PUBLIC HEALTH ASSESSMENT
GRANITE CITY, MADISON COUNTY, ILLINOIS
The tables mentioned in this section list the contaminants of interest in the different media. Thecontaminants of interest listed in this section will be evaluated to determine if they represent anexposure of public health significance. These chemicals were chosen based on the following criteria:
- Concentrations on and off the site.
- Field quality data, laboratory quality data, and sample design.
- Comparison of contaminant concentrations and background concentrations with health assessment comparison values for both carcinogenic and noncarcinogenic endpoints.
- Community health concerns.
In the tables and discussion that follow, a listed contaminant does not mean that it will causeadverse health effects from exposures. Instead, the list shows which contaminants will beevaluated further in this assessment.
|-||CEMEG||= Chronic Environmental Media Evaluation Guideline|
|-||CREG||= Cancer Risk Evaluation Guide|
|-||RfD||= Reference Dose|
|-||CRfD||= Chronic Reference Dose|
|-||RMEG||= Reference Dose Media Evaluation Guideline|
|-||EMEG||= Environmental Media Evaluation Guide|
|-||USEPA||= U.S. Environmental Protection Agency|
|-||IDPH||= Illinois Department of Public Health|
|-||IEPA||= Illinois Environmental Protection Agency|
|-||IMRL||= Intermediate Minimum Risk Level|
|-||LTHA||= Lifetime Drinking Water Health Advisory|
|-||MCL||= Maximum Contaminant Level|
|-||MCLG||= Maximum Contaminant Level Goal|
|-||PMCLG||= Proposed Maximum Contaminant Level Goal|
|-||ND||= No Data|
|-||NL||= Not Listed|
|-||F||= Frequency of detection|
|-||PPB||= Parts Per Billion|
|-||PPM||= Parts Per Million|
|RP||= Relative Potency|
|-||TEF||= Toxicity Equivalence Factor|
Environmental Media Evaluation Guides (EMEGs) are media-specific comparison values used to select contaminants of concern at hazardous waste sites. EMEGs are derived from Minimal Risk Levels (MRLs), developed by the Agency for Toxic Substances and Disease Registry (ATSDR), and are an estimate of human exposure to a compound that is not expected to cause noncancerous health effects at that level for a specified period. They are supposed to protect the most sensitive individuals (e.g., children). MRLs are guidelines and are not used to predict adverse health effects. MRLs do not take into account carcinogenic effects, chemical interactions, or multiple routes of exposure.
A Reference Dose (RfD) is a USEPA estimate of the daily exposure to a human population(including sensitive individuals) that is not expected to increase the risk of noncancerous adversehealth effects in that population over a lifetime.
Reference Dose Media Evaluation Guides (RMEGs) are comparison values developed to selectcontaminants of concern. They are derived from Reference Doses (RfD) developed by USEPA. They are not predictors of adverse health effects and do not take into account carcinogeniceffects, chemical interactions, or multiple routes of exposure.
Cancer Risk Evaluation Guides (CREGs) are based on a contaminant concentration estimated toincrease the cancer risk in a population by one individual in one million people over a lifetime ofexposure.
A Maximum Contaminant Level (MCL) is an enforceable maximum permissible level of acontaminant in a public drinking water supply. USEPA sets MCLs as close to the MaximumContaminant Level Goal (MCLG) as "feasible" based on the best technology, treatmenttechniques, and other means available, including cost.
Maximum Contaminant Level Goals (MCLGs) are drinking water health goals that differ fromMCLs because they do not take into account the feasibility of contaminant removal. USEPAsets them at a level at which there are no known or expected adverse health effects, and theyinclude a safety factor.
Lifetime Health Advisories (LTHAs) are contaminant concentrations in water that are notexpected to cause noncarcinogenic adverse health effects, over a lifetime's exposure, at thatlevel.
Relative Potency (RP) and Toxicity Equivalency Factors (TEF) are both used in riskcharacterization of mixtures. RPs and TEFs are both used for cancer evaluation; however, TEFscan also be used for noncancerous health effects. There is a set of grading criteria for TEFs. Ifnot all but some criteria are met, an RP for these compounds may be applied to the carcinogeniccompounds of this mixture.
IDPH examined the USEPA Toxic Chemical Release Inventory (TRI) to determine whatcompounds were released near the site by other industries. This database contains self-reportedinformation on releases of materials to air, water, and land, among other information. Thesedata were examined for Granite City (Zip Code 62040), Madison (Zip Code 62060) and Venice(Zip Code 62090). There were 52 reports for 10 separate industries in Granite City, Madison,and Venice. Total emissions were 520,725 pounds per year to the air, 77,392 pounds per year towaterways, and 4,662,979 pounds per year in landfills (Table 1). The top 5 companies withhighest releases were (from highest to lowest) Granite City Steel, Precoat Metals, ReillyIndustries, Spectralite Consortium, and Granite City Pickling.
Sampling was done at five different times between 1984 and 1992. On-site and off-sitesampling has included groundwater, soil, and surface wipes. Most contaminants found at the siteare associated with creosote, coal tar, PCP, and zinc naphthanate. Coal tar and creosote, adistillate of coal tar, are complex mixtures containing PAHs. Three hundred compounds havebeen identified in creosote, and there may be 10,000 more chemicals in the mixture. Chemicalsassociated with the PCP process include PCP and the constituents of diesel fuel or similarsolvents with which it was mixed during treatment. Contaminants of liquid PCP manufacturingthat can be found include dioxins and furans. The zinc naphthanate process used petroleumdistillates (aliphatic hydrocarbons).
Inorganic contaminants from on-site soils, off-site soils, background soils, and off-site wastedisposal areas were compared for the J-W site. Only 2 of the 12 inorganic contaminantsconcentrations were higher in the on-site surface soil versus off-site soil (Table 7). These twocontaminants were mercury and zinc. Except zinc, it appears that the sources of inorganiccompounds near J-W are not site-related. This conclusion is further supported by the presenceof many metal producing operations in Granite City in the past and present (Table 1), includingTaracorp, which is a secondary lead smelter and is on the NPL.
On-site media contaminated at the J-W facility include air, soil, groundwater, and surface water. Six areas on the site contain process wastes. Figure 2 identifies the on-site areas as the sludge pitin the Jennite process area, the zinc naphthanate and PCP process area, the general process area(including the creosote process area), the creosote cylinder pit, the oil/water separator pit, andthe treated tie storage area.
On-site wastes exist primarily as liquids and are contained in three areas: (1) the creosotecylinder pit (Area B), (2) the oil-water separator pit (Area D), and (3) the on-site sludgeDisposal Pit (Area E) (Figure 3). These on-site pits are unlined and, therefore, the contaminantscan come into direct contact with surface soil and groundwater. Contamination of these media isdiscussed in separate sections. Liquid wastes were also allowed to fall onto the ground surfacein treatment, process, and storage areas. Waste on the surface is discussed in On-Site SurfaceSoils. The liquid contamination in the three on-site pits is described in the following discussion.
In July 1991, as part of the Expanded Site Inspection, IEPA took four on-site waste samples (Figure 4):
- X113 - collected from inside the largest tank south of 22nd Street;
- X116 - collected from the buried tank car south of 22nd Street;
- X117 - collected from the smaller of the two tanks south of 22nd Street; and
- X118 - collected from the above-ground storage tank (17).
These samples were analyzed for volatile organic compounds (VOCs), semivolatile organiccompounds (SVOCs), inorganic compounds, dioxins, and furans (Table 2). In 1992, wastesamples were collected from the Jennite pit and 22nd Street lagoon and analyzed for dioxins andfurans. No dioxins or furans were detected.
The creosote cylinder pit was unlined and covered approximately 6,750 square feet. The depthof the pit varied from ground level to 3 feet below ground level. A modernization of thecreosote process included removing soil that could be seen to be contaminated and lining the pitwith concrete. This contaminated soil extended to the groundwater table at the creosote cylinderpit. No samples were taken of the liquid or sludge in the creosote pit before remediation becausethe liquid was almost pure creosote mixed with rain water.
