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PUBLIC HEALTH ASSESSMENT

RSR CORPORATION
DALLAS, DALLAS COUNTY, TEXAS


ENVIRONMENTAL CONTAMINATION AND OTHER HAZARDS

This section lists contaminants of concern at the RSR Corporation site. These contaminants wereselected by comparing contaminant concentrations to health assessment comparison (HAC)values for non-carcinogenic endpoints and carcinogenic endpoints. HAC values are mediaspecific contaminant concentrations that are used to screen contaminants for further evaluation.

The list below summarizes acronyms and symbols used to discuss contaminants of concern:

* HAC = Health Assessment Comparison Value
* MRL = Minimal Risk Level
* CREG = Carcinogenic Risk Evaluation Guide
* RfD = Reference Dose
* EMEG = Environmental Media Evaluation Guide
* ppm = parts per million
* mg/Kg = milligrams per kilogram (equal to ppm)
* µg/m3 = micrograms per cubic meter of air
* µg/dL = micrograms per deciliter

HAC values include non-cancer comparison values and carcinogenic risk evaluation guides(CREGs). Non-cancer comparison values are HAC values based on the Agency for ToxicSubstances and Disease Registry's (ATSDR's) minimal risk levels (MRLs), EPA's referencedoses (RfDs), or other non-carcinogenic health-based values. CREGs are HAC values based onEPA's chemical specific cancer slope factors and an estimated excess lifetime cancer risk ofone-in-one-million persons.

Exceeding a HAC value does not imply that a contaminant represents a public health threat butsuggests that the contaminant warrants further consideration. Subsequent sections of thisassessment will evaluate whether exposure to the contaminants at this site has public healthsignificance.

Although the data presented in this section were collected from areas outside the boundaries of the RSR Smelter facility site, for the purposes of this health assessment the term "on-site" refers to all areas within the defined 13.6 square-mile NPL site.

Sampling and analyses conducted at the RSR Corporation site primarily have evaluated thepresence of lead, cadmium, and arsenic in soil. HAC values for these contaminants in soil arelisted in Table 6.

Table 6.

Health Assessment Comparison Values For Contaminants of Concern in Soil
ContaminantHAC Value (ppm)Non-cancer HACValue Source
Non-cancerCREG1
Lead
Cadmium
Arsenic
500
40
20
NA2
NA
0.4
EPA/CDC
EMEGChild
EMEGChild

1 CREG value is based on EPA's chemical specific cancer slope factor.
2 NA = Not available.
3 EMEG = Environmental media evaluation guide; based on ATSDR's chronic oral minimal risk
level (MRL) of 0.0007 mg/kg/day for cadmium and 0.0003 mg/kg/day for arsenic.

A. On-site Contamination

Air

Historical ambient air monitoring data in the residential areas near the smelter are sparse. A well-documented history of the smelter's operations, however, indicates that the quantity of leademitted from the smelter was highest prior to 1968, when emissions were largely uncontrolled. Results of fenceline air monitoring by the City of Dallas indicate that emissions continued to bequite high throughout the 1970s, even after primary point source controls and initial sanitaryemission controls had been implemented [4].

A special enforcement study was conducted during a 30-day period in March 1973 by the City inpreparation for its 1974 lawsuit against the smelter. This study, which was implemented after the smelter had installed initial emission controls, recorded that the downwind lead concentration atthe fenceline of RSR averaged 44.6 µg/m3 and the upwind fenceline concentration averaged 20.9µg/m3. (According to descriptions of the sampling locations, the "upwind" measurement actuallywas collected between portions of the smelter complex and therefore reflects contaminant levelsassociated with the smelter). The City of Dallas standard for lead in air was 5 µg/m3 at that time[4].

The first adequate monitoring facilities were placed in the community near the smelter in 1982when the EPA installed three 24-hour ambient air monitors. The results of air monitoring for thesecond quarter of 1982 are presented in Table 7 below. This monitoring was conducted prior tothe closure of the RSR smelter facility and after the smelter had implemented the mostcomprehensive emission controls in its history of operation. Two of the monitors measured leadlevels in the air above 1.5 µg/m3, the National Ambient Air Quality Standard (NAAQS) for lead. These monitors were located 50 and 500 yard north of the smelter. Wind direction at the time ofmonitoring was not provided, but the prevailing wind direction at this site is north-northeast [4].

Since the smelter's closure in 1984, air samples taken before, during, and after remedial activities have never detected levels of lead above NAAQS for high volume sampling (1.5 µg/m3) [23]

Table 7.

Air Lead Values Measured by EPA Monitors April - July 1982 [4, 17]
Monitor/
Distance fromSmelter
Monitor A
50 yardsNorth
Monitor B
500 yardsNorth
Monitor C
150 yardsSouthwest
Monitor D
1 mile East
NAAQS
Value2.97 µg/m31.57 µg/m31.13 µg/m30.26 µg/m31.50 µg/m3

NAAQS = National Ambient Air Quality Standard.

Surface Soil

Soil samples have been collected during various periods over the past 12 years. We reviewedsamples collected before, during, and after both soil removal actions which were initiated in 1984 and in 1993. A summary of data associated with these removal efforts are presented below inchronological order.

The first soil samples were collected at this site in 1982 as part of the Dallas Area LeadAssessment Study. Sampling included soil grid sampling (750-feet grids) within a one-mileradius of the RSR Smelter. Analysis of the grid sampling produced isopleths (lines on the mapshowing the pattern of lead contamination in soil) consistent with the predominant wind directionfrom the RSR smelter. The isopleths are plotted on the map in Figure 4. The pattern of soil lead concentrations observed surrounding the smelter reflects the pattern of lead deposited from the smelter through the air. Lead concentrations in soil were highest near the RSR Smelter facility(up to 3,000 ppm) and decreased with increasing distance from the smelter (200 ppm atapproximately one-half mile). The mean lead concentration of soil in residential yards withinone-half mile of the smelter was 826 ppm; the mean soil lead concentration in yards locatedbetween one-half mile and one mile of the smelter was 192 ppm. In 1982, the overall mean soillead concentration of all yards sampled within one mile of the smelter was 489 ppm [17]. Leadlevels were higher north and northeast of the smelter, the direction of prevailing winds [6].

In 1984 and 1985, soil with lead levels of more than 1,000 ppm was removed from high use areaswithin one-half mile of the smelter. Soil was removed to a depth of six inches, replaced withseven inches of clean fill, and resodded. In public play areas and day care centers, contaminated soil was removed to a depth of 12 inches and replaced with washed sand. In gardens within a one-half mile radius of the smelter, 12 inches of soil were removed and replaced with clean fill. A vegetative barrier was established in less contaminated areas within a one-half mile radius ofthe smelter where soil was not removed [1,6]. Soil sampling data characterizing the site afterremoval were not available for review.

In 1991, TWC analyzed battery chips, slag material, and contaminated soil discovered by WestDallas residents. The chips and slag material contained lead levels as high as 64,000 ppm,arsenic in excess of 2,000 ppm, and cadmium above 100 ppm [24]. Between August and December 1991, EPA collected and analyzed approximately 1,200 additional soil samples. The majority of these samples contained less than 250 ppm of lead; lead levels ranged from levels below the detection limit up to 128,000 ppm. Approximately 16 percent of the samples contained 500 to 1,500 ppm of lead [7].

In 1992 and 1993, in an attempt to identify all properties containing battery chips and slag, TWC surveyed more than 6,800 properties within the 13.6 square-mile study area. Battery chips were identified on approximately 366 properties, including 282 residential properties, 53 vacant lots, 17 commercial properties, and 14 residential properties where the owner declined to sign asurvey form [25].

Table 8 is a compilation of the results of soil sampling conducted by EPA from August 1991through April 1993 and by TWC from September 8 through October 28, 1992 and February 23through March 16, 1993. Sample concentrations represent soil contamination resulting from airdeposition as well as the use of contaminated soil, slag, and battery chips as fill [26]. Only asmall percentage of samples were highly elevated and many were below detection limits, asevidenced by means which are low compared to the maximum concentration levels. For arsenic,the highest detected concentration was six times higher than the next highest measuredconcentration.

Table 8.

Contaminant Concentrations in Soil 1993 EPA Database1 [26]
ContaminantNumber of
Samples
Range2
(ppm)
Detection Limits
(ppm)
Mean3
(ppm)
Lead2,323BDL-128,0006 and 7740.18
Cadmium2,261BDL-20024.71
Arsenic2,275BDL-2,8806 and 714.62

1 Compilation of data from pre-excavation soil analysis performed by EPA from August 1991
through April 1993 and the Neighborhood Survey and Sampling performed by TWC from
September 8 through October 28, 1992 and February 23 through March 16, 1993.
2 BDL = Below Detection Limit.
3 Samples containing contaminants below detection limits were included in the calculation of
mean by using the value of the larger detection limit.

Between June 1992 and June 1993, approximately 206 properties with soil lead levels greaterthan 500 ppm were remediated. This removal action included properties within the high airdeposition area and all properties identified as high risk areas for children. In June 1993, EPAbegan to remediate an additional 194 properties where battery chips and slag had been identified. Soil with lead levels over 500 ppm, arsenic levels over 20 ppm, and cadmium levels over 30 ppmwas removed and replaced with clean fill [27].

Sampling collected during removal efforts indicated that lead exceeded action levels on mostproperties, but that arsenic was detected above its action level on only a few lots. All properties with elevated arsenic levels also had elevated lead levels; therefore, arsenic was removed during the excavation of soil to address elevated lead levels. A cadmium level above the 30 ppm action level was found on only two properties where elevated lead was not also found [26,28].

Table 9 is based on a subset of samples included in the compilation of data presented in Table 8. Table 9 includes results of 663 samples collected by an EPA contractor between September 1,1992 and April 30, 1993 [29]. These samples were collected where surveyors observed signs ofbattery chips and/or slag and in the yards of residents who requested sampling. This table reportsthe range of lead, arsenic, and cadmium concentrations observed in the samples collected.

ATSDR provided a health consultation to EPA for one West Dallas property where cadmiumlevels were found in concentrations ranging from 2.0 to 57.5 ppm [30].

