8.
Lead Poisoning
Authors
This chapter was prepared by Will Humble, R.S., M.P.H., Risk Assessment and Environmental Epidemiology, Arizona Department of Health
Health Effects of Lead
Lead, also known as lead metal, plumbum, and pigment metal, is an element found throughout the environment. It comes from the earth's crust and from processes initiated by humans. It is found in air, food, water, and dust.
The routes of exposure for lead include inhalation, ingestion, or dermal contact. If deposition of lead particles occurs in the lower respiratory tract, the particle absorption is almost total.
Fifty percent of the lead which is ingested by children is absorbed by the body with an 8% and a 15% rate of absorption, according to two separate studies examining ingestion exposure in adults. Ingestion is the most frequent exposure route for children. Fasting has been shown to enhance ingestion absorption by to up 45% in adults.
In animals, the absorption of alkyl lead (tetraethyl lead) occurred more rapidly by dermal application in rabbits than by ingestion. Since human's dermal absorption rate is lower, absorption in humans by dermal contact is less than by inhalation or ingestion.
Inorganic lead is not metabolized or bio-transformed. Metabolism does occur in the liver, however, with organic (alkyl) lead.
Regardless of the route of absorption, lead is distributed in the blood, soft tissue, and bone with the majority of the total body burden in the bone. Excretion in humans occurs through the urine and feces. Transplacental transfer has also been observed in humans.
A variety of toxic effects have been documented in humans from inhalation and ingestion exposures to lead. Severity of symptoms is dose-dependent, with higher doses of lead producing more severe symptoms. Consequences of exposure are:
o Impairment of heme synthesis with resultant anemia has been seen. Neurobehavioral toxicity has been documented in occupational groups mainly from inhalation but also from ingestion.
o Lead encephalopathy is the most serious neurobehavioral effect with symptoms of dullness, irritability, poor attention span, headache, muscular tremor, memory loss, and hallucinations. If the exposure concentration is high enough, the condition becomes quite severe, resulting in coma and death. Acute encephalopathy and death have been documented in children with mainly ingestion and secondarily inhalation exposure.
o At lower lead concentration levels, children have manifested neurological impairment (hyperactivity, peripheral neuropathy) and cognitive deficits (lower IQ).
o With inhalation and ingestion, some of the other consequences of lead exposure include:
Cardiovascular toxicity (abnormal EKGs, high blood pressure)
Nephropathy
Interference with Vitamin D metabolism
Gastrointestinal symptoms (colic)
Developmental toxicity (low birth weight)
Growth retardation
Compromise of the immune system
Reproductive toxicity (miscarriage)
Studies in these areas for dermal exposures were not available.
Data in epidemiologic studies were not adequate to establish an association between lead exposure and the development of cancer. Failure to document the specific lead compound, its dose, and the compound's exposure routes were all weaknesses of these studies.
An examination of lead production and battery workers who had inhaled lead in the workplace has demonstrated higher rates of total malignancies and mortality from total malignancies than would otherwise have been expected. For example, an increased number of renal cancers was observed in lead smelter workers.
In a number of animal studies, kidney tumors have consistently been reported with lead ingestion exposure. The EPA classifies lead as a probable human carcinogen (USDHHS, 1992).
The ADHS is the state agency mandated by Arizona law to maintain a registry for recording cases with elevated blood lead levels. In March, 1993, the Arizona lead poisoning reporting law was revised. The reporting level was changed from 25 microns/dL to 10 microns/dL.
Environmental Exposures to Lead
Exposure to environmental media containing lead is the primary source of elevated blood lead in children.
Sources of lead which may contribute to total lead exposure include water, air, soil, and dust.
Lead-based paint, ingested as paint chips or dust is the most common high dose source of lead nationwide. It is also the source most commonly identified in Arizona cases.
Other sources may include food, ceramic and pewter cooking utensils, home projects such as ceramics-making, and home remedies that contain lead.
Quantifying lead exposures from all sources is a critical part of estimating blood lead levels in children. This section analyzes and discusses the relative contributions made by each of these lead sources. Information about relative contributions may be used to effectively direct intervention resources.
The Committee used two methods to assess environmental exposure to lead.
o The first method uses the EPA Integrated Exposure Uptake Biokinetic (IEUBK) model to evaluate lead exposure (USEPA, 1994).
o The second method uses epidemiological data collected by the lead exposure registry at the ADHS as a measure of elevated blood lead levels in the population.
