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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.

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., (Copyright © 2016 Elsevier Inc. All rights reserved.)

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.

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.

Interior and exterior dust, soil and paint were analysed at five brick urban Sydney homes over 15 months to evaluate temporal variations and discriminate sources of lead (Pb) exposure. Exterior dust gauge Pb loading rates (μg/m(2)/28 days), interior vacuum dust Pb concentrations (mg/kg) and interior petri-dish Pb loading rates (μg/m(2)/28 days), were correlated positively with soil Pb concentrations. Exterior dust gauge Pb loading rates and interior vacuum dust Pb concentrations peaked in the summer. Lead isotope and Pb speciation (XAS) were analysed in soil and vacuum dust samples from three of the five houses that had elevated Pb concentrations. Results show that the source of interior dust lead was primarily from soil in two of the three houses and from soil and Pb paint in the third home. IEUBK child blood Pb modelling predicts that children's blood Pb levels could exceed 5 μg/dL in two of the five houses., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

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., (© 2013 Elsevier Ltd. All rights reserved.)

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.

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., (Published by Elsevier Ltd.)

Although significant headway has been made over the past 50 years in understanding and reducing the sources and health risks of lead, the incidence of lead poisoning remains shockingly high in urban regions of the United States. At particular risk are poor people who inhabit the polluted centers of our older cities without the benefits of adequate nutrition, education, and access to health care. To provide a future with fewer environmental and health burdens related to lead, we need to consider the multiple pathways of lead exposure in children, including their continued contact with dust derived from inner-city soils. Recent research into the causes of seasonal variations in blood-lead levels among children has confirmed the importance of soil in lead exposure. "Capping" lead-contaminated soil with lead-free soil or soil amendment appears to be a simple and cost-effective way to reduce the lead load for urban youth.

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., (Copyright 2010 Elsevier B.V. All rights reserved.)

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.