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Effects on Bone, on Vitamin D, and Calcium Metabolism
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
In this section we will briefly review the main features of Itai-itai disease and other manifestations of cadmium-induced bone effects and present the more recent data on cases occurring outside the original “endemic” area. A more detailed description of earlier studies of Itai-itai disease and a comprehensive list of references are given in the Appendix.
Introduction
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
A local physician, Dr. Hagino, reported on an unusually high occurrence of osteomalacia in the area in 1957.4 A few years later it was postulated that cadmium played a role in the etiology of Itai-itai disease.5 Since then there has been a great deal of debate about the etiology of Itai-itai disease. In 1968, the Japanese Ministry of Health and Welfare concluded that, “Itai-itai disease is caused by chronic cadmium poisoning, on condition of the existence of such inducing factors as pregnancy, lactation, imbalance in internal secretion, aging and deficiency of calcium.” In 1984, the Japanese Ministry has not changed this conclusion. However, the causal role of cadmium has not been unequivocally recognized. As late as 1975, Kodama referred to the disease as “a phantom pollution-originated disease”.6 The same year, a WHO task group in the preparation of an environmental health criteria document for cadmium concluded that, “cadmium was a necessary factor in the development of Itai-itai disease.” This task group11 also recognized that other factors, e.g., nutritional factors, had been of importance for the development of the disease.
Chronic cadmium exposure in Japanese quails perturbs serum biochemical parameters and enzyme activity
Published in Drug and Chemical Toxicology, 2020
Damir Suljević, Erna Islamagić, Anida Čorbić, Muhamed Fočak, Filip Filipić
Cadmium is a toxic heavy metal classified as a human carcinogen. Correlation between cadmium exposure and lung and prostate cancer in humans was found when inhaled cadmium in rodents caused pulmonary adenocarcinoma (Waalkes 2000). Besides the gastrointestinal system, the respiratory system is another pathway for cadmium entry into the body. About 50% of cadmium is absorbed from tobacco (Zalups and Ahmad 2003). Cadmium binds to the sulfhydryl cysteine radical in keratinocytes, then penetrates the blood by binding to metallothionein (Fasanya-Odewumi et al. 1998). Divalent metal transporter 1 (DMT1) and albumins have a high affinity for cadmium and distribute cadmium to different organs (Himeno et al. 2002). The biological half-life of cadmium is estimated at 15 to 20years (Kayankarnna et al. 2013). Cadmium also accumulates in the liver and kidneys due to the high content of metallothionein (Joseph 2009). Järup and Alfvén (2004) reported the connection between cadmium and diseases such as bone metabolism impairment and fragility, emphysema, immune system suppression and diabetes (Valko et al. 2005). Long-term exposure to cadmium in the Japanese population has led to the development of itai-itai disease. Characteristics of the disease include osteomalacia, osteoporosis, skeletal deformities, followed by changes in glucose, calcium, and amino acid levels (Inaba et al.2005).
Heavy metals in milk: global prevalence and health risk assessment
Published in Toxin Reviews, 2019
Amir Ismail, Muhammad Riaz, Saeed Akhtar, Joseph E. Goodwill, Jin Sun
Cd is another toxic contaminant reported in milk and milk products (Qin et al.2009, Najarnezhad and Akbarabadi 2013, Lutfullah et al.2014). Cd is mainly found in the kidneys and liver of human body, making them the major target organs of Cd toxicity. Cd toxicity is also linked with an aching disease called Itai-Itai disease (Malhat et al.2012). Moreover, Cd exposure has been attributed to bone demineralization, hypertension in pregnant women, disturbed calcium metabolism, stone formation, and hypercalciuria (Kosanovic et al.2002, Zaidan et al.2013)
Transcription profiling of cadmium-exposed livers reveals alteration of lipid metabolism and predisposition to hepatic steatosis
Published in Xenobiotica, 2021
Chenghui Ren, Longfei Ren, Jun Yan, Zhongtian Bai, Lei Zhang, Honglong Zhang, Ye Xie, Xun Li
Cadmium (Cd) is a nonessential element for the growth and development of organisms; its diffusion may cause tissue and cell damage (Liu et al.2018, Cosio and Renault 2020). The United Nations Environment Program (UNEP) and the Agency for Toxic Substances and Disease Registry (ATSDR) regard Cd as the first and the sixth hazardous substances with global significance, respectively (Inayat-Hussain et al.2018, Watson et al.2020). The long half-life of Cd (approximately 10–30 years) facilitates its accumulation in the kidneys, liver, bones, and reproductive organs after entering the body (Matović et al.2015, Yang and Shu 2015, Richter et al.2017, Liu et al. 2020, Yu et al. 2020). ‘Itai-Itai Disease’ incident in Japan in the last century has focused the scientists’ attention on the potential health effects of Cd, including liver toxicity (Scinicariello and Buser 2015, Shim et al.2017). The excessive accumulation of Cd in the liver can induce histopathological damage to the liver and immune disorders (Salah-Abbès et al.2015, Fu and Xi 2020). The authenticated mechanisms for its toxicity maybe: (1) Cd and calcium ions have a similar ion distribution, which may cause competitive interference with the normal biological function of calcium ions (Wang et al.2019, Gu et al.2020). (2) Cd ions can combine with the sulfhydryl groups of some biological macromolecules; the inactivation of the sulfhydryl groups affects the molecular function (Yu et al.2020). (3) Cd can induce oxidative stress and lipid peroxidation by depleting glutathione or by inhibiting the activity of antioxidant enzymes (Per et al.2017, Ren et al.2019). (4) Other mechanisms, such as epigenetics (Park et al.2017), gut microbes (He et al.2020), and immune response (Wang et al.2019).