Ingested plastic transfers hazardous chemicals to fish and induces hepatic stress

Abstract

Plastic debris litters aquatic habitats globally, the majority of which is microscopic (< 1 mm), and is ingested by a large range of species. Risks associated with such small fragments come from the material itself and from chemical pollutants that sorb to it from surrounding water. Hazards associated with the complex mixture of plastic and accumulated pollutants are largely unknown. Here, we show that fish, exposed to a mixture of polyethylene with chemical pollutants sorbed from the marine environment, bioaccumulate these chemical pollutants and suffer liver toxicity and pathology. Fish fed virgin polyethylene fragments also show signs of stress, although less severe than fish fed marine polyethylene fragments. We provide baseline information regarding the bioaccumulation of chemicals and associated health effects from plastic ingestion in fish and demonstrate that future assessments should consider the complex mixture of the plastic material and their associated chemical pollutants.

Figure 1. Schematic diagram of experimental design.

The diagram shows how we chose which contaminants to look for based upon our hypothesis.

Figure 2. Body burden of Oryzias latipes after the 1- and 2-month exposure.

Bar graphs show mean concentrations (ng/g lipid + s.e.m) of total PAHs (left), PCBs (middle) and PBDEs (right) in fish tissue (n = 3) after one (top) and two (bottom) months of exposure. White bars represent the negative control (NC), bars with diagonal lines represent the virgin-plastic (VP) and black bars represent the marine-plastic (MP) treatment. A 2-factor ANOVA showed no significant differences between treatments for total PAHs, PCBs or PBDEs after 1 month and for total PAHs and PCBs after 2 months, but showed a significant difference (P = 0.0003) between treatments for total PBDEs after 2 months. A post-hoc SNK distinguished the marine-plastic having greater concentrations than the virgin-plastic and control treatment.

Figure 3. Hepatic CYP1A expression in medaka.

The CYP1A value (y-axis) is given as the mean 2^−ΔCt value + s.e.m. (individual data points normalized to the internal control48) for the 1-month (left) and 2-month (right) exposure for males (M) and females (F) separately (n = 3). For all graphs the negative control (NC) treatment is depicted by white, the virgin-plastic (VP) treatment by diagonal and the marine-plastic (MP) treatment by black bars. For CYP1A expression, 1-factor ANOVAs showed no significant difference (P > 0.05) between treatments for either sex after both time periods.

Figure 4. Liver Histopathology in medaka sampled after 2 months.

Micrographs show livers that are glycogen-rich from the control treatment (a) and glycogen-depleted from the virgin-plastic (b) and the marine-plastic treatment (c). An eosinophilic focus of cellular alteration, a precursor to a tumor, was observed in one fish from the virgin-plastic treatment (b). The circle highlights eosinophilic (pinkish coloration) hepatocytes, approximately twice as large as the basophilic (blue coloration) glycogen-depleted hepatocytes. The progression of neoplastic hepatocytes is evidence by the presence of a tumor, a hepatocellular adenoma, in one fish from the marine-plastic treatment (encircled in panel c).