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At least 19 recordsLinked to original sources
PubMed1998

Environmental exposures to lead and urban children's blood lead levels.

Lead-contaminated water, soil, and paint have been recognized as potential sources of children's lead exposure for decades, but their contributions to lead intake among urban children remain poorly defined. This analysis was undertaken to estimate the relationship of environmental lead exposures to lead intake among a random sample of urban children, adjusted for exposure to lead-contaminated house dust. Analyses of 183 urban children enrolled in a random sample, cross sectional study were conducted. Children's blood and multiple measures of household dust, water, soil, and paint were analyzed for lead, and interviews were conducted to ascertain risk factors for childhood lead exposure. Environmental sources of lead, including house-dust, soil lead, and water lead, were independently associated with children's blood lead levels. In contrast, paint lead levels did not have a significant effect on blood lead levels after adjusting for other environmental exposures. An increase in water lead concentration from background levels to 0.015 mg/L, the current EPA water lead standard, was associated with an increase of 13.7% in the percentage of children estimated to have a blood lead concentration exceeding 10 micrograms/dL; increasing soil lead concentration from background to 400 micrograms/g was estimated to produce an increase of 11.6% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL, and increasing dust lead loading from background to 200 micrograms/ft2 is estimated to produce an increase of 23.3% in the percentage of children estimated to have a blood lead level exceeding 10 micrograms/dL. These data support the promulgation of health-based standards for lead-contaminated dust and soil and the progressive lowering of standards for lead-contaminated water as the definition of undue lead exposure has been modified.

Child, Preschool↗
PubMed1999

Environmental lead exposure and activity of delta-aminolevulinic acid dehydratase (ALA-D) in maternal and cord blood.

The hypothesis that environmental lead exposure measured from blood (Pb-B) inhibits delta-aminolevulinic acid dehydratase activity (ALA-D) from whole blood was tested in 241 urban mothers and their newborns. Geometric means and (5th and 95th Percentiles) for maternal and cord Pb-B were 6.4 microg dl(-1) (3.4-11.9) and 4.6 microg dl(-1) (2.8-9.2). Spearman correlations between mother and cord Pb-B and ALA-D were all negative but statistically significant only for cord Pb-B and mother ALA-D. A potential lead threshold, was identified between 3.2 and 4.8 microg dl(-1), above which ALA-D may be inhibited by lead, and below which ALA-D may be insensitive or even activated. In conclusion, low environmental exposure to lead is responsible for a demonstrable biochemical effect. This potential ALA-D inhibition may lead to neurotoxic effects, especially in newborns who have high level of neurogenesis.

Adult↗
PubMed1999

[Effects of environmental lead exposure in kindergartens on children's blood lead level].

OBJECTIVE: To determine if kindergartens' environmental status can influence children's lead exposure. METHODS: Environmental specimens, such as floor dust, peeled-off paint chip, soil and drinking water, as well as children's hand dust and blood samples, were collected and measured for their lead levels in 19 kindergartens, to analyze the relationship between children's blood lead levels and their environmental lead exposure. RESULTS: Geometric means of lead concentrations in indoor floor dust, peeled-off paint chip, dust fallout, outdoor floor dust, soil and drinking water were 86.5 microg/m(2), 235.5 microg/g, 445.9 microg/g, 172.4 microg/m(2), 70.1 microg/g and 12.5 microg/L, respectively. Lead level on children's hands averaged 3.4 microg at both hands. Blood lead levels in children correlated positively with the lead concentrations of outdoor floor dust and their hand dust, with correlation coefficients of 0.5186 and 0.2206, respectively. Multiple regression analysis showed that hand dust lead level in children entered the regression model with a largest standardized partial regression coefficient of 0.3842 and a coefficient of determination of 0.673 for the full equation with F = 6.52 and P < 0.01. CONCLUSION: Status of environmental health in kindergartens plays an important role in children's lead exposure. It is necessary to offer health education for children and make them wash their hands often and overcome unhealthy behavior of sucking their fingers.

Child Day Care Centers↗
PubMed1984

Environmental lead exposure of an urban Indian population.

