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Liver damage

The toxicity of chloronaphthalenes requires that special attention and caution be used during their manufacture and use acne is the most common result of excessive skin exposure to them and the most frequendy affected areas are the face and neck (16). Liver damage has occurred in workers who have been exposed repeatedly to vapors, particulady to those of penta- and hexachloronaphthalene [1335-87-1] (17,18). Uses for the chlorinated naphthalenes include solvents, gauge and instmment duids, capacitor impregnants, components in electric insulating compounds, and electroplating stop-off compounds. [Pg.483]

A comprehensive study of the tolerance of laboratory animals to vapors of 2-nitropropane was reported in 1952 (100). In a study pubHshed in 1979, rabbits and rats survived exposure to nitromethane for six months at 750 and 100 ppm, respectively, with no unexpected findings (101). Similarly, no compound-related effects were found for rabbits exposed to 2-nitropropane at 200 ppm or for rabbits or rats exposed at 27 ppm. Liver damage was extensive in male rats exposed at 207 ppm for six months, and hepatocellular carcinomas were observed. Subsequendy, the International Agency for Research on Cancer (lARC) found that there is "sufficient evidence" to conclude that 2-nitropropane causes cancer in rats but that epidemiologic data are inadequate to reinforce the conclusion in humans (102). The National Toxicology Program also concluded that it "may reasonably be anticipated to be a carcinogen" (103). [Pg.103]

Toxicity. Many /V-nitrosamines are toxic to animals and cells in culture (4,6—8,88). /V-Nitrosodimethy1amine [62-75-9] (NDMA) is known to be acutely toxic to the Hver in humans, and exposure can result in death (89). Liver damage, diffuse bleeding, edema, and inflammation are toxic effects observed in humans as a result of acute and subacute exposure to NDMA. These effects closely resemble those observed in animals dosed with NDMA (89,90). [Pg.109]

A second problem concerns delimiting the mechanisms of action which should be included in the definition, to exclude effects which are a secondary consequence of overt toxicity in other body systems. For example, disruption to the endocrine system caused by general metabolic disturbance, such as in severe liver damage, should not be grounds for calling a chemical an ED. [Pg.5]

A. Hepatotoxiiis Chemicals which produce liver damage ... [Pg.182]

Class and Definition Hepatotoxins - produce hepatic (liver) damage... [Pg.549]

Since no specific antidotes are known, symptomatic therapy must be accompanied by complete rest. Toxicity by Inhalation (ThresholdUmit Value)-. 0.5 mg/m Short-Term Exposure Limits 2 mg/m for 30 min Toxicity by Ingestion oral LD, = 283 mg/kg (rat) Late Toxicity Possible liver damage loss of appetite or weight. Vapor (Gas) Irritant Characteristics No data Liquid or Solid Irritant Characteristics No data Odor Threshold No data. [Pg.83]

Grade 0, LDjq > 15 g/kg Late Toxicity Liver damage in rats (from addition of oil to diet) Vapor (Gas) Irritant Characteristics Data not available Liquid or Solid Irritant Characteristics Data not available Odor Threshold Data not available. [Pg.292]

Heptachlor zero 0.0004 Liver damage risk of cancer Residue of banned termiticide... [Pg.21]

Heptachlor epoxide zero 0.0002 Liver damage risk of cancer Breakdown of hepatachlor... [Pg.21]

Acute Liver Damage Several compounds (e.g., dimethyl iiitrosoamine, carbon tetrachloride, and thioacetamide) cause necrosis of hepatocytes by inhibiting pro tein syndiesis at the translational level, i.e., by inhibiting the addition of new amino adds into the protein chain being sjTithetized. This is not, however, the only mechanism. Ethioiiine is a compound which inhibits protein synthesis bur doe not induce... [Pg.298]

TABLE 5.13 Examples of Drugs that Induce Intrahepatic Cholestasis or Liver Damage Resembling That Induced by Viral Hepatitis... [Pg.299]

Ulll TABLE S. 14 Chemical Compounds that Induce Chronic Liver Damage... [Pg.300]

TCDD is the most potent inducer of chloracne. This has been well known since the accident in Seveso, Italy, in 1976 in which large amounts of TCDD were distributed in the environment subsequent to an explosion in a factory that produced a chlorophenoxy herbicide, 2,4,5-T. TCDD is an impurity produced during the production of 2,4,5-T. The most common long-term effect of TCDD exposure was chloracne. Exposed individuals also suffered increased excretion of porphyrins, hyper-pigmentation, central nervous system effects, and liver damage and increased risk of cancer was a long-term consequence of the exposure. In addition to TCDD, polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans, and polychloronaphthalens cause chloracne as well as other effects typical of TCDD. 7i... [Pg.309]

A Mutant Protein That Folds Slowly Can Cause Emphysema and Liver Damage... [Pg.194]

The naproxen that you buy over the counter at your local pharmacy consists of a single enantiomer, which is an effective analgesic (pain killer). The other enantiomer is not a pain killer even worse, it can cause liver damage. [Pg.601]

Toxicity. Injection of aq Na perchlorate into rabbits caused no long term toxic effects. It behaved as a mild muscular poison, and large doses caused liver damage and diarrhea. Goldfish will live indefinitely in a 0.1% soln, but a 1% soln will cause asphyxia (Ref 4)... [Pg.645]


See other pages where Liver damage is mentioned: [Pg.199]    [Pg.312]    [Pg.110]    [Pg.110]    [Pg.111]    [Pg.139]    [Pg.4]    [Pg.80]    [Pg.81]    [Pg.91]    [Pg.124]    [Pg.142]    [Pg.143]    [Pg.186]    [Pg.194]    [Pg.286]    [Pg.288]    [Pg.288]    [Pg.367]    [Pg.391]    [Pg.397]    [Pg.397]    [Pg.398]    [Pg.298]    [Pg.299]    [Pg.300]    [Pg.304]    [Pg.334]    [Pg.194]    [Pg.323]    [Pg.582]    [Pg.874]    [Pg.1299]   
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