Microplastics in the environment produced by decomposition of globally increasing waste plastics have become a dominant component of both water and air pollution. To examine the potential toxicological effects of microplastics on human cells, the cultured human alveolar A549 cells were exposed to polystyrene microplastics (PS-MPs) of 1 and 10 μm diameter as a model of the environmental contaminants. Both sizes caused a significant reduction in cell proliferation but exhibited little cytotoxicity, as measured by the maintenance of cell viabilities determined by trypan blue staining and by Calcein-AM staining. The cell viabilities did not drop below 93% even at concentrations of PS-MPs as high as 100 μg/mL. Despite these high viabilities, further assays revealed a population level decrease in metabolic activity parallel in time with a dramatic decrease in proliferation rate in PS-MP exposed cells. Furthermore, phase contrast imaging of live cells at 72 h revealed major changes in the morphology of cells exposed to microplastics, as well as the uptake of multiple 1 μm PS-MPs into the cells. Confocal fluorescent microscopy at 24 h of exposure confirmed the incorporation of 1 μm PS-MPs. These disturbances at the proliferative and cytoskeletal levels of human cells lead us to propose that airborne polystyrene microplastics may have toxicologic consequences. This is the first report of exposure of human cells to an environmental contaminant resulting in the dual effects of inhibition of cell proliferation and major changes in cell morphology. Our results make clear that human exposure to microplastic pollution has significant consequence and potential for harm to humans.

Microplastics have gained much attention due to their prevalence and abundance in our everyday lives. They have been detected in household items such as sugar, salt, honey, seafood, tap water, water bottles, and food items wrapped in plastic. Once ingested, these tiny particles can travel to internal organs such as the kidney and liver and cause adverse effects on the cellular level. Here, human embryonic kidney (HEK 293) cells and human hepatocellular (Hep G2) liver cells were used to examine the potential toxicological effects of 1 μm polystyrene microplastics (PS-MPs). Exposing cells to PS-MPs caused a major reduction in cellular proliferation but no significant decrease in cell viability as determined by the trypan blue assay in both cell lines. Cell viability remained at least 94% for both cell lines even at the highest concentration of 100 μg/mL of PS-MPs. Phase-contrast imaging of both kidney and liver cells exposed to PS-MPs at 72 h showed significant morphological changes and uptake of PS-MP particles. Confocal fluorescent microscopy confirmed the uptake of 1 μm PS-MPs at 72 h for both cell lines. Additionally, flow cytometry experiments verified that more than 70% of cells internalized 1 μm PS-MPs after 48 h of exposure for both kidney and liver cells. Reactive oxygen species (ROS) studies revealed kidney and liver cells exposed to PS-MPs had increased levels of ROS at each concentration and for every time point tested. Furthermore, quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis at 24 and 72 h revealed that both HEK 293 and Hep G2 cells exposed to PS-MPs lowered the gene expression levels of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase ( GAPDH ), and antioxidant enzymes superoxide dismutase 2 ( SOD2 ) and catalase ( CAT ), thus reducing the potential of SOD2 and CAT to detoxify ROS. These adverse effects of PS-MPs on human kidney and liver cells suggest that ingesting microplastics may lead to toxicological problems on cell metabolism and cell–cell interactions. Because exposing human kidney and liver cells to microplastics results in morphological, metabolic, proliferative changes and cellular stress, these results indicate the potential undesirable effects of microplastics on human health.