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PubMed2004

Occurrence and determinants of increases in blood lead levels in children shortly after lead hazard control activities.

This study is an examination of the effect of lead hazard control strategies on children's blood lead levels immediately after an intervention was conducted as part of the US Department of Housing and Urban Development's Lead-Based Paint Hazard Control Grant Program. Fourteen state and local government grantees participated in the evaluation. The findings indicated an overall average reduction in the blood lead levels of 869 children soon after the implementation of lead hazard controls. However, 9.3% of these children (n = 81) had blood lead increases of 5 microg/dL or more. Data routinely collected as part of the evaluation, as well as additional information supplied by the individual programs, were used to determine potential reasons for these observed increases in blood lead. A logistic regression analysis indicated that three principal factors were associated with the blood lead increases: the number of exterior deteriorations present in the child's home (prior to intervention), the educational level of the female parent or guardian of the child, and the child's age. The statistical analysis did not find evidence that children living in households that either did not relocate or relocated for less than the full work period were significantly more likely to have a blood lead increase equal to or greater than 5 microg/dL than children living in households that fully relocated. Statistical analyses also did not reveal any single interior strategy to be more or less likely than others to be associated with a blood lead increase of 5 microg/dL or more.

Child↗
PubMed1985

Occupational lead exposure: studies in two brothers showing differential susceptibility to lead.

Unexpected differences in clinical and biochemical findings in two brothers occupationally exposed to the same source of lead for dissimilar lengths of time are presented. Only the brother with the shorter period of lead exposure was anemic and afflicted by nausea, vomiting, abdominal colic and arthralgia. His urinary PBG output yielded the high orders of magnitude found in acute intermittent porphyria in relapse. Prior to administration of a single dose of EDTA (1 g of the calcium disodium salt given intravenously in 325 mL 0.15 mol/L NaCl), his blood lead levels averaged 3.6 mumol/L. The amount of chelatable lead retrieved from his urine, 31 mumol/day, was more than twice that found in his asymptomatic counterpart who was exposed to lead for 13 months and whose pre-EDTA blood lead levels averaged 4.0 mumol/L. Not only the activity of delta-aminolaevulinic acid dehydratase, but also that of uroporphyrinogen I synthetase, was markedly inhibited by lead in red cells of both brothers. These activities were restored to normal levels in vitro by addition to the assay system of zinc and dithiothreitol. This ruled out a coexisting genetic deficiency of either enzyme. The anemia of the symptomatic brother with the shorter period of lead exposure was alleviated by folic acid, 15 mg/day. The differences in findings between the two brothers point to differential susceptibility to lead and illustrate the extent to which symptomatic lead poisoning may mimic biochemical and clinical features of the acute porphyrias.

Adult↗
PubMed2003

Blood lead levels and risk factors for lead poisoning among children in Jakarta, Indonesia.

The phase-out of leaded gasoline began in Jakarta, Indonesia on July 1, 2001. We evaluated mean blood lead levels (BLLs) and the prevalence of elevated BLLs of Jakarta school children and assessed risk factors for lead exposure in these children before the beginning of the phase-out activities. The study involved a population-based, cross-sectional blood lead survey that included capillary blood lead sampling and a brief questionnaire on risk factors for lead poisoning. A cluster survey design was used. Forty clusters, defined as primary schools in Jakarta, and 15 2nd- and 3rd-grade children in each cluster were randomly selected for participation in the study. The average age of children in this study was 8.6 years (range 6-12) and the geometric mean BLL of the children was 8.6 microg/dl (median: 8.6 microg/dl; range: 2.6-24.1 microg/dl) (n=397). Thirty-five percent of children had BLLs > or =10 microg/dl and 2.4% had BLLs > or =20 microg/dl. Approximately one-fourth of children had BLLs 10-14.9 microg/dl. In multivariate models, level of education of the child's primary caregiver, water collection method, home varnishing and occupational recycling of metals, other than lead, by a family member were predictors of log BLLs after adjustment for age and sex. BLLs of children who lived near a highway or major intersection were significantly higher than those of children who lived near a street with little or no traffic when level of education was not included in the model. Water collection method was a significant predictor of BLLs > or =10 microg/dl after adjustment for age and sex. BLLs in children in this study were moderately high and consistent with BLLs of children in other countries where leaded gasoline is used. With the phase-out of leaded gasoline, BLLs of children in Jakarta are expected to rapidly decline as they have in other countries that have phased lead out of gasoline.

Carcinogens↗
PubMed2003

Lead remediation and changes in human lead exposure: some physiological and biokinetic dimensions.

