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PubMed1977

Lead in enamel and saliva, dental caries and the use of enamel biopsies for measuring past exposure to lead.

Enamel biopsies taken from schoolchildren in a community where exposure to lead was a health hazard were analyzed for lead and fluoride. The children with high enamel lead had significantly higher caries scores than the children with low enamel lead, in spite of the fact that the high lead group also was higher in enamel fluoride. There was no increase in enamel lead with age. The lead in saliva was only a fraction of that in blood. Infants with lead poisoning showed higher saliva lead than a normal infant. The use of the lead in enamel biopsies and in saliva for measuring exposure to lead is discussed.

Adult↗
PubMed1996

Surveillance for waterborne-disease outbreaks--United States, 1993-1994.

PROBLEM/CONDITION: Since 1971, CDC and the U.S. Environmental Protection Agency have maintained a collaborative surveillance system for collecting and periodically reporting data that relate to occurrences and causes of waterborne-disease outbreaks (WBDOs). REPORTING PERIOD COVERED: This summary includes data for January 1993 through December 1994 and for previously unreported outbreaks in 1992. DESCRIPTION OF THE SYSTEM: The surveillance system includes data about outbreaks associated with water intended for drinking (i.e., drinking water) and those associated with recreational water. State, territorial, and local public health departments are primarily responsible for detecting and investigating WBDOs and voluntarily reporting them to CDC on a standard form. RESULTS: For the 2-year period 1993-1994, 17 states and one territory reported a total of 30 outbreaks associated with drinking water. These outbreaks caused an estimated 405,366 persons to become ill, including 403,000 from an outbreak of cryptosporidiosis in Milwaukee, the largest WBDO ever documented in the United States, and 2,366 from the other 29 outbreaks. No etiologic agent was identified for five (16.7%) of the 30 outbreaks. The protozoan parasites Giardia lamblia and Cryptosporidium parvum caused 10 (40.0%) of the 25 outbreaks for which the etiologic agent was identified. Two outbreaks of cryptosporidiosis occurred in large metropolitan areas (i.e., Milwaukee and Las Vegas/Clark County) and were associated with deaths among immunocompromised persons. The waterborne nature of these two outbreaks was not recognized until at least 2 weeks after the onset of the Milwaukee outbreak and until after the end of the Las Vegas outbreak. Campylobacter jejuni was implicated for three outbreaks and the following pathogens for one outbreak each: Shigella sonnei, Shigella flexneri, non-O1 Vibrio cholerae (in a U.S. territory; the vehicle was commercially bottled water), and Salmonella serotype Typhimurium (the outbreak was associated with seven deaths). Eight outbreaks of chemical poisoning were reported: three were caused by lead (one case each), two by fluoride, two by nitrate and one by copper. Twenty (66.7%) of the 30 outbreaks were associated with a well-water source. Fourteen states reported a total of 26 outbreaks associated with recreational water, in which an estimated 1,714 persons became ill. Fourteen (53.8%) of these 26 were outbreaks of gastroenteritis. The etiologic agent in each of these 14 outbreaks was identified; 10 (71.4%) were caused by G. lamblia or C. parvum. Six of these 10 were associated with chlorinated, filtered pool water, and three with lake water. One of the latter was the first reported outbreak of cryptosporidiosis associated with the recreational use of lake water. Four outbreaks of lake water-associated bacterial gastroenteritis were reported, two caused by S. sonnei, one by S. flexneri, and one by Escherichia coli O157:H7. Nine outbreaks of hot tub- whirlpool-, or swimming pool-associated pseudomonas dermatitis were reported. Two outbreaks of swimming pool-associated dermatitis had a suspected chemical etiology. The child who had the one reported case of primary amebic meningoencephalitis, caused by infection with Naegleria fowleri, died. INTERPRETATION: The number of WBDOs reported annually has been similar for each year during 1987-1994, except for an increase in 1992. Protozoan parasites, especially C. parvum and G. lamblia, remain important etiologic agents of WBDOs. The outbreaks of cryptosporidiosis in Milwaukee and Las Vegas demonstrate that WBDOs can occur in large metropolitan areas. Surveillance methods are needed that expedite the detection of WBDOs and the institution of preventive measures (e.g., boil-water advisories). ACTIONS TAKEN: Surveillance data that identify the types of water systems, their deficiencies, and the etiologic agents associated with outbreaks are used to evaluate the adequacy of current technologies for prov

Animals↗
PubMed1990

[The role of fluorides in the prevention of dental caries].

