PRELIMINARY PUBLIC HEALTH ASSESSMENT
U.S. SMELTER AND LEAD REFINERY, INC.
(a/k/a USS LEAD REFINERY INC.)
EAST CHICAGO, LAKE COUNTY, INDIANA
The tables in this section list the contaminants of concern. The contaminants will be evaluated insubsequent sections of this preliminary public health assessment to determine whether exposure tothem has public health significance. ATSDR selects and discusses contaminants using the followinginformation:
- Concentrations of contaminants on- and off-site.
- Field data quality, laboratory data quality, and sample design.
- Comparison of on-site and off-site concentrations with comparison values for both cancerous and non-cancerous effects.
- Community health concerns.
In the data tables that follow under both On-Site and Off-Site Contamination, the presence of alisted contaminant does not necessarily indicate that it will cause adverse health effects. Instead,the list indicates contaminants that will be evaluated further in this preliminary public healthassessment.
ATSDR uses comparison values -- contaminant concentrations in specific media that are consideredprotective of public health -- to select contaminants for further evaluation. ATSDR and otheragencies have developed the comparison values to provide guidelines for estimating contaminantconcentrations in media at which adverse health effects are not expected to occur. A standard dailyingestion rate and body weight are assumed in deriving these values. The following comparisonvalues are used in this section:
|=||Cancer Risk Evaluation Guide: Derived by ATSDR from the EPA cancer slopefactor. It represents a concentration in water, soil, or air at which excess cancerrisk is not likely to exceed one case of cancer in a million persons exposed overa lifetime.|
|=||Environmental Media Evaluation Guide: Derived by ATSDR from ATSDR'sminimal risk level (MRL). It is the concentration in water, soil, or air at whichdaily human exposure is unlikely to result in adverse noncancerous effects|
|=||Reference Media Evaluation Guide: Derived by ATSDR from the EPA oralreference dose. It is the concentration in water or soil at which daily humanexposure is unlikely to result in adverse noncancerous effects.|
|=||Proposed Maximum Contaminant Level Goal: Non-enforceable drinking waterhealth goal recommended by EPA and set at a level at which no known oranticipated adverse human health effects are expected.|
In addition, should no CREG be available for substances which may be carcinogenic (may causecancer), these substances are included as contaminants of concern regardless of the observedconcentrations.
The EPA maintains the Toxic Chemical Release Inventory (TRI), a database of over 320 differenttoxic substances released from facilities into the environment. Because USS Lead ceased operationsin 1985, the TRI was searched for information about releases that may have occurred up to andincluding 1987 in the area surrounding USS Lead. A large amount of metals were reportedlyreleased into both air and water. Lead, manganese, and aluminum oxide were released in largeamounts into the air (22,000 pounds, 18,000 pounds, and 48,000 pounds, respectively). Additionalmetals listed as air emissions were aluminum (1,400 pounds), antimony (250 pounds), andchromium (742 pounds). Water emissions listed were lead (2,050 pounds), zinc (1,000 pounds),and chromium (750 pounds).
|1)||Calcium sulfate (CaSO4) sludge generated from neutralizing battery acids. The sludge wasdried and stored in piles on the southern portion of the site. The sludge was contaminatedwith arsenic, cadmium, and lead. It was removed from the site in June 1992.|
|2)||Baghouse flue-dust generated by the blast furnace. Dust from the furnace exhaust wascollected by passing the exhaust through fabric bags, which acted as filters. Dust from thesebags was collected for recycling into the smelter. The dust contained large amounts of lead,arsenic, and antimony, and lesser amounts of cadmium and antimony. Up to 8,000 tons ofthe dust was stockpiled on-site. In 1982, the dust, which had been stored over a three to fiveacre area, was brought under cover in the Tank House building to prevent dispersion bywind and rain. The dust was removed from the site in June 1992.|
|3)||Slag generated from the blast furnace. The blast furnace slag has been disposed of primarilyin the southern area of the site. The slag was used as fill in the wetlands. It is contaminatedwith lead.|
|4)||Baghouse bags. The bags which were used to catch the flue-dust were emptied and storedon-site in large piles. These bags are believed to be contaminated with lead.|
Limited sampling has been completed on some of these wastes. Maximum observed concentrationsare listed in table 1.
