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In their article on seasonality and children’s blood lead (BPb) levels, Laidlaw et al. (2005) stated that “lead-contaminated soil in and of itself may be the primary driving mechanism of child BPb poisoning in the urban environment.” We believe that the data presented by Laidlaw et al. (2005) do not support this conclusion and that they misrepresent the many other studies of childhood lead poisoning, which support a more comprehensive, validated approach. To support their “soil-only” hypothesis, Laidlaw et al. (2005) made three primary arguments: a) soil lead represents a large and available reservoir of environmental lead; b) resuspension of lead from contaminated soil followed by inhalation of airborne particulate matter < 10 μm in diameter (PM10) and dust deposition on interior surfaces is the major source of lead exposure to children; and c) the major source of lead contaminated soil is fallout from the past use of tetraethyl lead in gasoline. Laidlaw et al. (2005) did not cite the compelling body of scientific evidence demonstrating that deteriorated lead-based paint and the contaminated dust and soil it generates is highly correlated with BPb levels in children. These have been reviewed at length elsewhere (National Academy of Sciences 1993; Jacobs 1995; President’s Task Force on Environmental Health Risks and Safety Risks to Children 2000). Indeed, Laidlaw et al. failed to recognize the enlightened statutory definition of the term “lead-based paint hazard,” which includes not only deteriorated lead-based paint but also interior settled house dust and bare soil. Together, these constitute the principal exposure sources and pathways for most (but not all) children today (Residential Lead-Based Paint Hazard Reducation Act of 1992—Title X 1992). Furthermore, documented evidence shows that soil lead levels are highest in soil at the house drip line and greatly decrease farther away from the house, regardless of whether or not the house is in a rural area or city (Jacobs 1995). Laidlaw et al. (2005) ignored confounding due to the coexistence of old, poorly maintained lead-painted housing and traffic congestion in urban areas. They failed to develop any rationale to exclude lead paint as a prominent source of lead exposure and should have included a measure of it in their models. Furthermore, they did not support their assumption that PM10 data can be used as a surrogate for airborne lead particulate. Laidlaw et al. should have used the more direct measures of airborne lead particulate levels, which are available from the U.S. Environmental Protection Agency’s (EPA) National Ambient Air Quality program (U.S. EPA 2004), rather than the convoluted indirect measures of particulate matter < 10 μm in diameter (PM10), soil moisture, and other variables. Studies of the effectiveness of soil removal in urban residential areas without addressing deteriorated lead paint have demonstrated that the “soil-only” approach being recommended by Laidlaw et al. (2005) is of limited value (U.S. EPA 1996). Even in Superfund sites where old mining and smelter wastes have resulted in very high soil lead levels, efforts that do not also address deteriorated lead paint often are disappointing. Furthermore, in the largest and most recent study of lead-based paint hazard control (which addressed lead paint hazards in > 3,000 homes in a dozen jurisdictions), house dust lead levels remained below preintervention levels for at least 3 years following the intervention (National Center for Healthy Housing and University of Cincinnati 2004). In a smaller follow-up study, dust lead levels remained between 11% and 75% lower than baseline levels for 6 years following lead-based paint hazard intervention (Wilson J, Pivetz T, Ashley P, Jacobs D, Strauss W, Menkedick J, et al., unpublished data). If the contention of Laidlaw et al. (2005) is correct (i.e., that urban soil lead is being resuspended and deposited inside homes), dust lead levels should have increased after intervention in these studies. In fact, they did not. This directly contradicts the authors’ conclusions. Finally, Laidlaw et al. (2005) erroneously cited a pooled analysis (Lanphear et al. 1998), which they believe supports their view that soil and dust lead are the most significant predictors of children’s BPb. In fact, the model used in that study also included paint lead and paint condition as variables. If the dust and soil lead terms are forced out of the model, paint lead becomes the most significant predictor, which is consistent with the now well-known pathway of paint to settled house dust and bare soil, to children’s hands, to ingestion through hand-to-mouth contact. The pooled analysis (co-authored by D.E.J.) cannot be used to justify Laidlaw et al.’s “soil-only” approach. The latest figures from the National Health and Nutrition Examination Survey indicate that the enormous disparity in the prevalence of BPb levels > 10 μg/dL once seen between African-American and white children has diminished greatly [Centers for Disease Control and Prevention (CDC) 2005]. Overall, the number of children in the United States with excessive BPb levels has declined from 890,000 in 1991–1994 to 310,000 in 1999–2002. Much of this is the result of federal, state, and local efforts to create a reservoir of lead-safe housing in communities at greatest risk. This success is tempered by recent evidence that a safe BPb level for children has not been demonstrated. The lack of a safe threshold reinforces the realization that to prevent the adverse health effects caused by lead exposure, we must exercise the wisdom to recognize and address the many sources of lead in children’s environments. The reality is too complicated and the cost of failure too devastating to reduce this to a one-source solution.