The depth of the oil/water separator pit was believed to be greater than the seasonal high watertable of 10 feet. The pit was an unlined 10 by 16-foot pit. Steam from heating coils in thecreosote tanks, boiler blow down liquids, and vacuum pump cooling water discharged into thispit and flowed through baffles before discharge to the municipal sewage treatment plant. Thiswater is occasionally contaminated with creosote after a leak. Staff from Ecology andEnvironment (E&E) collected one sludge and one liquid sample from the oil/water separator pitduring their remedial investigation in 1984 (2). The results of the sludge samples are shown inTable 2 under Area E and one sample in Area D. The only VOC identified in the sludgesamples was benzene at a concentration of 4.2 parts per million (ppm), which is less thancomparison values.
SVOCs identified in the oil/water separator pit sludge were acenaphthalene, naphthalene,chrysene, anthracene, fluorene, and pyrene. No insecticides were identified in the sludge. Dioxin and furans found in the subsurface soils were octachlorodibenzodioxin (OCDD),octachlorodibenzofuran (OCDF), heptachlorodibenzodioxins, heptachlorodibenzofurans, andhexachlorodibenzofurans.
The water sample from the oil/water separator contained two VOCs, methylene chloride andbenzene, at 21 and 79 parts per billion (ppb), respectively. The benzene concentration is abovethe drinking water comparison value. Two SVOCs, phenol and 2,4-dimethylphenol, weredetected at levels well above their comparison values. However, they are not included in thetable because the oil/water separator water is not used for drinking. A summary of the results iscontained in Table 3.
No pesticides were found in the oil/water separator liquid. Dioxins and furans were not analyzed in the sample. The inorganic compounds identified in the sample were antimony, cadmium,lead, and zinc, with all but zinc exceeding drinking water comparison values. These inorganiccompounds were not included in Table 3 because the separator liquid is not a drinking watersource.
The on-site sludge disposal pit (area E) is at the eastern edge of the property near the Jenniteprocess area. Its dimensions are approximately 30 by 80 by 10 feet deep. Creosote and Jenniteprocess wastes have been disposed of in the pit. Past observations indicate that wastes haveflowed off the site from the sludge disposal pit. The Jennite loading zone is next to the pit andhas a contaminated surface area of approximately 20 square feet. Obviously contaminated soilextends from the surface to the water table. One waste sample was taken from the Jennite pitand analyzed only for the presence of dioxins and furans. No dioxins or furans were detected inthe Jennite pit waste sample. No samples have been taken from the liquid in the pit.
The treated tie storage area covers approximately 7 acres north of 22nd Street. Soilcontamination occurred in this area from excess creosote dripping from ties during transport tothe area, off loading, and storage. Ties were stored for days to years. The area has variousdegrees of contamination, with the off-loading area having the highest contamination, storageareas having moderate contamination, and the other areas having light contamination. Theestimated areas covered by heavy, moderate, and light contamination are 22,000 square feet, 1.5acres, and 5 acres, respectively. Contamination was observed in the treated tie storage area fromthe surface to a depth of 5 feet. Surface samples and subsurface samples were taken fromcontaminated soil and analyzed for PAHs and PCP (Figure 3). Surface samples were generallymore heavily contaminated than subsurface samples, and surface and subsurface zones observedto be heavily contaminated had higher PAH concentrations than those observed to be less contaminated.
The PCP cylinder, which later became the zinc naphthanate cylinder, is along the western edgeof the site. Contamination occurred in this area from spills when the door was opened after thetreatment. In 1984, contamination was observed to extend toward the groundwater table. Soilcontaminants observed near the PCP treatment cylinder were light brown and oily. Subsurfacesoil sample results show high levels of PCP and PAHs. PCP levels ranged from 670 ppm (2 feetbelow the surface) to 0 ppm (at the water table).
The general process area is on approximately 3 acres south of 22nd Street, near the creosote andPCP/zinc naphthanate process areas. Contamination occurred because creosote, PCP, and zincnaphthanate dripped from treated wood during its transport to the storage area. Thecontamination is highest under and adjacent to the trolley tracks and other areas where drippingoccurred. Tracking may contaminate other areas. As expected, the SVOC analyses of surfaceand subsurface samples taken from underneath the drip track were higher than the other areas inthe general process area.
Very few samples were taken of the waste on the site unless special analyses were wanted (forexample, analyses for dioxin and furans). Apparently, contamination was readily seen on theground surface; and there was little reason to take waste samples. Instead of waste samples,most samples were taken from the contaminated media, primarily soil and groundwater.
Soil sampling in the treated tie storage area suggests that the source of contamination is fromspillage onto the surface. The results from different depths indicate differential migration of thecontaminants from the surface. The VOCs are leaching toward the groundwater at a higher ratethan the PAHs. Inorganic analyses in the treated tie storage area did not indicate the presence ofany metal concentrations above the background levels and were not included in Table 4. Additional surface soil samples were collected and analyzed for the presence of dioxins andfurans. The locations of these samples were the northeast corner of the site (Area H), the JennitePit area, south end of the site, and the area of the old PCP treatment cylinder. No dioxins orfurans were detected in these additional samples.
Composite surface soil samples were taken from Area A. The samples were taken by E&E inSeptember 1984 and were only analyzed for SVOCs. The SVOCs identified in these sampleswere naphthalene, acenaphthylene, acenaphthene, fluorene, anthracene, PCP, fluoranthene,pyrene, chrysene, benzo(b)fluoranthene, benzo(a)pyrene, indeno(1,2,3-cd)pyrene, benzo(g,h,i)perylene, and dibenz(a,h)anthracene. Of the SVOCs identified, only acenaphthene, fluorene,anthracene, PCP, fluoranthene, pyrene, and benzo(a)pyrene had soil comparison values. OnlyPCP, with a concentration of 24.9 ppm, exceeded its CREG. Table 10 contains the RP inbenzo(a)pyrene (BaP) equivalence for all carcinogenic PAHs, including BaP. The RP for PAHsin Area A was 7.2 ppm, which exceeds the CREG for BaP. These RP results make the mixtureof PAHs in surface soils in Area A contaminants of concern.
One Area B surface soil sample was taken by E&E. The sample was analyzed for organiccompounds (except dioxins and furans), and inorganic compounds. The only VOC found wasbenzene at a concentration of 0.007 ppm, which is well below its soil comparison value (Table4). SVOCs identified in the creosote cylinder area were naphthene, acenaphthene, fluorene,anthracene, fluoranthene, and benz(a)anthracene. Anthracene (4,500 ppm) and fluoranthene(4,300 ppm) were the only compounds identified in Area B above their soil comparison values. Aldrin was detected at a concentration of 7.8 ppm, which is well above its CREG. Surface soilsamples in Area B were not analyzed for chlorinated dioxins and furans. Table 10 contains theRP in BaP equivalence for all carcinogenic PAHs. The RP for PAHs in Area B was 2.8 ppm,which exceeds the CREG for BaP. The concentration of benz(a)anthracene (2.8 ppm - BaPequivalents) itself exceeds the CREG for BaP. BaP was not detected in Area B.
E&E and IEPA collected two surface soil samples from the PCP treatment cylinder area - AreaC - in 1992. Neither of the samples was analyzed for pesticides, dioxins, or furans. Only theE&E sample was analyzed for inorganic compounds. Table 10 contains the RP in BaPequivalence for all carcinogenic PAHs found in Area C. The RP for PAHs in Area C was 0ppm, and BaP was not detected in Area C.
Benzene was identified in one surface soil sample at a concentration of 0.028 ppm. Naphthalene, acenaphthalene, fluorene, anthracene, PCP, fluoranthene, and pyrene were theSVOCs identified in the samples (Table 4). As expected, PCP was detected in Area C withconcentrations of 40 and 19,500 ppm. The CREG is 6 ppm. The inorganic compounds detectedin the sample from Area B were antimony, arsenic, beryllium, cadmium, lead, mercury, nickel,thallium, and zinc.
