Lead exposure in the Roman Empire: a review of the written, material, and bioarchaeological evidence

All lead exposures matter – Authors' reply

Domestic dogs as sentinels of children lead exposure: Multi-pathway identification and source apportionment based on isotope technique

The objective of this paper was to determine the prevalence and sources of high lead (Pb) exposure among children in Bulacan, Philippines. A total of 150 children (6-7 years old) and their caregivers were studied. Lead was analyzed in children hair and deciduous teeth. Sources of lead exposure were determined by caregiver interview and Pb analysis of house soil, drinking faucet water, air, and water from seven Bulacan rivers. Lead was positive in 91.3% of children's hair (MC or median concentration = 8.9 μg/g; range = 0-38.29), in 46.2% of the teeth (MC = 0.000 μg/mg in positive samples; range = 0.00-0.020), in 100% of soil (MC = 27.06 mg/kg; range = 3.05-1155.80), in 21.1% of air (MC = 0 μg/Ncm; range = 0-0.10), in 4% of house, faucet water (MC = 0.0 ppm; range = 0-40). There was a significant correlation (Spearman's rho) between Pb in children's hair and soil (r = 0.195; p = 0.017) and between Pb in house water and outdoor air (r = 0.616; p = 0.005). There is no significant correlation between Pb in children's hair and teeth. None of the potential sources of Pb from interview were related to lead exposure in the children. Water from seven Bulacan rivers was 100% positive for lead (MC = 70.00 ppb; range = 30-90). Widespread flooding with river overflow occurred in Bulacan in 2009 which likely caused lead contamination of the soil. There was no significant difference in the lead concentration of the soil whether near or far from the river (p = 0.205, Mann-Whitney U test). High lead exposure in children in Bulacan is likely from soil contaminated by lead-polluted rivers during flooding. In areas where flooding is common, alluvial and riparian soils from polluted rivers are important sources of lead exposure in children.

Elevated Blood Lead Levels Related to the Use of Firearms.

This commentary is an investigation of sources of lead (Pb) exposure in West Africa. Pb is generally acknowledged as one of the most widespread environmental health hazards in West Africa, and there is heightened concern over adverse health effects at various levels of exposure (at doses once considered safe) in the West African region. A literature review for the possible health implications of Pb exposure on human health showed nervous system dysfunction, anemia, and potential cognitive diseases as the major health issues among children, while adults were found to suffer more from cardiovascular dysfunction, neurological decline, and reproductive diseases. Despite a decline in blood lead levels (BLLs), lead exposure continues to be a major public health concern as no level of Pb exposure can be considered safe. Moreover, lowering BLLs entails identifying various lead sources such as gasoline emissions, leaded paint, canned foods, and beverages, as well as plausible biological pathways of lead exposure and response. However, only countries such as Nigeria and Ghana have extensive research available regarding the different sources of Pb exposure. Further, it is not apparent which country is affected the most by Pb exposure. Therefore, this commentary was aimed to explore different literature sources to describe and list the different sources of Pb exposure in 15 West African countries. The findings indicated water, food, and occupational exposure as the major sources of Pb exposure in the region. People with occupations such as e-waste and Pb acid battery recycling, auto mechanics, fuel attending, welding, electronic repairing, farming/spraying, and mining were found to be at immediate risk. Tobacco, spices and paints constituted additional potential sources of exposure. For residents living near landfills or urban area, the major sources of Pb exposure were soil, air, and dust particles. The review revealed a vast research gap on the sources and implications of Pb exposure. Exposure to Pb could further increase due to uncontrolled traffic, urban growth, inadequate urban planning, and the inadequate enforcement of regulations. Therefore, more extensive research on the changing trends of Pb exposure among West African populations is needed.

Lead industries are one of the major sources of environmental pollution and can affect human through different activities, including industrial processes, metal plating, mining, battery recycling, etc. Although different studies have documented the various sources of lead exposure, studies highlighting different types of industries as sources of environmental contamination are limited. Therefore, this narrative review aims to focus mainly on lead industries as significant sources of environmental and human contamination. Based on the keywords searched in bibliographic databases we found 44 relevant articles that provided information on lead present in soil, water, and blood or all components among participants living near high-risk areas. We presented three case scenarios to highlight howlead industries have affected the health of citizens in Vietnam, Uruguay, and Malaysia. Factories conducting mining, e-waste processing, used lead-acid battery recycling, electronic repair, and toxic waste sites were the primary industries for lead exposure. Our study has shown lead exposure due to industrial activities in Vietnam, Uruguay, Malaysia and calls for attention to the gaps in strategic andepidemiologic efforts to understand sources of environmental exposure to lead fully. Developing strategies and guidelines to regulate industrial activities, finding alternatives to reduce lead toxicity and exposure, and empowering the public through various community awareness programs can play a crucial role in controlling exposure tolead.

