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Biomedical subjects

K R Mahaffey

Publications and source records attributed to K R Mahaffey.

At least 37 records · Page 2Linked to original sources
PubMed1990

Environmental lead toxicity: nutrition as a component of intervention.

The influence of nutritional status on susceptibility to the toxicity of lead is discussed. Emphasis is given to dietary factors of substantial clinical importance. Subtle changes in susceptibility are difficult to evaluate under conditions of overwhelming lead exposure. It is clear that subtle effects of lead exposure on neurobehavioral and cognitive development are a major concern. The role of nutrition is considered to be an adjunct to reduction of environmental lead exposure, which is the primary means of reducing adverse health effects of lead. Nutrition should be evaluated as a component of strategies to address this broad societal issue.

Calcium, Dietary↗
PubMed1986

Association of erythrocyte protoporphyrin with blood lead level and iron status in the second National Health and Nutrition Examination Survey, 1976-1980.

Both iron status and body burden of lead influence heme biosynthesis. Measurement of protoporphyrin IX in the circulating erythrocyte (EP) has been used to index the extent of lead exposure and iron deficiency. The association of iron status and blood lead level with the level of EP in whole blood for persons ages 6 months through 74 years in the general U.S. population has been investigated by using data obtained in the second National Health and Nutrition Examination Survey (NHANES II). Iron status was defined as a function of percentage transferrin saturation (%TS) and total iron-binding capacity (TIBC). Both low iron status (%TS less than or equal to 16.0 or TIBC greater than or equal to 450 micrograms/dl serum) and elevated blood lead levels (greater than or equal to 30 micrograms/dl) were associated with increased EP concentrations. The analysis of the proportions of persons in the U.S. population with EP levels above the 95th percentile (30 micrograms EP/dl of whole blood in the NHANES II data) support the concern that iron status has considerable influence on interpretation of EP levels recommended for use in screening programs aimed at identifying children with lead toxicity. With screening techniques based on EP only, currently used in various public health programs, a considerable number of children with blood lead levels of greater than or equal to 30 and less than or equal to 50 micrograms/dl are not referred for further diagnostic evaluation.

Adolescent↗
PubMed1986

Blood lead levels and dietary calcium intake in 1- to 11-year-old children: the Second National Health and Nutrition Examination Survey, 1976 to 1980.

Whether, and to what degree, dietary calcium is inversely associated with blood lead levels was examined in 2,926 black and white children, 1 to 11 years of age, from the Second National Health and Nutrition Examination Survey (NHANES II). Blood lead levels were significantly higher in black than in white children, whereas white children had significantly higher dietary calcium intake (P less than .0001). Using covariance analysis and multiple regression analysis, determinants of blood lead levels were assessed as follows. The dependent variable was log10 lead, with independent variables age, sex, race, height, Quetelet index, dietary intake of calcium, phosphorous, fat, carbohydrate, and calories, community size index, poverty index ratio, geographic region, urbanization index, and all two-way interactions of the preceding. In the multiple regression analysis, the following independent variables were significant, P less than .05. Race (black) and sex (male) were positively associated with blood lead level (P less than .0001 for both). The lower the family income and the more urban the family residence, the higher were the blood lead levels (P less than .0001, less than .008, respectively). A significant independent inverse association of blood lead levels with year of examination was noted, reflecting a downward secular trend in blood lead levels. Height was inversely associated with blood lead level (P less than .0001). Dietary calcium intake was also inversely associated with blood lead level (P = .028). Dietary intake of phosphorous, fat, carbohydrate, and total calories were not significantly associated with blood lead levels. The most direct strategy for prevention of childhood lead poisoning involves primary prevention to reduce exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Black People↗
PubMed1983

Biotoxicity of lead: influence of various factors.

