Skip directly to search Skip directly to A to Z list Skip directly to site content

PUBLIC HEALTH ASSESSMENT

CENEX SUPPLY AND MARKETING, INCORPORATED
(a/k/a WESTERN FARMERS, INCORPORATED)
QUINCY, GRANT COUNTY, WASHINGTON


DISCUSSION

Environmental investigations conducted since 1993 have confirmed the presence of contaminants in Cenex site soils, on-site and off-site shallow groundwater, and on-site and off-site subsurface soil gas. A limited-scale indoor air sampling investigation was conducted in and around the Quincy high school in 1998, followed by more comprehensive indoor air investigations in the summer of 2000 and fall of 2001.

The following section discusses how WDOH evaluates risk, the nature and extent of the contamination, the pathways of exposure, and the public health implications from exposure to the contaminants of concern. In other words, what contaminants are present, how people might come into contact with them, and the potential health effects that could result from exposure to the contaminants.

Contaminants of concern were assessed using various state (MTCA method B)10 and federal (ATSDR and EPA)11, 12 health-based criteria (comparison values). Comparison values are media-specific concentrations used to select environmental contaminants for further evaluation. Contaminant concentrations below comparison values are unlikely to pose a health threat. Contaminant concentrations exceeding comparison values do not necessarily pose a health threat, but are further evaluated to determine whether they are at levels observed to cause toxic effects (referred to as toxic effect levels) in human population and/or laboratory animal studies.

Evaluating noncancer risk

RfDs and MRLsTo evaluate the potential for noncancer health effects, a dose was estimated for each contaminant exceeding a comparison value. In estimating exposure doses, it was conservatively assumed that residents and workers were chronically exposed to the maximum detected contaminant concentrations in soil at the Cenex site, without regard to sample depth. In some cases, these samples were below ground surface, where exposures would have been unlikely. The estimated child and adult exposure doses for each contaminant were then compared to ATSDR's minimal risk level (MRL) or EPA's oral reference dose (RfD). MRLs and RfDs are estimates of daily exposure of a human to a chemical below which noncarcinogenic health effects are not expected. They are derived from human and laboratory animal studies. These studies provide either a lowest observed adverse effect level (LOAEL) or a no-observed adverse effect level (NOAEL). In human or animal studies, the LOAEL is the lowest dose at which an adverse effect is seen, while the NOAEL is the highest dose that did not result in any adverse health effects.

To account for uncertainty (i.e., intraspecies variability, interspecies variability and extrapolation of a subchronic effect level to its chronic equivalent), the LOAEL or NOAEL is divided by a safety factor (typically from 100 to 1,000) to provide the more protective MRL or RfD. If a dose exceeds the MRL or RfD, the potential exists for adverse health effects. Thus, a dose only slightly exceeding the MRL or RfD would fall well below a toxic effect level. The higher the estimated dose is above the MRL or RfD, the closer it will be to the toxic effect level. It is important to note that new analytical methods are now being employed that better utilize scientific studies by considering all of the dose-response data rather than just the LOAEL or NOAEL.

Evaluating cancer risk

For screening of chemicals that are known or expected to cause cancer, it is assumed that no "safe" level exists, and EPA cancer slope factors are used to calculate an estimated increased cancer risk. The slope factor is used to estimate an upperbound probability of an individual developing cancer as a result of exposure(s) to a particular level of a carcinogen(s). An exposure which results in an estimated increased cancer risk of one additional cancer in a population of 1 million people exposed, averaged over a 70-year lifetime, is considered an acceptable risk, and is used as the comparison value. This one additional cancer is in addition to the approximately one in four persons in the U.S. expected to develop cancer in their lifetime.13

A. Groundwater

A1. Nature and extent of contamination

For the general area encompassing Quincy, the U.S. Geological Survey (USGS) classifies the groundwater system as part of the Columbia Lava Plateau groundwater region. Two basic aquifers exist in the region, a shallow, unconsolidated aquifer zone and a deeper aquifer. However, restricting or confining layers in the unconsolidated materials result in perched water tables much closer to the soil surface (Figure 7). Due to input from irrigation project waters, shallow groundwater elevation levels have increased significantly. Quincy's five municipal wells are screened in the deeper aquifer, at depths ranging from 381 to 409 feet below ground surface (BGS). Groundwater flow in the unconsolidated shallow zone in this region is toward the southeast.3

