Environmental sources, fate, toxicological effects, and health risks of copper pyrithione: an overview

被引:0
|
作者
Tang, Can [1 ]
Qin, Xian [2 ]
Huang, Wenlong [3 ]
Debi, Sutapa [1 ]
Zhang, Zonghang [1 ]
Guo, Jiahua [4 ]
Liu, Wenhua [1 ]
Mo, Jiezhang [1 ]
机构
[1] Shantou Univ, Guangdong Prov Key Lab Marine Disaster Predict & P, Shantou 515063, Peoples R China
[2] City Univ Hong Kong, State Key Lab Marine Pollut, Hong Kong, Peoples R China
[3] Shantou Univ, Dept Forens Med, Med Coll, Shantou 515041, Peoples R China
[4] Northwest Univ, Coll Urban & Environm Sci, Shaanxi Key Lab Earth Surface Syst & Environm Carr, Xian 710127, Peoples R China
关键词
Copper pyrithione; Ecotoxicity; Environmental fate; Ecological risk assessment; Review; TEMPERATURE-DEPENDENT TOXICITIES; ANTIFOULING BOOSTER BIOCIDES; ZINC PYRITHIONE; METAL PYRITHIONES; BRINE SHRIMP; DEGRADATION COMPOUNDS; MARINE; SEA; COPEPOD; FISH;
D O I
10.1007/s11783-024-1892-4
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Copper pyrithione (CuPT) is an alternative to tributyltin that is widely used as an antifoulant and biocide in paint for ship hulls, fishing nets, and other marine environmental facilities. It gradually leaches from antifouling coatings into the aquatic environment, posing health risks to aquatic organisms. In recent years, there have been increasing concerns regarding the impacts of CuPT and its degradation products on organisms, as well as the associated health risks. Although the ecotoxicity of CuPT and its degradation products in various species has been studied, there are no comprehensive reviews in the literature that have collated and interpreted these data. This review provides a comprehensive summary of the ecotoxicological effects of CuPT and its degradation products on microorganisms, plants, invertebrates, fish, and mammals. CuPT and its degradation products can affect the light utilization of plants, thereby altering primary production in ecosystems. It can disrupt cell membranes, antioxidant capacity, and cellular pH gradients in animals, leading to developmental toxicity, deformities, morphological damages, endocrine disruption, reproductive toxicity, hepatotoxicity, and neurotoxicity. Mitochondria are believed to be the primary target of CuPT-induced toxicity in aquatic animals; however, further investigations are warranted to reveal the long-term (e.g., multigenerational and transgenerational) impacts and associated molecular mechanisms of CuPT and its degradation products-particularly at environmentally realistic levels. This will facilitate a more comprehensive understanding of the health effects (both in terms of toxicity and hormesis) and environmental risks of CuPT and its degradation products, facilitating more effective regulation and mitigation.
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