Bone Lead Levels Research Articles

Bone lead measurements of live condors in field to assess cumulative lead exposure.

Lead poisoning remains the leading cause of diagnosed death for critically endangered California condors, which are annually monitored for lead exposure via blood tests. Blood tests are generally reflective of acute lead exposure. Since condors are victims to both chronic and acute lead exposure, measuring bone, which in humans is reflective of years to decades worth of exposure, is a valuable biomarker. In this study, we measured bone Pb of the tibiotarsus of 64 condors in vivo using a portable x-ray fluorescence device. The average uncertainty for measurements, typically reflective of how effective the device performed, was found to be 3.8 ± 2.2µg/g bone mineral. The average bone lead level was found to be 26.7 ± 24.5µg/g bone mineral. Bone lead correlated significantly with a sum of all blood lead measures over the lifetime of each condor. In the future, bone lead can potentially be used to inform treatment planning and address the chronic health implications of lead in the species.

Improving prediction of linear regression models by integrating external information from heterogeneous populations: James-Stein estimators.

We consider the setting where (1) an internal study builds a linear regression model for prediction based on individual-level data, (2) some external studies have fitted similar linear regression models that use only subsets of the covariates and provide coefficient estimates for the reduced models without individual-level data, and (3) there is heterogeneity across these study populations. The goal is to integrate the external model summary information into fitting the internal model to improve prediction accuracy. We adapt the James-Stein shrinkage method to propose estimators that are no worse and are oftentimes better in the prediction mean squared error after information integration, regardless of the degree of study population heterogeneity. We conduct comprehensive simulation studies to investigate the numerical performance of the proposed estimators. We also apply the method to enhance a prediction model for patella bone lead level in terms of blood lead level and other covariates by integrating summary information from published literature.

Do we underestimate risk of cardiovascular mortality due to lead exposure?

BackgroundStudies using data from the National Health and Nutrition Examination Survey-III (NHANES-III) have demonstrated significant prospective associations between blood lead levels and increased mortality. Bone lead represents cumulative lead burden and thus is a better biomarker for assessing chronic impacts, but its in vivo assessment requires special K-x-ray fluorescence (KXRF) instrumentation. Our team recently developed an algorithm predicting bone lead levels from a combination of blood lead levels, age and other socioeconomic and behavioral variables. We examined the associations of our algorithm-estimated bone lead levels and mortality in NHANES-III. MethodsWe included 11,628 adults followed up to December 31, 2019. Estimated tibia lead and patella lead levels were calculated using our prediction algorithms. We used survey-weighted Cox proportional hazards models to compute hazard ratios (HRs) and 95 % confidence intervals (CIs). ResultsDuring the median follow-up of 26.8 years, 4900 participants died (mortality rate = 1398 per 100,000 adults/year). Geometric means (95 % CIs) of blood lead, predicted tibia lead, and predicted patella lead were 2.69 μg/dL (2.54, 2.84), 6.73 μg/g (6.22, 7.25), and 16.3 μg/g (15.9, 16.8), respectively. The associations for all-cause mortality were similar between blood lead and bone lead. However, the associations for cardiovascular mortality were much greater with predicted bone lead markers compared to blood lead: for comparing participants at the 90th vs. 10th percentiles of exposure, HR = 3.32 (95 % CI: 1.93–5.73) for tibia lead, 2.42 (1.56–3.76) for patella lead, 1.63 (1.25–2.14) for blood lead. The population attributable fractions for cardiovascular disease mortality if everyone's lead concentrations were declined to the 10th percentiles were 45.8 % (95 % CI: 28.1–59.4) for tibia lead, 33.1 % (18.1–45.8) for patella lead, and 22.8 % (10.4–33.8) for blood lead. ConclusionsThese findings suggest that risk assessment for cardiovascular mortality based on blood lead levels may underestimate the true mortality risk of lead exposure.

Metal Exposure and Risk of Parkinson Disease: A Systematic Review and Meta-Analysis.

