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Seasonality and Children’s Blood Lead Levels: Developing a Predictive Model Using Climatic Variables and Blood Lead Data from Indianapolis, Indiana, Syracuse, New York, and New Orleans, Louisiana (USA)
Mark A.S. Laidlaw, Howard W. Mielke, Gabriel M. Filippelli and 2 more
Environmental Health Perspectives · 2005 · Public domain
Abstract
On a community basis, urban soil contains a potentially large reservoir of accumulated lead. This study was undertaken to explore the temporal relationship between pediatric blood lead (BPb), weather, soil moisture, and dust in Indianapolis, Indiana; Syracuse, New York; and New Orleans, Louisiana. The Indianapolis, Syracuse, and New Orleans pediatric BPb data were obtained from databases of 15,969, 14,467, and 2,295 screenings, respectively, collected between December 1999 and November 2002, January 1994 and March 1998, and January 1998 and May 2003, respectively. These average monthly child BPb levels were regressed against several independent variables: average monthly soil moisture, particulate matter < 10 μm in diameter (PM10), wind speed, and temperature. Of temporal variation in urban children’s BPb, 87% in Indianapolis (R2 = 0.87, p = 0.0004), 61% in Syracuse (R2 = 0.61, p = 0.0012), and 59% in New Orleans (R2 = 0.59, p = 0.0000078) are explained by these variables. A conceptual model of urban Pb poisoning is suggested: When temperature is high and evapotranspiration maximized, soil moisture decreases and soil dust is deposited. Under these combined weather conditions, Pb-enriched PM10 dust disperses in the urban environment and causes elevated Pb dust loading. Thus, seasonal variation of children’s Pb exposure is probably caused by inhalation and ingestion of Pb brought about by the effect of weather on soils and the resulting fluctuation in Pb loading.
Full text
From PubMed Central, U.S. National Library of Medicine, as current on Oct 25, 2026. Paragraph numbers are ours, so an answer can point at one.
Lead poisoning causes permanent neurologic, developmental, and behavioral disorders, particularly in children. The identification and removal of new sources of human exposure to Pb over the past several decades have significantly reduced the percentage of Pb-poisoned children in the United States, although one remaining population that has not seen this improvement is urban children, particularly from minority groups or families with low socioeconomic standing. Although some of this continued Pb poisoning is due to remaining point sources (e.g., paint dust from poorly maintained homes), it appears that a significant additional source of Pb contamination is from soil—the legacy of 100 years of Pb use in cities linked to multiple sources (e.g., leaded gasoline, leaded paint, smelters). Recent work has suggested that seasonal increases in children’s blood Pb (BPb) levels relate to exposure via activity, that is, summer days of outdoor play and open windows and doors leading to increased contact with Pb-contaminated soils. Here we suggest an additional possibility—that higher children’s BPb levels may be related to a combination of weather, soil moisture, and wind that effectively remobilizes and makes more bioavailable the diffuse soil Pb. This process may exacerbate this usual summertime behavioral link, with added impacts on urban children’s health.
Urban Pb.
In the 1970s, the assumed source of soil Pb contamination was Pb-based house paint. An early study of garden soils conducted in metropolitan Baltimore, Maryland, raised questions about that assumption. Soil around Baltimore’s inner-city buildings, predominantly unpainted brick, exhibited the highest amounts of Pb, and soils outside of the inner city, where buildings were commonly constructed with Pb-based paint on wood siding, contained comparatively low amounts of Pb, suggesting that Pb-based house paint could not account for the observed pattern of soil Pb. Similarly, the same pattern was also found in Ottawa, Canada. The quantity and distribution of soil Pb have been studied in numerous places: cities in Minnesota; New Orleans, Louisiana; Milwaukee County, Wisconsin; Washington, DC; Indianapolis, Indiana; Syracuse, New York; Oslo, Norway; and Ibadan, Nigeria. All these cities exhibited the same distance decay characteristic of high soil Pb contamination in the inner city and decreasing contamination toward the outer parts of the city as initially identified in garden soils of Baltimore. Further, similarities in this distance decay pattern of soil Pb supports the idea that Pb-based house paint was not the sole source contributing to these observed differences.
Sources of Pb.
Except for storage batteries, paint and gasoline additives were the two major high-volume products containing Pb; about the same quantity of Pb, 5 to 6 million metric tons, was used to manufacture each. Lead-based house paint sales were phased out in 1978 in response to the Lead Paint Poison Prevention Act. The major processes that now release Pb-based house paint into the soil are deterioration and especially disturbance of old Pb-based paint by power sanding.
In the United States, motor vehicles used gasoline containing tetramethyl and tetraethyl Pb additives from the 1920s to 1986. By the 1950s, Pb additives were contained in virtually all grades of gasoline. By 1986, when leaded gasoline was banned, 5 to 6 million metric tons of Pb had been used as a gasoline additive, and about 75% of this Pb was released into the atmosphere. Thus, an estimated 4 to 5 million tons of Pb has been deposited into the U.S. environment by way of gasoline-fueled motor vehicles. Accumulation of soil Pb created by leaded gasoline is proportional to highway traffic flow.
Pb content and Pb loading of urban soils.
A critical aspect of Pb accumulated in soils is the relationship between Pb content and Pb loading. Studies in Minnesota and Louisiana examined the issue of Pb loading of the soil. In large cities of Minnesota and Louisiana, the median soil Pb for various site types measured from 6.0 to 32.25 g/m2, and the top 0.025 mm contained 6,000–32,250 μg Pb/m2 (557–2,996 μg Pb/ft2). When one compares this Pb loading rate with the U.S. Department of Housing and Urban Development’s guideline of 40 μg Pb/ft2 for interior floors, it becomes evident that soil is an enormous reservoir of Pb dust. Because of the low mobility of Pb in soil, all of the Pb that accumulates on the surface layer of the soil is retained within the top 20 cm. The half-life of Pb in surface soils has been estimated to be approximately 700 years, so without corrective action, Pb dust will persist for many generations. The persistence of the Pb burden that has accumulated in soil has significant long-term public health implications.
