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Prevalence of childhood lead poisoning in a lead mining area.

Introduction

Lead poisoning is a recognized threat to children living in urban areas of the United States (1). There is, however, little information available on the prevalence of lead poisoning in the rural areas of the United States, particularly as it relates to point sources such as lead mining and smelting. Ilene Danse, et al., reviewed published literature of blood lead surveys on persons residing in proximity to lead mining wastes and found evidence to suggest that lead found in mill tailings (lead sulfate) is not readily bioavailable and therefore poses a low risk for children (2). In contrast to tailings, Danse, et al., found that active smelter sites were more often associated with elevations in blood lead levels (2). A study of Swedish preschool children living in a community with high lead levels from mine waste found that there was no correlation between the mine waste and increased blood lead levels (3). The study presented here evaluates blood lead and urine cadmium levels in persons Diving in an abandoned lead mining, milling, and smelting area of southwestern Missouri that is on the National Priority List of hazardous waste sites (Superfund). A study by the EPA in 1986 reported lead soil levels from 73 to 7,300 ppm with a mean of 2,501 ppm and cadmium from 5.9 to 250 ppm with an average of 80 ppm (4).

The Jasper County Missouri Superfund Site is a portion of the old Tri-State Mining District of Missouri, Kansas, and Arkansas. From the 1840s through the Civil War years, over 200 widely dispersed primitive log smelting furnaces were operated in the Tri-State Mining District. Ore production consisted of mining, crushing, and grinding the rock to a standard size, ore separation, and tailings disposal. Environmental contamination with lead and cadmium was a common by-product of these operations. Mine production in the Missouri portion went on to reach its peak in 1916 when over 123 million rock-tons were processed to yield approximately 304 thousand tons of zinc concentrates and 41 tons of lead concentrates. The site is generally characterized by extensive surface land disturbances and piles of mine waste that resulted from the mining operations. Disturbed areas of the Jasper County Superfund Site in Missouri are spread over approximately 240 square miles. This mining waste contains differing levels of residual lead and cadmium depending upon when the mining took place. Smelting operations in the 1800s resulted in higher levels of residual lead and cadmium in the waste than modern smelting techniques.

Approximately eight million cubic yards of waste milling and mining products are scattered throughout the area. Some areas have been reclaimed for residential and industrial use by leveling the remaining piles of mine waste and incorporating the waste into the soil. Open mine shafts, subsided areas having steep, unstable slopes, and open pits containing deep pools of water exist throughout the region. The general site is primarily uncontrolled and routinely used for recreational purposes. In addition, water-quality problems result from artesian flow of mine waters from open shafts, rainwater runoff, and seepage from waste piles and settling ponds. Mine waste has been used as railroad ballast, road materials, and aggregates in asphalt paving and concrete. Sands and smaller sizes have been used for abrasives, roofing granules, pipe coatings, filter sands, and even children's sandboxes and play areas. Mine waste is also blown into the homes of residents in the area and is mixed with other materials originating inside and outside the home, including paint flakes, to form a mixture referred to in this paper as "dust".

This study hypothesized that the average soil, dust, and blood lead and urine cadmium levels would be higher in the lead mining area (study) than in a comparison community with no exposure to lead mining (control). This study also hypothesized that the proportion of children with blood lead levels above the level of concern established by the Centers for Disease Control and Prevention (CDC) - greater than or equal to 10 [[micro]gram]/dl - would be significantly greater in the study area than in the control area.

Methods

The sampling frame was determined through a census of all of the homes in both the study and control areas to ascertain individuals eligible for the study. Individuals stratified into three age groups, 6 through 71 months (children), 6 through 14 years (youth), and 15 through 44 years (adults), were randomly selected for the study if they had lived at their current residence at least 60 days before study commencement. Because our primary interest was childhood lead poisoning, children were over-sampled.
TABLE 1

Demographic Characteristics for Study and Control Groups

 Study Group Control Group
Characteristic Number Percent Number Percent

Gender

Male 207 50.2 140 49.5
Female 295 49.8 143 50.5

Age

6-71 months 243 59.0 138 48.8
6-14 years 117 28.4 95 33.6
15-44 years 52 12.6 50 17.6

Race

White 396 96.8 274 97.2
Black 3 0.70 3 1.10
Asian/Pacific Islander 1 0.20 0 0.00
Am. Indian/Alaskan Native 9 2.20 5 1.80

Income/year

[less than] $15,000 91 22.9 48 17.8
$15,000-24,999 106 26.7 71 26.3
[less than] $25,000 200 50.4 151 55.9