Metal exposure has been suggested as a possible environmental risk factor for Parkinson disease (PD). We searched the PubMed, EMBASE, and Cochrane databases to systematically review the literature on the relationship between metal exposure and PD risk and to examine the overall quality of each study and the exposure assessment method. A total of 83 case-control studies and 5 cohort studies published duringthe period 1963-July 2021 were included, of which 73 were graded as being of low or moderate overall quality. Investigators in 69 studies adopted self-reported exposure and biomonitoring after disease diagnosis for exposure assessment approaches. The meta-analyses showed that concentrations of copper and iron in serum and concentrations of zinc in either serum or plasma were lower, while concentrations of magnesium in CSF and zinc in hair were higher, among PD cases as compared with controls. Cumulative lead levels in bone were found to be associated with increased risk of PD. We did not find associations between other metals and PD. The current level of evidence for associations between metals and PD risk is limited, as biases from methodological limitations cannot be ruled out. High-quality studies assessing metal levels before disease onset are needed to improve our understanding of the role of metals in the etiology of PD.

The Influence of Environmental Exposure to Heavy Metals on the Occurrence of Selected Elements in the Maxillary Bone.

The elemental composition of the body's calcified tissues may reflect the environmental exposure of the population to heavy metals. The aim of the study was to assess whether the elemental composition of the maxillary bone from individuals belonging to a given population reflects the environmental exposure of this population to lead and cadmium. The research material consisted of cortical bone from the anterolateral walls of the maxilla collected from 126 patients during Caldwell-Luc maxillary sinus surgery on residents of two cities differing in terms of the lead and cadmium pollution of the natural environment. The content levels of lead, cadmium, iron, manganese, chromium, copper, and iron were determined by using atomic absorption spectrophotometry. The content levels of lead and cadmium in the samples of the maxillary bones of residents of Bielsko-Biala were 3.26 ± 2.42 µg/g and 0.74 ± 0.38 µg/g, respectively, whereas in the samples from the residents of Katowice, they were 7.66 ± 2.79 µg/g and 1.12 ± 0.08 µg/g, respectively. It was found that the lead and cadmium levels in the maxillary bone corresponded to the environmental exposure to these heavy metals in the place of residence, which was proven here via the example of the residents of two cities with different concentrations of these heavy metals in the air over long time periods. Additionally, higher content levels of essential metals such as manganese, chromium, copper, and iron are characteristic of the maxillary bone samples of residents of the area that is more polluted with heavy metals.

Comparison of levels of toxic trace elements in two most common spinal pathologies in three different tissues

Aim: The toxic trace element levels in serum, bone (lamina), and intervertebral disc tissues of patients with lumbar spinal stenosis and lumbar herniated nucleus pulposus (HNP) which are the two most common spinal pathologies were determined, and it was investigated whether they have a role in the pathophysiology of these pathologies. Materials and methods: Cadmium (Cd), aluminium (Al), arsenic (As), mercury (Hg), and lead (Pb) levels in serum, intervertebral disc, and bone (lamina) tissue of patients with HNP (=20) and 30 with lumbar spinal stenosis (LSS) (n=30) were determined by Inductively Coupled Plasma Mass Spectrometry technique. Results: LDH group Cd serum level was found to be significantly higher than LSS group Cd serum level (p=0.024). The Al disc level in the HNP group was found to be significantly higher than the Al disc level in the LSS group (p=0.038). While As serum level increased in LDH group, it was determined that As bone level increased very significantly (r= 0.699, p=0.001). In the LSS group, it was determined that the Hg disc level increased significantly as the Hg serum level increased (r=0.608, p<0.01). On the other hand, as the Hg serum level increased in the LDH group, the Hg disc level also decreased significantly (r= -0.579, p<0.01). Conclusion: The difference in toxic trace element levels seen in these pathologies has been discussed in terms of possible causes in light of current literature. The findings of our study support the hypothesis that toxic trace elements may be effective in lumbar disc degeneration.