Environmental lead exposure of the Greater Bombay population has been estimated by measuring lead concentrations in air particulates, water, food and cigarette smoke. Atmospheric lead concentrations in different zones of the city varied between 82 and 605 ng m-3. The dietary intake of lead is estimated to be 245 micrograms day-1 and is calculated from the lead content in different food groups and the amount of that group consumed by an average resident of the city. The uptake by a non-smoker living in the city area is estimated to be 33 micrograms of lead per day, 75% of which comes from food, 15% from air and 10% from water. For a suburban resident 85% of the lead intake comes from food. The blood lead measurements and the contribution of atmospheric lead to the blood lead level are discussed.

Air Pollutants↗
PubMed1999

The Yugoslavia Prospective Study of environmental lead exposure.

The Yugoslavia Prospective Study of environmental lead exposure has studied the associations between exposure to lead and pregnancy outcomes; childhood neuropsychological, behavioral, and physical development; and hematologic, renal, and cardiovascular function. The cohort comprises 577 children born to women recruited at midpregnancy in two towns in Kosovo, Yugoslavia; one town is the site of a lead smelter, refinery, and battery plant and the other is 25 miles away and relatively unexposed. A sample of these children has been followed at 6-month intervals through 7.5 years of age. Blood lead concentrations ranged from 1 to 70 microg/dl. Exposure to lead was not associated with adverse pregnancy outcomes. Exposure was associated with modest decrements in intelligence, small increases in blood pressure, higher risks of proteinuria, small increases in behavior problems, and perturbed hematopoiesis. Only at low level exposures (i.e., <16 microg/dl) were small associations with decreased height found. We discuss methodological problems that may hinder causal interpretation of these data, namely, use of blood lead concentration as an exposure measure, confounding, and town-specific associations. We conclude that while reported associations are small, collectively they lend support to the notion that lead is a toxicant with numerous adverse health effects.

Age Factors↗
PubMed2000

Environmental lead exposure: a public health problem of global dimensions.

Lead is the most abundant of the heavy metals in the Earth's crust. It has been used since prehistoric times, and has become widely distributed and mobilized in the environment. Exposure to and uptake of this non-essential element have consequently increased. Both occupational and environmental exposures to lead remain a serious problem in many developing and industrializing countries, as well as in some developed countries. In most developed countries, however, introduction of lead into the human environment has decreased in recent years, largely due to public health campaigns and a decline in its commercial usage, particularly in petrol. Acute lead poisoning has become rare in such countries, but chronic exposure to low levels of the metal is still a public health issue, especially among some minorities and socioeconomically disadvantaged groups. In developing countries, awareness of the public health impact of exposure to lead is growing but relatively few of these countries have introduced policies and regulations for significantly combating the problem. This article reviews the nature and importance of environmental exposure to lead in developing and developed countries, outlining past actions, and indicating requirements for future policy responses and interventions.

Adult↗
PubMed2002

Environmental lead exposure and urate excretion in the general population.

PURPOSE: Chronic occupational exposure to lead is related to low urate excretion and a high incidence of gout in lead workers. However, whether chronic low-level environmental lead exposure influences urate excretion in the general population remains unknown. SUBJECTS AND METHODS: We studied 111 healthy subjects with normal renal function (serum creatinine level < or =1.4 mg/dL) and no previous lead exposure or systemic diseases. All subjects had their blood lead levels measured, received ethylenediaminetetraacetic acid mobilization tests to assess their body lead burdens, and were investigated for renal function and urate excretion to assess the relation between lead and urate excretion. We studied urate excretion before and after lead chelation therapy in 24 subjects with high-normal body lead burden (>78 mg and <600 mg). RESULTS: Healthy subjects with gout (n = 27) manifested a higher body lead burden (84 +/- 42 mg vs. 45 +/- 30 mg, P <0.0001) and lower urate clearance (3.7 +/- 1.2 mL/min/1.73 m(2) vs. 6.0 +/- 2.8 mL/min/1.73 m(2), P <0.0001) than did those without gout (n = 84). Blood lead levels and body lead burden of all subjects were within the safe range. In analyses that adjusted for age, sex, body mass index, protein intake, and creatinine clearance, blood lead level was significantly related to serum urate level (beta coefficient [+/- SE] = 0.23 +/- 0.11, P = 0.03), and body lead burdens were related to all indices of urate excretion (serum urate: beta coefficient = 0.023 +/- 0.005, P <0.0001; daily urate excretion: beta coefficient = -1.55 +/- 0.40, P = 0.0002; urate clearance: beta coefficient = -0.030 +/- 0.006, P <0.0001; fractional urate excretion: beta coefficient= -0.034 +/- 0.006, P <0.0001). Following lead chelation therapy, urate clearance increased after body lead burden was reduced (3.4 +/- 1.2 mL/min/1.73 m(2) vs. 4.9 +/- 1.4 mL/min/1.73 m(2), P <0.005). CONCLUSION: Chronic low-level environmental lead exposure may inhibit urate excretion in the general population, and lead chelation therapy reduces this inhibition. These findings support efforts to reduce sources of environmental lead exposure and suggest alternative approaches to hyperuricemia and gout in the general population.

