The urban lead burden in humans, animals, and the natural world

The urban lead (Pb) burden in humans, animals and the natural environment

In Memoriam: Herbert L. Needleman

Good News and Bad News: Blood Lead Levels in the US Go Down, but Higher Levels Are Still Associated with a Higher Burden of CKD: Continued Decline in Blood Lead Levels among Adults in the United States: The National Health and Nutrition Examination Survey. Arch Intern Med 165: 2155-2161, 2005.

The burden of disease from pediatric lead exposure at hazardous waste sites in 7 Asian countries

Breast-feeding and Child Lead Exposure: A Cause for Concern

Getting the lead out: Can iron help?

Objective To assess the effect of protein kinase B(PKB)on the learning and memory functions of mice with chronic lead exposure. Methotis Since the first day after birth,50 Kunming mice were randomized into 5 groups(n=10)and exposed to a 6-week acetic lead exposure at the concentrations of 1.2,2.4,4.8,7.2,and 9.6 mmol/L administered in the drinking water,with another 10 having normal water as the control group.After the 6-week exposure.water maze test Was performed to assess the spatial learning and memory abilities of the mice.The total PKB(t-PKB) and phosphorylated PKB(p-PKB)in the cortical brain neurons were determined with Western bloRing.Results The mean latency of finding the platform in the lead exposure groups was significantly higher than that in the control group(P＜0.05).Chronic acetic lead exposure resulted in obviously impaired spatial learning and memory ability in the mice,and the severity ofthe damage was positively correlated to lead concentrations in the blood and brain tissue(r=678,P=0.000;r=0.643,P=0.000).Lead exposure caused a significant dose-dependent reduction in P-PKB level in the cortical neurons,and p-PKB level in the cortical neurons was inversely correlated to blood lead concentrations(r=0.820,P=0.028) and to the spatial learning and memory ability(r=-0.671,p=000).The level of t-PKB in the cortical brain neurons showed no significant changes in response to lead exposure. Conclusion Chronic acetic lead exposure can impair the learning and memory functions of mice possibly in association with reduced content of p-PKB in the cortical brain neurons. Key words: Protein kinase B; Lead intoxication; Cortical neuron

From the 1980s many well-designed epidemiological studies have confirmed that low-level, subclinical lead exposure in early life is associated with decrements in children's intelligence. Neurodevelopmental deficits from exposure to a low level of lead have been held to be not only an American problem, but also a worldwide issue in the past decade. Good epidemiological studies were reported from England, Scotland, Germany, Greece, Australia and New Zealand. Well-designed cross-sectional and prospective studies were carried out to quantify the magnitude of the relation between full scale IQ in children aged five years or more and the burden of lead (PbB or PbT) in early life of children. Of five cross-sectional studies of blood lead, two demonstrated a significant inverse association between lead and IQ even after adjustment for confounders. Two other studies, however, showed no firm evidence of inverse association after adjustment for confounders, and the remaining study demonstrated no significant inverse association of five cross-sectional studies of tooth lead, two indicated an inverse association between tooth lead and IQ, two others showed no significant inverse association after adjustment for confounders, and the remaining one manifested no association. Of four prospective studies, two revealed strong evidence of an inverse association between blood lead at the age of around two years and IQ. Another one, however, revealed an inverse association between mean postnatal blood level and IQ, while the remaining one demonstrated no significant inverse association between IQ and postnatal blood lead level after adjustment for confounders. In a comprehensive review of 26 epidemiological studies since 1979, including a meta-analysis, Pococok et al. indicated that doubling of the body lead burden (from 10 to 20 micrograms/dl) blood lead or (from 5 to 10 micrograms/g) tooth lead is typically associated with a mean deficit in full-scale IQ of around 1-2 IQ points. Lead in interior household dust, exterior surface soil, and old residential lead paint, which is deteriorated or removed, constitute the major sources of lead poisoning in children in the United States. Infants and children, who typically engage in hand to mouth activities, frequently come into contact with lead dust in soil and on the floor. Marked declines both in air lead and blood lead concentrations are evident parallel to the phase-down of lead in gasoline and soldered cans by U.S. food processors. The major source of lead in drinking water is from lead pipes used in household plumbing. The CDC revised its guidelines concerning childhood lead poisoning, stating that community prevention activities should be triggered when a large percentage of children in a community have blood lead levels of 10 micrograms/dl, the lowest level at which neurodevelopmental effects were believed to occur. For children with blood lead level concentrations between 10 and 14 micrograms/dl, more frequent rescreening may be needed. For concentrations between 15 and 19 micrograms/dl, in addition to more frequent screening, nutritional and educational advice should be given. In cases where these levels persist, there should be environmental investigation and intervention. All children with blood levels of 20 micrograms/dl or greater should receive environmental evaluation and medical examination. Such children may need pharmacological treatment.

