Search

In this study, the authors related blood lead concentrations to Apgar scores, birth weight, gestational age, small-for-gestational age, and hypertension in pregnancy (HIP)/toxemia. Data and blood were collected 4 times during pregnancy from 705 women, aged 12-34 yr. Blood lead concentrations, measured by atomic absorption spectrophotometry, were related to reproductive outcomes, abstracted from medical records. Average blood lead concentrations were 1.2 [micro]g/dl (standard error = [+ or -] 0.03). Maternal blood lead concentrations were related significantly to HIP/toxemia--before and after adjusting for age, calcium intake, and race/ethnicity (p < .03). Longitudinal regression analyses revealed that blood lead concentrations in women with HIP/toxemia changed by 0.02 [micro]g/dl for every 0.01 [micro]g/dl change in women without HIP/toxemia. Maternal blood lead concentration and its change were not significantly associated with other reproductive outcomes. Low levels of maternal blood lead concentrations were significantly associated with HIP/toxemia., LEAD is of the more extensively studied reproductive toxicants. (1) Lead readily crosses the placenta; therefore, it may cause fetal and maternal adverse outcomes, including low birth weight, preterm delivery, [...]

Increased bone turnover in pregnant women could release lead into their breast milk after birth, according to a study of 45 women. Lead is usually stored in bones, and can remain there for up to 20 years. However, the small amounts of lead in breast milk will probably have a minimal impact on the baby.

Many HIV-infected people may develop nutritional deficiencies that can be prevented with vitamin supplements. Researchers measured the level of 22 nutrients in blood samples from 64 HIV-positive people and 33 healthy HIV-negative people (the control group). Nineteen of the HIV-positive participants had AIDS, 18 had symptoms of HIV infection and 27 were asymptomatic. Compared to the control group, HIV-positive patients had lower blood levels of antioxidants such as vitamins A, C and E as well as carotene and glutathione. They also had lower magnesium levels. However, they were more likely to have high blood levels of choline and niacin. Those who were taking vitamins had higher levels of B vitamins and vitamin C than those who were not. However, 29% of those who took vitamins still had low blood levels of at least one antioxidant. AIDS patients were more likely to have low blood antioxidant levels than those who were asymptomatic.

A placebo-controlled double-blind trial of the effects of daily micronutrient supplements on circulating vitamin and trace metal concentrations and delayed-hypersensitivity skin test (DHST) responses was conducted. Subjects, aged 59-85 y, were randomly assigned to placebo (n = 27) or micronutrient (n = 29) treatment groups. DHST and circulating concentrations of nine micronutrients were measured before and after 6 and 12 mo of micronutrient ingestion. For the micronutrient group, there were statistically significant increases at 6 and/or 12 mo in the mean serum concentrations of ascorbate, [beta]-carotene, folate, vitamin B-6, and [alpha]-tocopherol. There was a significant increase at 12 mo in the number of subjects in the placebo group with one or more low concentrations. DHST responses to a panel of seven recall antigens were significantly increased at 12 mo in the micronutrient group but not the placebo group. This study demonstrates that daily supplementation with low-to-moderate doses of micronutrients can prevent low concentrations of some micronutrients and can improve DHST responses in healthy, independently living older adults. Am J Clin Nutr 1994;60:437-47.

This study was conducted to determine the effects of lead on Sertoli cell function. Androgen binding protein and inhibin in testicular fluids and classical parameters of the hypothalamic-pituitary-gonadal axis were measured in adult male rats. For 10 wk, the rats were given water that contained 0.05%, 0.1%, 0.5%, and 1% lead acetate. Serum follicle-stimulating hormone, luteinizing hormone, and testosterone levels in all animals that ingested lead were normal at the middle and end of the experiment, as was the pituitary content of follicle-stimulating hormone and luteinizing hormone. Histologic examination revealed no disruption of spermatogenesis. Distribution of androgen binding protein in serum, seminiferous tubular fluid, and interstitial fluid was normal, as was the concentration of inhibin in interstitial fluid and seminiferous tubular fluid. However, a significant increase in epididymal androgen binding protein level and a decrease in seminal vesicle weight were observed in rats that ingested water containing 1% lead acetate. These results suggest that the effect of lead on spermatogenesis is not marked in adult Sprague Dawley rats, nor does Sertoli cell function appear to be affected adversely. Lead has been reported to alter in vitro metabolic function of Sertoli cells obtained from 16- to 21-d-old Sprague Dawley rats, and the Sertoli cells of juvenile animals may be more susceptible to lead than those of adult animals. The significant decrease in seminal vesicle weight and the abnormal epididymal androgen binding protein content indicate that lead could affect the male reproductive function in Sprague Dawley rats via its action on male accessory organs., THE ADVERSE EFFECTS of permissible low-level occupational lead exposure on male reproductive function remain controversial. Difficulties in assessing total lead burden via occupational histories or serum lead levels, and the [...]

