The concurrent decline of soil lead and children's blood lead in New Orleans.

Lead (Pb) is extremely toxic and a major cause of chronic diseases worldwide. Pb is associated with health disparities, particularly within low-income populations. In biological systems, Pb mimics calcium and, among other effects, interrupts cell signaling. Furthermore, Pb exposure results in epigenetic changes that affect multigenerational gene expression. Exposure to Pb has decreased through primary prevention, including removal of Pb solder from canned food, regulating lead-based paint, and especially eliminating Pb additives in gasoline. While researchers observe a continuous decline in children's blood lead (BPb), reservoirs of exposure persist in topsoil, which stores the legacy dust from leaded gasoline and other sources. Our surveys of metropolitan New Orleans reveal that median topsoil Pb in communities (n = 274) decreased 44% from 99 mg/kg to 54 mg/kg (P value of 2.09 × 10-08), with a median depletion rate of ∼2.4 mg⋅kg⋅y-1 over 15 y. From 2000 through 2005 to 2011 through 2016, children's BPb declined from 3.6 µg/dL to 1.2 µg/dL or 64% (P value of 2.02 × 10-85), a decrease of ∼0.2 µg⋅dL⋅y-1 during a median of 12 y. Here, we explore the decline of children's BPb by examining a metabolism of cities framework of inputs, transformations, storages, and outputs. Our findings indicate that decreasing Pb in topsoil is an important factor in the continuous decline of children's BPb. Similar reductions are expected in other major US cities. The most contaminated urban communities, usually inhabited by vulnerable populations, require further reductions of topsoil Pb to fulfill primary prevention for the nation's children.

Blood lead and preeclampsia: A meta-analysis and review of implications.

BACKGROUND: Multiple cross-sectional studies suggest that there is an association between blood lead and preeclampsia. OBJECTIVES: We performed a systematic review and meta-analysis to summarize information on the association between preeclampsia and lead poisoning. METHODS: Searches of Medline, Web of Science, Scopus, Pubmed, Science Direct and ProQuest (dissertations and theses) identified 2089 reports, 46 of which were downloaded after reviewing the abstracts, and 11 studies were evaluated as meeting the selection criteria. Evaluation using the ROBINS-I template (Sterne, et al., 2016), indicated moderate risk of bias in all studies. RESULTS: We found that blood lead concentrations were significantly and substantially associated with preeclampsia (k = 12; N = 6069; Cohen's d = 1.26; odds ratio = 9.81; odds ratio LCL = 8.01; odds ratio UCL = 12.02; p = 0.005). Eliminating one study produced a homogeneous meta-analysis and stronger estimates, despite the remaining studies coming from eight separate countries and having countervailing risks of bias. CONCLUSIONS: Blood lead concentrations in pregnant women are a major risk factor for preeclampsia, with an increase of 1µg/dL associated with a 1.6% increase in likelihood of preeclampsia, which appears to be the strongest risk factor for preeclampsia yet reported. Pregnant women with historical lead exposure should routinely have blood lead concentrations tested, especially after mid-term. Women with concentrations higher than 5µg/dL should be actively monitored for preeclampsia and be advised to take prophylactic calcium supplementation. All pregnant women should be advised to actively avoid lead exposure.

Preliminary assessment of surface soil lead concentrations in Melbourne, Australia.