Surface Water and Sediment

The City of Dallas found no lead contamination in two surface water samples from Fish TrapLake, which is three-fourths of a mile northeast of the RSR Smelter [14,18]. According to a1992 ATSDR Public Health Consultation, a West Dallas resident stated that samples he hadtaken from Fish Trap Lake have shown elevated lead levels, but the citizen's data were notavailable for review. Additional surface water and sediment sampling data were not available forthis site.

Table 9.

Contaminant Concentrations in Soil Samples Collected Where
Battery Chips/Slag Were Observed1 [29]
ContaminantConcentration Range(ppm)Number of SamplesWithin Concentration RangePercentage ofSamples WithinConcentration Range
Lead0-249
250-499
500-749
750-999
1,000-1,499
1,500-1,999
2,000-5,000
5,000+
456
87
31
14
18
8
18
31
68.8%
13.1%
4.7%
2.1%
2.7%
1.2%
2.7%
4.7%
Arsenic0-2.49
2.5-4.9
5.0-7.49
7.5-9.9
10-14.9
15-19.9
20+
32
213
227
74
74
19
24
4.8%
32.1%
34.2%
11.2%
11.2%
2.9%
3.6%
Cadmium0-0.99
1.0-1.9
2.0-4.9
5.0-9.9
10.0-29.9
30+
476
108
51
14
10
4
71.8%
16.3%
7.7%
2.1%
1.5%
0.6%

1 Samples collected between September 1, 1992 and April 30, 1993 by EPA Contract Laboratory
in areas with visible contamination and where residents requested sampling.

In-Home Environmental Sampling

Walk-in Clinic Follow-up Data

In-home environmental sampling, including soil, dust, and water sampling, is offered to allindividuals with elevated blood lead levels identified at City of Dallas Walk-in Clinics (childrenwith15 µg/dL and adults with levels25 µg/dL). We reviewed data collected between 1991 and 1993 when 21 such follow-ups were conducted. There is no consistent relationship between anyof the measured parameters and observed blood lead levels; however, paint, which is commonlythe most significant source of childhood residential lead exposure, was tested for lead in onlythree of the homes. Data are presented in Table 10.

Biologic Indicators of Exposure Study Data

The most recent in-home sampling conducted in West Dallas was collected as part of the 1993Biological Indicators of Exposure Study. This study provided more comprehensiveenvironmental data than the Walk-in Clinic data and included soil, dust, water, and indoor andoutdoor paint sampling at the homes of the 305 West Dallas study participants. Environmentalsamples also were collected in the homes of 81 children from a comparison community. Asummary of the environmental sampling results are provided in Table 11.

As part of this study, 374 composite soil samples were collected from yards. The averageconcentration of lead in soil ranged from 70 ppm (in the "eastern low air dispersion area") up to148 ppm (in the comparison community).

In West Dallas, 576 dust samples were collected from children's bedrooms and the entryways ofhomes; in the comparison community, 323 dust samples were collected from children's bedroomsand the entryways of homes. The average concentration of lead in dust samples collected inchildren's bedrooms ranged from 80 ppm (in the area of West Dallas where chips and slag hadbeen identified) up to 146 ppm (in the area nearest the site). The average concentration of lead in dust collected from the entryways of homes ranged from 81 ppm (in the chips and slag area) to205 ppm (in the comparison community).

Approximately 386 indoor paint samples were collected. Approximately 9.6% of homes hadcontaminated paint on at least one indoor surface and the percentage of homes with contaminatedpaint ranged from 5.7% (in the homes where battery chips were used as yard fill) up to 16.1% (inthe comparison community). Exterior paint samples also were collected at 386 homes; 35.5%had lead-contaminated paint on exterior surfaces, with a range from 19.4% (in the western lowair dispersion area) up to 45.7% (in the comparison area).

The mean lead concentration from the 382 first-drawn cold water samples collected from thekitchen faucets of homes in the study was 3.5 mg/L. The lead concentrations in water rangedfrom 2.71 mg/L (in the high air dispersion area) up to 3.73 mg/L (in the eastern low airdispersion area).

All of the environmental sampling results were compared with the blood lead levels of childrenliving in the homes. The study did not find a statistically significant relationship between blood lead levels and any of the factors that were analyzed.

Table 10.

Follow-up Environmental Sampling in Homes of Individuals With Elevated Blood Lead Levels Identified at City of Dallas Walk-in Clinics, 1991 through 1993 [31]
Date SampledYearBornBloodLeadLevel(µg/dL)Soil in Yard(mg/kg)Dust (µg/sq ft)Paint Chips(mg/kg)Water(mg/L)
FrontBackFloorWindowSillIndoorOutdoorTap
>5001>200>500>5,000>0.015
08-26-918615395110<MDLNSNS<MDL
09-18-91892125395NS<MDLNSNS<MDL
09-18-91892125395NS<MDLNSNS<MDL
09-18-91842125395<MDLNSNSNS<MDL
10-10-9189163734<MDLNSNSNS0.005
11-04-91882488NS1010NSNS0.006
11-07-9191152291<MDL<MDL304NS<MDL
11-07-91622854121<MDL3,8003NS0.003
02-26-9290154424<MDL<MDLNSNS0.005
02-26-9288194424<MDL<MDLNSNS0.005
08-17-9291155360<MDL1.5NSNS0.005
09-16-9289194919712NSNS0.005
09-16-928627604098NSNS0.005
04-23-9392167516012112NSNS0.005
04-30-939320385NS321NSNSNSNS
06-25-93921578NS942NS17,900<MDL
08-12-93901750374764NSNS<0.005
08-16-93901944311631NSNS<0.005
09-02-938925143343<420.4NSNSNS
09-02-93921688.862.310651.6NSNSNS
09-02-939218401023014.8NSNSNS

1 Numbers in shaded row indicate general guides of comparison used by the City of Dallas to
identify levels of contamination that may be a cause for concern. Bolded numbers indicate
sample results exceeding these guides.
<MDL = less than the minimum detection limit.
NS = not sampled.

Table 11.

In-home Environmental Sampling Data for Lead Content from 1993 Biological Indicators of Exposure Study [22]
Type of SampleArea 1Area 2Area 3Area 4ComparisonAreaTotal
Composite Soil(averageconcentration)126 ppm 119 ppm70 ppm142 ppm148 ppm116 ppm
Dust in child's bedroom
(averageconcentration)
147 ppm84 ppm97 ppm80 ppm117 ppm99 ppm
Dust in entryway
(averageconcentration)
139 ppm179 ppm85 ppm81 ppm206 ppm136 ppm
Indoor paint
(% homes with leadpaint on at leastone surface)
7.6%12.7%5.8%5.7%16.1%9.6%
Outdoor paint
(% homes with leadpaint on at leastone surface)
37.7%37.8%19.4%42.9%45.7%35.5%
Water from kitchenfaucet
(average concentration)
2.71ppm 3.73 ppm3.70ppm3.47ppm3.70 ppm3.53 ppm

Other Sources of Contamination on Site

The Toxic Chemical Release Inventory (TRI) is an EPA database that documents contaminantsreleased by industrial facilities into the environment. TRI data is self-reported and only certaintypes of facilities are required to report. Table 12 lists all chemical releases reported to EPA inthe West Dallas area between 1987 and 1991.

According to TRI data, the Murmur Corporation released 500 pounds of lead between 1987 and1991. These emissions were reported by Murmur in association with its active reclamation andrecycling operation at the site; however, Murmur reported these releases to EPA under thecategory of environmental losses between 11 and 500 pounds per year and the actual amount thatwas released may be much less than 500 pounds. According to EPA, in 1993 the companyestimated that less than 100 pounds of lead per year were emitted to the environment (air, water,soil, etc.) from its processes and the site does not create detectable levels of lead air pollution. Air pollution monitors across the street from Murmur have not detected lead levels in air abovethe National Ambient Air Quality Standard since 1984 when the smelter closed. We willthoroughly evaluate the levels of lead contamination remaining on the smelter property when weaddress Operable Unit 4, which is currently being assessed and cleaned up by EPA. B. Off-site Contamination

Off-site sampling data were not available at this site. The boundaries of the 13.6 square mile sitewere drawn to include all areas potentially effected by the RSR Smelter.

Table 12.