|Chromium||Slag pile||320||8/80 ||none||carcinogen|
|Manganese||Slag pile||2,260||8/80 ||300||RMEG|
|Tungsten||Slag pile||200||8/80 ||none|
|Yttrium||Slag pile||372||8/80 ||none|
Surface Soil and Sediment
A few soil and sediment samples have been taken to confirm contamination at the site. Surface soil(0 to 1 inch deep) samples from various on-site locations indicate widespread contamination by lead,arsenic, and antimony. Sediment samples from the marsh which receives some of the stormwaterrun-off from the site indicate that marsh sediments are contaminated with lead, arsenic, antimony,and some mercury. Additional soil contamination occurs near the canal, where oil storage tankswere kept. Although no documentation could be found regarding fuel oil contamination in the area,visible contamination is present.
| Date and |
On-site surface water has become heavily contaminated with metals and fuel oils. A stormwateroutfall discharges into a canal, which flows directly into the Grand Calumet River. A few grabsamples and ten months of continuous monitoring during plant operations in 1984 indicate that thedischarge has been contaminated with lead, arsenic, and several other metals, as well as fluoride andsulfate. In addition, a black oily layer was observed on top of the canal water near the outfalldischarge. This area is near the oil storage tank locations. The canal water has becomecontaminated with similar metals as were observed in the discharge, but at lower concentrations. A marsh receives additional stormwater run-off from the site. Surface water collected from themarsh also contained contaminants similar to those observed in the outfall discharge.
Large amounts of lead-contaminated dust have been released in the past during normal operationsof the smelter. The Indiana State Board of Health conducted air monitoring on-site in 1985, andfound high levels of fugitive dust and lead suspended in the air. In addition, the practice of storingbaghouse flue-dust in open-air piles allowed dispersal of the dust. This practice ended in 1982,when the dust was moved into the Tank House. No air monitoring data is available for the periodprevious to 1982.
|Fugitive dust||218 downwind|
Surface soils were sampled for lead in 1985 at several locations off-site by the Indiana Air PollutionControl Board. The sampling was done to confirm the presence of lead. The number of samplesat each location were not sufficient for characterization of the off-site areas. Since the source of thelead contamination was most likely the deposition of flue-dust particulates out of the air, thenadditional contaminants found in the flue-dust may also be present in off-site surface soils. Surfacesoils at the E.C. DuPont facility, which is directly across Kennedy Avenue from USS Lead,contained extremely high amounts of lead. Several other off-site locations in residential areascontained high levels of lead contamination in surface soils, including the E.C. Rehabilitation Center(now the Lake County Rehabilitation Center), a playground, a schoolyard, and an area at theintersection of Melville and 151st Street. Concentrations tended to decrease rapidly with increasingdistance from the site.
|Lead||E.C. DuPont||300||32,087||4/85 ||none||carcinogen|
|Melville and 151st||800||1,541|
148th & Melville
148th & Carey
Sampling data for three sediment samples taken from the Grand Calumet River were found in theUS EPA's STORET database and presented in a site assessment plan for USS Lead . This dataprovides only a limited amount of information, indicating that there are several lead sources whichmay be affecting the river. The upstream lead concentration is 350 ppm, which is relatively high. Lead concentrations at the mouth of the canal as it exits USS Lead are much higher, at 1,177 ppm. However, the nearby sewage treatment plant also discharges large quantities of lead, and sedimentsfound near its discharge location were 4,758 ppm.