Urban soils in many cities have been found to be contaminated with lead from past usage of leaded petrol, deteriorating lead-based exterior paints and industrial sources. Currently, the spatial distribution of soil lead concentrations in the Melbourne metropolitan area is unknown. The objective of this study was to perform a preliminary assessment of the spatial distributions of the surface soil lead (Pb) concentrations in the Melbourne metropolitan area, Australia. Fifty-eight surface soil samples were collected at a depth of 0-2 cm along three linear transects oriented across the Melbourne metropolitan area. Surface soil samples were also collected at a higher density in five Melbourne suburbs. Soil cores (0-50 cm) were collected in four locations, soil transects were collected at intervals with distance away from the roadway (0-50 m) in two inner city parks, and one control soil sample was collected in a rural setting. The median soil Pb concentration of the soil transect samples was 173 mg/kg (range 32-710 mg/kg), and the median soil Pb concentration of the five suburbs was 69 mg/kg (range 9-1750 mg/kg). The suburb of Footscray had the highest soil Pb concentration with a median soil Pb concentration of 192 mg/kg (range 40-1750 mg/kg). Soil Pb concentrations were generally higher nearest the centre of the Melbourne metropolitan area and in the west of Melbourne and lower in the outer suburbs to the east and north of the city centre. Soil Pb concentrations decreased with distance from roadways in the two transects taken from urban parks, and soil lead decreased with depth in the four soil cores. The soil Pb concentrations in the Melbourne metropolitan area appear to be lower than soil lead concentrations observed in inner city areas of Sydney New South Wales (NSW) and Newcastle NSW. The spatial extent of the soil Pb hazard remains undefined in portions of the Melbourne metropolitan area.

Estimates of potential childhood lead exposure from contaminated soil using the USEPA IEUBK model in Melbourne, Australia.

Soils in inner city areas internationally and in Australia have been contaminated with lead (Pb) primarily from past emissions of Pb in petrol, deteriorating exterior Pb-based paints and from industry. Children can be exposed to Pb in soil dust through ingestion and inhalation leading to elevated blood lead levels (BLLs). Currently, the contribution of soil Pb to the spatial distribution of children's BLLs is unknown in the Melbourne metropolitan area. In this study, children's potential BLLs were estimated from surface soil (0-2 cm) samples collected at 250 locations across the Melbourne metropolitan area using the United States Environmental Protection Agency (USEPA) Integrated Exposure Uptake Biokinetic (IEUBK) model. A dataset of 250 surface soil Pb concentrations indicate that soil Pb concentrations are highly variable but are generally elevated in the central and western portions of the Melbourne metropolitan area. The mean, median and geometric soil Pb concentrations were 193, 110 and 108 mg/kg, respectively. Approximately 20 and 4% of the soil samples exceeded the Australian HIL-A residential and HIL-C recreational soil Pb guidelines of 300 and 600 mg/kg, respectively. The IEUBK model predicted a geometric mean BLL of 2.5 ± 2.1 µg/dL (range: 1.3-22.5 µg/dL) in a hypothetical 24-month-old child with BLLs exceeding 5 and 10 µg/dL at 11.6 and 0.8% of the sampling locations, respectively. This study suggests children's exposure to Pb contaminated surface soil could potentially be associated with low-level BLLs in some locations in the Melbourne metropolitan area.

Estimates of potential childhood lead exposure from contaminated soil using the US EPA IEUBK Model in Sydney, Australia.

Surface soils in portions of the Sydney (New South Wales, Australia) urban area are contaminated with lead (Pb) primarily from past use of Pb in gasoline, the deterioration of exterior lead-based paints, and industrial activities. Surface soil samples (n=341) were collected from a depth of 0-2.5cm at a density of approximately one sample per square kilometre within the Sydney estuary catchment and analysed for lead. The bioaccessibility of soil Pb was analysed in 18 samples. The blood lead level (BLL) of a hypothetical 24 month old child was predicted at soil sampling sites in residential and open land use using the United States Environmental Protection Agency (US EPA) Integrated Exposure Uptake and Biokinetic (IEUBK) model. Other environmental exposures used the Australian National Environmental Protection Measure (NEPM) default values. The IEUBK model predicted a geometric mean BLL of 2.0±2.1µg/dL using measured soil lead bioavailability measurements (bioavailability =34%) and 2.4±2.8µg/dL using the Australian NEPM default assumption (bioavailability =50%). Assuming children were present and residing at the sampling locations, the IEUBK model incorporating soil Pb bioavailability predicted that 5.6% of the children at the sampling locations could potentially have BLLs exceeding 5µg/dL and 2.1% potentially could have BLLs exceeding 10µg/dL. These estimations are consistent with BLLs previously measured in children in Sydney.