Since June 1996, Cenex has installed 29 on-site and off-site groundwater monitoring wells in the upper and lower parts of the shallow aquifer zone. Numerous VOCs and nitrates exceeding health comparison values and state and federal drinking water standards (maximum contaminant levels, or MCLs) were detected in the shallow groundwater. 1,2-dichloropropane (1,2-DCP) has been consistently detected at the highest concentration (up to 7,000 times the drinking water standard), although other VOCs have also been detected. Nitrate has been detected in groundwater underneath the site up to 28 times the federal drinking water standard. Monitoring well 9, an on-site well, was sampled for a full range of pesticides (EPA method 507 modified for pesticides) in September 1997, but none were detected. Maximum detected groundwater VOC and nitrate concentrations are presented in Table A5. The contaminated groundwater plume has migrated off-site, across Division Street and Sixth Avenue to the southeast (Figure 6).

A2. Pathways analysis and public health implications

Although the shallow groundwater has been significantly contaminated by past site activities, to date, these contaminants have not impacted the city's municipal drinking water supply wells. After a thorough review of county well logs, followed by field inspections, representatives of the Grant County Health District could not locate any private domestic wells in the vicinity of the site. As a result of their investigation, no private wells are believed to be used for domestic purposes in the vicinity of the Cenex groundwater plume. Residents downgradient of the site (and most, if not all, residents within the city limits) obtain their domestic water from the city's municipal wells (Grant County and City of Quincy staff, personal communications, 1997). No VOCs were detected in the most recent (January 22, 2001) water samples collected from Quincy well # 5.

B. Air: Onsite

B1. Nature and extent of contamination

VOC levels in ambient air at the Cenex site prior to site remediation activities in 1997 were limited to qualitative measurements taken with an Organic Vapor Analyzer (OVA). These measurements did not detect VOCs in on-site ambient air. Testing for 1,2-DCP at the Cenex property fence line with passive dosimeter badges also occurred during a limited-scale air sampling event in February 1998.14 No 1,2-DCP was detected during this event. On-site air sampling for pesticides or metals was not conducted.

An air model was used to predict concentrations of VOC emissions prior to startup of the on-site SVE system employed in November 1998.15 Air modeling results indicated that VOC concentrations were predicted to be below levels of health concern. The maximum modeled ground level concentration for these VOCs was estimated to be 24 meters from the stack.15

The SVE system was designed to remove VOCs, including the four primary contaminants of concern in the vadose zone vapors; 1,2-dichloropropane, chlorobenzene, chloroform, and vinyl chloride (i.e., VOCs previously detected during site subsurface soil gas tests).

After the SVE system became operational, air sampling for VOCs was conducted. VOCs were not detected in the stack effluent (i.e., the carbon system removed all VOCs). Modeled and measured air VOC concentrations, soil gas VOC concentrations, and health comparison values are presented in Table A8 and A9.

B2. Pathways analysis and public health implications

On-site air sampling for VOCs was conducted on several occasions, as described above. On the basis of the results of previous on-site ambient air sampling, VOCs do not appear to be a health concern to workers or residents near the site. Additionally, site soil gas remediation has been in effect for several years, and is ongoing. The soil gas removal effort is intended to further reduce the likelihood of VOCs present in subsurface soil gas from entering the groundwater and ambient air.

C. Air: Off-Site

C1. Nature and extent of contamination

February 1998 testing

RfCsBecause of community and school concerns about the potential for exposure to 1,2-DCP inside the Quincy high school, Cenex conducted a limited-scale air monitoring investigation at the school between February 18-23, 1998. Cenex installed 11 3-M passive organic vapor monitoring badges in and around the high school to determine the levels, if any, of this chemical.14 The badges were left in place for five days in an effort to achieve the required detection limit. 1,2-DCP, a primary chemical of concern, has been detected in soil, soil gas, and groundwater at the Cenex site, and in soil gas underneath the high school and adjacent Desert Electric property.

A low concentration of 1,2-DCP was detected in the staff lounge. The concentration was below ATSDR's minimal risk level (MRL), but exceeded EPA's inhalation reference concentration (RfC), and was further evaluated by WDOH to determine the potential health implications (see section C2 below).

