Lentza-Rizos C
Pesticide Residue Laboratory, Benaki Phytopathological Institute, Kiphissia, Greece.
Rev Environ Contam Toxicol. 1990;115:1-37. doi: 10.1007/978-1-4612-3416-6_1.
Degradation of ethylenebisdithiocarbamate fungicides (EBDCs) is known to produce ethylenethiourea (ETU). This article reviews the literature available on the toxicology of EBDCs and ETU, the sources in plants and persistence of ETU, and its formation during heat treatment of plant products. Detoxification techniques developed are mentioned, and Maximum Residue Limits and the results of monitoring studies are given for several countries. Some aspects of the methods of analysis are discussed. Although EBDCs have in the past been regarded as relatively harmless, data on their subchronic and chronic toxicity indicate that these toxicological features should not be ignored. ETU has low acute toxicity but possesses carcinogenic, goiterogenic, teratogenic, and mutagenic activity in animal tests. The most prominent aspect of its toxicology is its action on the thyroid gland, which causes hyperplasia and a decrease in thyroid hormone levels. It is a potent teratogen in pregnant rats after either acute exposure or administration throughout organogenesis, inducing a wide spectrum of malformations to the progeny. The teratogenic potential is specific to rat, whereas administration to pregnant mouse, hamster, guinea pig, and cat causes limited or no teratogenicity, except at very high dose levels. The mutagenicity of ETU has not been clearly established, although some data exist that indicate that it indeed has mutagenic potential. ETU can react with nitrites to form N-nitroso-ETU, which is a mutagenic and teratogenic compound. Most of the ETU present in fresh agricultural products treated with EBDCs arises from the presence of ETU in formulations. Surface deposits of EBDCs on plants may be a secondary source. ETU may also be taken up by plants from the soil following the breakdown of EBDCs, but conflicting results have been obtained on this phenomenon. ETU on plant surfaces undergoes subsequent degradation. Although small amounts may persist up to 30 d after spraying, there is no indication that it accumulates in plants. Initial findings that ETU is formed during the heat processing of EBDC-treated foods are confirmed by the more recent literature. However, the variability of the results indicates a wide range of conversion due to processing. Boiling of spinach, pears, grapes, tomatoes, and wheat, treated with different EBDCs, resulted in 3-30% conversion to ETU. Apple juice, dried pomace, and applesauce contained more ETU than the EBDC-treated apples, from which these products were produced. This was also true for tomato juice and canned whole tomatoes. ETU may be produced in the smoke of tobacco containing high EBDC residues.(ABSTRACT TRUNCATED AT 400 WORDS)
已知亚乙基双二硫代氨基甲酸盐类杀菌剂（EBDCs）降解会产生乙撑硫脲（ETU）。本文综述了关于EBDCs和ETU毒理学、ETU在植物中的来源及持久性、以及其在植物产品热处理过程中形成的现有文献。文中提到了已开发的解毒技术，并给出了几个国家的最大残留限量及监测研究结果。还讨论了分析方法的一些方面。尽管EBDCs过去被认为相对无害，但关于它们亚慢性和慢性毒性的数据表明，这些毒理学特征不应被忽视。ETU急性毒性较低，但在动物试验中具有致癌、致甲状腺肿、致畸和致突变活性。其毒理学最突出的方面是对甲状腺的作用，会导致甲状腺增生和甲状腺激素水平降低。在怀孕大鼠急性暴露或在整个器官形成期给药后，ETU是一种强效致畸剂，会导致后代出现广泛的畸形。致畸潜力是大鼠特有的，而对怀孕小鼠、仓鼠、豚鼠和猫给药，除了在非常高的剂量水平外，只会导致有限的致畸性或无致畸性。尽管有一些数据表明ETU确实有致突变潜力，但其致突变性尚未明确确定。ETU可与亚硝酸盐反应形成N-亚硝基-ETU，这是一种致突变和致畸化合物。用EBDCs处理的新鲜农产品中存在的大多数ETU来自制剂中ETU的存在。EBDCs在植物表面的沉积物可能是次要来源。EBDCs分解后，ETU也可能被植物从土壤中吸收，但关于这一现象的结果存在矛盾。植物表面的ETU会随后降解。虽然喷洒后少量ETU可能持续30天，但没有迹象表明它会在植物中积累。EBDC处理的食品在热处理过程中形成ETU这一初步发现得到了最新文献的证实。然而，结果的变异性表明由于加工导致的转化率范围很广。用不同EBDCs处理的菠菜、梨、葡萄、西红柿和小麦煮沸后，转化为ETU的比例为3% - 30%。苹果汁、干果渣和苹果酱中的ETU含量比生产这些产品所用的EBDC处理苹果中的含量更高。番茄汁和罐装整番茄也是如此。ETU可能在含有高EBDC残留的烟草烟雾中产生。（摘要截取自400字）
