Casarett and doulls toxicology torrent download

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Ivermectin is used Mechanism of Action Early studies, with a variety of inverte- for a wide range of ecto- and endoparasites of domestic and wild brate species and model systems, resulted in a number of possible animals.

A structural representation of the macrocyclic lactone avermectin B1a , abamectin B1b , and the semisynthetic insecticide ivermectin showing the structural differences at positions 22 to 23 and 25 of the ring. Newer Chemical Insecticides However, care must be taken in interpreting such results, since in- terneuronal and neuromuscular junctions are known to differ con- With the development of insect resistance to various classes of siderably between species Gerschenfeld, The low water sol- chemical insecticides, new approaches to insect control are needed.

Shown in Fig. While there may be different species-specific avermectin and 3 the phenylpyrazoles. They possess brane resistance, and increasing conductance inward. Such bind- unique and selective mechanisms of action and perhaps point the ing sites appear to be distinct from those of other effector mole- way to future insecticide development.

To date, there have been no cules and involve GABA-insensitive chloride channels Arena et reports of toxicity in humans. Explaining the selective specificity of avermectins wide range of nematodes, arthropods, Nitromethylenes A search for new classes of insecticides led to insects but not tapeworms, flukes, and adult filaria must await the a study of various aromatic heterocycles containing a nitrometh- molecular study of the receptor proteins in these species.

In ylene substituent, only those containing a pyridine system being mammals, in the nematode Caenorhabditis elegans, and the house insecticidal Fig. The ni- fly, avermectins interact with the GABA-receptor complex, as has tromethylene heterocycle NMH insecticides are fast-acting neu- been shown by avermectin-induced changes in GABA receptor— rotoxicants, effective by both contact or oral ingestion; they are rel- directed ligands Deng and Casida, ; Arena et al.

Schroeder and Flattum, The compound fipronil Fig. Fipronil is a noncompetitive inhibitor of GABA- induced effects, the effects in neurons being an increase in rapid Cl D bursts of electrical activity Gant et al. Fipronil, a sulfox- CN ide, is biotransformed to the corresponding sulfone in biological N systems, the latter compound still being a potent insecticide.

There is also a photoproduct, desulfinyl fipronil. Representative structures of the nitromethylene, chlor- brain receptors Cole et al. Comparing onicotinyl, and phenylpyrazole insecticides. The selectivity ratios rel- ganglion nerve preparation, various NMHs at micromolar con- ative to human GABA receptor are for fipronil, 17 for the sul- centrations produced a biphasic effect characterized by an initial fone, and 16 for the desulfinyl photoproduct Hainzl et al.

Elegant, classic neuropharmacologic experiments con- approach to insecticide development. The only worrisome concern ducted by these authors demonstrated that the NMHs acted as neu- is that, with increasing use and reliance on such agents, target in- rotransmitter mimics and had both excitatory depressant effects, sects may develop resistance to these new compounds through eventually blocking postsynaptic nicotinic receptors nAChR.

In More recent experiments with 2 nitromethylene tetrahydro-1,3- the meantime, the high insect selectivity, low mammalian toxicity, thiazine NMTHT Fig. These chemicals ranged from highly toxic agents oped in Japan in the mids. This agent combines high potency to both target and nontarget species , such as nicotine, to relatively to insects with exceptionally low mammalian toxicity and a favor- innocuous substances, such as derris root.

Interestingly, despite the able persistence Liu et al. The potency overwhelming number of synthetic insecticide formulations on the of imidacloprid and several analogs can be correlated with the bind- market, the two above-mentioned agents can still be purchased and ing affinity to house fly head membranes and mouse brain mem- are still considered effective insecticides.