This paper presents a qualitative and quantitative analysis of the various aspects of lead remediation effectiveness with particular reference to human health risk assessment. One of the key elements of lead remediation efforts at such sites as those under the Superfund program deals with populations at elevated exposure and toxicity risk in the proximity of, or at, the site of remediation, especially remediation workers, workers at other tasks on sites that were remediated down to some action level of lead concentration in soils, and groups at risk in nearby communities. A second element has to do with how one measures or models lead exposure changes with special reference to baseline and post-remediation conditions. Various biomarkers of lead exposure can be employed, but their use requires detailed knowledge of what results using each means. The most commonly used approach is measurement of blood lead (Pb-B). Recognized limitations in the use of Pb-B has led to the use of predictive Pb exposure models, which are less vulnerable to the many behavioral, physiological, and environmental parameters that can distort isolated or 'single shot' Pb-B testings. A third aspect covered in this paper presents various physiological factors that affect the methods by which one evaluates Pb remediation effectiveness. Finally, this article offers an integrated look at how lead remediation actions directed at one lead source or pathway affect the total lead exposure picture for human populations at elevated lead exposure and toxicity risk.

Biomarkers↗
PubMed1998

Lead poisoning of children in Africa, IV: Exposure to dust lead in primary schools in south-central Durban, South Africa.

Twenty primary schools in three areas (Merebank, Austerville and Bluff) of south-central Durban, South Africa were studied to determine if dust lead loading (microgram/m2) is high enough to constitute a risk to children. Atmospheric lead fallout rates in the schools varied from 9 to 264 micrograms/m2 per day and were higher than the values now being reported in the developed countries. Mean outside dust lead loadings were 425 micrograms/m2 in Merebank, 771 micrograms/m2 in Austerville and 1174 micrograms/m2 in Bluff areas, and 25% of the primary schools were found to have mean outside dust lead loading above 1000 micrograms/m2. Mean dust lead loadings inside classrooms were 2-4 times lower than the outside rates, and showed no significant difference among schools in the three areas. Dust lead loadings were correlated with lead concentrations in dust but not with distance from the highway or with atmospheric lead deposition rates. Exposure to dust lead in classrooms and in the school yard is considered to be an important contributor to blood lead levels in, and hence a potential health hazard to, children in many urban areas of the city.

Africa↗
PubMedDate not supplied

Relationship between lead mining and blood lead levels in children.

The authors studied blood lead levels of 226 randomly selected children, aged 6-92 mo, who lived in either a lead-mining area or a nonmining area, and 69 controls. The authors sought to determine to what extent mining activities contributed to blood lead levels in the children. The mean blood lead levels in the study and control groups were 6.52 microg/dl and 3.43 microg/dl, respectively. The corresponding proportions of children with elevated blood lead levels were 17% and 3%. Soil and dust lead levels were up to 10 times higher in the study than the control group. Elevated blood lead levels appeared to result from exposure to both lead-mining waste and lead-based paint. Mining waste was the cause of the higher prevalence of elevated blood lead levels in these children.

Case-Control Studies↗
PubMed2003

Lead exposure in radiator repair workers: a survey of Washington State radiator repair shops and review of occupational lead exposure registry data.

Radiator repair workers in Washington State have the greatest number of very elevated (> or =60 microg/dL) blood lead levels of any other worker population. The goals of this study were to determine the number of radiator repair workers potentially exposed to lead; estimate the extent of blood lead data underreporting to the Occupational Lead Exposure Registry; describe current safety and health practices in radiator repair shops; and determine appropriate intervention strategies to reduce exposure and increase employer and worker awareness. Lead exposure in Washington State's radiator repair workers was assessed by reviewing Registry data and conducting a statewide survey of radiator repair businesses. This study revealed that a total of 226 workers in Washington State (including owner-operators and all employees) conduct repair activities that could potentially result in excessive exposures to lead. Approximately 26% of radiator repair workers with elevated blood lead levels (> or =25 microg/dL) were determined to report to Washington State's Registry. This study also revealed a lack of awareness of lead's health effects, appropriate industrial hygiene controls, and the requirements of the Lead Standard. Survey respondents requested information on a variety of workplace health and safety issues and waste management; 80% requested a confidential, free-of-charge consultation. Combining data derived from an occupational health surveillance system and a statewide mail survey proved effective at characterizing lead exposures and directing public health intervention in Washington State.

Data Collection↗
PubMed1997

Lead exposure and children's intelligence: do low levels of lead in blood cause mental deficit?

