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PubMedDate not supplied

Durability of bipolar coaxial endocardial pacemaker leads compared with unipolar leads.

BACKGROUND: The coaxial design allows for thinner bipolar endocardial pacemaker leads, but recent reports have suggested a higher incidence of failure for this sophisticated configuration. OBJECTIVE: To compare the long-term survival of bipolar coaxial and unipolar leads. METHODS: Retrospective follow-up. RESULTS: Between January 1, 1980 and June 30, 1991, 1142 bipolar coaxial leads and 1181 unipolar leads were implanted at the Cleveland Clinic. The mean follow-up was 33 +/- 32 months (range 1 to 138 months). Ten bipolar coaxial leads failed (0.88%), as did 9 unipolar leads (0.76%). At 5 years the cumulative survival was 98.6% for both types of leads; however, at 10 years the survival of bipolar coaxial leads was only 92.4% compared with 98.6% of unipolar leads (P = .03; relative risk 2.7, 95% confidence interval = 1.1 to 6.9). CONCLUSIONS: The sophisticated design of bipolar coaxial leads could be the cause of their increased vulnerability. The benefit-to-risk ratio of this design should be prospectively reevaluated.

Electrodes, Implanted↗
PubMed1986

Chemical and biological monitoring of chronic lead poisoning in the rat. Implications to the assessment of hazard of low-level lead.

A study on rats of the effects of lead on delta-aminolevulinate dehydratase (ALA-D) activity, and its pH-dependent maximal enzyme activity is reported. Over a 5-week period, the lead burden and ALA-D activity in kidney, liver and brain are documented. Lead concentrations in the organs, expressed as micrograms/g protein are in the sequence kidney greater than liver greater than brain and reach essentially a constant level after 3 days of exposure. This is consistent with the existence of an efficient mechanism removing lead from these organs. Lead affects the ALA-D in all three organs by reducing the activity and shifting the pH of maximum enzyme activity to more acidic values. In common with the lead levels, the ALA-D activity does not deteriorate beyond the levels reached after 3 days of exposure. The existence of a mechanism removing lead from the organs is further supported in a recovery study on blood and kidney, in which both lead level and ALA-D activity return essentially to normal values after 7 days of no exposure to lead.

Animals↗
PubMed1995

Combined therapeutic potential of meso-2,3-dimercaptosuccinic acid and calcium disodium edetate on the mobilization and distribution of lead in experimental lead intoxication in rats.

Asymptomatic lead poisoning remains a serious public health problem in developed and developing countries. Chelation therapy particularly with calcium disodium ethelenediamine tetracetic acid (CaNa2EDTA) is often used therapeutically to reduce the body burden of lead. This chelating drug has serious side effects and drawbacks primarily related to redistribution of lead, nephrotoxicity, and essential metal depletion. The present study was planned to determine the effectiveness of CaNa2EDTA and meso-2,3-dimercaptosuccinic acid (DMSA) used in combination. Both drugs, when administered individually, resulted in significant urinary excretion of lead and lowered the tissue lead burden. Combined treatment with CaNa2EDTA and DMSA elicits an additive response in promoting urinary lead elimination, depleting body lead burden, and restoring altered lead-sensitive biochemical variables. Further, no redistribution of lead to brain or any other soft organ following combined DMSA-CaNa2EDTA treatment was observed indicating a definite advantage of combined therapy over the conventional treatment with CaNa2EDTA or DMSA alone. However, an elevation of serum transaminase activity, creatinine level, and depletion of blood zinc level may limit the usefulness of this combined treatment.

Alkaline Phosphatase↗
PubMed2003

Experimental study of blood lead kinetics in estuarine crocodiles (Crocodylus porosus) exposed to ingested lead shot.