Imidacloprid acts as a partial ago- contact insecticide, stomach poison, and fumigant in the form of nist at the nAChR channel, generating subconductance-state cur- nicotine alkaloid, the sulfate salt, or in the form of other deriva- rents Nagata et al. Characterization of cloned nAChRs tives. Nicotine makes up some 97 percent of the alkaloid con- at exactly the proper time. In the late s, many studies were tent of commercial tobacco. It is marketed under the trade name initiated to find agents that would selectively destroy certain plant of Black Leaf 40, an aqueous solution of the sulfate salt of nico- species.

Many of these early chemicals were more effective but tine, containing 40 percent nicotine. However, a few Nicotine is extremely toxic, the acute oral LD50 in rats being compounds served as prototype chemicals for further development. It is readily absorbed through the Summaries of the early days of herbicide development are pre- skin, and any contact with nicotine solutions should be washed off sented by Cremlyn l , McEwen and Stephenson , Kirby immediately.

Anecdotal accounts of experiences by people who , and Jager It func- vogue; and 2 mechanization of agricultural practices planting, tions as an insecticide in much the same manner, causing a block- tending, harvesting because of increased labor costs. The annual ade of synapses associated with motor nerves in insects. The result has been a plethora of chemically diverse struc- Six rotenoid esters occur naturally and are isolated from the plant tures rivaling the innovative chemistry of the insecticides, the aim Derris eliptica found in Southeast Asia or from the plant Lon- being to protect desirable crops and obtain high yields by selec- chocarpus utilis or Lonchocarpus urucu, native to South America.

It can be used ei- Herbicides may be classified by chemical structure, although ther as a contact or a stomach poison. However, it is unstable in this is not very enlightening because of overlapping biological ef- light and heat and almost all toxicity can be lost after 2 to 3 days fects for a variety of chemical structures. The second method of during the summer. Rotenone is very toxic to fish, and one of its classification pertains to how and when the agents are applied.

Pre- main uses by native people over the centuries was to paralyze fish planting herbicides are applied to the soil before a crop is seeded. The mammalian toxicity varies Preemergent herbicides are applied to the soil before the usual time greatly with the species exposed, the method of administration, and of appearance of the unwanted vegetation. Postemergent herbicides the type of formulation. Plant biochemists classify herbicides according to spectively Matsumura, Because the toxicity of derris pow- their mechanism of toxicity in plants; their action is referred to as ders exceeds that of the equivalent content of rotenone, it is obvi- selective toxic to some species , contact act when impinging on ous that the other esters in crude preparations have significant the plant foliage , or translocated being absorbed via the soil or biological activity.

Acute poisoning in animals is characterized by through the foliage into the plant xylem and phloem. The anesthetic-like action on nerves appears growth and development—interactions that result in severe injury to be related to the ability of rotenone to block electron transport to the plant and its eventual death. Although toxicity in laboratory and domestic animals has bicides and some examples of each class. The estimated fatal oral dose for a kg processes having no counterparts in mammalian systems, no risk man is of the order of 10 to g.

Rotenone has been used topically of mammalian toxicity is associated with these chemicals. With the for treatment of head lice, scabies, and other ectoparasites, but the exception of a few chemicals, the herbicides have demonstrated dust is highly irritating to the eyes potentially causing conjunc- low toxicity in mammals. The presence of some of these A herbicide, in the broadest definition, is any compound that is ca- contaminants has been largely ignored without any recognition that pable of either killing or severely injuring plants; it may be used the toxicities associated with them are different from those ob- for the elimination of plant growth or the killing off of plant parts served with the herbicidal chemical and frequently occur at far Jager, Many of the early chemicals—such as sulfuric acid, lower dosages.

Certain individuals, particularly those prone to chemically related to indoleacetic acid, that stimulate growth. No allergic reactions, may experience severe contact dermatitis, hormonal activity is observed in mammals and other species, and asthma-like attacks, and even anaphylactic reactions following der- beyond target organ toxicity that can be associated with the phar- mal or inhalation contact with formulated herbicides.