OBJECTIVE: It has come to be generally accepted that low levels of lead exposure may result in mental deficit. This causal inference is based on claimed time precedence of the lead exposure and on biological plausibility. The objective of this study is to argue that mental deficit causes pica which causes lead exposure (i.e. to support the theory of reverse causation). METHODOLOGY: The literature since the 1930s has been interpreted in the light of our own long experience in the investigation of lead exposure in children and adults to support the arguments in favour of reverse causation. RESULTS: The arguments for reverse causation are based on: (i) analogy with mental retardation which causes increased lead exposure; (ii) the results of published prospective studies that show a special relationship between blood lead levels at 24 months and intelligence tested later, exactly what would be predicted by the reverse causation theory; and (iii) on an alternative explanation for mental retardation following lead encephalopathy (i.e. that mental retardation following encephalopathy is due to anoxia and not due to a direct destructive effect on the brain neurones). The arguments, which have been proposed for the conventional view, are rejected for the following reasons: (i) none of the prospective studies have found a relationship between cord blood lead levels and intelligence tested later, undermining the argument based on time precedence of lead exposure; and (ii) there is no convincing evidence that lead poisoning, short of encephalopathy, causes mental retardation. CONCLUSION: We believe that the reverse causation hypothesis is a more plausible explanation of the facts.

Causality↗
PubMed1999

Dose dependent reduction of erythroid progenitor cells and inappropriate erythropoietin response in exposure to lead: new aspects of anaemia induced by lead.

OBJECTIVE: To determine whether haematopoietic progenitor cells and erythropoietin (EPO), which is an essential humoral stimulus for erythroid progenitor (BFU-E) cell differentiation, are affected by lead intoxication. METHODS: In male subjects chronically exposed to lead with and without anaemia, pluripotent (CFU-GEMM), BFU-E and granulocyte/macrophage (CFU-GM) progenitor cell counts in peripheral blood were measured with a modified clonal assay. Lead concentrations in blood (PbB) and urine (PbU) were measured by the atomic absorption technique, and EPO was measured with a modified radioimmunoassay. RESULTS: PbB in the subjects exposed to lead ranged from 0.796 to 4.4 mumol/l, and PbU varied between 0.033 and 0.522 mumol/l. In subjects exposed to lead with PbB > or = 2.896 mumol/l (n = 7), BFU-E cells were significantly reduced (p < 0.001) whereas the reduction in CFU-GM cells was only of borderline significance (p = 0.037) compared with the age matched controls (n = 20). The CFU-GEMM cells remained unchanged. Furthermore, BFU-E and CFU-GM cells were reduced in a dose dependent fashion, with increasing PbB or PbU, respectively. In the subjects exposed to lead EPO was in the normal range and did not increase in the presence of anaemia induced by lead. No correlations existed between EPO and PbB, PbU, or progenitor cells. CONCLUSION: The data suggest new aspects of lead induced anaemia besides the currently acknowledged shortened life span of erythrocytes and inhibition of haemoglobin synthesis. Two additional mechanisms should be considered: the reduction of BFU-E cells, and inappropriate renal EPO production in the presence of severe exposure to lead, which would lead to an inadequate maturation of BFU-E cells.

Adult↗
PubMed2001

A retrospective study on the disappearance of blood lead in cattle with accidental lead toxicosis.

Lead poisoning in cattle and other food animals is of public health significance because of the potential for human exposure to lead through ingestion of contaminated meat and milk products derived from lead-poisoned animals. In Michigan, lead poisoning in livestock is a reportable disease, and positive cattle are quarantined until they test negative (<0.05 ppm blood lead). There is surprisingly little information on blood lead kinetics in cattle. The half-life has been variably reported as 9 weeks and 1-2 months. Because these data did not fit those obtained from cases received at the Michigan State University Animal Health Diagnostic Laboratory, a retrospective study was conducted to review all cases of accidental lead poisoning in cattle between 1990 and 1998. This information is needed to estimate when quarantined lead-poisoned cattle can be released. The results showed that the half-life of blood lead was quite variable and ranged from 48 to 2,507 days. The shortest half-lives (48, 56, and 57 days) were found in a lactating herd of 20-month-old heifers. The longest half-life, 2,507 days, was found in a 9-month-old castrated bull, which ingested a discarded automobile battery. Of the 24 animals monitored, only 8/24 (33%) had half-lives between 6 and 14 weeks. In conclusion, the half-life of blood lead is difficult to predict in accidental cases of cattle poisoning.

Accidents↗
PubMed1974

Significance of high soil lead concentrations for childhood lead burdens.