A previous study of lead (Pb) contamination in estuarine crocodiles (Crocodylus porosus) in Kakadu National Park, Australia, found elevated Pb levels in bone and flesh from individuals caught in habitats where hunting with lead ammunition had occurred. Lead shot was suspected as the potential source of Pb in these animals. An investigation was designed to determine if crocodiles are capable of retaining and dissolving lead shot in their stomachs and absorbing the ionic Pb into the blood. Four of the six juvenile crocodiles (C. porosus) used in the experiment were fed an initial dose of five or ten lead shot each. Most of the lead shot were retained in the stomach over the 20-week experimental period, as confirmed by stomach lavage and radiography of the stomach region. From 13 to 30% of the original weight of individual lead shot had been eroded in that time. In vitro experiments confirmed that lead shot could be dissolved under conditions simulating those known for the crocodilian stomach. Blood Pb concentrations increased by an order of magnitude within a week after dosing three crocodiles with five lead shot each, and then attained steady-state equilibrium 5-20 weeks after dosing, with blood Pb steady-state levels ranging from 278 to 363 microg/dL. The blood Pb concentration-time curves in these crocodiles followed a one-compartment model with first-order loss kinetics that yielded an apparent biological half-life for Pb in blood of about 3.4 days. Throughout the experiment, the crocodiles remained in apparent good physical condition and displayed no clinical signs of Pb toxicosis. These observations, together with the very high blood Pb levels that were sustained for several months, suggest that crocodilians may possess a relatively high degree of resistance to Pb toxicity.

Administration, Oral↗
PubMed2004

Correlation between clinical indicators of lead poisoning and oxidative stress parameters in controls and lead-exposed workers.

The present study was undertaken to investigate the involvement of oxidative damage in lead-induced toxicity in humans and to enlighten whether oxidative stress indicators are correlated with the known indices of lead toxicity. For these purposes, selected oxidative stress parameters along with some clinical indices of lead poisoning were determined in blood of battery plant workers and control subjects. Workers had significantly increased erythrocyte malondialdehyde (MDA) levels, catalase and glucose-6-phosphate dehydrogenase (G6PD) activities, and decreased blood glutathione:glutathione disulfide ratio compared to the controls. Increased blood lead concentrations and zinc protoporphyrin (ZPP) levels, and decreased delta-aminolevulinic acid dehydratase (ALAD) activity were used as clinical indices of lead toxicity. Statistically significant correlation between oxidative stress parameters and clinical indices implies that disrupted prooxidant/antioxidant balance might contribute to lead-induced toxicity in erythrocytes. A significant correlation was found between ALAD activity and blood lead levels in human subjects. Similarly significant correlation between ALAD activity and erythrocyte MDA concentrations was shown. Present data indicates that ALAD can serve as a valuable biomarker of oxidative stress in lead-exposed hematological system as well as being a biochemical indicator of lead exposure.

Adult↗
PubMed2001

Environmental exposure to lead in a population of adults living in northern France: lead burden levels and their determinants.

As part of the assessment of a site in northern France polluted by metals from two smelters (in particular, lead, cadmium and mercury), a cross-sectional study was carried out which intended to estimate the levels of the lead burden of the adult population living on the site and the factors associated with these levels. The exposed zone included 10 municipalities in the Nord-Pas de Calais region, located in the vicinity of two non-ferrous metal smelters. The soils in these municipalities contained between 100 and 1700 ppm of lead. The non-polluted zone contained 20 municipalities from the same region, drawn randomly from those in the region of comparable size but free from any industrial lead exposure. The adult study population (301 men and 300 women) was stratified according to age, sex, employment status and exposure level. The inclusion criteria required subjects who were aged between 20 and 50 years and had been living in the exposed zone for at least 8 years; the exclusion criteria were pregnancy, cancer, kidney disease and diabetes. No more than 10% of the subjects participating could work at one of the two smelters. Data collection took place at home; visiting nurses interviewed subjects to complete a questionnaire and also took blood samples. The lead assay was performed by atomic absorption spectrometry. The geometric mean of the blood-lead levels was 74 microg/l, 95% CI = 69-80 among men and 49 microg/l, 95% CI = 46-53 among women. Blood-lead levels exceeding 100 microg/l were found among 30% of men and 12% of women. Several factors were associated with variation of the mean blood-lead level: the blood-lead level was significantly higher among the men for subjects living less than 1 km from the smelters (geometric mean x 1.3, 95% CI = 1.1-1.6), for those who drink alcoholic beverages (x 1.1, 95% CI = 1.0-1.2 for consumption of 30 g/day), those who smoke (x 1.2, 95% CI = 1.0-1.3 for 20 cigarettes/day), and for subjects with occupational exposure; among the women, for subjects living less than 1 km from the smelters (geometric mean x 1.5, 95% CI = 1.2-1.7), for those who drink alcohol (x 1.1, 95% CI = 1.1-1.2 for a daily consumption of 10 g), and for women living in a building constructed before 1948 (x 1.2, 95% CI = 1.0-1.4).

Adult↗
PubMed2004

High human exposure to lead through consumption of birds hunted with lead shot.

