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Dermal exposure residences

Gold, R.E. and T. Holcslaw (1985). Dermal and respiratory exposure of applicators to dichlorvos-treated residences, in Dermal Exposure Related to Pesticide Use, R.C. Honeycutt, G. Zweig and N.N. Ragsdale (Eds), ACS Symposium Series 273, American Chemical Society, Washington, DC, USA, pp. 253-264. [Pg.121]

Primary exposure routes to JP are inhalation and dermal exposure to the aircraft maintenance personnel working directly with the JP. Additionally, populations residing near air force bases may be exposed to the JP by inhalations route in the form of vapors and aerosol. [Pg.1469]

Dermal eoqposure to residents to DDVP oouH not be assessed however, it was noted that the environmental eaqxjsure pads received 0.31910.183 pg/on /hr during the application u)d the two hrs post-initiation. This r esents 63.9% of the total dermal exposure of the applicators. [Pg.262]

Twenty residential structures were treated with dichlorvos insecticide (DDVP) for (Serman cockroach control. Dermal exposure pads, air samplers, blood tests for sensn and erythrocyte acetyl-ciiolinesterase (oizyme) activity and urine analyses were used to monitor both c licators and residents for evidence of 9qx>sure to EDVP. [Pg.263]

Mirex has been found in human adipose tissue (Burse et al. 1989 Kutz et al. 1974). Although the route of exposure was not specified, exposure was probably via the inhalation, oral, and dermal routes. Levels of 0.16-5.94 ppm and 0.3-1.13 ppm in males and females, respectively, were found in tissue samples taken either from postmortem examinations or during surgery (Kutz et al. 1974). The adipose tissue samples came from individuals who lived in areas in which mirex was used extensively in a program to control fire ants. Adipose tissue levels of mirex ranging from 0.03 to 3.72 ppm have been found in residents living near a dump site in Tennessee (Burse et al. 1989). [Pg.110]

Human exposure to PFCs is likely to occur via a number of vectors and routes, for example food, drinking water, the ingestion of non-food materials, dermal contact and inhalation. Circumstantial factors such as place of residence, age, nature of PFCs vector, may also influence exposure. For example, according to Tittlemier et al. [27], food seems to represent the major intake pathway of PFAS in adult Canadians however, house dust, solution-treated carpeting and treated apparel might contribute a non-negligible 40% to the overall exposure. [Pg.366]

Distribution. Quantitative inhalation, oral, or dermal distribution studies in humans are not available for 1,4-dichlorobenzene. 1,4-Dichlorobenzene has been detected in human blood, adipose tissue, and breast milk after an assumed inhalation exposure in Tokyo residents (Morita and Ohi 1975 Morita et al. 1975), as well as people in some parts of the United States (EPA 1983b, 1986). The available data indicate that after inhalation, oral, and subcutaneous exposure, 1,4-dichlorobenzene preferentially distributes to the fat tissue and organ-specific sites within the body (Hawkins et al. 1980), following the order adipose > kidney > liver > blood (Charboimeau et al. 1989b Hawkins et al. 1980). Although... [Pg.116]

Okrent and Xing (1993) estimated the lifetime cancer risk to a future resident at a hazardous waste disposal site after loss of institutional control. The assumed exposure pathways involve consumption of contaminated fruits and vegetables, ingestion of contaminated soil, and dermal absorption. The slope factors for each chemical that induces stochastic effects were obtained from the IRIS (1988) database and, thus, represent upper bounds (UCLs). The exposure duration was assumed to be 70 y. Based on these assumptions, the estimated lifetime cancer risk was 0.3, due almost entirely to arsenic. If the risk were reduced by a factor of 10, based on the assumption that UCLs of slope factors for chemicals that induce stochastic effects should be reduced by this amount in evaluating waste for classification as low-hazard (see Section 7.1.7.1), the estimated risk would be reduced to 0.03. Either of these results is greater than the assumed limit on acceptable risk of 10 3 (see Table 7.1). Thus, based on this analysis, the waste would be classified as high-hazard in the absence of perpetual institutional control to preclude permanent occupancy of a disposal site. [Pg.346]

Exposure to benzene-contaminated water can also provide an opportunity for both inhalation and dermal absorption. In a series of experiments conducted in a single-family residence from June 11 to 13, 1991,... [Pg.141]

Fenske, R.A. and K.G. Black (1989). Dermal and respiratory exposures to pesticides in and around residences, in Measurement of Toxic and Related Air Pollutants Proceedings of the 1993 USEPA/A WMA International Symposium, Publication VIP-34, Air and Waste Management Association, Pittsburgh, PA, USA, pp. 853-858. [Pg.120]

Model 201 is independent of the other models, and the source of contamination considered in this model is contaminated soil in the outdoor vicinity of a residence. The exposure routes considered are dermal, ingestion and inhalation. Human physiological parameters, such as dermal exposed surface area, soil ingestion rate, inhalation rate and body weight, allow estimation of the dose for different age groups. [Pg.233]

This chapter describes and illustrates probabilistic approaches to aggregate and cumulative assessments of exposure, dose and risk. Aggregate assessments account for multiple sources (e.g. food, water, residence and occupation) and multiple routes (ingestion, dermal and inhalation) of exposure for a single pesticide. Cumulative assessments combine exposures for chemicals that share a... [Pg.275]


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