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Exposure analysis

Characterization of exposure is a straightforward determination of the environmental concentration range, or if available, the actual dose received by the biota of a particular stressor. Although simple in concept, determining or predicting the environmental exposure has proven to be difficult. [Pg.368]

However, as the material leaves the pipe and enters the ecosystem, it is almost immediately affected by both the biotic and abiotic components of the receiving system. All of the substrate and medium heterogeneity as well as the inherent temporal and spatial characteristics of the biota affect the incoming material. In addition to the state of the system at the time of pollution, the history of the environment as contained in the genetic makeup of the populations plus additional stressors in the past or present all impact the chemical-ecosystem interaction. The goal of the exposure analyses is to quantify the occurrence and availability of the stressor within the ecosystem. [Pg.369]

It should not be forgotten that a great deal of biotransformation does occur, especially for metals such as mercury and for many organics. In many cases, the result is a less toxic form of the original input, but occasionally more toxic materials are created. [Pg.369]

Lastly, models attempting to predict the fate and resultant exposure to a stressor can be used, and often they are applied in a variety of scenarios. Models, however, are simplifications of our imperfect understanding of exposure and should be tested whenever possible against comparable datasets. The reader should refer to the brief introduction of models found in Chapter 1. [Pg.369]

As the temporal and spatial distribution of the stressor has been quantified in the exposure analysis step, it should prove possible to provide the distribution curve for exposure of the biotic components of interest to the stressor. Dose and concentration probabilities are the typical units used in environmental toxicology. [Pg.369]

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]

Usage data. The concentrations of the food additive in foods plus, if available, the patterns of use. [Pg.64]

Food consumption data. The amounts of the affected foods eaten including, if necessary, consumption by sub-groups. [Pg.64]

The Estimated Daily Intake (EDI) can then be calculated using a relatively simple equation  [Pg.64]

The EDI is corrected for bodyweight so that a direct comparison with the ADI can be made. [Pg.64]

Having established some information about the relationship between dose and response it is necessary to determine the levels of actual doses to the human population. Two pieces of information are vital for this  [Pg.21]

Comprehensive data on the levels and frequency of occurrence of chemical contaminants in food are extremely expensive to obtain and are thus relatively rare. Nevertheless there are some reliable data sources and it is usually possible to acquire some data. Unfortunately, it is usually only possible to obtain data on average levels from many published sources. Even if ranges are published with the mean, interpretation is extremely difficult. [Pg.22]

In the UK the Joint Food Science and Safety Group of the Department of Health and the Ministry of Agriculture, Fisheries and Food have published the results of many analyses for chemical contaminants in food carried out under their Food Surveillance Programme. In many cases the raw data from these surveys are available for analysis. Table 2.1 lists the results of analyses for lead in some samples of cow, sheep and pig kidney obtained in Scotland and England.5 There are clear differences between species and some evidence of differences between sampling locations. What is not clear is the extent to which the variability observed is due to real and consistent differences between species and location or to normal biological variation. [Pg.22]

There is clearly considerable scope for producing a wide variety of intake estimates for any given scenario. It is therefore vital that the underlying [Pg.25]


If, on the other hand, it can be demonstrated that the particular N-nitroso contaminant is not an oncogen, the product will be cleared for registration without having to perform an exposure analysis. [Pg.388]

L.A. Burns and D.M. CUne, Exposure Analysis Modeling System Reference Manual for EXAMS2, EPA/600/3-85/038, NTIS Publication No. PB85-228138, Environmental Protection Agency, Washington, DC (1985). [Pg.907]

Shamoo, D.A., Johnson, T.R., Trim, S.C., Little, D.E., Linn, W.S., and Hackney, J.D., Activity patterns of a panel of outdoor workers exposed to oxidant pollution, Journal of Exposure Analysis and Environmental Epidemiology, 1(4), 423-438, 1991. [Pg.47]

This paper focuses on issues in the "dispersion" block of Figure 1. These issues must be addressed, however, in the context of a health effects problem. Some knowledge of the health risk is necessary to properly scope the exposure analysis. [Pg.69]

Appropriate methods of exposure analysis depend on the form of the health effect function, which must be presumed to depend on some function of the time history of concentration to which a person is exposed. Even... [Pg.69]

It is important in defining any analysis scheme that the analysis elements be consistent in scope, scale, and detail with each other and with the purposes of the analysis. Thus details of cohort exposure in microenvironments can provide valuable information on populations at risk if, in fact, pollutant concentrations are functions of micro-environments. It appears that micro-environments are clearly important in carbon monoxide (CO) exposure analysis because automobile generated CO concentrations are highly correlated with automobile usage patterns. It is not clear that ozone exposures are so correlated. Ozone commonly exists in "clouds" that are large compared to any one micro-environment, but drift over an area large compared to their size in the course of their formation and decay. [Pg.72]

