Hydrofluoric acid in the automotive industry: Epidemiology

Hydrofluoric acid in the automotive industry: Epidemiology

From these limited data it appears that sodium nitrite infusion resulted in lower than expected METHB levels, which occurred 35 to 70 minutes followin...

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From these limited data it appears that sodium nitrite infusion resulted in lower than expected METHB levels, which occurred 35 to 70 minutes following the nitrite infusion. The slow fall in METHB levels did not appear to be affected by HBO. Concerns about CAKinduced METHB adding to the toxicity of COHB m a y be unfounded.

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Hydrofluoric Acid in the Automotive Industry= Epidemiology

JM Heard, LK G a r r e r ~ C Siegel / Georgia Poison Control Center, Grady Memorial Hospital, Emory University; DeKalb Medical Center, Atlanta, Georgia In all 22 hydrofluoric acid exposures over an I 1-month period, circumstances of exposure and type of treatment were analyzed. Age distribution was even from 16 to 39 years. Ten of 22 occurred in June and July. Four of the 22 cases were women; one quarter were auto related. The site of exposure could not be determined in four. Fourteen of 18 (78%) occurred at work, with nine of 14 (64%) auto related, two air conditioner cleaners, two rust removers for fa~nc~, and-one jewelry cleaner. Four of 18 (22%) occurred at home, three of four with car products; two of four home exposures occurred with products brought from the workplace. Two of the exposures in unknown locations were with auto products. Thus, 14 of 22 (64%) were with auto products. All reported pain, erythema, or edema. The involved part of the body was: finger(s) only, nine of 22; hand and finger(s), eight; eye, two; abdomen, one; leg, one; arm, one. Eleven (65%) received intra-arterial calcium therapy. Three received subcutaneous and six received topical therapy only. Only one had symptoms suggestive of systemic hypocalcemia. The automotive cleaning products are a major source of hydrofluoric acid exposure. While concentrations are relatively low, exposure is often prolonged and injury may be severe.

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Subacute Home Chlordane Poisoning: Fact or Fallacy

DA Spyker, RR Bond, M Jylkka, PG Bernad / Pharmaceutical Research Associates Inc, Charlottesville, Virginia; Neurology Services Inc, Fairfax, Virginia Chlordane and heptachlor (C/H), currently the subject of a "no US distribution" agreement between Velsicol and the EPA, has been the termiticide of choice in the US since the 1940s. Due to its chemical stability, C/H persists in approximately 70% of the homes in the US. Unquestionably a potent neurotoxin and animal carcinogen, the frequency and severity of injury from inhalation exposure in the home remains unresolved. We report on 68 of the patients living in 30 domiciles from nine states whom we have examined with a chief complaint of chlordane exposure in their home. Their ages ranged from 2 to 63, with a mean of 33 years. Symptom frequency was headache in 67%, gastrointestinal difficulties 63%, fatigue 62%, m e m o r y deficits 57%, personality changes 54%, decreased attention span 52%, n u m b n e s s or paresthesias 45%, disorientation 36%, loss of coordination 30%, dry eyes 25%, and seizures 8%. EMG was abnormal in five of 23 (22%), current perception threshold in two of 11 (18%), electronystagmogram in eight of 13 [62%), and neuropsychiatric testing in nine of 16 (56%). Adipose biopsy in 22 patients showed C/H metabolites in the 11 to 73 percentile of adult normals, but ratio of C/H to DDT + metabolites ranged from 0.5 to 35 with a mean of 4.1 [1 expected). Our patients thus exhibited an elevated C/H body burden relative to DDT, and our findings support the presence of a neurotoxic syndrome with home C/H exposure.

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Field Trial of a Rapid Acetaminophen Meter

MW Shannon, R Saladino, DL McCarthy, KM Parker, LDL Scott, PA Vaughan / Department of Medicine, Children's Hospital, Boston, Massachusetts; Poison Control System, University of Oklahoma

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Health Sciences Center, Oklahoma City; MediSense (UK) Inc, Great Britain We conducted field trials of a newly developed meter that measures serum acetaminophen concentration (AC) after a 30-second analysis of one drop of whole blood (WB). Sixty-one WB samples from patients with known or suspected drug overdose were evaluated for acetaminophen overdose. In all cases a comprehensive toxic screen was sent with serum AC measured by high-performance liquid chromatography or TDx. AC was simultaneously tested with the meter. Twenty-five samples had a laboratory-confirmed elevated AC. The meter identified the elevated AC in all cases; there were no false-negatives (sensitivity, 100%). The rapid AC measurements correlated strongly with laboratory determinations (r = .983; P < .0001 ). Repeated testing (including with control solutions) documented the precision and reproducibility of the meter's results. Drug coingestion had no significant effect on the accuracy of the meter. These preliminary data identify the possibility of rapid determinations of AC after acute drug overdose. This meter would find its greatest value in the management of patients with acetaminophen overdose in whom expeditious but appropriate administration of antidotal therapy is desired.

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Cyanide Levels After Acetonitrile Exposure: An In.V'rtro Study

MK Kirk, SL Voorhees, K Kulig, BH Rumack / Rocky Mountain Poison and Drug Center, Denver General Hospital, University of Colorado Health Sciences Center; Analytitox Inc, Denver, Colorado Recent reports and one local case have demonstrated cyanide toxicity from ingestion of acetonitrile-containing products. Concern that cyanide quantitation performed locally was actually measuring acetonitrile or that cyanide was being generated in the blood specimen in vitro led us to assess the analytical method. Samples of whole blood from a normal volunteer and water samples were prepared by adding 5, 10, 25, 50, 100, and 150 ~g/mL of acetonitrile and analyzed immediately. An additional sample of blood was prepared with 500 ~g/mL, then analyzed five hours later. Cyanide levels were measured using the Conway microdiffusion technique. Detection limits for this method are 0.01 ~g/mL. A standard curve for cyanide was analyzed concurrently. Cyanide was not detectable in any of these specimens. These data suggest that the presence of acetonitrile in a whole blood sample does not generate cyanide in vitro within five hours when measured by this common analytical method. Detection of cyanide in whole blood after acetonitrile ingestion is therefore not likely to be a laboratory artifact when done by this technique.

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Liver Transplantation in Amanita Phalloides Poisoning

MR Daya, RL Norton, RD Fields, R Kao, JR Lake, NL Ascher, CW Pinson, KG Benner, EB Keefe / Oregon Poison Center, Oregon Health Sciences University, Portland; University of California at San Francisco Orthoptic liver transplantation (OLT) offers definitive therapy for selected cases of Amanita phalloides (AP) poisoning associated with irreversible hepatic failure. Since liver procurement can be a lengthy process, early identification of potential candidates is desirable. The clinical course of five severely poisoned individuals, four of whom had OLT, is reviewed. All five developed nausea, vomiting, abdominal pain, and diarrhea 7.5 to 10.5 hours following a cooked mushroom meal. Patients presented to the emergency department 12 to 24 hours following ingestion, where AP poisoning was confirmed by identification of an intact remaining mushroom. Initial management consisted of aggressive fluid resuscitation with forced diuresis, high-dose IV penicillin, and oral silymarin. The subsequent course was characterized by diarrhea, coagulopathy, reduced protein synthesis, and bone marrow toxicity with cytopenia. Laboratory abnormalities (mean _+ SE) common to all included profound hypophosphatemia (1.0 _+ 0. l mg/dL), elevated transaminases

Annalsof EmergencyMedicine

19:6 June 1990