August 2000 testing

In summer 2000, Cenex, with Ecology and school board oversight, conducted a more comprehensive indoor air investigation at the Quincy high school, the results of which were evaluated by ATSDR in a health consultation. No 1,2-DCP or other site-related chemicals were detected during that investigation. Several chemicals were detected, but were determined by ATSDR to be below levels of health concern. A similar, follow-up indoor air sampling investigation was conducted at the high school in fall 2001, the results of which will be evaluated by WDOH in a separate health consultation. The following section discusses the health implications associated with the 1998 1,2-DCP detection.

C2. Pathways analysis and public health implications

Before the early 1980s, 1,2-DCP was used in farming as a soil fumigant and was found in some paint strippers, varnishes, and furniture finish removers. 1,2-DCP has also been used as a solvent, photographic processing chemical, and as an intermediate in the formation of other chemicals.16

Breathing high levels of 1,2-DCP can cause dizziness, headache, nausea, eye and throat irritation, and injury to the liver and kidneys.16 There are no reports of health effects in humans following low-level exposure to 1,2-DCP for either short-or long-term time periods. Some animal studies indicate that inhalation of 1,2-DCP at high levels causes liver and kidney damage, as well as effects on the respiratory system.

EPA's RfC for 1,2-DCP is 4 µg/m3, and is based on increased cell growth in rat nasal mucosa following chronic high dose inhalation exposure.17 The 1998 detection in the staff lounge exceeded the RfC, indicating the possibility that continuous exposure over many years could result in adverse health effects for sensitive individuals. However, the level detected in the staff lounge was over 700 times lower than the lowest concentration at which actual health effects were observed in the studies used to derive the RfC. As a result, exposures would not be expected to result in chronic health effects for most people. As previously noted, more recent, and comprehensive indoor air sampling was conducted inside the high school in the summer of 2000. No 1,2-DCP or other site-related chemicals were detected during that event.

Although data exist on the carcinogenic potential from oral exposure to 1,2-DCP, data regarding the carcinogenic potency of 1,2-DCP following inhalation exposure are insufficient for estimation of carcinogenic potency.16, 17 No studies were located in the scientific literature regarding carcinogenic effects in humans following inhalation exposure to 1,2-DCP. A 1948 mouse study examined the hepatocarcinogenic (liver) effects of 1,2-DCP from intermediate-duration (25-30 weeks) inhalation exposures. In that study, some hepatomas were observed, but the results were inconclusive.16, 17 The concentration of 1,2-DCP administered in this study was over 100,000 times higher than the concentration measured in the high school staff lounge during the 1998 sampling event.

On the basis of available toxicological information, it is unlikely that short- or long-term exposures to 1,2-DCP at levels detected in the high school staff lounge during the 1998 sampling event would result in chronic health problems. 1,2-DCP air monitoring results, sampling locations, and health comparison values are presented in Table A10.

D. Soil Gas

D1. Nature and extent of contamination

VOCs were detected in subsurface soil gas, both on and off the Cenex site. The highest on-site VOC concentrations were detected between the former fumigant tank area and rinse pad. Lower concentrations were detected off-site, to the south and southeast, underneath the high school property, and underneath the Desert Electric property. The highest concentration of 1,2-DCP detected in subsurface soil gas underneath the high school property was 5.9 mg/m3. The highest concentration of 1,2-DCP in subsurface soil gas underneath the Cenex site was 3,010 mg/m3 (651 ppm). Chlorobenzene, chloroform, 1,1-DCE, and vinyl chloride were also detected in on-site soil gas, but at considerably lower concentrations. Soil gas results are presented in Table A8.

D2. Pathways analysis and public health implications

Site remediation workers are the most likely persons to come into direct contact with subsurface soil gas vapors. It is presumed they are aware of site conditions, and are taking the appropriate precautions to protect themselves from potential exposures. To mitigate further VOC contamination of the groundwater, and to reduce or eliminate the possibility of migration into the air, Cenex employed a soil vapor extraction system in fall 1998. The system continues to remove VOCs from site soil. 1,2-dichloropropane has not been detected in air samples collected after the system's carbon units, indicating that all of the VOCs being removed from the soil are being contained within the system's carbon media, and not being released into the air.

E. Soil

E1. Nature and extent of contamination

Most of the contaminated soil was excavated and removed from the site during the summer of 1997. Residual contaminant levels on the site are low, and do not pose a health threat. A 6-inch gravel layer was placed over the site, further reducing the chance for exposure.

