• Home
• About ATSDR
• Press Room
• A-Z Index
• Glossary
• Employment
• Contact Us
• CDC

ATSDR en Español

Search:

Skip directly to: content | left navigation | search

---

Find a Publication

1. ATSDR > Public Health Assessments & Consultations

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 were selected by comparing contaminant concentrations to health assessment comparison (HAC) values for non-carcinogenic endpoints and carcinogenic endpoints. HAC values are media specific 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 Toxic Substances and Disease Registry's (ATSDR's) minimal risk levels (MRLs), EPA's reference doses (RfDs), or other non-carcinogenic health-based values. CREGs are HAC values based on EPA's chemical specific cancer slope factors and an estimated excess lifetime cancer risk of one-in-one-million persons.

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

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 the presence of lead, cadmium, and arsenic in soil. HAC values for these contaminants in soil are listed in Table 6.

TABLE 6 - Health Assessment Comparison Values For Contaminants of Concern in Soil

Contaminant	HAC Value (ppm)		Non-cancer HAC Value Source
	Non-cancer	CREG1
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 lead emitted 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 be quite high throughout the 1970s, even after primary point source controls and initial sanitary emission controls had been implemented [4].

A special enforcement study was conducted during a 30-day period in March 1973 by the City in preparation 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 at the fenceline of RSR averaged 44.6 µg/m³ and the upwind fenceline concentration averaged 20.9 µg/m³. (According to descriptions of the sampling locations, the "upwind" measurement actually was collected between portions of the smelter complex and therefore reflects contaminant levels associated 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 1982 when the EPA installed three 24-hour ambient air monitors. The results of air monitoring for the second quarter of 1982 are presented in Table 7 below. This monitoring was conducted prior to the closure of the RSR smelter facility and after the smelter had implemented the most comprehensive emission controls in its history of operation. Two of the monitors measured lead levels 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 of monitoring 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]

NAAQS = National Ambient Air Quality Standard.

Surface Soil

Soil samples have been collected during various periods over the past 12 years. We reviewed samples 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 in chronological order.

The first soil samples were collected at this site in 1982 as part of the Dallas Area Lead Assessment Study. Sampling included soil grid sampling (750-feet grids) within a one-mile radius of the RSR Smelter. Analysis of the grid sampling produced isopleths (lines on the map showing the pattern of lead contamination in soil) consistent with the predominant wind direction from 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 at approximately one-half mile). The mean lead concentration of soil in residential yards within one-half mile of the smelter was 826 ppm; the mean soil lead concentration in yards located between one-half mile and one mile of the smelter was 192 ppm. In 1982, the overall mean soil lead concentration of all yards sampled within one mile of the smelter was 489 ppm [17]. Lead levels 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 areas within one-half mile of the smelter. Soil was removed to a depth of six inches, replaced with seven 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 of the smelter where soil was not removed [1,6]. Soil sampling data characterizing the site after removal were not available for review.

In 1991, TWC analyzed battery chips, slag material, and contaminated soil discovered by West Dallas 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 a survey form [25].

Table 8 is a compilation of the results of soil sampling conducted by EPA from August 1991 through April 1993 and by TWC from September 8 through October 28, 1992 and February 23 through March 16, 1993. Sample concentrations represent soil contamination resulting from air deposition as well as the use of contaminated soil, slag, and battery chips as fill [26]. Only a small percentage of samples were highly elevated and many were below detection limits, as evidenced 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 measured concentration.

TABLE 8 - Contaminant Concentrations in Soil 1993 EPA Database¹ [26]

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 greater than 500 ppm were remediated. This removal action included properties within the high air deposition area and all properties identified as high risk areas for children. In June 1993, EPA began 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 ppm was removed and replaced with clean fill [27].

Sampling collected during removal efforts indicated that lead exceeded action levels on most properties, 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 of battery chips and/or slag and in the yards of residents who requested sampling. This table reports the 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 cadmium levels 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 Trap Lake, which is three-fourths of a mile northeast of the RSR Smelter [14,18]. According to a 1992 ATSDR Public Health Consultation, a West Dallas resident stated that samples he had taken from Fish Trap Lake have shown elevated lead levels, but the citizen's data were not available for review. Additional surface water and sediment sampling data were not available for this site.