Anthropogenic soil Pb speciation and bioavailability.
Pb deposited by human activity onto and retained by surface soils has been added to the relatively small quantities of Pb naturally occurring in the soil. This anthropogenic Pb is generally speciated in the highly bioavailable carbonate, iron, and manganese hydroxide soil fractions, whereas the Pb in natural soils is speciated in the residual, or nonbioavailable fractions. Therefore, dust originating from urban soils contaminated by anthropogenic Pb is more toxic than naturally occurring Pb dust. Lead is associated with the smallest particles, the clay grain size fraction in urban soils; therefore, Pb in dust originating from urban soils is more potent and concentrated than would be expected from simple measurements of the Pb content of the soil.
Bioavailability is indicated by an isotope study of BPb and soil Pb. Each source of Pb has an isotopic signature that is unique to a particular mine. When this characteristic of Pb was first described, most manufacturers began interchanging Pb mining sources, and the effect was to scramble the isotope signatures and render Pb isotopes essentially useless for source identification. The former Soviet Union, however, did not scramble Pb sources that were used in gasoline. Armenia eliminated the use of leaded gasoline before 1997. The half-life of BPb is about 30 days and is therefore cleared from the blood in a matter of months. If Pb exposure continues, then BPb remains elevated. A study conducted in Yerevan, Armenia, 2 years after the elimination of leaded gasoline indicated that the soil Pb from previous gasoline Pb emissions persisted as a route of exposure for adults. The Pb isotopes of the BPb of adults and the Pb isotopes in contaminated soils were identical, and this provided strong evidence that prior leaded gasoline emissions persist and are highly bioavailable as a route of exposure.
Seasonal changes in BPb concentration.
Average monthly BPb of children from urban areas tends to increase significantly in summer months. Summertime increases of children’s BPb were so prominent over many years in Syracuse, New York, that researchers concluded that the phenomenon was probably caused by the interaction between climate and soils. The purpose of this study is to test the hypothesis that children’s exposure as measured by BPb is associated with climate and soil factors affecting Pb dust flux in three cities: Indianapolis, Indiana; Syracuse, New York; and New Orleans, Louisiana. Figure 1 presents a map illustrating the locations of the three cities.
Materials and Methods
This study differs from previous studies because it uses environmental variables as predictors of children’s BPb concentrations, which does not appear to have been attempted before using an ecologic study design. The U.S. EPA studies in Milwaukee and Boston attempted to model BPb using sinusoidal functions; however, it appears that multiple linear regression using climate and soil moisture variables may be more robust due the high percentage of variation explained in the model (up to 87%). The U.S. EPA models did not attempt to use environmental variables to predict BPb concentrations; however, both studies suggested that Pb from the environment might be causing the child BPb seasonality.
This study’s design is described as an analytic time-trend ecologic study. In ecologic studies, the unit of analysis is the group rather than the individual. The ecologic unit of analysis in this study is the group of children within the city limits of each city who have had their BPb measured. An ecologic design was selected because it is neither practical nor ethical to draw blood from large groups of children on a monthly basis over a long period. One potential limitation of ecologic studies is known as the ecologic fallacy: the failure of expected ecologic effect estimates to reflect biologic effects at the individual level. However, the biologic plausibility of the associations found at the ecologic level in this study have been found at the individual level in smaller studies. This supports the biologic plausibility of the suggested model. Another facet of this study is that it uses empiric data from three cities that differ in geographic location and climate. Syracuse (latitude 43° N and longitude 76° W) has a cold continental climate; Indianapolis (latitude 40° N and longitude 86° W) is located in the middle continent region; and, New Orleans (30° N latitude and 90° W longitude) has a southerly and warm Gulf Coast climate. The relationship between BPb, weather, and soil moisture is thus studied in geographically and hence climatically diverse locations.
Data Sources
The independent variables—average monthly soil moisture, particulate matter < 10 μm (PM10), wind speed, and temperature—were obtained from state or federal government data sources. Blood Pb databases for each city were obtained from local or state governmental sources as follows.
Indianapolis.
In Indianapolis, Indiana, BPb data for 15,944 children were obtained from the Marion County Health Department (personal communication). Nearly 15% of the children listed in the Indianapolis database were < 1 year (n = 2,320), 20% were 1–2 years (n = 3,202), 13% were 2–3 years (n = 2,078), 19% were 3–4 years (n = 3,050), 22% were 4–5 years (n = 3,476), and 11% were ≥5 years of age (n = 1,820). The BPb measurements were collected using the venous method. PM10 data were obtained from the Indiana Department of Environmental Management air monitoring station located at 3302 Englist Avenue (personal communication). Soil moisture data were obtained (personal communication) from actual field measurements of the top 6 inches of soil at Illinois Water Survey soil moisture monitoring site number 81 located near Champaign, Illinois, which is approximately 110 miles west of Indianapolis. Wind speed and temperature data were obtained from the National Oceanic and Atmospheric Administration (NOAA) National Climatic Data Center.
Syracuse.
In Syracuse, New York, child BPb data were obtained from the Onondaga County Health Department (personal communication). The child BPb screenings for the Syracuse BPb data set were collected from within the city limits of Syracuse. Approximately 90% of child BPb screenings were obtained from passive sources such as county clinics or physicians, and 10% of the screenings were collected from a mobile bus that screened children at locations including day care centers, prekindergarten centers, and Head Start centers. The bus schedule started in May and ended in September, operating full time in June, July, and August. The bus traveled to different locations each summer period. The bus sampling strategy typically targeted areas that had high percentages of BPb concentrations greater than 20 μg/dL. The child BPb screenings were conducted through a combination of capillary and venous methods. The BPb analysis was completed by laboratories certified by the New York State Department of Health. PM10 data were obtained from the New York State Department of Environmental Conservation’s Solvay High School air monitoring site located on Gertrude Avenue (personal communication). Soil moisture data were obtained from NOAA (Fan Y, personal communication), and wind speed and temperature data were obtained from the.