Motor neuron disease mortality and lifetime petrol lead exposure: Evidence from national age-specific and state-level age-standardized death rates in Australia.

BACKGROUND: The age standardized death rate from motor neuron disease (MND) for persons 40-84 years of age in the Australian States of New South Wales, Victoria, and Queensland increased dramatically from 1958 to 2013. Nationally, age-specific MND death rates also increased over this time period, but the rate of the rise varied considerably by age-group. The historic use of lead (Pb) additives in Australian petrol is a candidate explanation for these trends in MND mortality (International Classification of Disease (ICD)-10 G12.2). METHODS: Leveraging temporal and spatial variation in petrol lead exposure risk resulting from the slow rise and rapid phase-out of lead as a constituent in gasoline in Australia, we analyze relationships between (1) national age-specific MND death rates in Australia and age-specific lifetime petrol lead exposure, (2) annual between-age dispersions in age-specific MND death rates and age-specific lifetime petrol lead exposure; and (3) state-level age-standardized MND death rates as a function of age-weighted lifetime petrol lead exposure. RESULTS: Other things held equal, we find that a one percent increase in lifetime petrol lead exposure increases the MND death rate by about one-third of one percent in both national age-specific and state-level age-standardized models of MND mortality. Lending support to the supposition that lead exposure is a driver of MND mortality risk, we find that the annual between-age group standard deviation in age-specific MND death rates is strongly correlated with the between-age standard deviation in age-specific lifetime petrol lead exposure. CONCLUSION: Legacy petrol lead emissions are associated with age-specific MND death rates as well as state-level age-standardized MND death rates in Australia. Results indicate that we are approaching peak lead exposure-attributable MND mortality.

Lead exposure at firing ranges-a review.

BACKGROUND: Lead (Pb) is a toxic substance with well-known, multiple, long-term, adverse health outcomes. Shooting guns at firing ranges is an occupational necessity for security personnel, police officers, members of the military, and increasingly a recreational activity by the public. In the United States alone, an estimated 16,000-18,000 firing ranges exist. Discharge of Pb dust and gases is a consequence of shooting guns. METHODS: The objectives of this study are to review the literature on blood lead levels (BLLs) and potential adverse health effects associated with the shooting population. The search terms "blood lead", "lead poisoning", "lead exposure", "marksmen", "firearms", "shooting", "guns", "rifles" and "firing ranges" were used in the search engines Google Scholar, PubMed and Science Direct to identify studies that described BLLs in association with firearm use and health effects associated with shooting activities. RESULTS: Thirty-six articles were reviewed that included BLLs from shooters at firing ranges. In 31 studies BLLs > 10 µg/dL were reported in some shooters, 18 studies reported BLLs > 20 µg/dL, 17 studies > 30 µg/d, and 15 studies BLLs > 40 µg/dL. The literature indicates that BLLs in shooters are associated with Pb aerosol discharge from guns and air Pb at firing ranges, number of bullets discharged, and the caliber of weapon fired. CONCLUSIONS: Shooting at firing ranges results in the discharge of Pb dust, elevated BLLs, and exposures that are associated with a variety of adverse health outcomes. Women and children are among recreational shooters at special risk and they do not receive the same health protections as occupational users of firing ranges. Nearly all BLL measurements compiled in the reviewed studies exceed the current reference level of 5 µg/dL recommended by the U.S. Centers for Disease Control and Prevention/National Institute of Occupational Safety and Health (CDC/NIOSH). Thus firing ranges, regardless of type and user classification, currently constitute a significant and unmanaged public health problem. Prevention includes clothing changed after shooting, behavioural modifications such as banning of smoking and eating at firing ranges, improved ventilation systems and oversight of indoor ranges, and development of airflow systems at outdoor ranges. Eliminating lead dust risk at firing ranges requires primary prevention and using lead-free primers and lead-free bullets.

