Toxic Lead

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13 14 15 16 17 18 19 20
21 22 23 24 25
A1 A2 A3 A4 A5 A6 Bib Karl

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Toxic Metals Data

Life Flow One
The Solution For Heart Disease

by
Karl Loren

Toxic Lead

Results for your query on March 14, 1999:: Search all fields for: toxic lead; Published in 1966 through 1999; Only select references with abstracts available; Show references published in English only; Show references pertaining to humans

Documents: 1 to 100 of 1165

The Book
TOC Intro
Chapters:
1 2 3 4 5 6 7 8 9 10 11 12
13 14 15 16 17 18 19 20
21 22 23 24 25
A1 A2 A3 A4 A5 A6 Bib Karl

Vibrant Life Web

Family Of Three Chelation Formulas
Other VL Products
The Wednesday Letter
Frequently Asked Questions
Testimonials

Life Flow One, The Solution For Heart Disease Data Section

Shopping Cart

Use Separate Search Page or

Separate Search Page
or search below

Navigation Help

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Write To Karl Loren

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Number	Title	Comments
...1...	Assessment of toxic metal exposure following the Camelford water pollution incident: evidence of acute mobilization of lead into drinking water.
...2...	The present status of biological effects of toxic metals in the environment: lead, cadmium, and manganese.
...3...	Lead neuropathy in adults and children.
...4...	Tissue mineral levels in victims of sudden infant death syndrome II. Essential minerals: copper, zinc, calcium, and magnesium.
...5...	The role of vitamin D in toxic metal absorption: a review.
...6...	Indian herbal remedies for diabetes as a cause of lead poisoning [see comments]
...7...	Exposure to toxic elements via breast milk.
...8...	Monitoring for precursors of health impairment from toxic agents.
...9...	Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.	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).
...10...	The new CDC and AAP lead poisoning prevention recommendations: consensus versus controversy.	The problem of lead poisoning can be summarized best by a quote from a report of the Agency for Toxic Substances and Disease Registry to Congress, "Lead is toxic wherever it is found, and it is found everywhere."
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...11...	Neurological syndromes produced by some toxic metals encountered industrially or environmentally.
...12...	Metabolism and toxicity of cadmium, mercury, and lead in animals: a review.
...13...	Electromyographic changes in automechanics with increased heavy metal levels.
...14...	Long-term monitoring and prevention of occupational lead exposure in a production plant.
...15...	Application of pulse polarography with anodic stripping voltammetry to biological and toxicological analyses for lead and cadmium.
...16...	Lead poisoning [see comments]
...17...	Chromosome studies in human lymphocytes after in vitro exposure to metal salts.
...18...	Relation between quantities of lead ingested and health effects of lead in humans.
...19...	Is lead poisoning still a problem?
...20...	Tetramethyl lead absorption: a report of human exposure to a high level of tetramethyl lead.
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...21...	Atomic absorption analysis of some trace metals of toxicological interest.
...22...	Neurofibrillary changes following childhood lead encephalopathy.
...23...	Age and sensitivity to lead toxicity: a review.
...24...	Occupational lead intoxication: report of four cases.
...25...	Lead in pet foods and processed organ meats. A human problem?
...26...	History and background of protoporphyrin testing.
...27...	Depressed excretion of 6 beta-hydroxycortisol in lead-toxic children.
...28...	Nutritional factors in relation to heavy metal toxicants.
...29...	Neuropathology of the hippocampus and its susceptibility to neurotoxic insult.
...30...	The relationship of hyperactivity to moderately elevated lead levels.	The finding of statistically significant and obvious behavioral improvement reported by three separate evaluators (i.e., parent, teacher, and treating physician) of the child suggests that the presumption of a toxic relationship between moderately elevated lead levels and hyperactivity is supported.
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...31...	Cytotoxicity of heavy metals in the human small intestinal epithelial cell line I-407: the role of glutathione.
...32...	Azarcón por empacho--another cause of lead toxicity.
...33...	Engulfment and killing capabilities of neutrophils and phagocytic splenic function in persons occupationally exposed to lead.
...34...	Immunoglobulin levels and cellular immune function in lead exposed workers.
...35...	Kohl: a hazardous eyeliner.
...36...	The effect of lead exposure on target detection and memory scanning differs.
...37...	Erythrocyte fluorescence and lead intoxication.
...38...	Occupational lead exposure in Finland. VI. Final report.
...39...	Airborne concentrations of toxic metals resulting from the use of low melting point lead alloys to construct radiotherapy shielding.
...40...	Individual susceptibility in occupational and environmental toxicology.
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...41...	Reproductive ability of workmen occupationally exposed to lead.
...42...	Leaded eye cosmetics: a cultural cause of elevated lead levels in children.
...43...	Micro-scale blood lead determinations in screening: evaluation of factors affecting results.
...44...	A multivariate statistical method for the establishment of maximum allowable exposure to toxic materials in the workplace.
...45...	Occupational disease profile in Taiwan, Republic of China.
...46...	Intracellular sites of toxic metals.
...47...	The role of heavy metals in human health.
...48...	The role of the community health nurse in environmental health.
...49...	Increased lead absorption in children of workers in a lead storage battery plant.
...50...	Beverages as a source of toxic trace element intake.
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...51...	delta-Aminolaevulinic acid dehydratase as an index of lead toxicity. Time for a reappraisal?
...52...	Measurements of environmental lead contamination and human exposure.
...53...	Cytotoxicity and accumulation of Hg, Ag, Cd, Cu, Pb and Zn in human peripheral T and B lymphocytes and monocytes in vitro.
...54...	Evaluating the use of occupational standards for controlling toxic air pollutants.
...55...	Nutrient-toxicant interactions: susceptible populations.
...56...	Concentrations of cadmium, lead, selenium, and zinc in human blood and seminal plasma.
...57...	Blood lead levels of British competitive cyclists.
...58...	Metals in spinal cord tissue of patients dying of motor neuron disease.
...59...	Cord blood levels of potentially neurotoxic pollutants (polychlorinated biphenyls, lead and cadmium) in the areas of Prague (Czech Republic) and Katowice (Poland). Comparison with reference values in The Netherlands. The Czech/Polish/Dutch/German Research Team.
...60...	Urinary excretion of tubular brush-border antigens among lead exposed workers.
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...61...	Intrauterine cocaine, lead, and nicotine exposure and fetal growth.
...62...	General subcellular effects of lead, mercury, cadmium, and arsenic.
...63...	A nationwide survey of heavy metal absorption in children living near primary copper, lead, and zinc smelters.
...64...	Lymphocyte subpopulations of workers in a plant producing plastic materials (preliminary study).
...65...	Role of rice and cereal products in dietary cadmium and lead intake among different socio-economic groups in south India.
...66...	Lead levels in Birmingham dust.
...67...	An unknown risk group of lead poisoning: the gypsy children.
...68...	The relation of soluble lead to toxicity: an in vitro analysis.
...69...	L-line x-ray fluorescence of cortical bone lead compared with the CaNa2EDTA test in lead-toxic children: public health implications [published erratum appears in Proc Natl Acad Sci U S A 1989 Oct;86(19):7595]
...70...	The behavioral toxicology of metals.	Unwarranted loyalties to traditional psychological tests may be one source of the current dispute about safe levels of lead simply because parametric variations of clearly specified functions are beyond the scope of such instruments.
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...71...	Neurotoxic effects of selected metals.
...72...	Metabolic interactions between metals and metalloids.
...73...	Amplification of glutamate-induced oxidative stress.
...74...	Children and environmental toxins.
...75...	Nutrition of lead.
...76...	Effect of lead intoxication on calcium homeostasis and calcium-mediated cell function: a review.
...77...	Lead activates calmodulin sensitive processes.
...78...	Lead poisoning in inherited delta-aminolevulinic acid dehydratase deficiency.
...79...	Neurobehavioral toxicology of the organoleads.
...80...	Study and models of total lead exposures of battery workers.
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...81...	Early sensory-motor development and prenatal exposure to lead.
...82...	Tissue mineral levels in victims of sudden infant death syndrome I. Toxic metals--lead and cadmium.
...83...	A survey of the effects of lead on gunners.
...84...	Gasoline sniffing and lead toxicity in Navajo adolescents.
...85...	Simultaneous exposure to lead, arsenic and mercury from Indian ethnic remedies.
...86...	Role of DNA repair inhibition in lead- and cadmium-induced genotoxicity: a review.
...87...	Toxic metals in street and household dusts.
...88...	Diagnostic significance of edetate disodium calcium testing in children with increased lead absorption.
...89...	Graphite furnace atomic absorption spectroscopic measurement of blood lead in matrix-matched standards.
...90...	Lead screening among high-risk urban children. Are the 1991 Centers for Disease Control and Prevention guidelines feasible?
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...91...	Interactions of vitamin C with lead and mercury.
...92...	X-linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy.
...93...	Environmentally acquired lead, cadmium, and manganese in the cattle egret, Bubulcus ibis, and the laughing gull, Larus atricilla.
...94...	Neurotoxicity of lead, methylmercury, and PCBs in relation to the Great Lakes.
...95...	Copper jacketed bullets in the central nervous system.
...96...	Levels of lead in the United States food supply.
...97...	Toxic effects of lead impurities found in aluminum factories.
...98...	Toxic effects of lead impurities found in aluminum factories.
...99...	Predictors of lead stores in male veterans.
...100...	Effect of aluminum and lead salts on lipid peroxidation and cell survival in human skin fibroblasts.