The IEUBK model generates a probability distribution of blood lead levels for a group of children exposed to a particular concentration of lead in each media. The distribution reflects the variability of blood lead levels in several communities.
Methods
The IEUBK model was run four times using representative input parameters for environmental concentrations of lead which contribute to total lead exposure. The populations for which analyses were conducted include:
o Children living in areas with low background levels of soil lead whose homes do not contain lead-based paint;
o Children living in areas with low background levels of soil lead whose homes contain lead-based paint;
o Children living in areas with higher background levels of soil lead (e.g., smelter towns) whose homes do not contain lead-based paint;
o Children living in areas with higher background levels of soil lead whose homes contain lead-based paint.
The following subsections discuss each of the exposure media that may contribute to total lead exposure. IEUBK input parameters for each media are also discussed.
Water
Data from a computerized data base from the ADEQ were used to estimate lead exposures from water in Arizona and its contribution to total lead exposure. Data were available for 72% of the service population in Arizona. The results were:
o About 95% of the analyzed population in Arizona is being exposed to less than 0.01 mg/L.
o 99.2% of the analyzed population in Arizona is exposed to less than 0.02 mg/L.
o A subpopulation of approximately 7000 persons is being served by water systems with lead in excess of 0.06 mg/L.
The IEUBK model was run using a concentration of 0.01 mg/L as an estimate of state-wide lead exposure from water. This estimate is conservative and will tend to overestimate the contribution of lead exposure through water.
Air
Data from the ADEQ 1992) were used to estimate lead exposures from outdoor air in Arizona and its contribution to total lead exposure.
o Data collected from the Phoenix and Tucson metropolitan areas were used in the analysis as these data represent the majority of the population in Arizona. A total of 263 sample analyses were available for Phoenix and Tucson.
o Data from the Chiricahua National Monument was used in the Douglas/ Bisbee analysis. A total of 93 sample analyses were available for Chiricahua National Monument.
All data represented lead particles in the respirable fraction (less than 10 microns).
The mean of four quarterly averages from 263 samples at five sample locations was 0.83 micron/m3. This figure was used as the urban exposure concentration.
The mean of four quarterly averages from 93 samples at one location (4.5 microns/ m3) was used in the Douglas/Bisbee analysis.
The IEUBK model was run using 0.83 micron/m3 as the estimated lead concentration in air in urban areas.
A value of 4.5 microns/m3 was used for the Douglas/Bisbee analysis.
Soil
Data from the ADEQ (Earth Technology Inc., 1991) and a 1985 soil and blood lead investigation conducted by the ADHS in Douglas and Bisbee were used to evaluate lead exposures from soils.
The ADEQ data includes 62 soil samples from eight locations in the Phoenix and Tucson areas.
The Douglas/Bisbee data includes 126 soil samples from 126 locations. The urban and Douglas/Bisbee data were averaged in order to provide two estimates for input into the model.
The IEUBK model was run using the calculated mean of 7.7 mg/kg as the estimated lead concentration in soil in urban areas. A value of 303 mg/kg was used for the Douglas/Bisbee analysis.
House Dust
Lead in house dust is usually composed of lead from soils and airborne fallout. Other sources may include lead-based paint in the home.
No data are available on the concentration of lead in house dust. An estimate can be made, however, if soil and air concentrations are known.
Since lead-based paint in a home can significantly influence the amount of lead in the house dust, this analysis breaks lead exposure into homes with and without lead- based paint.
The IEUBK model uses a multiple source analysis to predict lead concentrations in house dust based upon the concentrations of lead in soil and air. Separate models were run for both the urban and Douglas/Bisbee assessment for homes with lead- based paint.
The IEUBK model was run using the soil lead concentrations discussed in the previous section as the concentration in house dust in homes without lead-based paint. The concentration of lead in house dust from paint was assumed to be 1200 mg/kg in homes with lead-based paint. The model integrates sources from soil and lead-based paint to obtain an estimate of lead in house dust.
Diet
The contribution of total lead exposure from food was assessed using the default parameters included in the IEUBK model. Exposure to lead from foods in the model is based on an analysis of the typical American diet and quarterly surveys of lead amounts in this diet.
