APPENDIX I
CADMIUM EXPOSURE ASSESSMENT, TRANSPORT, AND ENVIRONMENT FATE



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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests APPENDIX I CADMIUM EXPOSURE ASSESSMENT, TRANSPORT, AND ENVIRONMENT FATE

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests CADMIUM EPOSURE ASSESSMENT, TRANSPORT, AND ENVIRONMENT FATE THE PURPOSE OF THIS APPENDIX is to provide estimates of the magnitude of potential human contact with cadmium compounds as a result of the dispersion of zinc cadmium sulfide, ZnCdS, by the Army. EXPOSURE TO ENVIRONMENTAL CADMIUM Cadmium is a chemical element and a natural component of the earth's crust. Human activities can increase human exposure to cadmium through mining and combustion, which bring more cadmium into the air, water, and soil. In the sections below, we summarize sources of human exposure to cadmium in air, water, plants, animals, food, soil, and house dust. For each, we characterize likely magnitudes of human contact and the routes of contact—inhalation, ingestion, and dermal contact. CADMIUM IN OUTDOOR AIR Cadmium metal and cadmium salts have low volatility and exist in air primarily as fine suspended particulate matter. It enters the air from burning coal and household wastes, and from metal mining and refining processes. In the United States, mean levels of cadmium in ambient air range from less than 0.001 µg/m3 in remote areas to 0.005-0.04 µg/m3 in urban areas (Davidson and others 1985; Elinder 1985; EPA 1981; Saltzman and others 1985). Atmospheric concentrations of cadmium are generally highest in the vicinity of cadmium-emitting industries such as

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests smelters, municipal incinerators, or fossil fuel combustion facilities. Measurements of atmospheric cadmium up to 7 µg/m3 have been reported in these industrial types of areas in the United States (Schroeder and others 1987). When inhaled, some fraction of this particulate matter is deposited in the airways or lungs, and the rest is exhaled. Because most people spend only about 10% or less time outdoors per day, this issue is addressed in the exposure analysis. In the United States, a person who breathes 20 m3 of air per day and spends 10% of his or her time outdoors will have an estimated cadmium intake of 0.1-0.8 µg/day in urban cities or less than 0.02 µg/day in rural areas. CADMIUM IN WATER Cadmium enters drinking water directly from pollution-source releases to surface water and groundwater or from deposition from air to surface water, from soil runoff to surface water, or from leaching from rocks and soils into groundwater. The concentration of cadmium dissolved in the open ocean is less than 0.005 µg/L (IARC 1993; Nriagu 1980). The concentration of cadmium in drinking water is generally reported to be less than 1 µg/L, but it might increase to 10 µg/L as a result of industrial discharge and leaching from metal and plastic pipes (Friberg and others 1974). A person who consumes 2 L of water daily with a cadmium concentration of 1 µg/L will have an intake of 2 µg/d. UPTAKE IN PLANTS AND CADMIUM IN FOOD Plants are contaminated with cadmium via two routes—uptake of cadmium in soil through the roots and deposition of cadmium in air onto leaf surfaces followed by translocation to other plant parts. Cadmium residues in plants are typically less than 1 µg/kg (IARC 1993). Food is the main source of cadmium for nonoccupationally exposed people, although uptake of cadmium in the gut from food is generally less efficient than from water or air because cadmium binds to food constituents (IARC 1993). The average daily intake of cadmium through food varies among

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests countries, and varies among individuals in a given country or population group. In nonindustrialized rural areas away from mining operations, cadmium intake through food is estimated to be 10-60 µg/d; in polluted areas of Japan, values as high as 500 µg/d have been reported (Friberg and others 1974). There are several estimates of the daily adult intake of cadmium from food in the United States, but there is considerable variation among those estimates. Schroeder and Balassa (1961) reported a range of 4-60 µg per day and Nriagu (1981) reported a range of 38-92 µg, while estimated daily averages have been reported to be 30 µg (Gartrell and others, 1986), 38 µg (Duggan and Corneliussen, 1972), 50 µg (Duggan and Corneliussen, 1972), 51 µg (Mahaffey and others, 1975), and 92 µg (Murthy and others, 1971). A more recent estimate based on a Total Diet Study shows the daily dietary intake to be approximately 15 µg (Gunderson, 1995). Analysis of the earlier data shows that these discrepancies are probably due to different analytical methods. Cadmium contamination of food has been reduced over the years, presumably because of better technology. However, the cadmium contamination encountered in the 1950s and 1960s when the Army's dispersion tests were conducted are more relevant for risk assessment. On the basis of the U.S. data and data from other industrial nations from the northern hemisphere, the subcommittee believes that the daily cadmium intake from food ranges from 10 to 60 µg. CADMIUM IN SOIL (SOIL INGESTION AND DERMAL UPTAKE) Human intake of cadmium in soil occurs through soil ingestion that results from hand-to-mouth activities. Such intake is typically less important than the inhalation, water-intake, and food-consumption pathways associated with the same soil (McKone and Daniels 1991). Cadmium concentrations in soil vary widely. In nonpolluted areas, they are usually below 1 µg/g; in polluted areas, concentrations of up to 800 µg/g have been detected (Friberg and others 1974). The U.S. Environmental Protection Agency (EPA 1992) recommends that 0.2 g/d be used as an average soil-ingestion rate for children under