Two surface soil samples were taken near the on-site disposal pit (area E) in September 1984. The sample taken by IEPA was analyzed for VOCs, SVOCs, and inorganic compounds. Thesample taken by E&E was only analyzed for SVOCs. Methylene chloride was detected in thesample taken by IEPA; however, it was also detected in the blank sample. The SVOCsidentified in the sample taken by E&E were naphthalene, acenapthene, PCP, fluoranthene,pyrene, chrysene, benzo(b)fluoranthene, BaP, indeno(1,2,3-cd)pyrene, benzo(g,h,i)perylene,dibenz(a,h)anthracene. Table 8 contains the RP in BaP equivalence for all carcinogenic PAHs inarea E, excluding BaP. The RP for PAHs in area E was 0.4 ppm, which exceeds the CREG forBaP. These RP concentrations are based on the concentration of chrysene (0.43 ppm - BaPequivalents). BaP was not detected in area E. PCP was the only SVOC detected at aconcentration greater than its comparison value. No pesticides were analyzed in the surface soilsamples. No dioxins or furans were detected in the surface sample taken by IEPA. Inorganiccompounds detected in the sample, taken by IEPA were arsenic, barium, beryllium, cadmium,lead, manganese, mercury, nickel, and vanadium.
Two samples were taken in September 1984 in the general process area (area F) by E&E. OnlyVOCs and SVOCs were analyzed in these samples. No VOCs were detected. The SVOCsdetected included PAHs and PCP. The PAHs detected were naphthene, acenaphthalene,acenaphthene, fluorene, anthracene, fluoranthene, pyrene, chrysene, benzo(b)fluoranthene, BaP,indeno(1,2,3-cd)pyrene, benzo(g,h,i)perylene, and dibenz(a,h)anthracene (Table 4). Table 10contains the RP in BaP equivalence for all carcinogenic PAHs in area F. The RP for PAHs inarea F was 0.051 ppm, but this does not exceed the CREG for BaP.
IEPA collected more than 100 surface soil samples in July 1997. The surface soil samples werecollected to characterize the volume of waste at the site. The results of the sampling were notappreciably different from previous on-site soil samples.
Table 2 is a summary of data for subsurface soils on the site. Two VOCs, 2-butanone andbenzene, were identified in subsurface soil samples at concentrations above their comparisonvalues. A third VOC, 1,1,1-trichloroethane, does not have a comparison value. Table 2 showsthe concentration ranges and frequency of detections in each subsurface on-site area, and for allon-site areas combined.
SVOCs in subsurface soils on the site include PCP, 4-methyl phenol, 2, 4-dimethylphenol, and avariety of PAHs. Pesticides were analyzed for in 32 of the subsurface soil samples. Onlyheptachlor epoxide was above the comparison value. Heptachlor epoxide was only detected inone subsurface soil sample, which was taken at site E.
Table 8 contains the RP in BaP equivalence for all carcinogenic PAHs in on-site subsurfacesoils. The RP for benzo(b)fluoranthene (1.2 ppm BaP equivalent) exceeded the CREG for BaP. The total RP for PAHs in Area B was 7.7 ppm, which exceeds the CREG for BaP. These RPresults make the mixture of PAHs in subsurface soils in Area B contaminants of concern. TheBaP equivalents for benzo(b)fluoranthene (3.4 ppm) and dibenz(a,h)anthracene (0.35 ppm) wereeach above the CREG for BaP. BaP also exceeded the CREG.
The total RP for PAHs in Area C was 0.5 ppm, which exceeds the CREG for BaP. These RPresults make the mixture of PAHs in subsurface soils in Area C contaminants of concern. TheBaP equivalent for naphthalene (0.35 ppm) was above the CREG for BaP. BaP at 0.44 ppm alsoexceeded its CREG. The BaP equivalent concentrations in areas E and F at concentrations of1,359 ppm and 2.35 ppm greatly exceeded the CREG for BaP. Nearly all PAHs in areas Eindividually exceeded the CREG (Table 8).
Twelve subsurface soil samples were analyzed for the presence of 7 dioxins and furans. Thedioxins and furans analyzed were OCDD, OCDF, and total hexa- and hepta-chlorodibenzodioxins, and penta-, hexa-, and hepta-chlorodibenzo furans (Table 2). Pentachlorodibenzofurans were not detected in any of the samples. Table 9 contains the TEFsfor 2,3,7,8-TCDD for the dioxin and furan results in the on-site subsurface samples. The TEFsfor dioxins and furans in the on-site subsurface soils do not exceed the comparison value for2,3,7,8-TCDD.
Four inorganic compounds were identified in the subsurface soil samples at concentrations abovetheir comparison values. These compounds are arsenic, beryllium, mercury, and nickel.
IEPA collected subsurface soil samples in July 1997 to characterize the volume of waste at thesite. The sampling results were not appreciably different from those of previous samplingevents.
Contamination extending from the ground surface all the way to the water table has beenobserved in several areas including the creosote process area, near the Jennite process area, andin the PCP-zinc naphthanate process area (Figure 2). The groundwater under the site has beenmonitored at 27 locations. These monitoring wells consist of deep and shallow wells. Theupgradient wells consist of two shallow and two deep wells. The downgradient wells consist of12 shallow and 8 deep wells. The shallow and deep wells are nested together.
Shallow groundwater would be expected to have the highest levels of contamination with thedowngradient wells expected to have higher contaminant concentrations than the upgradientwells. The upgradient wells are very close to the site and would be expected to have backgroundlevels of contaminants in them. Table 3 shows the results of the shallow monitoring wells, whileTable 5 shows the analytical results of the deep water wells. The shallow wells were set justbelow the water table, while the deep wells were at the bedrock and soil interface.
Five shallow upgradient well samples were taken near the J-W site in 1984. All five sampleswere analyzed for VOCs, SVOCs, pesticides, and inorganic compounds. One upgradient,shallow well sample was analyzed for the presence of dioxins and furans. One SVOC and oneVOC were detected in the shallow upgradient wells. Methylene chloride, a laboratorycontaminant, was estimated in one sample at a concentration 1.2 ppb. Bis(2-ethylhexyl)phthalate was detected in one sample at a concentration of 20 ppb; however, it was also detectedin the blank. No pesticides were detected in shallow upgradient samples. No dioxins or furanswere detected in the one shallow upgradient sample. Inorganic compounds detected in shallowgroundwater, upgradient from the site were antimony, arsenic, beryllium, cadmium, lead,mercury, and nickel.
The shallow wells downgradient of the site had higher contaminant concentrations andfrequency of detections than the shallow upgradient wells. Fourteen downgradient shallow wellsamples were taken from 1984 to 1988, and all of them were analyzed for VOCs, SVOCs, andpesticides. Four samples were analyzed for dioxins and furans and 12 samples were analyzedfor inorganic compounds. VOCs detected in the samples were methylene chloride (110 ppb),chloroform (53 ppb), 2-butanone (22 ppb), 1,1,1-trichloroethane (2.7 ppb), benzene (1,200 ppb),and 2-hexanone (6.7 ppb). Many SVOCs were detected in the shallow downgradient wells.
Eleven wells are along the western fence line of the site, and these wells should showcontaminant migration from the site into the residential areas. The results of these well samplesshowed the presence of benzene and PAHs. Heptachlor and endrin also were detected indowngradient shallow wells. The highest concentrations each of heptachlor and endrin wereboth well above their comparison values. Dioxins and furans were also detected indowngradient shallow wells, although the water solubility of dioxins and furans is quite low. Inorganic compounds detected in the shallow downgradient groundwater were arsenic, lead,mercury, and nickel. The downgradient shallow wells are contaminated, while the compoundsin upgradient shallow wells are at or near background levels.