Linking source and effect: resuspended soil lead, air lead, and children's blood lead levels in Detroit, Michigan.

This study evaluates atmospheric concentrations of soil and Pb aerosols, and blood lead levels (BLLs) in 367839 children (ages 0-10) in Detroit, Michigan from 2001 to 2009 to test a hypothesized soil → air dust → child pathway of contemporary Pb risk. Atmospheric soil and Pb show near-identical seasonal properties that match seasonal variation in children's BLLs. Resuspended soil appears to be a significant underlying source of atmospheric Pb. A 1% increase in the amount of resuspended soil results in a 0.39% increase in the concentration of Pb in the atmosphere (95% CI, 0.28 to 0.50%). In turn, atmospheric Pb significantly explains age-dependent variation in child BLLs. Other things held equal, a change of 0.0069 µg/m(3) in atmospheric Pb increases BLL of a child 1 year of age by 10%, while approximately 3 times the concentration of Pb in air (0.023 µg/m(3)) is required to induce the same increase in BLL of a child 7 years of age. Similarly, a 0.0069 µg/m(3) change in air Pb increases the odds of a child <1 year of age having a BLL ≥ 5 µg/dL by a multiplicative factor of 1.32 (95% CI, 1.26 to 1.37). Overall, the resuspension of Pb contaminated soil explains observed seasonal variation in child BLLs.

Assessing Unequal Airborne Exposure to Lead Associated With Race in the USA.

Recent research applied the United States Environmental Protection Agency's Chemical Speciation Network and Interagency Monitoring of Protected Visual Environments monitoring stations and observed that mean concentrations of atmospheric lead (Pb) in highly segregated counties are a factor of 5 higher than in well-integrated counties and argument is made that regulation of existing airborne Pb emissions will reduce children's Pb exposure. We argue that one of the main sources of children's current Pb exposure is from resuspension of legacy Pb in soil dust and that the racial disparity of Pb exposure is associated with Pb-contaminated community soils.

Assessment of soil metal concentrations in residential and community vegetable gardens in Melbourne, Australia.

Gardening and urban food production is an increasingly popular activity, which can improve physical and mental health and provide low cost nutritious food. However, the legacy of contamination from industrial and diffuse sources may have rendered surface soils in some urban gardens to have metals value in excess of recommended guidelines for agricultural production. The objective of this study was to establish the presence and spatial extent of soil metal contamination in Melbourne's residential and inner city community gardens. A secondary objective was to assess whether soil lead (Pb) concentrations in residential vegetable gardens were associated with the age of the home or the presence or absence of paint. The results indicate that most samples in residential and community gardens were generally below the Australian residential guidelines for all tested metals except Pb. Mean soil Pb concentrations exceeded the Australian HIL-A residential guideline of 300 mg/kg in 8% of 13 community garden beds and 21% of the 136 residential vegetable gardens assessed. Mean and median soil Pb concentrations for residential vegetable gardens was 204 mg/kg and 104 mg/kg (range <4-3341 mg/kg), respectively. Mean and median soil Pb concentration for community vegetable garden beds was 102 mg/kg and 38 mg/kg (range = 17-578 mg/kg), respectively. Soil Pb concentrations were higher in homes with painted exteriors (p = 0.004); generally increased with age of the home (p = 0.000); and were higher beneath the household dripline than in vegetable garden beds (p = 0.040). In certain circumstances, the data indicates that elevated soil Pb concentrations could present a potential health hazard in a portion of inner-city residential vegetable gardens in Melbourne.

Children's Blood Lead Seasonality in Flint, Michigan (USA), and Soil-Sourced Lead Hazard Risks.