Policy statements providing health and environmental criteria for blood lead (PbB) often give recommendations on an acceptable distribution of PbB concentrations. Such statements may recommend distributions of PbB concentrations including an upper range (e.g., maximum and/or 90th percentile values) and central tendency (e.g., mean and/or 50th percentile) of the PbB distribution. Two major, and fundamentally dissimilar, methods to predict the distribution of PbB are currently in use: statistical analyses of epidemiologic data, and application of biokinetic models to environmental lead measurements to predict PbB. Although biokinetic models may include a parameter to predict contribution of lead from bone (PbBone), contemporary data based on chemical analyses of pediatric bone samples are rare. Dramatic decreases in environmental lead exposures over the past 15 years make questionable use of earlier data on PbBone concentrations to estimate a contribution of lead from bone; often used by physiologic modelers to predict PbB. X-ray fluorescent techniques estimating PbBone typically have an instrument-based quantitation limit that is too high for use with many young children. While these quantitation limits have improved during the late 1990s, PbBone estimates using an epidemiologic approach to describing these limits for general populations of children may generate values lower than the instrument's quantitation limit. Additional problems that occur if predicting PbB from environmental lead by biokinetic modeling include a) uncertainty regarding the fractional lead absorption by young children; b) questions of bioavailability of specific environmental sources of lead; and c) variability in fractional absorption values over a range of exposures. Additional sources of variability in lead exposures that affect predictions of PbB from models include differences in the prevalence of such child behaviors as intensity of hand-to-mouth activity and pica. In contrast with these sources of uncertainty and variability affecting physiologic modeling of PbB distributions, epidemiologic data reporting PbB values obtained by chemical analyses of blood samples avoid these problems but raise other issues about the validity of the representation of the subsample for the overall population of concern. State and local health department screening programs and/or medical evaluation of individual children provide PbB data that contribute to databases describing the impact of environmental sources on PbB. Overall, application of epidemiologic models involves fewer uncertainties and more readily reflects variability in PbB than does current state-of-the-art biokinetic modeling.

This study evaluates associations between soil lead concentrations (SPb), age of housing, and blood lead levels (BPb) of children in metropolitan New Orleans and Lafourche Parish, Louisiana. The database includes over 2,600 SPb and 6,000 BPb samples paired by their median values and pre-1940 housing percentages for 172 census tracts. Associations were evaluated with Fisher's exact test and Spearman's rho test and modeled with the least sum of absolute deviations regression. Census tracts with low SPb are associated with new housing, but census tracts with high SPb are evenly split between old and new housing [Fisher's exact test, p = 8.60 X 10(-13) for the percentage of housing built before 1940 (percent pre-1940 housing) versus SPb]. The p-value for SPb versus BPb is 12 orders of magnitude stronger than the p-value for percent pre-1940 housing versus BPb. Census tracts with low BPb are associated with new housing, but census tracts with high BPb are split evenly between old and new housing (Fisher's exact test, p = 1. 67 X 10(-12) for percent pre-1940 housing versus BPb). Census tracts with high SPb are associated with high BPb and census tracts with low SPb are associated with low BPb (Fisher's exact test, p = 3.18 X 10(-24) for BPb versus SPb). The Spearman's rho test of the association of SPb and BPb in Orleans and Lafourche Parishes yielded a p-value of 6.12 X 10(-24). The least sum of absolute deviations regression model of the data is BPb = 1. 845 + 0.7215 (SPb)0.4. A comparison of the modeled BPb versus observed BPb has an r(2) of 0.552 and a p-value of 2.83 X 10(-23) that this relation was due to chance. If blood lead in children is more closely associated to soil lead than to the age of housing, then primary lead prevention should also include soil lead. Images Figure 1.