Table 9 contains the TEFs for 2,3,7,8-TCDD for the dioxin and furan results in the upgradientand downgradient shallow well samples. The TEFs for dioxin and furans in both the upgradientand downgradient shallow wells did not exceed the comparison value for 2,3,7,8-TCDD.
The deep groundwater may be only slightly contaminated, if at all. Five upgradient and 14downgradient deep well samples were taken on and around the site from 1984 to 1988. Theupgradient wells were all sampled for organic compounds, but only one sample was analyzed forinorganic compounds. The only organic compound found in the upgradient deep wells waschloroform, which was also found in the blank. The estimated concentration of chloroform was0.03 ppb, which is below the drinking water comparison value. Arsenic was the only inorganiccompound detected in the deep upgradient well sample.
Fourteen downgradient deep well samples were taken from 1984 to 1988, and all were analyzedfor organic and inorganic compounds. Chloroform, benzene, and bis(2-ethylhexyl) phthalatewere detected in these samples. Because the concentrations were estimated and the compoundswere also detected in blank samples, the accuracy of the results was in question. Therefore, theconcentrations were not compared with their respective comparison values.
Heptachlor was detected in 1 of 14 samples at a concentration of 0.009 ppb. Chlorinateddioxins and furans were not analyzed in any of the deep groundwater samples. Arsenic andberyllium were the only inorganic compounds detected in the downgradient deep well samples.
In 1997, IEPA constructed several new, on-site groundwater wells and redeveloped some olderones. IEPA collected groundwater samples in July 1997. The groundwater sample results werenot extraordinarily different from previous results.
No on-site air sampling data were found for the J-W site. Since the site is no longer inoperation, exact airborne concentrations of contaminants that may have been present in air in thepast cannot be determined.
Two off-site waste disposal areas are east of the J-W site. These areas can be seen in Figure 2and are labeled as Areas G & H. Area G is a disposal pit east of the site and south of 22ndStreet. The wastes dumped in this area included creosote. Area H is a disposal area north andeast of the site. Creosote was apparently dumped in this disposal area also. The surface areas ofG and H are 7,200 and 4,600 square feet, respectively. Contamination exists in many off-siteareas in addition to the waste disposal areas. Runoff has been observed to flow from on-siteareas to off-site areas. Samples of the waste were not taken, but contaminated surface soils werecollected at these areas. In addition, one subsurface soil sample and one sludge sample weretaken from Area H.
Woodward and Clyde took surface samples in 1987, and IEPA took surface soil samples in1988. Surface soil samples were taken from a depth between 1 and 6 inches. Off-site surfacesoil sampling areas are divided into two areas: off-site disposal areas and residential areas. Thesurface soil samples taken from the disposal areas had much higher contaminant concentrationsthan other off-site areas. Soil comparison values used for the off-site surface disposal areas arefor children when using noncancer endpoints. The comparison values for carcinogens (CREGs)are based on adult exposure.
Six samples were taken from the off-site waste disposal areas. A fence was constructed aroundArea H in late 1994 or early 1995. Currently, no fencing is around Area G to prevent publicaccess. Table 6 contains a summary of the off-site data. The VOCs identified present atconcentrations above their comparison values are benzene, 2-butanone, and 2-hexanone. Of the19 SVOCs, 14 did not have a comparison value. The remaining 5 VOCs had comparison valuesand were detected in at least one sample at concentrations above their soil comparison values forchildren. Seventeen of the SVOCs were PAHs; six of these compounds exceeded theircomparison values, while the other 11 did not have soil comparison values. Five of the sixcomparison values used were for noncarcinogenic endpoints, and the BaP comparison value usedwas for cancer. RPs used for the other PAHs considered at least potential carcinogens. TheseRPs are expressed in BaP equivalences, and these values are compared with the CREG for BaP. The off-site waste disposal area had an RP concentration of 7,352 ppm, which was much greaterthan the BaP CREG of 0.1 ppm. In addition, the BaP concentration in one sample was 3,900ppm. All RPs for compounds in waste disposal areas exceeded the BaP CREG.
Pesticides were identified in the surface soil samples from the off-site waste disposal areas. Pesticides, dioxins, and furans were only analyzed in three of the six samples. Dioxins andfurans were detected in all three of these samples. Total TCDD concentrations were detected intwo of three samples at concentrations above the comparison value. The compound 2,3,7,8-TCDD exceeded comparison values in some off-site waste areas. In addition a TEF wasdetermined for other dioxins and furans in off-site waste areas. The TEF values for the otherdioxins and furans greatly exceeded the comparison value for 2,3,7,8-TCDD. Inorganiccompounds found in the surface soil samples at concentrations greater than their respectivecomparison values include arsenic, beryllium, lead, manganese, mercury, nickel, thallium, andvanadium. A summary of the analyses at the off-site disposal areas is found in Table 6.
Twenty-two surface soil samples were taken from residential areas between 1984 and 1991. VOCs detected at concentrations above their soil comparison values were 2-butanone and 1,1,1-trichloroethane. Thirteen of 18 analytes did not have comparison values, and the other five hadconcentrations that exceeded their comparison values. Nineteen SVOCs were reported for the22 residential soil samples. Of the seven SVOCs that had comparison values, only BaP, at 3.3ppm, exceeded the CREG. An RP for BaP was assigned to the other carcinogenic PAHs. Thetotal BaP equivalents for the PAHs in residential soils was 3.5 ppm, which exceeded the CREG. The mixture of PAHs in residential surface soils is a concern. The individual RP values forbenzo(b)fluoranthene and benzo(k)fluoranthene exceeded the CREG for BaP.
Pesticides were detected in 4 of the 22 residential samples, but none was above its comparisonvalue. Dioxins and furans were identified in all 19 samples in which they were analyzed. Thetotal 2,3,7,8-TCDD TEF for all dioxins and furans in residential soils exceeded the comparisonvalue for 2,3,7,8-TCDD. The individual TEF values for all three 2,3,7,8-HxCDD, 1,2,3,4,6,7,8-HpCDD, OCDD, 2,3,7,8-TCDF, 1,2,3,7,8-PeCDF, 1,2,3,4,7,8-HxCDF, 2,3,4,6,7,8 HxCDF,1,2,3,4,6,7,8-HpCDF, and OCDF all exceeded the 2,3,7,8-TCDD comparison value. The totalTEF for dioxins and furans does not include the 2,3,7,8-TCDD concentration of 0.00000172ppm, which alone is near the comparison value.
Inorganic compounds detected in residential surface soils at levels above comparison values arearsenic, beryllium, cadmium, lead, manganese, mercury, nickel, thallium, and vanadium. Off-site inorganic concentrations were higher in residential soils than they were in the on-site soils oroff-site waste areas.
Subsurface soil is soil taken from depths greater than 1 foot. Only one subsurface sample wastaken near J-W. This subsurface soil sample was taken in 1984 from Area H, a subsurfacedisposal area (Table 6). No VOCs were found in the sample. Five SVOCs were detected in thesamples with only three PAHs, anthracene, chrysene and benzo(b)fluoranthene, at concentrationsexceeding their comparison values.
Residential wells are within 200 feet of the western boundary of the site. IEPA sampled bothdowngradient wells in 1988. The sample results showed that no on-site contaminants werepresent in these wells. Methylene chloride was detected in both private well samples and in theblank. Diethylphthalate was estimated in one sample at a concentration well below itscomparison value. No other organic compounds, including pesticides, dioxins, and furans, weredetected in the residential wells. Inorganic compounds included arsenic, beryllium, cadmium,lead, manganese, mercury, nickel, and vanadium. The results of the shallow residential wells donot indicate that the groundwater contaminants on the site have migrated west of the site towardthese residential wells. The most recent sampling of these wells was 1988, so subsequentcontamination of these wells may have occurred.
No off-site air monitoring is known to have been conducted for PAHs, dioxins, or furans. Airsampling for metals in Granite City has been conducted but not within the immediate vicinity ofthe site.
