Absence of a Causal\nLink between Elemental Carbon\nExposure and Short-Term Respiratory Toxicity in Human-Derived Organoids\nand Cellular Models

Black carbon or elemental carbon (EC) in the atmosphere\nplays an\nambiguous role in acute respiratory toxic effects. Here, we evaluate\nthe contribution of EC to the short-term toxicity (including cytotoxicity\nand oxidative stress potency) of fine particulate matter (PM<sub>2.5</sub>) on the human respiratory tract using in vitro airway organoids\nand cell lines. The toxic potency of EC per unit mass, including char\nand soot, is more than 2 orders of magnitude lower than that of polycyclic\naromatic hydrocarbons (PAHs), which are coemitted from incomplete\ncombustion. EC contributes approximately 1 order of magnitude less\nto PM<sub>2.5</sub> toxicity than PAHs, despite its positive associations\nwith PM<sub>2.5</sub>-induced toxic potency (<i>p</i> <\n0.0001). Furthermore, PAHs contribute 71.9 ± 12.2% and 61.9 ±\n32.8% of the overall toxic potency of PM<sub>2.5</sub> emitted from\ntypical incomplete burning of solid and liquid fuels, respectively,\nwhile the PM<sub>2.5</sub> toxicity significantly correlates with\nPAHs content (<i>r</i> = 0.94, <i>p</i> = 0.002).\nHence, EC is not a cause of inducing acute toxicity, likely attributed\nto coemitted PAHs. These findings provide causal evidence for understanding\nthe respiratory health risks associated with exposure to PM<sub>2.5</sub> and further benefit to establishing efficient air pollution control\npolicies.