Educ. Head of Household

[greater than] 12th Grade 5 1.20 2 0.07
High School Graduate 210 51.9 130 45.9
Technical school 11 2.70 6 2.10
Some College or more 179 44.2 145 51.2

Year Home Built(*)

[greater than] 1960 151 62.1 42 30.8
1960-1979 40 16.5 73 52.9
1980-present 52 21.4 23 16.7

* p [less than] .001 (Chi square)


The study area was the Jasper County Missouri Superfund Site. It included portions of Webb City and Joplin and all of Duenweg, and Carterville, Missouri. The control area was chosen to be socio-economically similar, geographically close, but physically outside the Superfund and lead mining area. It included parts of Neosho and all of Goodman, Missouri.

Participants were interviewed and blood and urine were collected at sites centrally located to the study and control areas. Specimen collection and analysis were performed according to a standard protocol of the Environmental Health Laboratory Sciences Division of the CDC, which performed the urine cadmium and blood lead analyses using the Zeeman graphic furnace atomic absorption method. Quality control was established by duplicate analysis of whole blood pools, where target values were established by thermal ionization isotopic dilution mass spectroscopy.

This study also included environmental measurements in a sample of study and control homes for lead and cadmium in drinking water, soil, and house dust, and for lead in interior house paint. All environmental sampling and analysis was done by the Environmental Protection Agency (EPA) under a standard protocol. Soil and dust were analyzed for lead using digestion EPA SW-846 method 3050 and analysis EPA SW 846 method 7420.

Lead paint was classified as present in the home if it was detected by XRF in any areas inside the home in which the child played. The soil lead value of 150 ppm was chosen as the background level because this value was approximately equal to the mean plus two standard errors of the mean from the control area. It was also the value indicated by risk assessment to be associated with elevated blood lead levels (5).

Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS). Statistical significance was set at .05 with two-tailed tests of significance.

Results

Demographic and socio-economic characteristics of the study and control groups are presented in Table 1. The only characteristic that differed between groups was age of house. A higher percentage of homes in the study area were built prior to 1960 (p[less than].001), however a similar percentage of homes were built after 1980. There were 412 persons in the study group and 283 in the control group. Blood samples for lead were obtained from 391 study and 271 controls and urine samples for cadmium from 356 study and 249 controls. Blood samples could not be obtained from some young children because of small veins, nor could urine samples because some children were too young to provide adequate samples.

Table 2 presents blood lead, urine cadmium, and environmental lead and cadmium data by study group and age class. Environmental measurements were taken in 125 study and 26 control homes for lead and cadmium in drinking water, soil, and house dust, and for lead in interior house paint. Of the 125 study area samples, 105 were randomly selected using a table of random numbers from homes in which a child resided and 20 were tested because a child in the household had an elevated blood lead level. All 26 tested homes in the control area were randomly selected using a table of random numbers from homes in which a child resided. All homes where children with elevated blood lead levels resided received environmental testing.

All environmental measurements of lead and cadmium, except water, were higher in the study group compared to the controls. Lead in soil was over six times higher in the study area compared to the control area and lead in dust and interior paint was three times higher. Cadmium in soil and dust was also considerably higher in the study area.

Average blood lead levels in children were almost twice as high in study area children compared to controls. Analysis of covariance indicated that blood lead levels remained significantly higher in the study compared to the control group after controlling for indoor paint lead levels (p = .030, n = 179). Blood lead levels were also significantly higher after controlling for the age of the house (p [less than] .001, n = 353). In addition, average blood leads were significantly higher for youths and adults. Although soil and dust cadmium levels were significantly higher in the study group, urine cadmium levels were not statistically different between the study and control areas for any age group. Over 84% of all children tested did not have a detectable level of cadmium in their urine.

Figure 1 shows cumulative frequency for blood lead levels in children. In the study group, 14 percent of the children had blood lead levels greater than 10 [[micro]gram]/dl (the level of concern indicated by the CDC) and 5% had levels greater than 15 [[micro]gram]/dl. None of the control children had blood leads that were greater than 10 [[micro]gram]/dl. Children with elevated blood lead levels did not have other known sources of lead exposure such as parental occupation or hobbies, household renovation, use of lead cooking and storage containers, use of medicinal products containing lead, consumption of fish from contaminated streams, or any other identifiable sources of lead exposure.

