Characterizing Exposure

In exposure characterization, credible and relevant data are analyzed to describe the source(s) of stressors, the distribution of stressors in the environment, and the contact or co-occurrence of stressors with ecological receptors. An exposure profile is developed that identifies receptors and exposure pathways, describes the intensity and spatial and temporal extent of exposure, describes the impact of variability and uncertainty on exposure estimates, and presents a conclusion about the likelihood that exposure will occur. 

A source description identifies where the stressor originates, describes what stressors are generated, and considers other sources of the stressor. Exposure analysis may start with the source when it is known, but some analyses may begin with known exposures and attempt to link them to sources, while other analyses may start with known stressors and attempt to identify sources and quantify contact or co-occurrence. The source description includes what is known about the intensity, timing, and location of the stressor and whether other constituents emitted by the source influence transport, transformation, or bioavailabihty of the stressor of interest. 

Because exposure occurs where receptors co-occur with or contact stressors in the environment, characterizing the spatial and temporal distribution of a stressor is a necessary precursor to estimating exposure. The stressor s spatial and temporal distribution in the environment is described by evaluating the pathways that stressors take from the source as well as the formation and subsequent distribution of secondary stressors. For chemical stressors, the evaluation of pathways usually follows the type of transport and fate modeling described in Chapter 27. Some physical stressors such as sedimentation also can be modeled, but other physical stressors require no modeling because they eliminate entire ecosystems or portions of them, such as when a wetland is filled, a resource is harvested, or an area is flooded. 

The movement of biological stressors have been described as diffusion and/or jump-dispersal processes. Diffusion involves a gradual spread from the site of introduction and is a function primarily of reproductive rates and motility. Jump-dispersal involves erratic spreads over periods of time, usually by means of a vector. The gypsy moth and zebra mussel have spread this way the gypsy moth via egg masses on vehicles and the zebra mussel via boat ballast water. Biological stressors can use both diffusion and jump-dispersal strategies, which makes it difficult to predict dispersal rates. An additional complication is that biological stressors are influenced by their own survival and reproduction. 

The distribution of stressors in the environment can be described using measurements, models, or a combination of the two. If stressors have already been released, direct measurements of environmental media or a combination of modeling and measurement is preferred. However, a modeling approach may be necessary if the assessment is intended to predict future scenarios or if measurements are not possible or practicable. 

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FIGURE 7-1. Hazard Characterization Exposure Assessment Strategy... 

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. 

Large numbers of samples are required to characterize exposure distributions. Starling food items contained the highest diazinon concentrations and the highest... 

In this chapter the risk assessment is briefly introduced. Risk assessment is divided into four steps hazard identification, hazard characterization, exposure assessment, and risk characterization. This chapter also highlights five risk and life cycle impact assessment models (EUSES, USEtox, GLOBOX, SADA, and MAFRAM) that allows for assessment of risks to human health and the environment. In addition other 12 models were appointed. Finally, in the last section of this chapter, there is a compilation of useful data sources for risk assessment. The data source selection is essential to obtain high quality data. This source selection is divided into two parts. First, six frequently used databases for physicochemical... 

The exposure assessment should include a characterization of the exposure estimates with respect to quality and relevance of exposure data, assumptions, major uncertainties, etc. Guidance for characterizing exposure in US-EPA exposure assessments can be found in Guidance for Risk Characterization (US-EPA 1995). 

The exposure assessment could be performed for a single exposure scenario, or be more comprehensive including several exposure scenarios. In some simations, the estimated exposure from a single scenario is taken forward to the risk characterization while for other purposes, the estimated exposures from various scenarios form the basis for an estimation of a combined exposure to the chemical under evaluation from all characterized exposure scenarios. 

Polybrominated Biphenyls. A recent study has used caffeine as a potential tool to characterize exposure and/or effect of PBBs (Lambert et al. 1990). In this test, caffeine is used as a metabolic probe of cytochrome P-450 isozymes activity from the CYPIA family, which in animals is significantly induced by PBBs (Safe 1984). Tire caffeine breath test (CBT) is primarily useful for detecting induction of CYP1A2 activity in human liver, and for that reason, it also has been used as a marker for exposure to PCBs, CDDs, and CDFs (Lambert et al. 1992). A volunteer population of 50 Michigan subjects with previously high serum PBB levels and 50 with undetectable or low serum levels was compared to a control population not exposed to PBBs (Lambert et al. 1992). Two tests were conducted, the CYP1A2-dependent caffeine... 

Further studies on the transfer analytes that have been purged or extracted from a biological or environmental sample quantitatively and in a narrow band to the capillary GC would better characterize exposure. Improvements in cryofocussing of VOC analytes for capillary GC determination of VOCs (Washall and Wampler 1988) should improve sensitivity for the determination of chlorobenzene. 

Effect There are no specific biomarkers for the effects of tetryl. The toxic effects of tetryl, such as headaches, coughs, nausea, and dermatitis, are too general to be used to characterize exposure to this substance. Patch tests can be conducted in individuals who appear to be sensitive to tetryl (i.e., those who exhibit hypersensitivity-like reactions). Further studies are necessary to determine which types of biomarkers can be used to indicate effects caused by tetryl. 

Residential exposure should be estimated by taking into account distributions of exposure factors. Methods to assess distributions are through the deterministic or probabilistic approach (Figure 6.6). The former is often taken in preventive risk assessment in which each default value is determined from each distribution as a reasonable worst-case . The estimated exposures for the deterministic approach are expected to occur in the upper range. For actual risk assessments, the probabilistic approach directly uses the parameter distributions instead of single values to calculate distributions of exposure. To characterize exposure, an... 

As indicated by some of the examples described earlier, epidemiological studies can use a wide range of approaches for characterizing exposure to chemical agents such as pesticides (Table 7.1). 

Microposit 2400 resist, manufactured by Shipley Co., has been shown to be sensitive at this short wavelength ( ) and is being employed with the deep UV stepper. We report here the results of resist profile modeling for submicron photolithography at 248 nm. Various model parameters needed as input data were measured to characterize exposure and development of the resist. 

Salazar, M.H. and S.M. Salazar. 1997. Using caged bivalves to characterize exposure and effects associated with pulp and paper mill effluents. Water. Sci. Technol. 35 213-220. 

In the case of weathered releases, the fraction approach is likely to be the most useful. Analytical methods that support the fraction approach should be chosen to characterize exposures (Section 3.3, TPHCWG approach). The identity of the original contaminating product(s) need not be known. 

Olson, D. A., and Corsi, R. L. (2001). Characterizing exposure to chemicals from soil vapor intrusion using a two-compartment model. Atmos Environ 35, 4201-4209. 

Once all available and relevant information has been assembled, it can be critically analyzed for missing data elements or significant data gaps. The exposure assessor must determine where existing exposure measurements can be used directly and where other techniques must be applied to extrapolate or estimate the exposures of interest. Key types of data gaps that may need to be addressed include insufficient existing exposure data, inadequate information to characterize exposure scenarios for individual job tasks or titles, limited inputs for exposure models, or a lack of certainty regarding appropriate exposure classification. 

Exposed workers had significantly lower exposure duration-related mean values of thyroxine and higher mean values of free, esterified, and total cholesterol than controls. The study authors suggested that depression of serum thyroxine may be a key manifestation in hypercholesterolemia among carbon disulfide-exposed workers. The small sample size, lack of information on other exposures, and poorly characterized exposure concentrations preclude establishing conclusions from this study. 

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