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PubMed1983

Influence of dietary lead and calcium on tissue lead accumulation and depletion, lead metabolism and tissue mineral composition in sheep.

Two experiments were conducted to study the metabolism and tissue accumulation and depletion of dietary Pb in sheep. In Exp. 1, a feeding trial, 33 wethers, 56 kg initially, were assigned randomly to two dietary treatments: .25% Ca plus 1,000 ppm Pb or .50% Ca plus 1,000 ppm Pb. Supplemental Ca and Pb were supplied as reagent grade calcium carbonate or reagent grade lead acetate. The experiment was divided into two phases of 75 and 180 d; during the first phase, diets contained 1,000 ppm supplemental Pb and during the second phase, diets contained 3 ppm Pb. Calcium level remained constant within treatments throughout both phases. Sheep were slaughtered at various intervals during both phases and tissue samples taken. Lead increased in all tissues during the accumulation period and decreased during the depletion period; however, kidney was the only tissue in which Pb concentration declined to control values by 180 d. Dietary Ca reduced (P less than .05) the concentration of Pb deposited in liver, but not in other tissues. Interactions of dietary Ca and Pb on tissue concentration of various minerals occurred. In Exp. 2, a balance trial, 27 wethers, 53 kg initially, were allotted randomly to four treatments in a 2 X 2 factorial arrangement. Diets contained either 0 or 1,000 ppm supplemental Pb as reagent grade lead acetate and .25 or .50% total Ca with supplemental Ca from calcium carbonate. Increasing dietary Pb increased (P less than .05) percentage of Pb retained and increased (P less than .01) whole blood Pb concentration (1.0 vs 1.42 micrograms/ml).

Animals↗
PubMed2004

Terphenyl ligand stabilized lead(II) derivatives: steric effects and lead-lead bonding in diplumbenes.

The reaction of PbBr(2) with the lithium reagents LiC(6)H(3)-2,6-(C(6)H(3)-2,6-Pr(i)(2))(2) (LiArPr(i)(2)) and Et(2)O.LiC(6)H(3)-2,6-(2,6-Pr(i)-4-Bu(t)C(6)H(2))(2) (Et(2)O.LiArPr(i)(2)Bu(t)) furnished the bromide bridged organolead(II) halides [Pb(mu-Br)ArPr(i)(2)](2) (1) and[Pb(mu-Br)ArPr(i)(2)Bu(t)](2) (2) as orange crystals. Treatment of 1 with a stoichiometric amount of methylmagnesium bromide resulted in the "diplumbene" Pr(i)(2)Ar(Me)PbPb(Me)ArPr(i)(2) (3). The addition of 1 equiv of 4-tert-butylphenylmagnesium bromide to 1 afforded the feebly associated, Pb-Pb bonded species [Pb(C(6)H(4)-4-Bu(t))ArPr(i)(2)](2) (4), whereas the corresponding reaction of tert-butylmagnesium chloride and 1 afforded the monomer Pb(Bu(t))ArPr(i)(2) (5). The reaction of the more crowded aryl lead(II) bromide [Pb(mu-Br)ArPr(i)(3)](2) (Ar = C(6)H(3)-2,6(C(6)H(2)-2,4,6-Pr(i)(3))(2)) with 4-isopropyl-benzylmagnesium bromide or LiSi(SiMe(3))(3) yielded the monomers 6, [Pb(CH(2)C(6)H(4)-4-Pr(i))ArPr(i)(3)], or 7, [Pb(Si(SiMe(3))(3))ArPr(i)(3)]. All compounds were characterized with use of X-ray crystallography, (1)H, (13)C, and (207)Pb NMR (3-7), and UV-vis spectroscopy. The dimeric Pb-Pb bonded (Pb-Pb = 3.1601(6) A) structure of 3 may be contrasted with the previously reported monomeric structure of Pb(Me)ArPr(i)(3), which differs from 3 only in that it has para Pr(i) substituents on the flanking aryl rings. The presence of these groups is sufficient to prevent the weak Pb-Pb bonding seen in 3. The dimer 4 displays a Pb-Pb distance of 3.947(1) A, which indicates a very weak lead-lead interaction, and it is possible that this close approach could be caused by packing effects. The monomeric structures of 6 and 7 are attributable to steric effects and, in particular, to the large size of ArPr(i)(3).