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Documents

Record 1 from database: MEDLINE
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Title: Assessment of toxic metal exposure following the Camelford water pollution incident: evidence of acute mobilization of lead into drinking water.
Author: Powell JJ; Greenfield SM; Thompson RP; Cargnello JA; Kendall MD; Landsberg JP; Watt F; Delves HT; House I
Address: Gastrointestinal Laboratory, Range Institute, St. Thomas' Hospital, London, UK.
Source: Analyst, 1995 Mar, 120:3, 793-8
Abstract: Following the incident of acidic pollution of water by aluminium sulfate centred around Camelford in July 1988, we have carried out a retrospective analysis of the mobilization of toxic metals to residents of the area. An advanced nuclear technique was used to measure trace levels of elements within hair, thus, avoiding surface contamination. In contrast to controls, lead, but no other toxic metals, was consistently found within sections of hair that dated to mid-1988 from four residents; they must, therefore, have consumed this metal around the time of the incident. The source of this lead was probably local water pipe residue, and this was found on analysis to have a matrix specific to such soft-water areas that, prior to the incident, had slowly accumulated certain toxic metals such as cadmium and uranium and particularly lead. Lead is mobilized from such residues by acidic water and could, therefore, have heavily contaminated mains water after the incident. However, analyses of residents' plasma and whole blood, and of urine following a lead-chelation test, showed no evidence of either long-term increased body burdens of toxic metals or depletion of essential elements. In addition, we found no evidence of continued poor water quality in the area. In conclusion, during a short period following the pollution, some residents who consumed mains water would have been acutely exposed to lead and other toxic metals. Prediction of the scale of metal exposure to individuals was not possible owing to heterogeneity of the water distribution network, but long-term effects to residents from lead are not anticipated.(ABSTRACT TRUNCATED AT 250 WORDS)
Language of Publication: English
Unique Identifier: 95259797

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MeSH Heading (Major): Accidents|*; Environmental Exposure|*; Hair|*CH; Lead|AD/*AN/ME; Water Pollution|*
MeSH Heading: Absorption; Adult; Drinking; England; Female; Human; Lead Poisoning|DI; Male; Microscopy|MT; Middle Age; Support, Non-U.S. Gov't; Water Supply

Publication Type: JOURNAL ARTICLE
ISSN: 0003-2654
Country of Publication: ENGLAND

Record 2 from database: MEDLINE
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Title: The present status of biological effects of toxic metals in the environment: lead, cadmium, and manganese.
Author: Shukla GS; Singhal RL
Address
Source: Can J Physiol Pharmacol, 1984 Aug, 62:8, 1015-31
Abstract: The number of reports concerning the chemical toxicology of metals which are released in the environment by natural as well as anthropogenic sources, have been increasing constantly. Lead, cadmium, and manganese have found a variety of uses in industry, craft, and agriculture owing to their physical and chemical properties. The environmental burden of heavy metals has been rising substantially by smelter emission in air and waste sewage in water. Further, organic compounds of lead and manganese used as antiknock substances in gasoline are emitted into the atmosphere by automobile exhaustion. Such environmental contamination of air, water, soil, and food is a serious threat to all living kinds. Although these metals are known to produce their toxic effects on a variety of body systems, much emphasis has been placed on their effects on the nervous system owing to apparent association of relatively low or "subclinical" levels of metallic exposure with behavioral and psychological disorders. Clinical and animal data on environmental exposure show that while lead and manganese are most toxic to the nervous system, cadmium exerts profound adverse effects on kidney and the male reproductive system. It appears that the consequences of exposure to lead in adults are less severe than the types of exposure associated with hyperactivity in neonates. Except for a few reports, hyperactivity has indeed been observed in animals exposed to either of these three metals. Experimental work has also shown that these metals produce behavioral changes by altering the metabolism of brain neurotransmitters, especially catecholamines. Recently, it is hypothesized that these metals exert their toxic effect by damaging biological defences which exist in the body to serve as protective mechanisms against exogenous toxins. A voluminous publication list with diverse opinions on the biological effects of metals is available and there is an urgent need to compile assessment of the existing literature to identify the future theme of research work. The problem of metal toxicity becomes even more complex owing to simultaneous or successive exposure of the general population to different physical, chemical, biological, and psychological factors in the environment. The net toxic manifestations produced by multiple exposure should, therefore, be different from those produced by a single factor as the result of their additive, synergistic or antagonistic action. Even though a metal may not exist in sufficient amounts to cause any disability, the toxicity could result when a second factor is also present.(ABSTRACT TRUNCATED AT 400 WORDS)
Language of Publication: English
Unique Identifier: 85024374

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MeSH Heading (Major): Cadmium|*TO; Environmental Pollutants|*TO; Lead|*TO; Manganese|*TO
MeSH Heading: Aging; Animal; Behavior, Animal|DE; Brain Chemistry|DE; Cadmium Poisoning|PP; Human; Lead Poisoning|PP; Mice; Nervous System Diseases|CI; Neurotransmitters|ME; Rats; Species Specificity; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE; REVIEW
ISSN: 0008-4212
Country of Publication: CANADA
CAS Registry/EC Number: 0 (Environmental Pollutants); 0 (Neurotransmitters); 7439-92-1 (Lead); 7439-96-5 (Manganese); 7440-43-9 (Cadmium)

Record 3 from database: MEDLINE
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Title: Lead neuropathy in adults and children.
Author: Feldman RG; Hayes MK; Younes R; Aldrich FD
Address
Source: Arch Neurol, 1977 Aug, 34:8, 481-8
Abstract: All parts of the nervous systems can be affected, depending on the level and duration of exposure, by increased levels of lead. The occurrence of motor neuron disease, peripheral neuropathy, and encephalopathy are not mutually exclusive disorders for those individuals suffering from the toxic effects of lead. We present data that support the concept that increased absorption of lead produces changes in both central and peripheral nervous systems. Clinical and electrical evidence of subclinical involvement of peripheral nerves appears to be common to adults and children who are exposed to lead. These observations, accumulated from several possible sources of environmental hazard, also suggest that measurement of motor nerve conduction velocity may serve as an additional factor in the diagnosis of otherwise unrecognized toxic effects of lead.
Language of Publication: English
Unique Identifier: 77241330

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MeSH Heading (Major): Lead Poisoning|*CO/DI; Nervous System Diseases|*ET
MeSH Heading: Adult; Anemia|ET; Basal Ganglia Diseases|ET; Case Report; Colic|ET; Dementia|ET; Electromyography; Female; Human; Lead|BL/UR; Male; Middle Age; Motor Neurons; Muscle Spasticity|ET; Neural Conduction; Support, U.S. Gov't, Non-P.H.S.