For this health assessment, exposures to site soil contaminants were assumed to have occurred prior to site soil remediation in 1997. The higher of either the 1993 EPA soil/sludge or 1995 Cenex soil sampling results were used in the health assessment to evaluate potential health impacts, regardless of the depth or location of the soil samples. Persons assumed to be exposed include Cenex employees, adult residents, and children noted to occasionally have played on ramps and walked or bicycled across the site to and from school (Cenex Supply and Marketing, Inc., personal communication, 1997). The site was fenced in 1996, which effectively eliminated the potential for further residential direct contact exposures. Pre-remediated and post-remediated soil contaminant concentrations are presented in Tables A1 through A4, and A6 through A8.

Sixherbicide/pesticide compounds (trifluralin, vernolate, ethalfluralin, disulfoton, atrazine, and alachlor), one insecticide (chlorpyrifos), and four metals (chromium, beryllium, cadmium, and thallium) exceeded health comparison values in site soil, and were further evaluated in the health assessment. These 11 contaminants are discussed below relative to pathways of exposure and public health implications.

E2. Pathways analysis and public health implications

Trifluralin

Trifluralin is a selective preemergent herbicide used to control annual grasses and some broadleaf annual weeds. Trifluralin was detected in soil during both the 1993 EPA and 1995 Cenex sampling events. The highest concentration (349 mg/kg) was from a subsurface sample collected underneaththe former rinsate pond (EPA sample #RPS4). The highest concentration of trifluralin detected during the June 1997 (post-remediation) sampling event was 0.298 mg/kg, well below health comparison values.

Noncancer toxicity

Acute-duration laboratory animal tests have demonstrated trifluralin to have low to moderate acute toxicity by oral or dermal exposure, and moderate acute toxicity by inhalation.17, 18 EPA has not established an RfC for trifluralin. Exposure to high doses of trifluralin are associated with increases in kidney, bladder, and thyroid tumors. Dogs chronically exposed to trifluralin in their diet showed decreased weight gain, changes in hematological parameters, and increased liver weight.17 Skeletal abnormalities were observed in the offspring of mice exposed via gavage (experimentally introducing trifluralin into the stomach). The RfD for trifluralin is based on increased liver weights and an increase in methemoglobinemia in dogs.17 The estimated child and adult exposure doses were well below the chronic oral RfD, suggesting that noncancer health effects are unlikely.

Cancer toxicity

Cancer RiskEPA classifies trifluralin as a Group C (possible human) carcinogen. No studies were located in the scientific literature regarding the carcinogenicity of trifluralin in humans. Classification is based on the induction of urinary tract tumors (renal pelvis carcinomas and urinary bladder papillomas) and thyroid tumors (adenomas/carcinomas combined) in one rat study.17 Trifluralin did not produce statistically significant increases in tumors in other studies.17 For this health assessment, the estimated increased cancer risk for children and adults assumed to be exposed to trifluralin in soil was slight; approximately one additional cancer in a population of 1 million persons exposed. Because of the highly conservative exposure assumptions (i.e., that exposures occurred over many years to the highest detected concentration), the actual risk is likely even lower.

Ethalfluralin

Ethalfluralin is a selective preemergent herbicide, structurally similar to trifluralin. Like trifluralin, it is a dinitroaniline compound. Ethalfluralin is readily degraded in soil, both by microorganisms and by photodecomposition. Ethalfluralin was detected in site soil during both the 1993 EPA and 1995 Cenex sampling events. The highest concentration (1,530 mg/kg) was from a subsurface sample collected from the excavation on the north side of the former rinsate pond (EPA sample #RPS3). The highest concentration of ethalfluralin detected during the June 1997 sampling event, after soil removal, was 0.363 mg/kg, well below health comparison values.

Noncancer toxicity

Although no health comparison values exist for ethalfluralin, toxicological references suggest that, because of its chemical similarity to trifluralin, exposure would be expected to result in similar health effects. Limited rat studies have demonstrated several structurally similar urinary metabolites for these two compounds.17 Because of this similarity, the cancer slope factor established for trifluralin was also used in this health assessment to assess the cancer risk for exposure to ethalfluralin. Likewise, the RfD established for trifluralin was used to assess the potential for noncancer health effects from exposure to ethalfluralin. EPA has not established an RfC for ethalfluralin.

The estimated exposure doses were below the oral RfD, and were well below doses which caused health effects in laboratory animals, suggesting that noncancer health effects are unlikely.