We assess lead contamination of Greenland seabirds killed with lead shot having studied thick-billed murre and common eider, the two most important species in the diet. The lead concentration is very high in meat of eiders killed with lead shot (mean 6.1 microg/g-wet wt, 95% CL 2.1-12). This level is about 44 times higher than in drowned eiders and eight times higher than in shot murres. Analyzing whole breasts instead of sub-samples reveals about seven times higher lead levels in birds' meat. We conclude that in some cases the lead intake by Greenland bird eaters will largely exceed the FAO/WHO tolerable lead intake guideline and that lead shot is a more important source of lead in the diet than previously estimated.

Animals↗
PubMed1992

Experimental model of lead nephropathy. I. Continuous high-dose lead administration.

This study followed the progression of lead nephropathy in male Sprague-Dawley rats (E) administered lead acetate (0.5%) continuously in drinking water for periods ranging from 1 to 12 months. Control animals (C) were pair-fed. Observations included renal pathology by light and electron microscopy, wet and dry kidney weights, and glomerular filtration rate (GFR) to assess renal function. Urinary excretion of lead, the enzymes N-acetyl-beta-D-glucosaminidase (NAG) and glutathione-S-transferase (GST), and brush border antigens (BB50, CG9, and HF5) were utilized to explore possible markers of kidney injury. GFR was increased significantly after three months of lead exposure, but was decreased significantly after 12 months. Kidney wet weights were significantly greater in E than C from three months on. Kidney dry weight/wet weight ratio was constant up to three months, but decreased in E at 12 months. Glomerular diameters were normal at all time periods; the nephromegaly was related primarily to hypertrophy of proximal tubules. Lead inclusion bodies were found in nuclei of proximal convoluted tubules and pars recta at all times. Tubular atrophy and interstitial fibrosis first appeared at six months, and increased in severity thereafter. Brush borders of proximal tubules were disrupted at one and three months, but recovered thereafter. Focal and segmental glomerulosclerosis was observed in 2 of 10 rats at 12 months. Arteries and arterioles remained normal at all time periods. Urinary NAG was elevated in E above C after three months of lead exposure. However, urinary NAG in C also increased with age, obscuring changes in the 12 month E rats. GST was elevated after three months of lead administration in E, not without an attendant age-related increase in C rats. In three-month E rats, urinary brush border antigens were increased above C, but were decreased at six and 12 months, correlating with the morphologic changes in brush border. We conclude that a high dose of lead in rats may initially stimulate both renal cortical hypertrophy and an increase in GFR. Later, the adverse effects of lead on the tubulointerstitium predominate, and GFR falls. The urinary marker, NAG, was abnormal in the early stages of the disease, but age-related changes obscured its utility at later stages; urinary GST appeared to be a more consistent marker of injury.

Acetylglucosaminidase↗
PubMedDate not supplied

Lead in inner-city soil and its possible contribution to children's blood lead.

This study was designed to assess distribution and sources of lead in inner-city soils in Washington, D.C. Duplicate soil samples were collected randomly from 239 unpaved front yards of homes in Washington, D.C. Soil samples were collected 1 m from the houses. Lead concentration in soil was determined by flame atomic absorption spectrophotometry. Presence of lead detected in soil was correlated and traced to the anticipated source of origin. A significantly high concentration of lead was present in inner-city soils. Areas of the city in which the highest lead concentrations were found (Wards 1, 4, 5, 6, 7, 8) were determined to contain a large number of residents who had attained lower education levels than most residents in the remaining wards. It was concluded that lead concentration in inner-city soil plays a significant role in the incidence of lead poisoning in children in the District of Columbia and that paint is the main source of soil lead. Demographic characteristics of the residents appeared to enhance the distribution of lead poisoning.

Adolescent↗
PubMed1989

Lead poisoning among household members exposed to lead-acid battery repair shops in Kingston, Jamaica.

To investigate the risk of lead poisoning among household members exposed to 'backyard' battery repair shops (BBRS) in Kingston, Jamaica, environmental and blood lead (PbB) were measured at 24 households (112 individuals) with a BBRS worker or located at a BBRS premises and at 18 neighbourhood control households (74 individuals). Elevated PbB (greater than or equal to 25 micrograms per decilitre [micrograms/dl]) was common among subjects of all ages living at BBRS premises, especially among children less than age 12, 43% of whom had PbB greater than 70 micrograms/dl. Potentially hazardous soil and house dust lead levels were also common at BBRS premises, where 84% of yards had soil lead levels above 500 parts per million (geometric mean 3388 parts per million [ppm] at BBRS premises households with a BBRS worker). Geometric mean blood and environmental lead levels were significantly lower at control households, where less than 10% of subjects in all age groups had elevated PbB (maximum 33 micrograms/dl). Sharing a premises with a BBRS was a stronger determinant of household blood lead and environmental contamination than was the presence of a BBRS worker in a household. Blood lead levels were associated with soil and house dust lead levels in all age groups. We conclude that small battery repair shops, which have also been described in other developing countries, create a high lead poisoning risk for nearby residents.