Prenatal and Early Childhood Exposure to Lead and Repeated Measures of Metabolic Syndrome Risk Indicators From Childhood to Preadolescence

Background: Exposure to lead (Pb) during the early life stages has been associated with the development of metabolic syndrome (MetS). Longitudinal studies of Pb exposure in critical developmental windows in children are limited.Methods: Our study included 601 mother–child dyads from the PROGRESS (Programming Research in Obesity, Growth, Environment and Social Stressors) birth cohort. Blood lead levels (BLLs) were assessed during the second and third gestational trimesters, in cord blood at delivery, and at ages 1, 2, and 4 years. Bone lead levels in the patella and tibia were assessed at 1 month postpartum and evaluated in separate models. To account for cumulative exposure (prenatal, postnatal, and cumulative), we dichotomized the BLLs at each stage visit and determined the following: “higher” if a BLL was at least once above the median (HPb) and “lower” if all BLLs were below the median (LPb). We analyzed fasting glucose, HbA1c, triglycerides (TGs), total cholesterol (TC), high-density lipoprotein cholesterol (cHDL), low-density lipoprotein cholesterol (cLDL), body mass index, waist circumference (WC), body fat percentage, and systolic (SBP) and diastolic blood pressure (DBP) at two study visits between 6 and 12 years of age and created cutoff points based on the clinical guidelines for each indicator. Mixed effects models were used to analyze each outcome longitudinally for each BLL score, adjusting for child's sex, size for gestational age, child's age, maternal parity, mother's age, and socioeconomic status.Results: We observed associations for HPb exposure and TC in all stages (OR = 0.53, 95%CI = 0.32–0.86) and postnatally (OR = 0.59, 95%CI = 0.36–0.94) and for prenatal HPb and TGs (OR = 0.65, 95%CI = 0.44–0.95). HPb at all stages was associated with WC (OR = 0.27, 95%CI = 0.08–0.86), BMI (OR = 0.33, 95%CI = 0.11–0.99), SBP (OR = 0.53, 95%CI = 0.32–0.85), and DBP (OR = 0.57, 95%CI = 0.34–0.95). Pb levels in the patella were associated with cHDL (OR = 1.03, 95%CI = 1.00–1.07) and those in the tibia with TGs (OR = 0.95, 95%CI = 0.91–0.99).Conclusion: Early life exposure to Pb may alter early indicators of MetS. A follow-up of these children will allow for more definition on the impact of longer-term exposures.

Cumulative Lead Exposure Resulting from Coal Power Plants in India

BACKGROUND AND AIM: Coal pollution can lead to a myriad of toxic exposures and toxicity resulting from coal power generation has not been well-defined. As part of this study, we sought to identify cumulative lead exposure measured as bone lead in communities living near coal power plants. METHODS: We chose three communities at 1 km (n=50), 9 km (n=50), and 38 km (n=50) from coal power plants near Chennai, India and measured their bone lead using a portable x-ray fluorescence device. RESULTS:The bone lead identified in all participants was significantly higher than that found in typical occupationally exposed populations in the United States. We identified a dependency on location with the community living within 1 km of coal power plants experiencing higher cumulative lead exposure than the community farthest from the coal power plants. Lead exposure decreased at a rate of 0.92 ug/g/km. From our models, a 40-year-old adult at 1 km from a coal power plant would have an average bone lead level of 22.3 ug/g, whereas a 40-year-old at 10 km would have an average bone lead level of 14.3 ug/g. Further, we identified a population of over 704,185 that would be living in communities within 1 km of a coal power plant, equivalent to our highest exposure group. CONCLUSIONS:Our study was the first to identify a relationship between cumulative lead exposure and coal pollution, demonstrating a dramatic increase in lead exposure for communities near coal power plants. The community within 1 km of the coal power plants experienced bone lead on average 1.5 times higher than our control group. The control group had higher cumulative lead exposure than typical occupational exposures in the United States. These exposures would lead to drastic consequences throughout the body including cardiovascular and neurologic health impacts while ultimately increasing mortality from all causes. KEYWORDS: Coal, lead, cumulative, xrf, India, bone lead

Do We Underestimate Risk of Mortality due to Lead Exposure?