Publication Type: JOURNAL ARTICLE
ISSN: 0003-9942
Country of Publication: UNITED STATES

Record 4 from database: MEDLINE
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Title: Tissue mineral levels in victims of sudden infant death syndrome II. Essential minerals: copper, zinc, calcium, and magnesium.
Author: Erickson MM; Poklis A; Gantner GE; Dickinson AW; Hillman LS
Address
Source: Pediatr Res, 1983 Oct, 17:10, 784-7
Abstract: Deficiencies of various vitamin and minerals per se have been suggested as possible causes of sudden infant death syndrome (SIDS). Further, a deficiency of essential minerals may lead to enhanced toxicity of toxic elements, in particular, lead and cadmium to explore the possibility of mineral deficiencies or interactions with the toxic metals, lead and cadmium, lung, liver, kidney, and rib specimens were obtained at autopsy from 66 SIDS infants and 23 infants who died suddenly from other cases. Tissue copper, zinc, calcium, and magnesium were measured by atomic absorption spectroscopy. No differences were found between SIDS and non-SIDS for any element in any tissue except for more magnesium in the liver (P less than 0.0001) and less copper in the lungs (P less than 0.02) in the SIDS group. Only sporadic interactions between toxic and essential elements could be found. We found no evidence of any essential mineral deficiencies per se or significant interactions of essential and toxic minerals that might potentiate the effects of toxic metals. The physiologic significance, if any, of the higher liver magnesium and lower lung copper found in SIDS is unclear.
Language of Publication: English
Unique Identifier: 84041208

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MeSH Heading (Major): Calcium|*AN; Metals|*AN; Sudden Infant Death|*PP
MeSH Heading: Cadmium|AN; Comparative Study; Copper|AN; Human; Infant; Infant, Newborn; Kidney|AN; Lead|AN; Liver|AN; Lung|AN; Magnesium|AN; Ribs|AN; Spectrophotometry, Atomic Absorption; Support, U.S. Gov't, P.H.S.; Zinc|AN

Publication Type: JOURNAL ARTICLE
ISSN: 0031-3998
Country of Publication: UNITED STATES
CAS Registry/EC Number: 0 (Metals); 7439-92-1 (Lead); 7439-95-4 (Magnesium); 7440-43-9 (Cadmium); 7440-50-8 (Copper); 7440-66-6 (Zinc); 7440-70-2 (Calcium)

Record 5 from database: MEDLINE
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Title: The role of vitamin D in toxic metal absorption: a review.
Author: Moon J
Address: National College of Naturopathic Medicine, Portland Oregon 97216.
Source: J Am Coll Nutr, 1994 Dec, 13:6, 559-64
Abstract: Vitamin D increases intestinal calcium and phosphate absorption. Not so well known, however, is that vitamin D stimulates the co-absorption of other essential minerals like magnesium, iron, and zinc; toxic metals including lead, cadmium, aluminum, and cobalt; and radioactive isotopes such as strontium and cesium. Vitamin D may contribute to the pathologies induced by toxic metals by increasing their absorption and retention. Reciprocally, lead, cadmium, aluminum, and strontium interfere with normal vitamin D metabolism by blocking renal synthesis of 1,25-dihydroxyvitamin D. This is the first review of the role of the vitamin D endocrine system in metal toxicology.
Language of Publication: English
Unique Identifier: 95221746

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MeSH Heading (Major): Cadmium|ME/PD/*PK; Lead|ME/PD/*PK; Vitamin D|ME/*PH
MeSH Heading: Aluminum|ME/PD/PK; Body Burden; Human; Intestinal Absorption|PH; Strontium Radioisotopes|ME/PD/PK

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0731-5724
Country of Publication: UNITED STATES

Record 6 from database: MEDLINE
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Title: Indian herbal remedies for diabetes as a cause of lead poisoning [see comments]
Author: Keen RW; Deacon AC; Delves HT; Moreton JA; Frost PG
Address: Central Middlesex Hospital, London, UK.
Source: Postgrad Med J, 1994 Feb, 70:820, 113-4
Abstract: Herbal remedies from the Indian subcontinent have been found to have high concentrations of heavy metals and unsupervised treatment may result in toxicity. We report the case of an Indian patient with hepatitis who was found to have lead poisoning where the source was traced to ethnic remedies he had been taking for diabetes.
Language of Publication: English
Unique Identifier: 94224707

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MeSH Heading (Major): Diabetes Mellitus, Non-Insulin-Dependent|*TH; Lead Poisoning|*ET; Medicine, Traditional|*; Plants, Medicinal|*CH
MeSH Heading: Adult; Case Report; Hepatitis, Toxic|ET; Human; India; Lead|AN; Male

Publication Type: JOURNAL ARTICLE
ISSN: 0032-5473
Country of Publication: ENGLAND

Record 7 from database: MEDLINE
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Title: Exposure to toxic elements via breast milk.
Author: Oskarsson A; Palminger Hallén I; Sundberg J
Address: Toxicology Division, Swedish National Food Administration, Uppsala.
Source: Analyst, 1995 Mar, 120:3, 765-70
Abstract: Breast milk is the ideal nutrient for the newborn, but unfortunately also a route of excretion for some toxic substances. Very little attention has been paid to breast milk as a source of exposure to toxic elements. The dose-dependent excretion is breast milk and the uptake in the neonate of inorganic mercury, methylmercury and lead were studied in an experimental model for rats and mice. The transfer of mercury from plasma to milk was found to be higher in dams exposed to inorganic mercury than to methylmercury. In contrast, the uptake of mercury from milk was higher in the sucklings of dams exposed to methylmercury than to inorganic mercury. Pre- and postnatal exposure to methylmercury resulted in increased numbers and altered proportions of the thymocyte subpopulation and increased lymphocyte activities in the offspring of mice and also effects on the levels of noradrenaline and nerve growth factor in the developing brain of rats. Mercury in blood and breast milk in lactating women in Sweden was studied in relation to the exposure to mercury from, fish and amalgam. Low levels were found; the mean levels were 0.6 ng g-1 in milk and 2.3 ng g-1 in blood. There was a statistically significant correlation between mercury levels in blood and milk, showing that milk levels were approximately 30% of the levels in blood. Inorganic mercury exposure from amalgam was reflected in blood and milk mercury levels. Recent exposure to methylmercury from consumption of fish was reflected in mercury levels in the blood but not in milk.(ABSTRACT TRUNCATED AT 250 WORDS)
Language of Publication: English
Unique Identifier: 95259793

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MeSH Heading (Major): Lead|*AD/BL/PK; Mercury|*AD/BL/PK; Methylmercury Compounds|*AD/BL/PK; Milk|*/ME; Milk, Human|*/ME
MeSH Heading: Animal; Animals, Newborn; Female; Human; Infant, Newborn; Lactation; Mice; Rats; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE
ISSN: 0003-2654
Country of Publication: ENGLAND