TABLE 9 - Contaminant Concentrations in Soil Samples Collected Where
Battery Chips/Slag Were Observed¹ [29]

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 all individuals with elevated blood lead levels identified at City of Dallas Walk-in Clinics (children with15 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 any of the measured parameters and observed blood lead levels; however, paint, which is commonly the most significant source of childhood residential lead exposure, was tested for lead in only three 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 1993 Biological Indicators of Exposure Study. This study provided more comprehensive environmental data than the Walk-in Clinic data and included soil, dust, water, and indoor and outdoor paint sampling at the homes of the 305 West Dallas study participants. Environmental samples also were collected in the homes of 81 children from a comparison community. A summary of the environmental sampling results are provided in Table 11.

As part of this study, 374 composite soil samples were collected from yards. The average concentration of lead in soil ranged from 70 ppm (in the "eastern low air dispersion area") up to 148 ppm (in the comparison community).

In West Dallas, 576 dust samples were collected from children's bedrooms and the entryways of homes; in the comparison community, 323 dust samples were collected from children's bedrooms and the entryways of homes. The average concentration of lead in dust samples collected in children's bedrooms ranged from 80 ppm (in the area of West Dallas where chips and slag had been 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) to 205 ppm (in the comparison community).

Approximately 386 indoor paint samples were collected. Approximately 9.6% of homes had contaminated paint on at least one indoor surface and the percentage of homes with contaminated paint ranged from 5.7% (in the homes where battery chips were used as yard fill) up to 16.1% (in the 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 low air dispersion area) up to 45.7% (in the comparison area).

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

All of the environmental sampling results were compared with the blood lead levels of children living 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]

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]

Other Sources of Contamination on Site

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

According to TRI data, the Murmur Corporation released 500 pounds of lead between 1987 and 1991. These emissions were reported by Murmur in association with its active reclamation and recycling operation at the site; however, Murmur reported these releases to EPA under the category of environmental losses between 11 and 500 pounds per year and the actual amount that was released may be much less than 500 pounds. According to EPA, in 1993 the company estimated 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 above the National Ambient Air Quality Standard since 1984 when the smelter closed. We will thoroughly evaluate the levels of lead contamination remaining on the smelter property when we address 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 site were 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]

C. Quality Assurance and Quality Control

The EPA has approved all quality assurance and quality control (QA/QC) criteria contained in the referenced documents. In preparing this Health Assessment, TDH staff members relied on the information provided in the referenced documents and assumed that adequate QA/QC measures were followed with regard to chain-of-custody, laboratory procedures, and data reporting. The analyses and conclusions in this Health Assessment are valid only if the referenced 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 an adequate characterization of existing physical hazards. The buildings and facilities formerly associated with the RSR Corporation smelter are old and in poor condition; areas of the RSR property where slag, battery chips, and other waste materials may have been disposed have not been fully characterized; and the solid waste surface impoundment associated with RSR has not yet been remediated. These remaining structures and areas could present physical hazards if the areas were accessible to the public. To our knowledge, public access to the smelter and its associated facilities is effectively prohibited.

PATHWAYS ANALYSES

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

Exposure pathways are categorized as completed, potential, or eliminated. For a person to be exposed to a contaminant, the exposure pathway must be completed. An exposure pathway is considered to be completed when all five elements in the pathway are present and exposure has occurred, is occurring, or will occur in the future. An exposure pathway is considered to be a potential pathway when at least one of the five elements is missing but may be present in the future. An exposure pathway is eliminated when one or more elements are missing and will never be present to complete the pathway. Completed and potential exposure pathways at this site are presented in Table 12. Inclusion of a pathway in the table does not imply that the pathway presents a risk to public health. An evaluation of the public health significance of each pathway 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 to lead has occurred through the inhalation of contaminated air. The pattern of soil lead concentrations that resulted from air deposition of lead suggests that exposures most likely occurred north and northwest of the smelter in the direction of prevailing winds. Individuals who were 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 Corporation Smelter before 1984 while the smelter was operating. Approximately 10,000 people were potentially exposed through this pathway.

