Inorganic Chemical Pollutants
William J. Rea, Kalpana D. Patel in Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
Arsenic competes with selenium, and selenium is known to reduce arsenic toxicity. Arsenicals were used as medicine, and arsenic acid and nitrophenol forms of arsenic are used as growth enhancers and for feed efficiency of pigs and poultry.789–791 Arsenic is excreted, mainly through the urine, in its inorganic form and methylated derivatives. Because hair, nail, and liver show high levels of arsenic, they are considered excretory routes. Chronic toxicity is characterized by weakness, prostration, aching muscles, gastrointestinal upset, peripheral neuropathy (increased nerve conduction), and changes in pigmentation of the nails and skin. Arsenic antagonizes thyroid function with resultant goiter. It is a carcinogen or cocarcinogen.791 Certainly, excessive arsenic exposure will exacerbate chemical sensitivity.
The Esophagus
E. George Elias in CRC Handbook of Surgical Oncology, 2020
Alcohol and tobacco constitute the major risk factors in the U.S. and western Europe. Of the patients diagnosed with esophageal carcinoma, 80 to 90% have a history of high consumption of alcohol and tobacco. Some reports have suggested that there is a higher incidence of esophageal cancers in those who consume large amounts of whiskey or liquor when compared to those who drink beer or wine.2 Cigarette or cigar smoking, and even pipe smoking, increases the risk in the population especially if they have a high alcohol consumption. It is the general feeling that alcohol may act as a cocarcinogen or a promoter to other carcinogens. Alcohol may also play a mechanical role by affecting the permeability of the esophageal mucosa for other carcinogens to penetrate deep in the mucosa towards the target cells initiating carcinomas. In addition, high consumption of alcohol, particularly in association with liver disease, has been shown to be immunosuppressive. This may further add to the promoting effect of alcohol.
Liver Diseases
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Liver cancer is fairly common and associated with cirrhosis in alcoholics.103,278 Hepatocellular carcinoma also occurs in noncirrhotic alcoholics. Alcohol is considered as a cocarcinogen. In addition to the direct effects of ethanol, indirect consequences of malnutrition are associated with carcinogenesis. These include deficient intake of vitamins, riboflavin, pyridoxine, pantothenic acid, and essential trace metals. The effect of malnutrition in promoting cancer is very common. It is associated with oral, head, and neck cancer.314,387,606 In these cases, deficiencies are reported in iron, zinc, thiamin, riboflavin, ascorbic acid, and vitamin A. Alcohol may cause malnutrition and influence the absorption, distribution, metabolism, storage, and elimination of various essential nutrients.
Cell cycle dysregulation on prenatal and postnatal arsenic exposure in skin of Wistar rat neonates
Published in Xenobiotica, 2023
Navneet Kumar, Astha Mathur, Suresh Kumar Bunker, Placheril J. John
Arsenic is a transplacental carcinogen, thus prenatal arsenic exposure causes serious health impacts including cancer and other diseases (Rager et al. 2014; Liu et al. 2020). Several epidemiological and laboratory studies indicate that early life exposure to arsenic is a key factor in its detrimental consequences. These data are significant considering a general lack of cancer causing response by arsenic in rodent models (Rossman et al. 2001; Burns et al. 2004; Garry et al. 2015). A series of studies conducted by Waalkes group suggests that arsenic upon prenatal exposure can act as a complete carcinogen in rodents (Waalkes et al. 2003, 2004a, 2004b, 2004c). Interestingly, to adult mice similar doses were comparatively tolerable and were completely carcinogenic to them only in the presence of a cocarcinogen, confirming that early developmental period is specifically sensitive to arsenic (Waalkes et al. 2000, 2007). These studies show similar results as were obtained in ecological studies associated with arsenic induced carcinogenesis and use several strains of wild type mice, providing a direct indication that prenatal arsenic exposure alone can elevate the risk of cancer in exposed offspring (Farzan et al. 2013). Despite all these compelling studies, still it is not possible to conclude that in-utero only exposure of arsenic to humans would lead to tumorigenesis in later life, hence, more research in this direction is required (Garry et al. 2015). Thus, in the current study we evaluated the toxic effects of arsenic exposure during prenatal as well as post natal period on epidermal keratinocytes of Wistar rat neonates.
Medicinal plants in mitigating electromagnetic radiation-induced neuronal damage: a concise review
Published in Electromagnetic Biology and Medicine, 2022
Shamprasad Varija Raghu, Avinash Kundadka Kudva, Golgodu Krishnamurthy Rajanikant, Manjeshwar Shrinath Baliga
Additionally, RFR has co-carcinogenic effects (Soffritti and Giuliani 2019; Tillmann et al. 2010). Tillmann and colleagues (2010) reported in one of the first studies that combined exposure of embryo-fetus to ethylnitrosourea (carcinogen) and to 4.8 or 48 W/m2 of universal mobile telecommunications system (UMTS) for up to 24 months increased the incidence, multiplicity, and the number of metastasizing tumors, clearly indicating the co-carcinogenic effect of lifelong UMTS exposure (Tillmann et al. 2010). Lifelong exposure to Sinusoidal-50 Hz magnetic field (S-50 Hz MF) combined with acute exposure to gamma radiation or chronic administration of formaldehyde significantly increased the incidence of malignant tumours in both males and females when compared to sinusoidal-50 Hz magnetic field, gamma radiation, or formaldehyde alone (Soffritti and Giuliani 2019). Furthermore, exposure to 1.8 GHz of mobile phone radio base station either alone or in combination with acute gamma radiation causes a significant increase in the incidence of heart malignant schwannoma in males (Soffritti and Giuliani 2019). All of these observations collectively indicate that EMR may act as a co-carcinogen/enhancer/promoter of other chemicals, physical and biological carcinogens, and should be scientifically validated.
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