After a routine blood testing, a local pediatrician discovered that a 13-month-old boy had an elevated blood lead level (BLL) of 57 [micro]g/dL. Since the baby was mostly breast-fed, the pediatrician did a blood test on the mother, and the result showed a BLL of 85 [micro]g/dL As the mother denied any history of pica behavior, the pediatrician suspected a source of lead to which the entire family might have been exposed and tested the father's BLL. The results showed a BLL of 95 [micro]g/dL, and the pediatrician informed the poison center. The subsequent epidemiological investigation revealed that the parents had used a product called Sindoor for food coloring. Laboratory analyses showed that the product contains more than 57.8% of acid-extractable lead by weight. Given the extremely high content of Pb in this product, Sindoor poses a serious risk of lead poisoning if it is used for food coloring. Keywords Lead poisoning; Food coloring; Sindoor, INTRODUCTION While lead-based paint and lead in dust are still the most common causes for elevated blood lead levels (BLLs) in children, other unusual sources of lead may also pose [...]

Background: Immune function is highly dependent on nutritional status because the large mass and high rate of cellular turnover of the immune system make it a major user of nutrients. Furthermore, nutrient requirements may be increased during acute and chronic infections, including HIV-1 infection. Objective: The current study was designed to assess relations among HIV-1 progression and 11 nutritional and demographic variables. Design: The participants were 106 HIV-infected outpatients and 29 uninfected control subjects (n = 89 men and 46 women; age range: 35-57 y). The HIV-infected subjects represented a broad range of disease progression. Results: We found lower concentrations of plasma and erythrocyte magnesium and of erythrocyte reduced glutathione beginning early in the course of HIV-1 infection. Significantly decreased hematocrit and increased serum copper concentration developed only late in the course of the disease. Statistically significant univariate associations were found between the [CD4.sup.+] T lymphocyte count and hematocrit, plasma magnesium concentration, and plasma zinc concentration. The lowest erythrocyte magnesium concentrations occurred in HIV-infected subjects who consumed alcoholic beverages. Independent variables that were significant joint predictors of [CD4.sup.+] cell count in multiple regression analyses were hematocrit and plasma free choline and zinc concentrations. These 3 factors together explained 43% of the variability in [CD4.sup.+] cell counts. Conclusion: The results provide evidence that compromised nutritional and antioxidant status begin early in the course of HIV-1 infection and may contribute to disease progression. Am J Clin Nutr 2000;72:809-15. KEY WORDS HIV-1 infection, HIV infection, AIDS, HIV progression, glutathione, magnesium, hematocrit, choline, copper, zinc, ethanol, alcohol, antioxidants

Objectives:Little is known about the relationship between the renal and gastrointestinal excretion of potassium in humans. This information is important in light of strong associations of potassium intake with hypertension and occlusive stroke.Methods:We determined the relationship between fecal and urinary excretion of potassium under both fixed and variable potassium intakes using our unpublished archival data and published data of others. Twenty-five subjects were evaluated.Results:On a fixed, low oral potassium intake (61.2 ± 4.7 mmol/day; mean ± SD), there was an inverse relationship between fecal and urinary potassium excretion (r = −0.66, p = 0.040). In studies in which potassium intake varied between 61–135 mmol/day, fecal and urinary potassium excretions were positively correlated (r = 0.58, p = 0.024). Considerable within-and-between-subject variation was observed in the relationship between fecal and urinary potassium excretion.Conclusions:Inter-individual variation in fecal potassium excretion may arise from both variation in dietary potassium intake and intrinsic individual differences in the renal versus gastrointestinal handling of potassium.