Chemical Releases to Air and Land Reported in Toxic Release Inventory
West Dallas 1987 - 1991 [11]
DATESOURCE OF RELEASECONTAMINANTRELEASEDTOAMOUNT
lbs/yr
1987Roach Paint Co. Inc.
2121 French Settlement Road
Ethylene GlycolAir250
Lilly Industrial Coatings Inc.
2518 Chalk Hill Road
Xylene (mixedisomers)Air1,647
Dallas Woodcraft Inc.
2829 Sea Harbor Road
Xylene (mixed isomers)
Toluene
Acetone
Methyl Isobutyl Ketone
Methyl Ethyl Ketone
Air
Air
Air
Air
Air
390,250
71,250
23,250
37,250
10,150
Trinity Brass Copper Co., Inc.
2920 Sylvan
CopperAir1,350
Atlas Manufacturing Co.
2321 Beatrice Street
Dichloromethane
Phosphoric Acid
Sodium Hydroxide
1,1,1-Trichloroethane
Xylene (mixed Isomers)
Ammonia
Formaldehyde
Hydrochloric Acid
Methanol
Air
Air
Air
Air
Air
Air
Air
Air
Air
20
104
80
84
10
4
0
12
0
Blanks Engraving Co.
23443 North Beckley
Tetrachloroethylene
Trichlorethylene
Nitric Acid
Air
Air
Air
34,090
11,880
6,340
Oak Cliff Plating
2330 North Beckley
Sulfuric AcidAir
Land
500
6,000
1988Roach Paint Co. Inc.
2121 French Settlement Road
Ethylene GlycolAir250
Lilly Industrial Coatings Inc.
2518 Chalk Hill Road
Xylene (mixed isomers)
Ethylene Glycol
Toluene
Lead Compounds
Air
Air
Air
Air
2,044
1,530
2,861
1,000
Dallas Woodcraft, Inc.
2829 Sea Harbor Road
Xylene (mixed isomers)
Toluene
Acetone
Methyl Isobutyl Keytone
Methyl Ethyl Ketone
Air
Air
Air
Air
Air
640,250
63,250
8,550
47,250
7,950
Trinity Brass Copper Co. Inc.
2920 Sylvan
Copper Air1,200
Blanks Engraving Co.
2343 North Beckley
Tetrachloroethylene
Trichloroethylene
Nitric Acid
Air
Air
Air
18,579
7,840
3,005
1988Oak Cliff Plating
2330 North Beckley
Sulfuric Acid
Cyanide compounds
Air
Land
Air
Land
500
250
500
250
Murmur Corporation
2823 North Westmoreland
LeadAir500
Economy Forms Corporation
1915 West Commerce Street
Xylene (mixedisomers)Air11,196
1989Lilly Industrial Coatings Inc.
2518 Chalk Hill Road
Xylene (mixed isomers)
Barium
N-Butyl Alcohol
Methyl Isobutyl Ketone
Lead
Ethylene Glycol
Toluene
Ethylbenzene
Air
Air
Air
Air
Air
Air
Air
Air
2,553
1,875
1,000
1,419
1,000
1,275
4,047
500
Dallas Woodcraft, Inc.
2829 Sea Harbor Road
Xylene (mixed isomers)
Toluene
Methyl Isobutyl Ketone
1,1,1-TrichloroethaneGlycol Ethers
Air
Air
Air
Air
Air
60,250
35,250
12,250
24,250
28,005
Blanks Engraving Co.
2343 North Beckley
Tetrachloroethylene
Trichloroethylene
Nitric Acid
Air
Air
Air
15,086
11,880
16,417
Murmur Corporation
2823 North Westmoreland
LeadAir500
Economy Forms Corporation
1915 West Commerce Street
Xylene (mixedisomers)Air8,613
1990Lilly Industrial Coatings Inc.
2518 Chalk Hill Road
Xylene (mixed isomers)
Isopropyl Alcohol
N-ButylKetone
Methyl Isobutyl Ketone
Ethylene Glycol
Toluene
Lead Compounds
Barium Compounds
Ethylbenzene
Air
Air
Air
Air
Air
Air
Air
Air
Air
2,516
750
1,351
755
255
3,095
1,554
1,362
750
Dallas Woodcraft, Inc.
2829 Sea Harbor Road
Xylene (mixed isomers)
Toluene
Glycol Ethers
Air
Air
Air
15,250
18,250
43,005
Blanks Engraving Company
2343 North Beckley
Tetrachloroethylene
Trichloroethylene
Nitric Acid
Air
Air
Air
20,525
9,240
13,643
Murmur Corporation
2823 North Westmoreland
LeadAir500
Comet Steel Inc.
4846 Singleton Blvd.
TolueneAir11,000
1991Dallas Woodcraft, Inc.
2829 Sea Harbor Road
Toluene
Glycol Ethers
Air
Air
18,005
35,005
Blanks Engraving Company
2343 North Beckley
Trichlorethylene
Nitric Acid
Air
Air
15,000
2,600
Murmur Corporation
2823 North Westmoreland
LeadAir500
QDT LTD
1000 Singleton Blvd.
Freon 113
1,1,1-Trichloroethane
Air
Air
13,000
13,000

C. Quality Assurance and Quality Control

The EPA has approved all quality assurance and quality control (QA/QC) criteria contained inthe referenced documents. In preparing this Health Assessment, TDH staff members relied onthe information provided in the referenced documents and assumed that adequate QA/QCmeasures were followed with regard to chain-of-custody, laboratory procedures, and datareporting. The analyses and conclusions in this Health Assessment are valid only if thereferenced information is valid and complete.

D. Physical and Other Hazards

The extensive area contained within the RSR Corporation NPL site does not lend itself to anadequate characterization of existing physical hazards. The buildings and facilities formerlyassociated with the RSR Corporation smelter are old and in poor condition; areas of the RSRproperty where slag, battery chips, and other waste materials may have been disposed have notbeen fully characterized; and the solid waste surface impoundment associated with RSR has notyet been remediated. These remaining structures and areas could present physical hazards if theareas were accessible to the public. To our knowledge, public access to the smelter and itsassociated facilities is effectively prohibited.

PATHWAYS ANALYSES

We evaluated the environmental and human components required to determine the potential forhuman exposure to contaminants at the site. This process considers five elements of an exposurepathway: a source of contamination, transport through an environmental medium, a point ofexposure, a route of exposure, and an exposed population.

Exposure pathways are categorized as completed, potential, or eliminated. For a person to beexposed to a contaminant, the exposure pathway must be completed. An exposure pathway isconsidered to be completed when all five elements in the pathway are present and exposure hasoccurred, is occurring, or will occur in the future. An exposure pathway is considered to be apotential pathway when at least one of the five elements is missing but may be present in thefuture. An exposure pathway is eliminated when one or more elements are missing and willnever be present to complete the pathway. Completed and potential exposure pathways at thissite are presented in Table 12. Inclusion of a pathway in the table does not imply that thepathway presents a risk to public health. An evaluation of the public health significance of eachpathway will be presented in the following section.

A. Completed Exposure Pathways

Air

Based on ambient air levels observed in 1982 while the smelter was operating, past exposure tolead has occurred through the inhalation of contaminated air. The pattern of soil leadconcentrations that resulted from air deposition of lead suggests that exposures most likelyoccurred north and northwest of the smelter in the direction of prevailing winds. Individuals whowere exposed to site contaminants in the air include on-site workers and people who lived,visited, worked, or attended school within approximately one-half mile of the RSR CorporationSmelter before 1984 while the smelter was operating. Approximately 10,000 people werepotentially exposed through this pathway.

Although historical air sampling data were limited, exposure to lead through inhalation ofcontaminated air was probably higher prior to 1982 when emission controls were stepped up. Exposure to lead via this pathway was eliminated in 1984 when the smelter closed.

Soil

In the past, people living in the residential area just north and northeast of the smelter wereexposed to site contaminants in soil (primarily via incidental ingestion). This area was subject toair deposition of contaminants. Residents also were exposed to high levels of contaminants insoil on properties throughout the study area where battery chips, slag, or contaminated soils wereused as residential fill or disposed of improperly. The primary contaminants of concern includelead, arsenic, and cadmium.

Exposures to contaminants in soil were significantly reduced in 1984 and 1985 when all soil withlead levels above 1,000 ppm in the high deposition residential area and other high-use areas wasremoved. Additional remedial measures at that time, such as sodding and fencing ofunremediated areas, also reduced the potential for human exposure to contaminants in soil.

The recent remedial effort, initiated in 1991, further reduced the magnitude of exposure tocontaminants in soil. During these removal activities, contaminated soil has been removed frommost areas of the site that are readily accessible to the public, including areas where battery chipsand slag material have been identified. The ATSDR/City of Dallas exposure study which tookplace in 1993 and 1994 reports a mean soil concentration of 116 ppm in West Dallas.

Soil contamination in the residential areas of West Dallas has been reduced to a level that is notexpected to cause adverse health effects; however, human exposure to contaminants in soil maybe occurring and may occur in the future in several areas of the site. The exposed populationincludes trespassers to unremediated areas of the site, residents living on several properties whereproperty owners have refused remedial measures, and properties with soil lead levels below the500 mg/kg action level for lead. Unremediated areas also include the slag piles/dumps whichhave not yet been characterized, the former smelter facility, and other RSR property.

B. Potential Exposure Pathways

Air

Ambient air monitoring data collected while the smelter was operating did not measure levels of cadmium and arsenic; we were therefore unable to determine whether this pathway wascompleted. Although cadmium and arsenic were detected in soil near the smelter, we could notdetermine whether it was deposited from the air or associated with contaminated fill and otherdebris.

Sediment

Sampling data were unavailable for sediment in ponds, drainage ditches, and other surface watercollection areas. If runoff from contaminated areas resulted in contamination of sediments,human exposure would be possible via incidental ingestion of sediments. This exposure wouldbe most plausible for young children playing in areas with contaminated sediment. Exposurealso would be possible via consumption of contaminated fish.

Surface Water

Limited sampling by the City of Dallas found no lead contamination in surface water. Oneresident reported finding elevated levels of lead in Fish Trap Lake, but we were unable to obtaina copy of the sampling report for review. If surface water were contaminated, human exposurecould occur via incidental ingestion while playing in the water, but this type of activity isunlikely to result in significant levels of exposure.

Table 13.

Exposure Pathway Elements
PathwayNameSourceMediaPoint ofExposureRoute ofExposureExposedPopulationContaminants of ConcernTimeEstimatedNumberExposed
Completed Exposure Pathways
AirSmelterstacksAmbientairOn siteInhalationLocalresidentsOn-siteworkersLeadPast10,000
SoilSmelterstacksContaminatedfill/batterychips Slagpiles/disposal areasAirSoil/dustOn siteInhalationIngestionLocalresidents,especiallychildrenOn-siteworkersTrespassersLeadCadmiumArsenicPastPresentFuture1,000
Potential Exposure Pathways
AirSmelterAmbientairOn siteInhalationLocalresidentsOn-siteworkersCadmiumAresenicPast10,000
SedimentDrainageditches,pondsSediment FishOn siteIngestionLocalresidents,especiallychildrenLeadPresentFuture500
SurfaceWaterDrainageditches,pondsWaterOn siteIngestionLocalresidentsLeadPresentFuture500
PUBLIC HEALTH IMPLICATIONS

A. Toxicologic Evaluation

This section discusses the possible health effects that may result from exposure to specificcontaminants and the likelihood that adverse health effects will result from exposure tocontaminants at levels found on this site. The section also evaluates available health data andaddresses specific community health concerns.

To evaluate non-carcinogenic health effects, ATSDR has developed Minimal Risk Levels(MRLs) for contaminants commonly found at hazardous waste sites. The MRL is an estimate ofdaily human exposure to a contaminant below which non-cancer adverse health effects are notexpected to occur during a lifetime of exposure. MRLs are developed for each exposure, such asingestion and inhalation, and for different lengths of exposure, such as acute (less than or equalto 14 days), intermediate (15 to 364 days), and chronic (365 days or more). EPA's ReferenceDoses (RfDs) or Maximum Contaminant Levels (MCLs) are used to evaluate exposures when anMRL is not available for a specific compound.

Chemical-specific cancer slope factors and cancer unit risk factors are used to evaluatecarcinogenic health effects. EPA has developed these factors for contaminants commonly foundat hazardous waste sites to estimate the increased chance that a person exposed to contaminantswill develop cancer over the course of a lifetime.

