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S M Bradberry

Publications and source records attributed to S M Bradberry.

12 recordsLinked to original sources
PubMed2000

Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.

INTRODUCTION: Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation, and disruption of acetylcoenzyme A metabolism. Between January 1962 and January 1999, 66 cases of chlorophenoxy herbicide poisoning following ingestion were reported in the literature. FEATURES FOLLOWING INGESTION: Adjuvants in the formulations may have contributed to some of the features observed. Vomiting, abdominal pain, diarrhea, and, occasionally, gastrointestinal hemorrhage were early effects. When present, hypotension was predominantly due to intravascular volume loss, although vasodilation and direct myocardial toxicity may have contributed in some cases. Neurotoxic features included coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation, and paralysis. Hypoventilation occurred not infrequently, usually in association with central nervous system depression, but respiratory muscle weakness was a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, and myotonia were observed and increased creatine kinase activity was noted in some cases. Other clinical features reported included metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia, and hyperventilation. Twenty-two of 66 patients died. FEATURES FOLLOWING DERMAL AND INHALATIONAL EXPOSURE: Substantial dermal or inhalational 2,4-dichlorophenoxyacetic acid exposure has occasionally led to systemic features but no such reports have been published in the last 20 years and no fatalities have been reported at any time. Substantial dermal exposure has been reported to cause mild gastrointestinal irritation after a latent period followed by progressive mixed sensory-motor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have also occurred after occupational inhalation exposure, with or without dermal exposure. MANAGEMENT: In addition to supportive care, alkaline diuresis to enhance herbicide elimination should be considered in all seriously poisoned patients. Limited clinical data suggest that hemodialysis produces similar herbicide clearance to alkaline diuresis without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient. CONCLUSIONS: While chlorophenoxy herbicide poisoning is uncommon, ingestion of a chlorophenoxy herbicide can result in serious and sometimes fatal sequelae. In severe cases of poisoning, alkaline diuresis or hemodialysis to increase herbicide elimination should be considered.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2000

Chemical contamination of private drinking water supplies in the West Midlands, United Kingdom.

INTRODUCTION: In the United Kingdom, private drinking water supplies are subject to much less stringent sampling and testing regimes than are public supplies. Information regarding the quality of private drinking water supplies is disparate and poorly defined. The aim of this study was to collate the data for chemical contamination of private drinking water supplies in the West Midlands, a region of Central England with a population of 5.3 million. METHODS: The most recent year's data on the number of private supplies, the number of supplies sampled, and the number and type of failures for chemical parameters were obtained from District and Local Authorities in the West Midlands Region. RESULTS: Data covered 12-month periods during 1995-1996. Of the 6013 private supplies identified, samples from 1297 had been tested for chemical parameters during the period of the study. A total of 420 individual failures for chemical parameters were reported in 386 water supplies. The majority of breaches of United Kingdom and European Union standards were due to increased concentrations of nitrates (270), magnesium (21), manganese (17), and iron (15). Increased turbidity was present in 27 cases. Only 6 samples breached the standard for lead and 6 for pesticides. CONCLUSIONS: Over a quarter of the supplies tested during the period of the study were in breach of United Kingdom and European Union legislation. Of the reported failures, the high concentrations of nitrate and nitrite, lead, copper, and sulfate are of concern to health and remedial action is warranted. Regular sampling of private drinking water supplies remains necessary to prevent risk to health from a wide variety of toxic contaminants.

Environmental Monitoring↗
PubMed1999

Therapeutic review: is ascorbic acid of value in chromium poisoning and chromium dermatitis?

