Cases reported "Lead Poisoning"

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1/116. flour contamination as a source of lead intoxication.

    CASE REPORT: A 43-year-old man was hospitalized because of severe anemia and recurrent bouts of abdominal pain over 20 days. There was no known occupational exposure to toxins. Concomitantly, the patient's father complained of having the same symptoms. Familial lead poisoning was diagnosed when all 6 family members tested had high blood leads (31-64 micrograms/dL). RESULTS: Following detailed examination of the potential sources common to all members of the household, the cause of poisoning was determined to be corn flour containing 38.7 mg/g lead. physicians are reminded to consider lead poisoning in the differential diagnosis of individuals with unexplained symptoms, particularly those of abdominal discomfort and anemia.
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2/116. Lead induced anaemia due to traditional Indian medicine: a case report.

    Lead intoxication in adults without occupational exposure is a rare and unexpected event. The case of a western European is reported who had severe anaemia after ingestion of several ayurvedic drugs, obtained during a trip to india. Laboratory findings showed high blood lead concentrations, an increased urinary lead concentration, and an increased urinary excretion of delta-aminolaevulinic acid. Also, slightly increased urinary concentrations of arsenic and silver were found. physicians should be aware that with growing international travel and rising self medication with drugs from uncontrolled sources the risk of drug induced poisoning could increase in the future.
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3/116. lead poisoning: a disease for the next millennium.

    The decline in the prevalence of childhood lead poisoning is a public health success story. However, nearly a million preschool-aged children in the united states alone have elevated BPb levels. Toxicity correlates with BPb concentrations and progresses from biochemical and subclinical abnormalities at levels around 10 micrograms/dL to coma and death at levels over 100 micrograms/dL. Treatment consists of the elimination of exposure, interruption of the pathway into the child, modification of diet to ensure adequate essential metal intake (calcium, iron), and on occasion, chelation therapy. The identification of children with the most lead poisoning depends on screening for exposure (questionnaire) or evidence of increased absorption (BPb test). Follow-up is crucial to maximize the effectiveness of any intervention.
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4/116. Occupational and adult lead exposure in wisconsin.

    Lead is a versatile metal with many industrial applications. It is among the oldest recognized occupational health hazards. lead poisoning has been a reportable disease in wisconsin since 1911. Although reportable, it was not until wisconsin established an Occupational and environmental health epidemiology program in 1979 that modern reporting levels were adopted, physician and laboratory reporting promoted and publicized, and elevated blood lead report tracking initiated. With the federal funding from the National Institute of Occupational safety and Health (NIOSH), a comprehensive adult blood lead surveillance program was created in 1987. Eleven years of surveillance trend data reveal a wisconsin success story. Most wisconsin industries have made substantial strides toward reducing occupational lead exposure. The improvement is reflected in the reduced number of elevated blood lead levels in wisconsin's adult blood lead surveillance data. However, wisconsin must remain vigilant as new and re-emerging lead exposures continue to be identified through adult blood lead surveillance. wisconsin will also need to continue with its occupational lead exposure reduction efforts if it is to achieve the Federal Healthy People 2010 goals and objectives to have no adult blood lead level greater than 25 micrograms/dL.
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5/116. Poorly controlled hypertension in a painter with chronic lead toxicity.

    In 1984, a 56-year-old house painter developed intractable pain in his back and other joints. After several unrevealing medical work-ups, he was found to have a high blood lead level (122 microg/dL); he has a history of scraping and sanding lead paint without adequate protective measures. The patient was hospitalized and chelated with EDTA four times over the next 5 years; each time he felt better at the end of his treatment, but he returned to largely the same working conditions. He developed hypertension in April 1989, underwent a final chelation, and retired. He was subsequently followed on a regular basis with repeated measurement of lead levels in blood and bone (using a K-x-ray fluorescence instrument) as well as clinical parameters. In 1995 his blood pressure became difficult to control despite a sequential increase in his antihypertensive medication dosages and the addition of new medications. In 1997 he began calcium supplementation and a high-calcium diet; his blood pressure declined markedly, allowing him to taper off of two of his four antihypertensive medications. This case demonstrates an occupational activity (construction) that has now become the dominant source of lead exposure for U.S. adults, the importance of a good occupational history to suspecting and making a diagnosis, the possible outcomes of chronic lead toxicity, and the importance of preventing further exposure and using proper methods to treat acute toxicity. It also highlights a current major etiologic question, that is, whether and to what degree lead exposure contributes to the development of hypertension, and raises the issue of whether lead-induced hypertension constitutes a subset of hypertension that is especially amenable to therapy with dietary calcium.
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6/116. Occupational and take-home lead poisoning associated with restoring chemically stripped furniture--california, 1998.