The major cause of neonatal mortality and morbidity is preterm delivery in general (< 37 completed weeks), and especially very preterm delivery (< 32 completed weeks). The objective of this study is to determine if either thyroid hormonal dysfunction and/or the presence of thyroid autoantibodies in the mother are associated with an increased risk of preterm and/or very preterm delivery. Data were collected prospectively and analyzed as a nested-case control study. There were 953 delivered gravidas enrolled between 1996 and 2002. Samples were collected at entry to care and stored at –70°C. Cases included all women with preterm delivery (n= 124). Controls (n= 124) were randomly selected from among the 829 women who delivered at term (> 37 completed weeks). All samples were assessed for thyroid stimulating hormone, thyroperoxidase antibody, and thyroglobulin antibody. Gravidas with high thyrotropin (TSH) levels had a greater than threefold increase in risk of very preterm delivery. In some analyses, gravidas who tested positive for thyroglobulin antibody at entry to prenatal care also had a better than twofold increased risk of very preterm delivery. There were no significant associations between TSH level or thyroglobulin antibody positivity and the risk of moderately preterm delivery.

Three choroidal melanomas were detected in a 2.5-year period in a small community of 3,592 persons. This small cluster represented an incidence about 20 times that expected (P = .0006). The community has an isolated water supply and very little industry. We determined the incidence of cancer in this and two adjacent communities and found no other unexpectedly high incidence. The three patients had no common exposures. Analyses of air and water from the involved community by mass spectroscopy, chromatography, and Ames (mutagenicity) tests were noncontributory. Nine of 60 mice given community water after weaning developed lens opacities eight to 16 months later; electron microscopy showed an abnormal monolayer of cells on the outer surface of the anterior lens capsule. The genesis of this monolayer was not clear. None of the 30 controls showed such lesions

Background. Glutaraldehyde pretreatment of bioprosthetic heart valves is the major pathogenic factor in their calcific degeneration. This comparative study investigates the merit of the No-React aldehyde detoxification process as an alternative modifier of xenograft tissues.Methods. Glutaraldehyde- and No-React-pretreated porcine aortic valve cusps were implanted subcutaneously in 6-week-old rats (n = 20). At 3, 6, and 14 weeks, randomly selected animals were sacrificed and the explants underwent mineral and morphologic analyses. Glutaraldehyde- and No-React-treated bovine pericardium and porcine aortic valve cusp were incubated in fibroblast cell culture plates. Cell viability was observed under reversed microscope at 6, 24, 48, and 96 hours. Erythrosin B dye exclusion test was used to validate percent cell death.Results. Pretreatment with No-React significantly inhibited calcification of aortic cusp subcutaneous implants throughout the 14-week period (mean tissue Ca2+ content = 1.3 ± 0.7 μg/mg at 14 weeks.) Glutaraldehyde-treated cusps underwent protracted calcification (Ca2+ content = 190.6 ± 89.5 μg/mg; p < 0.01). Morphologic findings correlated with mineral analyses. One-hundred percent of fibroblast cells survived in the presence of No-React-treated tissue, with a growth pattern indistinguishable from control cell culture (ie, in the presence of no tissue). The cells incubated with glutaraldehyde-treated tissue showed signs of nonviability by 6 hours, with 100% cell death by 48 hours. Dye exclusion tests validated these findings.Conclusions. The No-React detoxification process completely abolishes the cytotoxicity of the xenograft tissue and inhibits calcific degeneration.