Prospectus on "Research and Development on an Exposure Analysis Modelling System (EXAMS) USEPA Athens, Ga., 1979. [Pg.195]

Exposure analysis summary including persistence evaluation... [Pg.253]

EPA. 1989g. Review of the national ambient air quality standard for lead Exposure analysis, methodology and validation. OAQPS staff report. Research Triangle Park, NC U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards. EPA-450/2-89-011. [Pg.515]

Klopffer, W. (1991) Photochemistry in environmental research Its role in abiotic degradation and exposure analysis. EPA Newsletter... [Pg.54]

Category C (possible human carcinogen) was evidenced by a dose-related increase in the incidence of leiomyosarcomas in the urinary bladder, a significant dose-related trend for combined hepatocellular adenomas and carcinomas in males, and a significantly higher incidence of combined lung adenomas and carcinomas in females. For the purpose of risk characterization, the RfD approach should be used for quantification of human cancer risk. The chronic exposure analysis revealed <100% RfD, and it is assumed that the chronic dietary endpoint is protective for cancer dietary exposure [64]. [Pg.94]

EPA. 1987a. Exposure analysis modeling system (EXAMSII). Center for Exposure Assessment Modeling, Ecosystems Research Division, National Exposure Research Laboratory, Office of Research and Development. U. S. Environmental Protection Agency. Athens, GA. [Pg.233]

Exposure analysis. The amount of any chemical that an individual is exposed to will depend upon the levels that occur in food and the amounts of those foods that are consumed. Different population groups will often have different levels of exposure and it is therefore necessary to identify such sub-groups. The exposure level for additives is frequently referred to as the Estimated Daily Intake (EDI). [Pg.61]

Environmental concentration Exposure analysis, biodegradation PEC Predicted environmental concentration... [Pg.78]

Golt, J. S., J. Lubin, et al. (2004). Gomparison of pesticide levels in carpet dust and self-reported pest treatment practices in four US sites. Journal of Exposure Analysis and Environmental Epidemiology 14(1) 74-83. [Pg.166]

The magnitude of the dose is a function of the amount of chemical in the medium of contact, the rate of contact with the medium, the route of exposure, and other factors as well. Experts in exposure analysis use various means to estimate the dose incurred by individuals exposed to chemicals. Exposure analysis is one of the critical steps in toxicological risk assessment. [Pg.28]

A similar set of defaults could be described for the human exposure assessment step. As noted, the regulatory approach tends to target those members of the population who are at the high end of exposures, and in some cases regulators, and other risk assessors, engage in something close to what is known as a worst-case exposure analysis. Here are three simple examples. [Pg.228]

Burns, L.A. Cline, D.M. Lassiter, R.R. "Exposure Analysis Modeling System (EXAMS) User Manual and System Documentation" U.S. Environmental Protection Agency, Environmental Research Laboratory Athens, GA, 1981. [Pg.296]

Emad A, Rezaian GR The diversity of the effects of sulfur mustard gas inhalation on respiratory system 10 years after a single, heavy exposure. Analysis of 197 cases. Chest 112(3) 734-738, 1997... [Pg.503]

Jarvholm et al. (1986) Sweden Cohort 219 men employed for at least one year on a machine using fluids containing ethanolamines and sodium nitrite 1966-83 No sub-group or exposure analysis. Population presumed to be exposed to TV-nitroso-diethanolamine... [Pg.410]

In our work with characterizing PAH in the work environment, we have felt that it is necessary to establish body doses through appropriate body fluid analysis for a better risk evaluation of occupational exposure. Analysis of metabolites and adducts between cellular macromolecules and -metabolites is in progress. [Pg.375]

Wenning RJ. 2002. Uncertainties and data needs in risk assessment of three commercial polybrominated diphenyl ethers probabilistic exposure analysis and comparison with European commission results. Chemosphere 46(5) 779-796. [Pg.457]


See other pages where Exposure analysis is mentioned: [Pg.387]    [Pg.6]    [Pg.213]    [Pg.35]    [Pg.39]    [Pg.73]    [Pg.90]    [Pg.64]    [Pg.78]    [Pg.77]    [Pg.163]    [Pg.166]    [Pg.61]    [Pg.129]    [Pg.64]    [Pg.346]    [Pg.404]    [Pg.292]   
See also in sourсe #XX -- [ Pg.61 , Pg.62 , Pg.64 , Pg.65 , Pg.66 , Pg.67 , Pg.68 , Pg.69 , Pg.70 , Pg.71 , Pg.72 , Pg.73 , Pg.74 ]

See also in sourсe #XX -- [ Pg.16 ]




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