive associations with PM_2.5-induced toxic potency (p < 0.0001). Furthermore, PAHs contribute 71.9 ± 12.2% and 61.9 ± 32.8% of the overall toxic potency of PM_2.5 emitted from typical incomplete burning of solid and liquid fuels, respectively, while the PM_2.5 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 PM_2.5 and further benefit to establishing efficient air pollution control policies.