The lead exposure of children and their mothers has been studied in two towns with mean soil lead contents of 900 and 400 ppm. No significant difference in blood or fecal lead contents was demonstrated between the two populations, but a small difference in hair lead content was shown. The blood lead content of children was greater than that of their mothers and was higher in the summer than in the spring samples. Children with pica for soil in the control area had increased lead content of blood and hair. Preliminary data for children and mothers from villages with mean soil lead contents of 500 ppm and 10,000 ppm are reported which show significant differences in blood and hair lead content within the normal range. The data suggest that soil lead content of 10,000 ppm may result in increased absorption of lead in children, but to a degree which is unlikely to be of biological significance.

Adult↗
PubMed1974

Role of airborne lead in increased body burden of lead in Hartford children.

The ingestion of airborne lead fallout is the mechanism responsible for increased lead body burdens found in 10 urban Connecticut children. The mean indoor lead levels found in housedust was 11,000 mug/g; highest concentrations occurred on windowsills and in floor dust. The mean lead content of Hartford street dirt was 1,200 mug/g; levels were highest near the street and next to the buildings. The mean lead concentration of hand samples taken from the subject children was 2,400 mug/g; the mean weight of hand samples was 11 mg. The concentration of lead in dirt and househould dust was high enough to theoretically result in excessive lead accumulation in young children who are putting their dusty, dirty hands in their mouths during play. While we believe that lead emitted from automobiles contributes significantly to air, dirt and dust lead levels the environmental impact of reducing or eliminating lead from gasoline is not yet completely understood.

Air Pollution↗
PubMed1992

Chelated lead and bone lead.

In this study a close correlation [correlation coefficient (r) = 0.86, P less than 0.001] was found between the blood lead level of 20 lead workers and their urinary excretion of lead for 24 h after intravenous infusion with 1 g of the chelating agent calcium disodium edetate. In addition, there were significant associations between lead levels in different bones (tibia/calcaneus: r = 0.93, P less than 0.001; tibia/phalanx: r = 0.67, P less than 0.002; calcaneus/phalanx: r = 0.80, P less than 0.001), as measured by in vivo X-ray fluorescence. Chelation produced no significant change in the lead level in either tibia or calcaneus. There was a significant correlation between chelated lead and bone lead (eg, for calcaneus, r = 0.62) in currently exposed workers. However, there was no significant relationship when a retired worker and an inactive worker were included (r = 0.14). It was concluded that chelatable lead mainly reflects the blood and soft-tissue lead pool, which is only partly dependent upon the skeletal lead content that comprises the biggest share of the total body burden.

Adult↗
PubMed2004

Blood lead levels in residents of homes with elevated lead in tap water--District of Columbia, 2004.

Lead exposure adversely affects intellectual development in young children and might increase the risk for hypertension in adults. In the District of Columbia (DC), of an estimated 130,000 residences, approximately 23,000 (18%) have lead service pipes (Daniel Lucey, MD, DC Department of Health [DCDOH], personal communication, March 24, 2004). The Environmental Protection Agency (EPA) requires water authorities to test tap water in 10-100 residences annually for lead. In March 2003, DC Water and Sewer Authority (WASA) expanded its lead-in-water testing program to homes with lead service pipes extending from the water main to the house. By late January 2004, results of the expanded water testing indicated that the majority of homes tested had water lead levels above EPA's action level of 15 parts per billion (ppb). On February 16, DCDOH requested CDC assistance to assess health effects of elevated lead levels in residential tap water. DCDOH also requested deployment of officers of the United States Public Health Service (USPHS) to assist in the investigations. This report summarizes the results of the preliminary investigations, which indicated that the elevated water lead levels might have contributed to a small increase in blood lead levels (BLLs). The investigation of elevated water lead levels is ongoing. In the interim, DCDOH has recommended that young children and pregnant and breast-feeding women refrain from drinking unfiltered tap water.

Adolescent↗
PubMed2004

[Multiple analysis of lead concentration in the air and renal function of lead exposure workers].