Background/Aim: Studies using data from the National Health and Nutrition Examination Survey-III (NHANES-III) have demonstrated significant associations between blood lead levels and increased mortality. However, blood lead reflects primarily recent exposure and lead mobilized from internal organs. Bone lead represents cumulative lead burden and thus is a better biomarker for assessing chronic impacts, but its in vivo assessment requires special K-x-ray fluorescence (KXRF) instrumentation. Our team used KXRF measurements of lead in bone and blood lead levels in participants of the Normative Aging Study to develop an algorithm predicting bone lead levels from a combination of blood lead levels and standard biochemical, hematologic, and questionnaire data. We examined the associations of our algorithm-estimated bone lead levels and mortality in NHANES-III.Methods: We included 11,065 adults followed up to December 31, 2015. Estimated tibia and patella bone lead levels were calculated using our prediction algorithm. We used survey-weighted Cox proportional hazards models to compute hazard ratios (HRs) and 95% confidence intervals (CIs).Results: During the median follow-up of 22.4 years (216,565 person-years), 4,103 participants died (mortality rate=1,895 per 100,000 adults/year). Means (95% CIs) of blood lead, tibia lead, and patella lead were 3.47 μg/dL (3.27-2.67), 2.98 μg/g (2.23-3.75), and 3.04 μg/g (1.94-4.14), respectively. After adjustment for potential confounders, the HRs comparing participants at the 90th vs. 10th percentiles of exposure with regards to all-cause mortality were 1.25 (95% CI: 1.05-1.50) for blood lead, 1.91 (1.36-2.68) for tibia lead, 2.00 (1.45-2.77) for patella lead; for CVD mortality, 1.67 (1.20-2.34) for blood lead, 1.89 (0.98-3.67) for tibia lead, 2.24 (1.26-4.00) for patella lead; and for cancer mortality, 1.35 (0.98-1.84) for blood lead, 2.52 (1.30-4.90) for tibia lead, 2.45 (1.29-4.66) for patella lead.Conclusions: These findings suggest that risk assessment based on blood lead levels may underestimate the true mortality risk of lead exposure.

Evidence of selected nephrotoxic elements in Sri Lankan human autopsy bone samples of patients with CKDu and controls

BackgroundThis article describes the analysis and interpretation of data relating to the presence of cadmium, lead, mercury and fluoride in human bone samples obtained from cadavers of patients dying of Chronic Kidney Disease of uncertain aetiology (CKDu) in a case-control study, which the authors believe to be the first in Sri Lanka.MethodsThis is a case-control study comparing selected nephrotoxins levels in autopsy samples of bones from persons confirmed to have died of CKDu, and who had lived in a CKDu hotspot and controls with no history of abnormal kidney functions who had lived in areas having a low prevalence of CKDu.ResultsThe average age at death of the cases was 59.6 ± 15.1 (±SD), while that for controls was 58.0 ± 19.3 (±SD) years with no significant statistical difference. Calcium adjusted bone lead and bone fluoride levels were significantly higher among CKDu cases (n = 14) than those of controls (n = 33). Further, younger and older clusters of CKDu cases can be differentiated when the calcium adjusted lead content was considered. Younger patients reported higher lead content compared to the older group. Cadmium and mercury content did not show a remarkable difference among cases and controls.ConclusionsOur results show a significant accumulation of lead in bone tissue in persons who have died of CKDu which indicates a higher chronic exposure of the CKDu victims, to lead. Fluoride content in the bones of cases is also significantly high. The results indicate that a gradual reduction of glomerular filtration rate (GFR) may have occurred with the chronic exposure to lead. At a certain point of the threshold of low GFR, excretion of fluoride may be impaired, since the main excretory pathway of fluoride is via the kidneys. Fluoride accumulation in blood in turn may exacerbate nephrotoxicity, triggering a synergistic cascade of events which may lead to a further deterioration in the GFR. The extremely high fluoride content detected suggests a cumulative effect in people exposed to comparatively higher fluoride levels, most probably from drinking water.

