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Experimental Lung Carcinogenesis by Intratracheal Instillation
Published in Joan Gil, Models of Lung Disease, 2020
Similarly to chromium compounds, cadmium is well known to be carcinogenic when it is injected parenterally (IARC, 1976). However, carcinogenic data from IT instillation or inhalation are limited. Sanders and Mahaffy (1983) examined the carcinogenic effects of low doses of cadmium oxide after single or multiple IT instillation. They found that cadmium oxide was not carcinogenic in the lung of rats. Recently, Pott et al. (1986) demonstrated a high incidence of lung tumors in rats by IT instillation of cadmium sulfide (a total dose, 0.63-50 mg). In the same series of experiments, Pott et al. examined carcinogenic effects of instilled cadmium chloride (maximal total dose, 135 μg/rat), and cadmium oxide (maximal total dose, 135 μg/rat) in rats. They found 6.4-7.5% incidences of lung tumor in about 40 rats. Adenomas, adenocarcinomas, and squamous cell carcinomas occurred in rats exposed to these cadmium compounds.
Respiratory Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
One of the first observations on the acute toxic effects of cadmium in the lung was published in 1932.85 Since that time several reports, using more sophisticated methods for examining the lung, have been published, most of them verifying the deleterious effects on the lung.6,36,75,91,99Table 1 presents data on the acute toxicity of cadmium oxide fumes for various animal species. Exposure periods ranged from 10 to 30 min. The LD50 (cumulative mortality) up to 7 and 28 days, varied between 500 and 15,000 min × mg cadmium oxide per cubic meter, depending on the species of animal used. Harrison et al.38 reported a 90% mortality among dogs exposed to 320 mg Cd per cubic meter in the form of cadmium chloride over a 30-min period (= 9600 min × mg/m3). Snider et al.91 mentioned that 17 out of 18 rats exposed to about 65 mg Cd per cubic meter in the form of chloride for 1 hr died within 3 days (= 3900 min × mg/m3). Hadley et al.36 exposed 61 rats to cadmium oxide at a concentration of 60 mg/m3 for 30 min. Twenty-seven of the exposed rats died from acute pulmonary edema within 3 days of exposure (= 1800 min × mg/m3). The average cadmium concentration in lungs from rats that had died was 26.9 mg/kg.
Cadmium: Uses, Occurrence, and Intake
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Cadmium is a soft, silvery, and ductile metal. Some of its physical and chemical properties are given in Table 1. Cadmium is readily volatilized at high temperatures, e.g., during welding or smelting, producing a fine dust of cadmium oxide particles with a typical yellow-brownish color. In most of its chemical properties, cadmium resembles zinc. Like zinc, cadmium is always divalent (2+) in stable compounds such as in the acetate, carbonate, chloride, oxide, stearate, sulfate, sulfide, and cadmium sulfoselenide compounds. The water solubility of inorganic cadmium compounds varies from the readily soluble acetate, chloride, and sulfate, to the almost insoluble carbonate, oxide, and sulfide. Certain organic cadmium compounds, in which cadmium is bound directly to a carbon atom, can be synthesized.
Mechanistic study of copper oxide, zinc oxide, cadmium oxide, and silver nanoparticles-mediated toxicity on the probiotic Lactobacillus reuteri
Published in Drug and Chemical Toxicology, 2023
Aya M. Eid, Osama M. Sayed, Walaa Hozayen, Tarek Dishisha
Ag NPs are mainly used in biomedical, nourishing, and textile applications due to their unique features, and they have been found to suppress Gram-negative and Gram-positive bacteria; thus, they can be used against bacterial pathogens in textile industries (Tharani et al.2020). Side by side, cadmium oxide (CdO) NPs have attracted significant attention due to their outstanding biological, chemical, and physical features (Ghotekar 2019). They have been extensively investigated and employed in paint pigments, electrical gadgets, and medicinal therapies. In addition, CdONPs have been utilized to create quantum dots, which are gaining popularity in medical diagnostic imaging and targeted therapies (Demir et al.2020). Accordingly, these inorganic NPs now have access to the human gastrointestinal tract (GIT) by ingestion as part of nano-enabled food and beverages, posing a risk to human health, microbial biodiversity, and the environment. (Gao et al.2018, Siemer et al.2018).
A murine model of the effects of inhaled CuO nanoparticles on cells of innate and adaptive immunity – a kinetic study of a continuous three-month exposure
Published in Nanotoxicology, 2019
Vladimir Holan, Eliska Javorkova, Kristyna Vrbova, Zbynek Vecera, Pavel Mikuska, Pavel Coufalik, Pavel Kulich, Radim Skoupy, Miroslav Machala, Alena Zajicova, Pavel Rossner
On day 3, a significant decrease in the proportion of neutrophils, macrophages and APC in the exposed group was detected. This decrease in the populations of cells of innate immunity observed in the spleen, could be due to a migration of these cells from the periphery to the lungs as the first defense line after inhalation. Certainly, an accumulation of eosinophils and neutrophils in the lungs shortly after the start of NP inhalation or intratracheal administration has been observed (Gustafsson et al. 2011; Jeong et al. 2016). However, even though there was no difference in the proportion of T or B cells between the exposed and control groups, T cells from NP exposed mice responded by a significantly enhanced proliferation, and B cells by a decreased proliferation to stimulation with T- and B-cell mitogens, respectively. In addition, T cells from the exposed mice produced higher concentrations of T-cell cytokines IL-2 and IFN-γ than cells from the control mice. These results indicate that already after 3 days of CuO NP inhalation, the reactivity of both T and B cells is influenced by NPs. These findings are in agreement with the observation of Blum et al. (2014) who showed that a short-term inhalation exposure to occupationally relevant concentrations of cadmium oxide NPs induced levels of proinflammatory cytokines one day after exposure. Similarly, the intravenous administration of ZnO NPs in mice resulted in an elevated production of TNF-α and IL-1β already 24 h post exposure (Fujihara et al. 2015).
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 (Cd) is a high density heavy metal frequently used in various industries, such as battery, pigments, alloy and multicolored glasses manufacturing. Cd is widely distributed in the environment via air, water and soil through mining, smelting, usage of phosphate fertilizers, and tobacco smoking, etc. (Jarup & Akesson, 2009). There are several forms of Cd generated, including cadmium chloride (CdCl2), cadmium oxide (CdO), cadmium nitrate (Cd(NO3)2) and cadmium sulfide (CdS). Cd and its derivative compounds are probably the most toxic metals that harm human health and are classified IB as human carcinogens by International Agency for Research on Cancer (IARC, 1993; Satarug et al., 2003). Exposure to Cd has been demonstrated to contribute to multi-organs damages, including kidney, liver, stomach, respiratory system and bone (Koyu et al., 2006; Nordberg et al., 2002; Schöpfer et al., 2010). Cd can accumulate in the brain tissue by transporting across the blood–brain barrier. In both human and animal models, exposure to Cd leads to long-term impairment of neurobehavioral functions, such as indisposition of attention and memory, alterations in the psychomotor and vasomotor functioning, peripheral neuropathy and olfactory dysfunction (Haider et al., 2015; Viaene et al., 2000). Cd(NO3)2, a compound generated from Cd, is the major product of tobacco smoking and was used in the nickel–Cd batteries. The most momentous source of human Cd absorption is from tobacco smoking and occupational exposure in the related job fields (Bernhoft, 2013; Nordberg et al., 2007). However, the pathologic characteristic of Cd(NO3)2 could be neurotoxicity which is the etiological factor in neurodegenerative diseases. However, the underlying mechanism remains unclear.