Cancer toxicity

Chronic mouse and rat-feeding studies indicate ethalfluralin has a low potential for carcinogenicity.18 One study demonstrated an increase in benign mammary tumors in female rats after high doses were administered over a 2-year period.18, 19 In addition, ethalfluralin produced a common urinary metabolite in rats (Dow specimen label for ethalfluralin, Pesticide Dictionary). The estimated increased cancer risk for children and adults assumed to be exposed to ethalfluralin in soil at the Cenex site was slight; approximately two additional cancers in a population of 1 million persons exposed. Because of the highly conservative exposure assumptions (ingestion of the highest detected concentration over many years), the actual risk is likely much lower. For example, the highest detected concentration of ethalfluralin in site surface soil, where exposures would be more likely to occur, was only one-third the maximum detected concentration evaluated in this health assessment (from a subsurface sample).

Disulfoton

Disulfoton is an organophosphate pesticide used to control a variety of harmful pests that attack many field and vegetable crops. Disulfoton binds moderately well to soil and typically does not readily migrate deep into the soil.17, 20, 21 Disulfoton was detected in soil during both the 1993 EPA and 1997 Cenex sampling events. The highest concentration (146 mg/kg) was from a subsurface sample collected in the excavation on the north side of the former rinsate pond (EPA sample #RPS2). Disulfoton was not detected after the June 1997 soil removal.

Noncancer toxicity

Health effects from exposure to high levels of disulfoton (much higher than levels detected at the Cenex site) include effects on the nervous system, narrowing of the pupils, vomiting, diarrhea, drooling, difficulty in breathing, tremors, convulsions, and even death.20, 21 The chronic oral MRL for disulfoton is based on decreased cholinesterase activity observed in female rats after a chronic feeding study.17 Although estimated adult and child exposure doses exceeded the chronic oral MRL and RfD by a factor of three to five, they were 350 to 450 times lower than the lowest dose that produced adverse health effects in the study. Disulfoton levels detected in surface soil, where exposures would have been more likely to occur, were much lower (from 3.4 mg/kg to 8.8 mg/kg). Estimated doses from exposure to disulfoton levels in surface soil were below the oral RfD, suggesting that adverse noncancer health effects were unlikely. EPA has not established an RfC for disulfoton.

Cancer toxicity

No studies were located in the scientific literature regarding cancer in humans after oral exposure to disulfoton.17, 20 There was no evidence of carcinogenicity in Beagle dogs fed disulfoton for two years at doses many times higher than were estimated for children or adults assumed to be exposed at the Cenex site.20 As a result, cancer effects would not be expected.

Vernolate

Vernolate is a thiocarbamate compound used as a selective soil-incorporated herbicide to control broadleaf and grassy weeds. Vernolate is registered in the United States for use on corn.17, 22, 23 Vernolate was detected in soil during both the 1993 EPA and 1995 Cenex sampling events. The highest concentration (112 mg/kg) was from a subsurface sample in the excavation on the north side of the former rinsate pond (EPA sample #RPS3). The highest concentration of vernolate detected during the June 1997 sampling event, after soil remediation, was 0.295 mg/kg, well below the health comparison value.

Noncancer toxicity

The RfD established for vernolate is based on a two-generation reproduction rat study which showed a statistically significant depression in the mean body weight of rats fed vernolate in their diet.17, 22 The estimated doses were 10 times less than the chronic oral RfD, suggesting that noncancer health effects are unlikely. EPA has not established an RfC for vernolate.

Cancer toxicity

No studies were located in the scientific literature regarding human carcinogenicity from exposure to vernolate. In a 24-month mouse study, no oncogenic/carcinogenic effects were observed at vernolate concentrations as high as 100 mg/kg/day (thousands of times higher than estimated Cenex site exposures).17, 23 Based on available information, cancer would not be expected for persons assumed to be exposed to the detected concentration of vernolate at the site.

Chlorpyrifos

Chlorpyrifos is an organophosphorus insecticide that has been widely used in the home and on farms. In the home, it has been used to control cockroaches, fleas, and termites. It has also been an active ingredient in some flea and tick collars. On farms, it is used to control ticks on cattle, and as a spray to control crop pests.24 In 1997, chlorpyrifos was voluntarily withdrawn from most indoor and pet uses by the manufacturer, DowElanco.

Chlorpyrifos adheres tightly to soil particles. Volatilization is the major route in which chlorpyrifos disperses after it is applied. Once in the environment, chlorpyrifos is broken down by sunlight, bacteria, or other chemical processes.24

Chlorpyrifos was detected in soil during the 1993 EPA sampling event. The highest concentration (162 mg/kg) was from a surface sample collected between the former rinse pad and old Telone plant (EPA sample # SS2).