Although historical air sampling data were limited, exposure to lead through inhalation of contaminated 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 were exposed to site contaminants in soil (primarily via incidental ingestion). This area was subject to air deposition of contaminants. Residents also were exposed to high levels of contaminants in soil on properties throughout the study area where battery chips, slag, or contaminated soils were used as residential fill or disposed of improperly. The primary contaminants of concern include lead, arsenic, and cadmium.

Exposures to contaminants in soil were significantly reduced in 1984 and 1985 when all soil with lead levels above 1,000 ppm in the high deposition residential area and other high-use areas was removed. Additional remedial measures at that time, such as sodding and fencing of unremediated 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 to contaminants in soil. During these removal activities, contaminated soil has been removed from most areas of the site that are readily accessible to the public, including areas where battery chips and slag material have been identified. The ATSDR/City of Dallas exposure study which took place 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 not expected to cause adverse health effects; however, human exposure to contaminants in soil may be occurring and may occur in the future in several areas of the site. The exposed population includes trespassers to unremediated areas of the site, residents living on several properties where property owners have refused remedial measures, and properties with soil lead levels below the 500 mg/kg action level for lead. Unremediated areas also include the slag piles/dumps which have 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 was completed. Although cadmium and arsenic were detected in soil near the smelter, we could not determine whether it was deposited from the air or associated with contaminated fill and other debris.

Sediment

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

Surface Water

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

TABLE 13 - Exposure Pathway Elements

PUBLIC HEALTH IMPLICATIONS

A. Toxicologic Evaluation

This section discusses the possible health effects that may result from exposure to specific contaminants and the likelihood that adverse health effects will result from exposure to contaminants at levels found on this site. The section also evaluates available health data and addresses 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 of daily human exposure to a contaminant below which non-cancer adverse health effects are not expected to occur during a lifetime of exposure. MRLs are developed for each exposure, such as ingestion and inhalation, and for different lengths of exposure, such as acute (less than or equal to 14 days), intermediate (15 to 364 days), and chronic (365 days or more). EPA's Reference Doses (RfDs) or Maximum Contaminant Levels (MCLs) are used to evaluate exposures when an MRL is not available for a specific compound.

Chemical-specific cancer slope factors and cancer unit risk factors are used to evaluate carcinogenic health effects. EPA has developed these factors for contaminants commonly found at hazardous waste sites to estimate the increased chance that a person exposed to contaminants will 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 of industrialization. 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 lead content 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 to deposition and accumulation of atmospheric particulates from numerous human activities associated with lead pollution, including driving automobiles. For example, the concentrations of lead in the upper layer of soil next to roadways are typically 30 to 2,000 ppm higher than natural 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 a variety of media including air, water, and soil, as well as through diet. The relative contribution of each of these sources to total lead intake varies with age and is dependent on site-specific characteristics.

Preschool-age children and fetuses are usually the most vulnerable segments of the population for exposures to lead. This increased vulnerability results from a combination of factors which include the following: 1) the developing nervous system of fetuses and neonates are more susceptible to the neurotoxic effects of lead; 2) young children are more likely to play in dirt and to place their hands and other objects in their mouths, increasing the opportunity for soil ingestion, (pica, the eating of dirt and other non-food items, also is more likely to occur in children); 3) the efficiency of lead absorption from the gastrointestinal tract is greater in children than 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 materials associated with normal early hand-to-mouth behavior. The degree to which hand-to-mouth behavior contributes to blood lead levels depends on the levels of lead in house dust, soil, and paint. In the United States, leaded paint continues to cause most of the severe lead poisoning in young children because it is the most widespread source and has the highest concentration of lead per unit of weight [33].

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

Absorption, Metabolism, and Excretion

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

Lead enters the bloodstream when it is first absorbed and is almost always carried bound to the red blood cell. It is distributed throughout different compartments of the body; the highest concentrations are in bone, teeth, liver, lung, kidney, brain, and spleen. These compartments and their interrelations have been used in metabolic models to qualitatively and quantitatively describe absorption, distribution, deposition, accumulation, and excretion of lead. Although the blood contains a small portion of the total body lead burden, it is easily accessible and is the fraction that most closely correlates with recent environmental exposures. The overall half-life of 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 for calcium in the bone matrix. Lead in bone has been estimated to represent approximately 95% of the 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 bone can 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, characterized initially 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 in intelligence and behavioral dysfunction. Acute encephalopathy is usually associated with high blood lead levels (over 150 µg/dL). Another effect of acute high dose lead exposure is the Fanconi 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 (red blood 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 and females. Lead is especially harmful to unborn children. Exposure to lead during pregnancy has been 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 been well-defined, reduced gestational age and reduced birthweight have been associated with blood lead levels of 10 to 15 µg/dL [33]. In addition, lead has been found to lower intelligence quotient (I.Q.) scores, slow growth, and cause hearing problems in children. These adverse effects can persist and lead to decreased performance in school.

