Effects Of Environmental Lead Exposure Research Articles

Identification of potential food sources affecting blood lead levels and their health hazards (CVD, respiratory diseases, cancer)

Environmental lead exposure is a well-known and significant public health concern. In areas with low lead exposure, comprehensive and detailed research and validation are needed to eliminate the adverse effects of environmental lead exposure. This study aims to understand the possible food pathways of environmental lead exposure by exploring the contribution of food to blood lead and the mediating effect of blood lead in the occurrence of diseases. Similarly, as lead is a heavy metal pollutant with good research foundation, fine analysis of lead in this period can also be a reference for other unknown pollutants. In this cross-sectional study of 1162 peoples, the data are taken from National Health and Nutrition Examination Survey (NANHES) 2015–2016, we grouped the population according to the median blood lead level (0.038 μmol/L) to screen the variables adjusted by the model. we grouped foods by code and used a generalized additive mixed model (GAMM) to study their relationship with blood lead levels, a correlation has been found between egg mixtures (p = 0.007) and legumes (p = 0.041) consumption and blood lead levels. We analyzed how metabolic status, exercise, and macronutrient intake modulate the impact of certain foods on blood lead levels to infer its possible process. To verify whether adverse effects are caused by lead, we explored the mediating effect of blood lead on the relationship between food intake and disease [cardiovascular diseases (CVD), respiratory diseases, cancer], however, no statistically significant mediating effect was found. Overall, environmental lead exposure through food still affects blood lead levels, but it has not led to adverse outcomes in blood, respiratory system, or cancers Under conditions where lead exposure levels were equivalent to those in the study (blood lead levels， mean = 0.052 μmol/L, standard deviation = 0.048 μmol/L, median = 0.038 μmol/L, min = 0.002 μmol/L, max = 0.904 μmol/L, skewness = 6.543, kurtosis = 89.391).

Adverse effects of environmental lead exposure on hepatic, renal and thyroid function of buffaloes

Lead emitting industries pose a risk of contamination of surface and ground water, soil and fodder by dissemination of the particles carrying lead by wind action and by runoff from the tailings which cause numerous biochemical, immunological and reproductive disturbances in animals. Samples (n-20) of tube-well water, surface soil and fodder were collected from an uncontaminated area with water lead level within the permissible limit (0.05µg/ml) which served as control, and from the lead contaminated area (n=25) of Ludhiana (Punjab) with water lead level above the permissible limit. Blood level of lead (>0.24µg/ml) was used to decide the exposure group. The biochemical profile of the buffaloes exposed to lead showed hypoproteinemia, hypoalbuminemia, hypercholesterolemia, hypertriglyridemia and hyperglycemia as compared to control group. The activity of serum enzymes viz alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase, alkaline phosphatase, lactate dehydrogenase and creatine kinase showed significant (p less than 0.05) elevation in lead exposed buffaloes. There was significant (p less than 0.05) increase in levels of plasma urea and creatinine, however, tri-iodothyrinine and thyroxine concentrations were significantly (p less than 0.05) declined in lead exposed buffaloes as compared to control animals. Blood lead levels were significantly correlated with alterations in different biochemical indices in lead exposed buffaloes indicating the adverse effect on hepatic, renal and thyroid function.

Diabetes and Exposure to Environmental Lead (Pb).

Although the increased incidence of type 2 diabetes since the 1950s is thought to be primarily due to coincident alterations in lifestyle factors, another potential contributing factor in industrialized countries is exposure of the population to environmental pollutants and industrial chemicals. Exposure levels of many environmental toxicants have risen in the same time-frame as the disease incidence. Of particular interest in this regard is the metal lead. Although overall lead exposure levels have diminished in recent decades, there is an under-recognized but persistent occurrence of lead exposure in poor underserved urban populations. Although the neural developmental pathologies induced by lead exposures have been well documented, very little is known about the effect of lead exposure on the incidence of chronic metabolic diseases such as type 2 diabetes. Although our understanding of the metabolic health effects of lead exposure is incomplete, there are studies in model systems and a small amount of epidemiological data that together suggest a deleterious effect of environmental lead exposure on metabolic health. This article reviews the human, animal and in vitro studies that have examined the effects of lead exposure on the development of diabetes and related metabolic conditions.