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests age 7 with 0.8 g/d as an upper bound. LaGoy (1987) suggests a soil-ingestion rate of 0.025 g/d for adults. On the basis of those values, we estimate that, in an area with soil cadmium of around 1 µg/g, cadmium intake as a result of soil ingestion is in the range of 0.02-0.2 µg/d. According to EPA (1992), an adult with a body surface area of 18,000 cm2 can have 5,000-5,800 cm2 of skin area exposed to soil contact and have a soil-to-skin adherence of 0.2-1 mg/cm2 with an exposure frequency of 40-350 events per year. That translates into an equivalent annual soil contact of 0.1-6 g/d. No human data on dermal uptake of cadmium are available, but animal data indicate that dermal uptake is slow, about 2% over 24 h of contact (ATSDR 1993). On the basis of these values, human contact with soil containing cadmium at 1 µg/g would result in annual dermal uptake of 0.002-0.12 µg/d. CADMIUM IN HOUSE DUST In recent years, it has been recognized that fine and coarse particles in the indoor environment have both air and soil sources and enter the indoor environment by such processes as resuspension, deposition, and soil tracking (Allott and others 1992; Nazaroff and Cass 1989). Friberg and others (1974) reported that the concentration of cadmium in the dust deposited in houses was related to concentrations in air particles more than to soil concentrations. In rural areas with cadmium concentrations in air of 0.005 µg/m3, cadmium was contributed to the house-dust pool at around 600 m/d. That implies that the cadmium deposition rate on household surfaces is about 3 µg/m2 per day in areas with an air concentration of 0.005 µg/m3. The resulting house-dust cadmium concentrations were in the range 13-14 µg/g of dust (Friberg and others 1974). That is much higher than the 1 µg/g typical of soil in the same areas and suggests the relative importance of deposition from air to house dust as a potential exposure pathway. The ratio of dust to air concentration suggests that cadmium concentrations could be from around 40 µg/g of dust in urban areas to as much as 140 µg/g of dust in industrialized areas, on the basis of air concentrations in these areas reported above. However, it should be noted that ambient air is not the only likely source of cadmium in indoor

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests air. Indoor sources, such as smoking and the agents used to color carpets and furniture, could result in increased cadmium in house dust. The loading of soil and dust on floors as reported in the recent literature varies from 0.136 to 0.870 g/m2 (Allott and others 1992; Nazaroff and Cass 1989). If we assume a dust inventory of 1 g/m2 on household surfaces, then, according to the air concentrations discussed above, the inventory of cadmium in the dust of household surfaces is about 14 µg/m2 in rural areas, 42 µg/m2 in urban areas, and as much as 140 µg/m2 in industrial areas. The residence time of cadmium in this dust is around 5 d; this is obtained by dividing the cadmium inventory, such as 14 µg/m2, by the rate of cadmium deposition on household surfaces, 3 µg/m2 per day. The soil ingestion and soil dermal-uptake calculations developed above for outdoor soils indicate that for soil ingestion the intake-to-concentration ratio is about 0.02-0.01 µg of cadmium ingested per day per 1 µg/g of soil and that for dermal contact the uptake-to-concentration ratio is about 0.002-0.12 µg of cadmium dermally adsorbed per day per 1 µg/g of soil. Because dust contacts indoors are likely to be lower than soil contact outdoors, consider the lower bound on these ranges to be appropriate for house dusts. In this case, the combined uptake from the two exposure routes is about 0.02 µg of cadmium per day per 1 µg/g of soil. If this ratio were applied to house dusts, the average ingestion and dermal uptake of cadmium from house dust would both be about 0.3 µg/d in rural areas, 0.8 µg/d in urban areas, and as much as 3 µg/d in industrial areas. CADMIUM IN INDOOR AIR In assessing the concentration of cadmium in indoor air, it is important to consider both outdoor air and house dust as sources. As noted above, cadmium concentrations in house dust are typically about 15 µg/g in rural areas, 40 µg/g in urban areas, and 140 µg/g in industrial areas. Assuming that the indoor air of the house has a dust loading of 50 µg/m3 and that that would be the same in household air would yield respective indoor air concentrations of 0.007 µg/m3 in rural areas, 0.02 µg/m3 in urban areas, and 0.07 µg/m3 in industrial areas. Given that these levels are comparable with those of outdoor air, resuspended dust inside homes is not likely