|Lead||Grand Calumet River,upstream||350||unknown ||none||carcinogen|
|Near discharge,sewage treatment plant||4,758|
During a preliminary site sampling study of USS Lead, water samples were taken from the GrandCalumet River, both upstream and downstream of the canal exiting the site. Aluminum, boron, lead,and manganese were present in both samples. There was no increase in the amount of metalcontamination observed in the downstream sample compared to the upstream sample. However,single sampling events for surface water are not conclusive.
|Contaminant||Maximum Concentration (ppb)||Date and|
Air monitoring for lead in off-site ambient air was conducted from 1985 through 1989 by theIndiana Department of Environmental Management. Air monitoring stations were placed at severallocations, including E.C. DuPont, the E.C. Rehabilitation Center, the East Chicago Post Office, anda location at 2401 Michigan Avenue. Data collected at three of these locations in 1985, when thesmelter was in operation, indicate that concentrations of airborne lead were relatively high, at anaverage of 16.1 µg/m3 at E.C. DuPont, and 1.3 µg/m3 at the E.C. Rehab Center and the East ChicagoPost Office. Subsequent sampling in 1986 through 1989 indicate that the concentrations of airbornelead quickly decreased after the smelter ceased operations. Lead concentrations averaged 0.12 to 0.46 µg/m3 in this time period.
|Lead||E.C. Dupont||16.1 average|
|E.C. Rehab||1.3 average|
In preparing this preliminary public health assessment, ATSDR relies on the information providedin the referenced documents. The Agency assumes that adequate quality assurance and qualitycontrol measures were followed with regard to chain-of-custody, laboratory procedures, and datareporting. The validity of the analysis and conclusions drawn for this preliminary public healthassessment is determined by the reliability of the referenced information.
Several physical hazards were noted during the ATSDR site visit. Buildings on the site havebecome dilapidated and unsafe through lack of maintenance and acts of vandals. Until 1991, accessto the site was unrestricted, and vandals frequently trespassed into the area. Although the electricalpower to USS Lead has been shut off, a transformer at the facility remains active. One trespasserwas electrocuted several years ago after apparently assuming that the transformer was no longer live.
To determine whether nearby residents and workers are exposed to contaminants migrating fromthe site, ATSDR evaluates the environmental and human components that lead to human exposure. This pathway analysis consists of five elements: A source of contamination, transport through anenvironmental medium, a point of exposure, a route of human exposure, and an exposed individualor population.
ATSDR categorizes an exposure pathway as a completed or potential pathway if it cannot beeliminated. Completed pathways require that the five elements exist and indicate that exposure toa contaminant has occurred in the past, is currently occurring, or will occur in the future. Potentialpathways, however, require that at least one of the five elements is missing, but could exist. Potential pathways indicate that exposure to a contaminant could have occurred in the past, couldbe occurring now, or could occur in the future. Eliminated pathways require that at least one of thefive elements is missing and will never be present. Table 9 identifies the completed exposurepathways. Table 10 estimates the number of exposed persons for completed exposure pathways andthe number of potentially exposed persons for potential exposure pathways. The discussion thatfollows incorporates only those pathways that are important and relevant to the site.
Surface Soil and Waste Pathways
Surface soils have become heavily contaminated with metals, both on-site and off-site. When USSLead was in production, its workers were exposed to elevated levels of lead, arsenic, and othermetals in surface soils and wastes stored on-site. After production at USS Lead ceased in 1985,trespassers began entering the facility to remove building materials and scrap. These trespasserswere also exposed to the contaminated soils and wastes. Extremely high levels of lead were foundin surface soils at the E.C. DuPont facility adjacent to USS Lead. This lead contamination was mostlikely deposited from past ambient air contamination emanating from USS Lead. Workers at theDuPont plant are exposed to lead-contaminated soils. Additional sampling in a nearby residentialarea indicates that the lead contamination extends for a distance of at least 3,000 feet (over half amile) to the north. Residents in this area have been exposed to soil contaminated with lead andpossible the other contaminants found in the flue-dust on-site. Exposure to the lead occurs throughincidental ingestion of and dermal contact with soils and wastes. Adults and especially childrenswallow small amounts of lead-contaminated soil because of hand to mouth activity. In addition,small children occasionally develop pica behavior, meaning that they swallow non-food items, suchas large amounts of soil. Pica behavior would greatly increase the amount of lead exposureexperienced by a child.