New Orleans.
In New Orleans, Louisiana, the child BPb data were obtained from the Louisiana Childhood Lead Poisoning Prevention Program Office of Public Health (personal communication). The screenings for the New Orleans BPb data set were collected from within the city limits. No known geographic or temporal sampling bias was reported. Eighty-four percent of the screenings originated from private providers such as pediatric clinics, physicians, and family practice physicians. Approximately 70% of the children whose BPb was screened were eligible or enrolled in Medicaid. The BPb levels were analyzed primarily by the following laboratories: Labcorp (Burlington, NC), Tamarac (Centennial, CO), Medtox (St. Paul, MN), Quest Diagnostics (Metairie, LA), and ARUP Laboratories (Salt Lake City, UT). The screening procedures were not reported to have changed between January 1998 and May 2003. The data set used in this study was screened for children that had blood drawn using the venous method. The PM10 data were obtained from the Louisiana Department of Environmental Quality (personal communication). The soil moisture data were obtained from NOAA (Fan Y, personal communication), and the wind speed and temperature data were obtained from the.
Statistical Analysis
We computed the average BPb concentration in each city using the child BPb measurements for each month. The outcome variable, children’s average monthly city BPb concentration for each city, was regressed against the independent variables average monthly soil moisture, PM10, wind speed, and temperature; interaction variables; and monthly dummy variables using backward elimination procedures. The independent variables temperature, PM10, and soil moisture were computed as the arithmetic mean, whereas the wind speed was computed as the median. Each model’s entry and criteria were 0.10 and 0.15, respectively. Backward variable elimination enters all of the variables in the block in a single step and then removes them one at a time based on removal criteria. Spearman’s rank correlation coefficient was used to assess the association between variables. Statistical analysis was performed using SPSS (version 11.5; SPSS Inc., Chicago, IL).
The Durbin-Watson (DW) and Lagrange multiplier (LM) statistics were calculated to assess the presence of serial autocorrelation. The LM was calculated by regressing the residuals of a model versus the same residuals shifted backward one value relative to the other residuals. The LM statistic is computed by multiplying the R2 value of this regression by the number of values in the regression. The DW statistic was calculated using SPSS.
Results
For each city, we calculated Spearman’s rank correlation coefficient matrices for the variables soil moisture, wind speed, PM10, and temperature; interaction variables; and monthly dummy variables (M1 to M11). In Indianapolis, Syracuse, and New Orleans, BPb concentration and soil moisture exhibited inverse correlations of –0.41, –0.75, –0.47, respectively. The correlations are presented in Tables 1–3.
Regression results: Indianapolis.
The time period of the regression consisted of 36 months between December 1999 and November 2002. The dependent variables for the first model consisted of the average monthly child BPb from a data set of 15,969 children. This model was run using backward elimination procedures.
This model indicates that the variables or interaction variables including soil moisture, wind speed, PM10, temperature, and the monthly dummy variables for March, April, June, July, August, and September explain 87% of the variation in the response variable, monthly average child BPb concentration (R2 = 0.87, p = 0.0004). The DW and LM statistics indicate that the model did not display serial autocorrelation (DW = 1.73, LM = 0.24). Figure 2 presents a chart of the average monthly child BPb concentration for the entire data set versus the predicted child BPb concentration.
The model regression coefficients indicate that the seven predictors with p-values less than 0.05 are temperature (p = 0.00093), wind speed (p = 0.00093), the interaction between temperature and wind (p = 0.002), soil moisture (p = 0.006), the interaction between soil moisture and temperature (p = 0.0076), the interaction between wind and soil moisture (p = 0.011), and the interaction between wind and PM10 (p = 0.016).
Regression results: Syracuse.
The time period of the regression consisted of 51 months from January 1994 through March 1998. The use of a mobile clinic to screen children in Syracuse in high-risk areas may have biased the high aggregate monthly average during the months of May through September. However, starting with the 1996 data, the universal screening requirement of the went into effect; subsequently, higher screening rates and more random sampling were apparent in the results. The dependent variables consisted of the average monthly child BPb concentration of a data set of 14,467 children from Syracuse. The model was run using backward elimination procedures. The time-series difference method was used to correct for serial autocorrelation.
This model indicates that the variables or interaction variables including soil moisture, wind speed, PM10, temperature, and the monthly dummy variables for January, March, April, May explained 61% of the variation in the response variable, monthly average child BPb concentration (R2 = 0.61, p = 0.0012). The DW and LM statistics indicate that the model did not display serial correlation (DW = 2.05, LM = 0.049). Figure 3 presents a chart of the average monthly child BPb concentration versus the predicted child BPb concentration.
The model regression coefficients indicate that the four predictors with p-values less than 0.05 are the interaction between temperature and PM10 (p = 0.0004), PM10 (p = 0.0047), wind speed (p = 0.029), and the interaction between soil moisture and temperature (p = 0.042).
Regression results: New Orleans.
The time period of the regression consisted of 65 months from January 1998 through May 2003. The dependent variable is the average monthly blood level of a data set of 2,295 children. This model was run using backward elimination procedures.
The model indicates that the variables soil moisture, wind speed, PM10, temperature, several interaction variables, and the monthly dummy variables for January, February, March, April, July, and October explained 59% of the variation in the response variable, monthly average child BPb concentration (R2 = 0.59, p = 0.0000078). The DW and LM statistics indicated that the model did not display serial autocorrelation (DW = 1.71, LM = 0.85). Figure 4 presents a chart of the average monthly child BPb concentration versus the predicted child BPb concentration.
The model regression coefficients indicate that the predictors with p-values < 0.05 are PM10 (p = 0.00003), the interaction between PM10 and wind (p = 0.00005), the interaction between PM10 and temperature (p = 0.0006), and soil moisture (p = 0.006). A summary of the statistics from the three cities is presented in Table 4.
Soil moisture and soil suspension.