Journal Article↗
PubMed1981

[Polymorphism of hemoglobins D in Ivory Coast: Hb Korle Bu (beta 73 (E17) Asp leads to Asn), Hb Avicenna (beta 47 (CD6) Asp leads to Ala) and Hb Cocody (beta 21 (B3) Asp leads to Asn) (author's transl)].

A recent screening performed at the CHU Cocody in Abidjan (Ivory Coast) revealed six cases of hemoglobin "D". The use of a rapid strategy based on isoelectric focusing studies, finger-printing, reverse phase high performance liquid chromatography and solid phase microsequence technique led to the characterization of three abdominal hemoglobins. The first variant corresponded to the Hb Korle Bu (beta 73 (E17) Asp leads to Asn) (pI = 7.210) which is common in this country. The second, Hb Avicenna (beta 47 (CD6) Asp leads to Ala) (pI = 7.225) has not yet been reported in Africa. The last one was a new variant, Hb Cocody (beta 21 (B3) Asp leads to Asn) (pI = 7.205). A large number of hemoglobin "D" have been detected in European, American negroes, Amerindian or Asiatic populations, but only few observations were reported in Africa. Large screenings and discriminative methodologists must provide information on the polymorphism of hemoglobin D in the African population.

Chemical Phenomena↗
PubMed1984

Hb J-Singa (alpha-78 Asn leads to Asp), a newly discovered hemoglobin variant with the same amino acid substitution as one of the two present in Hb J-Singapore (alpha-78 Asn leads to, alpha-79 Ala leads to Gly).

A new fast-moving alpha-chain Hb variant with an Asn leads to Asp substitution at position alpha-78 was found in a French-Acadian family living in Eastern Canada. The identical substitution was reported in Hb J-Singapore, which also had an additional Ala leads to Gly substitution at position alpha-79. The new variant, which did not result in any clinical symptoms, was named accordingly, Hb J-Singa.

Adult↗
PubMed1993

Bone lead content assessed by L-line x-ray fluorescence in lead-exposed and non-lead-exposed suburban populations in the United States.

Measurements of lead (Pb) in bone reflect cumulative Pb exposure, whereas blood Pb levels are indices of absorption during the previous 21-30 days. This study was undertaken to estimate bone Pb concentrations by L-line x-ray fluorescence (LXRF) in a United States suburban population which was exposed to unusually high levels of Pb in emissions from an adjacent factory during 1963-1981, compared with concentrations similarly estimated in a matched suburban community without unusual Pb exposure. The mean bone Pb value in 269 residents of the highly exposed suburb (15 ppm) was 3-fold greater than that of the reference suburb (5 ppm). LXRF estimates of bone Pb identified those individuals at risk for adverse effects of Pb, whereas blood Pb levels were uninformative. Average LXRF-estimated bone Pb concentrations in residents of the unusually exposed suburb approximated estimated values in workers at Pb-processing factories.

Adolescent↗
PubMed1976

Urinary non-precipitable lead in lead workers.