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests to increase cadmium concentrations in indoor air substantially. Instead, the figures suggest that cadmium enters the indoor air mainly from outside and not from dust resuspension. SMOKING It has been recognized for many years that smoking can be an important source of cadmium exposure of smokers. Friberg and others (1974) summarized a number of studies relating cadmium uptake to smoking. They reported that all the data agree well and show that 0.1-0.2 µg of cadmium can be inhaled by smoking 1 cigarette. Smoking habits to some extent affect the amount of cadmium taken up. However, it can be estimated that someone smoking 20-40 cigarettes per day will take in 2-8 µg of cadmium per day. SUMMARY Exposures to ambient cadmium result in a daily human intake in the range of 12-84 µg/d for an adult. For a 70-kg person, that corresponds to a potential dosage of about 0.2-1.2 µg/kg per day. The relative contributions of the various pathways to total potential dose for a 70-kg adult are as follows: Inhalation of cadmium in air indoors and outdoors 0.002-0.02 µg/d ~0.02% Water ingestion 2-20 µg/d ~20% Food products 10-60 µg/d ~76% Soil ingestion 0.02-0.2 µg/d ~0.2% Dermal contact 0.002-0.12 µg/d ~0.002% Contact with house dust 0.3-3 µg/d ~3% Smoking (2-8 µg/d) (for smokers) Total daily intake 12-84 µg/d   Food products and water contribute almost all the typical daily human

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests exposure. Inhalation exposures contribute a very small fraction. From our estimates here, contact with house dust is the third-ranking (for nonsmokers) potential exposure pathway for existing cadmium sources. TRANSPORT AND ENVIRONMENTAL FATE This section describes the sources, transport, environmental fate, and accumulation of ZnCdS and cadmium compounds in the environment. We begin by considering the sources and chemical properties of ZnCdS and cadmium compounds. Because ZnCdS does not occur naturally and little has been published on its environmental behavior, little can be reported here. For cadmium compounds, there is a rich, but still incomplete, literature on chemical properties, environmental concentrations, transport, and the global chemical cycle. Some relevant components of that literature are reported here. DISTRIBUTION COEFFICIENTS IN SOILS AND SEDIMENTS The distribution or sorption coefficient, Kd, is ratio of the concentration, at equilibrium, of a chemical species attached to solids or particles (in moles per kilogram) to chemical concentration in the solution, with which the particles have contact (in moles per liter). Several mechanisms define this partition relationship—including cation exchange, adsorption, speciation, coprecipitation, and organic complexation. Soil-water distribution coefficients are often modeled as independent of water-phase concentration, whereas in reality there often is a dependence of Kd on waterphase concentration. Bodek and others (1988) have reviewed and compared a number of sorption models for cadmium in soil-water and sediment-water systems. They report that in soils estimated Kd values range from 1 to 9,000 with a typical value (at low water concentrations) of about 1,000 and that in sediments estimated Kd values range from 1 to 160,000 with a typical value (at low water concentrations) of about 6,000.