Lead

Lead is naturally present in most soils and is widespread in the human environment as a result ofindustrialization. It is generally found in higher concentrations in urban environments,principally as a result of automobile emissions and the use of lead-based paint. The natural leadcontent of soil derived from crustal rock typically ranges from <10 to 30 parts lead per million parts soil (ppm). The concentration of lead in the top layers of soil varies widely due todeposition and accumulation of atmospheric particulates from numerous human activitiesassociated with lead pollution, including driving automobiles. For example, the concentrationsof lead in the upper layer of soil next to roadways are typically 30 to 2,000 ppm higher thannatural levels, although these levels drop drastically with increasing distance from the road [32].

Because of the prevalence of lead in the environment, humans are exposed to lead through avariety of media including air, water, and soil, as well as through diet. The relative contributionof each of these sources to total lead intake varies with age and is dependent on site-specificcharacteristics.

Preschool-age children and fetuses are usually the most vulnerable segments of the populationfor exposures to lead. This increased vulnerability results from a combination of factors whichinclude the following: 1) the developing nervous system of fetuses and neonates are moresusceptible to the neurotoxic effects of lead; 2) young children are more likely to play in dirt andto place their hands and other objects in their mouths, increasing the opportunity for soilingestion, (pica, the eating of dirt and other non-food items, also is more likely to occur inchildren); 3) the efficiency of lead absorption from the gastrointestinal tract is greater in childrenthan in adults; and 4) nutritional deficiencies of iron or calcium, which are prevalent in children,may facilitate lead absorption and exacerbate the toxic effects of lead [33].

Infants often are born with lead in their bodies due to their mother's past exposure to lead. Infants and children are exposed to lead mainly through diet and ingestion of non-food materialsassociated with normal early hand-to-mouth behavior. The degree to which hand-to-mouthbehavior contributes to blood lead levels depends on the levels of lead in house dust, soil, andpaint. In the United States, leaded paint continues to cause most of the severe lead poisoning inyoung children because it is the most widespread source and has the highest concentration oflead per unit of weight [33].

Most adults are exposed to lead from dietary sources. In some instances, occupational sourcesalso are a significant source of exposure. A great deal of information on the health effects of leadhas been obtained through years of medical observation and scientific research. Below is asummary of available toxicological information on lead.

Absorption, Metabolism, and Excretion

In adults, inorganic lead is readily absorbed through the lungs (approximately 40%), and lesswell absorbed through the gastrointestinal tract. Children absorb as much as 50% of ingestedlead. Inorganic lead is not absorbed through the skin. Absorption of lead from the lungs isdependent on the size of inhaled particulates. Particles in the range of 0.5 to 5.0 microns may bedeposited in the alveoli and absorbed. Larger particles are likely to be removed by ciliary actionand subsequently ingested.

Lead enters the bloodstream when it is first absorbed and is almost always carried bound to thered blood cell. It is distributed throughout different compartments of the body; the highestconcentrations are in bone, teeth, liver, lung, kidney, brain, and spleen. These compartments andtheir interrelations have been used in metabolic models to qualitatively and quantitativelydescribe absorption, distribution, deposition, accumulation, and excretion of lead. Although theblood contains a small portion of the total body lead burden, it is easily accessible and is thefraction that most closely correlates with recent environmental exposures. The overall half-lifeof lead in blood is estimated to be 36 days ± 5 days [32].

With prolonged exposure over time, most absorbed lead ends up in bone by substituting forcalcium in the bone matrix. Lead in bone has been estimated to represent approximately 95% ofthe total body lead burden [32] and is estimated to have a half-life as long as 10 years [34]. While lead in bone is not known to cause any harmful effects, the accumulation of lead in bonecan provide a source for remobilization of lead and continued toxicity after exposure has ceased.

Acute Toxicity

The most serious effects of acute high dose lead exposure is encephalopathy, characterizedinitially by headache and drowsiness, and in more severe cases by coma, convulsions, and death. Virtually all children who recover from acute lead encephalopathy exhibit residual reduction inintelligence and behavioral dysfunction. Acute encephalopathy is usually associated with highblood lead levels (over 150 µg/dL). Another effect of acute high dose lead exposure is theFanconi syndrome, an acute injury to the renal tubules, characterized by spillage of glucose,protein, amino acids, and phosphates into urine.

Chronic/Subchronic Toxicity

General

Chronic exposure to lead principally affects three organ systems: the hematologic system (redblood cells and their precursors), the central and peripheral nervous system, and the kidneys. Lead also has been shown to have adverse effects on the reproductive system in both males andfemales. Lead is especially harmful to unborn children. Exposure to lead during pregnancy hasbeen correlated with premature births, low birth weight infants, and spontaneous abortions. While the impact of maternal and cord blood lead levels below 10 µg/dL have not beenwell-defined, reduced gestational age and reduced birthweight have been associated with bloodlead levels of 10 to 15 µg/dL [33]. In addition, lead has been found to lower intelligencequotient (I.Q.) scores, slow growth, and cause hearing problems in children. These adverseeffects can persist and lead to decreased performance in school.

Hematologic

Anemia is the most serious effect of lead on the hematologic system. Lead-induced anemiaoccurs primarily by the lead-induced inhibition of several enzymes involved in the production ofhemoglobin. General population studies indicate that the activity of aminolevulinic aciddehydrogenase (ALAD) a heme biosynthetic enzyme is inhibited at very low blood lead levelswith no apparent threshold.

ALAD activity was inversely correlated with blood lead levels over the entire range of 3 to 34µg/dL in urban subjects never exposed occupationally [34]. Other reports have confirmed thecorrelation and apparent threshold in different age groups and exposure categories(children-[35,36]; adults-[37]). Lead begins to inhibit the enzyme ferrochelatase, whichcatalyzes the transfer of iron from ferritin into protoporphyrin to form heme, at blood lead levelsof 15 µg/dL in children and 25 to 30 µg/dL in adults. Another red blood cell enzyme,erythrocyte pyrimidine-5'-nucleotidase (EPN), is also inhibited in children at very low blood leadlevels. A significant negative linear correlation between EPN and blood lead level was seen in21 children with blood lead levels ranging from 7 to 80 µg/dL [38]. Similar findings werereported in 42 children whose blood lead levels ranged from <10 to 72 µg/dL [39].

Anemia, defined as a hematocrit of <35%, has not been observed at lead levels below 20 µg/dLalthough many of the enzymes involved in heme biosynthesis are affected at very low blood leadlevels. Heme synthesis is essential not only to hemoglobin but also to the synthesis ofcytochromes necessary for all oxidative reactions. In children, exposure to lead has been shownto inhibit formation of the heme-containing protein cytochrome P-450, as reflected in decreasedactivity of hepatic mixed-function oxygenases [40,41]. Impairment of cytochrome P-450 activitycould decrease the body's ability to detoxify other toxicants.

Central Nervous System

Chronic exposure to low lead levels has been shown to cause subtle effects on the centralnervous system which manifest as deficits in intelligence, behavior, and school performance[42]. Recent information indicates that children with blood lead levels as low as 10 µg/dL candevelop neurological and cognitive deficits [43]. Available evidence is not sufficient todetermine whether lead-associated deficits are irreversible [44].

Peripheral Nervous System

In the peripheral nervous system, lead can cause neuropathy which primarily affects the motornerves and appears to be axonal [45]. Lead targets motor axons and produces axonaldegeneration and segmental demyelination [46]. Clinically, the neuropathy is more severe in theupper extremity; in extreme cases this demyelination can produce palsy of the wrist and ankleextensor muscles, termed "wrist or ankle drop" or "painter's palsy." While the classic wrist drophas become exceedingly rare, subclinical neuropathy has been demonstrated at blood lead levelspreviously considered acceptable for workers [47]. Decreases in ulnar nerve conduction velocityare seen at blood lead levels of 30 to 40 µg/dL.

Renal

Renal effects of lead have been studied extensively in humans and animals. Exposure to lead hasbeen associated with hypertension, renal failure, and gout. Lead accumulates in the proximaltubular cells affecting urate excretion and forming densely staining intranuclear bodies. Systemic hypertension and interference with lipoprotein metabolism from lead toxicity canexacerbate chronic renal failure due to glomerular sclerosis. Exposure to high levels of lead cancause irreversible abnormalities in renal function including decreased glomerular filtration anddecreased tubular concentrating ability [48].

Cardiovascular

Information from both occupational and general population studies, including the NationalHealth and Nutrition Survey II (NHANES II), is sufficient to suggest a small but positiveassociation between blood lead levels and increased blood pressure. A simple correlationalanalysis of the NHANES II data in 1988 showed statistically significant associations betweenblood lead levels and systolic and diastolic blood pressure for both men and women, 12 to 74years of age [49]. Subsequent statistical analyses, controlling for a number of other potentiallyconfounding factors, indicated significant associations between blood lead and blood pressure inmen only. Additional analyses focusing on white men (40 to 59 years of age) revealedsignificant associations between blood lead and blood pressure, with no apparent threshold belowwhich blood lead level was not significantly related to systolic or diastolic blood pressure acrossa range of 7 to 34µg/dL [50]. Lead was a significant predictor of diastolic blood pressure greaterthan or equal to 90 mmHg, the criterion now used to define hypertension. A small but significantcorrelation between systolic blood pressure and blood lead levels also was found in a clinicalsurvey of 7,735 men between 40 and 49 years old [51,52].

Carcinogenicity

Lead has not been shown to be carcinogenic in humans; however, high doses of lead have beenfound to produce kidney tumors in laboratory studies of rats and mice. The extremely highcumulative doses of lead used in animal studies are difficult to extrapolate to low-level exposurein humans, and do not provide a sufficient basis for quantitative risk assessment. Based onanimal data, EPA currently classifies lead as a B2 carcinogen (probable human carcinogen).

Indices of Toxicity

Although no threshold level for adverse health effects has been established, evidence suggeststhat adverse effects occur at blood lead levels at least as low as 10 µg/dL. The Centers forDisease Control and Prevention (CDC) has determined that a blood lead level greater than orequal to 10 µg/dL in children indicates excessive lead absorption and constitutes the grounds forintervention. The 10 µg/dL level is based on observations of enzymatic abnormalities in the redblood cells at blood levels below 25 µg/dL and observations of neurologic and cognitivedysfunction in children with blood lead levels between 10 and 15 µg/dL [44].

