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Genotoxicity of polystyrene and polyethylene micro- and nanoparticles in human lung (A549) and liver (HepG2) cell lines
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Lab tests on human lung and liver cells exposed to tiny polystyrene and polyethylene plastic particles found modest reductions in cell survival and some DNA damage, more so in liver cells. Effects varied by plastic type and cell type, and were not clearly linked to oxidative stress.
Micro- and nanoplastics (MNPs) are widespread environmental pollutants that have raised concerns regarding their potential impact on human health. Among the most common plastic polymers, polystyrene (PS) and polyethylene (PE) are frequently detected in the environment, though comparative information on their biological effects remains limited. This study investigated the cellular responses to PS and PE MNPs in the A549 and HepG2 cell lines, with particular emphasis on cytotoxicity, primary DNA damage, oxidative stress, oxidative DNA damage, and particle uptake. Cytotoxicity was evaluated through dual acridine orange and ethidium bromide staining, while primary and oxidative DNA damage was measured using alkaline and Fpg-modified comet assays, respectively. Particle uptake and reactive oxygen species (ROS) generation were assessed by flow cytometry. Both PS and PE particles induced modest reductions in cell viability. HepG2 cells exhibited greater susceptibility to primary DNA damage, with PS particles inducing significant damage only in HepG2 cells, whereas PE particles induced significant DNA damage in both cell lines, particularly at higher concentrations. No consistent concentration-dependent increase in ROS levels or oxidative DNA damage was observed following exposure to PS and PE particles, despite statistically significant changes in DCF fluorescence under selected exposure conditions. Both particle types altered side-scattering (SSC) signal intensity in A549 and HepG2 cells, with a more pronounced signal observed in A549 cells. MNP-induced genotoxic responses varied according to polymer type and cellular model and were not consistently associated with ROS-mediated oxidative DNA damage.
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