The potential health implications of environmental micro/nanoplastics (MNPLs) are increasingly concerning. Beyond environmental exposure, other sources such as food packaging, including herbal/teabags, may also be significant. This study investigates the release of MNPLs from three commercially available teabags. By simulating tea preparation, MNPL samples were extracted and characterized using a range of analytical techniques: scanning electron microscopy (SEM), transmission electron microscopy (TEM), attenuated total reflectance/Fourier transform infrared spectroscopy (ATR-FTIR), dynamic light scattering (DLS), laser Doppler velocimetry (LDV), and nanoparticle tracking analysis (NTA). The results confirmed that the teabags were made of nylon-6 (NY6), polypropylene (PP), and cellulose (CL) and that microfibers and nano-range particles (NPLs) were present in the leachates. NTA data revealed that the number of released NPLs was 1.20 × 10⁹/mL (PP; 136.7 nm), 1.35 × 10⁸/mL (CL; 244 nm), and 8.18 × 10⁶/mL (NY6; 138.4). The leachate particles were then stained with iDye Poly-Pink and used to expose three human intestine-derived cell types (Caco-2, HT29, and HT29-MTX) to assess their biointeractions and the role of the mucosubstances in vitro. The results demonstrated that after 24 h of exposure to 100 μg/mL NPLs, there was significant uptake of PP-NPLs in HT29-MTX cells, as a model of cells segregating high amount of mucus. A similar uptake was observed for CL-NPLs in HT29 and HT29-MTX cells, while NY6-NPLs were internalized preferentially in Caco-2 cells. These findings underscore the importance of identifying new environmentally relevant MNPL exposure sources, for developing realistic MNPLs samples, and further investigating their potential human health effects.

This study examines the long-term impact of polyethylene terephthalate nanoplastics (PET-NPLs) and cigarette smoke condensate (CSC) on human lung BEAS-2B cells, focusing on key biological hallmarks of carcinogenesis. True-to-life PET-NPLs were generated from plastic water bottles and characterized to simulate environmental exposure conditions; and a comprehensive battery of assays was employed to assess genotoxicity, cellular transformation, and invasiveness. It was observed that, compared to passage control and individual exposures, co-exposure to PET-NPLs and CSC exacerbates oxidative stress, genotoxicity, and tumorigenic transformation, as evidenced by increased DNA damage, colony formation in soft agar, and enhanced cell migration and invasion. Transcriptomic analysis revealed a shift in cellular stress regulation including the upregulation of stress-response genes, including SLC7A11, NQO1, and HSPA1A, which are linked to oxidative stress adaptation and tumor survival. At the same time, key tumor-suppressor genes, such as LOX, and FN1, were significantly downregulated, promoting cellular transformation and invasiveness. These results provide compelling evidence that the combination of PET-NPLs and CSC enhances carcinogenic traits through oxidative stress, genomic instability, and disruption of tumor-suppressive pathways. This study underscores the importance of evaluating the synergistic effects of combined environmental exposures and their implications for human health.

Reproductive toxicity is of special concern among the harmful effects induced by environmental pollutants; consequently, further studies on such a topic are required. To avoid the use of mammalians, lower eukaryotes like Drosophila are viable alternatives. This study addresses the gap in understanding the link between reproductive adverse outcomes and the presence of pollutants in reproductive organs by using Drosophila. Silver nanoparticles (AgNPs) were selected for their ease of internalization, detection, and widespread environmental presence. Both male and female flies were exposed to AgNPs (28 ± 4 nm, 100 and 400 µg/mL) for one week. Internalization and bioaccumulation of AgNPs in organs were assessed using transmission electron microscopy, confocal microscopy, and inductively coupled plasma mass spectrometry. Substantial accumulation of AgNPs in the gastrointestinal tract, Malpighian tubules, hemolymph, reproductive organs (ovaries and testes), and gametes were observed. The highest AgNP content was observed in testes. Exposure to AgNPs reduced ovary size and fecundity, though fertility and gender ratios of the offspring were unaffected. Significant deregulation of reproductive-related genes was observed, particularly in males. These findings underscore the utility of Drosophila as a model for evaluating reproductive hazards posed by AgNP exposure. The ease of AgNP internalization in Drosophila reproductive targets could be extrapolated to mammalians, raising concerns about the potential impacts of nanoparticle exposure on reproduction toxicity in humans.

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.