Adult↗
PubMed1988

Environmental lead exposure and the kidney.

Lead and its components remain widely distributed in the environment and in some workplaces. Lead serves no useful physiological function, yet is potentially toxic to several organ systems. For many years human health effects have been recognized after heavy lead exposure. Recently more subtle human effects have been suggested invoking nervous system, reproductive and kidney function. Assessing lead body burden and dose-response relationships of this metal by blood lead determination, porphyrin assessments, chelation testing or bone lead studies may be difficult. Quantitative assessment of subtle changes in kidney function by routine BUN, creatinine, or urinalysis also poses problems. There is now mounting evidence that chronic low level environmental lead exposure may subtly effect kidney function. This paper first examines the history of lead and kidney function and then examines critically the evidence associating low-level environmental lead exposure and effects on renal function.

Animals↗
PubMed1997

Renal effects of environmental and occupational lead exposure.

Environmental and industrial lead exposures continue to pose major public health problems in children and in adults. Acute exposure to high concentrations of lead can result in proximal tubular damage with characteristic histologic features and manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. A high incidence of nephropathy was reported during the early part of this century from Queensland, Australia, in persons with a history of childhood lead poisoning. No such sequela has been found in studies of three cohorts of lead-poisoned children from the United States. Studies in individuals with low-level lead exposure have shown a correlation between blood lead levels and serum creatinine or creatinine clearance. Chronic low-level exposure to lead is also associated with increased urinary excretion of low molecular weight proteins and lysosomal enzymes. The relationship between renal dysfunction detected by these sensitive tests and the future development of chronic renal disease remains uncertain. Epidemiologic studies have shown an association between blood lead levels and blood pressure, and hypertension is a cardinal feature of lead nephropathy. Evidence for increased body lead burden is a prerequisite for the diagnosis of lead nephropathy. Blood lead levels are a poor indicator of body lead burden and reflect recent exposure. The EDTA lead mobilization test has been used extensively in the past to assess body lead burden. It is now replaced by the less invasive in vivo X-ray fluorescence for determination of bone lead content.

Adult↗
PubMed2003

Environmental lead exposure and progression of chronic renal diseases in patients without diabetes.

