Asbestos, carcinogenicity

Nickel may be a factor in asbestos carcinogenicity. The presence of chromium and manganese in asbestos fibers may enhance the carcinogenicity of nickel (USEPA 1980), but this relation needs to be verified. Barium-nickel mixtures inhibit calcium uptake in rats, resulting in reduced growth (WHO 1991). Pretreatment of animals with cadmium enhanced the toxicity of nickel to the kidneys and liver (USPHS 1993). Simultaneous exposure to nickel and cadmium — an industrial situation... 

Shabad EM, Pylev LN, Krivosheeva LV, et al. 1974. Experimental studies on asbestos carcinogenicity. J Natl Cancer Inst 52 1175-1180. 

Voytek P, Anver M, Thorslund T, et al. 1990. Mechanism of asbestos carcinogenicity. J Am Coll... 

Wagner JC. 1983. The risk assessment of asbestos carcinogenicity in the normal population. Animal to human correlations. VDI-Berichte Nr 475 305-308. 

Walker C, Everitt J, Barrett JC. 1992b. Possible cellular and molecular mechanisms for asbestos carcinogenicity. Am J Ind Med 21 253-273. 

Other fibrous and porous materials used for sound-absorbing treatments include wood, cellulose, and metal fibers foamed gypsum or Pordand cement combined with other materials and sintered metals. Wood fibers can be combined with binders and dame-retardent chemicals. Metal fibers and sintered metals can be manufactured with finely controlled physical properties. They usually are made for appHcations involving severe chemical or physical environments, although some sintered metal materials have found their way into architectural appHcations. Prior to concerns regarding its carcinogenic properties, asbestos fiber had been used extensively in spray-on acoustical treatments. 

A further consensus developed within the scientific community regarding the relative carcinogenicity of the different types of asbestos fibers. There is strong evidence that the genotoxic and carcinogenic potentials of asbestos fibers are not identical in particular mesothelial cancer is mostiy, if not exclusively, associated with amphibole fibers (43). 

Carcinogens Cancer-producing agents Skin Respiratory Bladder/urinary tract Liver Nasal Bone marrow Coal tar pitch dust crude anthracene dust mineral oil mist arsenic. Asbestos polycyclic aromatic hydrocarbons nickel ore arsenic bis-(chloromethyl) ether mustard gas. p-naphthylamine benzidine 4-am i nodi pheny lam ine. Vinyl chloride monomer. Mustard gas nickel ore. Benzene. 

Carotenoid oxidation products are also supposed to have detrimental effects in vivo. As mentioned earlier, they are suspected to be involved in the adverse effects of high doses of 3-carotene supplementation in smokers and asbestos workers (CARET and ATBC studies) and in smoke-exposed ferrets. The mechanisms potentially involved have been investigated in vitro. P-Apo-8 -carotenal, an eccennic cleavage oxidation product of P-carotene, was shown to be a strong inducer of CYPlAl in rats, whereas P-carotene was not active. Cytochrome P450 (CYP 450) enzymes thus induced could enhance the activation of carcinogens and the destruction of retinoic acid. ... 

Asbestos Reinforcing. Asbestos has been proposed as a reinforcing component [583]. However, asbestos is believed to be a carcinogen. 

Five recent studies investigated the potential toxic risk if CNTs reach the pleural cavity after inhalation exposure [6,88-91]. Three of these in vivo studies revealed that if CNTs are delivered to the abdominal cavity of mice or rats, they could induce a serious potential carcinogenic risk resembling that associated with exposure to certain asbestos fibers [6,88,89]. The other two studies described nontoxic responses [90,91]. 

Cigarette smoking is responsible for about 80% of lung cancer cases. Other risk factors include exposure to respiratory carcinogens (e.g., asbestos, benzene), genetic risk factors, and history of other lung diseases (e.g., tuberculosis, pulmonary fibrosis). 

Asbestos asbestos cement building materials like pipe lagging, ceiling tiles. carcinogenic asbestosis (a scarring of ling tissues). 

Three additional points need to be mentioned. First, if the observed cancer dose-response relationship derives from epidemiology data, the observed risks are relative, not absolute (the latter are usually reserved for data from animal experiments). Thus, for human carcinogens with reliable dose-response information (e.g., as exists for benzene, arsenic, chromium (+6), asbestos, and several other carcinogens), it is necessary to convert relative risks to absolute risks before extrapolating to low dose. 

Think how many carcinogens are household names asbestos, cigarette smoke (a mixture of several thousand chemical compounds), DES, dioxin, saccharin, arsenic, PCBs, radon, EDB, Alar. Hundreds more of these substances, some very obscure, are known to the scientific and medical community, and many of these are scattered throughout the land at thousands of hazardous waste sites similar to Love Canal. People are exposed to these dreadful substances through the air they breathe, the water they drink and bathe in, and the foods they eat. Chemicals can also produce many other types of health damage, some very serious, such as birth defects and damage to our nervous and immune systems. 

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