Department of Research, DNGM Research Foundation, Kolkata, India.
Kaohsiung J Med Sci. 2011 Sep;27(9):360-70. doi: 10.1016/j.kjms.2011.05.003. Epub 2011 Jul 27.
Chronic arsenic toxicity (arsenicosis) as a result of drinking arsenic-contaminated groundwater is a major environmental health hazard throughout the world, including India. A lot of research on health effects, including genotoxic effect of chronic arsenic toxicity in humans, have been carried out in West Bengal during the last 2 decades. A review of literature including information available from West Bengal has been made to characterize the problem. Scientific journals, monographs, and proceedings of conferences with regard to human health effects, including genotoxicity, of chronic arsenic toxicity have been reviewed. Pigmentation and keratosis are the specific skin diseases characteristic of chronic arsenic toxicity. However, in West Bengal, it was found to produce various systemic manifestations, such as chronic lung disease, characterized by chronic bronchitis, chronic obstructive and/or restrictive pulmonary disease, and bronchiectasis; liver diseases, such as non cirrhotic portal fibrosis; polyneuropathy; peripheral vascular disease; hypertension; nonpitting edema of feet/hands; conjunctival congestion; weakness; and anemia. High concentrations of arsenic, greater than or equal to 200 μg/L, during pregnancy were found to be associated with a sixfold increased risk for stillbirth. Cancers of skin, lung, and urinary bladder are the important cancers associated with this toxicity. Of the various genotoxic effects of arsenic in humans, chromosomal aberration and increased frequency of micronuclei in different cell types have been found to be significant. Various probable mechanisms have been incriminated to cause DNA damage because of chronic arsenic toxicity. The results of the study in West Bengal suggest that deficiency in DNA repair capacity, perturbation of methylation of promoter region of p53 and p16 genes, and genomic methylation alteration may be involved in arsenic-induced disease manifestation in humans. P53 polymorphism has been found to be associated with increased occurrence of arsenic-induced keratosis. Of the various genes involved in the regulation of arsenic metabolism, single-nucleotide polymorphisms of purine nucleoside phosphorylase, in one study, showed increased occurrence of arsenicosis.
慢性砷中毒（砷中毒）是由于饮用受砷污染的地下水而导致的一种主要的环境健康危害，在全世界范围内，包括印度，都存在这一问题。在过去的 20 年里，西孟加拉邦进行了大量关于健康影响的研究，包括慢性砷中毒的遗传毒性。对文献进行了综述，包括西孟加拉邦的信息，以描述这一问题。对涉及人类健康影响，包括慢性砷中毒的遗传毒性的科学期刊、专着和会议记录进行了综述。色素沉着和角化病是慢性砷中毒的特定皮肤疾病。然而，在西孟加拉邦，发现它会产生各种全身表现，如慢性肺病，表现为慢性支气管炎、慢性阻塞性和/或限制性肺病和支气管扩张；肝脏疾病，如非肝硬化性门脉纤维化；多发性神经病；外周血管疾病；高血压；手足非凹陷性水肿；结膜充血；虚弱；和贫血。研究发现，怀孕期间砷浓度高于或等于 200μg/L 与死产风险增加六倍相关。皮肤癌、肺癌和膀胱癌是与这种毒性相关的重要癌症。在人类中，砷的各种遗传毒性效应中，不同细胞类型中的染色体畸变和微核频率增加已被证明是显著的。已经有各种可能的机制被归咎于慢性砷中毒引起的 DNA 损伤。西孟加拉邦的研究结果表明，由于慢性砷中毒，DNA 修复能力的缺陷、p53 和 p16 基因启动子区域甲基化的扰动以及基因组甲基化改变可能与砷诱导的人类疾病表现有关。已经发现 p53 多态性与砷诱导的角化病的发生增加有关。在参与砷代谢调节的各种基因中，嘌呤核苷磷酸化酶的单核苷酸多态性在一项研究中显示砷中毒的发生率增加。