The fiers, cosolvents, and so-called inerts found in formulations has not chlorophenoxy herbicides are no longer the agents of choice be- been established. One such example is discussed below. In contrast, there are other herbicides that can elicit a range of acute and chronic effects following exposure, and it is on these chemicals that attention is focused here.

Chlorophenoxy Compounds During World War II, considerable effort was directed toward the development of effective, broad-spectrum herbicides in both the United States and the United Kingdom with a view to both increasing food production and finding potential chemical war- Figure The molecular structure of the three most common fare agents Kirby, The chlorophenoxy compounds chlorophenoxyacetic acid herbicides: 2,4-dichlorophenoxyacetic acid Fig.

Ester and amine salt derivatives are also mar- search in This class of herbicides has seen continuous, ex- keted. However, since they are still used herbicides from early production times, principally from a mixture in developing nations around the world, their toxicology cannot be of polychlorinated dibenzo-p-dioxins, the main one being TCDD, ignored. It is of interest to note that, in a recent toxicologic reeval- Courtney et al.

Recent in vitro uation of 2,4-D for the purposes of providing the U. EPA with a and in vivo genotoxicity studies of 2,4-D have proven negative new toxicity database for the chemical, an industry task force dis- Charles et al.

A subsequent review of the findings been established in rodent studies, that of TCDD has Van Miller suggested that this tumor incidence was not treatment-related et al. The toxicology of the polychlo- Koestner, ; Solleveld et al. The acute toxicity elicited rinated dioxins and furans is discussed in other chapters.

An industrial accident in in a 2,4,5-T manufacturing Tamburro, While exposure to this persistent contaminant plant in Nitro, West Virginia, presented the first large occupational can be verified by blood analysis of veterans, the multifaceted na- exposure, with acute symptoms of exposure to the reaction prod- ture of the adverse effects has precluded a definitive association ucts, including skin, eye, and respiratory tract irritation; headache; Ketchum et al.

In an epidemiologic study of these lymphoma HL without any definitive conclusions Hardell and same workers conducted in , clinical evidence of chloracne Sandstrom, ; Ott et al.

A study of wheat farmers Suskind and Hertzberg, There was no evidence of increased in western Canada, where 2,4-D has been used almost exclusively risk of cardiovascular, hepatic, or renal disease or of central or pe- from , showed an overall lower mortality and cancer rate than ripheral nervous tissue damage.

One study documented neurotox- expected Wigle et al. A review of published studies pre- icity, decreased peripheral conduction velocities being observed in sented evidence of an association between occupational exposure workers employed in the manufacture of 2,4-D and 2,4,5-T Singer to chlorophenoxy herbicides and an increased risk of NHL et al.

Earlier literature reported significant peripheral neu- Morrison et al. An in- Goldstein et al. Other studies of databases noxy herbicide exposure, although this is not a specific effect, being have suggested that the carcinogenic impact of chlorophenoxy caused by a number of halogenated aromatic compounds includ- compounds was negligible Munro et al. Since these chemicals are irri- tinues and in Vietnam, where exposure was so heavy.

At flammation in the terminal bronchioles Hayes, Hepatic and renal injury type I and type II alveolar epithelial cells, destruction of the in addition to irritation of the gastrointestinal mucosa have been epithelial membranes, and proliferation of fibrotic cells. Paraquat, a highly polar compound, is poorly absorbed from the gastrointestinal tract 5 to 10 percent Haley, Paraquat was first mulation concentrates may be enhanced by increased absorption synthesized in , but its pesticidal properties were not discov- due to the presence of emulsifiers and cosolvents.

Metabolism by ered until Haley, This agent, a nonselective contact mammalian tissue is not extensive, although intestinal microflora herbicide, is one of the most specific pulmonary toxicants known may account for 30 percent of the excreted metabolites in animal and has been the subject of intensive investigation because of the studies Daniel and Gage, Elevated levels of paraquat in re- startling toxicity observed in humans.

