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Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Arsenic has been used therapeutically for more than 2000 years (Frost, 1967). Medicinal uses of arsenic have ranged from treatment of syphilis to use as a tonic. Arsenicals act locally and are slow corrosives; they have been used in the treatment of skin cancer. In the United States there has been a decline in the use of arsenicals in human medicine but the decrease has not been as great in veterinarian or agricultural use (e.g., sodium arsenite as a weed killer).
Risk Characterization
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Arsenic may exist in either the +3 or +5 valence state. The binding of trivalent arsenic compounds to critical sulfhydryl groups is a likely event in the mode of action in both humans and rodents.105 Trivalent arsenicals may either be administered, produced metabolically, or occur naturally in water. In 2005, EPA’s Office of Pesticides concluded that the mode of action of arsenic for bladder cancer supported a nonlinear default approach and that a RfD/TDI was an appropriate TRV rather than a slope factor.105
A Review of Epidemiologic Studies with Regard to Routes of Exposure to Toxicants
Published in Rhoda G. M. Wang, James B. Knaak, Howard I. Maibach, Health Risk Assessment, 2017
In the majority of epidemiologic studies of humans, potential or actual routes of exposure are poorly defined. In some instances the route of human exposure can be inferred from the toxic agents involved, the nature of the exposure, and/or the associated health outcomes. The occurrence of nasal cancers in persons working in environments with wood dusts implies an inhalation route, while dermatitis in woodworkers is due to dermal exposure (Table 1).17 The association between acute exposure to phosgene gas (COCl2), mentioned earlier, and pulmonary edema is clearly due to inhalation (Table 1), as occurred among World War II workers exposed during the production of uranium chloride obtained by combining CC14 with uranium oxide.16,19 Exposure to arsenicals, associated with both lung and skin cancers, also occurs by inhalation and dermal contact. Various agents associated with lung cancer, such as nickel oxides, radon gas, and arsenic compounds, clearly reflect inhalation exposures (Table 1).
Sodium arsenite-induced detriment of cell function in Leydig and Sertoli cells: the potential relation of oxidative damage and antioxidant defense system
Published in Drug and Chemical Toxicology, 2020
Banu Orta Yilmaz, Nebahat Yildizbayrak, Melike Erkan
Arsenic is a common toxic agent naturally occurring in the environment. Arsenical compounds lead to various hazardous effects on human health through environmental and occupational exposure. Arsenic has a wide scope of industrial applications such as mining, smelting of metals, fossil fuels combustion, glass, and semiconductor production. Besides, arsenic frequently used in food preservatives, herbicides, insecticides, and fungicides (Hughes 2002). Around the world, the rising level of arsenic in drinking water has become major source of arsenic poisoning (Schulman 2000). Many developed and developing countries have endemic areas contaminated with a level of arsenic that is over the permissible limits for arsenic in drinking water by the World Health Organization (10 µg/L) (WHO 2011). China, Argentina, Mexico, Bangladesh, Turkey, Canada, and India can be listed among the countries that have high levels of arsenic in drinking water, ranging from 0.5 to 5000 µg/L (Altaş et al.2011).
Biotransformation of arsenic trioxide by AS3MT favors eradication of acute promyelocytic leukemia: revealing the hidden facts
Published in Drug Metabolism Reviews, 2020
Yasen Maimaitiyiming, Hong-Hu Zhu, Chang Yang, Hua Naranmandura
On one hand, it is well demonstrated that cytotoxicity of arsenicals is primarily dependent on their oxidation state and chemical structure (Shen et al. 2013). Many in vitro studies reported that trivalent methylated arsenicals (e.g. MMAIII and DMAIII) are much more toxic than their precursor iAsIII (Chen et al. 2003; Hayakawa et al. 2005; Naranmandura et al. 2006; Wang et al. 2015). This is also evidenced by the fact that MMAIII and DMAIII could inhibit the activity of many enzymes (Rehman and Naranmandura 2012; Shen et al. 2013; Fan et al. 2019; Lee and Levin 2019; Su et al. 2019). Darinaparsin (DAR) is a novel form of artificially designed organic arsenic derivative that was tested as a potent tumor-killing agent (Xu et al. 2019). To synthesize DAR, DMAIII was chemically conjugated with GSH to prevent its oxidization and increase stability in intracellular environment. DAR’s development is based on the strong toxicity of DMAIII. DAR has been evaluated against many different types of cancers and made it to phase II clinical trials (Wu et al. 2010; Hosein et al. 2012). These facts also reflect the appreciable contribution of AS3MT on increasing the anticancer effect of ATO through catalyzing generation of methylated trivalent metabolites.
Dose-response for assessing the cancer risk of inorganic arsenic in drinking water: the scientific basis for use of a threshold approach
Published in Critical Reviews in Toxicology, 2019
Joyce S. Tsuji, Ellen T. Chang, P. Robinan Gentry, Harvey J. Clewell, Paolo Boffetta, Samuel M. Cohen
The Efremenko et al. (2015) study was conducted as a complementary experiment to the Yager et al. (2013) study; the concentrations used in Efremenko et al. (2015) were the same as those in the human urothelial study (Yager et al. 2013). In addition to the arsenical trivalent mixture exposures, exposures to arsenic trioxide were also performed to compare responses for exposures of lung epithelial cells at the apical membrane from inhalation and exposures at the basal membrane from oral exposure. Similar analyses of the gene expression results were conducted as those in the Yager et al. (2013) study for urothelial cells, focusing on those genes expressed most in common among cells from three individuals. Benchmark dose analysis confirmed similarity in the concentration-response relationship between lung and bladder epithelial cells, with comparable benchmark dose estimates across tissue types for the trivalent mixtures, as well as comparable benchmark dose estimates following exposures of lung cells to either the trivalent mixture or arsenic trioxide. The consistency of the genomic responses in human primary cells from two different tissues (bladder and lung) and for two different trivalent arsenic exposures (arsenite and its trivalent metabolites vs. arsenite alone) supports the usefulness of this data to characterize the dose response for the cellular effects of trivalent inorganic arsenic.