Environmental lead exposure and pubertal trajectory classes in South African adolescent males and females

The effects of environmental lead exposure in the neuro-endocrine system have been shown to impact the maturation and tempo of puberty development in adolescents. In low and middle income countries very little is known regarding the detrimental health effects of childhood lead exposure with regard to the tempo of puberty development. To help address this gap in data, we examined the association between lead exposure and puberty progression in males and females.Study participants from the urban Birth to Twenty Plus (BT20+) birth cohort in Soweto-Johannesburg, South Africa with data for blood lead levels at age 13years, cord blood lead levels, pubic hair development and breast development in females, and pubic hair development and genital development in males, were included in this study. The sample comprised 1416 study participants (n=684 females). Pubertal development trajectory classes were defined using Latent Class Growth Analysis. Data were examined for (i) an association between cord blood lead levels and pubertal trajectory classes; and (ii) an association between blood lead levels at age 13years and pubertal trajectory classes.In females, there was an association between adolescent elevated blood lead levels (≥5μg/dL) and lower level of maturation at age 9years and slower progression of pubic hair and breast development (relative risk ratio (RRR)=0.45, p<0.0001; 95% CI (0.29–0.68)) and (RRR=0.46, p<0.01; 95% CI (0.27–0.77)), respectively. In males, elevated blood lead levels at birth were associated with slower tempo of pubic hair development (RRR=0.20, p<0.05).Findings from this study suggest a possible role for environmental lead in altering pubertal development in South African adolescents as shown by slower tempo of progression through the Tanner stages pubertal development in females and males. There were also gender-differences between the effects of prenatal and postnatal lead exposure during pubertal development.

Long-Term Effects of Environmental Lead Exposure on Blood Pressure and Plasma Soluble Cell Adhesion Molecules in Young Adults: A Follow-Up Study of a Prospective Cohort in Kosovo.

Background and Aims Epidemiologic studies examining the relationship between environmental lead (Pb) exposure and blood pressure (BP) generally report small associations between blood lead concentration (BPb) and BP. However, these studies are predominantly cross-sectional. In addition, no epidemiologic studies evaluate associations between either current or past Pb exposure and serum levels of markers of systemic inflammation and endothelial dysfunction, including soluble vascular adhesion molecule (sVCAM-1) and soluble intercellular cell adhesion molecule (sICAM-1). We prospectively investigate these associations later in life Methods. From our original prospective birth cohort study in Mitrovica (a mining town) and Prishtina (a control town), Kosovo, from 1985 to 1998, we located and assessed BPb and BP in 101 participants (mean age of 24.9 years old) in 2011. Results We found highly statistically significant association between concurrent BPb and sVCAM-1 in men and a marginally significant association between concurrent PBb and sICAM.-1 in women. We did not find evidence of mediation. Conclusion Current study results, along with previously reported findings on this cohort, provide evidence for the hypothesis that exposure to Pb leads to small increases in sBP and perhaps to increased circulating levels of sVCAM-1 and sICAM-1 later in life.

The Association between Environmental Lead Exposure and High School Educational Outcomes in Four Communities in New South Wales, Australia.

The associations between environmental lead exposure and high school educational outcomes in four communities located in New South Wales, Australia, were examined in this ecological study. A mixed model analysis was performed to account for each school’s results being more similar than results for other schools. The effect of environmental lead exposure on mean results for five educational outcomes was examined. ‘Leaded’ schools with more than five per cent of students living in the highest lead risk areas were tested against non-leaded ‘comparison’ schools that were matched by a pre-defined socio-educational advantage rating. A small disadvantage was found for leaded schools for four out of five outcomes, which was statistically significant for three outcomes: Higher School Certificate English (p < 0.01), School Certificate Mathematics (p < 0.05), and Australian Tertiary Admissions Rank eligibility rate (p < 0.01). This study adds to the large body of evidence in Australia and elsewhere supporting the importance of primary prevention to protect health at multiple stages of development.