BACKGROUND: Previous research suggests that environmental lead exposure correlates with age-related decreases in renal function. METHODS: Two hundred two patients with chronic renal insufficiency (indicated by a serum creatinine level between 1.5 mg per deciliter and 3.9 mg per deciliter) who had a normal total-body lead burden and no history of exposure to lead were observed for 24 months. After the observation period, 64 subjects with an elevated body lead burden were randomly assigned to the chelation control groups. For three months, the patients in the chelation group received lead-chelation therapy with calcium disodium EDTA, and the control group received placebo. During the ensuing 24 months, repeated chelation therapy was administered weekly to 32 patients with high-normal body lead burdens (at least 80 microg but less than 600 microg) unless on repeated testing the body lead burden fell below 60 microg; the other 32 patients served as controls and received weekly placebo infusions for 5 weeks every 6 months. The primary end point was an increase in the serum creatinine level to 1.5 times the base-line value during the observation period. A secondary end point was the change in renal function during the intervention period. RESULTS: The primary end point occurred in 24 patients during the observation period; the serum creatinine levels and body lead burden at base line were the most important risk factors. The glomerular filtration rate improved significantly by the end of the 27-month intervention period in patients receiving chelation therapy: the mean (+/-SD) change in the glomerular filtration rate in the patients in the chelation group was 2.1+/-5.7 ml per minute per 1.73 m2 of body-surface area, as compared with -6.0+/-5.8 ml per minute per 1.73 m2 of body-surface area in the controls (P<0.001). The rate of decline in the glomerular filtration rate in the chelation group was also lower than that in the controls during the 24-month period of repeated chelation therapy or placebo. CONCLUSIONS: Low-level environmental lead exposure may accelerate progressive renal insufficiency in patients without diabetes who have chronic renal disease. Repeated chelation therapy may improve renal function and slow the progression of renal insufficiency.

Adult↗
PubMed2001

Combining datasets to predict the effects of regulation of environmental lead exposure in housing stock.

A model for children's blood lead concentrations as a function of environmental lead exposures was developed by combining two nationally representative sources of data that characterize the marginal distributions of blood lead and environmental lead with a third regional dataset that contains joint measures of blood lead and environmental lead. The complicating factor addressed in this article was the fact that methods for assessing environmental lead were different in the national and regional datasets. Relying on an assumption of transportability (that although the marginal distributions of blood lead and environmental lead may be different between the regional dataset and the nation as a whole, the joint relationship between blood lead and environmental lead is the same), the model makes use of a latent variable approach to estimate the joint distribution of blood lead and environmental lead nationwide.

Biometry↗
PubMed2001

Environmental lead exposure and progressive renal insufficiency.

BACKGROUND: Several recent studies show that serum creatinine level or creatinine clearance is inversely associated with blood lead levels. However, the studies did not allow direct inferences about causality. OBJECTIVE: To evaluate the relation between body lead burden (BLB) and progressive renal insufficiency in patients without previous heavy lead exposure. DESIGN: A prospective, longitudinal study with a controlled clinical trial. PATIENTS: One hundred ten patients with chronic renal insufficiency (serum creatinine level, 133-354 micromol/L [1.5-4.0 mg/dL]) and normal BLB (EDTA mobilization tests, <600 microg per 72-hour urine collection) and without a history of previous heavy lead exposure were divided into 2 groups according to BLB: the high-normal BLB group (BLB > or =80 microg and <600 microg) and the low BLB group (BLB <80 microg). Patients were prospectively followed up for 2 years. MAIN OUTCOME MEASURES: The primary outcome was a 1.5 times increase in the initial creatinine level. The secondary outcome was a change over time in the value of creatinine clearance. At the end of follow-up, a 3-month clinical trial with chelation therapy for patients with high-normal BLB was performed to clarify the role of environmental lead exposure in progressive renal insufficiency. RESULTS: Fifteen patients (14 in the high-normal BLB group and 1 in the low BLB group) reached the primary outcome within 24 months. Renal outcome was significantly better in the low BLB group (P<.001). From month 12 to month 24, renal function of high-normal BLB patients had a greater rate of progressive renal insufficiency than that of low BLB patients. In the Cox multivariate regression analysis, BLB was the most important risk factor for determining the progression of renal insufficiency. After chelation therapy, significant improvement in renal function was noted. In addition, the effect of improving renal function lasted for more than 12 months in these patients. CONCLUSIONS: Long-term low-level environmental lead exposure may subtly affect progressive renal insufficiency in the general population. Progressive renal insufficiency may be improved for at least 1 year after lead chelating therapy. Further investigations are needed to clarify this observation.

Adolescent↗
PubMed1985

Condition and type of housing as an indicator of potential environmental lead exposure and pediatric blood lead levels.

