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Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells
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Scientists exposed human lung cells to tiny PET plastic particles (the type found in plastic bottles) continuously for over 20 weeks and found that these cells became worse at repairing their own DNA damage, essentially weakening the body's natural defense against cell mutations. When challenged with a DNA-damaging chemical, the plastic-exposed cells accumulated more lasting damage than normal cells, suggesting long-term nanoplastic exposure could make lung tissue more vulnerable to genetic errors over time. While this was a lab study on cells (not people), it raises real concerns about what breathing in plastic particles
Chronic inhalation exposure to nanoplastics, specifically polyethylene terephthalate (PET) nanoplastics (PET-NPLs) is an emerging health concern, yet the long-term consequences for genomic stability and DNA damage response (DDR) capacity in bronchial epithelial cells remain poorly characterized. For this study, human bronchial epithelial BEAS-2B cells were continuously exposed to PET-NPLs for over 20 weeks, after which elevated basal DNA genotoxic damage was observed, as assessed by the alkaline comet assay. In addition, a broad transcriptional suppression of the DDR, with 27 of 84 profiled genes involved in DDR showing reduced expression relative to passage-matched control was observed. The suppressed genes span ATM/ATR checkpoint signaling, homologous recombination (HR), base excision repair (BER), nucleotide excision repair (NER), and apoptotic pathways. To determine whether chronic PET-NPL exposure altered susceptibility to acute genotoxic challenge in a damage-type-specific manner, cells were treated with methyl methanesulfonate (MMS), ultraviolet-C (UV-C) radiation, or bleomycin. While MMS and UV-C induced comparable levels of DNA damage in control and PET-exposed cells, bleomycin produced significantly greater damage in PET-exposed cells, indicating selective sensitization to doble-strand breaks (DSB)-type and oxidative genotoxic insults. Transcriptional profiling during bleomycin challenge identified 18 DDR genes with relatively higher expression in PET-exposed cells compared to passage-matched controls, encompassing HR, BER, ATM/ATR signaling, the Fanconi anemia pathway, and apoptosis. Furthermore, PET-exposed cells retained significantly higher residual DNA damage after 3 h of bleomycin challenge, indicating a persistent early repair deficit. Together, these findings suggest that chronic PET-NPL exposure specifically compromises the bronchial epithelial DDR, with potential implications for long-term genomic stability in respiratory epithelia subjected to nanoplastic inhalation.
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This study tested nanoplastics made from ground-up PET food containers on human lung cells in the lab and found they caused DNA damage and increased harmful reactive oxygen species. Unlike most studies that use standard polystyrene particles, this research used real-world PET plastic from supermarket containers, making the results more relevant to actual human exposure. The findings suggest that inhaling tiny PET particles shed from everyday food packaging could pose a risk to lung health.
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This review looked at 36 lab studies testing tiny plastic particles (nanoplastics) on cells grown in dishes. It found that both polystyrene nanoplastics and plastics broken down from real PET bottles caused DNA damage, with immune cells showing more consistent effects than other cell types.
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Researchers exposed human nasal cells to nanoplastics made from real PET water bottles and found that the particles were absorbed into cells and triggered oxidative stress. The nanoplastics also disrupted mitochondrial function and activated the cell's autophagy cleanup pathway. Since the nose is the first barrier encountered when breathing in airborne plastic particles, these findings suggest that nasal tissues may be particularly vulnerable to nanoplastic exposure.
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