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Exposure routes dermal

Exposure medium environmental surfaces Enviromnental surfaces multiple Exposure route dermal contact Dermal surfaces multiple... [Pg.159]

Exposure medium environmental surface Environmental surface single Exposure route dermal contact Dermal surface single... [Pg.164]

EXPOSURE ROUTES dermal contact and inhalation during manufacture and formulation in polymers during use as a solvent... [Pg.253]

EXPOSURE ROUTES dermal contact with chemicals containing phenolic mixtures inhalation workers involved in fractionation and distillation of petroleum or coal exposure to commercial degreasing agents containing cresol cigarette and marijuana smokers those exposed to cigarette smoke inhale pg quantities... [Pg.307]

The most specific biomarker of exposure to methyl parathion is the presence of the compound in serum or tissue. This is an especially good biomarker for detection shortly after acute exposure. For example, methyl parathion levels were detected in the sera of five men who were exposed for 5 hours in a cotton field 12 hours after it was sprayed with methyl parathion. The route of exposure was dermal, through unprotected hands. Serum levels averaged 156 ppb after 3 hours of the 5-hour exposure, and averaged 101.4 and 2.4 ppb at 7 and 24 hours postexposure, respectively (Ware et al. 1975). [Pg.112]

These results are supported by studies in animals in which methyl parathion was detected 30-155 minutes after exposure (oral, dermal, inhalation, or intravenous routes) in plasma and liver (Abu-Qare et al. 2000 EPA 1978e). Due to extensive and rapid metabolism of methyl parathion (see Section 3.3), measurable levels are not expected to persist in tissue or serum for prolonged periods after exposure. [Pg.113]

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. [Pg.128]

There are insufficient data to determine potential daily inhalation and dermal exposure levels. However, based on the information presented in Seetions 6.3 and 6.4, exposure levels for the general population are probably very low by these routes. Inhalation exposure is not important for the general population, with the possible exception of those individuals living near areas where methyl parathion is frequently sprayed. Since methyl parathion is readily adsorbed through the skin, dermal eontact may be the most relevant exposure pathway. Dermal eontaet is most likely to oeeur in people who are occupationally exposed. [Pg.162]

The most important routes of exposure to endosulfan for the general population are ingestion of food and the use of tobacco products with endosulfan residues remaining after treatment. Farmers, pesticide applicators, and individuals living in the vicinity of hazardous waste disposal sites contaminated with endosulfan may receive additional exposure through dermal contact and inhalation. [Pg.221]

Bioavailability from Environmental Media. Endosulfan can be absorbed following inhalation of contaminated workplace air and ingestion of insecticide-contaminated food (Ely et al. 1967). Dermal contact with or ingestion of endosulfan that is tightly bound to soil particles is an exposure route of... [Pg.243]

Route Dependent Toxicity. The toxicity of trichloroethylene does not seem to be heavily dependent upon its route of entry. Inhalation and ingestion are the primary exposure routes, and the liver, heart, and central nervous system are the primary targets for both routes (Candura and Faustman 1991). Renal toxicity results principally from oral exposure, and dermal exposure generally confines its toxic effects to the skin, although broad systemic effects can be induced imder conditions of high exposure (Bauer and Rabens 1974). Attributing such effects solely to dermal exposure, however, is difficult because inhalation exposure is often a factor in these cases as well. [Pg.132]

Mineral Oil Hydraulic Fluids. Studies regarding cancer in humans or animals after inhalation exposure to mineral oil hydraulic fluids were limited to a single case-control study that examined associations between subjectively reported occupational exposure to petroleum-derived liquids and cancer at particular sites among 3,726 male cancer patients (Siemiatycki et al. 1987a). The study found no convincing associations between occupational exposure to hydraulic fluids and cancer at any site. This study is discussed in more detail in Section 2.2.3.8, because, while inhalation exposure was probable for the subject occupations, the authors reported that the exposure route was more often dermal contact. [Pg.67]

Mineral Oil Hydraulic Fluids. Mineral oil and water-in-oil emulsion hydraulic fluids are used extensively in virtually all heavy industries as well as in construction equipment, automobiles, tractors, trucks, and material handling equipment. Potentially exposed populations include workers in heavy and allied industries and the general population due to the use of hydraulic fluids in automobiles however, this profile does not focus on automotive fluids. The most common route of exposure is dermal contact with the neat fluid, although inhalation of oil mists and vapors may also occur. The components of mineral oil hydraulic fluids are present in many other petroleum-derived products including lubricating oils, so exposure to the major components of mineral oil hydraulic fluids is not limited to hydraulic fluid exposures. [Pg.290]

Exposure routes considered which may include ingestion, inhalation, dermal absorption, or any combination thereof. [Pg.288]

Human populations are likely to be exposed to a pollutant through more than one exposure route at a time. Total exposure may combine intake through ingestion of different substances, dermal absorption from surface water and water supply, and inhalation at different locations in the study area (e.g., work, home, recreational areas, commuting routes). Calculation of total exposure requires that the pharmacokinetics (absorption, metabolism, storage, excretion) for different exposure routes are understood for the pollutant of concern. Otherwise, only exposures by route can be combined. [Pg.296]