Hematologic

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

ALAD activity was inversely correlated with blood lead levels over the entire range of 3 to 34 µg/dL in urban subjects never exposed occupationally [34]. Other reports have confirmed the correlation and apparent threshold in different age groups and exposure categories (children-[35,36]; adults-[37]). Lead begins to inhibit the enzyme ferrochelatase, which catalyzes the transfer of iron from ferritin into protoporphyrin to form heme, at blood lead levels of 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 lead levels. A significant negative linear correlation between EPN and blood lead level was seen in 21 children with blood lead levels ranging from 7 to 80 µg/dL [38]. Similar findings were reported 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/dL although many of the enzymes involved in heme biosynthesis are affected at very low blood lead levels. Heme synthesis is essential not only to hemoglobin but also to the synthesis of cytochromes necessary for all oxidative reactions. In children, exposure to lead has been shown to inhibit formation of the heme-containing protein cytochrome P-450, as reflected in decreased activity of hepatic mixed-function oxygenases [40,41]. Impairment of cytochrome P-450 activity could 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 central nervous 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 can develop neurological and cognitive deficits [43]. Available evidence is not sufficient to determine whether lead-associated deficits are irreversible [44].

Peripheral Nervous System

In the peripheral nervous system, lead can cause neuropathy which primarily affects the motor nerves and appears to be axonal [45]. Lead targets motor axons and produces axonal degeneration and segmental demyelination [46]. Clinically, the neuropathy is more severe in the upper extremity; in extreme cases this demyelination can produce palsy of the wrist and ankle extensor muscles, termed "wrist or ankle drop" or "painter's palsy." While the classic wrist drop has become exceedingly rare, subclinical neuropathy has been demonstrated at blood lead levels previously considered acceptable for workers [47]. Decreases in ulnar nerve conduction velocity are 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 has been associated with hypertension, renal failure, and gout. Lead accumulates in the proximal tubular cells affecting urate excretion and forming densely staining intranuclear bodies. Systemic hypertension and interference with lipoprotein metabolism from lead toxicity can exacerbate chronic renal failure due to glomerular sclerosis. Exposure to high levels of lead can cause irreversible abnormalities in renal function including decreased glomerular filtration and decreased tubular concentrating ability [48].

Cardiovascular

Information from both occupational and general population studies, including the National Health and Nutrition Survey II (NHANES II), is sufficient to suggest a small but positive association between blood lead levels and increased blood pressure. A simple correlational analysis of the NHANES II data in 1988 showed statistically significant associations between blood lead levels and systolic and diastolic blood pressure for both men and women, 12 to 74 years of age [49]. Subsequent statistical analyses, controlling for a number of other potentially confounding factors, indicated significant associations between blood lead and blood pressure in men only. Additional analyses focusing on white men (40 to 59 years of age) revealed significant associations between blood lead and blood pressure, with no apparent threshold below which blood lead level was not significantly related to systolic or diastolic blood pressure across a range of 7 to 34µg/dL [50]. Lead was a significant predictor of diastolic blood pressure greater than or equal to 90 mmHg, the criterion now used to define hypertension. A small but significant correlation between systolic blood pressure and blood lead levels also was found in a clinical survey 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 been found to produce kidney tumors in laboratory studies of rats and mice. The extremely high cumulative doses of lead used in animal studies are difficult to extrapolate to low-level exposure in humans, and do not provide a sufficient basis for quantitative risk assessment. Based on animal 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 suggests that adverse effects occur at blood lead levels at least as low as 10 µg/dL. The Centers for Disease Control and Prevention (CDC) has determined that a blood lead level greater than or equal to 10 µg/dL in children indicates excessive lead absorption and constitutes the grounds for intervention. The 10 µg/dL level is based on observations of enzymatic abnormalities in the red blood cells at blood levels below 25 µg/dL and observations of neurologic and cognitive dysfunction 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 levels above 40 µg/dL to indicate excessive lead absorption in adults. Under regulations set forth by the OSHA, adult workers with blood lead levels above 50 µg/dL must be removed from occupational lead exposure until their blood lead levels have fallen to below 40 µg/dL. It is important to note that although this is the regulatory standard, biological effects have been reported 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 the environment [53]. In general, blood lead levels rise 3-7 µg/dL for every 1,000 ppm increase in soil or dust lead concentration. Assuming a background blood lead level of 6.6 µg/dL, a blood lead 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 a function of soil lead concentration is not linear. The rate of increase in blood lead levels at low concentrations of lead in soil is greater than at high concentrations of lead in soil. Based on data from exposure studies conducted at Helena Valley in Montana and Silver Valley in Idaho, a regression 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 blood lead level of 10.7 µg/dL.