A high mortality rate is en- nal tissue suggest the kidney as a primary route of excretion Rose countered in poisoning cases. Many countries have banned or se- et al.

Over a h posttreatment period, dispro- ; Davies et al. How- portionately high levels are found in the lung Sharp et al. Upon uptake, ers WHO, ; Ramasamy et al. In Taiwan, paraquat paraquat undergoes a NADPH-dependent one-electron reduction to accounted for 54 percent of the pesticide-related poisonings in the a free radical that reacts with molecular oxygen to regenerate the years to Yang et al.

The toxicology of this class paraquat cation plus a reactive superoxide anion O2. Alveolar cell membrane damage results in sia, diarrhea, ataxia, hyperexcitability, and convulsions, depending alveolitis, the destruction of alveolar cells, invasion of the space on the dosage and the species studied Smith and Heath, ; by fibrotic cells accompanied by a loss of pulmonary elasticity and Haley, Necropsy reveals hemorrhagic and edematous lungs, respiratory impairment, with an inefficient gas O2, CO2 exchange.

From a catalog of all the signs and Paraquat poisonings in children and adults have been de- symptoms, it is obvious that the lung is the most susceptible tar- scribed in detail in the literature Almog and Tal, ; Davies et get organ, and the same histopathologic picture of pulmonary le- al. Paraquat sions is observed in mice, rats, dogs, and humans Clark et al.

In poisonings, immediate effects are usually not seen in Wesseling et al. The ingestion of commercial paraquat concentrates is invari- ably fatal and runs a time course of 3 to 4 weeks. The initial irri- tation and burning of the mouth and throat, the necrosis and slough- ing of the oral mucosa, severe gastroenteritis with esophageal and gastric lesions, abdominal and substernal chest pains, and bloody stools give way to the characteristic dominant pulmonary symp- toms, including dyspnea, anoxia, opacity in the lungs seen in chest x-rays, progressive fibrosis, coma, and death.

While the pulmonary lesions are the most life-threatening, paraquat induces multiorgan toxicity with necrotic damage to the liver, kidneys, and myocar- dial muscle plus extensive hemorrhagic incidents throughout the body. Survivors of moderate-to-severe paraquat poisonings showed Figure The chemical structures of paraquat and diquat, marketed significant impairment in respiratory function tests, which im- as the dichloride and dibromide salts, respectively.

Swan found no detectable changes in workers ex- trol annual grasses and broad-leaf weeds in a number of crops posed to sprays 6 days per week for 12 weeks. Senanayake et al.

Subchronic Castro-Gutierrez et al. Neither were teratogenic effects seen in ration measured by oximetry during an exercise test Dalvie et al. More sensitive tests may be needed to assess long-term res- tagenicity studies. Revisiting the toxicity database and providing piratory disabilities.

Alachlor is considered to be a sorbed paraquat remaining in the gastrointestinal tract. Purgatives category 2B probable human carcinogen by the U. EPA, a risk may be given. Absorbed paraquat may be removed from the blood- to agricultural workers during mixing and loading, with levels of stream by aggressive, lengthy hemoperfusion through charcoal or exposure ranging from 0. To avoid excessive pulmonary damage, supple- exposure model used. The putative carcinogen metabolite, mental oxygen should be reduced to a level just sufficient to main- 2.

Even though these patients may suffer from humans Coleman et al. However, the human may form hypoxia and respiratory insufficiency, hyperbaric oxygen is con- DEBQ1 via another route. Studies of thyroid tumors in rats sug- traindicated because it appears to promote cellular toxicity. To date, there has been no evidence of an fore harvesting. Part of the reduced toxicity may be related to the fact that it is The discovery of alachlor in well water at levels of 0.