The National Institute of Occupational Safety and Health (NIOSH) considers blood lead levelsabove 40 µg/dL to indicate excessive lead absorption in adults. Under regulations set forth bythe OSHA, adult workers with blood lead levels above 50 µg/dL must be removed fromoccupational lead exposure until their blood lead levels have fallen to below 40 µg/dL. It isimportant to note that although this is the regulatory standard, biological effects have beenreported at blood lead levels below this value [32].

Blood Lead/Soil Lead Relationship

A number of studies are available relating blood lead levels in children to levels of lead in theenvironment [53]. In general, blood lead levels rise 3-7 µg/dL for every 1,000 ppm increase insoil or dust lead concentration. Assuming a background blood lead level of 6.6 µg/dL, a bloodlead level of 10 µg/dL would result from soil lead levels ranging from 485 ppm to 1,133 ppm. The results of several studies, however, have indicated that the increase in blood lead as afunction of soil lead concentration is not linear. The rate of increase in blood lead levels at lowconcentrations of lead in soil is greater than at high concentrations of lead in soil. Based on datafrom exposure studies conducted at Helena Valley in Montana and Silver Valley in Idaho, aregression model for the correlation between blood lead levels and soil lead levels was derived[54]. This approach predicts that a soil lead concentration of 500 ppm would result in a bloodlead level of 10.7 µg/dL.

A great deal of information is available on the absorption, distribution, and excretion of lead bythe body. Using this information, EPA has developed an Integrated Uptake/Biokinetic Model(IU/BK Model, Version 0.5) to estimate the effects of lead intake from various sources on thepotential blood lead levels in children under age seven [52]. The IU/BK model considers themonthly uptake of lead from diet, air, soil/dust, water, and paint sources, and media specificabsorption factors to estimate monthly blood-lead intake. Using default parameters suppliedwith the model an average exposure to a soil concentration of 500 mg/kg would result in ageometric mean (average) blood lead level of 5.78 µg/dL. Using the default geometric standarddeviation of 1.42, approximately 95% of the children exposed to this soil would be expected tohave blood lead levels below 10 µg/dL.

A recent study was conducted to evaluate the effectiveness of removing lead-contaminated soilon reducing blood lead levels [55]. The study was conducted among children with blood leadlevels ranging from 10 to 20 µg/dL, living in areas with multiple potential sources of leadexposure and high soil lead levels (the soil lead level at many residence was over 3,000 ppm). An average soil lead reduction of 1,790 ppm (down to a median level of 105 ppm) wasassociated with a decline in blood lead levels of only 0.8 to 1.6 µg/dL, independent of factorssuch as water, dust, and paint levels, children's mouthing behaviors, and other characteristics.

Based on soil lead levels measured in residential areas of West Dallas prior to the most recentremedial efforts, ingestion of contaminated soil could have resulted in elevated blood lead levels. Inhalation of contaminated air when the site was active also would have contributed significantlyto elevating blood lead levels in the past. Adverse health effects from past exposures, therefore,were possible. More recent soil sampling data suggest that average soil lead levels remaining inresidential areas of West Dallas are well below 500 ppm (average remaining soil lead levelsrange from 70 ppm to 142 ppm). Exposure to these levels of lead in soil would not be expectedto result in elevated blood lead levels.

Cadmium

Small amounts of cadmium occur naturally in all soils and rocks, including coal and mineralfertilizers. In the environment, cadmium usually is not found in the metallic state, but iscombined with other elements such as oxygen, chlorine, or sulfur. Most cadmium in theenvironment is released by human activities such as mining and smelting operations, fuelcombustion, disposal of metal-containing products, and application of phosphate fertilizer orsewage sludges. Cadmium is extracted from natural materials during the production of othermetals including lead, zinc, or copper [56].

Cadmium concentrations in non-polluted soil are highly variable, depending upon sources ofminerals and organic materials. The mean level of cadmium in uncontaminated topsoil in theU.S. is approximately 0.25 ppm. Soil becomes contaminated primarily through the deposition ofairborne cadmium, landspreading of municipal sludge, and the application of phosphatefertilizers. Cadmium enters the environment through the air as a result of burning coal andhousehold waste, and metal mining and refining processes.

Food is the major source of human exposure to cadmium in the general population. Averagecadmium levels in U.S. food range from 2 to 40 parts of cadmium per billion parts of food. Adults consume approximately 30 µg of cadmium in food each day, absorbing approximately 1to 3 µg. Vegetables generally contain the highest levels of cadmium, particularly leafyvegetables and potatoes. Liver, kidney, and shellfish contain higher levels (up to 1 ppm) ofcadmium than other meat and seafood products. For populations surrounding hazardous wastesites increased exposure can result from eating fruits and vegetables grown incadmium-contaminated soil, ingestion of cadmium-contaminated dust on food or hands, andfrom the direct ingestion of soil. In highly polluted areas, the daily intake of cadmium can be ashigh as 400 µg per day [56].

Inhalation is another major source of cadmium exposure. Average concentrations in air rangefrom less than 1 to 6 nanograms per cubic meter of air (ng/m3) in rural areas and from 20 to 700ng/m3 in industrial areas. For the general population, cadmium intake by inhalation averages0.02 µg/day but can be as high as 2 µg/day in highly polluted areas. Cigarette smokers absorb anadditional 1 to 3 µg per day (based on smoking one pack of cigarettes per day). Populationssurrounding hazardous waste sites can be exposed to higher levels of cadmium throughinhalation of fugitive dust emissions from cadmium-contaminated soil.

Absorption of cadmium depends to a great extent on the route of exposure and the type ofcompound containing the cadmium. It has been estimated that only about 5% of cadmiumingested as cadmium salts is absorbed. The amount of cadmium an individual absorbs followingingestion also depends upon factors such as age, pregnancy history, method of ingestion (food,water, soil), body stores of iron, calcium, and zinc, and the presence of other dietary componentsingested with the cadmium. Absorption of cadmium from the respiratory system is quitedifferent. More than 90% of inhaled cadmium can be absorbed, depending on the in vivosolubility of the inhaled compound. The amount of cadmium that is absorbed is also affected bythe availability of the cadmium to the lung, which is largely a function of particle size. Only 5%of particles greater than 10 microns in diameter are deposited in the lung, while up to 50% ofparticles less than 0.1 micron are deposited [56].

Once cadmium is absorbed, it is bound to red blood cells and serum albumin. Serum cadmium israpidly taken up by the liver and kidney. Since the half-life of cadmium is thought to be quitelong (25 to 30 years), cadmium accumulates in these tissues. Over 50% of the body burden ofcadmium is found in the liver and kidney. It has been hypothesized that there is a criticalconcentration of cadmium in the kidney above which cadmium-induced nephropathy will occur. The placenta appears to be an effective barrier to cadmium; however, fetal exposure can occurwith high maternal exposure.

The toxic effects of chronic exposure to cadmium occur primarily in the lungs and in the kidney. Effects on the lungs are associated solely with inhalation exposure, while the kidney effects mayoccur after oral or inhalation exposures. Chronic cadmium exposure also has been associatedwith cardiovascular disease and cancer of the lung, prostate, kidney, and stomach, although theseassociations are not well established.

The chronic pulmonary effects of cadmium exposure in humans is manifested as an obstructivelung disease. Long-term inhalation exposure to cadmium may cause decreased lung function andemphysema; Pulmonary assessment of patients with long-term inhalation exposure typicallyindicates a reduced vital capacity and an increased residual lung volume. The level ofobstructive disease appears to be related to the duration and level of cadmium exposure [57,58]. Studies on the effects of cadmium exposure via inhalation are often complicated by such factorsas cigarette smoking.

Long-term exposure to cadmium can effect the kidneys, causing proximal tubular necrosis,lesions in the renal cortex, and kidney dysfunction. Common laboratory findings include thepresence of protein, amino acids, and glucose in the urine. Damage is thought to occur when therenal cortical cadmium concentration exceeds the "critical" level of 200 µg/g (wet weight) [56]. Others have proposed that for the general population, the amount of cadmium accumulated in therenal cortex should not exceed 50 µg/g, a level corresponding to a urinary excretion of 2 µg ofcadmium per 24-hours [59]. Average levels in non-occupationally exposed 50 year-olds areapproximately 15-30 µg/g (wet weight) [60]. Cigarette smoking can double renal corticalcadmium concentrations. Because of the high amount of cadmium ingested through diet, themargin of safety for exposure to cadmium from other sources is very small, particularly forsmokers.

Studies on humans occupationally exposed to cadmium in the air report a No ObservableAdverse Effects Level (NOAEL) for kidney toxicity (proteinuria) of 0.017 mg/m3 [61]. Adjusting for continuous lifetime exposure and using an uncertainty factor of 10, ATSDR hasused this NOAEL to derive an inhalation MRL of 0.0002 mg/m3.

Studies on humans orally exposed to cadmium in cadmium-polluted areas of Japan report aNOAEL for kidney toxicity (proteinuria) of 0.0021 mg/kg/day [62]. Using an uncertainty factorof 3, ATSDR has used this NOAEL to establish a chronic oral MRL of 0.0007 mg/kg/day. TheEPA used a toxicokinetic model to determine the level of chronic human oral exposure whichwould result the highest renal cadmium level not associated with significant proteinuria (200µg/gram wet weight). Assuming 2.5% absorption of cadmium from food and 5% from water, themodel predicts a NOAEL for chronic cadmium exposure of 0.005 and 0.1 mg/kg/day from waterand food, respectively. Based on these NOAELs and an uncertainty factor of 10, the EPAcalculated a chronic oral reference dose (RfD) of 0.0005 mg cadmium/kg/day for water and anequivalent RfD for cadmium in food of 0.001 mg cadmium/kg/day [63].

Substantial evidence from laboratory studies suggests that cadmium inhalation can cause lungcancer in rats, but evidence that cadmium inhalation can cause lung cancer in humans is ratherweak. Evidence for evaluating potential carcinogenicity of cadmium by the oral and dermalroutes in both animals and humans is insufficient. Based on extensive animal data and limitedhuman data associating inhalation of cadmium with lung cancer, EPA classifies cadmium as a B1carcinogen (probable human carcinogen).

