Estimating Exposure Concentrations

Thus, tlie focus of tliis subsection is on qualitative/semiquantitative approaches tliat can yield useful information to decision-makers for a limited resource investment. There are several categories of uncertainties associated with site risk assessments. One is tlie initial selection of substances used to characterize exposures and risk on tlie basis of the sampling data and available toxicity information. Oilier sources of uncertainty are inlierent in tlie toxicity values for each substance used to characterize risk. Additional micertainties are inlierent in tlie exposure assessment for individual substances and individual exposures. These uncertainties are usually driven by uncertainty in tlie chemical monitoring data and tlie models used to estimate exposure concentrations in tlie absence of monitoring data, but can also be driven by population intake parameters. As described earlier, additional micertainties are incorporated in tlie risk assessment when exposures to several substances across multiple patliways are suimned. 

EEC Estimated exposure concentration NOEL No-observed-effect level... 

Resuspension accounts for contaminants deposited on soil that are resuspended in air by vrind, rainsplash, or physical disturbance and subsequently deposited on plant surfaces. When possible, samples of plants or plant products should be used to estimate exposure concentrations (EPA 1989c). 

The assessor combines the assumptions stated in the exposure scenario with information about the behavior of the chemical to perform a mass balance that produces an estimated exposure concentration, known as a predicted environmental concentration (PEC), in each of the relevant compartments. 

The risk assessors used the BUSES model to estimate exposure concentrations from these emissions. At steady state, the model predicted the following environmental concentrations (PECs) [57] ... 

The hazards need to be identified and the risks assessed for example, in fhe case of air contaminants the nature of the substance(s) present and the estimated exposure concentration, or, with noise, measurement of sound levels and frequency characteristics. 

Neal et al. attempted some rough quantification of the tremor by having the worker lift a flat wooden strip with a small block placed on one end, then return it to the table surface. Tremors were rated as slight, moderate, or severe, and the ratings revealed consistent relationships with the number of years employed in the industry and the estimated exposure concentration. 

It is estimated that concentrations of 3000 ppm cause unconsciousness in less than 10 minutes (39). Anesthetic effects have been reported at concentrations of 400 ppm after 20-min exposure. Decrease in psychomotor performance at a trichloroethylene concentration of 110 ppm has been reported in one study (33), whereas other studies find no neurotoxic effects at concentrations of 200 ppm (40—43). 

In this step, the assessor qiuuitifies tlie magnitude, frequency and duration of exposure for each patliway identified in Step 2. Tliis step is most often conducted in two stages estimation of exposure concentrations and calculation of intakes. The later estimation is considered in Step 4. In tliis part of step 3. the exposure assessor determines the concentration of chemicals tliat will be contacted over the exposure period. E.xposure concentrations are estimated using monitoring data and/or chemical transport and environmental fate models. Modeling may be used to estimate future chemical concentrations in media tliat are currently contaminated or tliat may become contaminated, and current concentrations in media and/or at locations for which tliere are no monitoring data. The bulk of the material in tliis chapter is concerned witli tliis step. 

Very few data are available on the effects of organotins in humans. Of the reported unintentional occupational exposures, none has an estimate of exposure concentration. Exposure was largely via the inhalation route, with some possibility of dermal exposure. Neurological effects were the most commonly reported, and these can persist for long periods. 

One of six workers died 12 days after exposure to a mixture of half dimethyltin dichloride and half trimeth-yltin chloride vapour during cleaning of a cauldron at a chemical plant in Germany in 1981. Maximum exposure time was 1.5 h over a 3-day period no estimates of exposure concentration were made. Symptoms preceding death included excretion of high levels of tin in the urine, respiratory depression, and coma (Rey et al.,... 

Exposures of Children. Data need to be developed to properly assess the exposure of infants who eat processed baby foods containing residues of pesticides such as endosulfan. Several studies have estimated exposure based on endosulfan concentration found in foods typically eaten by infants however, no studies that directly studied infant exposure could be located. Attention should also be given to infant formulas and to the tap water used to prepare infant formulas from condensed or powdered forms. More data are also required to properly assess endosulfan exposure to children who live, play, or attend school near farmlands that are treated with endosulfan. Maps that catalog endosulfan use on crops and present average application rates would better allow an assessment of the potential for children in farming communities to be exposed. The possibility that farming parents work clothes and shoes may carry endosulfan residues into the home also should be studied. In addition, home use of endosulfan, which may result in exposure of children, needs to be investigated. 