Adolescent↗
PubMed1981

Chelatable lead body burden (by calcium-disodium EDTA) and blood lead concentration in man.

The cheletable part of lead body burden was measured in 32 workers and seven office workers after an infusion test with CaNa2EDTA. The workers had been exposed to lead at a lead and zinc processing unit for one to three years (mean one year). There was good correlation (r = 0.87) between blood lead and chelatable urinary lead excretion described by the equation y = 0.07 . 10(0.46.x). From this equation it can be predicted that the generally accepted limit value for chelatable urinary lead excretion, 0.42 mumol/mmol CaNa2EDTA administered per 24 hours (3.1 mumol/24 hours or 650 micrograms/24 hours), corresponds to a blood lead concentration (PbB) of 1.7 mumol/l (or 35 micrograms/100 ml), which is lower than the commonly accepted limit value of 2.9 mumol/l (or 60 micrograms/100 ml) for occupationally lead-exposed persons. There was a better correlation between the cheletable lead excretion and the urinary ALA-excretion (r = 0.45; p less than 0.001) than between PbB and the urinary ALA-excretion (r = 0.26; p greater than 0.05).

Adult↗
PubMed1979

Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).

Air Pollutants, Occupational↗
PubMed1985

The "lead-induced colic" syndrome in lead intoxication.

Lead has a multiplicity of biologic effects. The universal occurrence of lead accounts for the continuous appearance of new instances of human lead poisoning. The most common and one of the earliest manifestations of lead intoxication in the adult is so-called lead-induced colic, which is a syndrome with a multiplicity of clinical patterns and at least three possible different pathogenic mechanisms. It may be caused by changes in the visceral smooth muscle tone secondary to the action of lead on the visceral autonomic nervous system, lead-induced alterations in sodium transport in the small-intestinal mucosa, and lead-induced interstitial pancreatitis. It should be considered in the differential diagnosis of abdominal pain of obscure etiology and whenever a disparity is observed between the symptoms and the abdominal findings in a patient with abdominal pain, especially in the presence of a history of occupational exposure to lead.

Abdominal Muscles↗
PubMed1988

Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning.

Microcytic anemia, long considered an effect of lead poisoning, may in fact result from coexisting iron deficiency. In this study, how RBC size, hemoglobin, and zinc protoporphyrin vary as a function of iron status in a group of children with high lead levels was examined. Charts of all children (N = 51) admitted to Cook County Hospital for treatment of lead poisoning in 1981 to 1983 were reviewed for data on age, blood lead level, hemoglobin concentration, MCV, transferrin saturation and zinc protoporphyrin level. The mean lead level was 86 micrograms/dL and the range was 63 to 190 micrograms/dL. Children with transferrin saturation values less than 7% had a mean MCV of 56 microL, hemoglobin of 8.9 g/dL, and zinc protoporphyrin of 693 micrograms/dL; for those with saturations of 7% to 16%, the values were 61 microL, 10.1 g/dL, and 581 micrograms/dL, respectively; the children with saturations greater than 16% had normal mean MCVs and hemoglobin concentrations (74 microL and 11.4 g/dL) and a mean zinc protoporphyrin value of 240 micrograms/dL (P less than .0005). Multiple linear regression was used to correct for effect of age, and transferrin saturation remained the most important predictor of MCV, hemoglobin, and zinc protoporphyrin levels; the addition of lead did not improve the models. Results of this study suggest that iron deficiency is strongly associated with some of the observed toxicities of lead. Also, lead poisoning can exist without producing microcytosis or anemia, and zinc protoporphyrin concentration may not be a sensitive indicator of lead level in the absence of iron deficiency.

Anemia, Hypochromic↗
PubMed1987

Excessive lead absorption resulting from exposure to lead naphthenate.