Risk-Factor Based Lead Screening and Correlation With Blood and Bone Lead Levels in Pregnancy [27K

INTRODUCTION: Lead exposure has devastating neurologic consequences for children and may begin in utero. The American College of Obstetricians and Gynecologists recommends prenatal lead screening using a risk factor-based approach rather than universal blood testing. The clinical utility of this approach has not been studied. We evaluated the association of bone and blood lead with a prenatal risk assessment questionnaire. METHODS: We enrolled a convenience sample of parturients ≥34 weeks’ gestation, with a singleton pregnancy, who were admitted from the obstetrical triage unit. We measured blood lead before delivery and bone lead ≤4 days postpartum using a portable X-ray spectrometer. We defined detectable blood lead as ≥2 ug/dL and detectable bone lead as ≥10 ug/g. The IRB approved the study. RESULTS: We enrolled 102 participants, of whom 100 had lead measured. We identified ≥1 risk factor among 78% of participants; none had clinical blood lead testing. The median blood lead was 0.2 ug/dL (0.2–0.4) and median bone lead was 3.8 ug/g (2.0–6.6). Blood lead, but not bone lead, was significantly higher for parturients born outside the US (P=.01). Two participants (2.2%) had detectable blood lead, while 16 (16.2%) had detectable bone lead. The questionnaire had good sensitivity but poor specificity when using blood (sensitivity 100%, specificity 22%), and bone (sensitivity 94%, specificity 25%) as the gold standard for lead exposure. CONCLUSION: This study showed that a risk-based approach for detecting lead exposure identifies parturients with high lead levels, but this approach was infrequently used clinically and has poor specificity.

Could Lifetime Lead Exposure Play a Role in Limbic-predominant Age-related TDP-43 Encephalopathy (LATE)?

Limbic-predominant Age-related TDP-43 Encephalopathy (LATE) is a disease in which the clinical presentation mimics that of Alzheimer's disease. TDP-43 proteinopathy associated with LATE has been identified in more than 20% of autopsies of community-dwelling adults over the age of 80. It is believed to contribute significantly toward tau-negative dementia. Heavy metals such as lead has also been linked to TDP-43 proteinopathy. In particular, lead triggers TDP-43 accumulation and disrupts TDP-43 homeostasis. However, the specific relationship between LATE and lead remains unknown. Before leaded gasoline was phased out during the 1970s and 1980s, average blood lead levels were 15 times what they are today. Thus, each successive birth cohort entering old age has had less cumulative lifeime exposure to lead. Lifetime exposure can be tracked in the tibia bone, where the half-life of lead is many decades. We hypothesize that lead plays a role in the development of LATE. There are two ways to explore the validity of this hypothesis. Generational differences in lead exposure should result in a steady decline in the prevalence of LATE among older adults. We propose the use of tibia bone lead levels be examined in conjunction with brain autopsies from different birth cohorts to examine the link between lead exposure and LATE prevalence, holding age constant. Furthermore, individuals with genetic polymorphisms that confer a greater lead absorption phenotype should display a higher degree of TDP-43 accumulation in autopsies. The results of such studies could provide insight into gene by environment interactions relevant to the development of LATE.

Prenatal lead exposure and cord blood DNA methylation in PROGRESS: an epigenome-wide association study.