In West Dallas, cadmium was detected at levels above the HAC value. Due to the cumulativenature of this toxin, however, adverse effects on the kidneys from low levels of exposure havebeen observed only after many years of exposure (i.e. fifty years). Based on availableinformation, exposure to cadmium at the levels detected in West Dallas would not be expected toproduce adverse health effects in most children and adults.

Arsenic

Arsenic is a naturally occurring element in the earth's crust, but is not common in theenvironment in elemental form. It is usually found in combination with other elements. Arseniccompounds can be classified into three main groups: 1) inorganic arsenic compounds, 2) organicarsenic compounds, and 3) arsine gas [64]. In the environment, arsenic is most often found asinorganic arsenic, which is formed when arsenic combines with other elements such as oxygen,sulfur, and chlorine. Inorganic forms of arsenic are usually more toxic than organic forms, whichare produced when arsenic forms stable bonds with carbon. Inorganic compounds are importantbecause they are the primary metabolites formed from inorganic arsenic in biological organisms. Arsine gas is the most toxic form of arsenic. In the United States, arsenic has been used ininsecticides, herbicides, desiccants in the cotton industry, wood preservatives, animal feedadditives, and more recently in the semiconductor industry. Environmental releases of arsenicare associated with application of pesticides, disposal of solid wastes, land applications ofmunicipal sludge, fossil fuel combustion, and industrial processes.

Since arsenic is a natural part of the environment, people are exposed to low levels of arsenic insoil, water, food, and air. The average adult takes in approximately 50 micrograms of arsenic perday from these sources, with food as a major contributor of total intake. Based on Food andDrug Administration (FDA) Market Basket Studies, adults ingest approximately 52.6 µg arsenicper day in food. However, since organic arsenic is the predominant form of arsenic in food, thedaily intake of inorganic arsenic from food is much lower (approximately 10-14 µg/day). Exposure to inorganic arsenic from other sources may range from 5 to 20 µg arsenic per daydepending upon the levels of arsenic in air and water. When arsenic levels in the environmentare higher than normal, greater exposure occurs. Exposure to arsenic among children living nearmetal smelters, particularly copper smelters, has also been reported [65].

Both inorganic and organic arsenic compounds are well absorbed. Over 90 percent of aningested dose of inorganic trivalent or pentavalent arsenic is absorbed. Most organic andinorganic arsenic leaves the body in urine within a few days of exposure, although some remainsin the body for several months or longer. The liver converts some arsenic to a less harmful

Very high doses of inorganic arsenic (above 60,000 ppb in food and water) can result in death.Lower levels (300 to 30,000 ppb in food or water) can cause stomach and intestinal irritation. Chronic exposure to arsenic through ingestion has been known to cause irritation of the digestivetract leading to pain, nausea, vomiting, and diarrhea. The minimal dose at which these effectsare usually observed in humans has ranged from 0.012 mg/kg/day to 0.05 mg/kg/day [66,67]. Other effects from swallowing arsenic include decreased production of red and white blood cells,abnormal heart function, blood vessel damage, and impaired nerve function causing a "pins andneedles" sensation in the hands and feet. Sensitive individuals often begin to show one or moreof the characteristic signs of arsenic poisoning at oral doses of about 0.02 mg/kg/day.

Although there is no evidence to suggest that arsenic can injure pregnant women or their fetuses,studies of animals show that doses large enough to cause illness in pregnant females may alsocause low birth weight, fetal malformations, or fetal death. The single most characteristic effectof long-term oral exposure to inorganic arsenic is a pattern of skin changes that includes adarkening of the skin similar to a corn or wart on the palms, soles, and torso [64].

EPA's reference dose for arsenic of 0.0003 mg/kg/day is based on two studies in whichhyperpigmentation, keratosis, and possible vascular complications were the critical effects[68,69]. The reference dose for arsenic was derived by dividing the estimated NOAEL for thesestudies, determined to be 0.0008 mg/kg/day, by an uncertainty factor of three to account forsensitive individuals and the lack of data on reproductive toxicity.

There is convincing evidence from a large number of epidemiologic studies and case reports thatingestion of arsenic increases the risk of developing skin cancer. The most common lesions aremultiple squamous cell carcinomas which appear to develop from hyperkeratotic warts or corns. Multiple basal cell carcinomas may also occur, usually from cells not associated withhyperkeratinization. In most cases, skin cancer develops only after prolonged exposure. However, several studies have reported skin cancer in people exposed for less than one year. Liver, bladder, kidney, and lung cancer also have been associated with exposure to arsenic, butthese associations are less well established [64].

In West Dallas, arsenic has been found at levels exceeding its HAC value. However, availabledata are insufficient to adequately assess the public health significance of this contaminant.

B. Health Outcome Data Evaluation

The following section discusses in greater detail the data presented previously in this document under the heading of Health Outcome Data.

Data indicate that blood lead levels among children in the West Dallas area have declinedsignificantly since 1982 when the first comprehensive blood lead study was conducted in thearea. In 1982, the mean blood lead level of 269 randomly-selected preschool children livingwithin one-half mile of the RSR Smelter was 20.1 µg/dL, with ten percent of children having blood lead levels greater than or equal to 30 µg/dL. These blood lead levels were high enough to be associated with effects on the central nervous system, which manifest as deficits in intelligence, behavior, and school performance, as well as subtle effects on the blood and the kidneys [44]. We were unable to evaluate the prevalence of these specific conditions which mayhave resulted from chronic exposure to lead in West Dallas because many of the effects are notreadily measurable and are associated with multiple potential causes.

In contrast to historical exposure data, the 1993 lead exposure study found that the average bloodlead level of 305 randomly-selected West Dallas preschool children was 5.5 µg/dL, with 26children (8.5 percent) having blood lead levels greater than or equal to 10 µg/dL (Table 14). Themaximum blood lead level measured in 1993 was below the average blood lead level measuredin 1982. In the 1993 study, blood lead levels observed among West Dallas children differed onlyslightly from blood lead levels of children in the Oak Cliff neighborhood, which served as acomparison community. The mean blood lead level of children in the comparison communitywas 5.4 µg/dL and 4.9 percent of tests were greater than or equal to 10 µg/dL.

In the 1992 study, the highest mean blood lead level (7.0 µg/dL) and the largest proportion ofchildren with elevated blood lead levels (10 of 53 children) in a single subarea were observed inArea 1. Although this area includes the residences nearest the smelter in the high air dispersionarea, the mean soil lead level reported for this area was only 126 ppm. The study did not find arelationship between blood lead concentrations and lead concentrations in residential soil, homedust, or other environmental media. The reason for the remaining elevated blood lead levels inthis area should be further explored.

The 1982 and 1993 exposure studies provide the most extensive information about lead exposureamong West Dallas children since each study includes a randomly-selected study group fromwithin the defined area of concern as well as environmental exposure data. Recent data collectedat Walk-in Clinics and by the EPSDT program are more difficult to interpret since they were notcollected randomly and do not include exposure data; but these data provide additional evidencethat lead levels among West Dallas children have decreased significantly in recent years (Table14).

Blood lead data collected at Walk-in Clinics are difficult to interpret since individuals may havebeen tested because they susp

Table 14.

Comparison of 1982 and 1993 Blood Lead Data for Randomly-Selected
West Dallas Children [17, 22]
Source of Data Elevated Tests Mean Blood Lead Level
(µg/dL)
10 µg/dL 30 µg/dL
# elevated/
# tested
percent
elevated
# elevated/
# tested
percent
elevated
1982 Lead Study na na 26/269 10 20.1
1993 Lead Exposure Study 26/305 8.5 na na 7.0

ected that exposure to lead had occurred; therefore blood lead levels reported by these clinics may not reflect blood lead levels found in the general population. Although the City of Dallas began to offer free-of-charge blood lead screening tests at voluntary walk-in clinics in 1984 for all residents of the West Dallas area, the earliest data from this program available for review were collected in 1991. Two periods of blood lead summary data were reviewed (July through December 1991 and July 1992 through December 1993). Among the 110 tests reported during the 1991 period for City of Dallas Walk-in Clinics, 33 children (30 percent) had elevated blood lead levels (10 µg/dL). These tests are particularly difficult to generalize to the larger population because the total number of West Dallas residents tested (110) was small. In the 1992/93 report, 158 (13.9 percent) of the 1,138 West Dallas children ages six and under who were tested at City of Dallas walk-in clinics had elevated blood lead levels (Table 15).

Table 15.

Comparison of Recent Blood Lead Data from West Dallas and
Other Areas of Dallas [17, 22]
West DallasOther Dallas
Source of DataNumber10 µg/dL
per numbertested
Percent
10 µg/dL
Number10µg/dL
per numbertested
Percent10 µg/dL
1992-1993 Walk-in Clinic
1993 EPSDT Program
158/1,138
125/1,126
13.9
11.1
59/486
330/5,361
17.9
9.1

While these walk-in clinic data may not accurately reflect rates of elevated blood lead levels inWest Dallas or in Dallas as a whole, it is unlikely that results underestimate the significance oflead as a public health problem in West Dallas compared with the rest of the city. Whencompared with blood lead results of residents from other parts of Dallas, the 1992/3 reportindicates that the mean blood lead levels of West Dallas residents tested during this period inWalk-in clinics was comparable or slightly higher than the mean blood lead level of other Dallasresidents tested during this period in every age group. These data also indicate that averageblood lead levels of children tested in walk-in clinics were significantly lower than levels foundthrough random testing in 1982.

The 1992/93 Walk-in Clinic data include the only available blood lead levels reported separatelyfor pregnant women. These data indicate that the mean blood lead level of the 19 pregnantwomen residing in West Dallas area who were tested was 3.5 µg/dL. The maximum blood leadlevel observed among these pregnant women was 8.0 µg/dL. While the impact of maternal andcord blood lead levels below 10 µg/dL have not been well defined, known fetal effects includingreduced gestational age and reduced weight at birth have not been associated with the blood leadlevels observed among West Dallas women [33].

Data collected through the EPSDT program during the period between January and June 1993also indicate that blood lead levels were not substantially different among West Dallas childrenand children from other parts of Dallas (Table 15). Among children living in West Dallas,approximately 11 percent had elevated blood lead levels, while approximately 9 percent ofchildren from other parts of Dallas had elevated blood lead levels (10 µg/dL).