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests BIOCONCENTRATION FACTORS FOR PLANT UPTAKE FROM SOIL The plant-soil partition coefficient, Kps, expresses the ratio of contaminant concentration in plant parts, both pasture and food, (in micrograms per gram of plant fresh mass) to the concentration in wet root-zone soil (in micrograms per gram). Cadmium is considered a potential essential trace element for plants and animals (Mertz 1981). Root uptake of cadmium as Cd2+ in plants is passive and occurs though uptake by roots of cadmium dissolved in water; cadmium is highly mobile in plants and readily translocated to other plant parts (Bodek and others 1988). Plant-soil partition coefficients have been reported in the range of 0.015-2.1 with a likely value of about 0.1 (Baes and others 1984; Bowen 1979; Nriagu 1980). BIOCONCENTRATION FACTORS FOR PLANT-LEAF CONCENTRATION RELATIVE TO AIR CONCENTRATION According to Bodek and others (1988), airborne deposition is believed to contribute to concentrations of cadmium found in plant leaves. At low concentrations, the ratio of plant-leaf concentration to air concentration when air and plant environments are in contact can be estimated as Cp/C = Vd/(Mp x Rp), where Cp is cadmium concentration in the plants in contact with contaminated air, mol/kg; Ca is the cadmium concentration in air above the plants, mol/m3; Vd is the deposition velocity that represents the rate of cadmium transfer from air to plant surfaces, m/d; Mp is the mass of the plants per unit area of land, kg/m2; and Rp is the first-order rate constant that accounts for all cadmium removals from plants (wash-off, biodegradation, and so on) per day. McKone and Ryan (1989) have estimated that, on the basis of the balance between deposition, weathering, and senescence processes in agricultural landscapes, this ratio can be estimated to have a mean value of 3,300 m3 (air)/kg (plants) and a geometric standard deviation of 3 for metal species.

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests BIOCONCENTRATION FACTORS FOR FISH The bioconcentration factor (BCF) is a measure of chemical partitioning between fish tissue based on chemical concentration in water and has a unit of moles per kilogram of fish per mol per liter of water. Bodek and others (1988) report ocean and freshwater fish BCFs in the range of 200-50,000, with 2,000 being a typical value in this range of reported values. SOURCES AND SINKS It is not clear from the current geochemical literature whether Zn0.8Cd0.2S occurs naturally and has its own biogeochemical cycle. In contrast, there has been extensive study of the natural and human biogeochemical cycles of cadmium (for example, Nriagu 1980). For Zn0.8Cd0.2S, our principal concern is the potential exposure to cadmium. That requires that we understand the local and regional scale distribution and fate of both Zn0.8Cd0.2S and the cadmium compounds formed from it. In the areas of small geographic extent to which it was dispersed, the persistence of cadmium will depend on the rate of atmospheric dispersion, the rate of deposition to surfaces (soil, snow, plants, and so on), and the rate of transformation from Zn0.8Cd0.2S to some other cadmium compound. Before the specific behavior of Zn0.8Cd0.2S in the environment can be fully characterized, there is a need to determine both the rates and end products of Zn0.8Cd0.2S transformation reactions in air, surface soil, vegetation surfaces, surface water (rivers, lakes, and ponds) and snow. Some possible reactions are listed below, but these are difficult to confirm. 5 Zn0.8Cd0.2S + 10 H2O + 5 O2 →4 Zn2+ + Cd2+ + 5 SO4-+ 10 H+ 5 Zn0.8Cd0.2S + 10 O2 + photon energy → 4 Zn2+ + Cd2+ + 5 SO4- Zn0.8Cd0.2S + biologic organisms → Zn2+? + Cd2+? + ? Although the actual degradation rate of Zn0.8Cd0.2S has not been measured in any environmental medium, the degradation of the fluorescence of Zn0.8Cd0.2S has been studied (Leighton and others 1965) and is likely related to the rate of transformation of Zn0.8Cd0.2S to other zinc and cad-

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests mium compounds. The degradation of Zn0.8Cd0.2S fluorescence has been attributed to photochemical reactions and found to vary with humidity and manufacturing lot (Leighton and others 1965). One study reported a loss of as much as 50% of Zn0.8Cd0.2S particles within 2 h of airborne travel in sunlight (Eggleton and Thompson 1961). Using the type of Zn0.8Cd0.2S used in several Army studies, Leighton and others (1965) reported only a 7% loss after a period of 19 h that included mostly daylight hours. The sources, sinks, and distribution of cadmium in many ecosystems have yet to be properly evaluated, and cadmium transfer rates between components of the earth system are only poorly known. Aspects of the global cycle of cadmium have been summarized by Nriagu (1980). Basically, a global model of an element consists of presumed reservoirs or compartments (atmosphere, lithosphere, ocean, lakes, soils, and so on), which can be active (available to the biota) or passive (unavailable to the biota). The total amount of cadmium in each compartment is referred to as the burden (or pool) and is obtained by multiplying the average concentration by the total mass (or volume) of the compartment. Reactions and advection processes in compartments can result in smaller-scale variations of cadmium concentration with both space and time. Table I-1 shows the principal compartments and concentrations of cadmium in the surface environment of the earth; the numbers are taken from Nriagu (1980). It should be noted that active pools—such as the atmosphere, soils, lakes, rivers, and ocean pools—are subject to large inputs of cadmium from human activities. The exchange of cadmium between compartments occurs along established pathways involving stream, ice, and groundwater flows; atmospheric transport and deposition; volcanism; uplift; weathering; sedimentation; and biologic mobilization. The residence time of each compartment gives a sense of how long that compartment takes to respond to a change in cadmium inventory. From the table we can conclude that the major natural sources of cadmium to the active parts of the environment are mobilization from the large reservoir that exists in the lithosphere. The major sink for cadmium that enters the active compartments is burial in freshwater or ocean sediments.