Environmental evaluations in a prospective behavioral study of children with blood lead levels up to about 50 micrograms/dl were performed by an intensive environmental survey and by exterior visual evaluation of housing quality. Serial blood lead values for infants in the study were compared to exterior housing type and quality, which itself was also compared with results of the intensive environmental evaluation. Five housing condition and type categories were defined: public housing; private housing (satisfactory, deteriorated, and dilapidated); and rehabilitated private housing. In this interim report on the first subset of available data, the housing categories were found to differ in paint and environment dust lead levels, with public and rehabilitated housing having lowest values. Blood lead concentrations of children differed across housing categories as early as 6 months of age, with children residing in public housing having lowest levels, followed by those in rehabilitated housing. The spread in mean blood lead concentrations among the housing quality categories increased with increasing age of the children. Housing category accounted for over one-half of the blood lead variability in 18-month-old children.

Dust↗
PubMed2002

Environmental lead exposure during early childhood.

OBJECTIVE: To determine the relative contribution of residential lead hazards to children's blood lead concentrations during early childhood. METHODS: We enrolled children 6 months of age and followed them until 24 months of age. Blood and samples of dust, soil, water and paint were analyzed for lead at 6-month intervals, and interviews were conducted to estimate nutritional, behavioral, and demographic factors linked with lead exposure. RESULTS: Of the 276 children enrolled, 249 (90%) were followed until 24 months of age. The geometric mean blood lead concentration of children at 6 months of age was 2.9 microg/dL (95% CI, 2.7-3.1). At 24 months of age, children's mean blood lead was 7.5 microg/dL; 82 (33%) had a blood lead level of > or = 10 microg/dL. In adjusted analyses, lead-contaminated floor dust, soil, and water contributed to children's lead intake throughout the first 2 years of life (P < .05). Lead-contaminated dust from window troughs was a source of lead exposure, especially in the second year of life. Dietary iron intake, but not calcium intake, was inversely associated with blood lead levels (P < .05). Blood lead concentration was over 50% higher in black than in white children (P = .0001). CONCLUSION: Lead-contaminated house dust is the major source of lead intake during early childhood. Black children remain at increased risk for higher blood lead concentration after adjusting for environmental lead exposures and dietary intake.

Age Factors↗
PubMed2005

Low-level environmental lead exposure and children's intellectual function: an international pooled analysis.

Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 microg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 microg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5-10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 microg/dL and declined to 9.4 microg/dL by 5-7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 microg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 microg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a log-linear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2-9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 microg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 microg/dL, 10 to 20 microg/dL, and 20 to 30 microg/dL were 3.9 (95% CI, 2.4-5.3), 1.9 (95% CI, 1.2-2.6), and 1.1 (95% CI, 0.7-1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 microg/dL was significantly greater than that observed for those with a maximal blood lead level > or = 7.5 microg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 microg/dL is associated with intellectual deficits.

Child↗
PubMed2004

Environmental exposure to lead and progression of chronic renal diseases: a four-year prospective longitudinal study.

Previous retrospective research suggests that low-level environmental lead exposure is associated with an acceleration of age-related impairment of renal function. For elucidating the long-term relationship between low-level environmental lead exposure and progression of chronic renal diseases in patients without diabetes, 121 patients who had chronic renal insufficiency, a normal body lead burden (BLB), and no history of exposure to lead were observed prospectively for 48 mo. Associations of both BLB and blood lead level (BLL) with renal function were evaluated, with reference to other covariates. The primary end point was an increase in the serum creatinine level to double the baseline value. Sixty-three patients had BLB > or =80 microg and < 600 microg (high-normal group), and 58 patients had BLB < 80 microg (low-normal group). The primary end point occurred in 17 patients. Fifteen of them had high-normal BLB, whereas two patients had low-normal BLB (hazard ratio [95% confidence interval]: 1.01 [1.00 to 1.01] for each increment of 1 microg; P = 0.002). The BLB and BLL at baseline were the most important risk factors to predict progression of renal insufficiency. Each increase of 10 microg in the BLB or 1 microg/dl in the BLL reduced the GFR by 1.3 (P = 0.002) or 4.0 ml/min (P = 0.01) during the study period. In conclusion, low-level environmental lead exposure is associated with accelerated deterioration of renal insufficiency. Even at levels far below the normal ranges, both increased BLL and BLB predict accelerated progression of chronic renal diseases.

Adult↗