Concerns about one analog of of the dose is eliminated via the urine following subcutaneous ad- a series has led to the examination of other chloracetanilides and ministration Daniel and Gage, A latency period of 24 h is closely related agents—e. Following acute, high-dose exposure or chronic exposure of animals to diquat, the major target organs were the gastrointesti- nal tract, the liver, and the kidneys Hayes, ; Morgan, Chronic feeding studies resulted in an increased incidence of cataracts in both dogs and rats Clark and Hurst, It is con- sidered that diquat can form free radicals and that the tissue necro- sis is associated with the same mechanism s of superoxide- induced peroxidation as observed with paraquat.

Unlike paraquat, diquat shows no special affinity for the lung and does not appear to involve the same mechanism that selectively concentrates paraquat in the lung Rose and Smith, Few diquat-related human intoxications have been reported to date Schonborn et al. In the few cases of suicidal intent described, ulceration of mucosal membranes, gastrointestinal symptoms, acute renal failure, hepatic damage, and respiratory difficulties were observed.

CNS effects Figure One individual died of cardiac arrest. Glyphosate was not teratogenic at et al. Glyphosate was not mutagenic in standard tests Ames and other No doubt, detailed mechanistic studies will reveal one or more bacterial assays, dominant lethal test in mouse Li and Long, modes of action. However, one study, with glyphosate iso- propylamine salt and Roundup formulation, showed weak muta- genic activity in the Ames test and a significant increase in chro- Phosphonomethyl Amino Acids mosomal aberrations in the Allium root cell when Roundup was tested Rank et al.

Carcinogenicity was not observed in Two agents, N-phosphonomethyl glycine glyphosate, Roundup, mice, rats or dogs, glyphosate being classified by the U. Moses has reported tumors in the pitu- must be considered because of their use in attempted suicides in itary and mammary glands in glyphosate-treated rats. Glyphosate southeastern Asia Fig. Both agents are broad-spectrum does not inhibit cholinesterases. While they exist as free acids, these agents are mar- dence of such poisonings increasing as paraquat is banned or is keted as the isopropylamine or trimethylsulfonium salts of more tightly controlled Talbot et al.

The for- concentrates of 41 percent and In con- mulation concentrate is used. Mild intoxications are characterized sidering any toxicity data, one must make the distinction whether by gastrointestinal symptoms nausea, vomiting, diarrhea, abdom- the data pertain to the acid, the salt, or the complete formulation s inal pain due to mucosal irritation and injury, with resolution containing what appear to be biologically active surfactants within 24 h Talbot et al.

In moderate intoxications, more Kamrin, ; Watanabe and Sano, Severe poisoning is characterized by pulmonary dys- zyme of the aromatic amino acid biosynthesis pathway essential function requiring intubation, renal failure requiring dialysis, hy- for protein synthesis in plants Haslam, Glyphosate is nontoxic by the dermal route, with ing in humans to be 17, 58, and mL, respectively.

Glyphosate is an ocu- ity of the surfactant polyoxyethyleneamine POEA in the formu- lations used currently Sawada and Nagai, ; Sawada et al. Tai et al. The chemical structures of glyphosate N-phospho- an important role in ammonia detoxification and amino acid me- nomethyl glycine and glufosinate N-phosphonomethyl homoalanine. In subchronic feeding stud- ies in rats, no agent-related deaths occurred, although body weight Fungicidal chemicals are derived from a variety of structures rang- gains in males were retarded in the ppm group.

Food con- ing from simple inorganic compounds, such as sulfur and copper sumption was reduced and water consumption increased and, at sulfate, through the aryl- and alkyl-mercurial compounds and chlo- this high dose, signs of CNS excitation and hypothermia were rinated phenols to metal-containing derivatives of thiocarbamic noted Hack et al. Glufosinate was not considered to be acid Fig. The chemistry of fungicides and their properties mutaginic, teratogenic, or carcinogenic in animal studies, although have been discussed by Cremlyn , Kramer , and Ed- in more recent studies using whole-embryo culture, teratogenic wards et al.