Sixty-six workers engaged in lead-glazing pottery with a presumed moderate exposure to lead were studied. The group comprised 20 men with long-term exposure to lead and positive laboratory signs of increased lead absorption (Group A); 22 with long-term exposure and negative laboratory signs (Group B); 11 with short-term exposure and positive laboratory signs (Group C); and 13 with short-term exposure and negative laboratory signs (Group D). In addition, 14 workers employed in casting the kelmet alloys with presumed heavy exposure to lead (Group E) and seven healthy individuals (Group F) were included. Urine samples from all the subjects were analysed to determine, first, the total lead using the ashing technique, and then the precipitable lead using the coprecipitation technique of Cholak, Hubbard, and Burkey (1948), but modified slightly by us. Thus, the non-precipitable lead fraction in urine was the difference between the two measurements and this was also expressed as a percentage of the total lead. The mean total lead and the mean proportion of non-precipitable lead were 0.62 mumol/l and 48.7%, 0.35 mumol/l and 44.9%, 0.40 mumol/l and 48.9%, 0.17 mumol/l and 24.6%, 1.43 mumol/l and 44.3%, 0.14 mumol/l and 18.8% for Groups A, B, C, D, E, and F respectively, showing that a large part of urinary lead was eliminated as precipitable lead in Groups D and F who had normal lead excretion, while about half was eliminated as non-precipitable lead in the other four groups who had excessive lead excretion. No essential difference in the proportion of non-precipitable lead among Groups A, B and C excluded the possibility that the proportion might be directly related to the period of exposure to lead and to the laboratory findings of excessive lead absorption. The mean proportion of non-precipitable lead for the physiological (up to 0.240 mumol/l), intermediate (0.241 to 0.721 mumol/l), and excessive (above 0.722 mumol/l) total lead levels was 26.7, 41.3, and 52.3% respectively, in the lead workers comprising Groups A, B, C, and E each showing increased lead excretion when grouped together. these data suggested that, when urinary lead is within the normal range, it is excreted largely as precipitable lead even in individuals exposed to lead, and that the principal conditions determining the excretion of non-precipitable lead would be the current or recent degree of lead absorption. The excretory mechanisms and the biological significance of the non-precipitable lead are also discussed.

Chemical Precipitation↗
PubMed2000

Effects of a thin-sized lead body of a transvenous single coil defibrillation lead on ICD implantation. Kainox RV Study Group.

In the interest of patients receiving implantable cardioverter defibrillators (ICDs), the clinical benefits of newer and thinner transvenous defibrillation leads have to be determined. The aims of this study were to evaluate the ICD procedure duration and the frequency of lead dislocation at the 3-month follow-up of a new defibrillation lead with a thin-sized lead body and its conventional-sized predecessor. The thin-sized single coil defibrillation lead (Kainox RV, Biotronik; lead body 6.7 Fr) was implanted in 61 patients and the conventional-sized defibrillation lead (SPS, Biotronik; lead body 7.8 Fr) in 60 patients. Both leads were connected to a left-sided, prepectorally implanted Phylax ICD (Biotronik) with active housing. The lead implantation time and total procedure duration were determined. Lead implantation time was defined as the time from lead insertion to the end of the pacing measurements. The total procedure duration spanned skin incision to closure. The incidence of lead repositioning during the lead implantation time and during ventricular fibrillation conversion testing was also assessed. The frequency of lead dislocations was recorded at the 3-month follow-up. Mean lead implantation time and total procedure duration of the thin-sized lead (23 +/- 22 minutes 76 +/- 37 minutes) were not statistically different from the time needed for the conventional-sized lead (22 +/- 20 minutes 81 +/- 34 minutes). The number of lead repositionings during the lead implantation time was similar (thin-sized lead: 1.4 +/- 2.4; conventional-sized lead: 1.1 +/- 1.9). An additional lead repositioning was not necessary during ventricular fibrillation conversion testing in 93.4% of the patients with thin-sized and in 94.4% with conventional-sized leads (not significant). At the 3-month follow-up, there were four (6.6%) lead dislocations in the thin-sized and four (6.7%) in the conventional-sized lead group. In conclusion, the down-sized lead body of the new defibrillation lead influenced neither ICD procedure duration nor the incidence of lead dislocation during follow-up.

Case-Control Studies↗
PubMed1994

Adjustment of QT dispersion assessed from 12 lead electrocardiograms for different numbers of analysed electrocardiographic leads: comparison of stability of different methods.