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests per unit of body weight per day (milligrams per kilogram per day) that enters the lungs (inhalation route), enters the gastrointestinal tract (ingestion route), or crosses into the stratum corneum (dermal route). The total potential dose is used as a basis for projecting the incidence of health effects within the population. In estimating the exposures to cadmium in areas where Zn0.8Cd0.2S was dispersed by the Army, it is important to assess not only the amount of material dispersed and the resulting short-term air concentrations, but also the extent to which this material was deposited on soil, vegetation, and snow and tracked into houses and other buildings. We explore here the premise that the effective persistence of the exposure concentrations in surface soil, house dust, and vegetation can be longer than those in the atmosphere, where cadmium persistence is measured in hours. Material transferred to soil surfaces, house dust, or plants could persist as an increased source of exposure for longer periods, perhaps days or weeks or months. In the sections below the potential exposure to cadmium in air is calculated for both the direct (inhalation) exposure pathway and the indirect exposure pathways, including dust resuspension, house-dust contacts, and deposition on vegetation used for food. For each pathway, we develop the potential dose ratio (Table 1-2), which is the ratio of cumulative intake for an exposure event, in micrograms of cadmium, divided by the overall product of concentration and time—the time integral of the exposure concentrations in air. DIRECT EXPOSURE: INHALATION OF CONTAMINATED AIR To determine the potential dose ratio, we first determine dose, which is the product of inhalation rate, IR, m3/h; the time-averaged cadmium air concentration during the exposure time, Cair, µg/m3; and the exposure time, ET, in h. The dose ratio is obtained by dividing the dose by the cumulative exposure, which is the product of average cadmium concentration in air, Cair, µg/m3, during the exposure time and the exposure time, ET. For direct exposure by inhalation, the potential dose ratio is obtained as follows:

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests potential dose ratio (inhalation) = (IR × ET × Cair)/(Cair × ET) = IR. For an adult breathing air at a rate of 1 m3/h, potential dose ratio (inhalation) = 1 µg/(µg/m3)-h. When this dose ratio is multiplied by the cumulative exposure for any exposure location, we obtain an estimate of inhalation dose for a person at that location for the period ET. TABLE 1-2 Summary of Potential Dose Ratios for Direct and Indirect Exposure Pathwaysa Exposure Pathway Direct or Indirect Contact with Air Potential Dose Ratio, µg ÷ µg-h/m3 of Cumulative Air Exposure Inhalation Direct 1.0 Inhalation of resuspended soil outdoors Indirect 0.0005-0.002 Dermal contact with and ingestion of house dust Indirect 2.5-5 Inhalation of resuspended house dust Indirect ≈ 0.12 Deposition on vegetation in home gardens Indirect 2.2 Deposition on surface drinking-water supplies Indirect 0.24-0.8 a Potential dose ratio is the ratio of total uptake or intake of cadmium in micrograms, divided by the integrated air exposure, in micrograms per cubic meter per hour.

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests INHALATION OF PARTICLES RESUSPENDED IN OUTDOOR AIR The Army risk assessment did not consider exposures to cadmium that was deposited on the ground and then resuspended in the air, where it could be inhaled after the main source had dispersed. The concentration of cadmium added to soil as a result of deposition from air can be estimated as Csoil = (Cair x Vdo x ET)/(Msoil), where Csoil is the concentration of cadmium added to soil, µg/g; Vdo is the outdoor deposition velocity of FP, assumed to be 20 m/h; Cair is the cadmium concentration in air during an event, µg/m3; ET is the exposure time, h; and Msoil is the mass inventory of surface soil, which, on the basis of soil depth of 1 cm and a soil density of 1,600 kg/m3, is 16,000 g/m2. Combining these values gives Csoil ≈ 0.00125 (Cair x ET) µg/g. Soil erosion rates in the United States due to wind and water are around 100 g/m2 per year. That implies that the residence time of soil particles deposited onto the soil surface is about 160 yr, that is, 16,000 g/m2 divided by 100 g/m2-yr. However, because of its relatively high solubility in water, cadmium species are eroded more rapidly from soil than is the bulk soil. Thus, cadmium has a residence time in soil that is more like 10-40 yr (Nriagu 1980). In urban areas, the concentration of particulate matter in air is about 100 µg/m3. If resuspended surface soil is assumed to be the source of all the particulate matter in air, the long-term concentration of cadmium in air resuspended from soil is given by Cresuspend = Csoil x 100 µg/m3 x 10-6 g/µg = 1.25 x 10-7 x (Cair x ET) µg/m3. For someone who breaths this at a rate of 20 m3/d for 10-40 yr, or 3,650-