Despite the historical reduction of blood lead levels in the West Dallas area demonstrated by allavailable blood lead data, a number of children continue to have elevated blood lead levels. Although these data do not indicate that elevated blood lead levels are associated withidentifiable environmental factors, we cannot identify, with certainty, the source of leadexposure.

C.Community Health Concerns Evaluation

We have addressed the community concerns about health as follows.

  1. Why is so much attention still focused on children?

Children in West Dallas are of particular concern because children experience many of theadverse health effects associated with lead at lower levels of exposure than adults. The increasedvulnerability of children results from a combination of factors: 1) the developing nervous systemis more susceptible to neurotoxic effects of lead; 2) young children are more likely than adults toexperience higher exposures to lead in soil, dust, and paint because of normal earlyhand-to-mouth behavior (pica, the eating of dirt and other non-food material, is also more likelyto occur among children); 3) children absorb lead more efficiently from the gastrointestinal tractthan adults; and 4) nutritional deficiencies of iron or calcium, which are prevalent in children,may increase the amount of lead that the body absorbs through the gastrointestinal tract. At theRSR site, children also may have been exposed to higher levels of cadmium and arsenic thanadults because of their frequent outdoor play and normal hand-to-mouth behavior.

  1. Should we be concerned about health effects among the residents who grew up in West Dallas and were exposed to lead all of their lives? Are they likely to develop illnesses resulting from their exposure to lead?

Residents who experienced exposure to lead during childhood are not likely to develop illnesseslater in life as a result of past exposure. When lead enters the human body, it travels to the softtissues, such as the liver, kidneys, lungs, brain, spleen, muscles, and heart. In adults, about 99%of lead that is taken in leaves the body in the waste within a couple of weeks; in children, about32% of lead is eliminated within a couple of weeks. Lead that remains in the body can be storedin the bones and teeth up to several decades, but lead stored in the body has no known healtheffects. The accumulation of lead in bone can provide a source for remobilization of lead toother parts of the body, but because the amount of lead remobilized is small, stored lead isunlikely to cause adverse health effects after exposure has ceased. According to availableinformation, only individuals with very high exposures (i.e. exposures indicated by blood leadlevels over 50 µg/dL) are at risk of continued toxicity after exposure has ceased.

Blood lead levels measure lead from both remobilized lead and lead from current exposures. Measures of blood lead level are easily obtainable with a blood lead test. If current blood leadlevels are not elevated (above 10 µg/dL for children and approximately 25 µg/dL for adults)adverse health effects should not be expected.

Since the past exposure levels of any given individual who grew up in West Dallas cannot bedetermined, it is difficult to know whether adverse health effects occurring in individuals are theresult of past exposures to lead. Many of the outcomes associated with lead exposure (such aseffects on kidneys, blood, and central nervous system, and particularly those associated withcognitive and physical development) that could occur at blood lead levels observed among WestDallas residents in the past are subtle and difficult to measure. These outcomes also can beassociated with many factors other than lead. While exposure to the levels of lead observed inWest Dallas in the past may have caused adverse health effects, residents who grew up in WestDallas are not likely to develop new illnesses resulting from their past exposure to lead.

Much of the published information about long-term effects of lead exposure has focused onpeople whose primary exposures occurred at work and who had chronically elevated blood leadlevels in the range of 50 to 60 µg/dL or higher. These blood lead levels have been associatedwith a general increased risk for developing kidney problems after many years of exposure. Some laboratory evidence suggests that effects on the kidneys can occur at blood lead levelsbelow this range, but there is no evidence that clinical illnesses or symptoms that could bedetected by a physician will occur. The blood lead levels reported among West Dallas residentswould not be expected to be associated with these types of problems. Studies of individuals whohave experienced lead levels below approximately 20 to 30 µg/dL generally do not indicate anyadditional risk for developing illnesses years after exposure.

  1. Should individuals with high blood lead levels be tracked for follow-up medical treatment?

Yes. Children with blood lead levels in the range of 10 to 14 µg/dL should be retested with avenous blood test to insure that the blood lead level does not increase. Adverse effects of bloodlead levels in this range are subtle and are not likely to be clinically recognizable or measurablein an individual child. Although an environmental history should be taken to determine anyobvious remediable source of lead, it is unlikely that there is a single predominant source ofexposure for these children.

Children with blood lead levels in the 15-19 µg/dL range need more careful follow-up. Thislevel of exposure indicates risk for decreased in IQ of up to several points and other subtleeffects. Parents and health care providers should seek interventions to reduce possible blood leadexposures among children with these levels. If levels persist at or above 15 µg/dL,environmental investigation and appropriate remediation should be completed.

Children with venous blood lead levels between 20 and 69 µg/dL should have a full medicalevaluation including a detailed environmental and behavioral history, physical examination, andtests for iron deficiency. The most important factor in managing childhood lead poisoning isreducing the child's exposure to lead, but some children with higher blood lead levels will benefitfrom chelation (treatment with oral medication that must be supervised by a physician). Health-care providers with limited experience in treating lead poisoning should considerreferring children needing urgent medical follow-up (those with blood lead levels 45 µg/dL), to aclinic with experience managing childhood lead poisoning.

Blood lead levels greater than or equal to 70 µg/dL in children constitute a medical emergency,requiring in-patient chelation therapy. The patient preferably must be managed by someone withexperience in treating children who are critically ill with lead poisoning. Medical andenvironmental management must begin immediately.

Medical follow-up generally is necessary for adults who experience significantly higher leadexposures than children. The CDC recommends retesting and monitoring for adults with bloodlead levels of 25 µg/dL and above. The Occupational Health and Safety Administration (OSHA)recommends that adults working around potential sources of exposure to lead receive annualblood lead screening tests and that medical consultations be obtained for workers with blood leadlevels above 40 µg/dL. OSHA requires medical removal for workers with blood lead levels of50 µg/dL.

More stringent medical guidelines should apply to pregnant women because of the unique risksassociated with fetal exposure to lead. Maternal blood lead levels between 10 and 15 µg/dL havebeen associated with fetal effects. In addition, effects on miscarriage rates and the ability tobecome pregnant have been detected among women with blood lead levels between 10 and 15µg/dL.

  1. Can residents be provided with free medical help for pollution-related illnesses?

Neither TDH nor ATSDR have resources to provide free medical assistance to citizens withpollution-related illnesses. If resources were available, it would be difficult to: a) diagnosemany illnesses and conditions which could be related to pollutants at this site; b) determinewhether the level of pollution to which an individual patient was exposed in the past wassufficient to cause illness; and 3) determine with certainty whether the diagnosed illness wascaused by the specific past exposure.

Lead is the principal pollutant identified at the RSR site at sufficient levels for causingpollution-related illnesses. While severe lead exposure in children (blood lead levels80 µg/dL)can cause coma, convulsions, and even death, the primary effects associated with lower levels oflead exposure, such as the levels observed among West Dallas residents, are much more subtleand difficult to measure. These outcomes include adverse effects on the central nervous system,kidneys, and blood. All of these effects can be associated with multiple causes and risk factors.

  1. Could exposure to lead in the environment during pregnancy cause learning disabilities and hearing problems for the unborn child?

Yes. In several, but not all studies, prenatal exposures have been associated with slowersensory-motor and delayed early cognitive development. One study suggests that with lowpostnatal exposures and favorable socioeconomic conditions, some of these early associationsmay decrease as children grow older.

  1. Is EPA's 500 ppm clean-up level adequate to protect public health?

Yes, while there is general agreement that children's exposure to lead should be reduced as much as possible, evidence from various sources suggests that under typical exposure scenarios,average soil lead concentrations of 500 ppm and less do not represent a threat to public health. In West Dallas, all available blood lead data suggest that the 500 ppm clean-up level has beenadequate to protect public health. The recent Biological Indicators of Exposure Study in WestDallas did not find any association between blood lead levels and remaining soil leadconcentrations.

It is also important to note that the clean-up level itself does not represent the average level oflead remaining in soil and that the average level of lead in soil is a more accurate reflection ofpotential exposure than the clean-up level. While the West Dallas clean-up level was 500 ppm,the most recent soil sampling results, collected in conjunction with the 1993 exposure study,indicate that average concentrations of lead remaining in soil were much lower than 500 ppm. The study reported remaining lead concentrations in residential areas for each subarea (1-4) ofthe study as follows: Area 1/high air dispersion area, 126 ppm; Area 2/eastern low air dispersionarea, 119 ppm; Area 3/western low air dispersion area, 70 ppm; and Area 4/area with slag orbattery chips, 142 ppm. The highest average soil concentration was found in the Oak Cliffcomparison community (148 ppm).

Next Section         Table of Contents

 
Source of DataElevated TestsMean BloodLead Level
(g/dL
)
10 g/dL30 g/dL
# elevated/
# tested
percent
elevated
# elevated/
# tested
percent
elevated
1982 Lead Studynana26/2691020.1
1993 Lead ExposureStudy26/3058.5nana7.0

Blood lead data collected at Walk-in Clinics are difficult to interpret since individuals may havebeen tested because they suspected that exposure to lead had occurred; therefore blood leadlevels reported by these clinics may not reflect blood lead levels found in the general population. Although the City of Dallas began to offer free-of-charge blood lead screening tests at voluntarywalk-in clinics in 1984 for all residents of the West Dallas area, the earliest data from thisprogram available for review were collected in 1991. Two periods of blood lead summary datawere reviewed (July through December 1991 and July 1992 through December 1993). Amongthe 110 tests reported during the 1991 period for City of Dallas Walk-in Clinics, 33 children (30percent) had elevated blood lead levels (10 g/dL). These tests are particularly difficult togeneralize to the larger population because the total number of West Dallas residents tested (110)was small. In the 1992/93 report, 158 (13.9 percent) of the 1,138 West Dallas children ages sixand under who were tested at City of Dallas walk-in clinics had elevated blood lead levels (Table15).