In Flint; MI; USA; a public health crisis resulted from the switching of the water supply from Lake Huron to a more corrosive source from the Flint River in April 2014; which caused lead to leach from water lines. Between 2010 and 2015; Flint area children's average blood lead patterns display consistent peaks in the third quarter of the year. The third quarter blood lead peaks displayed a declining trend between 2010 and 2013; then rose abruptly between the third quarters of 2013 from 3.6% blood lead levels ≥5 µg/dL to a peak of about 7% in the third quarter of 2014; an increase of approximately 50%. The percentage of blood lead level ≥5 µg/dL in the first quarter of 2015 then dropped to 2.3%; which was the same percentage as the first quarter of 2014 (prior to the Flint River water source change). The Flint quarterly blood lead level peak then rose to about 6% blood lead levels ≥ 5 µg/dL in the third quarter of 2015; and then declined to about 2.5% in the fourth quarter of 2015. Soil lead data collected by Edible Flint food collaborative reveal generally higher soil lead values in the metropolitan center for Flint; with lower values in the outskirts of the city. The questions that are not being asked is why did children's blood lead levels display a seasonal blood lead pattern before the introduction of the new water supply in Flint; and what are the implications of these seasonal blood lead patterns? Based upon previous findings in Detroit and other North American cities we infer that resuspension to the air of lead in the form of dust from lead contaminated soils in Flint appears to be a persistent contribution to lead exposure of Flint children even before the change in the water supply from Lake Huron to the Flint River.

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).

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 microm 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.

A Temporal Association between Accumulated Petrol (Gasoline) Lead Emissions and Motor Neuron Disease in Australia.

BACKGROUND: The age standardised death rate from motor neuron disease (MND) has increased from 1.29 to 2.74 per 100,000, an increase of 112.4% between 1959 and 2013. It is clear that genetics could not have played a causal role in the increased rate of MND deaths over such a short time span. We postulate that environmental factors are responsible for this rate increase. We focus on lead additives in Australian petrol as a possible contributing environmental factor. METHODS: The associations between historical petrol lead emissions and MND death trends in Australia between 1962 and 2013 were examined using linear regressions. RESULTS: Regression results indicate best fit correlations between a 20 year lag of petrol lead emissions and age-standardised female death rate (R² = 0.86, p = 4.88 × 10(-23)), male age standardised death rate (R² = 0.86, p = 9.4 × 10(-23)) and percent all cause death attributed to MND (R² = 0.98, p = 2.6 × 10(-44)). CONCLUSION: Legacy petrol lead emissions are associated with increased MND death trends in Australia. Further examination of the 20 year lag between exposure to petrol lead and the onset of MND is warranted.

Determining the relative importance of soil sample locations to predict risk of child lead exposure.

Soil lead in urban neighborhoods is a known predictor of child blood lead levels. In this paper, we address the question where one ought to concentrate soil sample collection efforts to efficiently predict children at-risk for soil Pb exposure. Two extensive data sets are combined, including 5467 surface soil samples collected from 286 census tracts, and geo-referenced blood Pb data for 55,551 children in metropolitan New Orleans, USA. Random intercept least squares, random intercept logistic, and quantile regression results indicate that soils collected within 1m adjacent to residential streets most reliably predict child blood Pb outcomes in child blood Pb levels. Regression decomposition results show that residential street soils account for 39.7% of between-neighborhood explained variation, followed by busy street soils (21.97%), open space soils (20.25%), and home foundation soils (18.71%). Just as the age of housing stock is used as a statistical shortcut for child risk of exposure to lead-based paint, our results indicate that one can shortcut the characterization of child risk of exposure to neighborhood soil Pb by concentrating sampling efforts within 1m and adjacent to residential and busy streets, while significantly reducing the total costs of collection and analysis. This efficiency gain can help advance proactive upstream, preventive methods of environmental Pb discovery.

Potential for childhood lead poisoning in the inner cities of Australia due to exposure to lead in soil dust.