Foliar fungicides are applied as liquids or pow- effects in mice have been observed, the effect being induced apop- ders to the aerial green parts of plants, producing a protective bar- tosis in the neuroepithelium of developing embryos Watanabe rier on the cuticular surface and systemic toxicity in the developing and Iwase, ; Watanabe, While glufosinate did not in- hibit brain cholinesterase, reductions in erythrocytic and serum cholinesterases have been seen in 7 of 16 patients affected by this herbicide Watanabe and Iwase, In contrast to plant metab- olism, glufosinate ammonium inhibited glutamine synthetase in an- imals, but this did not lead to a problem in ammonia metabolism, the mammal obviously compensating by using other metabolic pathways Hack et al.

Glufosinate ammonium has been involved in a number of poisoning cases, particularly in Japan Koyama et al. Early clinical symptoms included nausea, vomiting, and diarrhea associated with intestinal mucosal irritation but were followed in 24 h by neuro- logic signs, including impaired respiration, seizures, muscle weak- ness post—status epileptic myopathy , convulsions, and death within 4 days in 6 of 31 patients Koyama, Some survivors showed either a brief loss of memory or amnesia for 7 to 10 days after intoxication Koyama, Any significant role of gluta- mate in the neurologic events has not been confirmed.

Limited in- formation is available regarding glufosinate persistence in vivo, but urinary levels higher than concomitant blood levels have been re- ported and urinary excretion persisted for 3 to 5 days after inges- tion Watanabe and Iwase, Once again, concerns have been raised about the role of the surfactant.

The direct cause of death seemed to be circulatory dis- turbance, especially cardiac insufficiency, possibly related to the surfactant in the formulation involved in the intoxications Koyama et al. The absorption of glufos- inate in animals was 25 to 30 percent higher than the absorption rate of the agent when given alone Watanabe and Sano, This suggested that the glufosinate-related effects might be en- hanced by surfactant-induced penetration of the CNS, while the cardiovascular system effects were surfactant-related.

Many herbicides representative of several chemical classifi- cations and diverse structures have recently been introduced into agricultural practice Table Many of these newer chemicals are applied to crops or soil at exceedingly low application rates, minimizing nontarget species toxicity and avoiding environmental contamination. Present con- cerns focus on groundwater contamination and closer scrutiny of minor contaminants for mutagenic, teratogenic, and carcinogenic Figure Chemical structures of fungicides representative of vari- effects.

Poisonings in humans have usually been associated with ous chemical classifications. Soil fungicides are applied as liquids, dry powders, or gran- An effective fungicide must possess the following properties: ules, acting either through the vapor phase or by systemic proper- 1 low toxicity to the plant but high toxicity to the particular ties.

Dressing fungicides are applied to the postharvest crop ce- fungus; 2 activity per se or ability to convert itself by plant or real grains, tubers, corms, etc. The and 4 formation of a protective, tenacious deposit on the plant postharvest loss of food crops to disease is a serious worldwide surface that will be resistant to weathering by sunlight, rain, and problem Table Fungicides may be described as protective, wind Cremlyn, This list of properties is never fulfilled en- curative, or eradicative, according to their mode of action.

Protec- tirely by any single fungicide, and all commercially available com- tive fungicides, applied to the plant before the appearance of any pounds show some phytotoxicity, lack of persistence due to envi- phytopathic fungi, prevent infection by either sporicidal activity or ronmental degradation, and so forth. Thus, the timing of the by changing the physiologic environment on the leaf surface.

Cu- application is critical in terms of the development of the plant as rative fungicides are used when an infestation has already begun well as the fungus. With hyphae growing in the epidermis of the plant, preventing further a few exceptions, most of these chemicals have a low order of tox- development.

Eradicative fungicides control fungal development icity to mammals Table However, all fungicides are cyto- following the appearance of symptoms, usually after sporulation, toxic and most produce positive results in the usual in vitro mi- by killing both the new spores and the mycelia and by penetrating crobial mutagenicity test systems. Such results are not surprising the cuticle of the plant to the subdermal level Kramer, A safe Once used in tremendous volumes as a biocide in leather tanning, fungicide nonmutagenic in test cell systems would be useless for wood preservation, the paper and cellulose industry, and in paints, the protection of food and health.