Associations between lead concentrations and cardiovascular risk factors in U.S. adolescents

Little is known regarding the effects of environmental lead exposure on cardiovascular risk factors in the adolescent population. We studied 11,662 subjects included in the National Health and Nutrition Examination Survey (NHANES) 1999–2012. Blood lead levels were analysed for their association with cardiovascular risk factors (CVRF). Regression coefficients (Beta) and 95% confidence intervals (CIs) of blood lead in association with CVRF (e.g., total cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride, fasting glucose, glycohemoglobin, fasting insulin, and blood pressure) were estimated using multivariate and generalized linear regression after adjusting for age, gender, ethnicity, serum cotinine, body mass index (BMI), physical activity, and household income. We identified a strong positive association between blood lead (coefficient = 0.022, 95% CI 0.003, 0.041; P = 0.022) and LDL-cholesterol in adolescents (age 12–19 years). However, no associations with other CVRFs were found in the overall population. In the generalized linear models, participants with the highest lead levels demonstrated a 1.87% (95% CI 0.73%, 3.02%) greater increase in serum LDL-cholesterol (p for trend = 0.031) when compared to participants with the lowest lead levels. These results provide epidemiological evidence that low levels of blood lead are positively associated with LDL-cholesterol in the adolescent population.

Aging and neurobehavioral effects of environmental lead exposure

Aging and neurobehavioral effects of environmental lead exposure

Effects of environmental lead exposure on T-helper cell-specific cytokines in children

Lead (Pb) may alter T-lymphocyte reactivity in situ by preferentially enhancing the development of T-helper 2 (TH2)- and inhibiting TH1-lymphocyte development. These effects could result in dysregulation of the presence/availability of TH1- and TH2-associated cytokines. The aim of this study was two-fold, that is, to assess whole blood Pb levels in schoolchildren from Taiwanese communities that varied in degree of potential for Pb exposure and then ascertain if there were relationships between Pb exposure and changes in levels of key TH1 and TH2 cytokines. Grades 5 and 6 students were selected from four different community schools, i.e., one from: urban area with new homes; urban area with old homes; rural site with old homes; and area located near an oil refinery. Students at each site were further divided into healthy and respiratory allergy subgroups. Blood was collected and whole blood Pb levels and serum interferon (IFN)-γ, interleukin (IL)-12, -4, and -5 levels were determined. The results indicate no differences in whole blood Pb levels (<4 µg/dl) among students from urban and rural sites; these values were similar in the healthy and allergic subjects. Serum TH1 and TH2 cytokine levels also did not differ among/within the groups. In contrast, refinery children had significantly increased Pb levels (5.2–8.8 µg/dl) relative to any of the other sets’ levels. Of these, children with allergies had serum TH2 cytokine levels significantly higher and TH1 cytokine levels significantly lower than their healthy counterparts. Oddly, though having elevated Pb levels, healthy refinery students did not display altered TH1 or TH2 cytokine levels relative to control student values. From this, we conclude that substantively increased whole blood Pb levels may promote TH cell dysregulation and alter the availability of key TH1 and TH2 cytokines, effects that could ultimately contribute to development of pulmonary allergic diseases.

Present and Long Term Effect of Environmental Lead Exposure Over Intellectual Impairment in Children

ISEE-632 Objective: To determine if there is an association between early blood lead concentration and present intellectual ability in exposed schoolchildren, despite lead abatement in the area. Materials and Methods: 442 exposed children had blood lead evaluation in 1998. Of those, 47.5% had lead levels >10 μg/dL. After 7 years a cross-sectional study was conducted in 188 children between 7 and 16 years old, representing 43% of the group studied originally. We used past (1998) and current (2005) blood lead concentration as explanatory variables for intellectual ability (IQ) measured by the WISC-r test. Multiple regression models were used to evaluate the relationship between IQ and blood lead concentration, adjusting by maternal intelligence (WAIS scale), home stimulus (HOME questionnaire), sex, and SES. Results: Blood lead concentration was 3.6±2.3 μg/dL (range 0.5–14) in 2005 and 10.6 + 6.9 μg/dL (range 1–33) in 1998 with a correlation of 0.44 (P = 0.0001). Adjusting for the covariates, we found a significant inverse association between IQ and blood lead in 2005; however, we could not demonstrate a similar association with blood lead in 1998. An increase in the current blood lead concentration of 1 μg/dL was associated with a decrease of 1.03 IQ points (P = 0.012). The deleterious effect is greater the higher the blood lead level as shown through 4 categories of exposure: reference (1.4±0.41 μg/dL); low (2.6±0.37); medium (3.6±0.29) and high (6.5±2.5). Respectively the IQ deficits were: 1.9, 4.3, and 5.1 compared to the reference. Conclusions: Our findings provide additional evidence for deleterious effect of environmental lead on intellectual impairment at blood lead concentrations below 10 μg/dL. Recent blood lead seems more important than past blood lead. Policy efforts should target to prevent lead exposure to optimize children's intellectual potential.