INTRODUCTION: Repeated topical exposure to chromium(VI) may cause an allergic contact dermatitis or the formation of chrome ulcers. Systemic toxicity may occur following the ingestion of a chromium(VI) salt, from chromium(VI)-induced skin burns, or from inhalation of chromium(VI) occurring occupationally. Soluble chromium(VI) salts are usually absorbed more easily and cross cell membranes more readily than trivalent chromium salts, and, therefore chromium(VI) is more toxic than chromium(III). In experimental studies, endogenous ascorbic acid in rat lung, liver, and kidney and human plasma, effectively reduces chromium(VI) to chromium(III). The administration of exogenous ascorbic acid has been advocated therefore in the treatment of systemic chromium poisoning and chromium dermatitis to enhance the extracellular reduction of chromium(VI) to the less bioavailable chromium(III). REVIEW: In vitro experiments confirm that the addition of ascorbic acid to plasma containing chromium(VI) leads to a dose-dependent reduction of chromium(VI) to chromium(III). In animal studies, parenteral ascorbic acid 0.5-5 g/kg significantly reduced chromium-induced nephrotoxicity when administered 30 minutes before parenteral sodium dichromate and up to 1 hour after parenteral sodium chromate dosing. Parenteral ascorbic acid 0.5-5 g/kg also reduced mortality when given orally up to 2 hours after oral potassium dichromate dosing. However, the administration of parenteral ascorbic acid more than 2 hours after parenteral chromate in these experimental studies did not protect against renal damage, and parenteral ascorbic acid given 3 hours postparenteral chromate increased toxicity. In addition, there is no confirmed clinical evidence that the administration of ascorbic acid lessens morbidity or mortality in systemic chromium poisoning. A possible reason for the lack of benefit of ascorbic acid when administration is delayed, is that chromium(VI) cellular uptake has occurred prior to ascorbic acid administration. Topical 10% ascorbic acid has been claimed to reduce significantly the healing time of experimentally induced chrome ulcers in guinea pigs. The proposed mechanism is reduction on the skin surface of chromium(VI) to chromium(III). Several case reports suggest that topical ascorbic acid is effective in the management of chromium dermatitis but this has not been confirmed in controlled clinical trials and, moreover, the practical difficulties of frequent application are likely to limit its usefulness. DISCUSSION: Based on experimental studies, substantial amounts of ascorbic acid would need to be administered, preferably parenterally, soon after exposure to prevent systemic toxicity from chromium(VI) in humans. However, as ascorbic acid is a metabolic precursor of oxalate, the administration of ascorbic acid in high dose could lead to acute oxalate nephropathy, particularly in the presence of renal failure. While smaller doses of ascorbic acid (e.g., 10 g intravenously) are not toxic, such doses probably will not reduce the mortality from systemic chromium poisoning. CONCLUSION: There is currently insufficient evidence to advocate the use of ascorbic acid in the management of systemic chromium toxicity. Topical ascorbic acid may reduce dermal hexavalent chromium exposure, but this observation must be confirmed in controlled studies.

Animals↗
PubMed1999

Therapeutic review: do diethyldithiocarbamate and disulfiram have a role in acute nickel carbonyl poisoning?

INTRODUCTION: Sodium diethyldithiocarbamate and disulfiram have been proposed as effective nickel chelators. This paper examines the value of these compounds in the treatment of acute nickel carbonyl poisoning by reviewing published experimental and clinical data. REVIEW: In 2 studies, parenteral administration of diethyldithiocarbamate 50-100 mg/kg to rats immediately following nickel carbonyl exposure ensured the survival of all animals: Mortality fell from 73% to 8% when diethyldithiocarbamate was administered at 10 minutes in a third study. In the same study, there was no protection when diethyldithiocarbamate was administered at 6 hours, and the mortality was greater, though not significantly different, when diethyldithiocarbamate was administered at 24 hours. In another study in mice, total protection was afforded by diethyldithiocarbamate given at 8 hours but this protection was limited when diethyldithiocarbamate was administered at 24 hours, with diethyldithiocarbamate 100 mg/kg apparently being less protective than diethyldithiocarbamate 50 mg/kg. In 3 studies, oral diethyldithiocarbamate administration was less effective than parenteral administration. There are no adequately controlled clinical studies of the use of diethyldithiocarbamate in acute nickel carbonyl poisoning despite claims that this therapy has been effective in the treatment of several hundred such patients. Disulfiram, a metabolite of diethyldithiocarbamate, offered complete protection against nickel carbonyl-induced toxicity when administered in a dose of 1000 mg/kg to rats immediately following nickel carbonyl exposure. In contrast, disulfiram 500 mg/kg offered no protection and disulfiram 1500 mg/kg appeared to enhance mortality, possibly by increasing brain nickel accumulation. CONCLUSION: Animal studies demonstrate that diethyldithiocarbamate is an effective antidote in acute nickel carbonyl poisoning when it is administered parenterally soon after exposure. However, as no adequately controlled clinical studies have been performed, further clinical data are required before diethyldithiocarbamate can be recommended routinely in acute nickel carbonyl poisoning. If diethyldithiocarbamate is to be employed, it should be administered parenterally soon after exposure as delay in administration may increase nickel carbonyl toxicity. There are currently insufficient data to recommend disulfiram as an alternative to diethyldithiocarbamate even when diethyldithiocarbamate is not available.