I support the warning from Rabito et al. (2012) about the hazards of power sanding and their call for enforcing the New Orleans, Louisiana, Code of Ordinances (2001) and U.S. Environmental Protection Agency (EPA) Renovation, Repair, and Painting Rule (U.S. EPA 2008) for cleanup of residual lead dust at residential properties. Power sanding has been a scourge to the safety and well-being of children and pets in New Orleans for many years (Jacobs et al. 2003; Mielke et al. 2001). Unfortunately, Rabito et al. (2012) made a fundamental error by comparing medians from soil data (Mielke et al. 2005), which I shared with them, with principally foundation soil data. These medians included four sample locations: foundation, open space (i.e., mid-yard), residential-street side, and busy-street side. Comparing pre-Katrina median soil lead from our survey with foundation soil samples post-Katrina does not provide insight into foundation soil lead changes stemming from renovation. Furthermore, evidence from Louisiana blood lead surveillance shows decreasing—not increasing—exposure after Hurricane Katrina. The 2008 Orleans Parish results show that 38.5% of the children were tested, and 6.4% of these presented with lead concentrations ≥ 10 µg/dL (Louisiana Childhood Blood Lead Surveillance System 2009). In 2010, 40.0% of the children in Orleans Parish were tested, including a higher proportion of children from outer areas of New Orleans, and 3.3% presented with ≥ 10 µg/dL (Louisiana Childhood Blood Lead Surveillance System 2010). The continuing pattern of lead poisoning is uneven, with larger preva-lence in the interior of the city and lower prevalence in outer areas of the city (Zahran et al. 2011, their Figure 1). From the perspective of lead changes in soil and blood, both measurements decreased after Katrina (Zahran et al. 2010). Although large numbers of children are still at risk from lead poisoning, the blood lead trends reported for New Orleans do not support the future implications suggested by Rabito et al. (2012). Regarding the future, it is important to note that New Orleans is under-taking improvements to playgrounds so children will have lead-safe play areas in every neighborhood (Schleifstein 2011). A project is also under way to improve the quality of play areas at New Orleans child care centers (Mielke et al. 2011a). In addition, projects to eliminate lead-based paint and soil lead hazards at public housing properties are ongoing (Reckdahl 2011). The implications are that in the future, New Orleans will be safer with respect to lead. Private residential properties often have higher risk for lead poisoning than do public properties (Mielke et al. 2011b), and Rabito et al. have appropriately called attention to the need to address lead contamination of private residential properties.