A great deal of information is available on the absorption, distribution, and excretion of lead by the 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 the potential blood lead levels in children under age seven [52]. The IU/BK model considers the monthly uptake of lead from diet, air, soil/dust, water, and paint sources, and media specific absorption factors to estimate monthly blood-lead intake. Using default parameters supplied with the model an average exposure to a soil concentration of 500 mg/kg would result in a geometric mean (average) blood lead level of 5.78 µg/dL. Using the default geometric standard deviation of 1.42, approximately 95% of the children exposed to this soil would be expected to have blood lead levels below 10 µg/dL.

A recent study was conducted to evaluate the effectiveness of removing lead-contaminated soil on reducing blood lead levels [55]. The study was conducted among children with blood lead levels ranging from 10 to 20 µg/dL, living in areas with multiple potential sources of lead exposure 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) was associated with a decline in blood lead levels of only 0.8 to 1.6 µg/dL, independent of factors such 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 recent remedial 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 significantly to 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 in residential areas of West Dallas are well below 500 ppm (average remaining soil lead levels range from 70 ppm to 142 ppm). Exposure to these levels of lead in soil would not be expected to result in elevated blood lead levels.

Cadmium

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

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

Food is the major source of human exposure to cadmium in the general population. Average cadmium 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 1 to 3 µg. Vegetables generally contain the highest levels of cadmium, particularly leafy vegetables and potatoes. Liver, kidney, and shellfish contain higher levels (up to 1 ppm) of cadmium than other meat and seafood products. For populations surrounding hazardous waste sites increased exposure can result from eating fruits and vegetables grown in cadmium-contaminated soil, ingestion of cadmium-contaminated dust on food or hands, and from the direct ingestion of soil. In highly polluted areas, the daily intake of cadmium can be as high as 400 µg per day [56].

Inhalation is another major source of cadmium exposure. Average concentrations in air range from less than 1 to 6 nanograms per cubic meter of air (ng/m³) in rural areas and from 20 to 700 ng/m³ in industrial areas. For the general population, cadmium intake by inhalation averages 0.02 µg/day but can be as high as 2 µg/day in highly polluted areas. Cigarette smokers absorb an additional 1 to 3 µg per day (based on smoking one pack of cigarettes per day). Populations surrounding hazardous waste sites can be exposed to higher levels of cadmium through inhalation of fugitive dust emissions from cadmium-contaminated soil.

Absorption of cadmium depends to a great extent on the route of exposure and the type of compound containing the cadmium. It has been estimated that only about 5% of cadmium ingested as cadmium salts is absorbed. The amount of cadmium an individual absorbs following ingestion 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 components ingested with the cadmium. Absorption of cadmium from the respiratory system is quite different. More than 90% of inhaled cadmium can be absorbed, depending on the in vivo solubility of the inhaled compound. The amount of cadmium that is absorbed is also affected by the 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% of particles less than 0.1 micron are deposited [56].