By searching for the cause of mottled enamel--which was known already in Italy of the Roman period--the researchers Churchill, Smith, Lantz and Velu were almost simultaneously led to the recognition that the surplus fluoride in drinking water is the cause of the phenomenon. Thereafter, by Dean and his collaborators it was proved by means of mass caries screenings and chemical analyses of drinking water that if the drinking water contains 1 mg F-ion by litre then there is no mottle on the enamel while the condition of the teeth is substantially by about 50 to 60% better than those of consumers of drinking water poor in fluorine. The safely tolerable dose is 1.5 to 2.0 mg by litre. Obviously this is a populational resume drinking water which is natural or artificially enriched with fluoride. Employment of the fluorides has considerably been extended in the course of research and development. The methods can be grouped in several manners. In the author's opinion the best grouping is: a) collective and b) individual methods. The element F belongs to the group of the + type poisoning elements which, however, does not occur in nature because when getting into nature it immediately combines with ther elements and, therefore, in nature only its various salts are met with. Chronical fluorosis is caused by consuming 5 to 10 mg fluoride through many years. 100 to 200 mg is a lightly poisoning dose with children or adults. A mortal dose is 1200 to 2500 mg.

Administration, Oral↗
PubMed1976

[Effect of subacute fluorine poisoning in the rabbit on fluorine and phosphorus-calcium metabolism and on radiography of the skeleton].

Rabbit subacute fluoride intoxication effects (21,4 mg a day for 10 months) are researched on fluor, calcium and phosphorus metabolism and on skeletal radiology. Fluoremy increase (p less than 0.05) and there is a strong fluor retention (p less than 0.01), due to fluor digestive utilization coefficient increase (p less than 0.05), in spite of relative hyperfluorury (p less than 0.05). Calcemy decreases (p less than 0.01), but phosphatemy and alkaline phosphatasemy do not vary but a little. Calcium and phosphorus balances become negative (p less than 0.05), due to calcium digestive utilization coefficient inversion (p less than 0.05) and phosphorus digestive utilization coefficient decrease (p less than 0.05) and hypercalciury (p less than 0.05) and hyperphosphatury (p less than 0.05) with phosphorus renal reabsorption coefficient decrease (p less than 0.05). Some skeletal radiological abnormalities appear on rachis and limbs.

Alkaline Phosphatase↗
PubMed1988

Acute hydrofluoric acid exposure.

Significant local and systemic toxicity may occur from hydrofluoric acid by all routes of exposure. Prompt decontamination by removal from the source and copious irrigation of eyes and skin are essential to reduce morbidity and mortality. Ingestion of small amounts of HF can lead to rapid systemic poisoning and death. Calcium gluconate therapy has become the preferred method of detoxifying the fluoride ion, although its efficacy is based mainly on anecdotal reports and poorly controlled clinical studies. Therefore, more basic research is needed to elucidate the pathophysiology of local toxicity and the best therapeutic modalities to limit injury. All significant exposures should be evaluated by health care personnel familiar with the potential toxicity of this compound.

Accidents↗
PubMed1987

Effects of esterase inhibitors and buthionine sulfoximine on the prevention of acetaminophen hepatotoxicity by N-acetylcysteine.

Mice poisoned with acetaminophen were treated with esterase inhibitors, buthionine sulfoximine, and N-acetyl-L-lysine in experiments designed to explore the mechanism of N-acetylcysteine protection in vivo. Three esterase inhibitors, phenylmethylsulfonyl fluoride, bis-(p-nitrophenyl)-phosphate, and diisopropylfluorophosphate, had no effect on the antidote effectiveness of N-acetylcysteine, although each provided partial protection against acetaminophen poisoning. Buthionine sulfoximine, a specific inhibitor of gamma-glutamyl cysteine synthetase, antagonized the antidote effect of N-acetylcysteine. Acetaminophen-induced hepatotoxicity, as measured by plasma alanine aminotransferase activity, and mortality failed to decline, consistent with stimulation of glutathione synthesis as the primary mechanism of antidote protection. N-Acetyl-L-lysine was given at doses up to ten-fold higher than N-acetylcysteine yet had no effect on acetaminophen hepatotoxicity or its prevention by N-acetylcysteine. These results advance the view that N-acetylcysteine acts primarily as a glutathione precursor. They further suggest the esterase inhibitors limit poisoning by acetaminophen and may be useful agents in antagonizing the toxicity of other metabolically activated drugs.

Acetaminophen↗
PubMed1975

Transport of sugars and amino acids in bacteria. XV. Comparative studies on the effects of various energy poisons on the oxidative and phosphorylating activities and energy coupling reactions for the active transport systems for amino acids in E. coli.

