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Toxicity animal

Daylight fluorescent pigments (qv) are considered to be nontoxic. Since they are combinations of polymers and dyestuffs, the combined effect of the ingredients must be taken into account when considering the net toxic effect of these materials. Table 5 gives results of laboratory animal toxicity tests of standard modified melamine—formaldehyde-type pigments, the Day-Glo A Series, and the products recommended for plastic mol ding, Day-Glo Z-series. [Pg.304]

Table 5. Results of Laboratory Animal Toxicity Tests... Table 5. Results of Laboratory Animal Toxicity Tests...
Toxicological Information. The toxicity of the higher olefins is considered to be virtually the same as that of the homologous paraffin compounds. Based on this analogy, the suggested maximum allowable concentration in air is 500 ppm. Animal toxicity studies for hexene, octene, decene, and dodecene have shown Httle or no toxic effect except under severe inhalation conditions. The inhalation LD q for 1-hexene is 33,400 ppm for these olefins both LD q (oral) and LD q (dermal) are >10 g/kg. [Pg.442]

Safety is assessed by subjecting the antioxidant to a series of animal toxicity tests, eg, oral, inhalation, eye, and skin tests. Mutagenicity tests are also carried out to determine possible or potential carcinogenicity. Stabilizers are being granulated and Hquid products are receiving greater acceptance to minimize the inhalation of dust and to improve flow characteristics. [Pg.234]

AH four butanols are thought to have a generaHy low order of human toxicity (32). However, large dosages of the butanols generaHy serve as central nervous system depressants and mucous membrane irritants. Animal toxicity and irritancy data (32) are given in Table 4. [Pg.358]

Table 4.. Animal Toxicity and Irritancy Data for Butanols... Table 4.. Animal Toxicity and Irritancy Data for Butanols...
Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... [Pg.247]

Absorption, Distribution, Metabolism, and Excretion. There are no data available on the absorption, distribution, metabolism, or excretion of diisopropyl methylphosphonate in humans. Limited animal data suggest that diisopropyl methylphosphonate is absorbed following oral and dermal exposure. Fat tissues do not appear to concentrate diisopropyl methylphosphonate or its metabolites to any significant extent. Nearly complete metabolism of diisopropyl methylphosphonate can be inferred based on the identification and quantification of its urinary metabolites however, at high doses the metabolism of diisopropyl methylphosphonate appears to be saturated. Animal studies have indicated that the urine is the principal excretory route for removal of diisopropyl methylphosphonate after oral and dermal administration. Because in most of the animal toxicity studies administration of diisopropyl methylphosphonate is in food, a pharmacokinetic study with the compound in food would be especially useful. It could help determine if the metabolism of diisopropyl methylphosphonate becomes saturated when given in the diet and if the levels of saturation are similar to those that result in significant adverse effects. [Pg.108]

Schimmel, S.C., J.M. Patrick, Jr., and L.F. Fass. 1978. Effects of sodium pentachlorophenate on several estuarine animals toxicity, uptake, and depuration. Pages 147-155 in K.R. Rao (ed.). Pentachlorophenol Chemistry, Pharmacology, and Environmental Toxicology. Plenum Press, New York. [Pg.1233]

Among all chlorophenols, 2,4,6-trichlorophenol (TCP) and pentachlorophenol (PCP) are listed as priority pollutants by the US Environmental Protection Agency (EPA) (IRIS electronic database) and the EU [256]. In particular, PCP has been classified as a B2 probable carcinogen for humans from animal toxicity studies and human clinical data. [Pg.161]

See also Aminal growth studies Animal testing, cosmetics, 7 825 Animal toxicity, lindane and... [Pg.58]

The AEGL-2 value is supported by animal toxicity data, which produce a higher value. The threshold for narcosis for several animal species is approximately 200,000 ppm (Collins 1984 Silber and Kennedy 1979a). Adjustment by interspecies and intraspecies UFs of 3 each (for a total of 10) results in an AEGL-2 value of 20,000 ppm. [Pg.166]

TABLE 1.2. Synopsis of General Guidelines for Animal Toxicity Studies (U.S. FDA)... [Pg.8]

Lumley, C. E., and Walker, S. E. (1992). An international appraisal of the minimum duration of chronic animal toxicity studies. Hum. Exp. Toxicology, 11 155-162. [Pg.97]

One major purpose of preclinical (animal) toxicity studies of a potential new drug is to identify the toxic effects which most commonly occur at doses nearest to those to be used in humans. These observations serve to help ensure that care is taken to detect any such effects in humans. Additionally, a broad range of other indicators of adverse drug action may be identified to ensure that their occurrence is looked for. These are also commonly called safety parameters. [Pg.798]


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Acute toxicity animal studies

Acute toxicity tests, higher animals

Animal Models of Disease for Future Toxicity Predictions

Animal Toxicity Test

Animal models lead toxicity

Animal models toxicity studies

Animal studies aquatic toxicity

Animal studies cyanide toxicity

Animal studies nerve agents toxicity

Animal studies oximes toxicity

Animal toxic data

Animal toxicity data

Animal toxicity data extrapolation

Animals chronic toxicity studies

Animals vomitoxin toxicity

Control animals, repeat-dose toxicity testing

Developmental toxicity animal tests

Essentiality and Toxicity for Animals

Experimental Animal Toxicity Data

Extrapolation of Toxicity Values from Animals to Humans

FIGURE 4.4 Species sensitivity distributions for chronic toxicity of atrazine to plants and animals

Factors Determining the Toxicity of Organic Pollutants to Animals and Plants

Gastrointestinal Toxicity Reasons for Poor Translation from Animal to Human

Guidelines for animal toxicity studies

Health animal toxicity

Hepatic Toxicity Reasons for Poor Translation from Animal to Human

Higher animals, toxicity tests using

Human animal toxicity

Human epidemiology, animal toxicity

Ocular toxicity animal studies

Ocular toxicity animals

Potential for vitamin E toxicity in meat-producing animals

Pyrethroids toxicity animals

Radiation toxicity, animals

Renal Toxicity Reasons for Poor Translation from Animal to Human

Respiratory Toxicity Reasons for Adequate Translation from Animal to Human

Subacute toxicity from animals

Tannins animal toxicity

Target animal safety toxicity testing

Test Guidelines for Animal Toxicity Studies

The Cornerstone of Risk Assessment Toxicity Testing in Animals

Toxic Effects on Animals

Toxicity animal, study

Toxicity effects on animals

Toxicity in Animals and Man

Toxicity studies animal numbers

Toxicity test designs control animals

Toxicity to Animals

Toxicity to Animals and Humans

Toxicity to Soil-Dwelling Animals

Toxicity transgenic animal studies

Toxicity, evaluation animal

Toxicity, mechanisms animal data

Transgenic animals toxicity testing

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