Dermal exposure sensitization

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). 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been made for methyl parathion. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal exposure. 

The only study located regarding immunological effects in humans after dermal exposure to endosulfan was an account of the results of patch tests on the backs of 14 farm workers with work-related dermatitis and 8 controls who were not exposed to pesticides (Schuman and Dobson 1985). Skin sensitization was not observed in any of the subjects following a 48-hour, closed-patch exposure to an unspecified amount of 0.1 % endosulfan in petrolatum. 

Although human data are not extensive, the data suggest that dermal effects may be a concern for some humans exposed to trichloroethylene, particularly through bathing with contaminated water however, it is unlikely that exposure to trichloroethylene in the air or soil at hazardous waste sites would be irritating to human skin. Some people may develop immunological sensitivity to trichloroethylene which may manifest as a dermal response following inhalation, oral, or dermal exposure to trichloroethylene. 

Additional animal studies of trichloroethylene following intermediate-duration oral exposure are necessary to further define dose-response relationships. Because developmental neurotoxicity appears to be a sensitive end point, a focus on this end point would be useful. Animals studies following intermediate-duration dermal exposure are necessary. These studies would indicate whether targets following dermal exposure differ compared to inhalation and oral exposure. 

Quintolubric 95830W, displayed only weak skin sensitization (skin sensitization occurred in only 1 of 10 guinea pigs) (Kinkead et al. 1985, 1987a, 1988). No other studies were located regarding immunological effects in animals after dermal exposure to mineral oil hydraulic fluids. 

Mobile, colorless liquid with an odor like ammonia that is detectable at 2 ppm. The odor becomes annoying at 11 ppm. This material is hazardous through inhalation, skin absorption, penetration through broken skin, and ingestion, and produces local skin/eye impacts. Dermal exposure causes skin sensitization. 

Dermal exposure to chemicals is one of the leading causes of job-related illness as reported by the National Institutes for Occupational Safety and Health. As jet fuel is the primary occupational exposure of military and aviation industry personnel, there is elevated concern regarding JP-8 dermal exposures in the workplace. Several anecdotal reports confirm that persons exposed to jet fuel experience itching or burning skin, skin redness or rash, skin dryness or dermatitis, skin lesions or weeping, or skin sensitization [32,33,34], yet little is known regarding possible systemic effects following dermal exposure. 

Dermal toxicity due to JP-8 may also be attributed to increased free radical formation that may be involved in the development of skin sensitization [45], Following dermal exposure to JP-8, increasing levels of oxidative species are observed [46], In vitro studies with rat lung epithelial cells demonstrated that JP-8-induced cell death is inhibited by exogenous glutathione or the thiol-containing antioxidant N-acetyl-cysteine... 

Klink, K.J. and Meade, B.J., Dermal exposure to 3-amino-5-mercapto-l,2,4-triazole (AMT) induces sensitization and airway hyperreactivity in BALB/c mice, Toxicol. Sci., 75, 89, 2003. 

Howell, M.D., Weissman, D.N., and Jean, M.B., Latex sensitization by dermal exposure can lead to airway hyperreactivity, Int. Arch. Allergy Immunol., 128, 204, 2002. 

Modified Buehler. Buehler (1964) developed the first test system to use an occlusive patch to maximize dermal exposure and to increase the test sensitivity (Buehler, 1964). Although, this assay is still insensitive for some xenobiotics that may not sufficiently traverse the epidermis, it is particularly useful for compounds that are either highly irritating by intradermal injection or cannot be dissolved or suspended in a form that is conducive to injection. Other advantages are that the test produces few false positives, rarely overpredicts the potency of sensitizers, and is less likely to produce limiting system toxicity or ulceration at the induction sites. Figure 15.4 shows the test design in its current (OECD) form. 

Persons with a history of convulsive disorders would be expected to be at increased risk from exposure to endrin. Children may be more sensitive than adults to the acute toxic effects of endrin. In an endrin poisoning episode in Pakistan, children 1-9 years old represented about 70% of the cases of convulsions (Rowley et al. 1987). The causative factor responsible for the outbreak was not identified, however, and the age distribution of cases could be explained by age-specific exposure situations. In general, following oral administration, female animals appear to be more susceptible to endrin toxicity than males (Gaines 1960 Treon et al. 1955). The difference may be due to the more rapid excretion of endrin by male versus female rats (Hutson et al. 1975 Klevay 1971 Korte et al. 1970). A sex-related difference in toxicity was not apparent following dermal exposure (Gaines 1960, 1969). No sex-based differences in endrin-related... 

Uzodinma et al. 1984a Yarbrough et al. 1981), but no information was located for the inhalation or dermal exposure routes. Chlordecone may lead to death after oral administration, depending on dose (Larson et al. 1979b Simmons et al. 1987) pregnant animals may be more sensitive to lethal effects of chlordecone (Chernoff and Rogers 1976 Kavlock et al. 1985 Seidenberg et al. 1986). 

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