BackgroundArctic populations are exposed to mercury, lead and cadmium through their traditional diet. Studies have however shown that cadmium exposure is most often attributable to tobacco smoking. The aim of this study is to examine the trends in mercury, lead and cadmium exposure between 1992 and 2004 in the Inuit population of Nunavik (Northern Québec, Canada) using the data obtained from two broad scale health surveys, and to identify sources of exposure in 2004.MethodsIn 2004, 917 adults aged between 18 and 74 were recruited in the 14 communities of Nunavik to participate to a broad scale health survey. Blood samples were collected and analysed for metals by inductively coupled plasma mass spectrometry, and dietary and life-style characteristics were documented by questionnaires. Results were compared with data obtained in 1992, where 492 people were recruited for a similar survey in the same population.ResultsMean blood concentration of mercury was 51.2 nmol/L, which represent a 32% decrease (p < 0.001) between 1992 and 2004. Mercury blood concentrations were mainly explained by age (partial r2 = 0.20; p < 0.0001), and the most important source of exposure to mercury was marine mammal meat consumption (partial r2 = 0.04; p < 0.0001). In 2004, mean blood concentration of lead was 0.19 μmol/L and showed a 55% decrease since 1992. No strong associations were observed with any dietary source, and lead concentrations were mainly explained by age (partial r2 = 0.20.; p < 0.001). Blood cadmium concentrations showed a 22% decrease (p < 0.001) between 1992 and 2004. Once stratified according to tobacco use, means varied between 5.3 nmol/L in never-smokers and 40.4 nmol/L in smokers. Blood cadmium concentrations were mainly associated with tobacco smoking (partial r2 = 0.56; p < 0.0001), while consumption of caribou liver and kidney remain a minor source of cadmium exposure among never-smokers.ConclusionImportant decreases in mercury, lead and cadmium exposure were observed. Mercury decrease could be explained by dietary changes and the ban of lead cartridges use likely contributed to the decrease in lead exposure. Blood cadmium concentrations remain high and, underscoring the need for intensive tobacco smoking prevention campaigns in the Nunavik population.

Based on available evidence, household educational interventions and environmental interventions (namely dust control measures) show no evidence of a difference in reducing blood lead levels in children as a population health measure. The evidence of the effects of environmental interventions on cognitive and neurobehavioural outcomes and adverse events is uncertain too. Further trials are required to establish the most effective intervention for reducing or even preventing further lead exposure. Key elements of these trials should include strategies to reduce multiple sources of lead exposure simultaneously using empirical dust clearance levels. It is also necessary for trials to be carried out in low- and middle-income countries and in differing socioeconomic groups in high-income countries.

&lt;P&gt;Landmark studies identifying the unique susceptibility of the child’s developing brain to neurocognitive and neurobehavioral insults from lead have inspired a wealth of subsequent advances in our understanding of lead toxicity, exposure sources, screening approaches, treatment efficacy, and prevention strategies. However, ongoing data gaps are the source of healthy scientific debate regarding interpretation and clinical application of the current evidence base. This provides challenges to public health and medical practitioners striving for best evidence approaches to community and patient health.&lt;/P&gt; &lt;H4&gt;ABOUT THE AUTHOR&lt;/H4&gt; &lt;P&gt;Catherine Karr, MD, PhD, MS, is Assistant Professor, Department of Pediatrics, and Adjunct, Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA.&lt;/P&gt; &lt;P&gt;Address correspondence to: Occupational and Environmental Medicine Program, Box 359739, 325 9th Ave., Seattle, WA 98104; fax 206-744-9935; or e-mail &lt;a href="mailto:ckarr@u.washington.edu"&gt;ckarr@u.washington.edu&lt;/a&gt;.&lt;/P&gt; &lt;P&gt;Dr. Karr has disclosed no relevant financial relationships.&lt;/P&gt; &lt;H4&gt;EDUCATIONAL OBJECTIVES&lt;/H4&gt; &lt;OL&gt; &lt;LI&gt;Recognize the routes, sources, and patterns of lead exposure in children.&lt;/LI&gt; &lt;LI&gt;Discuss the current guidelines regarding screening children for lead exposure, delineating their strengths and limitations.&lt;/LI&gt; &lt;LI&gt;Review primary prevention strategies to reduce exposure to lead.&lt;/LI&gt; &lt;/OL&gt;

