Microplastics (MPs) pollution is a global paradigm that raises concern in relation to environment and human health. In order to investigate the molecular toxicity mechanisms of MPs, transcriptomic analyses were performed on in vitro Caco‐2 cell model. After observing that polystyrene microplastics (PS‐MPs) decreased cell viability in a dose‐dependent manner, the responsible genes and involved pathways that might make contribution to PS‐MBs‐induced toxicity to Caco‐2 cells were identified with Illumina RNA seq. A total of 442 genes including, 210 up‐regulated ones and 232 down‐regulated ones, showed differential expression after treatment by PS‐MPs with a concentration of 12.5 mg L−1 or 50.0 mg L−1 for 24 hours. Gene Ontology (GO) annotation enriched unigenes can be grouped into three separated clusters: cellular component (CC), biological process (BP), and molecular function (MF). The dominate pathways related to NF‐κB, MAPK signaling, cytokine‐cytokine receptor interaction, and toll‐like receptor were strongly influenced by PS‐MBs. These pathways are involved in modulating cell inflammatory and proliferation. The qPCR were applied to investigate the transcriptional level of five proliferation related genes (Ras, ERK, MER, CDK4, Cyclin D1) and four inflammation related genes (TRPV1, iNOS, IL‐1β, IL‐8), and the results were consistent with RNA‐seq data. This study has provided new insight into the understanding of the toxicity effects of PS‐MBs‐induced intestinal inflammatory diseases.

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The cellular toxicity response of human airway epithelial cells (A549) to tetrabromobisphenol (TBBPA) was assessed in vitro. Cell viability, levels of intracellular reactive oxygen species (ROS), lipid peroxidation (MDA), and caspase-3 activity were determined after A549 treated with varying concentrations of TBBPA. A comparative proteomic analysis was performed in cells treated with different concentrations of TBBPA (0, 10, and 40 μg/mL). Two-way anova analysis showed that cell viability was significantly decreased after treatment by TBBPA with a concentration of 16 μg/mL for 48 hr, however, the caspase-3 activities, ROS generation, and MDA content increased. Ultrastructural observation revealed that the cell was morphological damaged after exposure to 64 μg/mL TBBPA, with mitochondria seriously injured and the smooth endoplasmic reticulum dilated. There was a good correlation between ROS generation and mitochondrial dysfunction. Seventeen differentially expressed proteins involved in various biological processes were identified. These findings provide a basis for understanding the mechanisms of cell dysfunction and perturbation of antioxidant status induced by additive flame retardant on airway epithelial cells.

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Brominated flame retardants (BFRs) are supposed to act as disruptors of cell signaling, but the underlying mechanisms remain less clear. Human bronchial epithelial cells (BEAS‐2B) were used to investigate the toxic effect and gene expression changes induced by tetrabromobisphenol A (TBBPA). By genome‐wide approaches with Illumina RNA‐seq, 87 genes were identified to exhibit ≥1.5‐fold changes in expression after treatment by TBBPA for 48 h, among which, 79 were upregulated and 8 were downregulated. Gene ontology (GO) annotation enriched unigenes were divided into three clusters: biological process (BP), cellular component (CC) and molecular function (MF). Pathway analysis showed that NF‐κB, TNF signaling, toll‐like receptor, MAPK signaling and B‐cell receptor were the most prominent pathways affected by TBBPA, which play key roles in regulating cell proliferation and cell differentiation, inflammatory response. Finally, for verifying the accuracy of microarray analysis, qRT‐PCR was used to analyze the transcription level of key genes in the above signaling pathways, and ELISA assay confirmed the effect of TBBPA on the levels of CXCL‐2, CCL‐3, CCL‐4, IL‐1β, TNF‐α, and IL‐6. These findings provided important information for further exploitation of the mechanisms under‐lying BFR‐induced adverse health effects.