ADHD: Braun et al. Respond

We appreciate the comments of Brondum, and Konofal and Cortese, and the opportunity to clarify our results (Braun et al. 2006). It is common practice to select variables with a p-value of 0.2 for inclusion in multivariable models (Katz 1999). Although the association of blood lead levels and ADHD appeared “tenuous” in bivariate analysis (i.e., p = 0.19), this was largely an artifact of our decision to categorize blood lead levels. When we entered lead into our multivariable analysis as a continuous variable, we found a 1.2-fold increased odds [95% confidence interval (CI), 1.0–1.4; p = 0.02] of ADHD for each 1.0-μg/dL increase in blood lead levels. The blood lead quintiles were not divided into exactly equal sample sizes because we used weighted percentages to categorize the data. We decided a priori to present the analysis in quintiles to make the results easier to interpret and also to illustrate any dose–response relationships for blood lead levels and ADHD. As we noted in the “Discussion” of our article (Braun et al. 2006), a limitation of our study was the inability to adjust for parental psychopathology. This is an unfortunate trade-off when using a large nationally representative survey. In other studies, prenatal tobacco exposure has been shown to be a risk factor for the development of ADHD after controlling for parental psychopathology (Mick et al. 2002; Weissman et al. 1999). Although there is considerable experimental and epidemiologic evidence linking lead exposure with behaviors consistent with ADHD, future studies of childhood lead exposure will need to confirm our results by accounting for parental psychopathology and other potential confounders. The hypothesis proposed by Konofal and Cortese—that iron deficiency may play a role in symptom severity among children with ADHD—is intriguing. Indeed, it was their original research that prompted us to incorporate ferritin as a measure of iron status (Konofal et al. 2004). It is certainly plausible that iron deficiency may confound or modify the effects of environmental lead exposure on ADHD in children. Alternatively, lead exposure may act as a confounder or modifier for the observed effects of iron deficiency with ADHD. Unfortunately, we were not able to examine whether ferritin (or other indicators of iron status) was associated with ADHD symptom severity using the National Health and Nutrition Examination Survey. Nor did we specifically test for an association between iron deficiency and ADHD. Although iron or other micronutrient supplementation may protect children from lead toxicity, recent evidence from a double-blind randomized trial (Kordas et al. 2005) suggests that iron and zinc supplementation did not appreciably lower blood lead levels or improve child behavior, as measured by the Conners Rating Scales. However, Kordas et al. included only children without anemia in their trial.

ADHD: Braun et al. Respond

ADHD: Braun et al. Respond

Low-level lead exposure and children.

The adverse effects of environmental lead exposure on the mental development of young children are well established. There is no safe level of blood lead below which children are not affected. Recent research expands our understanding of the impact of lead exposure continuing into later childhood, as well as its effects on children's behaviour. However, social and other environmental factors also contribute to variance in measures of developmental and behavioural outcomes. Lead is associated with only modest effects on children's development, but is a potentially modifiable risk factor. As environmental exposure to lead declines for the whole population, continued specific attention is needed for children living in industrial areas.

Lead chelation therapy and urate excretion in patients with chronic renal diseases and gout