OBJECTIVE: Normal electrocardiographic recordings were analysed to establish the influence of measurement of different numbers of electrocardiographic leads on the results of different formulas expressing QT dispersion and the effects of adjustment of QT dispersion obtained from a subset of an electrocardiogram to approximate to the true QT dispersion obtained from a complete electrocardiogram. SUBJECTS AND METHODS: Resting 12 lead electrocardiograms of 27 healthy people were investigated. In each lead, the QT interval was measured with a digitising board and QT dispersion was evaluated by three formulas: (A) the difference between the longest and the shortest QT interval among all leads; (B) the difference between the second longest and the second shortest QT interval; (C) SD of QT intervals in different leads. For each formula, the "true" dispersion was assessed from all measurable leads and then different combinations of leads were omitted. The mean relative differences between the QT dispersion with a given number of omitted leads and the "true" QT dispersion (mean relative errors) and the coefficients of variance of the results of QT dispersion obtained when omitting combinations of leads were compared for the different formulas. The procedure was repeated with an adjustment of each formula dividing its results by the square root of the number of measured leads. The same approach was used for the measurement of QT dispersion from the chest leads including a fourth formula (D) the SD of interlead differences weighted according to the distances between leads. For different formulas, the mean relative errors caused by omitting individual electrocardiographic leads were also assessed and the importance of individual leads for correct measurement of QT dispersion was investigated. RESULTS: The study found important differences between different formulas for assessment of QT dispersion with respect to compensation for missing measurements of QT interval. The standard max-min formula (A) performed poorly (mean relative errors of 6.1% to 18.5% for missing one to four leads) but was appropriately adjusted with the factor of 1/square root of n (n = number of measured leads). In a population of healthy people such an adjustment removed the systematic bias introduced by missing leads of the 12 lead electrocardiogram and significantly reduced the mean relative errors caused by the omission of several leads. The unadjusted SD was the optimum formula (C) for the analysis of 12 lead electrocardiograms, and the weighted standard deviation (D) was the optimum for the analysis of six lead chest electrocardiograms. The coefficients of variance of measurements of QT dispersion with different missing leads were very large (about 3 to 7 for one to four missing leads). Independently of the formula for measurement of QT dispersion, omission of different leads produced substantially different relative errors. In 12 lead electrocardiograms the largest relative errors (> 10%) were caused by omitting lead aVL or lead V1. CONCLUSIONS: Because of the large coefficients of variance, the concept of adjusting the QT dispersion for different numbers of electrocardiographic leads used in its assessment is difficult if not impossible to fulfil. Thus it is likely to be more appropriate to assess QT dispersion from standardised constant sets of electrocardiographic leads.

Adult↗
PubMed2000

A comparison of different lead biomarkers in their associations with lead-related symptoms.

OBJECTIVES: To evaluate whether dimercaptosuccinic acid (DMSA) -chelatable lead, an estimate of current bioavailable lead stores, is a better predictor of lead-related symptoms than are other commonly used lead biomarkers. METHODS: A total of 95 male lead workers from three lead industries (one secondary lead smelting facility, one polyvinyl chloridestabilizer manufacturing plant, and one lead-acid storage battery factory), and 13 workers without occupational lead exposure recruited from an occupational health institute, were studied. Blood lead, blood zinc protoporphyrin (ZPP), 4 h DMSA-chelatable lead (after oral administration of 10 mg/kg DMSA), urine lead, and urinary delta-aminolevulinic acid levels were evaluated as predictors of 15 lead-related symptoms, assessed by self-administered questionnaire, with linear and logistic regression controlling for covariates. Total symptoms and symptoms in three categories (gastrointestinal, neuromuscular, and general) were evaluated. RESULTS: The mean (SD) 4 h DMSA-chelatable lead level was 288.7 (167.7) microg, with a range from 32.4 to 789 microg in the 95 lead workers. The mean (SD) in the non-exposed subjects was 23.7 (11.5) microg with a range from 10.5 to 43.5 microg. Blood lead, blood ZPP, and spot urine lead levels ranged from 21.4 to 78.4 microg/dl, 40 to 331 microg/l, and 7.5 to 153.0 micro/l, respectively, in the lead workers, and from 4.0 to 7.2 micro/dl, 27 to 52 microg/l, and 2.9 to 15.5 microg/l in the non-exposed controls, respectively. The overall mean symptom score (SD), derived as the sum of 0 or 1 point for absence or presence of 15 symptoms, of the lead workers was 3.7 (2.0), compared to 1.2 (1.5) for the non-exposed workers. DMSA-chelatable lead was the best predictor of symptom scores in both crude and adjusted analyses, compared with the other biomarkers. Lead workers with DMSA-chelatable lead values greater than the median (260.5 microg) were 6.2 times more likely to have frequent tingling or numbness of the arms or legs and 3.3 times more likely to have muscle pain than subjects with lower chelatable lead values. Three symptoms (tingling or numbness of arm or leg, muscle pain, and feeling irritation at the slightest disturbance) evidenced a dose-dependent relationship with DMSA-chelatable lead levels. CONCLUSIONS: DMSA-chelatable lead was found to be the best predictor of lead-related symptoms, particularly of both total symptom scores and neuromuscular symptoms, than were the other other lead biomarkers.