Noncancer toxicity

Short-term exposure to moderate levels of chlorpyrifos can cause dizziness, fatigue, runny nose or eyes, salivation, nausea, intestinal discomfort, sweating, and changes in heart rate. Short-term exposure to much higher levels of chlorpyrifos may cause paralysis, seizures, loss of consciousness, and death. Short-term exposure at high concentrations may cause muscle weakness weeks after the original symptoms have disappeared. Other effects include changes in behavior or sleeping patterns, mood changes, and effects on the nerves and/or muscles in the limbs.24 The EPA has not established an RfC for chlorpyrifos.

The MRL is based on acetylcholinesterase inhibition in rats. Estimated doses in this health assessment were well below the MRL and chronic oral RfD, suggesting that noncancer health effects are unlikely.

Cancer toxicity

No information was located in the scientific literature regarding carcinogenic effects of chlorpyrifos in humans following oral exposure. Chronic-duration exposure studies have shown no carcinogenicity in animals.24 The EPA has not classified chlorpyrifos for carcinogenicity (Class D).

Atrazine

Atrazine is an herbicide that selectively controls broadleaf (dicot) weeds, such as pigweed, cocklebur, velvetleaf and certain grass weeds in fields of corn and sorghum.

Atrazine was detected in soil during the 1993 EPA sampling event and 1995 Cenex sampling event. The highest concentration in soil (8.51 mg/kg) was from a surface sample collected by Cenex.

Noncancer toxicity

The RfD for atrazine is based on decreased body weight gain in rats chronically fed atrazine in their diet. The estimated child and adult exposure doses were well below the RfD, suggesting that noncancer health effects would not be expected.

Cancer toxicity

Since there is currently no oral cancer slope factor for atrazine, the former slope factor was used to estimate cancer risk. Using the former slope factor resulted in a slight estimated increased cancer risk for persons assumed to be exposed chronically to the single highest detection of atrazine in site soil.

Alachlor

Alachlor is an aniline herbicide used to control annual grasses and broadleaf weeds in field corn, soybeans, and peanuts. The highest detected concentration (19.8 mg/kg) was from a surface sample collected between the former rinse pad and old Telone plant (EPA sample # SS2).

Noncancer toxicity

The RfD is based on hemosiderosis observed in the kidney and spleen of beagle dogs and hemolytic anemia during a 1-year feeding study. Estimated doses for this health assessment were well below the RfD, indicating that noncancer health effects would not be expected.

Cancer toxicity

Although there is currently no oral cancer slope factor listed for alachlor, a previous slope factor for alachlor was located in EPA's 1997 Update Health Effects Assessment Summary Table (HEAST). EPA Region 3 also lists a health comparison value for alachlor (October 2000 RBC Table). Using the former slope factor, estimated past exposures to the highest detected concentration of alachlor were estimated to result in a slight additional increased cancer risk.

Cadmium

Cadmium is an element that occurs naturally in the earth's crust. It is one of many elements that are commonly called "heavy metals." Most cadmium in the United States is extracted as a by-product during the production of other metals such as zinc, lead, or copper. Cadmium is used in batteries, pigments, metal coatings, plastics, and some metal alloys.

Long-term exposure to lower levels of cadmium can lead to a buildup of cadmium in the kidney and possible kidney disease. Other potential long-term effects are lung damage and fragile bones. Skin contact with lower levels of cadmium is not known to affect the health of people or animals.25

The highest concentration of cadmium (25.2 mg/kg) was from EPA soil sample # RPS4, collected at the former rinsate pond. This concentration exceeded the 0.5 mg/kg mean background concentration of cadmium for the Yakima Basin region.

Noncancer toxicity

The EPA has established separate oral RfDs for cadmium in food and water. For this health assessment, the oral RfD for food was used to assess the potential for noncancer health effects, and is based on kidney effects in humans. The estimated doses were well below the oral RfD, suggesting that noncancer health effects are unlikely. The EPA has not established an RfC for cadmium.