Once cadmium is absorbed, it is bound to red blood cells and serum albumin. Serum cadmium is rapidly taken up by the liver and kidney. Since the half-life of cadmium is thought to be quite long (25 to 30 years), cadmium accumulates in these tissues. Over 50% of the body burden of cadmium is found in the liver and kidney. It has been hypothesized that there is a critical concentration 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 occur with 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 may occur after oral or inhalation exposures. Chronic cadmium exposure also has been associated with cardiovascular disease and cancer of the lung, prostate, kidney, and stomach, although these associations are not well established.

The chronic pulmonary effects of cadmium exposure in humans is manifested as an obstructive lung disease. Long-term inhalation exposure to cadmium may cause decreased lung function and emphysema; Pulmonary assessment of patients with long-term inhalation exposure typically indicates a reduced vital capacity and an increased residual lung volume. The level of obstructive 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 factors as 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 the presence of protein, amino acids, and glucose in the urine. Damage is thought to occur when the renal 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 the renal cortex should not exceed 50 µg/g, a level corresponding to a urinary excretion of 2 µg of cadmium per 24-hours [59]. Average levels in non-occupationally exposed 50 year-olds are approximately 15-30 µg/g (wet weight) [60]. Cigarette smoking can double renal cortical cadmium concentrations. Because of the high amount of cadmium ingested through diet, the margin of safety for exposure to cadmium from other sources is very small, particularly for smokers.

Studies on humans occupationally exposed to cadmium in the air report a No Observable Adverse 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 has used 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 a NOAEL for kidney toxicity (proteinuria) of 0.0021 mg/kg/day [62]. Using an uncertainty factor of 3, ATSDR has used this NOAEL to establish a chronic oral MRL of 0.0007 mg/kg/day. The EPA used a toxicokinetic model to determine the level of chronic human oral exposure which would result the highest renal cadmium level not associated with significant proteinuria (200 µg/gram wet weight). Assuming 2.5% absorption of cadmium from food and 5% from water, the model predicts a NOAEL for chronic cadmium exposure of 0.005 and 0.1 mg/kg/day from water and food, respectively. Based on these NOAELs and an uncertainty factor of 10, the EPA calculated a chronic oral reference dose (RfD) of 0.0005 mg cadmium/kg/day for water and an equivalent RfD for cadmium in food of 0.001 mg cadmium/kg/day [63].

Substantial evidence from laboratory studies suggests that cadmium inhalation can cause lung cancer in rats, but evidence that cadmium inhalation can cause lung cancer in humans is rather weak. Evidence for evaluating potential carcinogenicity of cadmium by the oral and dermal routes in both animals and humans is insufficient. Based on extensive animal data and limited human data associating inhalation of cadmium with lung cancer, EPA classifies cadmium as a B1 carcinogen (probable human carcinogen).

In West Dallas, cadmium was detected at levels above the HAC value. Due to the cumulative nature of this toxin, however, adverse effects on the kidneys from low levels of exposure have been observed only after many years of exposure (i.e. fifty years). Based on available information, exposure to cadmium at the levels detected in West Dallas would not be expected to produce 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 the environment in elemental form. It is usually found in combination with other elements. Arsenic compounds can be classified into three main groups: 1) inorganic arsenic compounds, 2) organic arsenic compounds, and 3) arsine gas [64]. In the environment, arsenic is most often found as inorganic 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, which are produced when arsenic forms stable bonds with carbon. Inorganic compounds are important because 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 in insecticides, herbicides, desiccants in the cotton industry, wood preservatives, animal feed additives, and more recently in the semiconductor industry. Environmental releases of arsenic are associated with application of pesticides, disposal of solid wastes, land applications of municipal sludge, fossil fuel combustion, and industrial processes.

Since arsenic is a natural part of the environment, people are exposed to low levels of arsenic in soil, water, food, and air. The average adult takes in approximately 50 micrograms of arsenic per day from these sources, with food as a major contributor of total intake. Based on Food and Drug Administration (FDA) Market Basket Studies, adults ingest approximately 52.6 µg arsenic per day in food. However, since organic arsenic is the predominant form of arsenic in food, the daily 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 day depending upon the levels of arsenic in air and water. When arsenic levels in the environment are higher than normal, greater exposure occurs. Exposure to arsenic among children living near metal smelters, particularly copper smelters, has also been reported [65].