Numerous studies have demonstrated that soil moisture concentration is a significant control of dust (PM10) suspension and loading (; Clausitzner and Singer 1996, 2000;; ). Soil moisture is a predictor of wind erosion because soil moisture contributes to bind particles together. Soil particles will become deflated when destabilizing forces such as drag, lift, and aerodynamic forces become greater than stabilizing forces such as particle weight and interparticle binding forces.
The threshold shear velocity of a particle is the wind velocity required to deflate (suspend) a particle in the atmosphere. Most models that predict wet threshold shear velocity (utw) of a particle take the form
where ut is the threshold shear velocity under dry conditions. The function f (moisture) is a function of the surface moisture expressed in terms of moisture content w (kilogram per kilogram) or capillary potential (Pascal).
Most models of the threshold shear velocity predict a rise in deflation threshold with increasing moisture content.
With decreasing soil matrix potential from a dry soil, the utw will increase exponentially until a soil matrix potential of –1.5 MPa occurs, at which no soil deflation takes place. The matrix potential (ψ) has been found to be a function of temperature (T ), air humidity (e/es), molar volume of water (Vw; 0.0224 m3/mol), and the universal gas constant (R; 8.3145 J/mol K):
These equations suggest that when temperature is high and soil moisture is low in the summertime, soils are susceptible to deflation. The modeling approach used in this study may have successfully explained the temporal variation in BPb because the matrix potential variables soil moisture (volumetric water content) and temperature were incorporated, which permits prediction of when soils are susceptible to dust emission. The variables PM10 and atmospheric Pb represent the end product of dust generation, and the variable wind speed may contribute to the explanation of the variance because of its effect on the PM10 (dust) deposition rate. Essentially, the high R2 values suggest that these variables predict temporal dust generation and exposure of children to Pb from dust in the environment.
The regression models indicate that environmental variables from outside the home, adjusted for seasonality, such as soil moisture, PM10, temperature, and wind speed, are significant predictors (p < 0.05) of children’s seasonal BPb fluctuations. This suggests that the Pb controlling the seasonal fluctuations originates from the outdoor environment. In the three cities studied here, the urban soils are highly contaminated by Pb. Thus, there is an abundant source of Pb in urban soils that could be suspended, resulting in elevated Pb dust loading rates during certain weather conditions.
The hypothesis that urban soils are being resuspended into the atmosphere is also supported by the literature that indicates a strong relationship between the suspension of surface soils and atmospheric particulates. In Bakersfield, California, 74% of PM10 from July through September 1988 was composed of geologically originated materials. One study estimated that street dust was composed of approximately 76% soil materials, and another study estimates that soil contributes between 57 and 90% of road dust. Finally, 43% of Pb emissions in the South Coast Air Basin in California resulted from the resuspension of soil and road dust.
Blood Pb seasonality.
Blood Pb seasonality suggests that Pb exposure varies over time. Thus, those who postulate that Pb-based paint is the primary source of Pb exposure also theorize that dust generation from Pb paint is somehow related to accelerated flaking from painted surfaces during summer months. Some have suggested that the opening and closing of windows painted with Pb paint may produce seasonal exposure to Pb dust. However, this study indicates that soil moisture, PM10, wind speed, and temperature fluctuations, adjusted for each other, are very strongly associated with children’s BPb levels. If these variables were noncausally associated with BPb fluctuations, and Pb paint was the source of the seasonality, this would imply that the opening and shutting of doors was associated with soil moisture, PM10, wind speed, and temperature. This appears to be counterintuitive because the opening and shutting of windows is likely temperature dependent and not dependent on soil moisture, PM10, and median wind speed.
We propose that BPb seasonality results from three or four exposure routes: First, children are likely seasonally exposed to elevated dust Pb loading on interior and exterior surfaces via hand-to-mouth processes, and the elevated Pb loading likely results from seasonal high Pb loading rates due to suspension of urban soils. Second, children are also exposed to direct ingestion of urban Pb-contaminated soil during warmer months. Third, it is possible that children are being seasonally exposed to Pb particles derived from the seasonal opening and shutting of windows painted with Pb paint. Fourth, children are exposed through inhalation to elevated atmospheric dust Pb concentrations resulting from seasonal soil suspension.
In addition, on the basis of the relationship between BPb, high temperatures, low soil moisture, and PM10 found in this study, we infer that arid climates with major urban areas and a long-term historical use of Pb in petroleum will experience high sustained rates of Pb loading that originate from Pb dust in soils. We also expect a more prolonged exposure when compared with colder climate areas, resulting in a muting of seasonality trends. These regions may include areas such as Los Angeles, California (USA), Mexico City and Tijuana, Mexico; arid areas of China, Pakistan, and India; and Nigeria, Saudi Arabia, and Cairo, Egypt. Furthermore, the aridity may exacerbate Pb exposure and childhood poisoning, particularly in emerging economies, where leaded gasoline is still in use. Soil Pb may be an important exposure variable in these environments, possibly overwhelming exposure to other sources of Pb.
Soil Pb and exposure.
A growing body of research supports the conclusion that urban soils contribute significantly to child BPb poisoning. Several ecologic studies have found associations between urban soil Pb concentrations and children’s BPb concentrations. A significant logarithmic relationship was reported between soil concentration (> 3,000 sampling points) and child BPb in New Orleans by census tract (R2 > 0.65). An independent study found a similar relationship in Syracuse (R2 > 0.65). Both these studies show that, non-temporally, soil accounts for a significant amount of the variation in BPb on a spatial basis. A study of urban dusts and soils in Britain found that soil and outdoor and indoor dusts were the most significant predictor variables in the regression model used to explain children’s BPb levels. The study also found that Pb in interior paint was not a strong independent variable in the final stepwise regression analysis used to explain children’s blood levels. A pooled study of 12 epidemiologic studies found that dust Pb loading and soil Pb concentration were the two most significant predictors of children’s BPb levels. In Bunker Hill, Idaho, structural equation modeling indicated that 40–50% of the BPb is from house dust, whereas approximately 30% was from community-wide soils and 30% from the yard at the home and the immediate neighborhood. In Tijuana, Mexico, several studies have found associations between soil Pb and children’s BPb levels.
