Abstract
The coking wastewater had a high chemical oxygen demand (COD) concentration (2 771 ± 397 mg/L) and was highly toxic to the zebrafish embryos. Although biological treatment removed over 80% of COD and almost all known toxic compound from the coking wastewater, the wastewater still caused nearly 90% mortality of zebrafish embryos, with severe cardiotoxicity and skeletal development toxicity, suggesting the presence of unknown toxic compounds in the biological effluent. Synchronized oxidation–adsorption (SOA) technology, i.e., Fenton-based oxidation coupled with hydroxyl radicals and adsorption through in-situ-formed hydrolyzed Fe3+ particles, was employed as a tertiary treatment, resulting in further COD removal from 315 ± 36 to 129 ± 9 mg/L. More importantly, SOA tertiary treatment greatly reduced the toxicity of the biological effluent, effectively improving the survival rate of zebrafish from 10% to 95% at 80% of the wastewater concentration. Toxicological analysis showed that SOA treatment of wastewater alleviated its cardiovascular and somatic skeletal toxicity in zebrafish. Notably, nkx2.5, which affects circulatory system development, and her12, which regulates the development of skeletal somites, remained at low levels, which explain the malformations observed in the final effluent-exposed zebrafish. In addition, wastewater exposure induced apoptosis in zebrafish. This study is the first to report on the effects of coking wastewater on the cardiovascular system, somite bone development, and apoptosis in zebrafish embryos at the genetic level.
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