Cancer toxicity

The EPA classifies cadmium as a probable human carcinogen by the inhalation route. Neither human nor animal studies provide conclusive evidence to determine whether or not cadmium is carcinogenic by the oral route. A few studies of cancer rates among humans orally exposed to cadmium have been performed. However, there is little evidence of an association between oral exposure to cadmium and increased cancer rates in humans. 25 In a 1992 rat study, oral exposure to very high doses of cadmium was associated with tumors of the prostate, testes, and hematopoietic (blood-forming) system.25 The estimated child and adult cadmium exposure doses were well below the cancer effect level (CEL) derived from the 1992 rat study. As a result, cancer effects would not be expected from exposure to even the highest level of cadmium detected.

Chromium

Chromium is a naturally occurring element found in rocks, animals, plants, soil, and in volcanic dust and gases. Chromium is present in the environment in several different forms. Trivalent chromium in small amounts is an essential nutrient.26 For this health assessment, it was conservatively assumed that 100% of the detected chromium was in the more toxic hexavalent form.

Chromium was detected in soil samples collected during both the 1993 and 1997 sampling events. One sample (sample # RPS4), collected at the former rinsate pond, slightly exceeded a noncancer comparison value.

Noncancer toxicity

Although ingesting small amounts of hexavalent chromium at low concentrations is not believed to be harmful, ingestion of large amounts of hexavalent chromium has caused stomach upsets, ulcers, convulsions, kidney and liver damage, and even death.26 There are no long-term studies of ingested hexavalent chromium. The respiratory system and the skin are the primary target organs for exposure to chromium and its compounds. Workers exposed to hexavalent chromium have developed skin ulcers and allergic reactions consisting of severe redness and swelling of the skin.26 The oral RfD for hexavalent chromium is based on systemic effects in rats exposed to hexavalent chromium in drinking water over a 1-year period.17, 26 The oral RfD for trivalent chromium also is based on systemic effects in rats. The estimated safe and adequate daily dietary intake for chromium of 50-200 µg/day has been established by the National Research Council, corresponding to 0.71-2.9 µg/kg/day for an adult.17 ATSDR has adopted the upper range of the estimated safe and adequate daily dietary intake of 200 µg/day as an interim guidance for oral exposure to hexavalent and trivalent chromium.26

The child and adult estimated exposure doses were well below the oral RfDs established for hexavalent and trivalent chromium, suggesting that noncancer health effects are unlikely.

Cancer toxicity

EPA classifies hexavalent chromium as a Class-A (human) carcinogen by the inhalation route of exposure, based upon both animal studies and studies of worker exposures in the chrome-plating industry. Long-term exposure to chromium has been associated with lung cancer in workers. Animal studies have not shown hexavalent chromium to be carcinogenic by the oral route of exposure.17, 26 No other studies were located in the scientific literature that suggests hexavalent chromium is carcinogenic by the oral route of exposure.

The levels of chromium detected at the site were not at levels expected to result in the development of cancer.

Beryllium

Pure beryllium is a hard, grayish metal. In nature, beryllium can be found in compounds in mineral rocks, coal, soil, and volcanic dust. Beryllium compounds are commercially mined, and the beryllium purified for use in electrical parts, machine parts, ceramics, aircraft parts, nuclear weapons, and mirrors. The greatest potential for exposure to beryllium is from occupational exposure (primarily in the form of beryllium oxide). Exposure to high levels of beryllium in air can cause lung damage and a disease that resembles pneumonia. Long-term exposure to beryllium or beryllium oxide at much lower levels has been reported to cause chronic beryllium disease in sensitive individuals, characterized by shortness of breath, scarring of the lungs, and berylliosis. In addition, a skin allergy has been shown to develop when soluble beryllium compounds come in contact with the skin of sensitized individuals. Animal studies have shown that only small amounts of beryllium are absorbed after ingestion of beryllium or its compounds.27

Beryllium was detected in soil samples collected during both the 1993 and 1997 sampling events. A single sample (EPA sample # RPS4), collected at the former rinsate pond in 1993, slightly exceeded a health comparison value. All detected concentrations, however, were within the 0.39 mg/kg to 2.79 mg/kg range of natural background beryllium concentrations for the Yakima Basin.28

Noncancer toxicity

An oral RfD has been established by EPA and is based on a 1976 study of exposure to beryllium that resulted in small intestinal lesions in male and female dogs. Adult and child estimated exposure doses were well below the chronic oral RfD, suggesting that noncancer health effects are unlikely.