Animals↗
PubMed1996

Elemental mercury-induced skin granuloma: a case report and review of the literature.

BACKGROUND: Injection of elemental mercury is rare and only some 72 cases have been reported in the literature over the period 1923-1995. Direct subcutaneous injection or extravasation of mercury injected into blood vessels can produce local granulomata and abscesses. Unless intravascular mercury injection has occurred, clinical signs of mercury toxicity are usually absent though four cases of systemic toxicity have been reported following isolated subcutaneous injection without evidence of elemental mercury dissemination. CASE REPORT: We report a further case of subcutaneous injection by gunshot of elemental mercury, with subsequent granuloma formation, in a 19-year old man who was admitted with an eight month history of a tender enlarging mass in his left antecubital fossa, while on active military service. Surgical removal of mercury from a presumed mercury-tipped bullet was undertaken but was incomplete and the patient declined further operative intervention as he remained asymptomatic. Chelation therapy was not instituted. Serum and urine mercury concentrations were measured for six years after presentation. CONCLUSIONS: We recommend that cases of subcutaneous metallic mercury injection should be managed by complete surgical excision of the granuloma under X ray control and serial monitoring of blood and urine mercury concentrations.

Adult↗
PubMed1995

Multiple-dose activated charcoal: a review of relevant clinical studies.

Although many studies in animals and volunteers have demonstrated that multiple-dose activated charcoal increases drug elimination significantly, this therapy has not been shown in a controlled study in poisoned patients to reduce morbidity and mortality. Further clinical studies are required to establish its role and the optimum dosage regimen of charcoal to be administered. Based on current evidence, multiple-dose activated charcoal should only be considered if a patient has ingested a life-threatening amount of phenobarbital (phenobarbitone), carbamazepine, theophylline, quinine, dapsone or salicylate. In all of these cases there are data to confirm enhanced elimination, though no controlled studies have demonstrated clinical benefit.

Charcoal↗
PubMed1995

Disturbances of potassium homeostasis in poisoning.

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.

Homeostasis↗
PubMed1994

Methemoglobinemia caused by the accidental contamination of drinking water with sodium nitrite.

Sodium nitrite is used commercially as a coloring agent, a food preservative and a corrosion inhibitor. Accidental poisoning usually results from the ingestion of contaminated food and water and causes gastrointestinal irritation, vasodilatation and methemoglobinemia with subsequent tissue hypoxia. We describe an unusual case of sodium nitrite-induced methemoglobinemia following the ingestion of drinking water contaminated with a corrosion inhibitor. To our knowledge this is the first report of such a case.

Adult↗
PubMed1994

Fatal methemoglobinemia due to inhalation of isobutyl nitrite.

Isobutyl nitrite is a popular recreational drug among both homosexuals and heterosexuals as it is alleged to enhance sexual pleasure and prolong orgasm. In contrast to the ingestion of this volatile nitrite, inhalation is associated only rarely with serious sequelae, though symptomatic methemoglobinemia may occur. The case reported is the first documented fatality from inhalation of isobutyl nitrite. The widespread use of isobutyl nitrite is a cause for concern and physicians should be aware of the potentially fatal consequence of abuse, particularly in those with ischemic heart disease, and its management.

Administration, Inhalation↗