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests 14,600 days (the assumed residence time in soil), the potential dose is potential dose ≈ Cresuspend x (3,650-14,600 d)= (0.0005-0.002) x (Cair x ET) µg, and thus the potential dose ratio for resuspension is estimated as potential dose ratio (inhalation) ≈ (0.0005-0.002) µg/(µg/m3)-h [over 10-40 yr]. That value is low relative to the direct exposure by inhalation of contaminated air during the exposure event and would apply only to people who lived in the contaminated area for a number of years after exposure. DERMAL CONTACT AND INGESTION OF HOUSE DUST It is difficult to estimate the house-dust impact because we do not have data on penetration and retention within the house. However, we can make a rough estimate of the likely levels of cadmium in house dust and the potential doses based on the existing information on house-dust exposure discussed previously. To estimate dermal and ingestion exposures to the cadmium transported to house dust, it is necessary to determine the cadmium concentration inside houses after dispersion and how much of this is deposited on household surfaces. To make this preliminary calculation, we assume that air concentrations of cadmium in houses went up in proportion to outdoor concentrations during the exposure time, ET, but that house dust is only 50% attributable to outdoor air. On the basis of that assumption, the added concentration of cadmium in house dust is calculated as Cdust ≈(0.5Cair x Vdh x ET)/(Mdust), where Cdust is the concentration of cadmium added to house dust, µ/g; 0.5Cair is the assumed cadmium concentration in indoor air during an event, µg/m3; Vdh is the indoor deposition velocity of ZnCdS on house-

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests hold surfaces, assumed as discussed above to be 25 m/h (600 m/d); ET is the exposure time, h; and Mdust is the mass inventory of dust on household surfaces, assumed as noted above to be about 0.5 g/m 2. Thus, Cdust ≈ 25 (Cair x ET) ≈g/g(dust). House dust has a likely residence time of 5 d (derived earlier). From the increased concentration of cadmium in house dust for 5 d and the previously derived dermal and ingestion uptake factor for house dust of 0.02 µg/d per 1 µg of cadmium per gram of dust, the 5-d effective dose for a single event of duration ET is potential dose ≈ Cdust x 5 d x 0.02 g(dust)/d = 2.5 x (Cair x ET) µg, so the potential dose ratio for dermal and ingestion contact with house dust is estimated as potential dose ratio (house dust) ≈ 2.5 µg/(µg/m3)-h [over ≈ 5 d]. That value is comparable with and slightly higher than the direct exposure to contaminated air by inhalation during the exposure event. However, there is much greater uncertainty associated with it than with the direct inhalation-dose estimate. INHALATION OF RESUSPENDED HOUSE DUST To make a preliminary estimate of the potential dose, we assume that air concentrations of cadmium in houses due to house dust are all attributable to resuspension of house dust and that the particle load indoors is around 50 µg/m3. Cdust to indoor air ≈ Cdust (µg/g) x 50 x 10-6 g/m3, where Cdust is the concentration of cadmium in house dust, µg/g. Because the breathing rate of occupants during this time is around 20 m3/d and the

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests estimated addition of cadmium to house dust during an event of duration ET is Cdust ≈ 25 (Cair x ET) µg/g(dust), the potential dose to occupants from breathing resuspended house dust is potential dose ≈ 25 (Cair x ET) x 50 x 1016 g/m3 x 20 m3/d x 5 d ≈ 0.12 x (Cair x ET) µg ≈ 0.12 µg/(µg/m3)-h [over ≈ 5 d]. That value is much lower than those for the other potential contacts with house dust. INDIRECT EXPOSURE FROM CONSUMPTION OF PLANTS AND ANIMALS In theory, plants can be contaminated with atmospheric cadmium either by uptake of cadmium from contaminated soil or by deposition of cadmium from air on leaf surfaces. As noted above, it is difficult to construct a scenario whereby cadmium in soil could be increased by only a small fraction above existing concentrations. Plant roots penetrate deeper into soil than the 1 cm assumed above, so there is no plausible mechanism by which plant tissues could be substantially contaminated by a short-term atmospheric exposure. However, when we consider deposition on leaf surfaces, there is a greater likelihood of vegetation contamination. The concentration of cadmium added to vegetation as a result of deposition from air can be estimated as Cveg = (Cair x Vdv x ET)/(Mveg), where Cveg is the concentration of cadmium added to vegetation during an exposure event, µg/kg; Cair is the average cadmium concentration in air during an event, µg/m3; Vdv is the deposition velocity of FP from air to vegetation, assumed to be 10 m/h; ET is the exposure time, h; and Mveg is