External lead contamination of women's nails by surma in Pakistan: Is the biomarker reliable?

BackgroundLow-level exposure to lead and to chronic stress may independently influence cognition. However, the modifying potential of psychosocial stress on the neurotoxicity of lead and their combined relationship to aging-associated decline have not been fully examined.ObjectivesWe examined the cross-sectional interaction between stress and lead exposure on Mini-Mental State Examination (MMSE) scores among 811 participants in the Normative Aging Study, a cohort of older U.S. men.MethodsWe used two self-reported measures of stress appraisal—a self-report of stress related to their most severe problem and the Perceived Stress Scale (PSS). Indices of lead exposure were blood lead and bone (tibia and patella) lead.ResultsParticipants with higher self-reported stress had lower MMSE scores, which were adjusted for age, education, computer experience, English as a first language, smoking, and alcohol intake. In multivariable-adjusted tests for interaction, those with higher PSS scores had a 0.57-point lower (95% confidence interval, −0.90 to 0.24) MMSE score for a 2-fold increase in blood lead than did those with lower PSS scores. In addition, the combination of high PSS scores and high blood lead categories on one or both was associated with a 0.05–0.08 reduction on the MMSE for each year of age compared with those with low PSS score and blood lead level (p < 0.05).ConclusionsPsychological stress had an independent inverse association with cognition and also modified the relationship between lead exposure and cognitive performance among older men. Furthermore, high stress and lead together modified the association between age and cognition.

Lead poisoning is a well-recognized public health concern for children living in the United States. In 1992, Health Care Financing Administration (HCFA) regulations required lead poisoning risk assessment and blood lead testing for all Medicaid-enrolled children ages 6 months to 6 years. This study estimated the prevalence of blood lead levels (BLLs) >/=10 microg/dL (>/=0.48 micromol/L) and the performance of risk assessment questions among children receiving Medicaid services in Alaska. Measurement of venous BLLs in a statewide sample of children and risk assessment using a questionnaire modified from HCFA sample questions. Eight urban areas and 25 rural villages throughout Alaska. Nine hundred sixty-seven children enrolled in Medicaid, representing a 6% sample of 6-month- to 6-year-old Alaska children enrolled in Medicaid. Determination of BLL and responses to verbal-risk assessment questions. BLLs ranged from <1 microg/dL (<0.048 micromol/L) to 21 microg/dL (1.01 micromol/L) (median, 2.0 microg/dL or 0.096 micromol/L). The geometric mean BLLs for rural and urban children were 2.2 microg/dL (0.106 micromol/L) and 1.5 microg/dL (0.072 micromol/L), respectively. Six (0.6%) children had a BLL >/=10 microg/dL; only one child had a BLL >/=10 microg/dL (11 microg/dL or 0.53 micromol/L) on retesting. Children whose parents responded positively to at least one risk factor question were more likely to have a BLL >/=10 microg/dL (prevalence ratio = 3.1; 95% confidence interval = 0.4 to 26.6); the predictive value of a positive response was <1%. In this population, the prevalence of lead exposure was very low (0.6%); only one child tested (0.1%) maintained a BLL >/=10 microg/dL on confirmatory testing; no children were identified who needed individual medical or environmental management for lead exposure. Universal lead screening for Medicaid-enrolled children is not an effective use of public health resources in Alaska. Our findings identify an example of the importance in considering local and regional differences when formulating screening recommendations and regulations, and continually reevaluating the usefulness of federal regulations.