Record 8 from database: MEDLINE
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Title: Monitoring for precursors of health impairment from toxic agents.
Author: Pfitzer EA
Address
Source: Ann Clin Lab Sci, 1976 Jul, 6:4, 318-21
Abstract: It is essential that one be able to diagnose when disorders are caused by drugs and toxic agents. It is also essential that scientists strive toward the ultimate goal of preventing such disorders. To this end, it is necessary to evaluate laboratory procedures for their capability to detect changes which precede disorders of health impairment. To accomplish this, some knowledge of the relationship between the exposure to a chemical agent and the effect owing to that exposure is required. The complexities of the dose-effect relationship are discussed with regard to the estimation of exposure, the effect owing to the exposure and the population exposed to the chemical agent.
Language of Publication: English
Unique Identifier: 76276407

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MeSH Heading (Major): Poisoning|*DI
MeSH Heading: Drug Therapy|AE; Heme|BI; Human; Lead|BL/PD; Lead Poisoning|DI; Pharmaceutical Preparations|AD

Publication Type: JOURNAL ARTICLE
ISSN: 0091-7370
Country of Publication: UNITED STATES

Record 9 from database: MEDLINE
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Title: Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.
Author: Baker EL Jr; Landrigan PJ; Barbour AG; Cox DH; Folland DS; Ligo RN; Throckmorton J
Address
Source: Br J Ind Med, 1979 Nov, 36:4, 314-22
Abstract: 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).
Language of Publication: English
Unique Identifier: 80065417

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MeSH Heading (Major): Lead|*BL; Lead Poisoning|*BL/EP; Occupational Diseases|*CI/EP
MeSH Heading: Air Pollutants, Occupational|AN; Anemia|CI; Blood Urea Nitrogen; Chemical Industry; Dose-Response Relationship, Drug; Gastrointestinal Diseases|CI; Human; Kidney Function Tests; Maximum Permissible Exposure Level; Metallurgy; Neuromuscular Diseases|CI; United States

Publication Type: JOURNAL ARTICLE
ISSN: 0007-1072
Country of Publication: ENGLAND

Record 10 from database: MEDLINE
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Title: The new CDC and AAP lead poisoning prevention recommendations: consensus versus controversy.
Author: Schaffer SJ; Campbell JR
Address: Department of Pediatrics, University of Rochester School of Medicine, New York.
Source: Pediatr Ann, 1994 Nov, 23:11, 592-9
Abstract: A considerable body of evidence has surfaced over the past several decades indicating that low-level lead exposure has detrimental effects for young children. As neurocognitive deficits have increasingly been found to be associated with lead levels as low as 10 micrograms/dL, the CDC has progressively lowered the threshold lead level designated as elevated to the present level of 10 micrograms/dL. The CDC also has recommended universal screening of all children for lead. These recommendations have engendered much controversy. After independently reviewing the relevant literature, the AAP and the National Academy of Science concurred with the CDC's conclusions and recommendations. As additional prevalence information becomes available, a more targeted approach to screening based on local prevalence data eventually may replace universal screening. However, as long as lead is found everywhere in the environment, children will continue to develop lead poisoning and suffer from its adverse effects. The problem of lead poisoning can be summarized best by a quote from a report of the Agency for Toxic Substances and Disease Registry to Congress, "Lead is toxic wherever it is found, and it is found everywhere."
Language of Publication: English
Unique Identifier: 95140510

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MeSH Heading (Major): Centers for Disease Control and Prevention (U.S.)|*; Lead Poisoning|BL/*PC; Pediatrics|*; Practice Guidelines|*; Societies, Medical|*
MeSH Heading: Child; Child, Preschool; Cognition Disorders|PC; Erythrocytes|CH; Human; Infant; Lead|AE/BL; Mass Screening|EC/MT; Nervous System Diseases|PC; Nutritional Status; Protoporphyrins|BL; Public Policy; Questionnaires; Risk Factors; United States

Publication Type: JOURNAL ARTICLE
ISSN: 0090-4481
Country of Publication: UNITED STATES

Record 11 from database: MEDLINE
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Title: Neurological syndromes produced by some toxic metals encountered industrially or environmentally.
Author: Bahiga LM; Kotb NA; El Dessoukey EA
Address
Source: Z Ernahrungswiss, 1978 Jun, 17:2, 84-8
Abstract: Toxic metals encountered industrially or environmentally may produce the following syndromes: 1) Peripheral neuropathy: which is mainly sensory in arsenic and entirely motor with inorganic lead, organophosphorus compounds and tallium produce a mixed form of peripheral neuropathy. 2) Encephalopathy: usually with lead poisoning where ataxia and hemiplegia or optic atrophy may occur. 3) Optic neuritis: transient or permanent impairment of vision in arsenic poisoning and blurring of vision followed by field fedects with thallium poisoning. 4) Cerebellar disturbances: in the form of ataxia in organic mercury. 5) Parkinsonism: extrapyramidal signs occurs in manganese poisoning shown as mask face and rigidity of muscles. 6) Mental changes: as acute psychosis in organic lead and erethism in organic mercury.
Language of Publication: English
Unique Identifier: 78252377

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MeSH Heading (Major): Nervous System Diseases|*CI; Poisoning|*CO
MeSH Heading: Adult; Arsenic|PO; Brain Diseases|ET; Cerebellar Diseases|ET; Child; Environmental Exposure; Human; Lead Poisoning|CO; Manganese|PO; Mental Disorders|ET; Mercury Poisoning|CO; Occupational Diseases|CO; Optic Neuritis|ET; Organomercury Compounds|PO; Organophosphorus Compounds|PO; Parkinson Disease|ET; Tetraethyl Lead|PO; Thallium|PO

Publication Type: JOURNAL ARTICLE; REVIEW
ISSN: 0044-264X
Country of Publication: GERMANY, WEST

Record 12 from database: MEDLINE
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Title: Metabolism and toxicity of cadmium, mercury, and lead in animals: a review.
Author: Neathery MW; Miller WJ
Address
Source: J Dairy Sci, 1975 Dec, 58:12, 1767-81
Abstract: Cadmium, mercury, and lead are toxic to humans and animals. Although cadmium and inorganic mercury toxicities occur in humans, they have not been observed in domestic livestock under practical conditions. In contrast, cattle, especially young calves, are extremely susceptible to lead toxicity. Apparently, cattle are more tolerant of cadmium than are other animal species. Due partially to higher absorption and longer retention times in the body, the alkyl mercuries, especially methyl mercury, are more toxic than inorganic mercury compounds. Inorganic forms of cadmium, mercury, and lead are poorly absorbed from the intestine. However, due to lack of effective homeostasis, after absorption retention time is long. Injected cadmium, mercury, and lead are metabolized differently from that naturally absorbed. Most cadmium and mercury are in kidney and liver (50 and 23% of total body in goats); but highest total load of methyl mercury is in muscle (72% in cows). With low to moderate body burden, most lead is retained in the skeleton. However, beyond a certain point, the kidney accumulates large quantities. Only minute amounts of cadmium and mercury are secreted into milk, but milk is only moderately well protected from dietary lead. Likewise, little cadmium and inorganic mercury pass the placental barrier whereas lead and methyl mercury pass more readily.
Language of Publication: English
Unique Identifier: 76095565

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MeSH Heading (Major): Cadmium|*/ME/TO; Lead|*ME; Lead Poisoning|*ET; Mercury|*ME; Mercury Poisoning|*ET
MeSH Heading: Animal; Birds; Cattle; Chickens; Environmental Exposure; Female; Food Contamination; Goats; Human; Lactation; Maternal-Fetal Exchange; Methylmercury Compounds|ME; Milk|ME; Pregnancy; Rabbits; Sheep; Species Specificity