The effects of prenatal lead exposure on child development include impaired growth and cognitive function. DNA methylation might be involved in the underlying mechanisms and previous epigenome-wide association studies reported associations between lead exposure during pregnancy and cord blood methylation levels. However, it is unclear during which developmental stage lead exposure is most harmful. Cord blood methylation levels were assayed in 420 children from a Mexican pre-birth cohort using the Illumina Infinium MethylationEPIC microarray. Lead concentrations were measured in umbilical cord blood as well as in blood samples from the mothers collected at 2nd and 3rd trimester and delivery using inductively coupled plasma-mass spectrometry. In addition, maternal bone lead levels were measured in tibia and patella using X-ray fluorescence. Comprehensive quality control and preprocessing of microarray data was followed by an unbiased restriction to methylation sites with substantial variance. Methylation levels at 202 111 cytosine-phosphate-guanine sites were regressed on each exposure adjusting for child sex, leukocyte composition, batch variables, gestational age, birthweight-for-gestational-age, maternal age, maternal education and mode of delivery. We find no association between prenatal lead exposure and cord blood methylation. This null result is strengthened by a sensitivity analysis showing that in the same dataset known biomarkers for birthweight-for-gestational-age can be recovered and the fact that phenotypic associations with lead exposure have been described in the same cohort.

Blood DNA methylation biomarkers of cumulative lead exposure in adults.

Background:Lead is a ubiquitous toxicant following three compartment kinetics with the longest half-life found in bones. Patella and tibia lead levels—validated measures of cumulative exposure—require specialized X-ray-fluorescence-spectroscopy available only in a few centers worldwide. We developed minimally-invasive biomarkers reflecting individual cumulative lead exposure using blood DNA methylation profiles—obtainable via Illumina450K or IlluminaEPIC bead-chip assays.Methods:We developed and tested two methylation-based biomarkers from 348 Normative Aging Study (NAS) elderly men. We selected methylation sites with strong associations with bone lead levels via robust regressions analysis and constructed the biomarkers using elastic nets. Results were validated in a NAS subset, reporting specificity and sensitivity.Findings:Participants were 73 years old on average (standard deviation, SD=6), with moderate lead levels of (mean±SD patella:27±18 μg/g; tibia:21±13 μg/g). Methylation-based biomarkers for lead in patella and tibia included 59 and 138 DNA methylation sites, respectively. Estimated lead levels were significantly correlated with actual measured values, (r=0.62 patella, r=0.59 tibia) and had low mean square error (MSE) (MSE=0.68 patella, MSE=0.53 tibia). Means and distributions of the estimated and actual lead levels were not significantly different across patella and tibia bones (p>0.05). Methylation-based biomarkers discriminated participants highly exposed (>median) to lead with a specificity of 74% and 73% for patella and tibia lead levels, respectively, with 70% sensitivity.Interpretation:DNA-methylation-based lead biomarkers are novel tools that can be used to reconstruct decades’ worth of individual cumulative lead exposure using only blood DNA methylation profiles and may help identify the consequences of cumulative exposure.

Blood DNA Methylation Biomarkers of Cumulative Lead Exposure in Adults

Lead is a ubiquitous toxicant following three compartment kinetics with the longest half-life found in bones. Patella and tibia lead levels—validated measures of cumulative exposure—require specialized X-ray-fluorescence-spectroscopy available only in a few centers worldwide. We developed minimally invasive biomarkers reflecting individual cumulative lead exposure using blood DNA methylation profiles—obtainable via Illumina 450K or IlluminaEPIC bead-chip assays. We developed and tested two methylation-based biomarkers from 348 Normative Aging Study (NAS) elderly men. We selected methylation sites with strong associations with bone lead levels via robust regressions analysis and constructed the biomarkers using elastic nets. Results were validated in a NAS subset, reporting specificity, and sensitivity. Participants were 73 years old on average (standard deviation, SD = 6), with moderate lead levels of (mean ± SD patella: 27 ± 18 µg/g; tibia:21 ± 13 µg/g). Methylation-based biomarkers for lead in patella and tibia included 59 and 138 DNA methylation sites, respectively. Estimated lead levels were significantly correlated with actual measured values, (r = 0.62 patella, r = 0.59 tibia) and had low mean square error (MSE) (MSE = 0.68 patella, MSE = 0.53 tibia). Means and distributions of the estimated and actual lead levels were not significantly different across patella and tibia bones (p > 0.05). Methylation-based biomarkers discriminated participants highly exposed (>median) to lead with a specificity of 74 and 73% for patella and tibia lead levels, respectively, with 70% sensitivity. DNA methylation-based lead biomarkers are novel tools that can be used to reconstruct decades’ worth of individual cumulative lead exposure using only blood DNA methylation profiles and may help identify the consequences of cumulative exposure.

