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Biomedical subjects

K R Mahaffey

Publications and source records attributed to K R Mahaffey.

At least 55 records · Page 3Linked to original sources
PubMed1979

Nutrient-toxicant interactions: susceptible populations.

Nutritional status can substantially modify the toxicity of environmental pollutants. Investigations with experimental animals and epidemiological observations on humans have established the role of nutrition in altering susceptibility to a variety of pollutants including pesticides and heavy metals. The degree of nutritional deficiency that alters susceptibility need not be severe. Frequently only biochemical indications of nutritional deficiency can be associated with changes in the dose-response of an animal or person to a toxic compound.

Adult↗
PubMed1978

Comparative effects of feeding lead acetate and phospholipid-bound lead on blood and tissue lead concentrations in young and adult rats.

Two different forms of lead, lead acetate and phospholipid-bound lead, were fed to young and adult male rats for 10 weeks at the 300 ppm dietary level. Based on the lead concentrations found in selected tissues, our results indicate that the bioavailability of phospholipid-bound lead is similar to that of lead acetate at the 300 ppm level. Young rats had higher concentrations of lead in tissues than did adult rats.

Aging↗
PubMed1978

Stimulation of lead absorption by vitamin D administration.

Two methods for the determination of lead absorption have been developed using the rat as the test animal. One is an everted intestinal sac method in which the time course of 210Pb transport across intestinal wall can be followed in vitro; and the other, 210Pb absorption from the intestine following gastric intubation can be followed in vivo. By using these techniques it can be clearly demonstrated that vitamin D markedly enhances lead absorption. Both techniques provide evidence that the distal small intestine is the major site of lead absorption and the site of greatest vitamin D stimulation. Lead acetate is apparently absorbed to the extent of 45% as it passes through the small intestine at a concentration of 0.01 mM.

Animals↗
PubMed1978

Interactions among lead, cadmium, and arsenic in relation to porphyrin excretion patterns.

This paper reviews the effects of lead (Pb), cadmium (Cd), and arsenic (As) on the mitrochondrion with emphasis on alteration of mitochondrial heme biosynthetic pathway. The information was used to examine results of a Pb x Cd x As interaction study which employed urinary porphyrin excretion patterns as one assessment criterion. Data from the study showed that dietary Pb produced increased urinary excretion of aminolevulinic acid (ALA) and coproporphyrin. Dietary exposure to organic or inorganic As caused increased excretion of uroporphyrin and to a lesser extent coproporphyrin, while dietary Cd caused no significant changes in urinary levels of any of the porphyrins measured. The combination of Pb plus As produced an additive effect on coproporphyrin excretion but not that of either ALA or uroporphyrin. These data are discussed in relation to utilization of urinary porphyrins for assessing toxicity and elemental interactions.

Animals↗
PubMed1977

Effects of concurrent administration of lead, cadmium, and arsenic in the rat.

Humans are exposed to a number of toxic elements in the environment; however, most experiments with laboratory animals investigate only one toxic element. To determine if concomitant exposure to lead (Pb), cadmium (Cd), and/or arsenic (As) modified the changes produced by any one metal in various parameters of toxicity, 168 male, Sprague-Dawley, young adult rats were fed nutritionally adequate diets to which had been added 0 or 200 ppm Pb as Pb acetate, or 50 ppm Cd as Cd chloride, or 50 ppm As as sodium arsenate or arsanilic acid in a factorial design for a period of 10 weeks. At these concentrations, Cd and As reduced weight gain even when differences in food intake were taken into account; 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 numbers of red blood cells (RBCs) were observed following administration of Pb, Cd, or As; usually more cells were observed when two or three metals were administered, compared to individual metals. Despite increasing numbers of circulating RBCs, hemoglobin and hematocrit were reduced, especially with the Pb-Cd combination and the Cd-arsanilic acid combination. Specific effects of Pb on heme synthesis were observed, including increased urinary excretion of delta-aminolevulinic acid; this increase was reduced by the presence of dietary cadmium. Analyses of blood showed values for the laboratory rat within normal ranges for blood urea nitrogen, creatinine, cholesterol, calcium, albumin, total protein, and bilirubin. Uric acid was increased by Pb, with little modification by dietary Cd or As content. Serum glutamate-oxalate transaminase activity was reduced by As. Serum alkaline phosphatase was greatly 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, with no effects of Cd or As alone or as interactions. Liver weight/body weight ratios were reduced in animals fed 50 ppm dietary Cd. Kidney histology shows predominantly Pb effects, namely, intranuclear inclusion bodies and cloudy swelling. Ultrastructural evaluation of kidneys from Pb-treated animals disclosed nuclear inclusion bodies of the usual morphology and mitochondrial swelling. Concurrent administration of Cd greatly minimized Pb effects on the kidney under conditions of this experiment. Liver histology suggests an increased rate of cell turnover with either As compound, but few specific changes.