We thank Mielke for his interest in our study of residential lead hazards in New Orleans (Rabito et al. 2012). In our study we found that most homes had either dust or soil lead above federal standards and concluded that children are at risk for lead exposure. Regarding the specific issue of whether soil lead has increased or decreased, we agree that a direct comparison between census-level soil lead survey data and direct measure-ments of residential samples has limitations. To reiterate the limitations outlined in our article (Rabito et al. 2012), differences in the number of soil samples, the sampling methodology, and the sample location limited our ability to directly measure any change in soil lead levels. Although it is of interest to know whether soil lead has increased or decreased as a result of Hurricane Katrina, our focus was to measure current residential lead hazards, because lead contamination in and around homes is the primary pathway of exposure for children (Lanphear and Roghmann 1997). Our finding that 61% of homes had lead levels above federal standards provides evidence that New Orleans children are at high risk of exposure. That the samples were collected from homes typically considered to be low risk (given the socio-demographic characteristics of the sample) is cause for added concern. In his letter, Mielke refers to trends in blood lead levels. The issue of whether blood lead levels are increasing or decreasing in New Orleans children—which was not within the scope of our study (Rabito et al. 2012)—is not easily addressed using surveillance data. Screening practices and rates drive the reported prevalence in any given year. Zahran et al. (2010) compared aggregate blood lead levels derived from the Louisiana Childhood Blood Lead Surveillance System (CBLSS) pre-Hurricane Katrina to levels post-Hurricane Katrina and found that median blood lead had decreased. However, profound changes in the socio-demographic makeup of the New Orleans population make the comparison vulnerable to significant bias (Bloomberg 2011). The surveillance data provided by Mielke supports our notion that the post-Hurricane Katrina population screened under the CBLSS is not stable from year to year. As stated by Mielke, 6.4% of children had elevated blood lead levels in 2008, but the estimate decreased to 3.3% in 2010. This decrease might not be valid because the majority of children in the 2008 cohort were from the inner city (with the highest prevalence of old housing) whereas the 2010 cohort included a higher proportion from outer areas of the city (considered low risk based on housing age). The assumption by Zahran et al. (2010) that soil lead serves as a proxy for length of lead exposure is likely not valid given the amount of housing destabilization and subsequent mobility of the population in the years following the storm. Finally, low screening rates, coupled with a reporting level of > 10 µg/dL (widely accepted as above the level of concern) does not allow for the valid estimation of the preva-lence of elevated blood lead levels in New Orleans children. Regardless of the inconclusive nature of blood lead data, given that 61% of sampled homes have significant lead hazards, we maintain that New Orleans children who live in old housing are at risk for lead exposure independent of race or income. We support the recent statement by the Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention that “the goal of primary prevention is to ensure that all homes become lead-safe and do not contribute to childhood lead exposure” (Centers for Disease Control and Prevention 2012). The City of New Orleans has made strides in its fight to reduce lead hazards in public places; however, they should not relax in their efforts to protect the environ-ment from further contamination.

Even as the Gulf Coast grapples with possibly its worst environmental catastrophe ever, a silver lining has emerged from the devastation of the stormy summer of 2005: both soil lead levels and children’s blood lead levels fell dramatically across New Orleans, Louisiana, after Hurricanes Katrina and Rita swept in clean sediment over the city’s lead-contaminated soil.1 This positive outcome bolsters the case for soil remediation as a way to protect children from lead poisoning. Howard Mielke, a research professor at the Tulane/Xavier Center for Bioenvironmental Research, says he and his colleagues “took advantage of a catastrophic natural event to examine changes in the environment and health.” Along with Sammy Zahran at Colorado State University and colleagues, Mielke measured soil lead levels at 46 New Orleans sites in 2000 and in 2006. The researchers obtained pre- and post-hurricane blood lead data for 13,306 children aged 6 years and younger from the Louisiana Childhood Lead Poisoning Prevention Program. After the hurricanes, only 6 of the 46 sites had soil lead concentrations above 400 mg/kg, compared with 15 of 46 sites before the hurricanes. The 400 mg/kg (ppm) cutoff is the point at which the U.S. Environmental Protection Agency recommends remediation of bare soil in children’s play areas; a cutoff of 1,200 ppm is recommended for other bare soil areas. Median soil lead levels fell 46% (from 328.54 mg/kg to 203.33 mg/kg), and median blood lead declined 33% (from 5.14 μg/dL to 3.45 μg/dL). In neighborhoods where soil lead declined by 50% or more, blood lead dropped by 53% on average. Children born after Katrina and Rita had the lowest blood lead levels of all those studied.1 “There’s a tremendous amount of lead in New Orleans’ soil—and all cities,” says Mielke. This toxic reservoir, which accumulated when lead was added to paint and gasoline, is constantly being redistributed by rain, wind, and construction activity. The hurricanes’ blanket of cleaner