In 1988, IEPA took two wipe samples from outdoor vertical surfaces in off-site areas. Thesewipe samples may represent airborne contaminant deposition. One sample was taken downwindof the site. The other was taken 4 blocks west of the site and is presumably a backgroundsample. Five compounds were found in the background sample at levels below detection limits. The downwind sample contained phenanthrene, pyrene, fluoranthene, and chrysene. Sevenother compounds were identified in the sample at levels below the detection limits of theinstrument. While the downwind samples seem to show wind-borne contaminants migratingfrom the site, the number of samples is far too small to draw any conclusions.
Air monitoring was conducted during the SACM removal action between November 1994 andFebruary 1995. Both on-site and off-site samples were collected during the removal action toidentify the levels of contaminants including dioxins, asbestos, and PAHs. No contaminantswere detected in the air at levels above comparison values.
There were three separate quality assurance/quality control (QA/QC) plans for the three studiesat the J-W site. The QA program was designed using the USEPA Handbook for Quality Controlin Water and Wastewater Laboratories, June 1977. The E&E laboratory was certified by theNew York State Department of Health under a USEPA approved accreditation program. Thatprogram involves on-site laboratory inspections and submission of the results of the analysis ofsemiannual performance evaluation samples. The Woodward-Clyde Consultants used IllinoisContract Laboratory Program procedures during their analyses. The IEPA screening siteinvestigation used a USEPA approved work plan.
Closing the plant eliminated those physical and chemical hazards associated with day-to-dayoperations. A chain link fence surrounds the site and limits access. However, unauthorizedaccess to the site has been reported. Hazards associated with unauthorized access includesdrowning in on-site waste pits and chemical burns from contacting on-site waste. A chemicalburn of the skin or eyes is also a potential hazard in contaminated areas off the site. Ingestion ofchemical compounds may also damage the gastrointestinal lining. The boiler building hascollapsed in several places. Trespassers entering the building are in danger of the buildingcollapsing on them. Razing the building would eliminate this hazard.
Exposure pathways are evaluated to determine if nearby residents are exposed to site-relatedcontaminants migrating off the site. An exposure pathway consists of five elements: a source ofcontamination, transport through an environmental media, a point of exposure, a route of humanexposure, and an exposed population. If any of these elements are missing, the exposurepathway is not complete.
Two types of pathways, complete and potential, are considered. Complete pathways requirethat the five exposure elements exist and that exposure has occurred in the past, is occurring, orwill occur in the future. Potential pathways have at least one of the five elements missing, butthe missing element(s) could exist. Potential pathways indicate that exposure could haveoccurred in the past, could be occurring, or could occur in the future. An exposure pathway iseliminated if one or more of the elements are missing and will never be present. Table 13identifies the complete exposure pathways while Table 14 identifies the potential pathways.
During site visits, the odor of creosote was always present and was sometimes very strong. Sources that have contributed to the ambient air contaminants include wastes, surface andsubsurface soil, site operations (particularly those using high heat and pressure), remedialactivities, and stored railroad ties. Residents interviewed complained about strong odors duringthe operating period, especially during the summer months. Exposure to these sources hasoccurred in the past. Those exposed were unprotected J-W employees, area residents, andindividuals working in area businesses. The site has since closed. Railroad ties are no longerstored on the site.
Soil and Sediments
Workers were exposed to on-site, contaminated soil in the past. Exposure occurred throughdermal contact if workers did not follow proper hygiene practices. Unprotected workers oremployees who currently visit the site or who may visit it in the future may be exposed to site-related contaminants.
Off-site soils are contaminated in areas surrounding the site. Residents and workers contactingcontaminated off-site soils were exposed in the past, are currently exposed, nd will be exposedin the future. Exposure to off-site, contaminated soils is through dermal contact. The extent ofexposure depends on a variety of factors, including the amount of time working or playing incontaminated soil. Behavioral factors, such as hand to mouth activity and pica tendencies(consuming nonfood items), can greatly increase exposure.
People were exposed to contaminated sediments in both on-site ponds and the contaminatedditch along the northeast boundary of the site (Area H). Residents have voiced concerns aboutchildren playing in contaminated ditches along the railroad tracks. J-W workers were exposed tothose sediments in the past, and nearby residents and children who played in the ditch were alsoexposed. The primary route of exposure was through direct dermal contact with soil andsubsequent absorption of contaminants. Current and future exposures will occur whenunprotected workers or trespassers contact on-site sediments or when residents contact off-sitesediments near Area H. No sediment sample analyses were done, so levels of exposure to thesediment cannot be estimated.
People were exposed to contaminants in surface water as they were exposed to sediments. Surface water contaminants consist of water soluble contaminants, while sediments contain theless water soluble contaminants, such as PAHs.
Workers excavating on-site areas with groundwater contamination were exposed tocontaminated groundwater. No known current exposure to contaminated groundwater isoccurring on the site. Future exposures will occur if unprotected remediation workers excavatedown to the groundwater. The groundwater exposure pathway is not expected to ever besignificant because the residents in the area have municipal water and the groundwater quality inthe Granite City area is generally poor. Therefore exposure to contaminated groundwater is notlikely, but IDPH will consider it a potential route of exposure should anyone ever decide to tapthe contaminated groundwater for domestic use.
People have been exposed to site-related contaminants in vegetables from neighborhood gardensin the past. The closest garden to the site is within 100 feet of the boundary. Past exposureswere through eating plants that uptake contaminants from soil and have contaminated surfacesbecause of air deposition of contaminants. No data exist for site-related contaminants in gardenvegetables near J-W. Current and future exposure to contaminants will occur primarily fromeating plants that have taken up contaminants from the soil. Based on the amount of off-site soilcontamination, this exposure pathway probably does not pose now, and did not pose in the past,a significant route of exposure because the types of contaminants present from the site are notbioaccumulated in plants at high enough levels to pose a concern.
Off-site groundwater exposure may occur if groundwater contaminants migrate to private wells. Data gathered during door to door interviews by IEPA and IDPH representatives show that theoff-site wells are currently used for watering yards and gardens and washing cars. The wells arenot used for drinking water. Potentially, other landowners around the site could drill wells anduse them for drinking water. Potential exposure routes from contaminated groundwater wouldinclude ingestion, dermal contact, and inhalation of contaminants present in the water. Anadditional potential exposure to groundwater would include off-site excavation into contaminated groundwater.
Potential exposures to contaminants in surface and subsurface soils are dependent on whetherremediation of the site will involve disturbing the soil and, if it is disturbed, what measures willbe taken to reduce exposures. Sources of contaminants in surface soils include wastes, surfacesoil, contaminated surface water runoff, and airborne deposition. Subsurface soil can becomecontaminated by the same sources listed for surface soils and would also include contaminationby groundwater. Potential exposures would occur by inhalation, ingestion, and direct contactwith contaminated soils. The population that could be potentially exposed would includeunprotected remediation workers, area residents, and employees in nearby businesses.
Exposure to subsurface contaminants may have occurred in the past to J-W workers, arearesidents, and to workers digging into contaminated subsurface soils off the site. Workerexposure to subsurface soils in the past may have been quite high when heavily contaminatedareas were excavated without proper protection. Exposure to subsurface contaminants on thesite will be completed if unprotected workers contact these subsurface soils. Exposure tosubsurface soil contaminants off the site would not be expected to be significant, except in theoff-site disposal areas.
Potential exposure to sediment contaminants would be much the same as for surface andsubsurface soils. These exposures would occur from remediation of sediments. The exposedpopulation would be the same as for soils.
Potentially, people may be exposed to airborne contaminants originating from surface wastes,contaminated surface soil, and contaminated subsurface soil suddenly exposed to the surface. Future exposure to airborne contaminants may continue to occur from surface wastes andcontaminated surface and subsurface soils.