Adult↗
PubMed1996

Comparative absorption of lead from contaminated soil and lead salts by weanling Fischer 344 rats.

A 44-day dosed feed study was performed to compare the bioavailability of lead from contaminated soil versus two lead salts and the effect of soil on gastrointestinal absorption of ingested lead. Male Fischer rats (approximately 4 weeks of age) received lead, 17, 42, or 127 ppm, in the form of lead acetate, lead sulfide, lead-contaminated soil, or combinations thereof in the diet for 7, 15, or 44 days. Control soil was added to the diets of some animals to determine how it might alter lead bioavailability. Blood Delta-aminolevulinic acid dehydratase (Delta-ALAD) and blood, bone, kidney, and liver lead were determined in groups of animals at each time-point. Blood Delta-ALAD was inhibited in a dose-dependent manner and to the greatest degree in the lead acetate and lead acetate/control soil groups, followed by the lead sulfide and lead-contaminated soil groups. Bone and tissue lead levels increased in a dose-dependent manner and were greatest in animals receiving lead acetate and significantly less in animals receiving lead sulfide and lead-contaminated soil. Blood lead levels were generally greatest by 7 days and stabilized at lower levels thereafter. Bone lead concentration-time patterns did not demonstrate the biphasic change seen with tissues and continued to increase in most treatment groups through the course of the study. The presence of soil in the diet clearly attenuated the absorption of lead acetate, but had little effect on the absorption of lead sulfide. Results of these studies confirm previous observations that lead absorption is highly dependent on the form of lead ingested and the matrix in which it is ingested. More important, these studies demonstrate that lead in soil may be significantly less available than estimated by current default assumptions and that the presence of soil may decrease the availability of lead from lead salts on which the default assumptions are based. Results presented here also demonstrate that the weanling rat may represent an appropriate model that could be used to obtain relatively rapid and economical estimates of the availability of lead in complex matrices such as soil.

Absorption↗
PubMed2004

Levels of lead in breast milk and their relation to maternal blood and bone lead levels at one month postpartum.