Ambient Air Pathways
Air sampling data indicates that lead-contaminated dusts contaminated ambient air, both on- and off-site. Concentrations were highest on-site, and decreased with increasing distance from the site. Thehighest documented concentrations occurred in 1985, when the site was in operation. After thistime, the concentrations decreased dramatically. Prior to 1982, the practice of storing baghouseflue-dust in open-air piles allowed dispersal of the dust into the air. This would have tended toincrease lead concentrations in the air until the piles were stored in the Tank House. The airsampling efforts focused on lead contamination. However, since most of this contaminationprobably came from particulates which escaped the baghouse, its constituents should be verysimilar, indicating that additional metals, such as arsenic and cadmium, were also present in the airat high concentrations. Workers at USS Lead while in operation experienced the greatest exposuresto lead. Off-site workers at E.C. DuPont also were exposed to very high levels of lead in theambient air. The limited information available for non-industrial off-site areas indicate that ambientair at these areas was also contaminated by lead. Exposure to the lead-contaminated dusts occursthrough inhalation.
No potential exposure pathways were found at USS Lead.
Public Supply Well Pathways
The Grand Calumet River flows into Lake Michigan through the Indiana Harbor. Lake Michiganprovides water to several municipal water supplies. These water distribution centers, however, arerequired to periodically sample water for several substances, including the contaminants of concernrelated to USS Lead. Should these contaminants be found at levels above the US EPA, Illinois, orIndiana regulatory values, the surface water source would be removed as a water source. For thisreason, the pathway for exposure through public supply wells is eliminated.
Biota (Food Chain) Pathways
Two possible pathways were considered for exposure through biota, or foods. Surface water andsediments in the USS Canal and the Grand Calumet River have become contaminated with metalsfrom USS Lead. These contaminants have some potential for bioconcentration within fish. However, since the community of East Chicago is a heavily industrial area, there is no fishing ofthe Grand Calumet River, or Indiana Harbor, into which the river flows. Therefore, this pathwaywas eliminated. An additional possibility for exposure through the food-chain is the through theconsumption of vegetables and fruits which have been grown in contaminated soils. There was noevidence, however, that residents in the area kept vegetable gardens.
|EXPOSURE PATHWAY ELEMENTS||TIME|
|POINT OF |
|ROUTE OF |
|Surface soils |
|surface soils, |
|surface soils |
|on- & off-site||ingestion |
|on-site workers |
|Ambient Air||on-site dust||ambient air||on- & off-site||inhalation||on-site workers |
|antimony, arsenic, cadmium, chromium, lead, manganese, mercury,selenium, tungsten, yttrium|
The contaminants of concern released into the environment at USS Lead have the potential to causeadverse health effects. However, for adverse health effects to occur the pathway for exposure mustbe completed. A release does not always result in exposure. A person can only be exposed to achemical if they come in contact with the chemical. Exposure may occur by breathing, eating, ordrinking a substance containing the contaminant or by skin (dermal) contact with a substancecontaining the contaminant.
Several factors determine the type and severity of health effects that occur from an exposure to acontaminant. Such factors include the exposure concentration (how much), the frequency and/orduration of exposure (how long), the route or pathway of exposure (breathing, eating, drinking, orskin contact), and the multiplicity of exposure (combination of contaminants). Once exposureoccurs, characteristics such as age, sex, nutritional status, genetics, life style, and health status of theexposed individual influence how the individual absorbs, distributes, metabolizes, and excretes thecontaminant. Together those factors and characteristics determine the health effects that may occuras a result of exposure to a contaminant.