Results
Input parameters for each population group were determined using the data presented above. The modeling results were as follows:
o Children living in areas with low background levels of lead in the soil, and whose houses do not contain lead-based paint, are unlikely to have elevated blood lead.
The probability distribution for this population indicates that 0.06 percent of the children under six-years old in this population will have blood lead concentrations in excess of 10 microns/dL. The geometric mean concentration of blood lead predicted by the model is 2.2 microns/dL.
o Some children living in areas with higher levels of lead in the soil, and whose houses do not contain lead-based paint may have elevated blood lead.
The probability distribution for this population indicates that about 13 percent of the children under six-years old in this population will have blood lead concentrations greater than 10 microns/dL. The geometric mean concentration of blood lead predicted by the model is 6 microns/ dL.
o Children living in areas with low background levels of lead in the soil, and whose houses contain lead-based paint are more likely to have elevated blood lead.
The probability distribution for this population indicates that about 34% of the children under six-years old in this population will have blood lead concentrations in excess of 10 microns/dL. The geometric mean concentration of blood lead predicted by the model is 8.5 microns/Dl.
o Children living in areas with higher background levels of lead in soil (303 mg/kg) and whose houses contain lead based paint are the group most likely to have elevated blood lead.
The probability distribution for this population indicates that about 50% of the children under six-years old in this population will have blood lead concentrations in excess of 10 microns/dL. The geometric mean concentration of blood lead predicted by the model is about 10 microns/ dL.
Model Estimate of Number of Children with Elevated Blood Lead
According to the IEUBK model, children living in homes that contain lead paint are at the highest risk of lead poisoning as measured by elevated blood lead.
Children living in areas with higher levels of soil lead are at some risk for lead poisoning. The likelihood of elevated blood lead in this population, however, is less than that of elevated blood lead in children in homes that contain lead paint.
Children living in areas with low background levels of lead in the soil, and whose houses do not contain lead-based paint, are unlikely to have elevated blood lead levels.
Lead was widely used as a major ingredient in most oil-based paints before the 1950s. In 1972, the Consumer Products Safety Commission limited lead content in new paint to 5,000 mg/kg, and to 600 mg/kg in 1978.
Due to the quantity of lead in paint before 1950, homes built before this time are the most likely to contain lead-based paint. Ninety percent of homes built before 1940 contain some lead-based paint.
According to 1990 census data, approximately 3.2% of the housing units in Arizona were built before 1940, and 6.8% were built before 1950.
o The data indicates that about 93,000 persons are living in pre-1950 houses in Arizona.
Assuming that approximately 11% of this population is under the age of six (ADES, 1993), approximately 10,230 children aged six and less are in the highest risk category.
The IEUBK model predicts that 34% of the 10,230 at-risk children, or 3,478 children, may have elevated blood lead in this category.
Assuming that the remainder of the under six population is in the lowest risk group (460,200), and that 0.06 percent of these children will have elevated blood lead, an additional 282 cases are predicted.
The total number of children with elevated blood lead estimated by the model is about 3,760.
The IEUBK model considers all of the environmental sources of lead, including air, water, food, soil and house dust. In addition, the model assumes an average maternal blood lead concentration of 2.5 microns/dL.
Analysis of the model results indicates that the majority of total lead exposure is by ingestion of lead containing soil and house dust.
Modeling Uncertainties
Because a child's exposure to lead involves a complex array of variables, results from the (IEUBK) model may differ from results of blood lead screening of children in a community (USEPA, 1994b). Variables include:
o Population sampling variability
o Variability in environmental lead measurements
o Variability in background levels of lead in soil, dust, food and drinking water
Possible sources of lead exposure that are not considered by the model include the use of ceramic or pewter cooking utensils, home projects such as ceramics-making, and the use of home remedies that contain lead.
Elevated Blood Lead Reporting and Investigations
National Trends
The concentrations of lead in the blood of children has declined substantially in recent years. A national survey of blood lead levels taken from 1988-1991 found that lead levels in children one through five years of age had decreased 88% since a survey conducted from 1976-1980 (USDHHS, 1994).
o The 1976-1980 study found that 53% of children aged one through five had blood lead levels over 15 microns/dL and 9.3% had levels over 25 microns/ dL.
o The 1988-1991 study found that 2.7% of children aged one through five had blood lead levels over 15 microns/dL, and 0.5 percent had levels over 25 microns/dL.