This article presents evidence demonstrating that the historical use of leaded gasoline and lead (Pb) in exterior paints in Australia has contaminated urban soils in the older inner suburbs of large cities such as Sydney and Melbourne. While significant attention has been focused on Pb poisoning in mining and smelting towns in Australia, relatively little research has focused on exposure to Pb originating from inner-city soil dust and its potential for childhood Pb exposures. Due to a lack of systematic blood lead (PbB) screening and geochemical soil Pb mapping in the inner cities of Australia, the risks from environmental Pb exposure remain unconstrained within urban population centres.

Estimation of leaded (Pb) gasoline's continuing material and health impacts on 90 US urbanized areas.

The subject of this paper is lead (Pb) additives in gasoline and their material and health impact from Pb dust inputs into 90 US urbanized areas (UAs). The mass of Pb additives for 90 UAs as a total of the US Pb additives in 1982 were estimated from vehicle travel, vehicle fuel economy (miles/gallon), ratio of leaded to unleaded fuel, and Pb/gallon. About 500 billion (109) miles of travel in 90 UA's during 1982 account for ~18,000 metric tons (MT), or nearly 30% of the US Pb additives in 1982. Applying the 1982 proportions to the 90 UAs for 1950 through 1982 fuel sales by state accounts for ~1.4 million MT Pb of the US national total of 4.6 million MT during the same years. Fates of Pb additives in engine systems were used to calculate Pb aerosol inputs into the 90 UAs. The inputs range from 100's to more than 100,000 MT of Pb depending on a given UA's traffic flow patterns. Soils are the reservoir of urban Pb dust. The median background soil Pb for the US is 16.5mg/kg (range 10.3 to 30.1mg/kg), and less by an order of magnitude or more than soil Pb within larger UAs. Recognizing the US input of massive gasoline Pb additives into UAs assists with comprehending soil Pb differences between large and small UAs, inner and outer areas of UAs, health disparities, and school achievement issues within UAs. The findings underscore the need for controlling accumulated exterior urban Pb dust from gasoline additives along with paint sources that have accumulated in soil to meet the goal of primary childhood Pb exposure prevention.

Lead (Pb) legacy from vehicle traffic in eight California urbanized areas: continuing influence of lead dust on children's health.

This article describes the magnitude of U.S. lead (Pb) additives in gasoline from 1927 to 1994 and estimated quantities of Pb dispersed by vehicle traffic in eight urbanized areas (UAs) of California from 1950 to 1982. The findings are the basis for predicting the health impact of Pb on children living in UA of California. Quantitative U.S. national data for 1927-1994 were from the U.S. Senate hearing of the 1984 Airborne Lead Reduction Act. Vehicle traffic data, fuel efficiency, percentage leaded gasoline, and quantities of Pb in gasoline were obtained for 1982 from public and corporate records to estimate vehicle Pb emissions for small to very large UAs of California. California fuel consumption records and yearly quantities of Pb additives per gallon were the basis for estimating the 1950-1982 dispersion of Pb in each UA. Lead additives were calculated by multiplying annual vehicle fuel used by average Pb per gallon. The proportion of Pb additive for each UA was calculated from vehicle miles traveled (VMT) driven in 1982 divided by miles per gallon fuel consumption times the ratio of leaded to unleaded fuel times Pb additive per gallon. U.S. Environmental Protection Agency calculations of the fates of Pb were used to estimate Pb aerosol dispersal in each UA. About 108 billion miles of travel in 1982 within 8 UAs accounts for 3200metric tons of Pb additives or approximately 60% total Pb additives in California. Between the 1950-1982 peak of Pb additives, about 258,000metric tons are accounted for out of the state 412,000metric tons total during the same time period. The estimates of the quantities of Pb dust that accumulated within various UAs in California assists with predicting the continuing influences of Pb on children's exposure. Mapping the soil Pb reservoir assists with establishing the priority for enhancing environments of children.