ATSDR considers the above physical and biological characteristics when developing healthguidelines. Toxicological profiles prepared by ATSDR summarize chemical specific toxicologicaland adverse health effects information. Health guidelines such as ATSDR's Minimal Risk Level(MRL) and EPA's Reference Dose (RfD) and Cancer Slope Factor (CSF) are included in thetoxicological profiles. Those health guidelines are used by ATSDR health professionals indetermining the potential for developing adverse noncarcinogenic health effects and/or cancer from exposure to a hazardous substance.
A Minimal Risk Level (MRL) provides a basis for comparison with concentrations of contaminantsin different environmental medium (soil, air, water, and food) to which people might be exposed. If daily exposure occurs at an amount below the MRL, harmful noncancerous health effects are notexpected to occur. If daily exposure exceeds the MRL, then ATSDR evaluates whether or not thatlevel of exposure is likely to cause adverse health effects by comparing the amount of exposure tolevels in animal and human studies. The method for deriving MRLs does not include informationabout cancer, therefore, an MRL does not imply anything about the presence, absence, or level ofcancer risk. An EPA Reference Dose is an estimate of the daily exposure for the human population,including sensitive sub-populations, that is likely to be without appreciable risk of adversenoncarcinogenic health effects during a lifetime (70 years). The RfD is a health guideline for theoral route of exposure. For carcinogenic substances, EPA has established the Cancer Slope Factor(CSF) as a health guideline. The CSF is used to determine the number of excess cancers expectedfrom exposure to a contaminant.
To link the site's human exposure potential with health effects that may occur under site-specificconditions, ATSDR estimates human exposure to the site contaminant from ingestion and/orinhalation of different environmental media . The exposure dose is related to the contaminantconcentration, the person's intake rate (for example, soil a person accidentally swallows), and that person's body weight.
ATSDR uses standard intake rates for ingestion of water and soil. The intake rate for incidentalingestion of soil is 100 mg/day for adults, 200 mg/day for children, and 5000 mg/day for childrenwith pica behavior, or the swallowing of non-food items such as soil. Standard body weights foradults and children are 70 kg and 10 kg, respectively. The maximum contaminant concentrationdetected at a site for a specific medium is commonly used to determine the estimated exposure. Useof the maximum concentration detected in a specific medium will result in the most protectiveevaluation for human health. When unknown the biological absorption from the environmentalmedium (soil, water) is assumed to be 100%.
Human exposure to antimony at USS Lead occurred through incidental ingestion of and dermalcontact with contaminated surface soils and wastes, and potentially through inhalation ofcontaminated air. Exposure occurred to on-site workers and trespassers and may have occurred to off-site workers and residents.
The general population is exposed to low levels of antimony in ambient air and food. The averagedaily intake from ingestion of food and water has been estimated to be 5 - 100 µg/day . Theingested dose which is estimated for workers at USS Lead is 480 µg/day. This dosage is 16 timeshigher than the US EPA's RfD. Non-cancerous adverse health effects may occur from exposure toantimony at the site through the incidental ingestion of soil.
Antimony and its compounds are currently used to treat two parasitic diseases, schistosomiasis andleishmaniasis. Toxic side effects in humans following injection with antimony-containing drugshave been reported. These effects include altered EKG, anemia, vomiting, diarrhea, joint andmuscle pain, and death. Altered EKG readings were observed after 4 days of trivalent antimonytreatment at a dosage over 100 times higher than that estimated for workers at USS Lead. However,for pentavalent antimony, a change in readings was not observed until after 3 weeks of injectionsat a dosage 1000 times higher than that for USS Lead workers . Amounts as low as 80 timesthe USS Lead dose have resulted in vomiting. In animal experiments, amounts as low as 40 timesthe estimated USS Lead dose caused a minor effect on blood vessels and the cardiovascular system. There is evidence that exposure to antimony might increase the severity of existing lung orcardiovascular disease. Dermal exposure to antimony has resulted in no reported effects in humans.
No information on the carcinogenic potential of antimony in humans was found. However,antimony has not produced cancer in rats or mice exposed by the oral route.