Much of the reduction in blood lead levels may be attributed to a 99.8% reduction in the amount of lead in gasoline and the virtual elimination of lead solder in food and soft-drink cans (USDHHS, 1994).
Further reductions in blood lead levels will require elimination of deteriorated leaded paint in older housing, and a reduction of lead concentrations in contaminated soils.
Statewide Reporting and Investigations
The number of reported lead poisoning cases in Arizona rose dramatically in 1993. The ADHS lead registry received 315 cases of elevated blood lead levels in 1993, a 573% increase over the previous year. This increase is due to the recent changes in reporting and screening (ADHS, 1993).
The Arizona Health Care Cost Containment System began screening Arizona children through the Early Periodic Screening, Diagnosis, and Treatment program in 1993. However, no rates can be determined using these data since the total number of children that have been screened is not available.
The primary suspected source of lead exposure in children during 1993 was lead- based paint. Other suspected sources included lead-containing soil, ceramic and pewter cooking utensils, ceramics-making, and take-home occupational exposures. In addition, a number of cases may have been caused by water stored in containers with lead-containing solder and brass fittings.
The majority of cases were from Maricopa (62%) and Pima Counties (23%). The distribution of elevated blood lead cases may reflect the size of the local populations and the numbers of children screened in each county.
In 1993, there were 144 children in Douglas and Pirtleville screened for elevated blood lead by the Arizona Health Care Cost Containment System. The screening found three (2%) with blood lead concentrations in excess of 10 microns/dL.
There have been seven reported cases of elevated blood lead in the Douglas area during 1994 (as of August 1, 1994). It is not known how many children were tested to yield these cases.
o Of the seven cases, four were sufficiently high to warrant environmental investigations.
o Paint and paint-contaminated soil were identified as the most likely sources for one case.
o The folk remedy Azarcon was implicated in three cases.
Estimated Number of Children with Elevated Blood Lead
While there is no published estimate of the rate of elevated blood lead levels in Arizona, estimates of the number of potential cases can be made by applying rates found in clinical settings to the number of children in Arizona.
The 1988-1991 NHANES study estimated that 2.7% of children nationally may have lead levels in excess of 15 microns/dL, with 0.5% of children having levels in excess of 25 microns/dL. The number of children under age six in Arizona in 1994 is estimated to be 470,430 (ADES, 1993).
Data collected by the University of Arizona Medical Center Pediatric Clinic for children screened for blood lead from March 1993 through January 1995 found:
o 2.3% of the 1,439 children had blood lead levels between 10 microns/dL and 14 microns/dL.
o 0.3% of 1,439 children had blood levels between 15 and 19 microns/dL.
o 0.1% of 1,439 children had levels between 20 and 24 microns/dL (University of Arizona, 1995).
The age distribution of the children screened is not provided. However, the majority of children screened were probably less than three years old.
The estimate of the number of children in Arizona with elevated blood lead made here uses the percentages from the University of Arizona study as a measure of the percentage of children with elevated blood lead in Arizona. If one assumes that the percentages found at the University of Arizona are representative of all children ages zero to six years old in Arizona, then the number of children with blood lead levels in excess of 10 microns/dL in Arizona may be 12,700, with 470 of these in excess of 20 microns/dL.
However, the vast majority of reported elevated blood lead cases to the ADHS registry are less than three years of age, and the majority of screening occurs in this population. Additionally, the vast majority of the screening data from the University of Arizona is in the zero to three age group.
If one assumes that the percentages found at the University of Arizona are representative of children aged zero to three years, then the number of children with blood lead levels in excess of 10 microns/dL in Arizona may be 6,350 with 235 of these in excess of 20 microns/dL.
Conclusion
Children with elevated blood lead levels are at risk of developing neurological damage, including peripheral neuropathy, hyperactivity, and cognitive deficits (decreased IQ).
The estimated number of children in Arizona with blood lead levels in excess of 10 microns/dL is 6,350. An estimated 235 of these children may have severely elevated blood lead (greater than 20 microns/dL).
Considerable progress has been made in reducing childhood exposure to lead through the phase-out of leaded gasoline, lead-soldered cans, and lead-based paint. However, residual lead contamination in houses with old lead-based paint remains in some areas in Arizona.
While there are a number of media through which children may be exposed to lead, eliminating exposure to lead-based paint and lead-contaminated soils will substantially reduce lead exposure in children.