When a chemical is emitted to the environment, it is distributed into different environmental matrices depending on the properties of the substance. When distributed in the environment, different organisms, including humans, can be exposed to the substance via different exposure routes such as ingestion, inhalation and dermal exposure. Depending on both species and substance characteristics, the exposure to a substance can give rise to different impacts. [Pg.124]

Recycling of printer circuit boards is deemed as the most important source of heavy metals to the ambient environment. These heavy metals may be entering into human body from various exposure routes such as ingestion, inhalation, and dermal absorption. Exposure to high levels of heavy metals can lead to acute and chronic toxicity, such as damage to central and peripheral nervous systems, blood composition, lungs, kidneys, liver, and even death [14],... [Pg.282]

Absorption, Distribution, Metabolism, and Excretion. Metabolism and excretion in animals exposed to acrylonitrile by the inhalation and oral routes have been studied extensively. However, only limited data on absorption and distribution are available. Some data on humans exposed by inhalation are available. No data are available on the toxicokinetics of acrylonitrile when the exposure route is dermal. More extensive information on absorption and distribution of acrylonitrile would be valuable to fully understand the toxicokinetics of acrylonitrile. Some data on the toxicokinetics of acrylonitrile... [Pg.70]

Dermal nickel sulfate hexahydrate dose equivalent to 40, 60, or 100 mg Ni/kg BW daily for 30 days (rats licked skin so exposure route may be oral in part)... [Pg.505]

Disparate effects on T-cell proliferative responses have been reported following exposure to JP-8. Significant suppression of T-cell proliferation is reported following either inhalation or dermal exposure to JP-8 [ 18,20,36], while the response is unaffected following either the oral or dermal exposure routes in other studies [66,71,72], These differences may be explained by variations in exposure routes and in assay methodology, as agents used to evaluate T-lymphocyte activation and proliferation were diverse and included Con A plus IL-2 [18,20], anti-CD3 [36], or Con A only [66,71,72],... [Pg.232]

Despite wearing protective equipment that included disposable overalls and compressed-air-fed visors or full-facepiece masks with filters for dusts and vapors, hexachloroethane was detected in the plasma of exposed workers (Selden et al. 1993). After 5 weeks of exposure, plasma levels of hexachloroethane in 12 workers were 7.3 + 6 pg/L. Mild dermal irritation was also noted. If the skin irritation was a response to hexachloroethane rather than trauma from the protective clothing, the irritation suggests that the principal exposure route may have been dermal. Absorption of a saturated hexachloroethane solution across human skin was estimated to be 0.0230 mg/cm2/hour based on the physical properties of hexachloroethane (Fiserova-Bergerova et al. 1990). [Pg.74]

Intermediate-Duration Exposure. A study (Selden et al. 1994) of 11 workers who wore protective equipment while being exposed to hexachloroethane for 5 weeks showed no respiratory, hematological, liver, or kidney effects at plasma levels of 7.3 + 6 pg/L (Selden et al. 1993). Because mild dermal effects were noted, the principal exposure route may have been dermal. The dermal effects may also have been a result of trauma from the protective equipment. Because of the protective equipment, it is not possible to determine exposure levels. [Pg.105]

Chronic-Duration Exposure and Cancer. No studies were located in humans following chrome-duration exposure to hexachloroethane for any exposure route. No chronic animal studies were conducted using the inhalation route of exposure. In oral studies with rats, the kidney was identified as a primary target organ in males and females (NTP 1989). The kidney damage in male rats was the result of hyaline droplet nephropathy and, accordingly, was not suitable as the basis for an oral MRL. In contrast to acute- and intermediate-duration oral exposure, liver toxicity was not evident in rats following chronic oral exposure. There were no studies of chronic dermal exposure to hexachloroethane. [Pg.106]

A case can often be made to omit studies as scientifically unnecessary, because it is possible to conduct an adequate risk assessment without them. This is most often the case if the substance decomposes to degradants of known hazardous properties. For example the substance may hydrolyse rapidly to non-toxic products, so the key issue is to establish that this happens rapidly in the stomach before the parent substance can be absorbed. There may then be a case for omitting the expensive long-term animal studies, providing it is also established that there is no dermal or inhalation absorption from these exposure routes. In a similar way, it may be justified to omit ecotoxicity studies on a substance which hydrolyses or otherwise decomposes in the aquatic environment to stable products that have already been tested. [Pg.16]

In the pharmaceutical industry, the two most common routes of administration are via diet and gavage (PMA, 1988). Some compounds are given by drinking water, topical (dermal) application, or injection, depending on the expected clinical exposure route, which is the primary criterion for determining the route of administration in carcinogenicity studies. When more than one clinical route is anticipated for a drug, the dietary route is often chosen for practical reasons. [Pg.306]


See other pages where Exposure routes dermal is mentioned: [Pg.937]    [Pg.937]    [Pg.257]    [Pg.320]    [Pg.307]    [Pg.48]    [Pg.108]    [Pg.123]    [Pg.127]    [Pg.169]    [Pg.107]    [Pg.936]    [Pg.118]    [Pg.159]    [Pg.109]    [Pg.289]    [Pg.49]    [Pg.300]    [Pg.818]    [Pg.6]    [Pg.82]    [Pg.88]    [Pg.102]    [Pg.160]    [Pg.163]    [Pg.19]   
See also in sourсe #XX -- [ Pg.21 , Pg.266 ]




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