Blood lead, bone lead and child attention-deficit-hyperactivity-disorder-like behavior

Background and objectiveMounting evidence showed that lead exposure increased the risk of child attention-deficit-hyperactivity disorder (ADHD). Epidemiologic studies have typically used the blood-lead as a biomarker of lead exposure; blood-lead levels mostly reflect recent lead exposure. However, few studies have examined the relationship between bone-lead, a biomarker of cumulative exposure, and ADHD. Therefore, we aimed to compare the associations of bone-lead vs blood-lead levels with child ADHD symptoms and comorbidities. MethodsA total of 164 children aged 3–15 years were enrolled during 2014–2015. The Vanderbilt-ADHD-Diagnostic-Parent-Rating Scale (VADPRS) was used to evaluate the children's ADHD symptoms and comorbidities. Children's blood and bone lead concentrations were assessed, the latter using a non-invasive K-X-ray-fluorescence technique. According to blood-lead levels, children were classified into high (blood-lead ≥ 10.0 μg/dL) and low (blood-lead < 10.0 μg/dL) blood-lead groups. According to bone-lead levels, children were classified into high (bone-lead ≥ 2.66 μg/g) and low (bone-lead < 2.66 μg/g) bone-lead groups. We associated blood/bone lead with VADPRS data using multi-variable binary logistic regression models. ResultsChildren in the high blood-lead group had higher hyperactivity/impulsivity (P = 0.02) scores than the corresponding low blood-lead group. Children in the high bone-lead group had higher hyperactivity/impulsivity (P = 0.02) and oppositional-defiant-disorder (ODD) (P = 0.03) scores than the corresponding low bone-lead group. After adjusting for relevant confounders, children in the high bone-lead group were more likely to have ODD-behavior than the low group (OR = 6.7, 95%CI: 1.2–36.5). However, no adjusted association was observed between blood-lead and any ADHD-domain score. ConclusionHigh levels of cumulative lead exposure in children may be an independent risk factor of ODD-behavior.

Lead Exposure in the Critically Endangered Bearded Vulture (Gypaetus barbatus) Population in Southern Africa

Lead poisoning is an important threat to some raptor species, and the primary source of lead is through the ingestion of carcasses that have been shot with lead, which makes scavengers such as vultures particularly vulnerable. We examined the concentrations of lead in blood and bone tissue samples collected throughout the range of the Bearded Vulture (Gypaetus barbatus) in southern Africa. This population is regionally critically endangered and it is not known to what extent lead poisoning may be a threat. Blood lead levels (0.62 ± 0.81 μg dL−1) from six live birds tested in 2017 indicated background levels of exposure to lead. Similarly, five live birds tested in 2009 using a less sensitive method all had blood lead levels <3 μg dL−1. Bone lead levels (11.79 ± 8.34 μg g−1) from eight birds that had died indicated lead exposure and accumulation over time, suggesting that lead may have contributed to their deaths. These levels of lead may be detrimental to the survival and fecundity of this small and declining population. Recommendations to address this threat include banning hunting and culling with lead ammunition, which is the most likely source of this pollutant. Such actions may reduce the population's susceptibility to other threats, which may be compounded by high lead levels, and help ensure the success of planned reintroduction programs.