Environmental sources of lead are multiple, and a number of factors influence their toxicity. However, with the exception of tetramethyl and tetraethyl lead, the particular compound of lead seems to have relatively little influence on toxicity compared with the particle size of the source and the route and frequency of exposure. Susceptibility to lead toxicity is greater among immature animals and very young children because of their higher levels of lead ingestion, greater absorption from the gastrointestinal tract, higher percent lead retention in tissues, and greater reactivity of organs, particularly the central nervous system. Marginal nutritional status also increases susceptibility to lead toxicity. Dietary factors influencing toxicity of lead include total calories, calcium, iron, zinc, fat, ascorbic acid, and protein. Although vitamin D, specifically the metabolite 1,25-dihydroxycholecalciferol, increases lead absorption in vitamin D-deficient animals, clinical studies have shown that lead-burdened children have reduced rather than elevated plasma 1,25-dihydroxycholecalciferol levels. Bioavailability of lead, as shown by tissue lead concentrations, is not always an adequate predictor of lead toxicity. For example, concurrent exposure to cadmium results in higher toxicity of lead to the hematopoietic system, but lowers tissue lead levels substantially. Low dietary calcium increases the total body burden of lead but disproportionately increases the deposition of lead in nonosseous tissues.

Age Factors↗
PubMed1982

National estimates of blood lead levels: United States, 1976-1980: association with selected demographic and socioeconomic factors.

Data from the second National Health Nutrition Examination Survey showed that 22 per cent of persons six months through 75 years old had blood lead levels under 10 micrograms per deciliter; 1.9 per cent had elevated levels (greater than or equal to 30 micrograms per deciliter [greater than or equal to 1.45 mumol per liter]). Among children six months through five years old the prevalence of elevated levels was significantly higher (4 per cent) than previously predicted on the basis of fewer data. The prevalence of elevated lead levels was 12.2 per cent in black children and 2.0 per cent in white children. Mean levels of blood lead were higher in blacks than white among children and adults, among young children living in urban and rural areas, and among members of low-income, moderate-income, and higher-income families. These racial contrasts may reflect different lead exposure or absorption (or both). Young children from families (both white and black) whose incomes were under $6,000 had a significantly higher prevalence of elevated lead levels than those from households with incomes of $6,000 or more.

Adolescent↗
PubMed1982

Association between age, blood lead concentration, and serum 1,25-dihydroxycholecalciferol levels in children.

Serum levels of 1,25-dihydroxycholecalciferol (1,25-CC), the form of vitamin D active in stimulating intestinal absorption of calcium, phosphorus, and lead, were determined in 177 human subjects ages 1 to 16 yr. Significant negative association (r = -0.88) was observed between serum 1.25-CC levels and blood lead concentrations over the entire range of blood lead levels, 12 to 120 micrograms/dl. Adolescents ages 11 to 16 yr had serum 1,25-CC levels higher than those observed among children 10 yr old or younger. No effect of sex or season on serum 1,25-CC level was observed. When the 1,25-CC values for children with blood lead concentrations greater than 30 micrograms/dl were excluded from the analysis, no significant effect of geographic location on 1,25-CC levels was observed.

Adolescent↗
PubMed1982

Effect of lead acetate on rats fed diets containing low levels of folic acid.

Nutritional factors such as deficiencies of calcium, iron, and protein alter susceptibility to the toxic effects of lead. While the suggestion has been made that vitamins may also influence lead toxicity, possible interactions have not been well documented. The present studies were performed to determine if a dietary deficiency of folic acid enhances the susceptibility to rats of the toxic effects of lead acetate. Lead exposure during the development of folate deficiency resulted in alterations in two of the parameters diagnostic of the individual conditions. Decreases in erythrocyte mean corpuscular volume (MCV) occur during lead poisoning, while increases occur during the development of folate deficiency. In the present study, significant reductions in MCV were observed in both the control + lead and in the low folate + lead groups. The increased MCV characteristic of folate deficiency was prevented by the concomitant lead exposure. Elevations in free erythrocyte protoporphyrin (FEP) levels are characteristic of lead intoxication; in contrast, FEP levels decline during folate deficiency. In the present study, FEP levels were significantly elevated only in the control + lead group. Values in the low folate + lead group were intermediate between those of the control and the control + lead groups, but did not differ significantly from those in the low folate group. The expected lead-induced elevation in FEP levels was diminished by the reduced erythropoiesis characteristic of folate deficiency.

Aminolevulinic Acid↗
PubMed1981

Effect of lead ingestion on functions of vitamin D and its metabolites.

