Parental transfer of nanopolystyrene-enhanced tris(1,3-dichloro-2-propyl) phosphate induces transgenerational thyroid disruption in zebrafish

Plastic is a globally recognized superwaste that can affect human health and wildlife when it accumulates and is amplified in the food chain. Microplastics (plastic particles < 5 mm) and nanoplastics (plastic particles < 100 nm) can interact with organic pollutants already present in the aquatic environment, potentially acting as carriers for pollutants entering organisms and thus influencing the bioavailability and toxicity of those pollutants. In this study, we investigated the transfer kinetics and transgenerational effects of exposure to tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) and polystyrene nanoplastics (PS-NPs) in F1 offspring. At 90 days postfertilization, zebrafish (Danio rerio) strain AB was exposed to either TDCIPP (0, 0.47, 2.64, or 12.78 μg/L) or PS-NPs (10 mg/L) or their combination for 120 days. The results showed that TDCIPP and PS-NPs accumulated in the gut, gill, head, and liver of the zebrafish in a sex-dependent manner. The presence of PS-NPs promoted the bioaccumulation of TDCIPP in the adult fish and increased the parental transfer of TDCIPP to their offspring. We demonstrate that parental exposure to TDCIPP alone or in combination with PS-NPs induces thyroid disruption in adults, and then leads to thyroid endocrine disruption in their larval offspring. Reduced thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels contributed to the observed transgenerational thyroid dysfunction, which inhibited developmental growth and disturbed the transcription of genes and expression of proteins involved in the hypothalamic–pituitary–thyroid (HPT) axis in the F1 larvae. The increased transfer of TDCIPP to the offspring in the presence of PS-NPs also enhanced transgenerational thyroid endocrine disruption, demonstrated by a further reduction in T4 and the upregulation of thyroglobulin (tg), uridine diphosphate-glucuronosyltransferase (ugt1ab), thyroid-stimulating hormone (tshβ), and thyroid hormone receptor (trα) expression in the F1 larvae compared with the effects of parental TDCIPP exposure alone. Overall, our results indicate that the presence of PS-NPs modifies the bioavailability of TDCIPP and aggravates transgenerational thyroid disruption in zebrafish.