soil—sediment from Lake Pontchartrain and nearby wetlands that was carried through the city’s breached levees by the storm surge—likely will not persist, predicts Mielke. However, the natural effect of the blanket of sediment is duplicated by soil remediation, in which clean soil with no more than 5 ppm lead is hauled in and deposited on a geotextile barrier. The barrier allows water to pass through but contains the lead and prevents anyone from digging into contaminated soil underneath. Soil is often an underappreciated source of childhood lead exposure in cities, relative to lead paint in homes,2 yet “both are to blame for childhood blood lead elevation,” says Rudolph Jaeger, a research professor of environmental medicine at New York University Medical School. Exposure to lead in soil contributes to elevated blood lead, which in turn is associated with reduced educational outcomes.3 Mielke has worked with New Orleans area child-care centers where soil has contained 500–5,000 mg/kg lead. “If we pay attention to environments where children play in the very early years of life, we may reduce their blood lead levels,” Mielke says. Mielke also thinks the current blood lead level of concern of 10 μg/dL—the level at which the Centers for Disease Control and Prevention recommends medical intervention—is too high. Studies show that just 2 μg/dL adversely impacts the heart,4 kidney,5 and child intelligence,6 and many researchers believe there is no safe level of exposure.7 “If we lower this threshold, there may be more interest in primary prevention measures like soil remediation,” Mielke says.

Our article (Laidlaw et al. 2005) is about seasonality of blood lead (BPb) and developing a predictive model using climatic variables. It is a new and unique finding about lead, marked particularly by the fact that it identifies diffuse soil lead as a significant component of lead sources in urban children. In the article, we argued that meteorologic factors can be robustly applied as a predictor for seasonal variations in children’s BPb, which can be used as a potential tool for health care clinicians in the fight to eliminate lead poisoning in youth. We did not intend to review the literature on lead sources; a vast literature already exists of such studies. Suggesting that we propose the “soil-only hypothesis” completely misconstrues our work. Brown and Jacobs fail to appreciate our argument that lead accumulation in soil is from a combination of lead-based paint, leaded-gasoline, and many other sources, but is clearly not from lead-based paint alone. They fail to understand the fact that soil normally contains very small amounts of lead, and research from many cities has shown that there has been an excessive accumulation of lead in inner-cities (Filippelli et al. 2005; Mielke 2005). We acknowledge that multiple exposure routes for lead exist for children and likely influence the observed seasonality trends in BPb levels (Laidlaw et al. 2005). We seek to assist with scientific understanding of how and why inner-city children are commonly excessively exposed to lead, and we seek a solution to that problem. We are concerned that people working at agencies that should champion the reduction of lead exposure do not appreciate the fact that multiple sources of lead have accumulated in urban environments and that all major sources and reservoirs need full attention if we expect to meet the goals of Healthy People 2010 (2005). Our work suggests that, to fully address the childhood lead exposure problem in the United States, a paradigm shift is required that includes all major reservoirs of active lead dust.

In this study we estimated the number of housing units in the United States with lead-based paint and lead-based paint hazards. We included measurements of lead in intact and deteriorated paint, interior dust, and bare soil. A nationally representative, random sample of 831 housing units was evaluated in a survey between 1998 and 2000; the units and their occupants did not differ significantly from nationwide characteristics. Results indicate that 38 million housing units had lead-based paint, down from the 1990 estimate of 64 million. Twenty-four million had significant lead-based paint hazards. Of those with hazards, 1.2 million units housed low-income families (< 30,000 US dollars/year) with children under 6 years of age. Although 17% of government-supported, low-income housing had hazards, 35% of all low-income housing had hazards. For households with incomes greater than or equal to 30,000 US dollars/year, 19% had hazards. Fourteen percent of all houses had significantly deteriorated lead-based paint, and 16% and 7%, respectively, had dust lead and soil lead levels above current standards of the U.S. Department of Housing and Urban Development and the U.S. Environmental Protection Agency. The prevalence of lead-based paint and hazards increases with age of housing, but most painted surfaces, even in older housing, do not have lead-based paint. Between 2% and 25% of painted building components were coated with lead-based paint. Housing in the Northeast and Midwest had about twice the prevalence of hazards compared with housing in the South and West. The greatest risk occurs in older units with lead-based paint hazards that either will be or are currently occupied by families with children under 6 years of age and are low-income and/or are undergoing renovation or maintenance that disturbs lead-based paint. This study also confirms projections made in 2000 by the President's Task Force on Environmental Health Risks and Safety Risks to Children of the number of houses with lead-based paint hazards. Public- and private-sector resources should be directed to units posing the greatest risk if future lead poisoning is to be prevented.