Cancer toxicity

No studies were located in the scientific literature regarding cancer in humans after oral exposure to beryllium or its compounds. Chronic oral ingestion studies did not result in increased incidences of tumors in rodents.27 The EPA recently reclassified beryllium from a B2 (probable human carcinogen, sufficient evidence in animals, and inadequate or no evidence in humans) to a B1 (probable human carcinogen, limited human data are available) carcinogen on the basis of the inhalation route of exposure.17 Because there is currently no oral slope factor listed, the former oral slope factor was used.

The estimated increased child and adult cancer risk from exposure to the highest detected concentration of beryllium in soil (1.39 mg/kg) is slight; approximately one additional cancer in a population of 1 million persons exposed. This slight increased cancer risk can be attributed entirely to natural background beryllium concentrations in the native soil.

Thallium

Thallium is used mostly in manufacturing electronic devices, switches, and closures, primarily for the semiconductor industry. It also has limited use in the manufacture of special glass and for certain medical procedures.

The highest concentration of thallium detected at the site was 6.7 mg/kg from EPA sample # RPS4, collected at the former rinsate pond. The concentration was determined by the lab to be above the instrument detection limit, but below the minimum quantitation limit.

Noncancer toxicity

The single highest concentration of thallium detected slightly exceeded the MTCA method B noncarcinogenic soil clean-up level of 5.6 mg/kg. The estimated exposure dose, assuming chronic exposure to the highest detected thallium concentration, was below the oral RfD for the five thallium compounds listed in EPA's Integrated Risk Information System (IRIS). As a result, noncancer health effects would not be expected.

Cancer toxicity

The Department of Health and Human Services, the International Agency for Research on Cancer, and the EPA have not classified thallium as to its human carcinogenicity. No studies are available in people or animals on the carcinogenic effects of breathing, ingesting, or touching thallium.


MULTIPLE CHEMICAL EXPOSURE

A person can be exposed by more than one pathway and to more than one chemical. Exposure to multiple pathways occurs if a contaminant is present in more than one medium (i.e., air, soil, surface water, groundwater, and sediment). For example, the dose of a contaminant received from drinking water might be combined with the dose received from contact with that same contaminant in soil.

For many chemicals, much information is available on how the individual chemical produces effects. It is much more difficult, however, to assess exposure to multiple chemicals. The vast number of chemicals in the environment make it impossible to measure all of the possible interactions between these chemicals. The potential exists for these chemicals to interact in the body and increase or decrease the potential for adverse health effects. Individual cancer risk estimates can be added since they are measures of probability. When estimating noncancer risk, however, similarities must exist between the chemicals if the doses are to be added. Groups of chemicals that have similar toxic effects can be added, such as volatile organic compounds (VOCs) which cause liver toxicity. Polycyclic aromatic hydrocarbons (PAHs) are another group of chemicals that can be assessed as one combined dose based on similarities in chemical structure and metabolites. Although some chemicals can interact to cause a toxic effect that is greater than the added effect, there is little evidence demonstrating this at concentrations commonly found in the environment.

Tables A13 and A14 summarize estimated total cancer and noncancer risks for adults and for children, assuming concurrent exposure to the highest detected concentrations of all 11 contaminants of concern detected in site soil. The total estimated increased cancer risk was low; approximately five to seven additional cancers in a population of 1 million persons exposed. Individual noncancer risk estimates (hazard quotients) were conservatively added to assess the likelihood of adverse noncancer health effects. Although the total noncancer risk estimates slightly exceeded a hazard quotient of one (suggesting the possibility of noncancerous health effects), upon careful review of the relevant toxicity studies, adverse health effects would not be expected. The combined exposure doses were still well below the toxic effect levels observed in the toxicity studies. In addition, disulfoton was the only contaminant responsible for the hazard quotient exceedence, and it was detected in a subsurface soil sample, where exposure is unlikely to occur.



Next Section     Table of Contents

  
 
USA.gov: The U.S. Government's Official Web PortalDepartment of Health and Human Services
Agency for Toxic Substances and Disease Registry, 4770 Buford Hwy NE, Atlanta, GA 30341
Contact CDC: 800-232-4636 / TTY: 888-232-6348

A-Z Index

  1. A
  2. B
  3. C
  4. D
  5. E
  6. F
  7. G
  8. H
  9. I
  10. J
  11. K
  12. L
  13. M
  14. N
  15. O
  16. P
  17. Q
  18. R
  19. S
  20. T
  21. U
  22. V
  23. W
  24. X
  25. Y
  26. Z
  27. #