Low-Level Cumulative Lead and Resistant Hypertension: A Prospective Study of Men Participating in the Veterans Affairs Normative Aging Study.

BackgroundBone lead offers a better method over blood lead measurement to discern long‐term lead exposure and accumulation. We examined the risk of resistant hypertension based on bone lead levels in a prospective cohort study of NAS (Normative Aging Study).Methods and ResultsParticipants had clinic data on hypertension (systolic blood pressure, diastolic blood pressure, and antihypertension medication), lead (blood, bone‐patella, bone‐tibia), and demographic and confounding variables. Cases of resistant hypertension were identified by meeting criteria for: (1) inadequate systolic blood pressure (>140 mm Hg) or diastolic blood pressure (>90 mm Hg) while taking 3 medications or (2) requiring >4 medications for blood pressure control. A modified Poisson regression was used for model analysis. Of the 475 participants, 97 cases of resistant hypertension (20.4%) were identified. Among the cases of resistant hypertension, the median tibia and patella lead levels were 20 μg/g and 25 μg/g, respectively, while median tibia and patella lead levels were 20 μg/g and 27.5 μg/g, respectively, in participants without resistant hypertension. Tibia lead demonstrated a significant association with resistant hypertension (relative risk, 1.19; 95% confidence interval, 1.01–1.41 [P=0.04]) per interquartile range increase in tibia lead (13–28.5 μg/g). Patella lead was not associated with resistant hypertension (relative risk, 1.10; 95% confidence interval, 0.92–1.31 [P=0.31]) per interquartile range increase in patella lead (18–40 μg/g). Blood lead levels were not significantly associated with resistant hypertension (relative risk, 1.11; 95% confidence interval, 0.88–1.40 [P=0.38]).ConclusionsTibia lead represents a novel risk factor for resistant hypertension. Our study demonstrates an increased association between tibia lead and resistant hypertension status, with an increased risk of 19% per 1 interquartile range increase in tibia lead.

Acute and Chronic Lead Exposure in Four Avian Scavenger Species in Switzerland.

Despite irrefutable evidence of its negative impact on animal behaviour and physiology, lethal and sublethal lead poisoning of wildlife is still persistent and widespread. For scavenging birds, ingestion of ammunition, or fragments thereof, is the major exposure route. In this study, we examined the occurrence of lead in four avian scavengers of Switzerland and how it differs between species, regions, and age of the bird. We measured lead concentration in liver and bone of the two main alpine avian scavengers (golden eagle Aquila chrysaetos and bearded vulture Gypaetus barbatus) over the entire area of the Swiss Alps and two of the main avian scavengers occurring in the lowlands of Switzerland (red kite Milvus milvus and common raven Corvus corax). Of those four species, only the bearded vulture is an obligate scavenger. We found that lead burdens in the two alpine avian scavengers were higher than those found for the same species elsewhere in Europe or North America and reached levels compatible with acute poisoning, whereas lead burdens of the two lowland avian scavengers seemed to be lower. Several golden eagles, but only one red kite with abnormally high bone lead concentrations were found. In all four species, a substantial proportion of birds had elevated levels which presumably represent recent (liver lead levels) or past (bone lead levels) uptake of sublethal doses of lead.

Lead poisoning

Lead is not known to have any physiological role in the body but is ubiquitous in nature. In our country there are many sources of lead exposure, in particular paints and recycling of batteries. Lead is a persistent metal and is present in water, soil and dust. After being absorbed through the gastrointestinal tract (GIT) or respiratory system, it is stored in soft tissues as well as bones. Lead tends to affect many organ systems in the body particularly the nervous system and kidneys. There are no safe levels and data suggests that low level exposure to lead may also affect health of individuals. The diagnosis of lead toxicity can be done by measuring blood lead levels and K x ray fluorescence (KXRF) instruments which measure lead levels in bone. The treatment consists of chelating agents like BAL, EDTA & DMSA. Eliminating lead from potential sources of exposure would go a long way in preventing effects of lead toxicity.