Figure 2 indicates that 76% of children with blood lead levels greater than 10 [[micro]gram]/dl lived in homes in which the soil lead was greater than 150 ppm and there was lead-based paint in the home. Twenty-four percent of the children with elevated blood lead levels came from homes with lead levels greater than [TABULAR DATA FOR TABLE 2 OMITTED] 150 ppm in the soil, but no lead-based paint in the home. This is probably due to the fact that approximately 31% of indoor dust has an origin of outdoor soil (6). None of the 17 children living in homes with lead-based paint but without elevated levels of lead in the soil (greater than 150 ppm) had elevated blood leads.

Discussion

The primary objective of this study was to determine the prevalence of blood lead levels greater than the CDC level of concern (10 [[micro]gram]/dl) among children living in an old lead mining area and to compare this to the prevalence in an area not affected by mining. The results indicate that children living in the study area had greater exposure to lead as indicated by the significantly higher prevalence of elevated blood lead levels - 14% compared to 0%. Mean blood lead levels were almost twice as high in children living in the study area (6.25 [[micro]gram]/dl) compared to children living in the control area (3.59 [[micro]gram]/dl).

Environmental sampling indicated that soil lead levels in the study area were over six times higher than in the control area. Lead levels in dust and paint samples were also significantly higher in the study area. Indoor dust derives from both indoor and outdoor sources. As previously stated, it has been estimated that approximately 31% of indoor dust comes from exterior soil (6).

Both the number of persons with elevated blood lead levels and the mean blood lead levels for the mining area were significantly greater than those for the control area. These mean differences continued to be statistically significant after controlling for indoor paint levels and age of the home. Age of home was controlled for because more homes in the study area were built prior to 1960, the year that lead was beginning to be phased out of residential paint. As indicated in Figure 2, all of the children with elevated blood lead levels lived in homes that had soil lead levels greater than background levels of 150 ppm and most of these also had lead paint in the home. None of the 60 children from the study and control areas who lived in homes without lead paint or soil lead had elevated blood lead levels.

It is not possible to determine from this study what proportion of the biological lead burden results from mining and smelting waste and what proportion comes from other sources such as paint and gasoline residue deposited in soil. The evidence suggests that some portion of the difference in blood lead levels between the mining and non-mining areas is the result of exposure to the mining waste, since the difference can not be accounted for by differences in paint lead levels between the two areas. Although paint lead levels were somewhat higher in the study area, blood lead levels continue to be significantly higher in the study area after controlling for paint lead levels and after controlling for an indicator of lead paint - age of house. Also, some of the children with elevated lead levels came from homes in which leaded paint was not found but elevated soil lead levels were.

Although both dust and soil cadmium levels were significantly higher in the study area, the urine cadmium levels were not different between the study and control children. This is possible due to the lack of biological availability of cadmium from soil since cadmium could not be detected in the urine of 84% of the children.

Conclusion

Children living in the Jasper County Superfund Site where soil is contaminated with lead from mining and smelting operations have a higher prevalence of elevated blood lead levels compared to children living in areas without soil contamination. The data suggest that this increased prevalence of elevated blood lead levels may be due to a combination of soil lead from mining and smelting operations and other sources of lead, such as household lead paint.

Corresponding Author: Ana Maria Murgueytio, M.D., M.P.H., School of Public Health, Saint Louis University, 3663 Lindell Blvd., St. Louis, MO 63108.

Acknowledgements

This study was supported by a grant from the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, Department of Health and Human Services.

REFERENCES

1. Centers for Disease Control (1991), Preventing Lead Poisoning in Young Children, U.S. Department of Health and Human Services.

2. Danse, I.H.R., L.G. Garb, and R.H. Moore (1995), "Blood Lead Surveys of Communities in Proximity to Lead-Containing Mill Tailings," Am. Ind. Hyg. Assoc. J., 56(4):384-393.

3. Bjerre, B., M. Berglund, K. Harsbo, and B. Hellman (1993), "Blood Lead Concentrations of Swedish Preschool Children in a Community With High Lead Levels from Mine Waste in Soil and Dust," Scand. J. Work Environ. Health, 19 (3):154-161.

4. U.S. Environmental Protection Agency (1986), Final Report for the Tri-State Mining Area Joplin, Missouri, Region VII, Kansas City, Ks.

5. Bassinger-Daniels, Sherry (Jan. 5, 1995), Personal Communication, Missouri Dept. of Health.

6. Calabrese, E.J., and E.J. Stanek (1992), "What Proportion of Household Dust is Derived from Outdoor Soil," J. Soil Cont, 1(3):253-263.
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Author:Moehr, Tony
Publication:Journal of Environmental Health
Date:Jun 1, 1996
Words:2736
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