Exposure estimates concepts

Exposure Estimation Concept 237 Model Utility Concept 238 REFERENCES 239... 

Each application has revealed new aspects that had not been considered previously (Table I). Nevertheless, the examples share one characteristic common to toxic chemical risk analysis an acceptable exposure level must be combined with a relationship between source concentration and estimated degree of exposure. This concept has been published previously(1,2,3) ... 

It is not possible to quantify all sources of uncertainty. Therefore, expression of uncertainty, variability or both in exposure estimates may be qualitative or quantitative, but uncertainty should be quantified to the extent that is scientifically achievable. The concepts of variability and uncertainty are distinct, and typically there will be a need to distinguish these based upon the problem formulation. 

Terrestrial wildlife movements are such that site-specific tools are more efficiently used to refine exposure estimate. In this case, site-specific exposure estimates are used and compared with safe thresholds for toxicity, termed toxicity reference values (TRVs). Toxicity reference values for wildlife have been developed for energetic compounds. This chapter presents a brief overview of the processes used to establish these tools for ERA for explosives and related soil contaminants that are frequently of potential ecological concern at the affected military sites. This chapter also provides recommendations for use of these values in the ERA process. Investigations addressing the importance and extent of habitat disturbance as a component of the ERA process on explosives-contaminated ranges are reviewed in Chapter 11. General bioaccumulation principles and applications of the bioaccumulation factor and bioconcentration factor (BAF and BCF, respectively) concepts that are often employed in the ERA process to determine bioaccumulation potential of MC for terrestrial receptors are reviewed in Chapter 10. 

The process whereby the risks associated with the use of pesticides are assessed has become Increasingly complex over the years, and even the definition of the term risk assessment Is widely variable. However, most Include the concepts of hazard and probability of occurrence and require Information on toxicology and exposure. In the Ideal situation there should be accurate data on the actual amount of pesticide to which the worker was exposed. Including the primary route of exposure, the absorption should be known, enabling correction of the exposure estimate, and the amount of pesticide necessary to cause toxic effects In test animals should be known. From these data. It could be determined whether the product could be used safely. 

Acceptable Daily Intake (ADI) An estimate similar in concept to the RfD, but derived using a less strictly defined methodology. RfDs have replaced ADIs as the USEPA s (Agency) preferred values for use in evaluating potential noiicarcinogenic health effects resulting from exposure to a chemical. 

Development of subchronic RfDs parallels the development of chronic reference doses in concept the distinction is one of e.xposurc duration. Appropriate studies are evaluated and a subchronic NOAEL is identified. The RfD is derived from the NOAEL by the application of the UFs and MF, as outlined above. When experimental data arc available only for shorter e.xposurc durations than desired, an additional uncertainly factor is applied. This is similar to the application of the uncertainly factor for duration differences when a chronic RfD is estimated from subchronic animal data. On the other hand, if subchronic data are missing and a chronic oral RfD derived from chronic data exists, the chronic oral RfD is adopted as the subchronic oral RfD. Ill this instance, there is no application of an uncertainly factor to account for differences in exposure duration. 

Chapter 2 offers a unifying exposure to the relevant concepts of estimability and redundancy, in particular their importance in the decomposition of the general data processing problem. 

Environmental risk assessment of substances is nowadays based on an evaluation of exposure pathways and concentrations on the one hand and identification and selection of sensitive endpoints on the other. The concept is operationalised by comparing real or estimated (predicted) exposure concentrations (PEC) with calculated no-effect concentrations (NEC or PNEC, predicted NEC). The comparison can be made by calculating the quotient of exposure and no-effect concentration. If the quotient is less than one, then the substance poses no significant risk to the environment. If the quotient is greater than one, the substance may pose a risk, and further action is required, e.g. a more thorough analysis of probability and magnitude of effects will be carried out. 

This form of risk assessment is based on the concept of defining an exposure level, the derived standard, expressed usually on a temporal basis (e.g., daily, weekly), which is considered to offer sufficient reassurance of protection of human health, and then comparing this with an estimated level of exposure. If the estimated exposure is higher than the standard, then further regulatory intervention may be needed. Please see Section 5.12 for a discussion of the health implications of exceeding the tolerable intake. 

The US-EPA (1986) applied the concept of response addition to the determination of cancer risks, assuming a complete negative correlation of tolerance. This assumption is considered to contribute to a conservative estimation of risk, since the correlation of tolerances may not be strictly negative in inbred homogenous experimental animals. There is a major difference between the concepts of response addition and dose addition when the human simation of low exposure levels is assessed. Response addition implies that when doses of chemicals are below the no-effect levels of the individual compounds (i.e., the response of each chemical equals zero), the combined action of aU compounds together wdl also be zero. In contrast, dose addition can also occur below the no-effect level and the combined toxicity of a mixture of compounds at individual levels below the no-effect level may lead to a response. 

The explanation of the pharmacokinetics or toxicokinetics involved in absorption, distribution, and elimination processes is a highly specialized branch of toxicology, and is beyond the scope of this chapter. However, here we introduce a few basic concepts that are related to the several transport rate processes that we described earlier in this chapter. Toxicokinetics is an extension of pharmacokinetics in that these studies are conducted at higher doses than pharmacokinetic studies and the principles of pharmacokinetics are applied to xenobiotics. In addition these studies are essential to provide information on the fate of the xenobiotic following exposure by a define route. This information is essential if one is to adequately interpret the dose-response relationship in the risk assessment process. In recent years these toxicokinetic data from laboratory animals have started to be utilized in physiologically based pharmacokinetic (PBPK) models to help extrapolations to low-dose exposures in humans. The ultimate aim in all of these analyses is to provide an estimate of tissue concentrations at the target site associated with the toxicity. 

Sir Edward Pochin (1978) Why be Quantitative about Radiation Risk Estimates Hymer L. Friedell (1979) Radiation Protection-Concepts and Trade Offs Harold O. Wyckoff (1980) From Quantity of Radiation and Dose to Exposure and Absorbed Dose -An Historical Review James F. Crow (1981) How Well Can We Assess Genetic Risk Not Very Eugene L. Saenger (1982) Ethics, Trade-offs and Medical Radiation Merril Eisenbud (1983) The Human Environment-Past, Present and Future Harald H. Rossi (1984) Limitation and Assessment in Radiation Protection John H. Harley (1985) Truth (and Beauty) in Radiation Measurement Herman P. Schwan (1986) Biological Effects of Non-ionizing Radiations ... 

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