The epidemiology literature has also indicated that the removal of Pb-contaminated soil results in significant reductions in child BPb concentration and supports the causal spatial relationship between soil Pb and BPb that has been found in the ecologic studies. Soil Pb abatement resulted in a 2.25–2.70 μg/dL reduction in BPb levels when a randomized trial of soil abatement was conducted. Logistic regression indicated that soil Pb > 165 mg/kg was independently associated with BPb concentrations > 10 μg/dL [odds ratio (OR) = 4.1; 95% confidence interval (CI), 1.3–12.4]. Yard soil removal resulted in a 3-fold reduction in the child BPb concentrations of children in the Silver Valley of Idaho, located near the Bunker Hill Superfund site, and reduced the dust Pb levels inside the homes. Removal of soil from children’s yards reduced the children’s BPb when compared with controls (OR = 0.28; 95% CI, 0.08–0.92). A study conducted on the effect of soil removal on child BPb concentrations at homes where the soil Pb concentration was greater than 500 mg/kg showed a statistically significant difference between BPb concentrations in homes in which soil was removed versus those where contaminated soil was not removed (p < 0.05).
Integrated Exposure Uptake Biokinetic Model for Lead in Children.
The degree to which the proposed exposure hypotheses result in reasonable predictions for BPb levels can be examined with the U.S. EPA’s Integrated Exposure Uptake Biokinetic Model for Lead in Children (IEUBK). To develop an exposure regime for the IEUBK model input, we note that indoor residential dusts generally show Pb concentrations about two times higher, on average, than the corresponding outdoor soils, although these results may have been influenced by fine particulate automotive Pb emissions. More recent data are available as summaries from 299 residential locations in eight different Idaho communities for the Human Health Risk Assessment for the Coeur d’Alene Basin showed an average enrichment factor of 1.6 for Pb concentration in carpet dusts compared with outdoor soils. Studies also indicate that dust Pb loading was 1.2 times higher in spring and fall than in winter and that in summer the loading was 1.6 times higher than in winter. Model predictions were obtained by specifying seasonal dust concentration differences that would result in the observed dust Pb loading differences. Using the IEUBK default values for Pb in air, water, food, and soil, soil and dust ingestion rates, and with soil representing 45% of the combined soil and dust ingestion, dust Pb concentration was specified as 333 ppm or 550 ppm. For children 1–2 years of age, this increased BPb values from 5.5 μg/dL (winter) to 7.0 μg/dL (summer). When the soil ingestion was specified as 25% of the combined soil/dust intake, the predictions ranged from 5.8 μg/dL (winter) to 7.8 μg/dL (summer).
A more realistic exposure regime for Syracuse might specify a soil Pb concentration of 150 mg/kg, with a winter–summer range of 200–320 mg/kg for the indoor dusts. If the ingested soils are limited to 10% of the total ingestion for combined soils and dusts, the predicted BPb values range from 4.5 to 5.9 μg/dL. This corroborates the range of observations for the 1997–1998 monitoring (Figure 3). Mean observed BPb values for recent Indianapolis data are lower than the 1994–1998 results in Syracuse, so IEUBK model input values would have to be lower to replicate the observations. If one assumes soil Pb is 100 mg/kg and ingestion of soil represents 10% of the total soil/ dust ingestion, and the dust concentration varies from 100 to 180 mg/kg and is associated with a bioavailability of 40% instead of the 30% default value, predicted BPb values range from 3.6 to 4.9 μg/dL. This shows reasonable agreement with the observations (Figure 2).
These exploratory uses of the IEUBK are meant only to indicate the types of concentration values and changes in physiochemical parameters that might provide a mechanistic explanation for the correlations observed in this work. A temporal structure in BPb levels can be modeled by the multicompartmental biokinetic IEUBK model using a wide variety of ingestion rates, soil and dust concentration values, and bioavailability parameters. Because we posit the seasonal variations in PM10, it is not unreasonable to consider changes in model default parameters for bioavailability. Small particle size is known to increase Pb uptake from particles. The potential influence of soil resuspension processes in modulating BPb levels needs careful examination, and future studies should incorporate detailed monitoring for temporal resolution of suspended Pb per volume of air, seasonal influences on residential dust Pb loading and concentration, and measures of Pb bioavailability. Further discussion about the many influences that the natural environment has on public health may be found in.
Conclusion
A conceptual model of child BPb seasonal Pb poisoning is suggested. Lead from multiple sources has accumulated in soils of urban environments. The seasonal resuspension of Pb-contaminated soil in urban atmospheres appears to be controlled by soil moisture and climate fluctuations. This study indicates that higher urban atmospheric Pb loading rates are experienced during periods of low soil moisture and within areas of Pb-contaminated surface soils. Children and adults living in urban areas where surface soils are contaminated with Pb may become exposed through indoor and outdoor inhalation of Pb dust and ingestion of Pb deposited within homes and outdoor surfaces. Because resuspension of Pb from contaminated soil appears to be driving seasonal child BPb fluctuations, concomitantly, we suggest that Pb-contaminated soil in and of itself may be the primary driving mechanism of child BPb poisoning in the urban environment.
References 80
- 1.
Aschengrau A, Beiser A, Bellinger D, Copenhafer D, Weitzman M. The impact of soil lead abatement on urban children’s BLL levels. Environ Res. 1994;67(2):125-148.
Not in our library10.1006/enrs.1994.1069
- 2.
Billick IH, Curran AS, Shier DR. Analysis of pediatric blood lead levels in New York City for 1970–1976. Environ Health Perspect. 1979;31:83-90.
Not in our library10.1289/ehp.7931183
- 3.
Blatt SD, Weinberger HL. Prevalence of lead exposure in a clinic using 1991 Centers for Disease Control and Prevention Recommendations. Am J Dis Children. 1993;147:761-763.
Not in our library10.1001/archpedi.1993.02160310063019
- 4.
