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Modeling dermal exposure

McKone TE. 1993. Linking a PBPK model for chloroform with measured breath concentrations in showers implications for dermal exposure models. J Expo Anal Environ Epidemiol 3(3) 339-365. [Pg.277]

For a better idea of the toxicity of VOCs, we can look more closely at some studies of TCE (Bogen et al., 1998). In vitro uptake of C-14-labeled trichloroethylene (TCE) from dilute (similar to 5-ppb) aqueous solutions into human surgical skirt was measured using accelerator mass spectrometry (AMS). The AMS data obtained positively correlate with (p approximate to 0) and vary significantly nonlinearly with (p = 0.0094) exposure duration. These data are inconsistent (p approximate to 0) with predictions made for TCE by a proposed EPA dermal exposure model, even when uncertainties in its recommended parameter values for TCE are considered but are consistent (p = 0.17) with a 1-compartment model for exposed skin-surface. This study illustrates the power of AMS to facilitate analyses of contaminant biodistribution and uptake kinetics at very low environmental concentrations. Eurther studies could correlate this with toxicity. [Pg.35]

Versar, Inc. (1995). DERMAL Exposure Model Description and User s Manual, USEPA Contract No. 68-D3-0013, Springfield, VA, USA. [Pg.242]

The RISKOFDERM Dermal Exposure Model [53] is a model for estimating potential dermal exposure, i.e. the total amount of a substance coming into contact with the protective clothing, work clothing and exposed skin. It is based on statistical analysis of data gathered in the RISKOFDERM project, a European project on dermal exposure. The model originally consists of a set of equations as reported in the deliverables of the RISKOFDERM project. These equations have been entered into a user-friendly spread sheet in Excel. [Pg.568]

TNO/HSL (2008) RISKOEDERM potential dermal exposure model 2006. Download as www.tno.nl/downloads/RISKOFDERM potential dermal exposure model vs 2.1t.xls... [Pg.583]

Skinner CS, Kilgore WW. 1982b. Application of a dermal self-exposure model to worker reentry. J Toxicol Environ Health 9 461-481. [Pg.231]

W.J. Popendorf, Advances in the unified field model for reentry hazards, in Dermal Exposure Related to Pesticide Use Discussion of Risk Assessment, ed. R.C. Honeycutt, G. Zweig, and N.N. Ragsdale, ACS Symposium Series 273, American Chemical Society, Washington, DC, pp. 323-340 (1985). [Pg.1025]

The relation between the calculated amount of IPP excreted in urine resulting from dermal exposure and actual exposure of the hands was studied for both work clothing and protective clothing trials using the regression model ... [Pg.75]

Type IV Hypersensitivity. There are several well-established preclinical models for assessing Type IV (delayed-type) hypersensitivity reactions following dermal exposure, but not for predicting this response after systemic exposure. [Pg.572]

Risk Assessment. The Chinery-Gleason model has the greatest potential for use in estimating exposures to chloroform in a household environment as well as for occupational exposures that result from dermal exposure. [Pg.135]

Interroute Extrapolation. The Chinery-Gleason model examined two routes of exposure, inhalation-only exposure and inhalation/dermal exposure. The model was useful in predicting the concentration of chloroform in shower air and in the exhaled breath of individuals exposed by the dermal and inhalation routes. [Pg.136]

Risk Assessment. The McKone model has some use in human chloroform risk assessments, in that the model defined the relationship between the dermal and inhalation exposure to measures of dose and the amounts that can be metabolized by the liver by each route. The model also provided information about the inhalation and dermal exposure concentrations at which chloroform metabolism becomes nonlinear in humans. [Pg.136]

Comparative Toxicokinetics. A limited number of studies exist regarding the comparative toxicokinetics of orally administered silver compounds in rats, dogs, monkeys, and humans. A more complete comparison of the absorption and elimination of silver in humans and rats may be warranted given that much of the toxicokinetic data comes from rats. It would also be useful to acquire data on the comparative toxicokinetics of various silver compounds in several species of experimental animals and in humans following inhalation and dermal exposure in order to model the kinetics of silver deposition across different exposure scenarios and within sensitive populations. [Pg.69]

Maximum value for total absorbed dose for each individual calculated by three methods based on the pharmacokinetic model for clearance after dermal exposure to 2,1+,5-T (l6). [Pg.143]


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Dermal

Exposure model

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