General toxicity

Health Hazards Information - Recommended Personal Protective Equipment None needed Symptoms Following Exposure No toxicity General Treatment for Exposure None needed Toxicity by Inhalation (Threshold limit Value) Not pertinent Short-Term Exposure Limits Not pertinent Toxicity by Ingestion None Late Toxicity None Vapor (Gas) Irritant Characteristics Not pertinent liquid or Solid Irritant Characteristics None Odor Threshold Not pertinent. 

Acetaminophen may worsen kidney function and increase blood pressure.1516 Nevertheless, acetaminophen remains the preferred analgesic for mild to moderate pain in patients with hypertension or kidney disease owing to the greater risks associated with NSAID use.17 Monitoring specifically for these toxicities generally is unnecessary. 

The manufacturer s own toxicologists will begin testing with a determination of acute toxicity. If it appears the chemical is not unduly toxic, general subchronic and chronic, and a variety of specialized tests will be planned. A number of design issues need to be considered. 

Characteristics of toxicity for a number of metals are presented in Table 7.5. While the exact tissue and molecular site of the toxic action of each metal is different, toxicity generally results from interaction of the metal with specific functional groups on macromolecules in the cell. These groups include sulfhydryl, carboxyl, amino, phosphoryl, and phenolic moieties. Interactions of such groups with metals can lead to disruption of enzyme activities and transport processes and eventually... 

Mild nephrotoxicity occurs in 25% of renal transplant patients, 38% of cardiac transplant patients, and 37% of liver transplant patients, generally 2-3 mo after transplantation (more severe toxicity generally occurs soon after transplantation). Hepatotoxicity occurs in 4% of renal transplant patients, 7% of cardiac transplant patients, and 4% of liver transplant patients, generally within the first mo after transplantation. Both toxicities usually respond to dosage reduction. 

Disease/pathological conditions. Disposition of chemicals is potentially altered by disease and hence toxicity. Generalization, however, is difficult as the effects are unpredictable. Thus liver disease may decrease metabolism, but this depends on type of disease and particular pathway of metabolism. Disease in one organ may affect the response of another, for example, chronic renal disease decreases hepatic cytochrome P-450. 

Impurities Easy to qualify toxicity testing may be required Difficult to qualify toxicity generally not an issue but may affect immunogenicity... 

Species specificity Species independent preclinical assessments for generally toxicity generally performed in one rodent (generally rat) and one nonrodent (generally dog) Species specific nonhuman primates often the only relevant species or design of specific animal models... 

Mechanism of Toxicity (general background interspecies and individual variabibties, especially as they pertain to AEGL derivation)... 

SAFETY PROFILE Salts of iodic acid. Variable toxicity. Generally eye, skin, and mucous membrane irritants. Powerful oxidizers. Similar to bromates and chlorates. Contamination of iodates with organic matter may produce explosive mixtures. Iodates are used in bread as an improving agent for the dough. When heated to decomposition they emit toxic fumes of I . See also specific compounds. 

Tienilic acid (ticrynafen) is a uricosuric diuretic that was initially marketed in the United States in 1979. It was withdrawn a few months later because of hepatitis-like adverse reactions that developed in approximately 1 of 1000 patients treated with the drug but were fatal in 10% of the patients who developed overt jaundice (48). The onset of overt toxicity generally occurred 1 to 6 months after starting therapy with... 

Coprine (506) was isolated from the inky cap mushroom Coprinus atramentarius 416,613 mushroom proved to be non-toxic generally, but it caused severe illness when taken together with alcohol. It was found that semiaminal 4, the product of hydrolysis of 506, was the active substance inhibiting acetaldehyde dehydrogenase 61 -624... 

Definitive information regarding the acute toxicity of di-N-octylphthalate is not available. An estimated lethal oral dose in humans is between 0.5 and 15gkg, or between 1 oz equivalent to 29.6 mis and 1 qt equivalent to 0.96 liters in a 70 kg adult. Compounds that are structurally similar to di-N-oct-ylphthalate are known to irritate mucous membranes resulting in irritation of the eyes, throat, and upper respiratory tract passages and in gastrointestinal disturbances. There is evidence that some phthalates, such as di-s-octylphthalate, may be reproductive and developmental toxicants. Generally, the acute oral toxicity of alkylphthalates is low and the acute oral toxicity decreases as molecular weight increases. 

Mild toxicity generally results from oral or dermal exposure. Triadimefon may cause dermal sensitization and moderate irritation of the eyes. 

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