• • HCBD is unintentionally formed during chlorination stages of carbon tetrachloride, dichloroacetylene, tri-/tetrachloroethylene, and chlorobenzene production, via free-radical mechanisms, and is released through waste gas, wastewater, and solid waste, necessitating multi-pathway emission controls.
• • HCBD undergoes long-range atmospheric transport and adsorbs onto soil and sediments, leading to multi-media contamination; its bioaccumulation and food-chain magnification amplify ecological risks, with documented toxicity to aquatic organisms and hepatic/renal damage in mammals.
• • Chronic toxicity studies in rats (Kociba et al., 1977) provide critical dose-response data for HCBD, underpinning risk assessment and regulatory limit setting for occupational and environmental exposure.
• • Effective mitigation requires integrated process optimization and end-of-pipe treatment technologies, coupled with stringent emission standards and life-cycle management, as demonstrated by the reviewed literature.
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