Dermal following

Health and Safety Factors. See "General Health and Safety Eactors." The following toxicides for adiponitrile have been reported oral LD q (rats), 300 mg/kg dermal LD q (rabbits), 2,134 mg/kg and inhalation 4-h LC q (i ts), 1.7 mg. NIOSH has proposed an exposure limit of 4 ppm as a TWA (68). 

The importance of hydrolysis potential, ie, whether moisture or water is present, is illustrated by the following example. In the normal dermal toxicity test, namely dry product on dry animal skin, sodium borohydride was found to be nontoxic under the classification of the Federal Hazardous Substances Act. Furthermore, it was not a skin sensitizer. But on moist skin, severe irritation and bums resulted. 

Endrin [72-20-8] is l,2,3,4,10,10-hexachloro-l,4,4t ,5,8,8t -hexahydro-6,7-epoxy-l,4- <7o, <7o-5,8-dimethanonaphthalene (35) (mp 245 dec, vp 0.022 mPa at 25°C) and is soluble in water to 23 / g/L. It is produced by a Diels-Alder reaction of hexachloronorbomadiene with cyclopentadiene, followed by epoxidation. This reaction produces the endo,endo isomer of dieldrin, which is less stable and more toxic with rat LD q values of 17.8 and 7.5 (oral) and 15 (dermal) mg/kg. It is used as a cotton insecticide but because of its high toxicity to fish it has been restricted. 

Eye and Skin Contact. Some nickel salts and aqueous solutions of these salts, eg, the sulfate and chloride, may cause a primary irritant reaction of the eye and skin. The most common effect of dermal exposure to nickel is allergic contact dermatitis. Nickel dermatitis may occur in sensitized individuals following close and prolonged contact with nickel-containing solutions or metallic objects such as jewelry, particularly pierced earrings. It is estimated that 8—15% of the female human population and 0.2—2% of the male human population is nickel-sensitized (125). 

Syndet bar soaps were developed for sensitive skin. Their pH value usually is around 5-6, far less than that of the normal soaps (pH 9-10), which is the reason for the latter causing dermal fissures with people who need frequent washing of their hands. The manufacture of syndet bar soaps requires special attention to methodology. A typical raw material composition of a syndet bar soap is as follows ... 

Death from a combination of inhalation and dermal exposures has been reported by Fazekas (1971) in four individuals who used methyl parathion (Wofatox) spray in a careless manner. These individuals were part of a larger series of 30 cases (20 men, 10 women) of fatal methyl parathion intoxication reported by Fazekas (1971). Since 26 of these fatalities followed oral exposure, this report is discussed in detail in Sections 3.2.2.1 and 3.2.2.2. 

Two of seven children who ingested methyl parathion in contaminated drinking water, and also were exposed by inhalation and possibly by dermal contact following spraying of methyl parathion inside a house, died (Dean et al. 1984). Additional details are provided in Section 3.2.1.1. 

Although the extent of absorption was not measured, the above evidence suggests that absorption in humans occurs rapidly following dermal exposure to commercial pesticide formulations of methyl parathion. 

Following single dermal applications of 10 mg/kg of radiolabeled methyl parathion to pregnant rats, methyl parathion was found to be widely distributed to all major tissues and organs. Concentrations were highest in plasma and kidney, maximum levels measured 2 hours postapplication. Peak levels in liver, brain, fetus, and placenta, were measured 2 to 10 hours later, at which times the highest concentration of methyl parathion was in the fetus (Abu-Quare et al. 2000). 

Based on the rapid appearance of clinical signs and cholinesterase inhibition, methyl parathion appears to be readily absorbed by humans and animals following inhalation, oral, and dermal exposure. Following oral administration of methyl parathion to animals, the extent of absorption was at least 77-80% (Braeckman et al. 1983 Hollingworth et al. 1967). No studies were located regarding the extent of absorption following inhalation and dermal exposure, or the mechanism of absorption. 

Procedures that have been used to reduce absorption of methyl parathion include the following. In inhalation and dermal exposures, the exposed person is first removed from the source of exposure. 

Absorption, Distribution, Metabolism, and Excretion. Evidence of absorption comes from the occurrence of toxic effects following exposure to methyl parathion by all three routes (Fazekas 1971 Miyamoto et al. 1963b Nemec et al. 1968 Skiimer and Kilgore 1982b). These data indicate that the compound is absorbed by both humans and animals. No information is available to assess the relative rates and extent of absorption following inhalation and dermal exposure in humans or inhalation in animals. A dermal study in rats indicates that methyl parathion is rapidly absorbed through the skin (Abu-Qare et al. 2000). Additional data further indicate that methyl parathion is absorbed extensively and rapidly in humans and animals via oral and dermal routes of exposure (Braeckman et al. 1983 Flollingworth et al. 1967 Ware et al. 1973). However, additional toxicokinetic studies are needed to elucidate or further examine the efficiency and kinetics of absorption by all three exposure routes. 

No studies were located regarding excretion of methyl parathion in humans following inhalation exposure. The limited information available from human case studies indicates that the chemical s metabolites are rapidly excreted primarily in the urine in humans following oral (Morgan et al. 1977) or dermal (Ware et al. 1974, 1975) exposure and in animals following oral (Hollingworth et al. 1973) or dermal (Abu-Qare et al. 2000) exposure. 

Dermal Effects. No studies were located regarding dermal effects in humans following oral exposure to endosulfan. 

The primary systemic targets of endosulfan toxicity in animals following dermal exposure are the liver and kidney. Adverse hematological effects have also been observed following dermal administration of endosulfan. No studies were located regarding musculoskeletal effects in humans or animals after dermal exposure to endosulfan. 

The adrenals of rabbits given a single dermal dose of 100 mg/kg of endosulfan exhibited microscopic changes, including swollen cells with foamy cytoplasm and eccentric nuclei (Gupta and Chandra 1975). Also, release of lipids from the adrenal cortex was observed in rats that died following daily application... 

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