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Mirex toxicity

Yarbrough, J.D., J.E. Chambers, J.M. Grimley, E.G. Alley, M.M. Fang, J.T. Morrow, B.C. Ward, and J.D. Conroy. 1981. Comparative study of 8-monohydromirex and mirex toxicity in male rats. Toxicol. Appl. Pharmacol. 58 105-117. [Pg.1158]

Yarbrough JD, Chambers JE, Grimley JM, et al. 1981. Comparative study of 8-monohydromirex and mirex toxicity in male rats. Toxicol Appl Pharmacol 58 105-117. [Pg.293]

Tvede KG, Loft S, Poulsen HE, et al. 1989. Methyl parathion toxicity in rats is changed by pretreatment with the pesticides chlordecone, mirex and linuron. Arch Toxicol Suppl 13 446-447. [Pg.234]

The insecticide heptachlor oxidizes in the soil, and becomes a more toxic epoxide, capable of remaining for a long time. The insecticide aldrin transforms in the soil into dieldrin, maintaining its toxicity [15, 30]. Mirex (FDso=300-600 mg/kg), used to fight ants, just like kelevan (FDS0=255-325 mg/kg), used to fight the Colorado beetle, transform in the soil into the more toxic chlordekon (FD50 decreases to 95-140 mg/kg) [30]. [Pg.38]

Acute oral toxicity of mirex to birds and mammals... [Pg.28]

Acute oral toxicity of mirex to warm-blooded organisms was low, except for rats and mice, which died 60 to 90 days after treatment with 6 to 10 mg mirex/kg body weight (Table 21.1). Birds were comparatively resistant. The red-winged blackbird (Agelaius phoeniceus) was unaffected at 100 mg mirex/kg body weight, although it was considered the most sensitive of 68 species of birds tested with 998 chemicals for acute oral toxicity, repellency, and hazard potential (Schafer et al. 1983). [Pg.1136]

Table 21.1 Acute Oral Toxicity of Mirex to Birds and Mammals... Table 21.1 Acute Oral Toxicity of Mirex to Birds and Mammals...
Table 21.2 Dietary Toxicity of Mirex to Vertebrate Organisms... [Pg.1137]

The maximum acceptable toxicant concentration (MATC) values calculated for mirex and various freshwater species were ... [Pg.1137]

Mirex has considerable potential for chronic toxicity because it is only partly metabolized, is eliminated very slowly, and is accumulated in the fat, liver, and brain. The most common effects observed in small laboratory mammals fed mirex included weight loss, enlarged livers, altered liver enzyme metabolism, and reproductive failure. Mirex reportedly crossed placental membranes and accumulated in fetal tissues. Among the progeny of mirex-treated mammals, developmental abnormalities included cataracts, heart defects, scoliosis, and cleft palates (NAS 1978 Blus 1995). [Pg.1138]

Gaines, T.B. and R.D. Kimbrough. 1969. The oral toxicity of mirex in adult and suckling rats. Toxicol. Appl. Pharmacol. 14 631-632. [Pg.1154]

Ludke, J.L., M.T. Finley, and C. Lusk. 1971. Toxicity of mirex to crayfish, Procambarus blandingi. Bull. Environ. Contam. Toxicol. 6 89-96. [Pg.1156]

Lue, K.Y. and A. de la Cruz. 1978. Mirex incorporation in the environment toxicity in Hydra. Bull. Environ. Contam. Toxicol. 19 412-416. [Pg.1156]

Commercial PCB mixtures frequently contain impurities that may contribute to the 2,3,7,8-TCDD toxic equivalency factor. These impurities may include other PCBs, dioxins, dibenzofurans, naphthalenes, diphenyl ethers and toluenes, phenoxy and biphenyl anisoles, xanthenes, xanthones, anthracenes, and fluorenes (Jones etal. 1993). PCB concentrations in avian tissues sometimes correlate positively with DDE concentrations (Mora et al. 1993). Eggs of peregrine falcons (Falco peregrinus) from California, for example, contained measurable quantities of various organochlorine compounds, including dioxins, dibenzofurans, mirex, hexachlorobenzene, and / ,//-DDE at 7.1 to 26.0 mg/kg FW PCB 126 accounted for 83% of the 2,3,7,8-TCDD equivalents, but its interaction with other detectable organochlorine compounds is largely unknown (Jarman et al. 1993). [Pg.1286]

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and other interested individuals and groups with an overall perspective of the toxicology of mirex and chlordecone. It contains descriptions and evaluations of toxicological studies and epidemiological investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. [Pg.18]

Mirex and chlordecone are structurally similar insecticides. The only structural difference is that mirex has two bridgehead chlorine atoms where chlordecone has a carbonyl oxygen atom. As suggested by this similarity in structure, these two chemicals produce similar toxicities in a number of organs. Flowever, several aspects of the toxicity of mirex are distinctly different from those of chlordecone, and vice versa. Because the toxicity profiles of mirex and chlordecone differ significantly, each chemical will be discussed separately below. [Pg.18]

No studies were located regarding hepatic toxicity in animals following inhalation exposure to mirex or chlordecone. [Pg.22]

In addition to the adaptive effects described above, marked hepatic toxicity has been observed after acute-duration oral exposure of animals to mirex. The primary form of hepatotoxicity observed in... [Pg.82]


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See also in sourсe #XX -- [ Pg.113 ]




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