Lead exposure can have serious consequences for health and development. The neurological and behavioral effects of lead are considered irreversible. Young children are particularly vulnerable to lead poisoning. In 2020, Pure Earth and UNICEF estimated that one in three children had elevated blood lead levels above 5 µg/dL. The sources of lead exposure vary around the world and can range from household products, such as spices or foodware, to environmental pollution from nearby industries. The aim of this study was to analyze common products from markets in low- and middle-income countries (LMICs) for their lead content to determine whether they are plausible sources of exposure. In 25 LMICs, the research teams systematically collected consumer products (metal foodware, ceramics, cosmetics, paints, toys, spices and other foods). The items were analyzed on site for detectable lead above 2 ppm using an X-ray fluorescence analyzer. For quality control purposes, a subset of the samples was analyzed in the USA using inductively coupled plasma mass spectrometry. The lead concentrations of the individual product types were compared with established regulatory thresholds. Out of 5007 analyzed products, threshold values (TV) were surpassed in 51% for metal foodware (TV 100 ppm), 45% for ceramics (TV 100 ppm), and 41% for paints (TV 90 ppm). Sources of exposure in LMICs can be diverse, and consumers in LMICs lack adequate protection from preventable sources of lead exposure. Rapid Market Screening is an innovative, simple, and useful tool to identify risky products that could be sources of lead exposure.

Source apportionment based on lead isotope ratios: Could domestic dog's blood lead be used to identify the level and sources of lead pollution in children?

Lead and noise, via different mechanisms, may damage hearing ability, and, in some cases, cause severe and irreversible damage. To explore possible independent and synergistic effects of lead and noise on auditory function, the authors conducted a cross-sectional study in two lead-battery manufacturing factories. Lead and noise were the two most common sources of occupational exposures in the factories. Blood lead level, ambient lead concentration, noise exposure level, and hearing thresholds of 339 lead-battery workers-including clerical and managerial staffs-were measured. The authors obtained demographics and working histories via an interview-based structured questionnaire. A total of 220 lead-battery workers were exposed to high levels of lead and noise; their average blood lead concentration was 56.9 microg/dl, and their average noise exposure level was 86.0 dBALeq. Multivariate analysis, in which possible risk factors of hearing ability were considered, demonstrated a significant correlation between a high, long-term lead exposure index (defined by duration of employment and ambient lead concentration) and decreased hearing ability. In contrast, such a correlation between short-term lead exposure (defined by blood lead level) and hearing ability was not significant. Furthermore, neither noise exposure level alone nor the interaction between noise exposure level and short- or long-term lead exposure was correlated significantly with hearing ability. The present study raises an important, but typically ignored, issue: lead exposure might precipitate a more severe auditory than noise-exposure effect. The preservation of workers' hearing ability requires that preventive measures be taken against noise exposure, which is as essential as measures taken against lead exposure.