Publication Type: JOURNAL ARTICLE; REVIEW
ISSN: 0022-0302
Country of Publication: UNITED STATES

Record 13 from database: MEDLINE
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Title: Electromyographic changes in automechanics with increased heavy metal levels.
Author: Melgaard B; Clausen J; Rastogi SC
Address
Source: Acta Neurol Scand, 1976 Sep, 54:3, 227-40
Abstract: Twenty automechanics possessing increased whole blood values of one or more of the following heavy metals; chromium, copper, lead, manganese and nickel, were studied for peripheral nerve affection by means of electromyography (both sensoric and motoric nerve potentials were recorded). The heavy metal contents were related to the findings of denervation, distal motor latency, distal sensory latency, motoric and sensoric conduction velocities. Apart from two workers, in whom only lead was assayed, the remaining group of 18 were assayed for all heavy metals under study. Six workers showed increased distal motor and/or sensory latency and seven decreased nerve conduction velocity (four motoric and three sensoric affections). Of the workers with nerve affection, three showed increased levels of lead (nickel and chromium also raised). Four workers showed increased lead, nickel and chromium and one of lead, chromium and manganese. All in all, 10 out of 20 workers (50 percent) with elevated lead levels showed definite signs of peripheral neuropathy and seven out of 14 with raised nickel values showed these signs but they could all be accounted for by the increased lead levels. All except seven workers with raised lead levels in the whole group showed values above the critical limit of 80.0 mug/100 ml in whole blood. The data argue for the highly toxic effect of lead and other heavy metals on the peripheral nervous system and stress the diverse toxic exposure which automechanics undergo during their work. The possibility of there being a synergistic action between heavy metals and components of mineral oil and petroleum is discussed.
Language of Publication: English
Unique Identifier: 76274372

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MeSH Heading (Major): Metals|*/BL; Occupational Diseases|*CI; Peripheral Nervous System Diseases|*CI
MeSH Heading: Action Potentials; Adult; Aged; Chromium|BL; Copper|BL; Electromyography; Environmental Exposure; Erythrocytes|EN; Female; Human; Lead|BL; Levulinic Acids|UR; Male; Manganese|BL; Middle Age; Neural Conduction; Nickel|BL; Oils|AN; Oxidoreductases|BL

Publication Type: JOURNAL ARTICLE
ISSN: 0001-6314
Country of Publication: DENMARK

Record 14 from database: MEDLINE
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Title: Long-term monitoring and prevention of occupational lead exposure in a production plant.
Author: Jaremin B; G…ombiowski P; Winnicka A; Starnawska M; Widuch H
Address: Clinic of Occupational and Tropical Diseases, Institute of Maritime and Tropical Medicine in Gdynia.
Source: Bull Inst Marit Trop Med Gdynia, 1995, 46:1-4, 31-42
Abstract: During 19 years of monitoring and prevention of occupational lead exposure in a production plant the authors studied lead emission sources and exposure intensity encountered in the work place, the indices of current and long-term lead exposure, and markers of toxic effects of lead in 132 persons examined together 935 times. Lead poisoning was confirmed in 20 persons, i.e. about 2 per cent of examinations, whereas in 12 per cent signs of enhanced lead absorption were found. Based on a complex simultaneous assessment of many parameters, appropriate prophylaxis and therapy were applied to lessen the toxic effects of lead exposure. It is pointed out that technical improvements are fundamental for limiting lead emission and absorption in the work place. As it has been demonstrated, the proper cooperation between the physician, the toxicological laboratory, occupational safety service and the plant administration effectively contribute to the limitation or even elimination of lead exposure, thus reducing the possible future health effects of long-term lead exposure.
Language of Publication: English
Unique Identifier: 96288582

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MeSH Heading (Major): Air Pollutants, Occupational|*AN; Environmental Monitoring|*MT; Lead|*AN; Lead Poisoning|*PC; Occupational Diseases|*PC; Occupational Exposure|*PC
MeSH Heading: Adult; Dose-Response Relationship, Drug; Human; Male; Metallurgy; Poland; Powders; Risk Factors

Publication Type: JOURNAL ARTICLE
ISSN: 0324-8542
Country of Publication: POLAND

Record 15 from database: MEDLINE
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Title: Application of pulse polarography with anodic stripping voltammetry to biological and toxicological analyses for lead and cadmium.
Author: Herbeuval X; Maso JL; Baudot P; Hutin MF; Burnel D
Address
Source: Pathol Biol (Paris), 1975 May, 23:5, 379-86
Abstract: The development of polarographic techniques within the last thirty years has made possible exceptional increases in sensitivity ; thus the order of concentration studied has passed from 10-3 g ion/1. to 10-10 g ion/1. Pulse polarography with anodic stripping voltammetry is, therefore, particularly suitable for the determination of a large number of the so-called " biologically essential " and " highly toxic " metals, more often than not present in extremely low concentrations in biological samples which may be of limited volume (blood, for example). Our principal concern has been to describe and apply a method for the determination of lead and cadmium, sufficiently sensitive, precise, practical and rapid for everyday use by biologists and toxicologists. A fortiori this method is applicable in hydrology to the determination of traces of these metals in water.
Language of Publication: English
Unique Identifier: 76076765

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MeSH Heading (Major): Cadmium|*AN/BL/PO/UR; Lead|*AN/BL/UR; Polarography|*MT
MeSH Heading: Cadmium Poisoning|DI; Electrolysis; Human; Lead Poisoning|DI; Microchemistry; Water|AN; Water Pollutants, Chemical|AN

Publication Type: JOURNAL ARTICLE
ISSN: 0369-8114
Country of Publication: FRANCE

Record 16 from database: MEDLINE
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Title: Lead poisoning [see comments]
Author: Landrigan PJ; Todd AC
Address: Department of Community Medicine, Mount Sinai School of Medicine, New York, New York 10029.
Source: West J Med, 1994 Aug, 161:2, 153-9
Abstract: Lead poisoning is the most common disease of environmental origin in the United States today. Adult lead poisoning results primarily from exposure by inhalation in the workplace. Pediatric lead poisoning results principally from the ingestion of lead from environmental media, including paint chips, dust, soil, drinking water, ceramics, and medications. Lead is toxic to many organ systems, among them developing erythrocytes, the kidneys, and the nervous system. Lead-induced toxicity to the central nervous system causes delayed development, diminished intelligence, and altered behavior. In young children, this effect has been demonstrated convincingly to occur at blood lead levels between 10 and 20 micrograms per dl. The Centers for Disease Control and Prevention has recommended that a blood lead level of 10 micrograms per dl or higher be considered evidence of increased lead absorption, and the National Academy of Sciences has concurred in that recommendation. Unresolved issues in need of further study include the frequency of screening young children for lead, the question of whether women should be offered screening for lead before conceiving a pregnancy, the role of x-ray fluorescence analysis in assessing lead in bone, and the appropriate legislative response of the United States government to lead-based paint abatement.
Language of Publication: English
Unique Identifier: 95027943

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MeSH Heading (Major): Lead Poisoning|*/DI/EP/ET/ME/PC
MeSH Heading: Adult; Body Burden; Child; Environmental Monitoring|LJ/MT; Environmental Pollution|AE; Female; Human; Lead|ME/PK; Mass Screening; Preconception Care; Research; Support, U.S. Gov't, P.H.S.; United States

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0093-0415
Country of Publication: UNITED STATES