Brinkmann R. Lead pollution in soils in Milwaukee County, Wisconsin. J Environ Sci Health. 1994;A29(5):909-919.
Not in our library
- 5.
Chaney RL Mielke HW 1986. Standards for soil lead limitations in the United States. In: Proceedings of the University of Missouri’s 20th Annual Conference on Trace Substances in Environmental Health (Delbert D, Hemphill DD, eds). Columbia, MO:University of Missouri Press, 357–377.
Not in our library
- 6.
Chen WN, Dong ZB, Li ZS, Yang ZT. Wind tunnel test of the influence on the erodibility of loessial sandy loam soils by wind. J Arid Environ. 1996;34(4):391-402.
Not in our library
- 7.
Chlopecka A, Bacon JR, Wilson MJ, Kay J. Forms of cadmium, lead, and zinc in contaminated soils from southwest Poland. J Environ Qual. 1996;25:69-79.
Not in our library
- 8.
Clark CS Bornschein R Succop P Peace B 1988. The Cincinnati soil-lead abatement demonstration project. In: Lead in Soils: Issues and Guidelines (Davies BE, Wixson BG, eds). Northwood, UK:Science Reviews Ltd, 287–300.
Not in our library
- 9.
Clausnitzer H, Singer MJ. Respirable-dust production from agricultural operations in the Sacramento Valley, California. J Environ Qual. 1996;25(4):877-884.
Not in our library
- 10.
Clausnitzer H, Singer MJ. Environmental influences on respirable dust production from agricultural operations in California. Atmos Environ. 2000;34(11):1739-1745.
Not in our library
- 11.
Cornelis W, Gabriels D. The effect of surface moisture on the entrainment of dune sand by wind: an evaluation of selected models. Sedimentology. 2003;50:771-790.
Not in our library
- 12.
Culbard E, Thornton I, Watt J, Wheatley M, Moorcroft S, Thompson M. Metal contamination in British urban dusts and soils. J Environ Qual. 1988;17:226-234.
Not in our library
- 13.
Dong A, Chesters G, Simsiman GV. Metal composition of soil, sediments, and urban dust and dirt samples from the Menomonee River Watershed, Wisconsin, U.S.A. Water Air Soil Pollut. 1984;22:257-275.
Not in our library
- 14.
Edlefson NE, Anderson ABC. Thermodynamics of soil moisture. Hilgardia. 1943;15:31-298.
Not in our library
- 15.
Elhelu MA, Caldwell DT, Hirpassa WD. Lead in inner-city soil and its possible contribution to children’s blood lead. Arch Environ Health. 1995;50(2):165-169.
Not in our library10.1080/00039896.1995.9940894
- 16.
Ericson JE, Gonzalez EJ. Hierarchical sampling of multiple strata: an innovative technique in exposure characterization. Environ Res. 2003;92:221-231.
Not in our library10.1016/s0013-9351(02)00088-9
- 17.
Ericson JE, Mishra SI. Soil lead concentrations and prevalence of hyperactive behavior among school children in Ottawa, Canada. Environ Int. 1990;16:247-256.
Not in our library
- 18.
Filippelli GM, Laidlaw M, Latimer J, Raftis R. Urban lead poisoning and medical geology: an unfinished story. GSA Today. 2005;15:4-11.
Not in our library
- 19.
Gonzalez EJ, Pham PG, Baker DB, Ericson JE. Tijuana childhood lead risk assessment revisited: validating a GIS model with environmental data. Environ Manag. 2002;29(4):559-565.
Not in our library10.1007/s00267-001-0007-1
- 20.
Haley VB Talbot TO 2004. Seasonality and trend in blood lead levels of New York State children. BMC Pediatrics 48 (10.1186/1471–2431–4–8).
Not in our library10.1186/1471-2431-4-8
- 21.
Hayes EB, McElvaine MD, Orbach HG, Fernandez AM, Lyne S, Matte TD. Long term trends in blood lead levels among children in Chicago: relationship to air lead levels. Pediatrics. 1994;93(2):195-200.
Not in our library
- 22.
Hollinger SE, Isard SA. A soil moisture climatology of Illinois. J Climat. 1994;7:822-833.
Not in our library
- 23.
Hopke PK, Lamb RE, Natusch DFS. Multielemental characterization of urban roadway dust. Environ Sci Technol. 1980;14:164-172.
Not in our library
- 24.
Hunt A, Johnson DL, Thornton I. Apportioning the sources of lead in house dusts in the London borough of Richmond, England. Sci Total Environ. 1993;138:183-206.
Not in our library10.1016/0048-9697(93)90414-2
- 25.
Hunter JM. The summer disease; an integrative model of the seasonality aspects of childhood BLL poisoning. J Soc Sci Med. 1977;11:691-703.
Not in our library10.1016/0037-7856(77)90155-x
- 26.
Hwang YH, Wang JD. Temporal fluctuation of the lead level in the cord blood of neonates in Taipei. Arch Environ Health. 1990;45(1):42-45.
Not in our library10.1080/00039896.1990.9935923
- 27.
Iverson JD, Pollack JB, Greenley R, White BR. Saltation threshold on Mars: the effect of interparticle force, surface roughness, and low atmospheric density. Icarus. 1976;29:318-393.
Not in our library
- 28.
Johnson D, Bretsch J. Soil lead and children’s BLL Levels in Syracuse, NY, USA. Environ Geochem Health. 2002;24(4):375-385.
Not in our library
- 29.
Johnson D, McDade K, Griffith D. Seasonal variation in paediatric blood levels in Syracuse, NY, USA. Environ Geochem Health. 1996;18(2):81-88.
Not in our library10.1007/bf01771136
- 30.
Kimbrough RD, LeVois M, Webb DR. Management of children with slightly elevated BLL levels. Pediatrics. 1994;93:188-191.
Not in our library
- 31.
Kurkjian CR, Flegal AR. Isotopic evidence of the persistent dominance of blood lead concentrations by previous gasoline lead emissions in Yerevan, Armenia. Environ Res. 2003;93(3):308-315.