There are no reported studies of the relationship between exposure to lead naphthenate and lead absorption in humans. In an aluminum forging operation where lead naphthenate was sprayed without local ventilation, the mean concentration of lead in air was 96 micrograms/m3 with a range of 12-430 micrograms/m3. The 29 forge operators who worked in this area had a mean blood lead concentration of 63 micrograms/dl, which was statistically significantly (P less than .001) higher than the mean blood lead concentration of 17 micrograms/dl among the 103 unexposed workers. Similarly, the mean zinc protoporphyrin concentration among the forge operators was 265 micrograms/dl, which was statistically significantly (P less than .001) higher than the mean concentration of 26 microgram/dl among the unexposed workers. Nineteen workers, all of whom worked in the forge areas, had blood lead concentrations in excess of 60 micrograms/dl, with the highest concentration being 108 micrograms/dl. This is the first reported instance in which the use of lead naphthenate has been associated with increased lead absorption in humans.

Absorption↗
PubMed1984

Inhibition of the pentose phosphate shunt by lead: a potential mechanism for hemolysis in lead poisoning.

Recent investigations have disclosed a decrease in pentose phosphate shunt activity in hereditary pyrimidine 5'-nucleotidase deficiency. Clinical lead poisoning is associated with an acquired decrease in pyrimidine 5'-nucleotidase activity. The current investigations were undertaken (1) to determine if pentose shunt activity was decreased in erythrocytes exposed to lead, and (2) to compare the mechanism of inhibition to that seen in hereditary pyrimidine 5'-nucleotidase deficiency. Normal erythrocytes incubated with lead acetate in vitro demonstrated increased Heinz body formation, decreased reduced glutathione, a positive ascorbate cyanide test, and a reversible suppression of pentose shunt activity in the intact erythrocyte. Lead acetate added to normal red cell hemolysates markedly inhibited the activities of glucose-6-phosphate dehydrogenase (G6PD) and phosphofructokinase. The mean Kis of lead for glucose-6-phosphate and nicotinamide adenine dinucleotide phosphate (NADP) for G6PD were 1.5 microM and 2.1 microM, respectively, which is within the range of intraerythrocytic lead concentrations found in clinical lead poisoning. Magnesium enhanced the ability of lead to inhibit G6PD. Thus, the shortened erythrocyte survival in lead poisoning appears to be due, in part, to increased oxidant sensitivity secondary to inhibition of G6PD and the pentose shunt. The mechanism of shunt inhibition is, in part, similar to that seen in hereditary pyrimidine 5'-nucleotidase deficiency.

5'-Nucleotidase↗
PubMed1984

Iron depletion and blood lead levels in a population with endemic lead poisoning.

The effect of iron depletion on blood lead levels was studied in a group of 558 schoolchildren aged 10 to 18 residing in two West Bank Arab villages with a high prevalence of excessive lead exposure and clinical lead poisoning. Thirty percent of the subjects studied had whole-blood lead levels greater than 30 micrograms/dl, and 45% had whole-blood zinc erythrocyte protoporphyrin greater than 50 micrograms/dl. The percentage of abnormal blood lead values in subjects with normal serum ferritin and transferrin saturation (31%) was similar to that in subjects with one (28%) or two (25%) abnormal iron parameters. Likewise, there was no correlation between serum ferritin and blood lead levels in individual patients (r = 0.059). Normal distribution plots and mean levels of blood lead (27.3 micrograms/dl) were identical in the iron-deficient and iron-replete groups. These findings indicate that iron depletion does not affect blood lead levels and suggest that in man, unlike in experimental animals, iron depletion may not have a significant effect on lead absorption.

Adolescent↗
PubMedDate not supplied

[Factors related to the blood lead level in children 6 to 30 months old in the Prospective Lead Study in Mexico City].

A majority of the sample of children (N = 160-121, ages 6-30 months) from the Mexico City Prospective Lead Study exceeds the lowest limit action level (10 micrograms/dl) of the Centers for Disease Control standards for childhood lead exposure. Over one-third of the sample at 18 months and 24 months exceeds the action level (15 micrograms/dl) for aggressive intervention. Diet plays an important role in regulating early childhood blood lead levels. Fresh milk and breast feeding are associated with lower lead levels, but extended breast feeding is related to elevated lead levels. Low income and poor maternal education are associated with higher lead concentration in children. Child consumption of canned milk and juice, up to this date, is associated with elevated child lead levels. Canned products sealed with lead are disappearing from Mexican markets. Efforts to improve childhood nutrition and poverty may be expected to have the additional benefit of lowering lead levels of Mexican children.

Analysis of Variance↗