Both inorganic and organic arsenic compounds are well absorbed. Over 90 percent of an ingested dose of inorganic trivalent or pentavalent arsenic is absorbed. Most organic and inorganic arsenic leaves the body in urine within a few days of exposure, although some remains in the body for several months or longer. The liver converts some arsenic to a less harmful organic form, but large doses can cause adverse health effects [64].

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 digestive tract leading to pain, nausea, vomiting, and diarrhea. The minimal dose at which these effects are 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 and needles" sensation in the hands and feet. Sensitive individuals often begin to show one or more of 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 also cause low birth weight, fetal malformations, or fetal death. The single most characteristic effect of long-term oral exposure to inorganic arsenic is a pattern of skin changes that includes a darkening 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 which hyperpigmentation, keratosis, and possible vascular complications were the critical effects [68,69]. The reference dose for arsenic was derived by dividing the estimated NOAEL for these studies, determined to be 0.0008 mg/kg/day, by an uncertainty factor of three to account for sensitive individuals and the lack of data on reproductive toxicity.

There is convincing evidence from a large number of epidemiologic studies and case reports that ingestion of arsenic increases the risk of developing skin cancer. The most common lesions are multiple squamous cell carcinomas which appear to develop from hyperkeratotic warts or corns. Multiple basal cell carcinomas may also occur, usually from cells not associated with hyperkeratinization. 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, but these associations are less well established [64].

In West Dallas, arsenic has been found at levels exceeding its HAC value. However, available data 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 declined significantly since 1982 when the first comprehensive blood lead study was conducted in the area. In 1982, the mean blood lead level of 269 randomly-selected preschool children living within 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 may have resulted from chronic exposure to lead in West Dallas because many of the effects are not readily measurable and are associated with multiple potential causes.

In contrast to historical exposure data, the 1993 lead exposure study found that the average blood lead level of 305 randomly-selected West Dallas preschool children was 5.5 µg/dL, with 26 children (8.5 percent) having blood lead levels greater than or equal to 10 µg/dL (Table 14). The maximum blood lead level measured in 1993 was below the average blood lead level measured in 1982. In the 1993 study, blood lead levels observed among West Dallas children differed only slightly from blood lead levels of children in the Oak Cliff neighborhood, which served as a comparison community. The mean blood lead level of children in the comparison community was 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 of children with elevated blood lead levels (10 of 53 children) in a single subarea were observed in Area 1. Although this area includes the residences nearest the smelter in the high air dispersion area, the mean soil lead level reported for this area was only 126 ppm. The study did not find a relationship between blood lead concentrations and lead concentrations in residential soil, home dust, or other environmental media. The reason for the remaining elevated blood lead levels in this area should be further explored.

The 1982 and 1993 exposure studies provide the most extensive information about lead exposure among West Dallas children since each study includes a randomly-selected study group from within the defined area of concern as well as environmental exposure data. Recent data collected at Walk-in Clinics and by the EPSDT program are more difficult to interpret since they were not collected randomly and do not include exposure data; but these data provide additional evidence that lead levels among West Dallas children have decreased significantly in recent years (Table 14).

TABLE 14 - Comparison of 1982 and 1993 Blood Lead Data for Randomly-Selected
West Dallas Children [17, 22]

Blood lead data collected at Walk-in Clinics are difficult to interpret since individuals may have been tested because they suspected 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]

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

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

Data collected through the EPSDT program during the period between January and June 1993 also indicate that blood lead levels were not substantially different among West Dallas children and 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 of children 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 all available 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 with identifiable environmental factors, we cannot identify, with certainty, the source of lead exposure.

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 the adverse health effects associated with lead at lower levels of exposure than adults. The increased vulnerability of children results from a combination of factors: 1) the developing nervous system is more susceptible to neurotoxic effects of lead; 2) young children are more likely than adults to experience higher exposures to lead in soil, dust, and paint because of normal early hand-to-mouth behavior (pica, the eating of dirt and other non-food material, is also more likely to occur among children); 3) children absorb lead more efficiently from the gastrointestinal tract than 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 the RSR site, children also may have been exposed to higher levels of cadmium and arsenic than adults because of their frequent outdoor play and normal hand-to-mouth behavior.