Despite the many well-recognized benefits of breast-feeding for both mothers and infants, detectable levels of lead in breast milk have been documented in population studies of women with no current environmental or occupational exposures. Mobilization of maternal bone lead stores has been suggested as a potential endogenous source of lead in breast milk. We measured lead in breast milk to quantify the relation between maternal blood and bone lead levels and breast-feeding status (exclusive vs. partial) among 310 lactating women in Mexico City, Mexico, at 1 month postpartum. Umbilical cord and maternal blood samples were collected at delivery. Maternal breast milk, blood, and bone lead levels were obtained at 1 month postpartum. Levels of lead in breast milk ranged from 0.21 to 8.02 microg/L (ppb), with a geometric mean (GM) of 1.1 microg/L; blood lead ranged from 1.8 to 29.9 microg/dL (GM = 8.4 microg/dL); bone lead ranged from < 1 to 67.2 microg/g bone mineral (patella) and from < 1 to 76.6 microg/g bone mineral (tibia) at 1 month postpartum. Breast milk lead was significantly correlated with umbilical cord lead [Spearman correlation coefficient (rS) = 0.36, p < 0.0001] and maternal blood lead (rS= 0.38, p < 0.0001) at delivery and with maternal blood lead (rS = 0.42, p < 0.0001) and patella lead (rS= 0.15, p < 0.01) at 1 month postpartum. Mother's age, years living in Mexico City, and use of lead-glazed ceramics, all predictive of cumulative lead exposure, were not significant predictors of breast milk lead levels. Adjusting for parity, daily dietary calcium intake (milligrams), infant weight change (grams), and breast-feeding status (exclusive or partial lactation), the estimated effect of an interquartile range (IQR) increase in blood lead (5.0 microg/dL) was associated with a 33% increase in breast milk lead [95% confidence interval (CI), 24 to 43%], whereas an IQR increase in patella lead (20 microg/g) was associated with a 14% increase in breast milk lead (95% CI, 5 to 25%). An IQR increase in tibia lead (12.0 microg/g) was associated with a 5% increase in breast milk lead (95% CI, -3% to 14%). Our results indicate that even among a population of women with relatively high lifetime exposure to lead, levels of lead in breast milk are low, influenced both by current lead exposure and by redistribution of bone lead accumulated from past environmental exposures.

Adolescent↗
PubMed1986

A low molecular weight lead-binding protein in brain attenuates lead inhibition of delta-aminolevulinic acid dehydratase: comparison with a renal lead-binding protein.

A low molecular weight high-affinity lead-binding protein (PbBP) in kidney appears to account, at least in part, for the relative insensitivity of renal delta-aminolevulinic acid dehydratase (ALAD) to Pb inhibition. A PbBP is also known to exist in brain cytosol but is not a major Pb-binding constituent in liver. This study was undertaken to examine the relative sensitivity of brain and liver ALAD to Pb inhibition in vitro and to determine if inhibition of hepatic ALAD by Pb could be reversed by addition of partially purified brain PbBP to liver cytosol. This effect was also compared with that of a previously described renal PbBP. Finally, the mechanism(s) of reversal of Pb inhibition of ALAD by these tissue-specific PbBPs were studied. A concentration-dependent reversal of Pb-induced inhibition of hepatic ALAD activity was observed for both brain and kidney PbBPs. Inhibition of hepatic ALAD activity by 0.1 to 1.6 microM Pb was partially reversed by a single concentration of brain PbBP. No differences in sensitivity of ALAD to Pb inhibition in various brain regions were observed. Kinetic analysis of both brain and liver ALAD activity at an IC50 Pb showed a "mixed" or noncompetitive inhibition pattern. Addition of brain PbBP reduced markedly the inhibitory effects of Pb on the Vmax of the liver enzyme. Incubation of 65Zn-labeled PbBP fractions from brain and kidney with purified bovine liver ALAD demonstrated that the PbBPs donate Zn to ALAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

In vivo measurements of lead in bone in long-term exposed lead smelter workers.

In-vivo measurements of lead concentrations in calcaneus (mainly trabecular bone) and tibia (mainly cortical bone) were performed by x-ray fluorescence (XRF) in 70 active and 30 retired lead smelter workers who had long-term exposure to lead. Comparison was made with 31 active and 10 retired truck assembly workers who had no known occupational exposure to lead. After physical examination, all participants provided blood and urine samples and answered a computerized questionnaire. Since 1950, blood lead has been determined repeatedly in lead workers at the smelter, which made it possible to calculate a time-integrated blood lead index for each worker. Lead concentrations in blood, urine, calcaneus, and tibia in active and retired lead workers were significantly higher than in the corresponding control groups (p < .001). The highest bone lead concentrations were found among retired lead workers (p < .001), which was the result of considerably higher lead exposure during 1940 to 1960. Lead concentrations in calcaneus in active lead workers were significantly higher than in tibia when expressed in ug of lead per gram of bone mineral, which suggests a quicker absorption over time in this mainly trabecular bone. The estimated biological half-times were 16 y in calcaneus (95% confidence interval [95% CI] = 11-29 y) and 27 y in tibia (95% CI = 16-98 y). A strong positive correlation was found between lead concentrations in calcaneus and tibia for all lead workers (r = 0.54; p < .001). A strong positive correlation was also found between the bone lead concentrations and the cumulative blood lead index. Blood lead, at the time of study, correlated well with bone lead concentrations in retired--but not in active--workers, reflecting the importance of the endogenous (skeletal) lead exposure. The findings in this study indicate that bone lead measurements by XRF can give a good index of long-term lead exposure. Tibia measurements offer a higher precision than calcaneus measurements. The method is of particular interest in epidemiologic studies of adverse health effects caused by long-term lead exposure.

