Airborne emissions from combustion of graphene nanoplatelet/epoxy composites and their cytotoxicity on lung cells via air-liquid interface cell exposure in vitro

Graphene nanoplatelet (GNP) as a nanofiller improves the mechanical strength, electrical conductivity, and flame retardancy of the polymers significantly. With an increasing number of GNP-reinforced products, a careful safety assessment is needed to avoid social and economic setbacks. However, no study has addressed the effects of combustion-generated emissions from GNP-reinforced products in the lung, the most sensitive exposure route to airborne particles. Therefore, we studied the influence of GNP as a nanofiller on the emitted particles and polycyclic aromatic hydrocarbons (PAHs), and cytotoxicity of the emissions from the combustion of pure epoxy (EP) and GNP-reinforced epoxy (EP-GNP). GNP was not detected in the airborne emissions. PAHs were found in airborne particles of both emissions from EP and EP-GNP, with some differences in their concentrations. A first hazard assessment was performed on human alveolar epithelial cells exposed to the airborne emissions at airliquid interface conditions. At 24 h and 96 h after the exposure, similar responses were observed between EP and EP-GNP except an acute transient decrease in mitochondrial activity after exposure to the emissions from EPGNP. Both emissions from EP and EP-GNP had no acute effects on membrane integrity, cell morphology or expression of anti-oxidative stress markers (HMOX1 and SOD2 genes). Meanwhile, both emissions induced the activation of the aryl hydrocarbon receptor (CYP1A1 gene) and a transient (pro-) inflammatory response (MCP1), but the effects between EP and EP-GNP were not significantly different.

Automated summary

This study investigated the emissions of particles and polycyclic aromatic hydrocarbons (PAHs) from the combustion of graphene nanoplatelet (GNP)-reinforced products, as well as the cytotoxicity of these emissions on lung cells. GNP was not detected in the emissions, but PAHs were found in both emissions from pure epoxy (EP) and GNP-reinforced epoxy (EP-GNP). The exposed cells showed no acute effects but exhibited activation of the aryl hydrocarbon receptor and a transient (pro-) inflammatory response.