Dermal exposure USEPA

USEPA. 1992. "Dermal Exposure Assessment Principles and Application." United States Environmental Protection Agency (USEPA), report no. EPA/600/8-91/011B (January, 1992). U.S. EPA, Washington, D.C. 

Table 1.2 Surface areas for regions of the adult body and locations of dermal exposure pads that represent these regions (USEPA, 1987)...

The SCIES and MCCEM models give only inhalation exposure, but the simulated results can be incorporated into a whole-risk assessment in the residential space such as the USEPA SOP framework (USEPA, 1997b) which estimates multiple exposure levels via all routes (i.e. inhalation, dermal and oral). THERdbASE is capable of estimating inhalation and dermal exposures based on the simulated airborne concentration and the film-thickness theory, and InPest estimates all exposures, including oral routes, based on the simulated concentration in the air and amounts on the room materials (Matoba et al., 1998c). 

Versar, Inc. (1995). DERMAL Exposure Model Description and User s Manual, USEPA Contract No. 68-D3-0013, Springfield, VA, USA. 

The present OECD and USEPA protocols typically focus on dermal uptake expressed as percentage of dose. In general, no information is provided on the rate of absorption (peak profile or sustained presence) and the metabolites formed, although some guidance on these issues exists (USEPA, 1998). This additional information on the behavior of the test substance could be very useful in (refinement oO the risk assessment. For instance, information on the metabolites formed after dermal exposure could be very helpful in addressing the question as to what extent oral toxicity studies could be used to assess the risk of the dermally exposed population. Information on the rate of absorption could be employed in a similar manner. This latter value can easily be obtained from in vitro smdies. 

USEPA (1992). Dermal Exposure Assessment Principles and Applications, Interim report EPA/600/8-91.001B, United States Environmental Protection Agency, Office of Research and Development, Washington, DC, USA. 

Dermal exposure The quantifiable measure of the amount of residue deposited on skin, normally expressed as a density, or mass per unit time, deposited on a defined skin surface area (e.g. mg/h hand exposure) equivalent to potential dose for the dermal route (USEPA, 1998). 

Intake rate Rate of inhalation, ingestion and dermal contact depending on the route of exposure. For ingestion, the intake rate is simply the amount of food containing the contaminant of interest that an individual ingests during some specific time-period (units of mass/time). For inhalation, the intake rate is the rate at which contaminated air is inhaled. Factors that affect dermal exposure are the amount of material that comes into contact with the skin, and the rate at which the contaminant is absorbed (USEPA, 1997c). 

SADA provides a full human health risk assessment module and associated databases. The risk models follow the USEPA s Risk Assessment Guidance for Superfund (RAGS) and can be customized to fit site-specific exposure conditions. It calculates risks based on the following exposure pathways ingestion, inhalation, dermal contact, food consumption, and also a combined exposure. 

About 727,000 workers were potentially exposed to nickel metal, nickel alloys, or nickel compounds during the period 1980 to 1983 (USPHS 1993). Worker exposure differs from that of the general population in that the major route of exposure for nickel workers is inhalation and for the general population it is dermal contact (Sevin 1980). Nickel workers with lung cancer had elevated concentrations of 1.97 mg/kg DW in their lungs when compared to the general population (0.03 to 0.15 mg/kg DW USPHS 1977). Plasma concentrations of nickel quickly reflect current exposure history to nickel (USEPA 1980). Mean nickel concentrations in plasma of humans occupationally exposed to nickel have declined by about 50% since 1976, suggesting decreased exposure due to improved safety (Boysen et al. 1980). 

In mammals, the toxicity of nickel is a function of the chemical form of nickel, dose, and route of exposure. Exposure to nickel by inhalation, injection, or cutaneous contact is more significant than oral exposure. Toxic effects of nickel to humans and laboratory mammals are documented for respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, dermal, ocular, immunological, developmental, neurological, and reproductive systems (NAS 1975 Nielsen 1977 USEPA 1980, 1986 WHO 1991 USPHS 1993). 

Animal experimental models of nickel-induced skin sensitivity are few and have been conducted only under very specialized conditions (USEPA 1986). Studies examining the mechanism of nickel contact sensitization and its extent in wildlife are needed (USPHS 1993). The importance of the surface properties and crystalline structure of nickel compounds in relation to their reactivity and protein-binding activities is well documented. It is therefore necessary to identify clearly the nickel compounds to which exposure occurs (Sunderman etal. 1984). Acute and chronic dermal and... 

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