OBJECTIVE: To determine the lead concentration in the air (pbA) at the workplace and the renal function of lead exposure workers. METHODS: The lead concentration in the air of 11 printing plants, 4 smelteries and 2 lead mines were measured. Screening urinalysis was performed in 1190 long term lead exposed workers with urine sugar, protein and sigements. It one of the three was abnormal, the workers were given examination of renal function. The relationship between pbA and renal function were confirmed by mutiple linear. RESULTS: The concentrations of pbA in the printing plants, smelteries and lead mines were 0.07 mg/m3, 0.26 mg/m3 and 0.66 mg/m3 respectively. Altogether 157 cases had one and more abnormal renal function. The correlation of concentration PbA in the workplace and the renal function of lead exposure workers was shown (R = 0.894, P < 0.001, R2 = 0.799). The correlation coefficient of skewness of showed that PbA and Bpb. Upb. Bun Scr Usug. Ubeta2MG were positively correlated (P < 0.01 approximately 0.001); Ccr was negatively correlated (P =0.05). Upro, UNAG and Ualb were nonsignificant. CONCLUSION: The lead concentration in the air at the workplace is related to the renal functions of lead exposure workers. It is important to decrease the lead environment and to prevent renal damage.

Adult↗
PubMed2005

Effect of environmental lead pollution on blood lead levels in traffic police constables in Islamabad, Pakistan.

OBJECTIVE: To determine the blood lead levels and trace elements (copper and manganese) in traffic police constables in Islamabad in order to assess the effects of environmental pollution on the levels of metals in body fluids. METHODS: Blood samples were collected from 47 male traffic police constables, 21 to 45 years of age, posted in different areas of Islamabad and controlling traffic from 3 months to 18 years, 8 hours/day, 6 days/week. Adolescent males (13-19 years), residing in comparatively clean and very low traffic areas were included as controls. Blood lead, copper, and manganese concentrations were estimated by atomic absorption spectrophotometry. RESULTS: The mean blood lead level among constables (27.27 microg/dl) was significantly (p<0.0001) high as compared to controls (3.22 microg/dl). Twenty one percent constables had elevated blood lead levels (over 25 microg/dl) and 13% had levels above the safety limit (40 microg/dl). No correlation was found between blood lead levels and length of service. No significant difference was found in the mean values for copper between traffic constables (93.49 microg/dl) and controls (71.15 microg/dl). The mean blood manganese levels in traffic constables (21.94 microg/dl) were significantly (p<0.0001) higher than in controls (1.70 microg/dl). The mean blood lead levels were significantly high in traffic constables of Karachi (47.7 microg/dl) as compared to Islamabad (27.2 microg/dl), which shows direct relation of rise in blood lead levels with vehicle exhaust. CONCLUSION: Environmental lead pollution is associated with an increased blood lead concentration in those who are regularly exposed to vehicle exhaust in high traffic areas. The degree of lead pollution arising from vehicle exhaust differs in Karachi and Islamabad. Exposure to air containing dust particles rich in manganese may affect blood manganese levels.

Adolescent↗
PubMed1974

Lead poisoning in chickens and the effect of lead on interferon and antibody production.

The effect of aqueous lead acetate given per os to chickens for 35 consecutive days and the effect of lead on interferon and antibody production was investigated. Chickens were found to tolerate levels of lead as high as 160 mg/kg/day without exhibiting clinical signs or hematological changes in spite of very high levels of lead in the blood (6.2 ppm). It is apparent from these findings that chickens are more resistant to lead poisoning than humans, horses, dogs and wild fowl such as ducks. Subclinical lead doses did not affect interferon induction in response to statolon and Newcastle Disease virus (NDV)-B(1). Interferon concentrations and duration in serum were markedly decreased in chickens which received lead at the 320 mg/kg level. Long time lead exposure had no marked effect on antibody production to NDV in chickens. No consistent correlation was observed between blood lead concentration and antibody titer. The results of these studies indicate that long term subclinical lead intake suppresses neither interferon nor antibody production in chickens.

Acetates↗
PubMedDate not supplied

Renal function impairment in secondary lead smelter workers: correlations with zinc protoporphyrin and blood lead levels.

Potential kidney function decrement with long-term lead exposure is important in the overall assessment of adverse health effects of lead in industrial workers or other exposed groups. Two clinical field studies of secondary lead smelter workers have shown that a significant proportion of workers had slightly to moderately elevated BUN and creatinine levels; the prevalence was higher in those with longer lead exposure. Since a decrement of kidney function with age has been documented, and, since duration of lead exposure may also be strongly related to age, it was necessary to assess the age dependent renal function decrement in a control (non-lead-exposed) population. BUN and creatinine levels in the lead-exposed workers showed a much more significant correlation with age than that which was found in the non-exposed population; the correlations between the indicators of renal function, BUN and creatinine, and duration of lead exposure remained statistically significant after removing the age-dependent decrement derived from the control population. Moreover, a highly significant correlation between BUN and zinc protoporphyrin levels was found. The results indicate a sizeable and significant decrement in kidney function in the secondary lead smelter workers studied; this effect was found to be lead-induced, by removing its age-dependency.

Aging↗