TABLE 15 - Comparison of Recent Blood Lead Data from West Dallas and
Other Areas of Dallas [17, 22]

West DallasOther Dallas
Source of DataNumber10 g/dL
per numbertested
Percent
10 g/dL
Number10g/dL
per numbertested
Percent10 g/dL
1992-1993 Walk-in Clinic
1993 EPSDT Program
158/1,138
125/1,126
13.9
11.1
59/486
330/5,361
17.9
9.1

While these walk-in clinic data may not accurately reflect rates of elevated blood lead levels inWest Dallas or in Dallas as a whole, it is unlikely that results underestimate the significance oflead as a public health problem in West Dallas compared with the rest of the city. Whencompared with blood lead results of residents from other parts of Dallas, the 1992/3 reportindicates that the mean blood lead levels of West Dallas residents tested during this period inWalk-in clinics was comparable or slightly higher than the mean blood lead level of other Dallasresidents tested during this period in every age group. These data also indicate that averageblood lead levels of children tested in walk-in clinics were significantly lower than levels foundthrough random testing in 1982.

The 1992/93 Walk-in Clinic data include the only available blood lead levels reported separatelyfor pregnant women. These data indicate that the mean blood lead level of the 19 pregnantwomen residing in West Dallas area who were tested was 3.5 g/dL. The maximum blood leadlevel observed among these pregnant women was 8.0 g/dL. While the impact of maternal andcord blood lead levels below 10 g/dL have not been well defined, known fetal effects includingreduced gestational age and reduced weight at birth have not been associated with the blood leadlevels observed among West Dallas women [33].

Data collected through the EPSDT program during the period between January and June 1993also indicate that blood lead levels were not substantially different among West Dallas childrenand children from other parts of Dallas (Table 15). Among children living in West Dallas,approximately 11 percent had elevated blood lead levels, while approximately 9 percent ofchildren from other parts of Dallas had elevated blood lead levels (10 g/dL).

Despite the historical reduction of blood lead levels in the West Dallas area demonstrated by allavailable blood lead data, a number of children continue to have elevated blood lead levels. Although these data do not indicate that elevated blood lead levels are associated withidentifiable environmental factors, we cannot identify, with certainty, the source of leadexposure.

C.Community Health Concerns Evaluation

We have addressed the community concerns about health as follows.

  1. Why is so much attention still focused on children?

Children in West Dallas are of particular concern because children experience many of theadverse health effects associated with lead at lower levels of exposure than adults. The increasedvulnerability of children results from a combination of factors: 1) the developing nervous systemis more susceptible to neurotoxic effects of lead; 2) young children are more likely than adults toexperience higher exposures to lead in soil, dust, and paint because of normal earlyhand-to-mouth behavior (pica, the eating of dirt and other non-food material, is also more likelyto occur among children); 3) children absorb lead more efficiently from the gastrointestinal tractthan adults; and 4) nutritional deficiencies of iron or calcium, which are prevalent in children,may increase the amount of lead that the body absorbs through the gastrointestinal tract. At theRSR site, children also may have been exposed to higher levels of cadmium and arsenic thanadults because of their frequent outdoor play and normal hand-to-mouth behavior.

  1. Should we be concerned about health effects among the residents who grew up in West Dallas and were exposed to lead all of their lives? Are they likely to develop illnesses resulting from their exposure to lead?

Residents who experienced exposure to lead during childhood are not likely to develop illnesseslater in life as a result of past exposure. When lead enters the human body, it travels to the softtissues, such as the liver, kidneys, lungs, brain, spleen, muscles, and heart. In adults, about 99%of lead that is taken in leaves the body in the waste within a couple of weeks; in children, about32% of lead is eliminated within a couple of weeks. Lead that remains in the body can be storedin the bones and teeth up to several decades, but lead stored in the body has no known healtheffects. The accumulation of lead in bone can provide a source for remobilization of lead toother parts of the body, but because the amount of lead remobilized is small, stored lead isunlikely to cause adverse health effects after exposure has ceased. According to availableinformation, only individuals with very high exposures (i.e. exposures indicated by blood leadlevels over 50 g/dL) are at risk of continued toxicity after exposure has ceased.

Blood lead levels measure lead from both remobilized lead and lead from current exposures. Measures of blood lead level are easily obtainable with a blood lead test. If current blood leadlevels are not elevated (above 10 g/dL for children and approximately 25 g/dL for adults)adverse health effects should not be expected.

Since the past exposure levels of any given individual who grew up in West Dallas cannot bedetermined, it is difficult to know whether adverse health effects occurring in individuals are theresult of past exposures to lead. Many of the outcomes associated with lead exposure (such aseffects on kidneys, blood, and central nervous system, and particularly those associated withcognitive and physical development) that could occur at blood lead levels observed among WestDallas residents in the past are subtle and difficult to measure. These outcomes also can beassociated with many factors other than lead. While exposure to the levels of lead observed inWest Dallas in the past may have caused adverse health effects, residents who grew up in WestDallas are not likely to develop new illnesses resulting from their past exposure to lead.

Much of the published information about long-term effects of lead exposure has focused onpeople whose primary exposures occurred at work and who had chronically elevated blood leadlevels in the range of 50 to 60 g/dL or higher. These blood lead levels have been associatedwith a general increased risk for developing kidney problems after many years of exposure. Some laboratory evidence suggests that effects on the kidneys can occur at blood lead levelsbelow this range, but there is no evidence that clinical illnesses or symptoms that could bedetected by a physician will occur. The blood lead levels reported among West Dallas residentswould not be expected to be associated with these types of problems. Studies of individuals whohave experienced lead levels below approximately 20 to 30 g/dL generally do not indicate anyadditional risk for developing illnesses years after exposure.

  1. Should individuals with high blood lead levels be tracked for follow-up medical treatment?

Yes. Children with blood lead levels in the range of 10 to 14 g/dL should be retested with avenous blood test to insure that the blood lead level does not increase. Adverse effects of bloodlead levels in this range are subtle and are not likely to be clinically recognizable or measurablein an individual child. Although an environmental history should be taken to determine anyobvious remediable source of lead, it is unlikely that there is a single predominant source ofexposure for these children.

Children with blood lead levels in the 15-19 g/dL range need more careful follow-up. Thislevel of exposure indicates risk for decreased in IQ of up to several points and other subtleeffects. Parents and health care providers should seek interventions to reduce possible blood leadexposures among children with these levels. If levels persist at or above 15 g/dL,environmental investigation and appropriate remediation should be completed.

Children with venous blood lead levels between 20 and 69 g/dL should have a full medicalevaluation including a detailed environmental and behavioral history, physical examination, andtests for iron deficiency. The most important factor in managing childhood lead poisoning isreducing the child's exposure to lead, but some children with higher blood lead levels will benefitfrom chelation (treatment with oral medication that must be supervised by a physician). Health-care providers with limited experience in treating lead poisoning should considerreferring children needing urgent medical follow-up (those with blood lead levels 45 g/dL), to aclinic with experience managing childhood lead poisoning.

Blood lead levels greater than or equal to 70 g/dL in children constitute a medical emergency,requiring in-patient chelation therapy. The patient preferably must be managed by someone withexperience in treating children who are critically ill with lead poisoning. Medical andenvironmental management must begin immediately.

Medical follow-up generally is necessary for adults who experience significantly higher leadexposures than children. The CDC recommends retesting and monitoring for adults with bloodlead levels of 25 g/dL and above. The Occupational Health and Safety Administration (OSHA)recommends that adults working around potential sources of exposure to lead receive annualblood lead screening tests and that medical consultations be obtained for workers with blood leadlevels above 40 g/dL. OSHA requires medical removal for workers with blood lead levels of50 g/dL.

More stringent medical guidelines should apply to pregnant women because of the unique risksassociated with fetal exposure to lead. Maternal blood lead levels between 10 and 15 g/dL havebeen associated with fetal effects. In addition, effects on miscarriage rates and the ability tobecome pregnant have been detected among women with blood lead levels between 10 and 15g/dL.

  1. Can residents be provided with free medical help for pollution-related illnesses?

Neither TDH nor ATSDR have resources to provide free medical assistance to citizens withpollution-related illnesses. If resources were available, it would be difficult to: a) diagnosemany illnesses and conditions which could be related to pollutants at this site; b) determinewhether the level of pollution to which an individual patient was exposed in the past wassufficient to cause illness; and 3) determine with certainty whether the diagnosed illness wascaused by the specific past exposure.

Lead is the principal pollutant identified at the RSR site at sufficient levels for causingpollution-related illnesses. While severe lead exposure in children (blood lead levels80 g/dL)can cause coma, convulsions, and even death, the primary effects associated with lower levels oflead exposure, such as the levels observed among West Dallas residents, are much more subtleand difficult to measure. These outcomes include adverse effects on the central nervous system,kidneys, and blood. All of these effects can be associated with multiple causes and risk factors.

  1. Could exposure to lead in the environment during pregnancy cause learning disabilities and hearing problems for the unborn child?

Yes. In several, but not all studies, prenatal exposures have been associated with slowersensory-motor and delayed early cognitive development. One study suggests that with lowpostnatal exposures and favorable socioeconomic conditions, some of these early associationsmay decrease as children grow older.

  1. Is EPA's 500 ppm clean-up level adequate to protect public health?

Yes, while there is general agreement that children's exposure to lead should be reduced as much as possible, evidence from various sources suggests that under typical exposure scenarios,average soil lead concentrations of 500 ppm and less do not represent a threat to public health. In West Dallas, all available blood lead data suggest that the 500 ppm clean-up level has beenadequate to protect public health. The recent Biological Indicators of Exposure Study in WestDallas did not find any association between blood lead levels and remaining soil leadconcentrations.

It is also important to note that the clean-up level itself does not represent the average level oflead remaining in soil and that the average level of lead in soil is a more accurate reflection ofpotential exposure than the clean-up level. While the West Dallas clean-up level was 500 ppm,the most recent soil sampling results, collected in conjunction with the 1993 exposure study,indicate that average concentrations of lead remaining in soil were much lower than 500 ppm. The study reported remaining lead concentrations in residential areas for each subarea (1-4) ofthe study as follows: Area 1/high air dispersion area, 126 ppm; Area 2/eastern low air dispersionarea, 119 ppm; Area 3/western low air dispersion area, 70 ppm; and Area 4/area with slag orbattery chips, 142 ppm. The highest average soil concentration was found in the Oak Cliffcomparison community (148 ppm).

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