Human exposure to arsenic at USS Lead occurred through incidental ingestion of and dermal contactwith contaminated surface soils and wastes, and potentially through inhalation of contaminated air. Exposure occurred to on-site workers and trespassers and may have occurred to off-site workers andresidents.
Arsenic is a naturally occurring element that is normally found combined with other elements. Theexact forms of arsenic at USS Lead are unknown. Arsenic toxicity varies depending upon its form. The soluble inorganic forms are well absorbed from the digestive tract and distributed widelythroughout the body. Arsenic is cleared rapidly from the blood. Most arsenic that is absorbed intothe body is converted to a less toxic form and excreted; consequently, arsenic does not accumulatein the body during exposures to low levels. Although arsenic may concentrated in small amountsin the liver, kidney, lung, spleen, aorta, and upper gastrointestinal tract, it is also rapidly clearedfrom these tissues. Arsenic which remains and accumulates in the body is stored mainly in the skinand hair.
Studies of the chronic oral effects of arsenic show that although some people can ingest up to 150µg/kg/day (microgram of arsenic per kilogram of body weight every day) without noticeableill-effects, doses as low as 20 to 60 µg/kg/day may result in one or more signs of arsenic toxicityin more sensitive individuals. EPA's RfD for arsenic is 0.4 µg/kg/day. Adverse health effects fromarsenic exposure include: digestive tract irritation, disturbances of the blood and nervous systems,skin and blood vessel injuries, and liver or kidney injury. The severity of these symptoms generallydepends upon the duration of exposure. In most cases of chronic (many years) exposure, many orall of the signs of arsenic toxicity are detected together, indicating that the dose-responserelationships for the various systemic end points are fairly similar. The most sensitive effects arethe changes in pigmentation of the skin and the appearance of calluses. The incidental ingestion ofsoil and wastes containing the maximum levels detected on-site results in exposures which exceedthe RfD by a factor of nine. The doses at which health effects have been noted are not exceeded. People exposed to similar levels as are estimated for workers at this site did not experience adverseeffects. However, the estimated exposure in workers is about 10 times less than levels that causeblackfoot and Raynaud's diseases in humans. Some uncertainty exists in estimating the amount ofworker exposure, since contaminant concentration may have been higher or lower. Workers alsomay have received additional exposures from breathing arsenic-contaminated dust. The total arsenicexposure, therefore, may be high enough to cause blackfoot and Raynaud's diseases and skindiscoloration.
People who may show increased sensitivity to arsenic include those on protein-poor diets or thosewith choline (a B-vitamin) deficiency. Inorganic arsenic is detoxified in humans by liver enzymes. Those individuals with low liver enzyme activity or liver damage such as alcoholic- or viral-inducedcirrhosis, may be more sensitive to the effects of arsenic than are people with normal liver enzymeactivity .
Arsenic has been classified by the US EPA and the Department of Health and Human Services asa known human carcinogen. Inhalation exposure to arsenic has been associated with lung cancer. This has been seen in people exposed to arsenic in or around smelters. Ingestion of arsenic has beenassociated with an increase in the rates of cancers of the skin, liver, bladder, kidney, and lung. Theingestion exposure of on-site workers to the maximum levels of arsenic observed in flue-dust maylead to a high increase in these cancers, especially skin cancer.
Human exposure to cadmium at USS Lead occurred through incidental ingestion of and dermalcontact with contaminated surface soils and wastes, and potentially through inhalation ofcontaminated air. Exposure occurred to on-site workers and trespassers and may have occurred to off-site workers and residents.
The estimated exposure dose for on-site workers through incidental soil ingestion is four timeshigher than ATSDR's chronic oral MRL, and slightly higher than the US EPA's RfD. Mild damageto the kidney could have occurred to workers at USS Lead because of that exposure. This damageshould be very mild because the exposures are very low. Cadmium accumulates in soft tissue suchas the kidney. Because it is a cumulative toxin which is highly retained, long-term exposure to lowdoses produces similar effects as short-term exposure to high doses. Little cadmium is absorbedthrough the skin, thus dermal exposure is not of great concern.