A study of the effect of ingestion of lead on the metabolism and function of vitamin D was carried out in rats fed diets varying in calcium and phosphorus content. The ingestion of 0.82% lead as lead acetate suppressed plasma levels of 1,25-dihydroxycholecalciferol in rats fed either a low phosphorus or a low calcium diet while it had no effect on this parameter in rats fet either a high calcium diet or a normal phosphorus diet. Most important, the ingestion of lead totally blocked the intestinal calcium transport response to cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. On the other hand, the ingestion of lead acetate had no influence on the mobilization of calcium from bone, the elevation of serum inorganic phosphorus and in the mineralization of rachitic bone in the same animals. Thus by the feeding of 0.82% lead on the intestinal responses to vitamin D and its metabolites was greatest in animals fed a low calcium or a low phosphorus diet, it was present with all diets tested.

Animals↗
PubMed1981

Comparative toxicity and tissue distribution of lead acetate in weanling and adult rats.

The relative toxicity of low doses of lead acetate provided steadily in drinking water or by mouth once per week was studied in weanling and adult rats. Free erythrocyte protoporphyrin and urinary delta-aminolevulinic acid levels were measured, as well as lead levels in blood and kidney. The accumulation of lead in brain tissue and in bone (femur) was measured to determine the effect of age and schedule of administration on tissue distribution and retention of lead. Total intakes of lead during the 60-week experimental period were: weanling and adult rats exposed to drinking water supplemented with 200 microgram of lead acetate/ml: 127 +/- 10 mg and 160 +/- 16 mg, respectively; weanling and adult rats dosed with lead acetate orally once per week: 132 mg and 161 mg, respectively. Increased toxic effects of lead in the weanling animals were apparent in most of the parameters measured (urinary delta-aminolevulinic acid and blood, brain, femur and kidney lead levels). This pattern was observed in weanling rats exposed to lead steadily through drinking water or dosed orally with an equivalent quantity of lead once per week. Lead levels in blood were highly correlated with the accumulation of lead in brain, femur, and kidney tissue in both groups of weanling rats. In adult rats, significant correlations between blood lead and kidney lead and between blood lead and femur lead were found only in the rats receiving lead steadily in drinking water.

Aging↗
PubMed1981

Concurrent exposure to lead, cadmium, and arsenic. Effects on toxicity and tissue metal concentrations in the rat.

Male rats were exposed to dietary Pb (200 ppm), Cd (50 ppm), or As (50 ppm) as arsenate either alone or in combination for 10 weeks using a 2 x 2 x 2 factorial design. Cd and As reduced weight gain even when differences in food intake were taken into account, and administration of both Cd and As depressed weight gain more than did either metal alone. Pb did not adversely affect food consumption or weight gain. Increased RBCs were observed after administration of Pb, Cd, or As, and more cells were observed when two or three metals were concomitantly administered. Despite increased numbers of circulating RBCs, hemoglobin and hematocrit were reduced, especially with the Pb-Cd combination. Analysis of blood chemistries showed normal ranges for blood urea nitrogen, creatinine, cholesterol, calcium, albumin, total protein, and bilirubin. Uric acid was increased by Pb, but not by Cd or As. SGOT activity was reduced by As alone. Serum alkaline phosphatase was reduced by either As or Cd but not Pb. Combinations of As and Cd did not further reduce the activity of this enzyme. Kidney weight and kidney weight/body weight ratios were increased by Pb alone, but Cd or As alone or in combination had no effect. Liver weight/body weight ratios were reduced in animals fed Cd. Kidney histology showed predominantly Pb effects, i.e., intranuclear inclusion bodies and cloudy swelling. Ultrastructural evaluation of kidneys from Pb-treated animals disclosed nuclear inclusion bodies and mitochondrial swelling. Concurrent administration of Cd reduced total mean bone and kidney Pb levels by 50% and 60%, respectively, and this was associated with a decrease in kidney intranuclear inclusions. Cd exposure also reduced renal, femur, and liver concentrations of Fe by 33%, 43%, and 63%, respectively, decreased femur Zn by 27%, but increased renal Zn by 20%. Administration of As produced mild swelling of tubule cell mitochondria, increased mean total renal Cu to 200% of control, and increased liver Fe by 44%. Dietary Pb produced increased urinary excretion of ALA and coproporphyrin. Dietary exposure to As caused increased urinary excretion of uroporphyrin and to a lesser extent coproporphyrin, whereas dietary Cd caused no significant changes in urinary levels of any of the porphyrins measured. Pb plus As produced an additive effect on coproporphyrin excretion but not that of ALA or uroporphyrin. These studies indicate that interactions between common toxic elements do occur and are characterized by alterations in both tissue trace metal levels and toxicity.

Animals↗