Adult↗
PubMed2004

Effect of breast milk lead on infant blood lead levels at 1 month of age.

Nursing infants may be exposed to lead from breast milk, but relatively few data exist with which to evaluate and quantify this relationship. This route of exposure constitutes a potential infant hazard from mothers with current ongoing exposure to lead as well as from mothers who have been exposed previously due to the redistribution of cumulative maternal bone lead stores. We studied the relationship between maternal breast milk lead and infant blood lead levels among 255 mother-infant pairs exclusively or partially breast-feeding through 1 month of age in Mexico City. A rigorous, well-validated technique was used to collect, prepare, and analyze the samples of breast milk to minimize the potential for environmental contamination and maximize the percent recovery of lead. Umbilical cord and maternal blood lead were measured at delivery; 1 month after delivery (+/- 5 days) maternal blood, bone, and breast milk and infant blood lead levels were obtained. Levels of lead at 1 month postpartum were, for breast milk, 0.3-8.0 microg/L (mean +/- SD, 1.5 +/- 1.2); maternal blood lead, 2.9-29.9 microg/dL (mean +/- SD, 9.4 +/- 4.5); and infant blood lead, 1.0-23.1 microg/dL (mean +/- SD, 5.5 +/- 3.0). Infant blood lead at 1 month postpartum was significantly correlated with umbilical cord (Spearman correlation coefficient rS = 0.40, p < 0.0001) and maternal (rS= 0.42, p < 0.0001) blood lead at delivery and with maternal blood (rS= 0.67, p < 0.0001), patella rS = 0.19, p = 0.004), and breast milk (rS = 0.32, p < 0.0001) lead at 1 month postpartum. Adjusting for cord blood lead, infant weight change, and reported breast-feeding status, a difference of approximately 2 microg/L (ppb; from the midpoint of the lowest quartile to the midpoint of the highest quartile) breast milk lead was associated with a 0.82 microg/dL increase in blood lead for breast-feeding infants at 1 month of age. Breast milk lead accounted for 12% of the variance of infant blood lead levels, whereas maternal blood lead accounted for 30%. Although these levels of lead in breast milk were low, they clearly have a strong influence on infant blood lead levels over and above the influence of maternal blood lead. Additional information on the lead content of dietary alternatives and interactions with other nutritional factors should be considered. However, because human milk is the best and most complete nutritional source for young infants, breast-feeding should be encouraged because the absolute values of the effects are small within this range of lead concentrations.

Adolescent↗
PubMed2001

[Evaluation of inferior wall myocardial infarctions by ECG using 5 unipolar retrocardial leads in addition to the standard 12 leads].