Record 17 from database: MEDLINE
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Title: Chromosome studies in human lymphocytes after in vitro exposure to metal salts.
Author: Deknudt G; Deminatti M
Address
Source: Toxicology, 1978 May, 10:1, 67-75
Abstract: The toxic concentration of different heavy metal salts was determined in normal stimulated human lymphocyte cultures and was found to be 3 X 10(-3), 1 X 10(-2) and 5 X 10(-4) for zinc chloride, lead acetate and cadmium chloride respectively. Furthermore 3 subtoxic doses of each salt (2, 10 and 100 times less than the toxic dose) were added to 48- and 72-h cultures at 0 h and 24 h after initiation. Chromosome preparations were made and 100 well spread metaphases from each culture were analysed for the presence of numerical and structural aberrations. The most common aberration found for all tested metal salts was the occurrence of chromosome fragments. Dicentric chromosomes were only recorded in lymphocyte cultures treated with the lowest concentration of zinc chloride (3 X 10(-5) M) added at time 0, regardless whether the cultures were fixed after 48 or 72 h.
Language of Publication: English
Unique Identifier: 78229519

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MeSH Heading (Major): Cadmium|*PD; Chromosomes|*DE; Lead|*PD; Lymphocytes|DE/*UL; Zinc|*PD
MeSH Heading: Cells, Cultured; Chromosome Aberrations; Human; In Vitro; Mitosis|DE; Time Factors

Publication Type: JOURNAL ARTICLE
ISSN: 0300-483X
Country of Publication: NETHERLANDS

Record 18 from database: MEDLINE
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Title: Relation between quantities of lead ingested and health effects of lead in humans.
Author: Mahaffey KR
Address
Source: Pediatrics, 1977 Mar, 59:3, 448-55
Abstract: 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.
Language of Publication: English
Unique Identifier: 77124880

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MeSH Heading (Major): Lead Poisoning|*/CO/ME
MeSH Heading: Child, Preschool; Feces|AN; Heme|BI; Human; Infant; Kidney Diseases|ET; Lead|ME/TO; Maximum Permissible Exposure Level; Neurologic Manifestations

Publication Type: JOURNAL ARTICLE
ISSN: 0031-4005
Country of Publication: UNITED STATES

Record 19 from database: MEDLINE
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Title: Is lead poisoning still a problem?
Author: Chisolm JJ Jr
Address
Source: Clin Chem, 1977 Feb, 23:2 PT. 1, 252-5
Abstract: Today, health professionals are concerned about whether asymptomatic or mildly symptomatic increases in lead absorption in preschool children is one of the important factors causing minimal brain dysfunction, which only becomes evident later during the school years. This concern arises, in part, because current screening data show that 5 to 10% of the children tested recently in the United States have a degree of increase in lead absorption sufficient to cause metabolic derangement in heme synthesis, but insufficient, with rare exception, to cause classical acute clinical symptoms of plumbism. These screening data are disturbing because similar increases in lead absorption in suckling (but not older) experimental animals have been shown in some studies to be followed by the delayed appearance of subtle deficits in learning ability and aberrations in behavior. Derangement of hemoglobin synthesis is the first adverse effect of increased lead absorption now detectable. Intervention on the basis of the first or critical effect of a toxic agent before more serious effects occur has advantages from the viewpoint of preventive medicine. Current CDC guidelines for prevention of childhood lead poisoning are based on this concept and recommend the use of micro-scale erythrocyte protoporphyrin tests in conjunction with micro blood lead tests for early detection of children with disturbed heme synthesis caused by lead.
Language of Publication: English
Unique Identifier: 77089837

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MeSH Heading (Major): Lead|BL/*ME; Lead Poisoning|*/CO/PP
MeSH Heading: Aminolevulinic Acid|UR; Animal; Attention Deficit Disorder with Hyperactivity|ET; Child; Child, Preschool; Dose-Response Relationship, Drug; Environment; Erythrocytes|ME; Human; Protoporphyrins|BL

Publication Type: JOURNAL ARTICLE
ISSN: 0009-9147
Country of Publication: UNITED STATES

Record 20 from database: MEDLINE
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Title: Tetramethyl lead absorption: a report of human exposure to a high level of tetramethyl lead.
Author: Gething J
Address
Source: Br J Ind Med, 1975 Nov, 32:4, 329-33
Abstract: Accidental human exposure to a high level of tetramethyl lead is described. Tetramethyl lead is blended with petrol as an antiknock agent, and it has similar physical properties to tetraethyl lead. The patient had high levels of lead in urine, averaging 4-75 mumol (983 mug) daily for the first four days after exposure and he continued to have raised levels of urinary lead for six months. He had no symptoms or physical signs of lead poisoning and comparisons are made between this case and previously reported cases of poisoning by tetraethyl lead. In the cases of tetraethyl lead poisoning all the patients had symptoms, some severe, yet in no instance did the urinary lead levels approach those described in this patient. The effects of chelation therapy with calcium disodium versenate are discussed and the results are similar to those found in tetraethyl lead poisoning. Blood lead levels of up to 3-91 mumol/l (81 mug/100 g) occurred but these levels were not raised commensurate with the urinary lead output. The levels of deltaaminolaevulinic acid (ALA) in the urine were not significantly raised and this report shows that the urinary lead levels give a better guide to the degree of absorption of tetramethyl lead compared with the blood lead or urinary ALA levels. The report illustrates that tetramethyl lead is less toxic to man than tetraethyl lead.
Language of Publication: English
Unique Identifier: 76062265

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MeSH Heading (Major): Organometallic Compounds|*AA; Tetraethyl Lead|*AA/ME/PO/TO
MeSH Heading: Accidents, Occupational; Adult; Aminolevulinic Acid|UR; Case Report; Chelating Agents|TU; Comparative Study; Edetic Acid|TU; Feces|AN; Human; Lead|AN/BL/UR; Lead Poisoning|DT; Male; Penicillamine|TU

Publication Type: JOURNAL ARTICLE
ISSN: 0007-1072
Country of Publication: ENGLAND

Record 21 from database: MEDLINE
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Title: Atomic absorption analysis of some trace metals of toxicological interest.
Author: Van Ormer DG
Address
Source: J Forensic Sci, 1975 Oct, 20:4, 595-623
Abstract: A selective and critical review, mainly from 1971 to 1974, of atomic absorption applied to the determination of eight toxic metals (lead, mercury, cadmium, thallium, arsenic, bismuth, beryllium, and boron) in blood, urine, and tissue is presented. Discussion involves both flame and flameless atomization, sample preparation, matrix modification, background correction, and contamination. Advantages of other atomic spectrometric techniques and use of recent confirmatory instrumental methods are included. Some normal and toxic levels are mentioned.
Language of Publication: English
Unique Identifier: 76026441

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MeSH Heading (Major): Metals|*AN; Spectrophotometry, Atomic Absorption|*/IS/MT
MeSH Heading: Arsenic|AN; Beryllium|AN; Bismuth|AN; Boron|AN; Cadmium|AN; Comparative Study; Forensic Medicine; Human; Lead|AN; Mercury|AN; Organometallic Compounds|AN; Specimen Handling; Thallium|AN; Trace Elements|AN

Publication Type: JOURNAL ARTICLE; REVIEW
ISSN: 0022-1198
Country of Publication: UNITED STATES

