Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells

Area of Science:

• Environmental Health
• Toxicology
• Genetics

Background:

• Nanoplastics (NPs) are emerging environmental contaminants.
• Chronic inhalation of polyethylene terephthalate nanoplastics (PET-NPLs) is a growing health concern.
• Long-term effects of PET-NPLs on genomic stability and DNA damage response (DDR) in bronchial epithelial cells are largely unknown.

Purpose of the Study:

• To investigate the long-term effects of chronic PET-NPL inhalation exposure on human bronchial epithelial cells.
• To assess the impact of PET-NPLs on basal DNA damage and the DDR capacity.
• To determine if chronic PET-NPL exposure alters cellular susceptibility to specific genotoxic agents.

Main Methods:

• Human bronchial epithelial BEAS-2B cells were continuously exposed to PET-NPLs for over 20 weeks.
• Alkaline comet assay was used to assess DNA genotoxic damage.
• Transcriptional profiling of 84 DDR genes was performed.
• Cells were challenged with methyl methanesulfonate (MMS), UV-C radiation, or bleomycin to assess genotoxic insult response.

Main Results:

• Chronic PET-NPL exposure led to elevated basal DNA damage and suppressed expression of key DDR genes (27/84 genes).
• PET-NPL-exposed cells showed selective sensitization to bleomycin (inducing double-strand breaks and oxidative damage), but not MMS or UV-C.
• PET-NPL-exposed cells exhibited a persistent early repair deficit, retaining higher residual DNA damage after bleomycin challenge.

Conclusions:

• Chronic PET-NPL inhalation compromises the bronchial epithelial DNA damage response.
• This impairment may lead to increased susceptibility to specific genotoxic agents and affect long-term genomic stability in the respiratory tract.