OBJECTIVE: This study was planned to evaluate the change patterns in 5 unipolar retrocardial leads (taken from back) in addition to standard 12 leads ECG in subjects with inferior myocardial infarction (IMI) and to see whether these patterns, if there are any, could be useful to assess the cases with IMI. METHODS: A hundred forty two cases were included to study. At first, in order to determine the normal ECG configurations in 5 unipolar retrocardial leads 30 subjects with normal standard 12 lead ECG and normal physical findings were studied. The normal configurations of retrocardial leads were then determined and retrocardial leads were expressed as RE1-5. Later, 60 subjects with chronic IMI and 52 with acute IMI were evaluated. RESULTS: The QS or Qr in VRE1, QR or qR in VRE2, qRs in VRE5 and transitional patterns in VRE3-4 were accepted as normal configurations of the retrocardial leads. Pre- and retrocardial derivations of 60 cases who had old IMI were normal in 21(35%) cases. There were pathologic Q waves in VRE1-VRE2 leads in 5 (8.3%) cases, in VRE3-VRE4 leads in 11(18.3%) cases, in V5-V6 and VRE5 leads in 3 (5%) cases, in V5-V6 and VRE1-VRE5 leads in 12 (20%) cases, in VRE1-VRE4 leads in 8 (13.3%) cases. Pre- and retrocardial leads of 52 cases with acute IMI were normal in 10 (19.5%) cases. There were ST segment depression in V1-V2 and ST segment elevation in VRE-VRE2 leads in 4 (7.6%) cases, ST segment depressions in V3-V4 derivations and ST segment elevations in VRE3-VRE4 leads in 5 (9.6%) cases, ST segment depression in V2-V6, VRE5 leads and ST segment elevation in VRE1-VRE4 leads in 8 (15.3%) cases, ST segment depression in V1-V4 leads and ST segment elevations in RE1-VRE4 in 12 (23%) cases. ST segment depression in V1-V4 leads and ST segment elevation in V5-V6 and VRE1-VRE5 were found in 13 (25%) cases. CONCLUSION: According to ECG findings which were taken from pre- and retrocardial leads of IMI cases were classified as follows; ST elevation or Q wave or both in DII, DIII, AVF(-)+; 1--Pre and retrocardial leads are normal; 2--ST depression in V1 (sometimes ST elevation if there is right ventricular involvement)--V2, ST elevation or Q wave or both in VRE1-VRE2); 3--ST depression in V3-V4 and ST elevation or Q wave or both in VRE3-VRE4); 4--ST depression in V1-V4 and ST elevation or Q wave or both in VRE1-VRE4); 5--ST depression in V1-V4, ST elevation or Q wave or both inV5-V6 and ST elevation or Q wave or both in VRE1-VRE5); 6--ST depression in V1-V6 and ST elevation or Q wave or both in VRE1-VRE4 and ST depression in VRE5). It is concluded that, in addition to standard 12 lead ECG, retrocardial 5 leads could be recorded and interpreted easily. ECG patterns taken from 5 unipolar retrocardial leads in patients with IMI are not homogeneous. Different groups of ECG findings in certain leads were determined. Further investigations to clarify these different groups ECG findings are needed and these might bring a new approach to assess the subjects with IMI.

Adult↗
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↗
PubMed2005

A noninvasive isotopic approach to estimate the bone lead contribution to blood in children: implications for assessing the efficacy of lead abatement.

Lead hazard control measures to reduce children's exposure to household lead sources often result in only limited reductions in blood lead levels. This may be due to incomplete remediation of lead sources and/or to the remobilization of lead stores from bone, which may act as an endogenous lead source that buffers reductions in blood lead levels. Here we present a noninvasive isotopic approach to estimate the magnitude of the bone lead contribution to blood in children following household lead remediation. In this approach, lead isotopic ratios of a child's blood and 5-day fecal samples are determined before and after a household intervention aimed at reducing the child's lead intake. The bone lead contribution to blood is estimated from a system of mass balance equations of lead concentrations and isotopic compositions in blood at the different times of sample collection. The utility of this method is illustrated with three cases of children with blood lead levels in the range of 18-29 microg/dL. In all three cases, the release of lead from bone supported a substantial fraction of the measured blood lead level postintervention, up to 96% in one case. In general, the lead isotopic compositions of feces matched or were within the range of the lead isotopic compositions of the household dusts with lead loadings exceeding U.S. Environmental Protection Agency action levels. This isotopic agreement underscores the utility of lead isotopic measurements of feces to identify household sources of lead exposure. Results from this limited number of cases support the hypothesis that the release of bone lead into blood may substantially buffer the decrease in blood lead levels expected from the reduction in lead intake.

Bone and Bones↗