2. 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 illnesses later in life as a result of past exposure. When lead enters the human body, it travels to the soft tissues, 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, about 32% of lead is eliminated within a couple of weeks. Lead that remains in the body can be stored in the bones and teeth up to several decades, but lead stored in the body has no known health effects. The accumulation of lead in bone can provide a source for remobilization of lead to other parts of the body, but because the amount of lead remobilized is small, stored lead is unlikely to cause adverse health effects after exposure has ceased. According to available information, only individuals with very high exposures (i.e. exposures indicated by blood lead levels 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 lead levels 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 be determined, it is difficult to know whether adverse health effects occurring in individuals are the result of past exposures to lead. Many of the outcomes associated with lead exposure (such as effects on kidneys, blood, and central nervous system, and particularly those associated with cognitive and physical development) that could occur at blood lead levels observed among West Dallas residents in the past are subtle and difficult to measure. These outcomes also can be associated with many factors other than lead. While exposure to the levels of lead observed in West Dallas in the past may have caused adverse health effects, residents who grew up in West Dallas 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 on people whose primary exposures occurred at work and who had chronically elevated blood lead levels in the range of 50 to 60 µg/dL or higher. These blood lead levels have been associated with 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 levels below this range, but there is no evidence that clinical illnesses or symptoms that could be detected by a physician will occur. The blood lead levels reported among West Dallas residents would not be expected to be associated with these types of problems. Studies of individuals who have experienced lead levels below approximately 20 to 30 µg/dL generally do not indicate any additional risk for developing illnesses years after exposure.

3. 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 a venous blood test to insure that the blood lead level does not increase. Adverse effects of blood lead levels in this range are subtle and are not likely to be clinically recognizable or measurable in an individual child. Although an environmental history should be taken to determine any obvious remediable source of lead, it is unlikely that there is a single predominant source of exposure for these children.

Children with blood lead levels in the 15-19 µg/dL range need more careful follow-up. This level of exposure indicates risk for decreased in IQ of up to several points and other subtle effects. Parents and health care providers should seek interventions to reduce possible blood lead exposures 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 medical evaluation including a detailed environmental and behavioral history, physical examination, and tests for iron deficiency. The most important factor in managing childhood lead poisoning is reducing the child's exposure to lead, but some children with higher blood lead levels will benefit from chelation (treatment with oral medication that must be supervised by a physician). Health-care providers with limited experience in treating lead poisoning should consider referring children needing urgent medical follow-up (those with blood lead levels 45 µg/dL), to a clinic 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 with experience in treating children who are critically ill with lead poisoning. Medical and environmental management must begin immediately.

Medical follow-up generally is necessary for adults who experience significantly higher lead exposures than children. The CDC recommends retesting and monitoring for adults with blood lead 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 annual blood lead screening tests and that medical consultations be obtained for workers with blood lead levels above 40 µg/dL. OSHA requires medical removal for workers with blood lead levels of 50 µg/dL.

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

4. 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 with pollution-related illnesses. If resources were available, it would be difficult to: a) diagnose many illnesses and conditions which could be related to pollutants at this site; b) determine whether the level of pollution to which an individual patient was exposed in the past was sufficient to cause illness; and 3) determine with certainty whether the diagnosed illness was caused by the specific past exposure.

Lead is the principal pollutant identified at the RSR site at sufficient levels for causing pollution-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 of lead exposure, such as the levels observed among West Dallas residents, are much more subtle and 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.

5. 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 slower sensory-motor and delayed early cognitive development. One study suggests that with low postnatal exposures and favorable socioeconomic conditions, some of these early associations may decrease as children grow older.

6. 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 been adequate to protect public health. The recent Biological Indicators of Exposure Study in West Dallas did not find any association between blood lead levels and remaining soil lead concentrations.

It is also important to note that the clean-up level itself does not represent the average level of lead remaining in soil and that the average level of lead in soil is a more accurate reflection of potential 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) of the study as follows: Area 1/high air dispersion area, 126 ppm; Area 2/eastern low air dispersion area, 119 ppm; Area 3/western low air dispersion area, 70 ppm; and Area 4/area with slag or battery chips, 142 ppm. The highest average soil concentration was found in the Oak Cliff comparison community (148 ppm).

Next Section           Table of Contents