Alzaben Mohammad, Burve Regina, Loeschner Katrin, Møller Peter, Roursgaard Martin
Department of Public Health, Section of Environmental Health, University of Copenhagen, Øster Farimagsgade 5A, DK-1014 Copenhagen K, Denmark.
Department of Energy Conversion and Storage, Technical University of Denmark, Anker Engelunds Vej 301, DK-2800, Lyngby, Denmark.
Mutat Res Genet Toxicol Environ Mutagen. 2023 Nov-Dec;892:503705. doi: 10.1016/j.mrgentox.2023.503705. Epub 2023 Oct 10.
The ubiquitous pollution of plastic particles in most environmental matrices leads to concern about any potential adverse effects on human health. Most studies on the toxicological effect of nanoplastics has focused on standard particles of polystyrene. In reality humans are exposed to a large variety of different types and sizes of plastic material via oral intake and inhalation. In this study, we investigated the effect of polyethylene terephthalate (PET) nanoplastic particles from ground food containers from a supermarket. The aim was to investigate a possible link between exposure to PET nanoplastics and genotoxic response in a cell model of the human airway epithelial (A549) cells. Further, we investigated the combined effect of PET and chemicals known to alter the cellular redox state, as a model of partially compromised antioxidant defense system. DNA damage was assessed by the alkaline comet assay. The ground PET nanoplastics have a mean hydrodynamic diameter of 136 nm in water. The results showed that PET exposure led to increased reactive oxygen species production (approximately 30 % increase compared to unexposed cells). In addition, exposure to PET nanoplastic increased the level of DNA strand breaks (net increase = 0.10 lesions/10 base pair, 95 % confidence interval: 0.01, 0.18 lesions/10 base pair). Pre- or post-exposure to hydrogen peroxide or buthionine sulfoximine did not lead to a higher level of DNA damage. Overall, the study shows that exposure to PET nanoplastics increases both intracellular reactive oxygen production and DNA damage in A549 cells.
大多数环境介质中普遍存在的塑料颗粒污染引发了人们对其对人类健康可能产生的任何潜在不利影响的担忧。大多数关于纳米塑料毒理学效应的研究都集中在聚苯乙烯标准颗粒上。实际上，人类通过口服和吸入接触到各种各样不同类型和尺寸的塑料材料。在本研究中，我们调查了来自超市磨碎食品容器中的聚对苯二甲酸乙二酯（PET）纳米塑料颗粒的影响。目的是研究在人气道上皮（A549）细胞的细胞模型中，接触PET纳米塑料与遗传毒性反应之间的可能联系。此外，作为部分受损抗氧化防御系统的模型，我们研究了PET与已知会改变细胞氧化还原状态的化学物质的联合作用。通过碱性彗星试验评估DNA损伤。磨碎的PET纳米塑料在水中的平均流体动力学直径为136纳米。结果表明，PET暴露导致活性氧生成增加（与未暴露细胞相比增加约30%）。此外，接触PET纳米塑料会增加DNA链断裂水平（净增加=0.10个损伤/10个碱基对，95%置信区间：0.01，0.18个损伤/10个碱基对）。预先或事后接触过氧化氢或丁硫氨酸亚砜胺不会导致更高水平的DNA损伤。总体而言，该研究表明，接触PET纳米塑料会增加A549细胞内的活性氧生成和DNA损伤。