Potential ambient air exposure would occur from substances released into the air if the wastesand contaminated media are disturbed. The route of exposure would be inhalation and ingestionof the contaminated dust particles. The exposed population could include nearby residents,employees in the area, businesses, and unprotected remediation workers. Exposure to indoor aircontaminants may occur in area homes if site-related, contaminated dust has entered homesthrough doors or windows, or if contaminated soil gas migrates to homes.
This section includes discussions on the health effects in persons exposed to specific site-relatedcontaminants, an evaluation of any applicable state and local health databases, and a response tospecific community health concerns. The health effects discussions are in the ToxicologicalEvaluation subsection, state database discussions are in the Health Outcome Data Evaluationsubsection, and the responses to community concerns are in the Community Concerns Evaluationsubsection.
To evaluate health effects, ATSDR has developed Minimal Risk Levels (MRLs) for compoundscommonly found at hazardous waste sites. An MRL estimates the daily human exposure to acontaminant below which adverse, noncancerous, health effects are not likely to occur. MRLsare developed for different routes of exposure, including ingestion and inhalation, and for threedifferent exposure periods: acute (less than 14 days), intermediate (15-364 days), and chronic(365 days or more).
ATSDR developed Toxicological Profiles for contaminants that are common at hazardous wastesites. The Toxicological Profiles are specific for individual chemicals and some mixtures. TheToxicological Profiles used in this discussion are: benzene, creosote, naphthalene/2-methylnaphthalene, PCP, PAHs, and 2,3,7,8-tetrachlorodibenzo-para-dioxin. The PAHsincluded in the PAH Toxicological Profile were acenaphthene, acenaphthylene, anthracene,benz(a)anthracene, BaP, benzo(b)fluoranthene, benzo(g,h,i)perylene, benzo(k)fluoranthene,chrysene, dibenzo(a,h)anthracene, fluoranthene, fluorene, indeno(1,2,3-cd)pyrene, phenanthrene,and pyrene. The profiles contain information on health effects, environmental transport, humanexposure, and regulatory status of each chemical.
Many compounds associated with wood treating were found both on and off the site. Mostwood treating substances have many compounds associated with them. For example, creosote isa complex mixture containing 300 identified compounds and perhaps as many as 10,000unidentified compounds. The compounds of concern at this site are the PAHs associated withcreosote, zinc naphthanate, PCP, dioxins, and furans.
Exposure to site-related compounds occurs as a mixture of chemicals. Generally, human andanimal studies are performed using one chemical compound. The toxicology of mixtures has notbeen well studied and, therefore, determining the possible adverse health effects associated withthese mixtures is difficult. The toxicological data used in this report has come primarily fromthe ATSDR Toxicological Profiles. The toxicology of the chemicals selected for furtherevaluation are divided into three groups: creosote/PAHs, PCP, and dioxins/furans. Manycompounds do not have data on toxicological effects for the different exposure routes andvarious target organs.
This discussion is further divided into noncarcinogenic and carcinogenic effects. Thepopulations that are considered are the on-site workers and nearby residents. Children areconsidered as exposure to nearby residents is evaluated. Maximum exposures would haveprobably occurred while the plant was in operation. The past exposures may have been highestdue to more lenient rules regarding releases, fewer safeguards in the work place, and no fencingalong the property's border. Exposures on and off the site would have been through dermalcontact, inhalation, and ingestion of contaminated environmental media. Workers would haveprobably had the highest exposure, followed by children who may have played in the contaminated wastes or runoff areas.
Many potential health effects that workers and children may be or may have been at risk ofdeveloping would already have occurred. Most of the health effects due to this exposure, exceptcancer, are probably reversible.
The toxicological evaluation discussed in this section is based on past exposures of workers toon-site air, direct skin contact, and soil exposure to on-site contaminants and the exposures ofresidents to contaminated air and soil. The exposure to site-related contaminants was onlycalculated for on-site soil, residential soils, and off-site soil in the waste disposal Area G. Exposures to site-related compounds have occurred through direct skin contact with on-sitechemicals, inhalation of airborne contaminants, and contact with and ingestion of soils. Exposure through direct contact with on-site chemicals and inhalation were not calculated due toa lack of data.
Worker exposures are calculated for soil ingestion on the site; however, this probably was notthe primary source of exposure. The highest worker exposures would have been from inhalationand direct contact with the chemicals. Past exposures to workers and residents are assumed to behigher than they are now or will be in the future. This assumption is based on highercontaminant levels present in the air and soil due to site activities and processes andenvironmental degradation of many contaminants in the soil.
Current exposures are expected, primarily, in area residents. Since the site has closed, noworkers are present on the site. Current exposures to residents are from contact with andingestion of contaminated soils and breathing site-related compounds.
Future exposures involve area residents and remediation workers. Future exposures to residentsmay include contact with contaminated soils and airborne contaminants. Airborne exposures canbe calculated if air monitoring is done. Additionally, air monitoring can be done duringremediation activities to determine both worker and resident exposures.
Exposures to groundwater were not calculated due to the low probability of exposure tocontaminants. Off-site residential wells do not appear to be contaminated. Surface water andsediment exposures were not calculated. Except for background benzene air samples taken morethan 0.5 miles away, no air data exist for site-related contaminants and, therefore, no exposurescould be calculated due to a lack of data.
Exposure to asbestos has been shown to cause asbestosis, a form of pneumoconiosis. Asbestosisfrom on-site sources would not be expected to occur because asbestosis occurs from exposure tohigh concentrations. Asbestos is a human lung carcinogen when inhaled. Inhalation of asbestoshas resulted in mesotheliomas in humans. Removal of the visible asbestos insulation reducedexposures and, thus, reduced health risk.
Exposure to benzene has occurred in both workers and residents. Benzene is a common VOCfound in gasoline and other products. The primary exposure to benzene is through the air. Airborne benzene from J-W is probably only a fraction of the total benzene exposure toresidents. In 1989, while J-W was still in operation, TRI data show two companies releasedbenzene into the air. These businesses were Granite City Steel at 22,000 pounds per year andReilly Industries Inc. at 11,330 pounds per year. These releases, along with other benzenesources such as gasoline, probably contribute much more to the total benzene exposure of arearesidents than any exposures due to releases from J-W.
In an airborne VOC study conducted by Sweet and Vermette from May 1986 to April 1990, theaverage benzene concentration for Granite City was 1.3 micrograms per cubic meter (µg/m3). The benzene monitor is more than one quarter of a mile from the site boundary at 20th andAdams. The study also identified a rural airborne benzene concentration of 1.3 µg/m3.
At these air levels, the primary concern would be an increase in cancer risk. Long-termexposure to high levels of benzene can cause leukemia. However, the cancer risk from exposureto this background level would result in no apparent increased cancer risk.
This air level of 1.3 µg/m3 is much lower than the level that has caused hematological effects inhumans and is considerably lower than the level that has caused immunological effects inanimals. No long-term, noncancerous, health effects would be expected at this air concentration. Chronic exposure to benzene in on-site and off-site soils does not exceed the chronic referencedose for benzene ingestion. Benzene would not be expected to cause chronic health effects as aresult of soil ingestion in either workers or area residents, including children. Exposure tobenzene in soils around the site would not be expected to increase the incidence of cancer around the site.
IDPH has not calculated ingestion of benzene from groundwater because benzene was notdetected in off-site wells and because off-site well water is not used as drinking water.
Polycyclic Aromatic Hydrocarbons (PAHs)
Exposure to PAHs at the site would have occurred as a mixture, primarily creosote. Theavailable human data are also primarily for mixtures of PAHs. Little data exist for individualPAH exposures. The noncarcinogenic health effects associated with naphthalene and 2-methylnaphthalene are more well studied than the other 15 PAHs and are discussed separately.
