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Public Health Issues Emanating from Heavy Metal Contamination of Freshwater Ecosystems and Groundwater
Published in Abhik Gupta, Heavy Metal and Metalloid Contamination of Surface and Underground Water, 2020
Non-Indian childhood cirrhosis (NICC) is a form of early childhood liver cirrhosis, which is known to be caused by excess Cu in drinking water. However, when an epidemiological study in Berlin, Germany, investigated the link between Cu concentrations in drinking water and signs of liver damage in infants, it could not establish any dose relation between Cu intake and serum parameters. Infants whose food was prepared with water containing 0.8 mg L–1 Cu did not show any sign of liver malfunction (Zietz et al. 2003). In contrast, Dieter et al. (1999) had found cases of early childhood cirrhosis in Germany coinciding with high hepatic Cu contents and Cu plumbing/acid well water. Genetic factors, age, and level of Cu intake could all influence Cu-induced hepatic damage in humans. Effects on liver in infants and children were usually manifested through three syndromes: Wilson’s disease, Indian childhood cirrhosis, and idiopathic copper toxicosis, of which the latter two were caused by an autosomal recessive, the manifestations of which were associated with a high level of dietary Cu from milk stored in copper or brass containers or drinking water. Pericellular fibrosis of liver, abnormal biomarkers of liver damage, and high levels of Cu in liver were observed in such cases. In contrast, infants having 0.8 ppm Cu in drinking water did not reveal any evidence of liver damage (ATSDR 2004).
Clinical Toxicology of Copper
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Sonal Sekhar Miraj, Mahadev Rao
Indian childhood cirrhosis causes elevated Cu levels without a decrease in the levels of ceruloplasmin unlike Wilson’s disease. Histopathological changes in the Indian childhood cirrhosis comprise of prominent degenerative ballooning of the hepatocytes, diffuse Mallory bodies, marked neutrophilic infiltrate in acini, and severe micronodular fibrosis. The presence of coarse dark-brown orcein staining and intralobular pericellular fibrosis differentiates Indian childhood cirrhosis from Wilson’s diseases. The absence of steatosis and the presence of cholestasis late in the disease course features in India childhood cirrhosis.
Biosorption of heavy metals from water: mechanism, critical evaluation and translatability of methodology
Published in Environmental Technology Reviews, 2022
Risha Jasmine Nathan, Arvind Kumar Jain, Rhonda J. Rosengren
Copper: Cu is an essential trace element [54]. However, chronic Cu toxicity results in diseases such as Wilson’s disease (mental alterations, dysarthria, dysphagia, ataxia, difficulty in writing, haemolytic anaemia, renal tubular dysfunction, renal stones, and fulminant hepatic failure) and Indian childhood cirrhosis (inflammation of the hepatocytes and a severe micronodular fibrosis) resulting in poor hepatocyte regeneration and fibrosis [55–57]. Additionally, exposure to Cu through contaminated drinking water has been associated with neurodegenerative diseases such as Alzheimer’s disease [58], Parkinson’s disease [59], memory and learning dysfunction [60], arteriosclerosis, diabetes mellitus [61].
Equilibrium study of dried orange peel for its efficiency in removal of cupric ions from water
Published in International Journal of Phytoremediation, 2018
Kiran Kumar, Sachin S. Patavardhan, Saritha Lobo, Richard Gonsalves
The presence of heavy metals in water is an important environmental and social problem. Some metals, such as Fe, Zn, Cu, Co, Cr, Mn, and Ni, are required for biological metabolism in trace amounts; however, their higher dose may cause toxic effects. Among the heavy metals, copper is the major available type of heavy metal in the aquatic environment. Copper is involved in hydroxyl-free radical production via the Haber-Weiss reaction that results in mitochondrial damage, neuronal injury, and DNA breakage (Linder 2012, Xu, Barrientos; Andrews 2013), and higher doses of copper exposure lead to “Indian childhood cirrhosis.” It is a chronic liver disease in 1 to 3-year-old children, considered to be endemic in India (Nayak and Chitale 2013.). In the body, 85–95% of the copper is bound to ceruloplasmin, remaining occurs as free or loosely bound to albumin and other small molecules. Free Cu+2 ions normally reduce oxidative stress via Cu-Zn dependent superoxide dismutase-mediated metabolic elimination of reactive oxygen species. Excessive free copper effects zinc homeostasis, which in turn impairs the antioxidant enzyme functionality, thereby increasing oxidative stress (Sahawneh et al.2010). Higher levels of free Cu+2 in the blood cause zinc deficiency. Drinking water that contains higher than 3 mg/L Copper concentration causes nausea, diarrhoea, abdominal pain, and vomiting (Ashish, Neeti and Himanshu 2013). The world health organization recommended that acceptable concentration of copper in drinking water be 2 mg/L (Cockell, Bertinato and L'Abbé 2008). According to specifications of Indian standard, the limit of copper in drinking water is 0.05 mg/L (Central Ground Water Board, Ministry of Water Resources, RD & GR Government of India. Retrieved from http://cgwb.gov.in/). Hence it is necessary to remove excess of copper from water to make it fit for portability.