ILSl, A Framework for Estimating Pesticide Concentrations in Drinking Water for Aggregate Exposure Assessments, Workshop Report 5/19/99. International Life Sciences Institute, Washington, DC (1999). 

A variety of modeling approaches may be used to estimate pollutant concentrations in exposure media. These range from qualitative estimates extrapolated from case examples or environmental scenarios, simple analytical equilibrium or transport models, to complex multi-media models. In selecting an approach or approaches, it is important that ... 

Exposure estimation is the next logical step in an exposure assessment. In this step, the data and methods developed in the previous steps dre linked together so that the relationship between pollutant sources and human exposure can be examined. Through estimation of the degree of exposure rather than just estimation of concentrations in environmental media, a more detailed analysis of a pollution problem is possible, including ... 

Exposure assessment is the process of predicting or estimating the concentration or amount of an agent, the frequency, and the duration that reaches the receptor. 

Kleinfeld (1980) reported a case of arsine poisoning in a 31-y-old man. The exposure to arsine occurred from a leaking canister thought to be empty. The exposure duration was estimated to be 1-2 min, but no actual or estimated arsine concentrations were available. The victim presented with hematuria. On hospital admission, no intact erythrocytes were present in the urine, hematocrit was 43%, and hemoglobin was 9.8 g/ dL. The hematocrit dropped to as low as 18%, the correction of which required one unit of packed cells. Based upon the exposure history and the subject s note of a "garlicky" odor, the diagnosis was arsine-induced hemolytic anemia. Urinary arsenic was 7.2 mg/L on admission and 0.1 mg/L 4 d later. The patient was subsequently discharged. 

Numerous case reports are available regarding the lethal and nonlethal toxicity of arsine in humans, but definitive exposure concentration or duration data are lacking. Although the case reports are of limited use for quantitative estimates of exposure limits, they do provide qualitative information about the nature of arsine poisoning in humans. Some estimated human toxicity values are available and are summarized in Table 2-3. 

For AEGL-3, the 1-h LC50 of 82 ppm for squirrel monkeys (Haun et al. 1970) was reduced by a factor of 3 to estimate a lethality threshold (27.3 ppm). Temporal scaling to obtain time-specific AEGL values was described by C% t=k (where C=exposure concentration, t=exposure duration, and k=a constant). The lethality data for the species tested indicated a near linear relationship between concentration and exposure duration (n=0.97 and 0.99 for monkeys and dogs, respectively). The derived exposure value was adjusted by a total uncertainty factor of 10.2 An uncertainty factor of 3 was applied for... 

The AEGL-3 values were derived based upon the 1-h LC50 value of 82 ppm reported for squirrel monkeys (Haun et al. 1970). As previously noted, there appears to be a critical and narrow threshold between an exposure that induces only minimal toxicity and one that causes death. For squirrel monkeys, 1-h exposure to a mean concentration of 82 ppm (range, 70-95 ppm) killed two of four animals. For derivation of the AEGL-3, the lethality threshold for squirrel monkeys was estimated by a 3-fold reduction of the LC50 (82 ppm) to obtain a value of 27.3 ppm. This estimate can be justified by the known steep exposure-response relationship for the toxic effects of monomethylhydrazine, and the fact that the resulting 27.3-ppm value represents an exposure concentration that does not produce overt toxicity in test animals. 

Estimate the exposure concentration in ppm that will result in fatalities for 80% of the exposed individuals if they are exposed to phosgene for 4 min. 

Although a great many deaths have occurred from accidental, intentional, or occupational exposures to HCN, in only a few cases are specific exposure concentrations known. In a review of human fatalities (ATSDR 1997), it was stated that exposure to airborne concentrations of HCN at 180 to 270 ppm were fatal, usually within several minutes, and a concentration of 135 ppm was fatal after 30 min. The average fatal concentration for humans was estimated at 546 ppm for 10 min. The latter data point is based on the work of McNamara (1976), who considered the resistance of man to HCN to be similar to that of the goat and monkey and four times that of the mouse. Fatal levels of HCN cause a brief period of central nervous system stimulation followed by depression, convulsions, coma with abolished deep reflexes and dilated pupils, and death. Several review sources, such as Dudley et al. (1942),... 

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