The noncarcinogenic health effects of acenaphthene, acenaphthylene, anthracene,benz(a)anthracene, BaP, benzo(b)fluoranthene, benzo(g,h,i)perylene, benzo(k)fluoranthene,chrysene, dibenzo(a,h)anthracene, fluoranthene, fluorene, indeno(1,2,3-cd)pyrene, phenanthrene,and pyrene have not been well studied. The noncarcinogenic health effects associated with these15 compounds are discussed by exposure route.
While still in operation in 1989, J-W reported releasing 4,371 pounds of naphthalene into the airper year. Naphthalene levels were not monitored in the Granite City area. No airbornenaphthalene exposures were calculated because data were not available. Naphthalene has thehighest vapor pressure of the PAHs, which means that it will volatilize more readily than otherPAHs.
Ingestion exposures to naphthalene in on-site waste disposal areas were calculated for on-siteworkers and residents. No health guidelines have been established for naphthalene ingestion. The highest exposure is for children exposed to soil in the waste area with an estimated dose of2.2 milligrams per kilogram per day (mg/kg/day). The MRL for naphthalene is 0.02 mg/kg/dayfor intermediate exposures, and 0.05 mg/kg/day for acute exposures. The waste areas are on theeastern boundary of the site, and children would probably not frequent these areas as much asthey would residential soils. Still, children frequently trespassing and playing in waste areascould be at risk.
The exposure dose to naphthalene for children in residential soils is 0.000085 mg/kg/day. Thehighest adult exposure would be for residents exposed to soils near the waste disposal area alongthe northwestern corner of the site. Worker exposures to naphthalene in soil were estimated tobe 0.00014 mg/kg/day. Worker exposure to naphthalene by direct contact with creosote wouldresult in a higher exposure by both absorption and ingestion.
Naphthalene exposures in humans at levels well above those levels found at J-W have causedhemolytic anemia, nausea, vomiting, diarrhea, kidney damage, jaundice, and liver damage. Theeffects are seen from both inhalation and ingestion. These effects would not be expected to beexhibited from exposure to naphthalene contaminated soils around J-W. There are not enoughanimal or human data to classify the carcinogenicity of naphthalene.
In the 10 on-site surface soil samples, 2-methylnaphthalene was not detected. On-site exposureto 2-methylnaphthalene by workers occurred when workers contacted creosote. Additional on-site exposures would have occurred by inhalation, especially by workers in the creosote workareas. Exposure to 2-methylnaphthalene by workers was not calculated.
Residential exposure has occurred in the past, is occurring, and will continue in the future. Exposure routes are by air and soil. Residential exposure cannot be calculated due to a lack ofair data.
No health guidelines were available for 2-methylnaphthalene ingestion or inhalation. Chronichealth effects associated with 2-methylnaphthalene were not found.
Exposure to coal tar creosote has been little studied in either man or animals for certainsymptoms. No studies have been done to identify neurological, immunological, reproductive, orgenotoxic effects from creosote exposure.
The noncarcinogenic effects of PAHs are based primarily on animal studies where the animalswere exposed to much higher levels than those associated with J-W. BaP caused reproductivedifficulties in mice and their offspring. These offspring also exhibited birth defects anddecreased body weight. Animal studies with other PAHs produced a variety of health effects,including adverse effects to skin, body fluids, and the immune system. BaP has an acute MRLof 0.1 mg/kg/day. This acute MRL was not exceeded in any of the exposure estimates. Noacute health effects would be expected from BaP.
Inhalation exposure to creosote and associated PAHs continues to occur in off-site areas due tolarge quantities on top of the soil. Most information on exposure to compounds in creosoteinvolves PAHs. Inhalation of PAHs in humans has been associated with the followingsymptoms: headache, nausea, vomiting, abdominal pain, malaise, ocular effects, confusion,anemia, jaundice, and renal disease. Inhalation of naphthalene has reportedly resulted incataracts, retinal hemorrhaging, and chorioretinitis. The primary exposure route in these caseswas assumed to be inhalation, but it is possible that exposure was also dermal or ocular. Noncarcinogenic effects through inhalation are little studied since the primary chronic inhalationend point is lung and respiratory cancer. Inhalation exposures in residents and workers cannotbe calculated since no air data are available for the site.
Except reports of fatal doses, oral exposure studies to coal tar creosote have not been found foreither humans or animals. Fatal doses of creosote ingestion have been reported for humans andanimals. Death has occurred 14 to 36 hours after ingestion of 7 grams in adults and 1 to 2 gramsin children. The actual dose that induces death in humans is not precisely known. The acutefatal dose for sheep and calves are 4 to 6 g/kg and more than 4 g/kg, respectively. The LD50(50% deaths in studied animals) in five rodent studies varied from 0.43 g/kg to 1.7 g/kg. Othereffects of creosote ingestion are limited. Some effects of chronic creosote exposures in animalsinclude increased liver weight-body weight ratio, loss of weight, and increased brain weight-body weight ratio.
Inadequate human and animal information exists for oral exposure to dibenzo(a,h)anthracene orchrysene. Both short-term and intermediate high-level oral exposures have resulted in death toexperimental animals. The deaths were apparently due to bone marrow depression. Oral BaPstudies in mice and rats have shown evidence of adverse reproductive and developmental effects.
Exposures to PAHs have elicited responses in several organs. Gastrointestinal effects fromingestion are possible in humans. This is based on alteration of enzyme activity in animals. Animals given anthracene, benz(a)anthracene, BaP, and phenanthrene had changes ingastrointestinal mucosa enzymes. The data suggest that oral exposure in humans may lead toadverse health effects. Adverse health effects associated with ingestion of these PAHs are fromanimal studies because no human data were identified.
None of the health guidelines were exceeded for worker exposure to PAHs from soil ingestion. The additive exposures of PAHs in soil for noncarcinogenic endpoints were not done for thispublic health assessment. In addition, dermal and inhalation exposure doses were not calculatedfor on-site workers due to a lack of data. These exposures would probably represent muchhigher doses than the soil estimates.
Dermal exposure in humans is known to affect skin and eyes. Burns and irritation of skin andeyes are the most common symptoms of coal tar creosote exposure. Coal tar creosote can inducephototoxicity of the skin. The dermal effects of creosote are exacerbated by exposure tosunlight. Several cases of acute allergic dermatitis have been reported.
Based on off-site ingestion of soils from residential areas, chronic noncancerous health effectsare not expected to occur, based on the PAHs individually. However, this is based only on soilingestion and does not take into account inhalation exposures, dermal absorption from soil, oradditive or synergistic effects from exposure to a mixture of PAHs.
Exposures of residents to off-site waste disposal area soils were calculated for residents. Thecalculated exposures for both adults and children for fluorene, anthracene, phenanthrene, andpyrenes exceeded their respective health guidelines. Acenaphthylene from the waste pilesamples exceeded the chronic RfD for children. Since off-site waste disposal areas are no longeraccessible to the area residents, particularly young children, the exposure estimates wouldrepresent past exposures. Based on the calculations, some chronic health effects would bepossible in exposed individuals.
The estimated total PAH exposure was also calculated for on-site soils, off-site wastes, andresidential soils. The estimated total PAH worker exposure is 0.0017 mg/kg/day and wasderived by adding all the PAH exposure estimates. At this concentration, past on-site soilexposure would be a concern. This does not take into account other on-site exposures,particularly during the operating period when risk exposure to PAHs in air and waste was muchhigher.
Off-site waste disposal area exposures calculated for both children and adults were 9.2mg/kg/day and 0.68 mg/kg/day respectively. Chronic health effects, especially in children,would be expected to be observed at these concentrations. Since off-site waste disposal areas areno longer accessible to the area residents, particularly young children, the exposure estimateswould represent past exposures. The total exposure to PAHs in residential soils for children andadults were 0.00093 mg/kg/day and 0.00006 mg/kg/day, respectively. IDPH would not expectadverse health effects from chronic exposure at these levels.
