Mukerjee D
National Center for Environmental Assessment, United States Environmental Protection Agency, Cincinnati, Ohio, USA.
J Air Waste Manag Assoc. 1998 Feb;48(2):157-65. doi: 10.1080/10473289.1998.10463655.
Polychlorinated dibenzo-p-dioxins (PCDDs), commonly known as dioxins, form as unwanted impurities in the manufacturing of chlorophenol and its derivatives--pulp and paper--and in the combustion of municipal, sewage-sludge, hospital, and hazardous waste. Combustion, in presence of a chlorine donor, seems to be a major source of these compounds. High levels of dioxins are also emitted from metallurgical industries including copper smelters, electric furnaces in steel mills, and wire reclamation incinerators. Trace levels are detectable in emissions from motor vehicles using leaded gasoline or diesel fuel, in forest fires, and in residential wood burning. Extremely persistent and widely distributed in the environment, PCDDs have been detected in all three primary and many secondary media. Releases into the air occur mainly from combustor emissions. Atmospheric dispersion, deposition, and subsequent accumulation in the food chain seem to be the major pathways of exposure to the general population. Residues of these chemicals have been detected in soil, sediment, fish, meat, cow's milk, human adipose tissue, and mothers' milk. In general, these chemicals have high lipophilicity. The elimination half-life of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in humans is approximately 7-11 years. Very little human toxicity data from exposure to PCDDs are available. Health-effect data obtained from occupational settings in humans are based on exposure to chemicals contaminated with TCDD. It produces a spectrum of toxic effects in animals and is one of the most toxic chemicals known. Most of the toxicity data available on TCDD are from high-dose oral exposures to animals. Very few percutaneous and no inhalation exposure data are available in the literature. There is a wide range of difference in sensitivity to PCDD lethality in animals. The signs and symptoms of poisoning with chemicals contaminated with TCDD in humans are analogous to those observed in animals. Dioxin exposures to humans are associated with increased risk of severe skin lesions such as chloracne and hyperpigmentation, altered liver function and lipid metabolism, general weakness associated with drastic weight loss, changes in activities of various liver enzymes, depression of the immune system, and endocrine- and nervous-system abnormalities. It is a potent teratogenic and fetotoxic chemical in animals. A very potent promoter in rat liver carcinogenesis, TCDD also causes cancers of the liver and other organs in animals. Populations occupationally or accidentally exposed to chemicals contaminated with dioxin have increased incidences of soft-tissue sarcoma and non-Hodgkin's lymphoma. No comprehensive studies have been conducted to determine any health impact to the general population from environmental exposure to PCDDs. This paper presents a brief review of relevant animal and human data for projecting any possible health effects from environmental exposures to PCDDs.
多氯二苯并 - 对 - 二噁英（PCDDs），通常被称为二噁英，在氯酚及其衍生物（纸浆和造纸）的制造过程中，以及城市垃圾、污水污泥、医院废物和危险废物的燃烧过程中，作为不需要的杂质形成。在有氯供体存在的情况下燃烧似乎是这些化合物的主要来源。包括铜冶炼厂、钢铁厂的电炉和电线回收焚烧炉在内的冶金工业也会排放高浓度的二噁英。在使用含铅汽油或柴油燃料的机动车排放物、森林火灾和居民燃木中可检测到痕量水平。PCDDs在环境中具有极强的持久性且分布广泛，在所有三种主要介质和许多次要介质中都已被检测到。向空气中的排放主要来自燃烧器排放。大气扩散、沉降以及随后在食物链中的积累似乎是一般人群接触的主要途径。在土壤、沉积物、鱼类、肉类、牛奶、人体脂肪组织和母乳中已检测到这些化学物质的残留。一般来说，这些化学物质具有高亲脂性。2,3,7,8 - 四氯二苯并 - 对 - 二噁英（TCDD）在人体中的消除半衰期约为7 - 11年。关于人类接触PCDDs的毒性数据非常少。从职业环境中获得的人体健康影响数据是基于接触受TCDD污染的化学物质。它在动物中会产生一系列毒性作用，是已知毒性最强的化学物质之一。现有关于TCDD的大多数毒性数据来自对动物的高剂量口服暴露。文献中很少有经皮暴露的数据，且没有吸入暴露的数据。动物对PCDD致死性的敏感性差异很大。人体接触受TCDD污染的化学物质中毒的症状与在动物中观察到的症状相似。人类接触二噁英会增加患严重皮肤病变（如氯痤疮和色素沉着过度）、肝功能和脂质代谢改变、与体重急剧下降相关的全身虚弱、各种肝酶活性变化、免疫系统抑制以及内分泌和神经系统异常的风险。它在动物中是一种强效致畸和胚胎毒性化学物质。TCDD是大鼠肝癌发生的一种非常强效的促进剂，还会导致动物肝脏和其他器官的癌症。职业性或意外接触受二噁英污染化学物质的人群软组织肉瘤和非霍奇金淋巴瘤的发病率增加。尚未进行全面研究以确定环境接触PCDDs对一般人群的任何健康影响。本文简要回顾了相关的动物和人体数据，以预测环境接触PCDDs可能产生的任何健康影响。