Not in our library10.1016/s0013-9351(03)00066-5
- 32.
Laidlaw M 2001. Distribution and Sources of Metals in Soils of Marion County, Indiana [Master’s Thesis]. Indianapolis, IN:Indiana University.
Not in our library
- 33.
Lankey RL, Davidson CI, McMichael FC. Mass balance for lead in the California south coast air basin: an update. Environ Res. 1998;78:86-93.
Not in our library10.1006/enrs.1998.3853
- 34.
Lanphear BP, Matte T, Rogers J, Clickner R, Dietz B, Bornschein R, et al. The contribution of lead-contaminated house dust and residential soil to children’s blood lead levels: a pooled analysis of 12 epidemiological studies. Environ Res A. 1998;79:51-68.
Not in our library10.1006/enrs.1998.3859
- 35.
Lanphear BP, Succop P, Roda S, Henningsen G. The effect of soil abatement on BLL levels in children living near a former smelting and milling operation. Pub Health Rep. 2003;118(2):83-91.
Not in our library10.1016/s0033-3549(04)50223-6
- 36.
Lee Pyeong-Koo, Touray JC, Baillif P, Ildefonse JP. Heavy metal contamination of settling particles in a retention pond long the A-71 motorway in Sologne, France. Sci Total Environ. 1997;201:1-15.
Not in our library10.1016/s0048-9697(97)84048-x
- 37.
Lejano RP, Ericson JE. Tragedy of the temporal commons: soil-bound lead and the anachronicity of risk. J Environ Plan Manag. 2005;48(2):299-318.
Not in our library
- 38.
Macey GP, Her X, Reibling ET, Ericson JE. An investigation of environmental racism claims: testing environmental management approaches with a geographic information system. Environ Manag. 2001;27(6):893-907.
Not in our library10.1007/s002670010197
- 39.
Maisonet M, Bove FJ, Kaye WE. A case-control study to determine risk factors for elevated blood lead levels in children, Idaho. Toxicol Ind Health. 1997;13(1):67-72.
Not in our library10.1177/074823379701300106
- 40.
Malcoe LH, Lynch RA, Keger MC, Skaggs VJ. Lead sources, behaviors, and socioeconomic factors in relation to blood lead of Native American and white children: a community-based assessment of a former mining area. Environ Health Perspect. 2002;110(suppl 2):221-231.
Not in our library10.1289/ehp.02110s2221
- 41.
Marrero O, Meigs JW, Stark AD, Quah RF. Seasonal patterns in children’s blood lead levels: a second peak in late winter. Conn Med. 1983;47(1):1-5.
Not in our library
- 42.
McKenna-Neuman C, Nickling WG. A theoretical and wind tunnel investigation of the effect of capillary water on the entrainment of sediment by wind. Can J Soil Sci. 1989;69:79-96.
Not in our library
- 43.
Mielke HW. Lead dust contaminated USA communities: comparison of Louisiana and Minnesota. Appl Geochem. 1993;8(suppl 2):257-261.
Not in our library
- 44.
Mielke HW. Lead in New Orleans soils: new images of an urban environment. Environ Geochem Health. 1994;16(3/4):123-128.
Not in our library10.1007/bf01747908
- 45.
Mielke HW, Adams JE, Huff B, Pepersack J, Reagan PL, Stoppel D, et al. Dust control as means of reducing inner-city childhood Pb exposure. Trace Subst Environ Health. 1992;25:121-128.
Not in our library
- 46.
Mielke HW, Anderson JC, Berry KJ, Mielke PW, Chaney RL, Leech M. Lead concentrations in inner-city soils as a factor in the child lead problem. Am J Public Health. 1983;73:1366-1369.
Not in our library10.2105/ajph.73.12.1366
- 47.
Mielke HW, Barroughs S, Wade R, Yarrow T, Mielke PW. Urban lead in Minnesota: soil transect results of four cities. J Minn Acad Sci. 1984/85;50:19-24.
Not in our library
- 48.
Mielke HW, Dugas D, Mielke PW, Smith KS, Smith SL, Gonzales CR. Associations between soil lead and children’s blood lead in urban New Orleans and rural Lafourche Parish of Louisiana. Environ Health Perspect. 1997;105:950-954.
Not in our library10.1289/ehp.97105950
- 49.
Mielke HW, Powell ET, Shah A, Gonzales CR, Mielke PW. Multiple metal contamination from house paints: consequences of power sanding and paint scraping in New Orleans. Environ Health Perspect. 2001;109:973-978.
Not in our library10.1289/ehp.01109973
- 50.
Mielke HW, Reagan PL. Soil is an important pathway of human lead exposure. Environ Health Perspect. 1998;106(suppl 1):217-229.
Not in our library10.1289/ehp.98106s1217
- 51.
Mielke HW, Smith MK, Gonzales CR, Mielke PW. The urban environment and children’s health: soils as an integrator of lead, zinc and cadmium in New Orleans, Louisiana, U.S.A. Environ Res. 1999;80(2):117-129.
Not in our library10.1006/enrs.1999.3966
- 52.
Morgenstern H 1998. Ecological studies. In: Modern Epidemiology (Rothman KJ, Greenland S, eds). 2nd ed. Philadelphia: Lippincott-Raven, 459–480.
Not in our library
- 53.
NCDC (National Climatic Data Center) 2004. Climate Resources. Available: http://www.ncdc.noaa.gov/oa/climate/climateresources.html [accessed 27 April 2005].
Not in our library
- 54.
New York State Department of Health 2002. Screening for Lead Poisoning. Albany:New York State Department of Health. Available: http://www.health.state.ny.us/nysdoh/lead/handbook/phc4.htm [accessed 25 April 2005].
Not in our library
- 55.
Nickovic S, Kallos G, Papadopoulos A, Kakaliagou O. A model prediction of desert dust cycle in the atmosphere. J Geophys Res. 2001;106:18113-18130.
Not in our library
- 56.