The effects of various energy poisons on oxidation of respiratory substrate, synthesis of cellular ATP, and energy transformation reaction in intact Escherichia coli cells were studied systematically. Various mutants were, therefore, used in which specific functions in the energy-transducing reactions were defective or altered. The energy poisons examined were: sodium azide. DPPA and azidebenzenes which are inhibitors of respiratory-chain phosphorylation, SF6847, and CCCP which are known to be uncouplers, zinc sulfate which is an inhibitor for certain dehydrogenases, and sodium arsenate and sodium fluoride which are inhibitors of glycolytic synthesis of ATP. The preferential inhibitions occurred in the oxidation reactions with certain respiratory substrates by energy poisons used. DPPA inhibited glycerol oxidation much more strongly than succinate oxidation. However, DPPA could inhibit the oxidation of both glycerol 3-phosphate and succinate by membrane fraction strongly while the oxidation of NADH and D-lactate slightly. It inhibited glycerol 3-phosphate dehydrogenase [EC 1.1.2.1] strongly as well as succinate dehydrogenase [EC 1.3.99.1],.but not D-lactate dehydrogenase of membrane fraction. MAB and other azidebenzene derivatives inhibited succinate oxidation preferentially. SF6847 and CCCP inhibited succinate oxidation strongly, while sodium azide inhibited it weakly and these three poisons were less inhibitory for glycerol oxidation. DPPA, sodium azide, SF6847, and CCCP inhibited the synthesis of ATP coupled with respiration but not with glycolysis. Zinc sulfate inhibited the cellular ATP synthesis coupled with either respiration or glycolysis.

Adenosine Triphosphate↗
PubMed1957

Facts and fallacies on industrial poisoning.

Misdiagnosis of diseases as due to industrial poisoning leads to much misunderstanding, higher taxes and insurance rates and "compensation neuroses." It is important to know the concentration of the suspected poison and its specific effects in order to logically indict it as the cause of illness. Examples discussed to illustrate some of the pitfalls of diagnosis in industrial medicine are methylbromide, carbon monoxide, ozone, oxides of nitrogen and of sulfur, hydrogen sulfide, benzene analogs, boron and fluorides.

Carbon Monoxide↗
PubMed2004

Position Paper on urine alkalinization.

This Position Paper was prepared using the methodology agreed by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT). All relevant scientific literature was identified and reviewed critically by acknowledged experts using set criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not considered. A draft Position Paper was then produced and presented at the North American Congress of Clinical Toxicology in October 2001 and at the EAPCCT Congress in May 2002 to allow participants to comment on the draft after which a revised draft was produced. The Position Paper was subjected to detailed peer review by an international group of clinical toxicologists chosen by the AACT and the EAPCCT, and a final draft was approved by the boards of the two societies. The Position Paper includes a summary statement (Position Statement) for ease of use, which will also be published separately, as well as the detailed scientific evidence on which the conclusions of the Position Paper are based. Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis is the prime objective of treatment; the terms forced alkaline diuresis and alkaline diuresis should therefore be discontinued. Urine alkalinization increases the urine elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, mecoprop, methotrexate, phenobarbital, and salicylate. Based on volunteer and clinical studies, urine alkalinization should be considered as first line treatment for patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior. Supportive care, including the infusion of dextrose, is invariably adequate in chlorpropamide poisoning. A substantial diuresis is required in addition to urine alkalinization in the chlorophenoxy herbicides, 2,4-dichlorophenoxyacetic acid, and mecoprop, if clinically important herbicide elimination is to be achieved. Volunteer studies strongly suggest that urine alkalinization increases fluoride elimination, but this is yet to be confirmed in clinical studies. Although urine alkalinization is employed clinically in methotrexate toxicity, currently there is only one study that supports its use. Urine alkalinization enhances diflunisal excretion, but this technique is unlikely to be of value in diflunisal poisoning. In conclusion, urine alkalinization should be considered first line treatment in patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization and high urine flow (approximately 600 mL/h) should also be considered in patients with severe 2,4-dichlorophenoxyacetic acid and mecoprop poisoning. Administration of bicarbonate to alkalinize the urine results in alkalemia (an increase in blood pH or reduction in its hydrogen ion concentration); pH values approaching 7.70 have been recorded. Hypokalemia is the most common complication but can be corrected by giving potassium supplements. Alkalotic tetany occurs occasionally, but hypocalcemia is rare. There is no evidence to suggest that relatively short-duration alkalemia (more than a few hours) poses a risk to life in normal individuals or in those with coronary and cerebral arterial disease.

Alkalies↗