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Population exposures

Figures 16-3 through 16-5 present the decision network for screening contaminant fate in air, surface water, ground water, and biota. Pathways must be further evaluated to determine the likelihood of population exposure. Figures 16-3 through 16-5 present the decision network for screening contaminant fate in air, surface water, ground water, and biota. Pathways must be further evaluated to determine the likelihood of population exposure.
CASRAM predicts discharge fractions, flash-entrainment quantities, and liquid pool evaporation rates used as input to the model s dispersion algorithm to estimate chemical hazard population exposure zones. The output of CASRAM is a deterministic estimate of the hazard zone (to estimate an associated population health risk value) or the probability distributions of hazard-zones (which is used to estimate an associated distribution population health risk). [Pg.351]

Mining Waste Estimated 10-20 eaneers aiuiually, largely due to arsenie. Remote loeations and small population exposure reduee overall risk though individual risk may be high. [Pg.411]

E1 The Extent of Population Exposure to Assess Clinical Safety for Drugs Intended for Long-Term Treatment of Non-Life Threatening Conditions E2A Clinical Safety Data Management Definitions and Standards for Expedited Reporting... [Pg.80]

Exposure to endosulfan residues in tobacco products could be another important source of general population exposure. Endosulfan residues in tobacco leaves and finished tobacco products were reviewed by EPA (1982a). Eor example, auction market tobacco had a mean residue of <0.2-14 ppm endosulfan and endosulfan sulfate in the early 1970s, and cigarettes sold in 1973 contained a mean residue of 0.83 ppm endosulfan. No information was found in the available literature regarding endosulfan concentrations in cigarette smoke. [Pg.236]

Skender L, Karacic V, Bosner B, et al. 1994. Assessment of urban population exposure to trichloroethylene and tetrachloroethylene by means of biological monitoring. Arch Environ Health 49 445-451. [Pg.290]

Vartiainen T, Pukkala E, Rienoja T, et al. 1993. Population exposure to tri- and tetrachloroethylene and cancer risk Two cases of drinking water pollution. Chemosphere 27 1171-1181. [Pg.294]

Polyalphaolefin Hydraulic Fluids. Polyalphaolefin hydraulic fluids find significant use in a number of applications including situations where cold temperature operation is important. Applications include construction equipment and other machinery that is designed to operate in cold conditions. No estimates of either occupational or general population exposure to these hydraulic fluids were found in the available literature. [Pg.312]

T. Johnson and J. Capel, "Population Exposure to Ozone in the Northeast Corridor from May through October, 1979," PEDCo Environmental, Inc., Durham, North Carolina, 1980. [Pg.88]

The output of an exposure and risk assessment will usually describe the levels of exposure and quantity the population exposed for both humans and other biota, and will estimate the associated probabilities of the incidence of adverse health effects. Population exposure or risk, obtained by multiplying the individual (per capita) exposure or risk by the numbers exposed at each level of exposure, may also be a useful measure of impact. Various analyses can be performed on the results, for example, comparison of exposures in a particular geographic area against national average exposure levels. Likewise, for the same pollutant, environmental risks due to a particular industry might be compared against risks associated with occupational or household activities. In addition, the health risk of different substances could be compared for priority setting. [Pg.289]

The purpose of an Exposure Route and Receptor Analysis is to provide methods for estimating individual and population exposure. The results of this step combined with the output of the fate models serve as primary input to the exposure estimation step. Unlike the other analytic steps, the data prepared in this step are not necessarily pollutant-specific. The two discrete components of this analysis are (1) selection of algorithms for estimating individual intake levels of pollutants for each exposure pathway and (2) determination of the regional distribution of study area receptor populations and the temporal factors and behavioral patterns influencing this distribution. [Pg.292]

The magnitude of exposure in a geographic area is a function not only of the amount of pollutant to which a "typical" individual is exposed but also of the size of the population exposed. This is especially important in the calculation of risk for an area or subpopulation. The resulting quantity is a population exposure factor which is the product of the individual pollutant intake level per unit time (average or maximum) multiplied by the population size exposed. [Pg.293]

For a limited number of exposure pathways (primarily inhalation of air in the vicinity of sources), pollutant fate and distribution models have been adapted to estimate population exposure. Examples of such models include the SAI and SRI methodologies developed for EPA s Office of Air Quality Planning and Standards (1,2), the NAAQS Exposure Model (3), and the GEMS approach developed for EPA s Office of Toxic Substances (4). In most cases, however, fate model output will serve as an independent input to an exposure estimate. [Pg.295]