Thirty-six weanling male Sprague-Dawley rats were randomly assigned to one of four treatment groups: 1) SE rats received 4.0 ppm selenium as sodium selenite in drinking water containing 1% sucrose; 2) 15MO rats received 15 ppm molybdenum as sodium molybdate in the drinking water; 3) 45MO rats received 45 ppm molybdenum in their water; and 4) CON rats received distilled-deionized water containing only 1% sucrose. The esophageal carcinogen methylbenzylnitrosamine (MBN) was administered intragastrically in 10% ethanol twice per week for 5 wk at a dose of 2.5 mg/kg. MBN dosing was followed by a 12-wk period for tumor promotion. After this, heart, lungs, liver, spleen, kidneys, testes, tibia, muscle, brain and esophagus were excised. The esophagus was examined for MBN-induced lesions using dissecting and light microscopes and a portion was analyzed for Se. All other tissues were analyzed for Cu, Zn, Fe and Mn; some were also analyzed for Se and Mo. Most rats had precancerous lesions, and all rats had papillomas. There were no significant differences among the four treatment groups in the incidence and number per rat of precancerous lesions or gross papillomas. The SE group had significantly fewer carcinomas per rat than the other groups. The SE rats exhibited a number of significant differences in tissue trace element concentrations; in particular, they had higher Fe concentrations in heart, kidney and spleen than the other rats. The SE rats also had significantly greater urinary excretion of Mn and Fe, and excretion of the latter elements was significantly correlated with that of selenium. It is possible that the antitumor activity of Se is related to its effects of the metabolism of other essential trace elements.

• A child with hypogammaglobulinemia and intractable diarrhea underwent parenteral alimentation for five months. A clinical syndrome of acrodermatitis enteropathica subsequently developed associated with a depression in thymus-dependent lymphocyte (T cell) numbers, abnormal T-cell mitogen-induced blast transformation, and anergy to skin test antigens. Plasma zinc levels were found to be abnormally low. Zinc therapy resulted in dramatic resolution of the clinical manifestations of acrodermatitis enteropathica. Cell-mediated immune function was also restored to normal, suggesting an important role for zinc and possibly other trace metals in cellular immune responses.(Am J Dis Child 133:915-918, 1979)

To determine whether zinc has a specific role on weight gain and intestinal disaccharidase activity, 42 male Sprague-Dawley rats were assigned to one of seven groups (n6 each). These were a baseline control group (O) that was killed to analyze initial intestinal disaccharidase (sucrase and maltase) activity, a second group (A) fed a zinc-deficient diet for 1 week, a third group (B) pair-fed control for A, a fourth group (C) fed a zinc-deficient diet for 2 weeks, a fifth group (D) pair-fed control for C, a sixth group (E) fed a zinc-deficient diet for 3 weeks, and a seventh group (F) pair-fed control for E. All experimental groups received distilled deionized drinking water, whereas control groups received zinc-enriched (25 μg of zinc/ml) distilled deionized water. Water was given ad libitum. After killing, the mucosa of the proximal half of the small intestine was analyzed for protein and disaccharidase activity, and liver, kidney, and heart were analyzed for zinc concentration. Protein content and disaccharidase activity of the jejunal mucosa in the experiment and control groups did not differ significantly. However, animals on the zinc-deficient diet demonstrated mildly depressed growth rates that were proportional to the duration of the experiment, and significantly lower zinc concentration in the kidney in the experimental groups. The data indicate that administration of a zinc-deficient diet for up to 3 weeks did not result in significant changes in intestinal mucosa protein content or in disaccharidase activity.

To determine whether zinc has a specific role on weight gain and intestinal disaccharidase activity, 42 male Sprague-Dawley rats were assigned to one of seven groups (n=6 each). These were a baseline control group (O) that was killed to analyze initial intestinal disaccharidase (sucrase and maltase) activity, a second group (A) fed a zinc-deficient diet for 1 week, a third group (B) pair-fed control for A, a fourth group (C) fed a zinc-deficient diet for 2 weeks, a fifth group (D) pair-fed control for C, a sixth group (E) fed a zinc-deficient diet for 3 weeks, and a seventh group (F) pair-fed control for E. All experimental groups received distilled deionized drinking water, whereas control groups received zinc-enriched (25 µg of zinc/ml) distilled deionized water. Water was given ad libitum. After killing, the mucosa of the proximal half of the small intestine was analyzed for protein and disaccharidase activity, and liver, kidney, and heart were analyzed for zinc concentration. Protein content and disaccharidase activity of the jejunal mucosa in the experiment and control groups did not differ significantly. However, animals on the zinc-deficient diet demonstrated mildly depressed growth rates that were proportional to the duration of the experiment, and significantly lower zinc concentration in the kidney in the experimental groups. The data indicate that administration of a zinc-deficient diet for up to 3 weeks did not result in significant changes in intestinal mucosa protein content or in disaccharidase activity.