Impairment of lung function is associated with chronic inhalation exposure to low cadmium levels. Bronchiolitis and alveolitis may occur and impaired respiratory function and emphysema havebeen observed in persons occupationally exposed to cadmium. Since there is no ambient air datafor cadmium, the level of exposure and consequent health effects cannot be determined.
It is not known if cadmium exposure causes cancer in humans. Some epidemiological studies ofworkers exposed to cadmium suggest a possible link between cadmium inhalation and lung andprostatic cancer . Animal study evidence shows that chronic inhalation of cadmium chlorideproduces an increased frequency of lung cancer in animals. There is not any human or animalevidence demonstrating that oral or dermal exposure to cadmium causes cancer. Based on animalsstudies, the EPA has classified cadmium as a probable human carcinogen when inhaled. Workersare unlikely to get cancer from ingesting cadmium. Because sufficient air data is not available, nodetermination can be made about whether that exposure would have been at high enough levels tocause lung cancer in workers.
Several populations may be sensitive to cadmium exposure. Those with dietary deficiencies incalcium and protein, renal disease, and those who smoke are at an increased risk to the adverseeffects of cadmium. The limited amount of cadmium exposure to workers at this site might add to any existing sensitivity to cadmium.
Human exposure to chromium at USS Lead occurred through incidental ingestion of and dermalcontact with contaminated surface soils and wastes, and potentially through inhalation ofcontaminated air. Exposure occurred to on-site workers and trespasser and may have occurred tooff-site workers and residents.
Chromium is present in the environment in several different forms. The most common forms arechromium 0, chromium III, and chromium VI. Chromium III occurs naturally in the environment,whereas Chromium VI and chromium 0 are generally produced by industrial processes. Amaximum of 47% of the total chromium in ferrochrome smelter dust may be bioavailable (capableof being absorbed by an exposed human or animal). Of this amount, about 40% may exist aschromium VI, and the remainder as chromium III [. Based on these assumptions, the estimated dosefor the on-site workers through incidental soil ingestion is far below the US EPA's RfD for bothchromium III and chromium VI. Therefore, non-cancerous adverse health effects should not occurto on-site workers and trespassers through soil ingestion.
Long-term exposure to high levels of chromium in the air has been associated with lung cancer inpeople. It is not clear which form of chromium is capable of causing lung cancer, althoughchromium VI is believed to be primarily responsible. There is no evidence that chromium in anyform may cause cancer when exposure occurs through ingestion. The US EPA and the Departmentof Health and Human Services have determined that chromium VI is a known human carcinogen. No data exists for chromium levels in air, therefore, no determination can be made about whether workers might get cancer from inhalation exposure while working at USS Lead.
On-site workers and trespassers and off-site workers and residents were exposed to lead throughincidental soil ingestion, dermal contact with contaminated soils and wastes, and inhalation ofairborne lead-contaminated dust. There are no MRLs or RfDs for lead.
The estimated exposure for on-site workers and off-site pica children far exceeds levels in animaland human studies that caused impaired learning and behavioral tasks in monkeys. The estimatedexposure is also high enough to cause mild changes in enzyme activity in the blood, heme synthesisin the blood, and alter motor activity . The highest estimated exposure in workers at the E.C.DuPont plant and in off-site children is similar to these exposure levels.
Additional exposure to lead occurred to both children and adults through the inhalation of aircontaminated with lead dust. The amount of lead which would be absorbed through inhalation isnot known. The limited air monitoring data available on-site did not exceed occupational standards. However, continuous monitoring conducted off-site at E.C. DuPont exceeded the OccupationalSafety and Health Administration's Permissible Exposure Limit for workers of 50 µg/m3 one dayin 1985 .