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests the average density of growing vegetation, which is about 3 kg/m2. Combining those values yields Cveg 3.3 (Cair x ET) µg/L. On the basis of data from Nriagu (1980), we estimate that particles deposited on vegetation could persist for some 20 d. The important question regarding exposure to vegetation is how much consumption of vegetation would take place among the local populations. EPA data suggest that in urban areas, less than 10% of consumed vegetation is homegrown. Combining that 10% factor, cadmium persistence on plants, and the observation that a typical adult consumes fruits and vegetables at roughly 125 kg/yr, or 0.34 kg/d, we obtain the following estimate of potential dose: potential dose ≈ Cveg x 20 d x 0.10 x 0.34 kg/d = 2.2 x (Cair x ET) µg. Thus, the potential dose ratio for ingestion of homegrown vegetables is potential dose ratio (homegrown foods) ≈ 2.2 µg/(µg/m3)-h [over ≈ 20 d]. That value is comparable with and higher than the direct exposure to contaminated air by inhalation during the exposure event. However, there is much greater uncertainty associated with it than with the direct inhalation-dose estimate. Our estimate of exposures through food is likely to be a high-end estimate, because we ignore seasonal effects, we ignore removal of cadmium from plant surfaces by rain and wind, and we assume a relatively high fraction of homegrown food consumption. INDIRECT EXPOSURE FROM DEPOSITION ON SURFACE WATERS The concentration of cadmium added to surface water as a result of deposition from air can be estimated as

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests Cwater = (Cair x Vdo x ET)/(Vwater), where Cwater is the concentration of cadmium added to surface water during an exposure event, µg/L; Cair is the average cadmium concentration in air during an event, µg/m3; Vdo is the outdoor deposition velocity of FP, assumed to be 20 m/h; ET is the exposure time, h; and Vwater is the mass inventory of surface water, L/m2. On the basis of data in the Water Encyclopedia, we estimate the average depth of surface water as 5 m, which gives a typical value of Vwater of 5,000 L/m2. Combining these values yields Cwater ≈ 0.004 (Cair x ET) µg/L. The residence time of surface waters—such as lakes, ponds, and rivers—ranges from days to a year. Assuming that added cadmium persists in a surface drinking-water supply for 30-100 d and that someone drinks 2 L/day from this supply, we get an estimated contact with the deposited cadmium of 60-200 L for a single event. For that person, the potential dose for a single event is potential dose ≈ Cwater x (60-600) L = (0.24-0.8) x (Cair x ET) µg [over ≈ 30-100 d]. That value is comparable with and slightly lower than the direct exposure to contaminated air by inhalation during the exposure event. However, there is greater uncertainty associated with this value than with the direct inhalation-dose estimate. This pathway is relevant only in cities like Fort Wayne, IN, where a public water supply was exposed to the same degree of air concentration as the population. In most of the cities under consideration, that was not the case. REFERENCES Allott, R.W., M. Kelly, and C.N. Hewitt. 1992. Behavior of urban dust contaminated by chernobyl fallout: Environmental half-lives and transfer coef-

