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Risk Characterization
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Chlorine has been a commodity chemical for over 100 years. Most often, chlorine is produced by the chlor-alkali process by electrolytic decomposition of brine or seawater. One of the past uses of chlorine was the production of pesticides, specifically the pesticide toxaphene, first introduced in 1945. Toxaphene was widely used as an insecticide on cotton, soybeans, and corn.47
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Toxaphene: For several years, toxaphene insecticide ranked first in quantity used in the United States, with an estimated annual production of 75–95 million pounds.127 The exact formula is unknown, but, empirically, it is listed as C10H10C118. It appears to be a cytochrome P-450 stimulator and to be oxidized and gluconated. Its presence in the Fort Worth Rolling Hills water supply is discussed elsewhere. Toxaphens has been shown to cause liver tumors in mice and is mutagenic to salmonella (Tables 7.14 through 7.17, Figures 7.10 through 7.12).
Halogenated insecticides
Published in Bev-Lorraine True, Robert H. Dreisbach, Dreisbach’s HANDBOOK of POISONING, 2001
Bev-Lorraine True, Robert H. Dreisbach
Toxaphene consists of chlorinated terpenes, with chlorinated camphene predominating. It is stable for 1–6 months after application and is fat-soluble and water-insoluble. Toxaphene is available for insecticidal use in the form of wettable powders, dusts, emulsion concentrates, and concentrated solutions in oil. The fatal dose of toxaphene for an adult is estimated to be around 2 g. Several members of one family were non-fatally poisoned after eating greens contaminated with toxaphene to the extent of 3 g/kg of greens. The maximum dose ingested by one person was thought to be approximately 1 g. Several fatalities in children have followed ingestion of larger but undetermined amounts. The tolerance of toxaphene in foods is 7 ppm. At least three fatalities from toxaphene ingestion have been reported. The exposure limit for toxaphene is 0.5 mg/m3.
Veterinary utility of dried blood spots for detailed analysis of chlorinated pesticides and polychlorinated biphenyls by gas chromatography tandem mass spectrometry
Published in Toxicology Mechanisms and Methods, 2020
Andreas F. Lehner, Lauren Stensen, Alan Zimmerman, Adam Bush, John Buchweitz
Organochlorine pesticides such as aldrin, dieldrin, DDT and its derivatives (4,4′-dichlorodiphenyldichloroethane [4,4′-DDD] and 4,4′-dichlorodiphenyldichloroethylene [4,4′-DDE]), lindane, hexachlorobenzene, and polychlorinated biphenyls (PCBs) are of particular concern due to their highly bioaccumulative properties and toxicities (Chopra, et al 2011). These chemicals persist in nature, biomagnify in the food web, and impose toxic effects in marine and other organisms (El-Shahawi et al. 2010). The Stockholm Convention on Persistent Organic Pollutants (POPs) has issued recommendations aimed at restricting and eliminating highly dangerous, long-lasting chemicals, and of 21 listed chemicals, 14 are chlorinated pesticides (aldrin, chlordane, chlordecone, DDT, dieldrin, endrin, heptachlor, hexachlorobenzene, lindane and its alpha- and beta-isomers, mirex, pentachlorobenzene and toxaphene), with the remainder including PCBs, polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, polybrominated diphenyl ethers (PBDEs), perfluorooctane sulfonic acid (PFOS) and perfluorooctane sulfonyl fluoride (PFOS-F) (Stockholm Convention Factsheet 2011).
Porcine interleukin-6 enhances the expression of CYP2C33 through a constitutive androstane receptor/retinoid X receptor-mediated pathway
Published in Xenobiotica, 2019
Lixia Xie, Yucheng He, Xiaoqiao Zhou, Xiaowen Li, Xiue Jin, Xiliang Wang, Deshi Shi
NRs are a large protein family of transcription factors that act by binding to the DNA sequence of the target gene promoter (Mo & He, 2014; Xiao et al., 2013). The CAR xenobiotic receptor in the liver acts as a drug transporter to regulate the expression of phases I and II drug-metabolizing enzymes (Yan & Xie, 2016). TCPOBOP (3,3′,5,5′-tetrachloro-1,4-bis(pyridyloxy)benzene)-activated CAR also promotes liver growth by upregulating the expression of c-Myc, which drives proliferating cells into the S phase by increasing the expression of glucose transporter and glycolytic genes (Yarushkin et al., 2016), as well as that mitochondrial pyruvate-metabolizing genes, and by downregulating the expression of gluconeogenic genes. In addition, the expression of Pkm2, which modulates glucose metabolism and cell proliferation, is upregulated by CAR activation. In mice, CAR plays an important role in tumour development induced by phenobarbital, toxaphene and imazalil in the liver (Wang et al., 2017; Yamamoto et al., 2004).
Critical evaluation of the human relevance of the mode of action for rodent liver tumor formation by activators of the constitutive androstane receptor (CAR)
Published in Critical Reviews in Toxicology, 2021
Tomoya Yamada, Samuel M. Cohen, Brian G. Lake
While PB has been shown to produce liver tumors in a number of mouse strains, two studies have demonstrated that PB did not produce liver tumors in the Syrian hamster (Diwan et al. 1986; Stenbäck et al. 1986). In addition, unlike the mouse and rat, PB has been shown not to promote liver tumors in the Syrian hamster after initiation with DEN or other genotoxic carcinogens (Tanaka et al. 1987). While PB is known to stimulate RDS in cultured mouse and rat hepatocytes, PB has been shown not to stimulate RDS in cultured Syrian hamster and guinea pig hepatocytes (James and Roberts 1996). Like PB, chronic studies with four other CAR activators, namely 1,1′-(2,2,2-trichloroethylidene)-bis[4-chlorobenzene] (DDT) (Graillot et al. 1975; Cabral et al. 1982; Rossi et al. 1983), dieldrin (Stevenson et al. 1999; Wang et al. 2020), toxaphene (Goodman et al. 2000), and diazepam (IARC 1996), performed in the Syrian hamster did not result in liver tumor formation. However, one metabolite of DDT, namely 1,1′-(2,2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE), was found to be weakly carcinogenic to the liver in Syrian golden hamsters whereas DDT was negative in the same study (Rossi et al. 1983). A chronic study with DDT was also performed in primates (24 animals comprising 13 Cynomolgus and 11 Rhesus monkeys) where only one Cynomolgus monkey developed hepatocellular carcinoma (HCC) after an observation period of almost 20 years and total dose of 292 g DDT, with no tumors being detected in the control group of 17 monkeys, comprising nine Cynomolgus and eight Rhesus monkeys (Takayama et al. 1999). However, as noted by the authors, it is unclear whether the single case of HCC with such long latent period was actually associated with DDT treatment.