Administration, Oral↗
PubMed1977

Quantities of lead producing health effects in humans: sources and bioavailability.

Levels of lead ingestion and inhalation producing increased body burden of lead and clinical toxicity in adults and children are compared with usual levels of exposure. The magnitude of lead exposure from air, water, and food is estimated. Sources of high level exposure to lead are described; urban street dirt, house dust, and paint are particularly common sources of high concentrations of lead. The bioavailability of different lead compounds is reviewed as well as factors affecting susceptibility to lead.

Adult↗
PubMed1977

Delta-aminolevulinic acid dehydratase--a sensitive indicator of lead exposure in Japanese quail.

Red blood cell delta-aminolevulinic acid dehydratase (RBC-ALAD) activity has proven to be a sensitive indicator of lead exposure in humans. The depressed enzyme activity and its negative correlation to blood lead concentrations are well-known effects of lead exposure in man. The sensitivity of RBC-ALAD activity in young Japanese quail exposed to low levels of lead as lead acetate was investigated. Two groups of nine birds each were fed purified diets containing either no added lead or 25 micrograms of lead per g. of diet. After 2 weeks, blood samples for hematocrit, hemoglobin, and enzyme determinations and renal, hepatic, duodenal, and tibial tissues were collected. There were no significant differences between controls and lead-fed birds in body, kidney, duodenal, and tibial weights, or in hematocrit and hemoglobin concentrations. However, the renal, hepatic, duodenal, and tibial lead concentrations were significantly (P less than 0.001) greater in the lead-treated birds. The activity of RBC-ALAD in the group fed lead was 45% of that in the control group; these values were significantly different (P less than 0.001). RBC-ALAD activity expressed as the log. base 10 showed significant (P less than 0.02) negative correlation with both hepatic and tibial lead. The study demonstrates that the activity of RBC-ALAD in the Japanese quail is a very sensitive indicator of lead exposure.

Animals↗
PubMed1977

Relation between quantities of lead ingested and health effects of lead in humans.

Major metabolic effects of lead are briefly reviewed and available data on quantitative relationships between lead ingestion and development of toxicity in adults and children are discussed. Levels of lead ingestion producing clinical toxicity in adults are compared with normal levels of exposure. For children, comparison of levels of lead ingestion and quantities of lead producing toxic effects is not currently possible, as information on levels of lead producing clinical toxicity appears to be highly variable on the basis of the small amount of data available. However, recommendations on tolerable levels of lead exposure for childrne are proposed, based on estimates of lead exposure for children having normal and elevated body burdens of lead.

Child, Preschool↗
PubMed1975

Heavy metal exposure from foods.

The Food and Drug Administration has a continuing program of monitoring foods for their content of lead, cadmium, mercury, zinc, arsenic, and selenium to determine trends of increasing or decreasing levels. The monitoring protocol is that of the Total Diet Study, in which "market baskets" of typical foods and beverages consumed by 15- to 20-year-old American males are collected in various geographical locations at regular intervals during the year, divided into food classes, composited, and analyzed. Cadmium has the most widespread distribution of the six heavy metals and mercury the most limited. The analytical values for lead may be underestimated because of limitations of the methodology; these do not apply to the other five elements. A tabulation by year shows that the levels of these elements in foods do not vary significantly from one year to the next. Average intakes of lead, cadmium, and mercury are below the WHO/FAO tolerable intakes for adults; such tolerable intakes have not been established for arsenic and selenium. Increases in concentrations of these elements in foods would be considered undesirable, however.

Adolescent↗
PubMed1974

Nutritional factors and susceptibility to lead toxicity.

Although the quantities of lead (Pb) to which individuals are exposed vary widely, susceptibility of an individual to the effects of a specific level of exposure is another highly important factor in development of lead toxicity. For example, susceptibility to lead toxicity can be modified by several dietary factors. Low dietary intakes of calcium or iron (20% of recommended levels) substantially increase the toxicity of the same level of lead exposure to rats. In the studies of calcium effect, when calcium was fed to rats at (1/5) of the recommended intake, 12 mug Pb/ml drinking water produced the same degree of toxicity as did 200 mug Pb/ml with a normal calcium diet. The maximal dose for a 10-week period that does not impair heme synthesis or renal function in the rat has been established to be 200 mug Pb/ml drinking water. The role of low calcium diet on increasing susceptibility to lead has been confirmed in several species. Mechanisms explaining the effect of calcium on lead toxicity may be related to absorption of lead from the gastrointestinal tract or renal tubule or to function of the parathyroid. Preliminary histological investigations on the parathyroids of control and lead-treated rats on normal and low calcium diets show no effect of lead. Studies are currently underway to evaluate the lead, calcium and iron contents of the diets of children with normal and elevated concentrations of blood lead.

Animals↗