Very little data exists concerning adverse effects associated with inhalation exposures of lead. However, maximum concentrations on-site and at E.C. DuPont (38.2 and 16.1 µg/m3, respectively)exceed the concentration of 11 µg/m3 at which some minor hematological changes were observedin people after long exposures.
Children are more sensitive to the adverse health effects from lead exposure than are adults. Thecentral nervous system is the primary target organ for lead toxicity in children [20-24]. Recentstudies have indicated the adverse effects on the function of the central nervous system will persistinto adulthood . Current information has shown that disturbances in neurobehavioraldevelopment occur in children with lead levels in the range of 10 to 25 µg/dl and in children whosemothers had blood lead levels in that range during pregnancy. There has been some indication thateffects occur at blood lead levels even below 10 µg/dl . The Centers for Disease Control andPrevention has recommended that the intervention level be established at 10 µg/dl . Suggestedactions are the education of parents on simple modifications in food storage and housekeepingactivities that will reduce the potential for exposure to lead. In addition, the child's blood lead levelshould be retested in 3 months if it was between 10 and 14 µg/dl .
High levels of lead exposure can cause reproductive effects. The incidence of miscarriages andstillbirths is increased in women exposed to high levels of lead during pregnancy. An increasedfrequency of spontaneous abortion has been reported in women living near a lead smelter . Studies of male lead workers indicates that male fertility is adversely affected by lead exposure. Itis not known whether exposure levels at the site are high enough to cause these effects.
Studies of humans exposed to lead have not established what concentrations of lead present in soilmay result in blood lead concentrations associated with adverse noncarcinogenic health effects. Therefore, soil guidelines for protection of public health have not been determined for lead.
The potential for exposure to lead from dermal contact is considered insignificant because little leadpasses through the skin . Therefore, adverse health effects from dermal contact with leadcontaminated soils and wastes is not expected to be of public health concern.
Case reports have implicated lead as a potential kidney carcinogen in humans . The EPA hasconcluded that human data are inadequate to determine the potential carcinogenicity of leadexposure. However, based on animal studies,the EPA has classified lead as a probable humancarcinogen . Health guidelines for possible cancerous effects in humans resulting from leadexposure have not been established. Therefore, the cancer risk associated with lead exposure at USSLead cannot be evaluated.
Individuals have been exposed to multiple contaminants at USS Lead by ingestion, inhalation, anddermal contact with contaminated soil and dust. However, data are very limited on the health effectsof multiple contaminant exposure. The effects of multiple contaminant exposure can be additive,synergistic (greater than the sum of the single contaminant exposures), or antagonistic (less than thesum of the single contaminant exposures). Also, simultaneous exposure to contaminants that areknown or probable human carcinogens could increase the risk of developing cancer. ATSDR'sevaluation of exposures in this preliminary public health assessment is limited to individualcontaminant exposures; multiple exposures have not been evaluated because of the limitedknowledge that exists about the toxicity from multiple exposures. The only available informationregarding interactions between two or more of the metals at this site is for cadmium and lead. Cadmium may act synergistically with lead, when a person is exposed to both metalssimultaneously. Increased mortality rates and behavioral changes have been reported in animalstudies using both metals . No information is available regarding other possible interactions,or the lack of interactions between the metals at this site.
The Indiana State Board of Health conducted blood lead screening for children in East Chicago . The study included children aged six months to six years, and was performed over a two day periodin June, 1985. USS Lead was still in operation at the time of the study. It is not clear what criteriawere used in selecting the children for this study. Fifty-three children were tested by finger-stickfor elevated blood lead levels. Two children were found to have class II blood lead levels,indicating that they were moderately increased, between 10 to 20 µg/dl. The home environmentsof both children were investigated by the East Chicago Health Department. No conclusive resultswere found regarding the sources of the lead contamination. One home was built in 1977, with nolead found in paint or soil. The other residence was an apartment undergoing remodeling. Noconclusions regarding the impact of the site on children in the area can be drawn from the limitedinformation currently available about this study.
No community concerns have been identified.