In response to the growing body of scientific evidence about effects of exposure to low levels of lead,1 the U.S. Centers for Disease Control and Prevention (CDC) has announced it is changing its guidelines for children’s exposure to the toxic metal, reducing by half the blood lead level at which intervention is recommended.2 According to CDC spokesman Jay Dempsey, the agency estimates the change will increase the number of affected children from fewer than 100,000 to 372,979. Recommended intervention involves identifying and removing sources of lead exposure and follow-up blood lead monitoring. Since 1991 the CDC’s “level of concern” for lead in children’s blood had been set at 10 µg/dL. At the recommendation of its Advisory Committee on Childhood Lead Poisoning Prevention, the agency is dispensing with the use of a static number. Instead, its new reference value of 5 µg/dL is based on the 97.5th percentile of blood lead levels in U.S. children aged 1–5 years, as measured by the agency’s National Health and Nutrition Examination Survey (NHANES). The reference value will be updated every four years based on the two most recent iterations of the NHANES.2 The CDC has moved away from the “level of concern” terminology because it “gives a false sense of security to people” whose children’s blood lead fell below the cutoff, says Christopher Portier, director of the agency’s National Center for Environmental Health. The agency and its advisory committee can find no evidence that there is a safe level of lead exposure for children, he says. Lead-based paint remains the most important source of lead poisoning for U.S. children.1 Despite the great reductions in exposure that followed the removal of lead from gasoline, an estimated 37.1 million U.S. homes still contain lead paint.6 Ingestion ... A host of studies now link exposure to lower levels of lead with behavior problems, attention deficit/hyperactivity disorder, and adverse cardiovascular, immunological, and endocrine effects, says Bruce Lanphear of Simon Fraser University. Lanphear led a 2005 study in which seven different longitudinal cohorts from multiple countries reported very similar decreases in intelligence in association with blood lead levels below 10 µg/dL.3 In June 2012 the National Toxicology Program concluded that adverse health effects occur at levels below even 5 µg/dL.4 Homes can be a major source of lead exposure, and the CDC is focused on primary prevention, says Mary Jean Brown, chief of the agency’s Lead Poisoning Prevention Branch. “We have to develop an agenda that controls or eliminates lead hazards before children are poisoned,” she says. The CDC is working with the U.S. Department of Housing and Urban Development and the U.S. Environmental Protection Agency to identify communities where high proportions of children have elevated lead levels and to take actions to remediate the sources of exposure, she says. “For most children, the majority of their exposure is from household dust that is a consequence of the decay of old lead-based paint,” says Michael Weitzman, a professor of environmental medicine and pediatrics at New York University’s Langone Medical Center. Old windows are a major source of exposure; another is renovating older homes without taking proper precautions, according to the nonprofit National Center for Healthy Housing (NCHH). However, less is known about how to clean up these sources of lead. Lanphear points to the need for effective, evidence-based methods for reducing lead in house dust, soil, water, and consumer products. He is working on a study that he says demonstrates the efficacy of lead hazard controls to reduce children’s blood lead levels. Despite dramatic cuts to the CDC’s Healthy Homes/Lead Poisoning Prevention Program in fiscal year 2012,5 the May 2012 announcement of the new reference value constitutes a promise of action, Portier says. He says the agency will develop educational materials to explain to health departments, pediatricians, nongovernmental organizations, and other groups what the change means and how to act on it. However, 80% of the program budget supported state and local lead-poisoning prevention programs that will no longer be funded, says Dempsey. Portier says he is beginning to see many of these programs wind down. No matter how the new guidelines are ultimately implemented, NCHH executive director Rebecca Morley hopes more families will start to understand that even very low lead exposures can cause harm. She says the decision will prompt follow-up educational activities to help ensure that “parents are going to begin to get the information that they deserve.”

African American men have the highest incidence of prostate cancer in the world and have substantially higher rates of prostate cancer when compared to white men in the U.S. The cause(s) for this race disparity remains elusive. A single nucleotide polymorphism (SNP), rs10486567, in intron 2 of juxtaposed with another zinc finger protein 1 (JAZF1) has been associated with increased risk of prostate cancer in genome-wide association studies (GWAS) and may be key to uncovering reasons for disparities in the disease. JAZF1 is a cysteine-hystidine structured zinc finger protein, a type of protein that has been shown to interact with lead in vitro. Lead is recognized as a probable carcinogen in humans and African American men who are residentially segregated to industrialized urban environments in the U.S. have higher blood lead levels on average compared to white men. In a case-only study of 228 African American men with prostate cancer diagnosed at a large health system in the Detroit Metropolitan area, we assessed gene-environment interactions (GxE) between rs10486567 (CC vs. CT/TT genotype) and two sources of lead exposure. Lifetime occupational lead exposure was determined through industrial hygiene review of extensive face-to-face interviews. Neighborhood lead exposure, defined as the median proportion of census tract housing built before 1950 (≥ 47% vs. &amp;lt;47%), was derived from subjects address at time of diagnosis. Generalized estimating equation (GEE) modeling was used for analyses that included nested census data. In younger African American cases (&amp;lt;62 years of age), we found a significant gene-environment interaction between rs10486567 CC carriers and high occupational-respiratory lead exposure when compared to those with no respiratory lead exposure (OR 2.68, CI 1.05-6.88, p=.04). A significant GxE interaction was also observed between CC carriers and residence in a neighborhood with a large proportion of older housing in all cases and younger cases (all OR 1.92, CI 1.12-3.29, p=.017, younger OR 2.64, CI 1.21-5.73, p=.014, older OR 1.64, CI 0.73-3.70, p=.23). The interaction between rs10486567 and housing remained significant even after adjustment for occupational lead exposure. Combining lead exposure from occupation and neighborhood housing into a four category index showed even stronger interactions between the polymorphism and the highest lead exposed group compared to the lowest exposure group (all OR 3.13, CI 1.22-7.99, p=.017). These findings indicate that lead may be an important risk factor for prostate cancer in carriers of the rs10486567 CC genotype. Future studies of race disparities in prostate cancer should further assess interactions between lead and JAZF1 and lead and other zinc containing proteins. Focusing on genes and polymorphisms identified in GWAS studies might help to identify environmental risk factors for prostate cancer. Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):PR-8.