This review shows the equal or greater importance of leaded gasoline-contaminated dust compared to lead-based paint to the child lead problem, and that soil lead, resulting from leaded gasoline and pulverized lead-based paint, is at least or more important than lead-based paint (intact and not pulverized) as a pathway of human lead exposure. Because lead-based paint is a high-dose source, the biologically relevant dosage is similar to lead in soil. Both lead-based paint and soil lead are associated with severe lead poisoning. Leaded gasoline and lead in food, but not lead-based paint, are strongly associated with population blood lead levels in both young children and adults. Soil lead and house dust, but not lead-based paint, are associated with population blood lead levels in children. Most soil lead and house dust are associated with leaded gasoline. Lead-based paint dust is associated with cases of renovation of either exterior or interior environments in which the paint was pulverized. Based upon the limited data to date, abatement of soil lead is more effective than abatement of lead-based paint in reducing blood lead levels of young children. About equal numbers of children under 7 years of age are exposed to soil lead and lead-based paint. Seasonality studies point to soil lead as the main source of population blood lead levels. Soil lead is a greater risk factor than lead-based paint to children engaged in hand-to-mouth and pica behavior. In summary, soil lead is important for addressing the population of children at risk of lead poisoning. When soil lead is acknowledged by regulators and the public health community as an important pathway of human lead exposure, then more effective opportunities for improving primary lead prevention can become a reality. Images Figure 1

The costs of lead-based paint hazard control in housing are well documented, but the costs of cleanup after improper, inherently dangerous, methods of removing lead-based paint are not. In this article we report a case of childhood lead poisoning and document the costs of decontamination after uncontained power sanding was used to remove paint down to bare wood from approximately 3,000 ft(2) of exterior siding on a large, well-maintained 75-year-old house in a middle-income neighborhood. After the uncontrolled removal of lead-based paint, interior dust lead levels ranged from 390 to 27,600 micro g Pb/ft(2) (on floors and windowsills) and bare soil lead levels ranged from 360 ppm in the yard to 3,900 ppm along the foundation to 130,000 ppm in the child's play area, well above applicable U.S. Department of Housing and Urban Development/U.S. Environmental Protection Agency standards. The hard costs of decontamination were over $195,000, which greatly exceeds the incremental cost of incorporating lead-safe work practices into repainting. This case report highlights the need to incorporate lead-safe work practices into routine repainting, remodeling, and other renovation and maintenance jobs that may disturb lead-based paint.

The lead exposure of children and their mothers has been studied in two towns with mean soil lead contents of 900 and 400 ppm. No significant difference in blood or fecal lead contents was demonstrated between the two populations, but a small difference in hair lead content was shown. The blood lead content of children was greater than that of their mothers and was higher in the summer than in the spring samples. Children with pica for soil in the control area had increased lead content of blood and hair. Preliminary data for children and mothers from villages with mean soil lead contents of 500 ppm and 10,000 ppm are reported which show significant differences in blood and hair lead content within the normal range. The data suggest that soil lead content of 10,000 ppm may result in increased absorption of lead in children, but to a degree which is unlikely to be of biological significance.