Cimetidine is a histamine H2-receptor antagonist that is used in the treatment of patients with gastric and duodenal ulcers and other hypersecretory conditions. This drug has a structure that suggests that it could act as a chelating agent. To examine its effects on trace metal and mineral metabolism, 38 weanling male Sprague-Dawley rats were assigned to one of five treatment groups. These were a high dose [(HD) 1750 mg/(kg·d)] group, HD pair-fed control (HDPF) group, intermediate dose [(ID) 875 mg/(kg·d)] group, ID pair-fed (IDPF) group and low dose [(LD) 87.5 mg/kg·d)] group. In a separate experiment, 20 female Sprague-Dawley rats were assigned to one of two treatment groups: a high dose cimetidine group [(HDFem) 1750 mg/kg·d)] and a pair-fed control group (PFFem). Cimetidine was administered intragastrically four times per week for 5 wk. Significant differences (P< 0.05) found among groups for the male rats studied included higher plasma copper in the HD and the ID groups, higher plasma sodium, liver copper, heart calcium and heart zinc in the HD group and a lower percentage of fecal excretion of all the divalent metals studied in the HD and the ID groups than in their pair-fed controls. Pathologic examination of the liver revealed extensive fatty infiltration of liver cells, liver cell necrosis and disrupture of liver lobular architecture in the HD group. Cimetidine-dosed females had higher zinc in heart and plasma, higher copper in heart, kidney, liver, jejunum, ileum and uterus, higher manganese in stomach and ileum, lower iron in kidney and liver, lower kidney calcium and higher stomach calcium and lower liver magnesium compared with their pair-fed controls. Levels of liver and kidney metallothionein in the two groups were comparable. Male and female rats receiving high dose cimetidine experienced significant changes in tissue concentrations of some of the trace metals and minerals studied.

Calcific degeneration is the most frequent cause of clinical dysfunction of glutaraldehyde (GA)-pretreated bioprosthetic heart valves. The No-React (NR) process has been shown to be a promising anticalcification treatment. In this comparative study, our objective was to delineate the advantages of the NR treatment over GA.

Forty-six female Sprague-Dawley rats (170–200 g) were randomly assigned to one of six treatment groups receiving 0.1, 5.0, or 25.0 ppm dietary vanadium with either normal (0.13 mEq/g) or high (1.82 mEq/g) dietary potassium. Supplemental vanadium was administered as sodium metavanadate. These diets were fed for 2 weeks, and all feces and urine collected. At the end of the treatment period, brain, liver, renal cortex and medulla, whole blood, and plasma were obtained and analyzed for vanadium by atomic absorption spectrophotometry, as were the urine and feces samples. Tissue vanadium concentrations increased significantly (P< 0.00001) with increasing food vanadium content, but were not affected by dietary potassium in spite of the polyuria induced in animals on the high potassium diets. The highest vanadium concentrations were found in the renal cortex and the lowest in the brain. Although urinary vanadium excretion was higher in animals fed the high potassium diets, a relatively small percentage of ingested vanadium was excreted in the urine. Rats fed diets containing no supplementa sodium metavanadate (0.1 ppm vanadium) were in negative vanadium balance, but their growth was not inhibited. Animals receiving 5.0 and 25.0 ppm vanadium diets retained 39.7 ± 18.5% of ingested vanadium and excreted 59.1 ± 18.8% of ingested vanadium in the feces. These values indicate greater absorption and retention of ingested vanadium than found in previously reported investigations.