Public concern has focused on this chemical has been phased out of use because many commer- the positive mutagenicity tests obtained with many fungicides and cial products were contaminated by polychlorinated dibenzo- the predictive possibility of both teratogenic and carcinogenic dioxins and dibenzofurans, predominantly by hexachlorinated, potential.

The fact that nearly 90 percent of all agricultural fungi- heptachlorinated, and octachlorinated congeners. While these cides are carcinogenic in animal models has not reassured the pub- congeners are considerably less toxic than TCDD, evidence from lic, especially when this is translated into the fact that some 75 animal studies has pointed to the fact that the contaminants in com- million pounds of the fungicides used annually fall into this cate- mercial- or technical-grade PCP were responsible for the toxicity gory NAS, An evaluation of 11 fungicides concluded that, observed.

Technical-grade PCP fed to rats caused altered plasma although the areas treated with these chemicals represented only enzymes, increased hepatic and renal weights, and caused hepato- 10 percent of the acreage treated annually with pesticides, they cellular degeneration in addition to changes in blood biochemistry could account for 60 percent of the total estimated dietary car- decreased erythrocyte count, decreased hemoglobin and serum al- cinogenic risk. The administration of purified PCP resulted only in in- While a number of different chemicals are shown in creased liver and kidney weight.

Prolonged treatment of female Fig. Other fungi- studied Goldstein et al. Pentachlorophenol was not ter- cides are undergoing reevaluation because of suspected toxicity, atogenic in rats and is not considered to be carcinogenic in mice particularly as teratogens or carcinogens and incomplete or out- or rats Innes et al. A number of environmental problems have been associated with PCP Eisler, Human poisoning by commercial PCP has occurred, usually Hexachlorobenzene associated with occupational exposure and instances of sloppy han- From the s through the s, HCB saw extensive use as a dling and neglect of hygienic principles Jorens and Schepens, fungidical dressing applied to seed grain as a dry powder.

Between The chemical is absorbed readily through the skin, the most and , an epidemic of poisoning occurred in Turkey, ul- usual route of acquisition, with several products, including PCP, timately involving some individuals who consumed treated detected in the urine. Both adults and vomiting, headache, incoordination, generalized weakness, and and children were afflicted, young children and nursing infants be- early coma Hayes, Pentachlorophenol acts cellularly to ing at particular risk Schmid, ; Wray et al.

Survivors frequently display being used in developing countries and still presents a health haz- dermal irritation and exfoliation, irritation of the upper respiratory ard.

Like other organochlorine compounds, HCB possesses all of the properties of chemical sta- Phthalimides bility, slow degradation and biotransformation, environmental per- sistence, bioaccumulation in adipose tissue and organs containing Of this class of chemicals, folpet and captofol, true phthalimides, a high content of lipid membranes, and the ability to induce a range have been deregistered and only captan, being structurally differ- of tissue cytochrome-P as well as conjugative enzymes.

Re- ent with a cyclohexene ring Fig. Earl Gray Jr. Toxic Responses of the Endocrine System. Hoyer and Jodi A. Flaws Unit V Toxic Agents Toxic Effects of Pesticides.

Costa Toxic Effects of Metals Erik J. Tokar, Windy A. Boyd, Jonathan H. Freedman, and Michael P. Waalkes Bruckner, S. Satheesh Anand, and D. Alan Warren Toxic Effects of Radiation and Radioactive Materials. Hoel Watkins, III Toxic Effects of Calories Martin J. Ronis, Kartik Shankar, and Thomas M. Kane, Rebecca D. Klaper, and Robert H. Hurt Air Pollution. Di Giulio and Michael C. Newman Food Toxicology.

Kotsonis and George A.