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Respiratory Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
The first report on chronic respiratory effects of cadmium was published by Friberg.28-30 He reported an increased quotient between residual volume and total lung capacity for workers exposed to cadmium dust in comparison to sawmill workers of similar ages. This residual quotient was estimated as the ratio between the residual volume (RV) and the total lung capacity (TLC) in percent (100% × RV/TLC). It is however, likely that Seiffert87 as early as 1897 actually observed chronic cadmium poisoning and not plumbism, as he thought, among workers in a zinc smelter. Zinc ore often contains considerable amounts of cadmium and significant cadmium exposure may therefore occur in zinc smelters (Chapter 3). Seiffert reported emphysema among 83% and proteinuria among 82% of the workers examined. As discussed by Friberg,29 there may well have been considerable exposure to cadmium as the symptoms described agree with those of chronic cadmium poisoning.
Kinetics and Metabolism
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Gunnar F. Nordberg, Tord Kjellström, Monica Nordberg
Combined treatment with two or more chelating agents has been tried in acute cadmium poisoning in animals. Although an advantage of such combined treatment has been reported, this report has later been shown to be erroneous and there is no advantage of, e.g., a combination of EDTA and salicylic acid compared to EDTA alone.28
Heavy Metals
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Cadmium poisoning is associated with tobacco smoke (as tobacco leaves accumulate cadmium), ingestion of foods containing cadmium (grains, legumes, leafy vegetables, fish, and shellfish), and contact with cadmium-containing products (electric batteries and solar panels) [9].
Assessment of the concentrations and health risk of some heavy metals in cowpea (Vignus unguiculata) in Gwagwalada, Nigeria
Published in Drug and Chemical Toxicology, 2021
M. G. Akande, F. S. Sanni, N. G. Enefe
In the present study, the results indicated that the two types of cowpea contained Cd at concentrations above the FAO/WHO permissible limit of 0.2 mg/kg (FAO/WHO 2001). The high levels of Cd reported in this study could be due to contamination of the farms or the soils where the two cowpea types were cultivated with metal based fertilizers or sewage sludge, or from pollution by haphazard fumes from the exhaust of vehicles (Ladipo and Doherty 2011). Cadmium poisoning in humans could lead to anemia, renal damage, bone disorder, cancer of the lungs and death (Muntean et al. 2013, Garba et al. 2015). However, in a study conducted by Adepoju et al. (2018), the level of Cd detected in beans collected from three different markets in Ibadan, Oyo State, was below the permissible limit set by FAO/WHO (2001) and this result is contrary to what was obtained in our study.
Cadmium nitrate-induced cytotoxicity and genotoxicity via caspases in Neuro-2A neurons
Published in Toxin Reviews, 2018
Chuan-Cheng Wang, Ming-Ling Yang, Ching-Ping Yang, Ching-Hui Liang, Chien-Ying Lee, Hui-Wei Lin, Yu-Hsiang Kuan
Cadmium poisoning has been known to induce dysfunction of physiological, biochemical and behavioral capabilities in experimental animals and humans since ancient times. Cd exists in several commodities, such as televisions, batteries, cosmetics, paint pigments and tobacco smoking (Jarup & Akesson, 2009). Cd is rarely absorbed through skin, about 5–10% is absorbed through ingested Cd, a greater ratio arises in people with deficiency of iron, calcium or zinc. The primary way of Cd absorption, which constitutes about 10–50%, occurs through inhalation of Cd dust (Bernhoft, 2013; Nordberg et al., 2007). Therefore, tobacco smoking can be considered as the major source of human Cd absorption (Bernhoft, 2013). Cd(NO3)2 is the major product of tobacco smoking and is used in the manufacturing of nickel–Cd batteries (Bernhoft, 2013; Nordberg et al., 2007). Recent study has reported that pretreatment with another cd compound cadmium diacetate (Cd(CH3COO)2) at 10 μM for 24 h will significantly induce cell death in neuron-like rat pheochromocytoma cell line, PC12 (Yuan et al., 2016). Our findings appeared to be similar in that Cd(NO3)2 could also induce neurotoxicity. For the present, it may be useful to look more deeply at various concentrations and time durations applied on Cd(NO3)2 treated neuron-like cells, i.e. the N2A murine neuroblastoma. Our results had shown that Cd(NO3)2 exhibited a concentration- and time-dependent cytotoxicity to N2A cells.
Cadmium exposure induces cardiac glucometabolic dysregulation and lipid accumulation independent of pyruvate dehydrogenase activity
Published in Annals of Medicine, 2021
Olufemi I. Oluranti, Ebunoluwa A. Agboola, Nteimam E. Fubara, Mercy O. Ajayi, Olugbenga S. Michael
Studies have documented stimulating evidence connecting environmental exposure to heavy metals with increased risks of cardiovascular disease, hypertension, metabolic syndrome and diabetes [16,17]. Cadmium (Cd), a heavy metal and an environmental pollutant, known to cause toxic effects in humans at relatively low exposure in all its biological types [18]. This pollutant, however, is ubiquitous, not biodegradable and has a long environmental life [19]. Cd accumulates in the human body, particularly in the liver and kidneys, which are vital organs for acute toxicity-induced detoxification processes, causing severe health problems [20,21]. The Joint FAO/WHO Expert Committee on Food Additives (2004) set a provisional tolerable intake of Cd at 7μg kg−1 body weight per week. In this sense, as a result of growing levels of toxic metals and contaminants in terrestrial and marine environments from natural and anthropogenic sources, the importance of monitoring the impact of toxic elements on living organisms has increased in recent years. Water, soil, environment, plants, livestock, vegetables, meat and seafood are all showed by survey data to be the possible risk of exposure to Cd [22]. Cd-induced toxicity is mediated by free radical generation and subsequent accumulation of reactive oxygen species (ROS), which plays a crucial role in tissue damage [23]. The major events caused by cadmium poisoning include oxidative stress, cell cycle progression, DNA damage and apoptosis [24]. A correlation has been identified between exposure to Cd and the possibility of cardiovascular diseases such as hypertension, myocardial infarction, cardiomyopathy, stroke, heart failure, arteriosclerosis and peripheral arterial disease [25].