Record 22 from database: MEDLINE
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Title: Neurofibrillary changes following childhood lead encephalopathy.
Author: Niklowitz WJ; Mandybur TI
Address
Source: J Neuropathol Exp Neurol, 1975 Sep, 34:5, 445-55
Abstract: This report details the findings in a patient who survived severe lead encephalopathy at age 2 1/4 years, to die 42 years later in a state of severe mental deterioration. The brain revealed diffuse cortical atrophy, most severe in the temporal lobes, followed by hippocampi, amygdaloid nuclei and frontal cortex. Numerous pyramidal cells of the forebrain grisea contained Alzheimer's neurofibrillary tangles. The remaining pyramidal cells of the hippocampi exhibited granulo-vacuolar degeneration. Many senile plaques were present predominantly in the atrophic temporal cortex. Electron microscopic examination revealed many 800 A twisted tubules in the tangles. Atomic absorption spectrophotometry disclosed a tenfold increase of lead in frontal and temporal cortices as compared to suitable controls. The possibility that toxic levels of lead in any form could result in the formation of Alzheimer's fibrillary tangles is discussed.
Language of Publication: English
Unique Identifier: 76026642

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MeSH Heading (Major): Brain|*PA/UL; Lead Poisoning|ME/*PA; Neurofibrils|*UL
MeSH Heading: Adult; Aluminum|AN; Alzheimer Disease|PA; Amygdaloid Body|PA; Animal; Brain Chemistry; Case Report; Cerebellum|PA; Cerebral Cortex|PA; Hippocampus|PA; Human; Lead|AN; Male; Rabbits; Sclerosis; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE
ISSN: 0022-3069
Country of Publication: UNITED STATES

Record 23 from database: MEDLINE
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Title: Age and sensitivity to lead toxicity: a review.
Author: McCabe EB
Address
Source: Environ Health Perspect, 1979 Apr, 29:, 29-33
Abstract: During the past 20 years considerable attention has been focused on the epidemiologic features of childhood lead poisoning in the United States. Large numbers of children with symptomatic intoxication, as well as those with incipient symptoms, were commonplace a decade ago for physicians working in inner-city hospitals. With the recent availability of improved screening techniques, as well as a variety of environmental control measures, the incidence of symptomatic lead poisoning in children has diminished significantly in recent years. With the focus shifting from children with dangerously elevated body lead burdens to those with less significant exposures, increased attention has been directed to the various inherent metabolic and physical characteristics of the young that may influence the toxic effects of lead exposure. A number of differences with respect to lead exposure, absorption and retention, and varying nutritional conditions between children and older individuals are discussed. Experimental studies dealing with age differences of lead-treated animals are examined, and relevant human studies are reviewed.
Language of Publication: English
Unique Identifier: 80068793

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MeSH Heading (Major): Lead Poisoning|*EP/ME
MeSH Heading: Adolescence; Adult; Age Factors; Child; Digestive System|ME; Environmental Exposure; Female; Human; Lead|ME; New York; Nutrition; Pregnancy; Suburban Population; United States; Urban Population

Publication Type: JOURNAL ARTICLE
ISSN: 0091-6765
Country of Publication: UNITED STATES

Record 24 from database: MEDLINE
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Title: Occupational lead intoxication: report of four cases.
Author: Grimsley EW; Adams Mount L
Address: Department of Internal Medicine Education, Memorial Medical Center, Savannah, Ga 31403-3089.
Source: South Med J, 1994 Jul, 87:7, 689-91
Abstract: We discuss the cases of four immigrant workers in whom lead intoxication developed via inhalation while they were cutting steel beams removed from a dismantled bridge. They all had toxic lead levels with symptoms and received chelation therapy; the therapy was followed by a decrease in blood lead levels. Rebound increases in their blood lead levels and return of the symptoms necessitated two additional chelation treatments. Prevention is certainly superior to treatment, and these cases underscore the importance of prevention of occupational lead exposure. These workers should have been provided with protective clothing to minimize the accumulation of lead on their skin and hair. This clothing should have been left at the work site to protect the members of the workers' households. They should also have been provided with respiratory protection by the strict use of respirators and by engineering controls. Physicians should be aware of the potential health problems related to lead intoxication.
Language of Publication: English
Unique Identifier: 94294855

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MeSH Heading (Major): Lead Poisoning|DT/*ET/PC; Occupational Diseases|DT/*ET/PC
MeSH Heading: Adult; Case Report; Chelating Agents|AD; Human; Lead|BL; Male; Middle Age

Publication Type: JOURNAL ARTICLE
ISSN: 0038-4348
Country of Publication: UNITED STATES

Record 25 from database: MEDLINE
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Title: Lead in pet foods and processed organ meats. A human problem?
Author: Hankin L; Heichel GH; Botsford RA
Address
Source: JAMA, 1975 Feb, 231:5, 484-5
Abstract: The finding that canned pet foods contain considerable amounts of lead is important, since it had been alleged that some of these products are used for human consumption. The lead content of canned dog and cat food ranged from 0.9 to 7 ppm, and ingestion of 170 gm (6 oz) could provide up to 0.95 mg of this toxic element. The lead probably comes from organ meats used in the manufacture of pet foods. The lead content of liverwurst ranged from 1.6 to 7.6 ppm.
Language of Publication: English
Unique Identifier: 75097952

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MeSH Heading (Major): Animal Feed|*AN; Lead|*AN/ME
MeSH Heading: Age Factors; Animal; Cats; Dogs; Food Contamination; Food-Processing Industry; Human; Hyperkinesis|ET; Kidney|ME; Lead Poisoning|CO; Liver|ME; Spectrophotometry, Atomic Absorption; United States

Publication Type: JOURNAL ARTICLE
ISSN: 0098-7484
Country of Publication: UNITED STATES

Record 26 from database: MEDLINE
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Title: History and background of protoporphyrin testing.
Author: Labbé RF
Address
Source: Clin Chem, 1977 Feb, 23:2 PT. 1, 256-9
Abstract: Lead intoxication was first associated with increased coproporphyrin excretion almost 100 years ago; but not until the 1930's were abnormalities in blood protoporphyrin detected. These later findings have been interpreted as an inhibition by lead of iron incorporation into protoporphyrin during heme synthesis. The testing and application of this hypothesis had to await three more decades of research during which prophyrin/heme biosynthesis was elucidated, control of the pathway was intensively studied, and methodology was greatly improved. The heme biosynthetic pathway is uniquely affected by lead at several sites. These toxic effects can be manifested as increased coproporphyrin and delta-aminolevulinate excretion, decreased erythrocyte delta-aminolaevulinate dehydratase activity, and increased erythrocyte protoporphyrin concentration, all of which have been used and promoted as diagnostic tests for lead intoxication. Among these, the last appears to be becoming the test of choice. The historical background of this development is discussed from a biochemical viewpoint.
Language of Publication: English
Unique Identifier: 77089839

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MeSH Heading (Major): Lead Poisoning|*DI; Porphyrins|*AN; Protoporphyrins|*AN/BL
MeSH Heading: Erythrocytes|ME; Ferrochelatase|ME; Heme|BI; Human; Iron|ME; Lead|PD; Porphobilinogen Synthase|BL; Zinc|ME

Publication Type: JOURNAL ARTICLE
ISSN: 0009-9147
Country of Publication: UNITED STATES

Record 27 from database: MEDLINE
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Title: Depressed excretion of 6 beta-hydroxycortisol in lead-toxic children.
Author: Saenger P; Markowitz ME; Rosen JF
Address
Source: J Clin Endocrinol Metab, 1984 Feb, 58:2, 363-7
Abstract: 6 beta-Hydroxycortisol (6 beta OHF) is a highly polar metabolite of cortisol, probably formed in the endoplasmic reticulum of hepatocytes by cytochrome P-450-dependent microsomal monoxygenases. Lead decreases the activity of cytochrome P-450-dependent microsomal hydroxylases in vivo and in vitro. To examine possible inhibitory effects of lead on 6 beta OHF metabolism, urinary 6 beta OHF excretion was measured in 26 children with mild to moderate increases in blood lead concentrations. Children were divided into 2 groups on the basis of their response to the EDTA provocative test. This test was used to assess the size of chelatable and potentially toxic lead stores in such children. Children with elevated urinary lead excretion after an EDTA provocative test, i.e. elevated tissue lead stores, had markedly decreased urinary excretion of 6 beta OHF (178 +/- 15 micrograms/m2 X 24 h) compared to children who had negative tests (333 +/- 40 micrograms/m2 X 24 h; P less than 0.01); their urinary cortisol excretion was not different from that of age-matched controls. These findings suggest that lead, at relatively low concentrations, may interfere with hepatic microsomal formation of a cortisol metabolite.
Language of Publication: English
Unique Identifier: 84111936