We studied the effects of dietary calcium on kidney, femur, testis, liver, heart and brain concentrations of lead, magnesium, iron, copper, calcium and zinc in rats exposed to lead for 1 y. Renal levels of the 28,000 Da, vitamin D-dependent, calcium-binding protein calbindin-D28K were also measured. Seventy-two weanling male Sprague-Dawley rats were randomly assigned to one of nine treatment groups. Rats were fed diets containing 0.1, 0.5 or 2.5% Ca for 52 wk and were simultaneously given either 0, 50 or 100 mg lead/L in their drinking water. Rats fed the 0.1% Ca diet had organ lead concentrations that were two- to 20-fold greater than the corresponding animals fed 0.5% Ca. Rats fed diets containing 2.5% Ca had the lowest organ lead concentrations. Despite substantial effects of diet Ca on organ lead concentrations, Ca did not significantly influence concentrations of most other divalent metals studied with the exception of kidney calcium and magnesium, testis iron, plasma ionic calcium and magnesium, and several femur metals. Kidney calcium concentrations were lower in rats fed 2.5% Ca diets than in those fed 0.1 or 0.5% Ca diets. For rats not given lead, renal calbindin concentrations were highest in rats fed 0.1% Ca, and lowest in rats fed 2.5% Ca. Lead inhibited an increase in renal calbindin in the rats fed 0.1% Ca, but paradoxically increased renal calbindin levels in animals fed 2.5% Ca.

Sweat volume and ionic composition depend to a large extent upon the cytosolic free calcium level in secretory sweat cells and sodium and potassium transport in the reabsorptive sweat duct. Since essential hypertension and its treatment with antihypertensive drugs is likely to be associated with altered cellular ionic regulation, the objective of this research was to explore sweat formation and sweat parameters in hypertensive and normotensive subjects.

We examined the potential of increased Ca in the diet to modify the effects of Pb on tissue metal concentrations, blood pressure and the incidence of renal tumors. We randomly assigned 48, 5-wk-old male Wistar rats to one of six treatment groups. They were fed a low (0.2%) or high (4.0%) Ca diet for 31 wk and given 0, 1.0 or 100 µg Pb/mL in drinking water. In the low Ca groups, increasing concentrations of Pb produced graded increases in mean blood pressure. Rats receiving 4.0% Ca had higher mean blood pressures than the animals fed the 0.2% Ca diet. The 4.0% Ca diet also caused renal and urinary bladder stones to develop in some rats. The high Ca diet did not prevent dose-dependent increases in tissue Pb accumulation, but it caused significant decreases in kidney Cu, femur Mg and Fe in kidney, liver and testis. Femur Mg and Fe and liver Fe concentrations were lowest in rats receiving 4.0% Ca and 100 µg Pb/mL. Precancerous and cancerous renal lesions occurred to the greatest extent in the rats receiving 100 µg Pb/mL and the high Ca diet. These results suggest that high dietary Ca does not protect against Pb-induced increases in blood pressure or Pb accumulation in tissues and may often produce nephrocalcinosis. In addition, high dietary Ca in the presence of Pb may increase the incidence of renal tumors.

Excessive and dangerous lead contents have recently been found in a number of unexpected sources, including colored printing inks1 and toothpaste.2 The pervasiveness of lead contamination suggested an examination of the lead content of aspirin. Aspirin was chosen because of its high rate of consumption in the United States, because of its ready availability as a nonprescription drug, and because of the possibilities for lead contamination during its manufacture. Dust in the manufacturing plants or corrosion of pipes and vessels with the sulfuric or acetic acids used could result in lead contamination of aspirin.Surprisingly, the United States Pharmacopeia specifies that aspirin may contain as much as 10 ppm of lead.3 This represents a daily intake of 50μg of lead if ten ½-gm tablets are taken daily. This would be a substantial amount of ingested lead, especially when added to the 200μg to 300μg ingested daily from

To the Editor.—I read with considerable interest the article by Dr. Barltrop in the February issue of the Journal (127:165, 1974). The article appears to be an excellent evaluation of current thinking about environmental sources of lead. However, the author states that the very diversity of the studies in progress has a negative aspect in that it tends to divert attention from the continuing problems of lead-based paint in the home. Lead paint remains the major lead hazard for children and is virtually the only source of lead associated with symptomatic poisoning.Some very recently available evidence suggests that other sources of lead besides paint chips may contribute significantly to the daily ingestion of the 1,000μg of lead that Barltrop indicates is sufficient to cause symptomatic lead poisoning if ingestion continues for several months.Colored printed matter (especially reds, yellows, oranges, and greens) has recently been shown to contain