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests ficients. Environ. Sci. Technol. 26:2142-2147. ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profile for Cadmium. TP-92/06. Atlanta, Ga.: Agency for Toxic Substances and Disease Registry. Baes, C.F. III, R.D. Sharp, A.L. Sjoreen, and R.W. Shor. 1984. A Review and Analysis of Parameters for Assessing Transport of Environmentally Released Radionuclides Through Agriculture. ORNL-5786/NTIS DE85-000287. Oak Ridge National Laboratory, Oak Ridge, Tenn. Bodek, I., W.J. Lyman, W.F. Reehl, and D.H. Rosenblatt, eds. 1988. Environmental Inorganic Chemistry: Properties, Processes, and Estimation Methods. New York: Pergamon. Bowen, H.J.M. 1979. Environmental Chemistry of the Elements. New York: Academic. Davidson, C.I., W.D. Goold, T.P. Mathison, G.B. Wiersma, K.W. Brown, and M.T. Reilly. 1985. Airborne trace elements in Great Smoky Mountains, Olympic, and Glacier National Parks. Environ. Sci. Technol. 19(1):27-35. Duggan, R.E., and P.E. Corneliussen. 1972. Dietary intake of pesticide chemicals in the United States (III), June 1968-April 1970. Pestic. Monit. J. 5:331-341. Eggleton, A.E.J., and N. Thompson. 1961. Loss of fluorescent particles in atmospheric diffusion experiments by comparison with radioxenon tracer. Nature 192:935-936. Elinder, C.-G. 1985. Cadmium: Uses, occurrence, and intake. In Cadmium and Health: A Toxicological and Epidemiological Appraisal. Vol. 1. Exposure, Dose, and Metabolism. Effects and response. L. Friberg, C.-G. Elinder, T. Kjellström, G.F. Nordberg, eds. Boca Raton, Fla.: CRC Press. EPA (U.S. Environmental Protection Agency). 1981. Health assessment document for cadmium. EPA-600/8-81-023. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office. EPA (U.S. Environmental Protection Agency). 1992. Dermal Exposure Assessment: Principles and Applications EPA/600/8-91/011B. Office of Health and Environmental Assessment, U.S. Environmental Protection Agency, Washington, D.C. Friberg, L., Piscator, M., Nordberg, G. F., and others. 1974. Cadmium in the Environment, 2nd Ed. Boca Raton, Fla.: CRC. Gartrell, M.J., J.C. Craun, D.S. Podrebarac, and E.L. Gunderson. 1986. Pesticides, selected elements, and other chemicals in adult total diet samples, October 1980-March 1982. J. Assoc. Off. Anal. Chem. 69:146-159.

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Toxicologic Assessment of the Army's Zinc Cadmium Sulfide Dispersion Tests Gunderson, E.L. 1995. Dietary intakes of pesticides, selected elements, and other chemicals: FDA total diet study, June 1984-April 1986. J. AOAC Int. 78(4):910. IARC (International Agency for Research on Cancer). 1993. Beryllium, Cadmium, Mercury, and Exposures in the Glass Manufacturing Industry. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 58. Lyon, France: International Agency for Research on Cancer. LaGoy, P. K. 1987. Estimated soil ingestion rates for use in risk assessment. Risk Anal. 7:355-359. Leighton, P.A., W.A. Perkins, S.W. Grinnell, and F.A. Webster. 1965. The Fluorescent particle atmospheric tracer technique. J. Appl. Meteorol. 4:334-335. Mahaffey, K.R., P.E. Corneliussen, C.F. Jelinek, and J.A. Fiorino. 1975. Heavy metal exposure from foods. Environ. Health Perspect. 12:63-69. McKone, T.E., and P.B. Ryan. 1989. Human exposures to chemicals through food chains: An uncertainty analysis . Environ. Sci. Technol. 23:1154-1163. McKone, T.E., and J.I. Daniels. 1991. Estimating human exposure through multiple pathways from air, water, and soil. Regul. Toxicol. Pharmacol. 13:36-61. Mertz, W. 1981. The essential trace elements. Science 213:1332-1338. Murthy, G.K., U. Rhea, and J.T. Peeler. 1971. Levels of antimony, cadmium, chromium, cobalt, manganese, and zinc in institutional total diets. Environ. Sci. Technol. 5:436. Nazaroff, W.W., and G.R. Cass. 1989. Mathematical modeling of indoor aerosol dynamics. Environ. Sci. Technol. 23:157-166. Nriagu, J.O. 1980. Cadmium in the Environment. Part I: Ecological Cycling. New York: John Wiley & Sons. Nriagu, J.O. 1981. Cadmium in the Environment. Part II: Health Effects. New York: John Wiley & Sons. Saltzman, B.E., J. Cholak, and L.J. Schafer. 1985. Concentrations of six metals in the air of eight cities. Environ. Sci. Technol. 19:328-333. Schroeder, H.A., and J.J. Balassa. 1961. Abnormal trace metals in man: Cadmium. J. Chron. Dis. 14:236-258. Schroeder, W.H., M. Dobson, and D.M. Kane. 1987. Toxic trace elements associated with airborne particulate matter: A review. JAPCA 37:1267-1285.

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