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MeSH Heading (Major): Hydrocortisone|*AA/UR; Lead Poisoning|DT/EN/*ME; Microsomes, Liver|*EN
MeSH Heading: Child; Child, Preschool; Cytochrome P-450|ME; Edetic Acid|DU; Female; Human; Lead|ME; Male; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE
ISSN: 0021-972X
Country of Publication: UNITED STATES
CAS Registry/EC Number: 50-23-7 (Hydrocortisone); 53-35-0 (6 beta-hydroxycortisol); 60-00-4 (Edetic Acid); 7439-92-1 (Lead); 9035-51-2 (Cytochrome P-450)

Record 28 from database: MEDLINE
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Title: Nutritional factors in relation to heavy metal toxicants.
Author: Levander OA
Address
Source: Fed Proc, 1977 Apr, 36:5, 1683-7
Abstract: An increased environmental exposure to various toxic heavy metals such as lead, cadmium, or mercury seems to be a fact of 20th-century life. But relatively little attention has been paid to the possible implications of sucy exposure for the nutritional status of humans and animals. This review summarizes the information available concerning the effect of various nutritional factors in resistance to metal toxicants and the effect of heavy metal toxicity on nutritional status. In particular, the following questions are considered: 1) Are there any examples of heavy metal toxicity that are potentiated by a nutritional deficiency? 2) Is there any evidence that nutritional deficiency can be caused by heavy metal toxicity? 3) Is there any proof that heavy metal toxicity can be decreased by an excess intake of nutrients: 4) Is there any proof that heavy metal toxicity can be increased by an excess intake of nutrients? The discussion is focused primarily on studies with animal models but, wherever possible, implications for human health are pointed out.
Language of Publication: English
Unique Identifier: 77138686

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MeSH Heading (Major): Metals|PO/*TO; Nutrition|*
MeSH Heading: Animal; Ascorbic Acid|TU; Cadmium|ME; Cadmium Poisoning|CO/DH; Calcium|DF/PD; Copper|DF; Dose-Response Relationship, Drug; Human; Iron|DF/PD; Lead|ME; Lead Poisoning|CO; Mercury Poisoning|PC; Molecular Weight; Protein Deficiency|CO; Selenium|TU; Vitamin E Deficiency|CO; Zinc|ME/PD

Publication Type: JOURNAL ARTICLE
ISSN: 0014-9446
Country of Publication: UNITED STATES

Record 29 from database: MEDLINE
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Title: Neuropathology of the hippocampus and its susceptibility to neurotoxic insult.
Author: Stoltenburg Didinger G
Address: Institute of Neuropathology, Free University, Klinikum Steglitz, Berlin.
Source: Neurotoxicology, 1994 Fal, 15:3, 445-50
Abstract: The hippocampal formation and its cholinergic input are an important neurobiological substrate for learning and memory processes. Since alterations in learning and memory are a common consequence of toxicant exposure it is possible that the hippocampus is an important target site for neurotoxicity. In fact, the hippocampus has been shown to be preferentially susceptible to a wide variety of toxic insults. For example, the hippocampus is damaged by environmental toxicants such as heavy metals, drugs of abuse such as alcohol and by cerebrovascular insufficiency finally resulting in hypoxia. The NMDA subtype of glutamatergic receptor plays a major role in learning and memory and in excitoxicity secondary to ischemia, hypoglycemia and trauma. The nature of the adverse effects of neurotoxins at this receptor site may be linked to the neurobiological characteristics that make this structure uniquely susceptible to toxic insult.
Language of Publication: English
Unique Identifier: 95157801

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MeSH Heading (Major): Hippocampus|AH/*DE/PH
MeSH Heading: Animal; Ethanol|TO; Human; Lead|TO; Long-Term Potentiation; Receptors, N-Methyl-D-Aspartate|AN

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0161-813X
Country of Publication: UNITED STATES

Record 30 from database: MEDLINE
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Title: The relationship of hyperactivity to moderately elevated lead levels.
Author: David OJ; Hoffman SP; Clark J; Grad G; Sverd J
Address
Source: Arch Environ Health, 1983 Nov-Dec, 38:6, 341-6
Abstract: Controversy exists with respect to whether moderately elevated lead levels are toxic in certain children with various central nervous system dysfunctions. One way of addressing this controversy is to remove the lead; if the condition is ameliorated a presumption of toxicity becomes reasonable. Such a strategy is reported herein. Children with an operationally defined central nervous system dysfunction (hyperactivity) and moderately elevated lead levels were treated with a lead chelating agent in a random allocation double blind treatment regimen. The finding of statistically significant and obvious behavioral improvement reported by three separate evaluators (i.e., parent, teacher, and treating physician) of the child suggests that the presumption of a toxic relationship between moderately elevated lead levels and hyperactivity is supported.
Language of Publication: English
Unique Identifier: 84126972

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MeSH Heading (Major): Hyperkinesis|*BL/DT; Lead|*BL
MeSH Heading: Analysis of Variance; Child; Child Behavior|DE; Child, Preschool; Double-Blind Method; Female; Human; Male; Methylphenidate|TU; Penicillamine|TU; Socioeconomic Factors; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type: CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
ISSN: 0003-9896
Country of Publication: UNITED STATES
CAS Registry/EC Number: 113-45-1 (Methylphenidate); 52-67-5 (Penicillamine); 7439-92-1 (Lead)

Record 31 from database: MEDLINE
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Title: Cytotoxicity of heavy metals in the human small intestinal epithelial cell line I-407: the role of glutathione.
Author: Keogh JP; Steffen B; Siegers CP
Address: Institute for Toxicology, Medical University of LÂubeck, Germany.
Source: J Toxicol Environ Health, 1994 Nov, 43:3, 351-9
Abstract: Cytotoxicities of metal salts were determined in the intestinal epithelial cell line I-407 in microwell culture plates over 48 h using the widely utilized and accepted neutral red uptake procedure. Rank order cytotoxicities induced by the metal salts (in terms of LC50 values) were found to be HgCl2 (32 microM) > CdCl2 (53 microM) > CuCl2 (156 microM) > T12SO4 (377 microM) > Pb(NO3)2 (1.99 mM). Combined administration of the two most toxic metals at their LC50's showed that their toxicities were not additive or synergistic. The role of glutathione in determining toxicity induced by the metal salts in these cells was assessed by inhibition of its synthesis. Buthionine sulfoximine pretreatment at 1 mM, which was not toxic to the cells, caused sustained reduction in cellular glutathione content (to 13.8% after 48 h) and increased toxicities induced by HgCl2 (5.7-fold) and CuCl2 (1.44-fold) as shown by reductions in the LC50 values. Toxicity induced by the other metals remained unaffected. Administration of glutathione with either HgCl2 or CdCl2 did not protect the cells against their toxicity, and in the case of cadmium its toxicity was exacerbated. N-Acetylcysteine diminished toxicity induced by mercury but not cadmium.
Language of Publication: English
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