PAHs known or suspected to cause cancer in humans include benz(a)anthracene, BaP,dibenzo(a,h)anthracene, and benzo(b)fluoranthene. PAH mixtures that may potentially beassociated with respiratory tract cancers are BaP, fluoranthene, chrysene, benz(a)anthracene,benzo(b)fluoranthene, and dibenzo(a,h)anthracene. In mixtures, estimating the carcinogeniccontribution of a particular substance to the total carcinogenicity of the mixture is impossible. Chronic oral exposure to PAHs in animals suggests that benz(a)anthracene, BaP,dibenzo(a,h)anthracene, and possibly others are carcinogenic.
No apparent increased cancer risk to on-site workers would have resulted from past exposure tocontaminated soil in Area E, and Area F. Worker exposure to soils in Areas A, B, and C mayhave resulted in a low increased risk of cancer.
Cancer risks were also calculated for off-site exposure to residents. The increased cancer riskfrom exposure in the off-site disposal area is very high. This risk represents past exposures tothe residents as the off-site disposal areas are now fenced. There may be a low increased cancerrisk for residents exposed to PAHs in the residential soils.
The most significant risk of increased cancer comes from the off-site waste disposal areas. Theother areas of on-site and off-site soils represent low to no increased cancer risk. These cancerrisks do not take into account inhalation exposures or the effects of other carcinogens such as PCP.
Intermediate and long-term low-level dermal exposures to BaP in animals have been associatedwith cancer. Human studies are not available. Long-term exposure studies in animals consist ofdermal exposures using BaP, chrysene, or dibenzo(a,h)anthracene. In these studies only BaP hasbeen shown to induce cancer in laboratory animals by dermal exposure. Dermal exposure tomixtures of PAHs has been associated with cancer in humans.
Dermal exposure to PAHs in animals has resulted in skin tumors. In humans, skin tumors aremore prevalent among individuals exposed to PAH mixtures. Scrotal cancer in chimney sweepsmay be caused by PAHs. Animal studies have shown that benz(a)anthracene, BaP, chrysene,benzo(b)fluoranthene, and dibenzo(a,h)anthracene may induce skin tumors followingintermediate dermal exposure. PAHs that do not act as complete animal carcinogens includeanthracene fluoranthene, fluorene, indeno (1,2,3-cd) pyrene, phenanthrene, and pyrene.
The cancer risk for airborne exposures was not calculated due to a lack of data.
Occupational inhalation exposures to PCP cause inflammation of the upper respiratory tract andbronchitis. Cardiovascular effects include tachycardia from acute exposure and toxicmyocarditis has resulted from longer exposures. Anecdotal reports of abdominal pain, nausea,and vomiting in humans from inhalation of PCP during occupational exposure were the onlygastrointestinal effects associated with that route of exposure. Hematological effects from acuteexposures include decreased hemoglobin levels and hemolytic anemia; intermediate and long-term effects include aplastic anemia and death. Acute inhalation has resulted in jaundice. Long-term exposure has resulted in enlargement of the liver. Chronic occupational exposure to PCPhas resulted in the reduction of glomerular filtration rate and tubular function.
The liver is a target organ in animals exposed to PCP. Neurological effects from clinicalobservations included pyrexia, diaphoresis, hyperkinesis, muscle twitching and tremors,epigastric tenderness, leg pain, tachypnea, and tachycardia. There are no studies ondevelopmental and reproductive effects. Dermal exposures have essentially the same symptomsas inhalation and ingestion.
PCP exposure estimates were calculated for workers exposed to on-site soils. No exposureestimates were made for air because the data do not exist. The estimated worker exposure to on-site soils is 0.0039 mg/kg/day, which exceeds the intermediate MRL of 0.001 mg/kg/day. Worker exposures represent past exposures. The health effects associated with these levels mayinclude liver and kidney effects, including increased organ weight.
Groundwater exposure pathways were not calculated because, as of the last testing, theresidential wells were not contaminated. Exposures to residential soil and soils in off-site wastedisposal areas were calculated (Table 16). PCP exposure estimates from the off-site wastedisposal for adults and children are 0.0006 mg/kg/day and 0.00004 mg/kg/day, respectively. These levels are less than the intermediate MRL. The intermediate MRL for PCP does notinclude chronic effects and lower doses.
Estimated ingestion doses for residential surface soils are summarized in Table 17. Theestimated ingestion for adults and children are 0.0000023 mg/kg/day and 0.000052 mg/kg/day. These levels are well below the intermediate MRL of 0.001 mg/kg/day.
PCP is also a probable human carcinogen. The cancer risk for PCP was calculated for pastexposure of workers and residents, as well as off-site residential soils. There was a lowincreased cancer risk for past exposure of workers to surface soils. There was no increasedcancer risk for adult residents from exposure to the waste disposal areas and residential soils.
Dioxins and Furans
No data were found for inhalation of dioxins or furans. Symptoms experienced by humansexposed to dioxins include chloracne, immunotoxicity, hyperpigmentation, hyperkeratosis,hirsutism of the skin, possible hepatotoxicity, hypertriglycerid, and hypercholesteremia, achingmuscles, loss of appetite, weight loss, digestive disorders, headaches, neuropathy, insomnia,sensory changes, and loss of libido. The primary route of exposure is probably dermal withsome exposures from inhalation and ingestion. No animal studies on dermal exposure to dioxinswere identified in the literature.
The carcinogenicity of dioxins is not known. It has been suggested that there is a relationshipbetween dermal exposure and soft tissue sarcomas and increased non-Hodgkins lymphomas. There are several limitations to these studies; the major limitations include the fact that exposureto other chemicals (e.g., pesticides) may have occurred and there is a lack of quantitative data forexposed individuals.
Dioxin exposure estimates for soils were below the minimum risk level for chronic exposures. Adverse health effects would not be expected to occur from TCDD in soils. This does not takeinto account additive exposures to other polychlorinated dioxins and furans or exposures fromother sources.
The more chlorinated dioxins and furans were analyzed in the samples. The only MRL thatexists for these groups of compounds is a chronic MRL for 2,3,7,8-TCDD of 0.000000001mg/kg/day and an intermediate MRL of 0.00003 mg/kg/day for 2,3,4,7,8-PeCDF. Neither ofthese MRLs was exceeded for exposure to on-site surface soil, off-site waste disposal area soil,or residential soil.
Health outcome data have not been evaluated for this site because no specific health outcomedata that are appropriate for this site have been identified. In addition, an analysis of healthoutcome data for an estimated exposed population of this size would not provide statisticallysignificant results.
The community health concerns have been addressed as follows:
- How can the contaminants at the site affect my children's health? Currently, the most prominent exposure to children who are not trespassing into fenced areas is from residential soil. The contaminant concentrations of concern in off-site soils do not appear to be at levels that would cause adverse health effects, even after exposures over a long period.
- I played in areas that were visibly contaminated and had direct contact with these substances. Am I going to get cancer? The incidence of cancer for an individual cannot be predicted. The risk increases with higher exposures over longer periods. Exposure to highly contaminated soils or wastes for brief periods may not increase your cancer risk at all.
- Are there any long-term health effects associated with site-related contaminants? Yes, the primary long-term health effect associated with PAHs, PCP, and dioxins and furans at the levels identified in the off-site areas is cancer. The cancer risk calculated for off-site soils for PAHs and PCP varied from no apparent increased risk to a low increased risk of cancer.
- Will exposure to these compounds cause cancer? Exposure to many of these site-related contaminants may increase the risk of getting cancer. The amount of increased risk depends on several factors, including exposure dose and duration, and the effects of chemical mixtures on the carcinogenicity of the compounds. Cancer risk estimates for exposure to off-site residential soils suggested insignificant to low increased risk. Exposure data for airborne compounds are not available, and thus cancer risk via this exposure route cannot be determined. Please note that the presence of carcinogens does not necessarily indicate an increased cancer risk.
- How will dioxin (specifically 2,3,7,8-TCDD) affect my health andthat of my children? The health effects of TCDD are discussed in theToxicological Evaluation section.