Lead Exposure Survey Tool (LEST): A methodological approach to highlight the invisible lead poisoning

Objective To evaluate the effect of curcumin on the lead burden in lead-exposed rats, and to study whether curcumin can influence the lipid peroxidation caused by lead exposure. Methods A total of 70 rats of 21-day-old rats were divided randomly to 7 groups, the control group was given normal diet and drinking water, the curcumin group was given curcumin only 1 month after normal drinking water being given; the other 5 lead-exposed groups were given 2 g/L of acetate lead in free drinking water for 1 month and then randomly divided into lead-exposed group, low, medium and high concentration curcumin groups and Dimercaptosuccinic acid(DMSA) group, relatively.Lead levels of lead-exposed rats were determined by using inductively coupled plasma mass spectrometry, and commercial kit was used to detect antioxidant enzymes, and glutathione related enzymes and lipid peroxides. Results The lead concentrations in the blood, hippocampus, liver and kidney of lead-exposed group increased, the levels of each group were (221.76±12.59) μg/L, (1.10±0.11) μg/g, (1.40±0.12) μg/g, (8.26±0.47) μg/g, and (57.58±6.09) μg/g, respectively; compared with the lead-exposed group, the lead concentrations reduced in the blood, hippocampus, liver and kidney significantly (F=90.67, 39.07, 27.34, 86.04, all P=0.000) in the curcumin-treated group, while the effect of curcumin in the bones showed no significant difference between groups(F=5.65, P=0.230). Lead could significantly improve the level of lipid peroxides in the serum and hippocampus, and curcumin-treated groups could significantly reduce the level of lipid peroxidation(F=58.03, 19.25, 32.27, 24.83, all P=0.000) and (F=28.18, 33.71, 38.95, 32.11, all P=0.000); lead could also reduce the antioxidant enzyme activity in the serum and hippocampus; curcumin-treated groups could significantly increase the antioxidant enzyme activity (F=18.24, 78.65, all P=0.000) and (F=13.68, 17.04, all P=0.000), respectively.The concentration in the curcumin group was better than that of DMSA group (P<0.05). Conclusions Curcumin can downregulate the lead concentrations in the blood, hippocampus, liver and kidney and improve the activity of antioxidant enzymes, inhibit the oxidative stress induced by lead, and thus resist the lead-induced damage. Key words: Lead; Curcumin; Neurologic damage; Reactive oxygen species

Cardiovascular diseases (CVD) are the leading causes of death and disability worldwide. Lead exposure is an important risk factor for CVD. In our study, we aimed to estimate spatial and temporal trends in the burden of cardiovascular disease associated with chronic lead exposure. The data collected for our study were obtained from Global Burden of Disease (GBD) study 2019 and analyzed by age, sex, cause, and location. To assess the temporal trends in burden of CVD attributable to chronic lead exposure over 30 years, we used Joinpoint regression analysis. In 2019, the number of lead exposure-attributable CVD deaths and disability-adjusted life-years (DALYs) were 0.85 and 17.73 million, 1.7 and 1.4 times more than those observed in 1990, respectively. However, the corresponding age-standardized rates (ASR) of death and DALY gradually decreased from 1990 to 2019, especially from 2013 to 2019. Over the last 30 years, among 21 GBD regions and 204 countries and territories, the High-income Asia Pacific and the Republic of Korea experienced the largest reductions in age-standardized DALY and death rates, while Central Asia and Afghanistan experienced the largest increases. Males and the elderly population suffered higher death rates and DALY burdens than females and the young population. Furthermore, we observed that higher socio-demographic index (SDI) regions demonstrated lower ASR of death and DALY rates. In 2019, the low and low-middle SDI regions, especially South Asia, exhibited the highest burden of CVD attributable to lead exposure. Our study provides a thorough understanding of the burden of CVD attributable to chronic lead exposure. The findings confirm the significance of implementing lead mitigation strategies and increasing investment in CVD prevention and treatment. These measures are crucial in reducing the burden of CVD and promoting public health on a global scale.

Sniffing is a behaviour which can be induced by dopamine D1/D2 receptor agonists. In order to test the effect of chronic lead exposure on dopamine receptor subtypes, we studied the effects of acute and chronic lead exposure on sniffing induced by apomorphine, a dopamine receptor agonist. Intraperitoneal injection of the dopaminergic receptor agonist, apomorphine (0.25-1 mg/kg), induced dose-dependent the sniffing behaviour in rats. Acute administration of lead acetate (50, 100 and 200 mg/kg) deceased the apomorphine-induced sniffing. Chronic lead (0.25%) exposure also decreased the apomophine response Dopamine D1 or D2 receptor antagonists reduced the apomorphine effect. Lead exposure could not potentiate the blockade induced by the dopamine receptor antagonists. It is concluded that the response of lead is not mediated by alteration of dopamine receptors.