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Evaluating the Effects of a Plastics Additive on Avian Physiology

Medicine International 2025
Phoebe Aurora Johnson

Summary

Captive mallards exposed to UV-328, a plastic additive and persistent organic pollutant, showed hepatic lipidosis and elevated liver damage markers at environmentally relevant doses that persisted through a 16-day recovery period. The study provides early in vivo evidence that UV-328 is hepatotoxic to birds, filling key knowledge gaps on plastic additive risks to wildlife health.

Study Type In vitro

Plastic pollution is a growing and global concern, with ingestion by wildlife documented in numerous species. Wild birds have some of the highest ingestion rates of plastics among wildlife and are of special interest due to this high ingestion rate. However, when ingesting plastics, they are also being exposed to numerous chemicals that can be associated with plastics, including potentially harmful additives such as UV-328 (2-(2H-Benzotriazol-2-yl)-4,6-di-tert-pentylphenol). UV-328 is added to plastics and various consumer products to help prevent solar degradation and discolouration and enters the environment on plastic debris and in wastewater treatment plant discharges. In the spring of 2023, UV-328 was declared a persistent organic pollutant of emerging concern by international regulatory processes, due to its persistent, bioaccumulative, and toxic properties. UV-328 has been detected in blood and liver samples of numerous wildlife species, including wild birds, thus posing a potential risk to these species. However, the toxicological effects of this compound remain widely unknown, beyond in vitro studies and laboratory model organisms. To understand how UV-328 impacts avian physiology, captive mallards (Anas platyrhynchos) were administered an environmentally relevant dose of UV-328 orally for 10 days, followed by a 16-day post exposure period, and compared to an untreated group. To assess the toxicological impacts of UV-328 on tissue structure, liver and heart tissues were examined using histopathology. At the given dose, there were no observable changes to normal heart architecture. However, liver tissue from ducks exposed to UV-328 had increased lipid accumulation consistent with hepatic lipidosis, often displayed in periportal patterns reflecting direct toxicity to hepatocytes. These changes were observed in UV-328 exposed mallards with and without a recovery period, demonstrating the ability of this compound – or its effects – to persist. In female birds from both control and UV-328 exposure groups, liver biochemistry data revealed levels of glutamate dehydrogenase (GLDH) to be above reference values, with exposed ducks extending slightly above control ducks. Increased GLDH concentrations reflect hepatocellular damage, as observed during histopathological examinations. To further evaluate changes to avian physiology related to UV-328 exposure, I conducted untargeted metabolomic examination of fecal and serum samples of mallards, using 1H 600 MHz nuclear magnetic resonance spectroscopy. Metabolomics allows for detection, identification, and quantification of metabolites present in a biological sample, which gives an overview of physiology and mechanisms of action for pollutants. I predicted that lipid metabolism would be promoted in ducks exposed to UV-328, however I detected no differences in either fecal or serum metabolomes of the treatment groups. However, there were a few upregulated pathways and metabolites, demonstrating possible liver lipid accumulation. My study analyzed the physiological impacts of UV-328 on mallards to fill key knowledge gaps on plastic pollution and avian health. Overall, I found that an environmentally relevant dose of UV-328 has a hepatotoxic effect in this species, potentially impacting liver function. Future work should examine lipidomics, to fully explore liver functions, and to improve our understanding of the potential hazards of UV-328 in the context of wildlife health.

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