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Pulmonary toxicology assessment of polyethylene terephthalate nanoplastic particles in vitro
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Researchers evaluated the lung toxicity of polyethylene terephthalate nanoplastics on human lung cells and found that these particles entered cells but showed relatively low toxicity at environmental concentrations. At higher concentrations, the nanoplastics reduced cell survival and triggered significant oxidative stress. The study suggests that while routine exposure levels may pose limited immediate risk to lung cells, higher or accumulated exposures could cause oxidative damage worth monitoring.
Nanoplastics are more likely to be suspended in air and pose a risk of respiratory exposure. However, the early health effects of low-dose nanoplastics on the respiratory system, which are expected to reflect the risk of atmospheric nanoplastics, need to be further evaluated. In this study, nanoparticles of polyethylene terephthalate, a representative plastic polymer in air, were prepared by a precipitation method. The toxicity impacts of nano-PET at environmental concentrations on the human lung carcinoma cell A549 cells were evaluated. Although the nano-PET was identified to enter the cells by confocal microscope observation and alkali-assisted thermal depolymerization coupled with LC-MS/MS analysis, the nano-PET exhibited low toxicity on mitochondrial membrane potential levels and cell apoptosis. At low concentrations of 0.10 and 0.98 μg/mL, the nano-PET had a slight promotion effect on cell viability, while an inhibitory effect on cell viability presented at higher nano-PET concentrations of 98.40 and 196.79 μg/mL. The cell survival rate at 98.4 and 196.79 μg/mL of nano-PET are lower than that of the control, and significant oxidative stress in cells caused by the nano-PET exposure at 49.2 μg/mL was observed. A decrease tendency of mitochondrial membrane potential with the increasing nano-PET exposure presents, which is consistent with the change of reactive oxygen species. Furthermore, nano-PET at ≦ 98.4 μg/mL could not increase the sum of apoptotic in the cells, but the late apoptotic cells increased with the increase of the exposure dose. The major mechanism of the toxic effect of nano-PET on cells may be the increase of reactive oxygen species caused by oxidative stress, which in turn induces a decrease in the mitochondrial membrane potential. This study provides information on the toxicity of nano-PET at environmental concentrations in human lung cells, which helps to enrich the risk cognition of nanoplastics in the respiratory system.
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