Dermal occupational exposure limits

Bos, P.M.J., D.H. Brouwer, H. Stevenson, P.J. Boogaard, W.L.A.M. de Kort and J.J. van Hemmen (1998). Proposal for the assessment of quantitative dermal exposure limits in occupational environments Part I. Development of a concept to derive a quantitative dermal occupational exposure limit, Occup. Environ. Med., 55, 795-804. 

This should be the case even if exposure to the substance at that level occurs repeatedly or over a long period of time, even a worker s entire working life (8 h a day, 40 years). Some authors proposed the use of Dermal Occupational Exposure Limits (DOEL) [81]. 

Generic Exposure Values (GEVs) are generic threshold values for occupational exposure (and derived dermal values) derived from OELs (Occupational Exposure Limits). The effects used to estimate GEVs are acute and repeated dose toxicity for a total of 63 organic and nonorganic substances, both volatile and nonvolatile. 

The use of personal protection equipment (PPE) is not allowed as a permanent measure. It should not be a substitute for necessary technical improvements to reach the state of the art In practice, in most cases it is used as an additional supplementary protection measure to give protection against unexpected or accidental incidents, e. g., a sudden leakage. In the case of exceeding the occupational exposure limit or a risk of dermal exposure, personal protection equipment (PPE) must be used. The duration of this must be restricted to the period of necessity. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of methyl parathion in humans and animals by various routes of exposure. The available literature reviewed concerning the health effects of methyl parathion in humans described case reports of longer-term studies of pesticide workers and case reports of accidental or intentional ingestion of methyl parathion. The occupational exposure is believed to be via the dermal and inhalation routes. The information on human exposure is limited in that the possibility of concurrent exposure to other pesticides or other toxic substances cannot be quantified. 

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. 

Mineral Oil Hydraulic Fluids. There is limited information on the toxicity of mineral oil hydraulic fluids in humans. A single case report of a child accidentally ingesting a single dose of automotive transmission fluid provides limited information on death and systemic effects. A case-control study provides some information on the carcinogenicity of mineral oil hydraulic fluids. The study population was exposed via inhalation and dermal routes. An occupational exposure study provides information on neurotoxicity following chronic dermal exposure. Information on the toxicity of mineral oil hydraulic fluids is limited to a series of inhalation, oral, and dermal acute-duration exposures. These studies provide information on death, systemic effects, and neurotoxicity by inhalation, oral, and dermal routes, and immunotoxicity following dermal exposure. 

Mineral Oil Hydraulic Fluids. Two human studies involving exposure to mineral oil hydraulic fluids were located. One was a case report of a child who accidentally ingested a lethal dose of automotive transmission fluid (Perrot and Palmer 1992). The other is an occupational exposure in which workers were dermally exposed to mineral oil hydraulic fluids (Jarvholm et al. 1986). Both of these studies are limited because only a small number of end points were examined and there is no accurate reporting of dose levels. Because mineral oil hydraulic fluids are widely used, the potential for human exposure is great. 

Research studies investigating exposure to JP-8 via oral administration offers an alternative examination of the systemic effects of JP-8 on immune function. Admittedly, this does not ideally mimic occupational exposures, but it does eliminate technical limitations associated with inhalation and dermal penetration of JP-8. It has been suggested that the only route available that can assess the whole mixture (JP-8 in its entirety), without fractionation due to volatilization of components, is the oral route [1] as select components of JP-8 may have increased permeability during dermal exposure, other specific components may be enriched following inhalation exposures[71]. 

To date, very little quantitative data exist regarding the toxicokinetics of endrin and its metabolites. Limited data were found regarding the absorption, distribution, metabolism, and excretion of endrin in humans and animals after inhalation, oral, or dermal exposure, which is especially relevant to occupational exposure scenarios. Endrin appears to be well absorbed orally, and distribution is primarily to fat and skin. Endrin is excreted in urine and feces, and the major biotransformation product is anti-12-hydroxy-... 

Nervous system effects may occur in humans after occupational exposure to disulfoton (Wolfe et al. 1978). In this study, mean disulfoton concentrations of 0.460.633 mg/m caused a 22.8% depression in erythrocyte cholinesterase activity in workers at a pesticide-fertilizer mixing operation. The workers were exposed to disulfoton for 9 weeks, and there were no reports of adverse clinical signs due to disulfoton exposure. The study was limited in that baseline blood cholinesterase activities were obtained 2 weeks after the initial exposure and were compared with cholinesterase activities at 9 weeks. Therefore, the actual depression in cholinesterase activity over a 9-week period was probably >22.8%. In addition, these workers were also dermally exposed to disulfoton (see Section 2.2.3.4) therefore, the 22.8% depression in cholinesterase activity was probably due to both inhalation and dermal exposure. Despite these limitations, the study concluded that because this depression in cholinesterase activity was only associated with dry mixing operations, the wet mixing operations are less hazardous to workers. 

Hepatic Effects. No studies were located regarding hepatic effects in humans after dermal exposure to 1,3,5-TNB. In one case report of occupational exposure to 1,3-DNB (Ishihara et al. 1976), the exposed worker had palpable liver while her liver function tests were negative. This study is limited in that only a single case was described and functional tests were performed 10 days after the exposure. 

Distribution data are limited to qualitative information derived from cases of accidental ingestion of food contaminated with PBBs, cases of occupational exposure via dermal contact (Eyster et al. 1983 Landrigan... 

White Phosphorus. Studies of human exposure to white phosphorus are limited to those examining occupational exposure to white phosphorus for intermediate or chronic durations. Most of the information on the effects of occupational exposure of humans to white phosphorus was from case reports, rather than epidemiology studies. Phosphorus oxidizes rapidly when exposed to air, and fumes/vapors in phosphorus factories probably contained phosphorus, phosphoric oxide, and phosphorus oxide (Heimann 1946 Hughes et al. 1962 Ward 1928). Exposure levels for white phosphorus and phosphorus compounds were not reported in the occupational studies. However, workers at phosphorus plants were probably also exposed to white phosphorus by the dermal and oral routes. 

Studies regarding dermal (nonbum) exposure of humans to white phosphorus were limited to those involving occupational exposure. In one study, the workers hands were regularly in contact with paste containing phosphorus (Ward 1928). The extent of dermal exposure in the other occupational studies was not clear, although it is likely there was dermal exposure to airborne particles (Heimann 1946 Hughes et al. 1962 Kennon and Hallam 1944). 

Most of the information on the toxicity of white phosphorus in humans comes from case reports of individuals who intentionally or accidentally ingested a single dose of phosphorus that was a component of poison or fireworks. These case reports provide information on acute systemic effects, possible immunological effects, neurological effects, reproductive effects, and death in humans. In addition to these case reports of single exposures, there are several case reports of children ingesting white phosphorus for an intermediate duration these studies provide information on intermediate systemic effects and developmental effects. Information on chronic oral and dermal exposure in humans is limited to occupational exposure studies in which workers were exposed to white phosphorus via inhalation, oral, or dermal routes. Some limited information on chronic systemic effects is available from these studies. There is limited information on the toxicity of inhaled white phosphorus in humans. Several occupational exposure studies are available however, only a limited number of parameters were assessed in these studies. 

Some information on health effects in humans following dermal bum exposure is available. As with the occupational exposure studies identified for inhalation, oral, and dermal (nonbum), these studies examined a limited number of systemic parameters. 

There is little information regarding health effects in humans following inhalation, oral, or dermal exposure to barium (Figure 2-2). Inhalation studies are limited to several case reports of individuals exposed acutely or chronically through occupational exposure (Doig 1976 Essing et al. 1976 ... 

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