Lead poisoning is associated with physical, cognitive and neurobehavioural impairment in children and trials have tested many household interventions to prevent lead exposure. This is an update of the original review by the same authors first published in 2008. To determine the effectiveness of household interventions in preventing or reducing lead exposure in children as measured by reductions in blood lead levels and/or improvements in cognitive development. We identified trials through electronic searches of CENTRAL (The Cochrane Library, 2010, Issue 2), MEDLINE (1948 to April Week 1 2012), EMBASE (1980 to 2012 Week 2), CINAHL (1937 to 20 Jan 2012), PsycINFO (1887 to Dec week 2 2011), ERIC (1966 to 17 Jan 2012), Sociological Abstracts (1952 to 20 January 2012), Science Citation Index (1970 to 20 Jan 2012), ZETOC (20 Jan 2012), LILACS (20 Jan 2012), Dissertation Abstracts (late 1960s to Jan 2012), ClinicalTrials.gov (20 Jan 2012), Current Controlled Trials (Jan 2012), Australian New Zealand Clinical Trials Registry (Jan 2012) and the National Research Register Archive. We also contacted experts to find unpublished studies. Randomised and quasi-randomised controlled trials of household educational or environmental interventions to prevent lead exposure in children where at least one standardised outcome measure was reported. Two authors independently reviewed all eligible studies for inclusion, assessed risk of bias and extracted data. We contacted trialists to obtain missing information. We included 14 studies (involving 2656 children). All studies reported blood lead level outcomes and none reported on cognitive or neurobehavioural outcomes. We put studies into subgroups according to their intervention type. We performed meta-analysis of both continuous and dichotomous data for subgroups where appropriate. Educational interventions were not effective in reducing blood lead levels (continuous: mean difference (MD) 0.02, 95% confidence interval (CI) -0.09 to 0.12, I(2) = 0 (log transformed); dichotomous ≥ 10µg/dL (≥ 0.48 µmol/L): relative risk (RR) 1.02, 95% CI 0.79 to 1.30, I(2)=0; dichotomous ≥ 15µg/dL (≥ 0.72 µmol/L): RR 0.60, 95% CI 0.33 to 1.09, I(2) = 0). Meta-analysis for the dust control subgroup also found no evidence of effectiveness (continuous: MD -0.15, 95% CI -0.42 to 0.11, I(2) = 0.9 (log transformed); dichotomous ≥ 10µg/dL (≥ 0.48 µmol/L): RR 0.93, 95% CI 0.73 to 1.18, I(2) =0; dichotomous ≥ 15µg/dL (≥ 0.72 µmol/L): RR 0.86, 95% CI 0.35 to 2.07, I(2) = 0.56). When meta-analysis for the dust control subgroup was adjusted for clustering, no statistical significant benefit was incurred. The studies using soil abatement (removal and replacement) and combination intervention groups were not able to be meta-analysed due to substantial differences between studies. Based on current knowledge, household educational or dust control interventions are ineffective in reducing blood lead levels in children as a population health measure. There is currently insufficient evidence to draw conclusions about the effectiveness of soil abatement or combination interventions.Further trials are required to establish the most effective intervention for prevention of lead exposure. Key elements of these trials should include strategies to reduce multiple sources of lead exposure simultaneously using empirical dust clearance levels. It is also necessary for trials to be carried out in developing countries and in differing socioeconomic groups in developed countries.