Nriagu JO, Blackson MI, Ocram K. Childhood lead poisoning in Africa: a growing Public Health Problem. Science Total Environ. 1996;181(2):93-101.
Not in our library10.1016/0048-9697(95)04954-1
- 57.
Rabinowitz MB, Leviton A, Needleman H, Bellinger D, Waternaux C. Environmental correlates of infant blood lead levels in Boston. Environ Res. 1985;38:96-107.
Not in our library10.1016/0013-9351(85)90075-1
- 58.
Rabinowitz MB, Needleman HL. Temporal trends in the lead concentration of umbilical cord blood. Science. 1982;216:1429-1431.
Not in our library10.1126/science.7089532
- 59.
Rieuwerts JS, Farago MA. Lead contamination in smelting and mining environments and variations in chemical forms and bioavailability. Environ Geochem Res. 1995;7(4):113-123.
Not in our library
- 60.
Rothenberg SJ, Williams FA, Delrahim S, Khan F, Kraft M, Lu M, et al. Blood levels in children in South Central Los Angeles. Arch Environ Health. 1996;51(5):383-388.
Not in our library10.1080/00039896.1996.9934426
- 61.
Selinus O Alloway B Centeno JA Finkelman RB Fuge R Lindh U 2005. Essentials of Medical Geology: Impacts of the Natural Environment on Public Health. Amsterdam:Elsevier Academic Press.
Not in our library
- 62.
Semlali RM, Dessogne JB, Monna F, Bolte J, Azimi S, Denaix L, et al. Modeling lead input and output in soils using lead isotopic geochemistry. Environ Sci Technol. 2004;38:1513-1521.
Not in our library10.1021/es0341384
- 63.
Sheldrake S, Stifelman M. A case study of lead contamination cleanup effectiveness at Bunker Hill. Sci Total Environ. 2003;303(1–2):105-123.
Not in our library10.1016/s0048-9697(02)00354-6
- 64.
Sridhar M, Adogame L, Olawuyi J. Lead exposure in urban centres: a case study from Ibadan, Nigeria [Abstract]. Epidemiology. 2000;11(4):S62.
Not in our library
- 65.
Stark AD, Quah RF, Meigs JW, De Louise ER. Season as a factor in variability of blood lead levels in children. Conn Med. 1980;44(7):1-5.
Not in our library
- 66.
Steele MJ, Beck BD, Murphy BL, Strauss HS. Assessing the contribution from lead in mining wastes to blood lead. Reg Toxicol Pharmacol. 1990;11(2):158-190.
Not in our library10.1016/0273-2300(90)90019-8
- 67.
Ter Haar G, Aronow R. New information on lead in dirt and dust as related to the childhood lead problem. Environ Health Perspect. 1974;7:83-89.
Not in our library10.1289/ehp.74783
- 68.
TerraGraphics and URS Greiner 2001. Final Baseline Human Health Risk Assessment for the Coeur d’Alene Basin Extending from Harrison to Mullan on the Coeur d’Alene River and Tributaries, Remedial Investigation/Feasibility Study. Prepared for Idaho Department of Health and Welfare, Division of Health, Idaho Department of Environmental Quality, and U.S. Environmental Protection Agency, Region 10. Moscow, ID:TerraGraphics Environmental Engineering Inc.; Washington, DC:URS Greiner Inc.
Not in our library
- 69.
Thornton I, Davies DJA, Watt JM, Quinn MJ. Lead exposure in young children from dust and soil in the United Kingdom. Environ Health Perspect. 1990;89:43-48.
Not in our library10.1289/ehp.908955
- 70.
Tijhuis L, Brattli B, Saether OM. A geochemical survey of topsoil in the City of Oslo, Norway. Environ Geochem Health. 2002;24:67-94.
Not in our library
- 71.
Tong S. Roadside dust and soil contamination in Cincinnati, Ohio, USA. Environ Manag. 1990;14:107-113.
Not in our library
- 72.
Requirements for notification, evaluation and reduction of lead-based paint hazards in federally owned residential property and housing receiving federal assistance. Fed Reg. 1999;64(178):50140-50231.
Not in our library
- 73.
U.S. EPA 1994. Guidance Manual for the Integrated Exposure Biokinetic Model for Lead in Children. EPA/540/R-93/049F. Washington, DC:Office of Emergency and Remedial Response, U.S. Environmental Protection Agency.
Not in our library
- 74.
U.S. EPA 1995. Seasonal Rhythms of BLL Levels: Boston, 1979–1983: Final Report. EPA 747-R-94-003. Washington, DC:U.S. Environmental Protection Agency.
Not in our library
- 75.
U.S. EPA 1996. Seasonal Trends in BLL Levels in Milwaukee: Statistical Methodology. EPA 747-R-95-010. Washington, DC:U.S. Environmental Protection Agency.
Not in our library
- 76.
Lead: Identification of Dangerous Levels of Lead; Final Rule. 40CFR745. Fed Reg. 2001;66:6763-6765.
Not in our library
- 77.
von Lindern I, Spalinger S, Petroysan V, von Braun M. Assessing remedial effectiveness through the blood lead:soil/dust lead relationship at the Bunker Hill Superfund Site in the Silver Valley of Idaho. Sci Total Environ. 2003;303(1–2):139-170.
Not in our library10.1016/s0048-9697(02)00352-2
- 78.
Wixson BG, Davies BE. Guidelines for lead in soil: proposal of the Society for Environmental Geochemistry and Health. Environ Sci Technol. 1994;28(1):26A-31A.
Not in our library
- 79.
Yiin LM, Rhoads GG, Lioy PJ. Seasonal influences on childhood lead exposure. Environ Health Perspect. 2000;108:177-182.
Not in our library10.1289/ehp.00108177
- 80.
Young TM, Heeraman DA, Sirin G, Ashbaugh LL. Resuspension of soil as a source of airborne lead near industrial facilities and highways. Environ Sci Technol. 2002;36(11):2484-2490.
Not in our library10.1021/es015609u
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