As discussed in the introduction to Section 2.2, the bulk of the human data on the health effects of lead are expressed in terms of internal exposure, or PbB levels, rather than external exposure levels (i.e., mg/m3 or mg/kg/day). For the general population, exposure to lead occurs primarily via the oral route with some contribution from the inhalation route, whereas occupational exposure is primarily by inhalation with some oral. Therefore, it is difficult to distinguish specific routes and levels of exposure. For this reason, the human health effects data for lead will be presented in terms of PbB levels in this section. Health effects associated with human exposures to lead and internal lead doses are shown in Table 2-1. [Pg.37]

This inverse relationship between equilibrium factor and "unattached" fraction and their relationship to the resulting dose is important in considering how to most efficiently and effectively monitor for exposure. This inverse relationship suggests that it is sufficient to determine the radon concentration. However, it is not clear how precisely this relationship holds and if the dose models are sufficiently accurate to fully support the use of only radon measurements to estimate population exposure and dose. [Pg.11]

Variations in radiation doses to individuals within exposed populations also occur. Based upon previous exposures of people to Pu and Sr in fallout and exposures of laboratory animals to Ce, the dispersion of individual doses in a population is expected to be significant and should be considered in the formulation of population exposure guidelines. [Pg.21]

Mioduszewski, R.J., S.A. Reutter, L.L. Miller, E.J. Olajos, and S. A. Thomson. Evaluation of Airborne Exposure Limits for G-Agents Occupational and General Population Exposure Criteria, Edgewood Arsenal Report No. ERDEC-TR-489. April 1998 with Erratum Sheet dated April 17,2000. [Pg.103]

The extent of population exposure to assess clinical safety Clinical safety data management Definitions and standards for expedited reporting... [Pg.76]

Having identified information about the relationship between dose of a food additive and any toxicological response, and determined an ADI, it is necessary to investigate the levels of actual doses in the human population. Exposure analysis is used to find out if any individuals have potential intakes that might exceed the ADI for a particular additive and if so, by how much. Two pieces of information are vital for this ... [Pg.64]

General population exposure to mirex has been determined as a result of several monitoring studies (EPA 1986b Kutz et al. 1979 Stehr-Green 1989). Levels of mirex in most tissues are very low (at or near the detection limit). Examination of the 1982 National Adipose Tissue Survey failed to detect mirex in the adipose tissues of children less than 14 years old although mirex residues were detected in adults. People who live in areas where mirex was manufactured or used have higher levels in their tissues. Women who live in these areas were found to have detectable levels of mirex in their milk that could be passed on to their infants. Since mirex is no longer manufactured, occupational exposure currently is limited to workers at waste disposal sites or those involved in... [Pg.173]

General population exposure to chlordecone has not been determined because this compound has not been monitored in any national program (EPA 1986b Kutz et al. 1979 Phillips and Birchard 1991a Stehr-Green 1989). Levels of chlordecone were detected in 9 of 298 samples of human milk... [Pg.175]

EPA. 1978e. Human population exposures to mirex and Kepone. Washington, DC U.S. Environmental Protection Agency. Document No. ISS EPA/600/1-78/045, CRESS-26. [Pg.251]

Balonov M., Jacob P., Likhtarev I., Minenko V., 1996. Pathways, levels and trends of population exposures from consumption of agricultural and semi-natural products, The radiological consequences of the Chernobyl accident Proc. of the 1-st Intern. Conference (Minsk, Belarus, 18-22 March, 1996), Luxembourg, pp. 235-251. [Pg.42]

Exposures in the population of interest will generally reveal that incurred dose is only a small fraction, and sometimes a very tiny fraction, of that at which toxic responses has been or can be directly measured, in either epidemiology or animal studies. Occupational populations (Table 8.1, Scenario C) may be exposed at doses close to those for which data are available, but general population exposures are usually much smaller. Thus, to estimate risk it will be necessary to incorporate some form of extrapolation from the available dose-response data to estimate toxic response (risk) in the range of doses expected to be incurred by the population that is the subject of the risk assessment. [Pg.227]


See other pages where Population exposures is mentioned: [Pg.368]    [Pg.77]    [Pg.525]    [Pg.217]    [Pg.97]    [Pg.355]    [Pg.169]    [Pg.245]    [Pg.220]    [Pg.926]    [Pg.193]    [Pg.289]    [Pg.311]    [Pg.435]    [Pg.67]    [Pg.76]    [Pg.11]    [Pg.24]    [Pg.443]    [Pg.187]    [Pg.90]    [Pg.153]    [Pg.340]    [Pg.346]    [Pg.236]    [Pg.240]   
See also in sourсe #XX -- [ Pg.16 , Pg.286 ]




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Carcinogenic effects general population exposures

Data bases exposure, general population

Exposure Characterizations for Lead in Specific Human Populations

Exposure and the Population at Risk

Exposure general population

Occupational lead exposures population studies

Population exposure estimates

Population exposure model

Potential Population Exposure

Sample Distributions of Exposure Assumptions in Human Populations

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