It is known that chronic renal insufficiency (CRI) patients with gout may have subtle lead poisoning. In addition, gout episodes frequently aggravate progressive renal insufficiency because of the use of nephrotoxic drugs and urate deposition. Our study was arranged to evaluate the causal effect of environmental lead exposure on urate excretion in CRI patients. A cross-section study and a randomized, controlled trial were performed. Initially, 101 patients with CRI and without a history of previous lead exposure received ethylenediaminetetraacetic acid mobilization tests to assess body lead stores (BLS). Then, a clinical trial was performed; 30 CRI patients with gout and high-normal BLS and the changes of urate excretion in these patients were compared before and after lead chelating therapy. The treated group received four-week chelating therapy, and the control group received a placebo therapy. The BLS of patients with CRI and gout was higher than that of patients with CRI only, and none had subtle lead poisoning. The BLS, not the blood lead level (BLL), significantly correlated to indices of urate excretion in all CRI patients after related factors were adjusted. In addition, after lead chelating therapy, urate clearance markedly improved after a reduction of the BLS of patients with CRI and gout (study group 67.9 +/- 80.0% vs. control group 1.2 +/- 34.0%, P = 0.0056). Our findings suggest that the chronic low-level environmental lead exposure may interfere with urate excretion of CRI patients. Importantly, the inhibition of urate excretion can be markedly improved by lead chelating therapies. These data shed light on additional treatment of CRI patients with gout; however, more studies are needed to confirm our findings.

Elevated immunoglobulin E (IgE) levels in children with exposure to environmental lead

Lead has been reported to be an immunosuppressive agent in animal systems at levels far below those recognized as overtly toxic. Little data exist on lead’s effects on the human immune system, especially in young children who are at greatest risk for exposure to this environmental hazard. The effects of environmental lead exposure on the human immune system were examined in a population of young children, age 9 months–6 years, from the urban population of Springfield–Greene County, Missouri. Reported here are data from 279 children with blood lead levels ranging from 1 to 45 μg/dl. White blood cell populations have been enumerated and examined for cell–surface expression of activation markers. Serum has been analyzed for IgE, specific titers to Rubella vaccine, sCD25 (the soluble form of the IL2 receptor), sCD27 (the soluble form of the lymphocyte specific member of the tumor necrosis factor receptor family), and IL4 (the cytokine interleukin 4). Variation of these assays with age of the child was considered in statistical analysis of data. A statistically significant relationship of IgE and blood lead level was found in this population; as blood lead (PbB) level increases, IgE level increases. No other statistically significant differences between risk categories or other associations with blood lead level were found. The exact mechanism for this apparent stimulus of IgE-producing B cells remains to be elucidated. The development of allergic symptoms is often preceded by an increase in IgE. These data indicate that ingested lead could play a role in this process by stimulating IgE production.

The magnitude, persistence and public health significance of cognitive effects of environmental lead exposure in childhood

Although much research has been done on the effects of lead exposure on cognitive development, the magnitude, persistence and public health implications of such effects remain controversial. A literature search, in conjunction with our own work, was conducted to review these issues. Currently available evidence suggests that early exposure to environmental lead may cause a discernible effect on cognitive development, and this effect seems to persist into later childhood. No threshold is evident down to a blood lead concentration of 5 μg dl−1, although there is a paucity of epidemiological data at these lower levels. An economic loss could be serious for children exposed to an excess of lead in their environment. The environmental lead problem is preventable, or, where it is already established, is remediable. It should therefore be addressed, especially in developing countries where rapid industrialisation and increased use of motor vehicles are occurring. There is clear evidence that excessive lead exposure is still a significant public health issue in most countries, particularly developing countries. The formulation of a public health strategy should seek a balance between consideration of the nature and extent of the risk to human population health, knowledge of any dose-effect threshold, estimation of socio-environmental benefits, and commitment to making the best use of existing resources. The development of such a strategy should take into account the views and priorities of all interested parties, and—most certainly—those of communities directly at risk from lead exposure. Copyright © 1999 John Wiley & Sons, Ltd.

The magnitude, persistence and public health significance of cognitive effects of environmental lead exposure in childhood

Although much research has been done on the effects of lead exposure on cognitive development, the magnitude, persistence and public health implications of such effects remain controversial. A literature search, in conjunction with our own work, was conducted to review these issues. Currently available evidence suggests that early exposure to environmental lead may cause a discernible effect on cognitive development, and this effect seems to persist into later childhood. No threshold is evident down to a blood lead concentration of 5 μg dl−1, although there is a paucity of epidemiological data at these lower levels. An economic loss could be serious for children exposed to an excess of lead in their environment. The environmental lead problem is preventable, or, where it is already established, is remediable. It should therefore be addressed, especially in developing countries where rapid industrialisation and increased use of motor vehicles are occurring. There is clear evidence that excessive lead exposure is still a significant public health issue in most countries, particularly developing countries. The formulation of a public health strategy should seek a balance between consideration of the nature and extent of the risk to human population health, knowledge of any dose-effect threshold, estimation of socio-environmental benefits, and commitment to making the best use of existing resources. The development of such a strategy should take into account the views and priorities of all interested parties, and—most certainly—those of communities directly at risk from lead exposure. Copyright © 1999 John Wiley & Sons, Ltd.

Environmental Lead and Renal Effects in Children

The effect of lead on five renal-effect parameters was studied in 151 children (i.e., 3-6-y-olds) who resided at different distances from a lead smelter in Baia Mare, Romania. A relationship was found between concentration of lead in blood (mean +/- standard deviation: 342 +/- 224 microgram/l) and the activity of N-acetyl-beta-D-glucosaminidase in urine, as demonstrated by a 14% increase of N-acetyl-beta-D-glucosaminidase per 100 micrograms/l blood lead that was indicative of renal tubular damage. No relationship was found between blood lead level and the renal-effect parameters albumin, alpha-1-microglobulin, retinol binding protein, or alanine aminopeptidase in urine. Cadmium in blood was not elevated. It is well known that N-acetyl-beta-D-glucosaminidase is a sensitive parameter for renal effects, resulting from lead exposure in adults and from diabetes and nephrotoxic medicines in children. This study is the first to demonstrate an effect of environmental lead exposure on renal integrity in children.

Results from the European multicenter study on lead neurotoxicity in children: Implications for risk assessment

In order to improve dose-response information on neurobehavioral effects of environmental lead exposure in children, the World Health Organization, Regional Office for Europe (WHO/EURO), in collaboration with the Commission of the European Communities, initiated this international study which was planned, executed and evaluated between 1984 and 1989. Eight groups from eight European countries (Bulgaria, Denmark, Greece, Hungary, Italy, Roumania, W. Germany and Yugoslavia) took part. A common study protocol with inherent quality assurance elements was developed to achieve comparability. Blood-lead concentrations (PbB) were the main markers of exposure. The WISC (4 subtests) for psychometric intelligence, the Bender Gestalt test (GFT version) and the Trail-Making test for visual-motor integration, the Vienna Reaction Device and a delayed RT task for reaction performance, and the Needleman scales for behavior ratings served as behavioral endpoints. All individual studies taken together represent a sample size of 1879 school-age children and cover a PbB range from below 5 to about 60 micrograms/100 ml. Overall statistical evaluation of outcome was done by multiple regression analysis using a uniform confounder model. The strongest and most consistent effects occurred for the Bender Gestalt test (GFT version) and for serial choice reaction performance (Vienna Device). The degree of association with PbB was significant for these variables, although the contribution of PbB to the observed variance never exceeded 0.8%. Psychometric intelligence was also negatively affected, although the consistency of outcome between studies was poor, and the association with PbB only borderline. An effort towards risk assessment was made by calculating the proportion of children at risk, using the observed regression coefficients as well as means and standard deviations.

Issues in environmental epidemiological research: the example of environmental lead and health.

Modern environmental epidemiology encompasses the "traditional" area of physico-chemical hazards, along with health hazards in the societal environment (e.g. noise, stress, social organisation), and, increasingly, supranational problems (e.g. ozone depletion, global warming). As governments undertake environmental management, improved quantitative estimates of environmental risks to health are needed. Methodological difficulties of environmental epidemiological research include problems of exposure measurement, of estimating exposure at the level of the individual, and of detecting relatively small effects (particularly at low exposure levels). The health hazards of occupational lead exposure are well documented. The health hazards of environmental exposure to lead, within the general population, remain a focus of continuing epidemiological research. Indeed, the reported adverse effects upon the developing central nervous system of young children are now central to public health debate about environmental lead exposure standards. Recent evidence from cohort studies in several countries indicates adverse effects of environmental lead exposure upon early childhood mental development. In South Australia, a cohort study of children born in a lead smelter community, Port Pirie, has revealed evidence of such an effect. After controlling for many potential confounding factors (social, behavioural, family, and medical), cumulative postnatal lead exposure was found to be weakly associated with an adverse effect upon mental development at age two years and, more strongly, at age four years. The relations between environmental epidemiological research and public health policy are discussed.