    The Occupational lead poisoning Prevention Program (OLPPP) of the california Department of health services and a county health department investigated cases of lead poisoning in six furniture workers and their families in 1998. The investigation, initiated after a blood test of a worker's child revealed an elevated blood lead level (BLL), found that lead remaining in previously painted or coated stripped wood was carried from the workplace on clothes and shoes and was the source of the child's lead exposure and subsequent poisoning. Employers in industries in which workers restore or build using stripped wood should assess lead exposure and, when necessary, should establish a comprehensive lead safety program.
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7/116. Peripheral neuropathy in chronic occupational inorganic lead exposure: a clinical and electrophysiological study.

    BACKGROUND AND OBJECTIVES: Traditionally the neuromuscular disorder associated with lead poisoning has been purely motor. This study assessed peripheral nerve function clinically and electrophysiologically in 46 patients with neuropathic features out of a total population of 151 workers with raised blood and/or urinary lead concentrations. RESULTS: Average duration of occupational exposure for the neuropathic group ranged from 8-47 years (mean 21.7). Their mean blood lead concentration (SD) was 63.9 (18.3) microg/dl (normal <40), urinary lead 8.6 (3.3) microg/dl (normal<5.0), urinary coproporphyrins 66.7 (38.4) microg/g creatinine (20-80), urinary aminolaevulinic acid 1.54 (0.39) mg/g creatinine (0.5-2.5). All 46 had distal paraesthesiae, pain, impaired pin prick sensation, diminished or absent ankle jerks, and autonomic vasomotor or sudomotor disturbances. Reduced vibration sensation and postural hypotension were present in all 20 studied. None of these 46 patients had motor abnormalities. Motor conduction velocity and compound muscle action potential amplitudes were normal, with marginally prolonged distal motor latencies. Sensory nerve action potential amplitudes lay at the lower end of the normal range, and the distal sensory latencies were prolonged. No direct correlation was found between the biochemical variables, and the clinical or electrophysiological data. CONCLUSIONS: One additional patient was seen with shorter term exposure to lead fumes with subacute development of colicky abdominal pain, severe limb weakness, and only minor sensory symptoms. Unlike the patients chronically exposed to lead, he had massively raised porphyrins (aminolaevulinic acid 21 mg/g creatinine, coproporphyrins 2102 microg/g creatinine). patients with unusually long term inorganic lead exposure showed mild sensory and autonomic neuropathic features rather than the motor neuropathy classically attributed to lead toxicity. It is proposed that the traditional motor syndrome associated with subacute lead poisoning is more likely to be a form of lead induced porphyria rather than a direct neurotoxic effect of lead.
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keywords = occupational exposure, exposure
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8/116. Neuro-ototoxicity in andean adults with chronic lead and noise exposure.

    Brainstem auditory evoked responses and audiological thresholds were used as biomarkers for neuro-ototoxicity in adults with chronic lead (Pb) intoxication from long-term Pb exposure in ceramic-glazing work. Venous blood samples collected from 30 adults (15 men and 15 women) indicated a mean blood Pb level of 45.1 micrograms/dL (SD, 19.5; range, 11.2 to 80.0 micrograms/dL) and in excess of the world health organization health-based biological limits (men, 46.2 micrograms/dL; SD, 19.6; range, 18.3 to 80.0 micrograms/dL; women, 44.0 micrograms/dL; SD, 20.1; range, 11.2 to 74.2 micrograms/dL). Mean auditory thresholds at frequencies susceptible to ototoxicity (2.0, 3.0, 4.0, 6.0, and 8.0 kHz) revealed sensory-neural hearing loss in men, which may be attributable to occupational noise exposure in combination with Pb intoxication. Bilateral brainstem auditory evoked response tests on participants with elevated blood Pb levels (mean, 47.0 micrograms/dL) showed delayed wave latencies consistent with sensory-neural hearing impairment. The results suggest that environmental noise exposure must be considered an important factor in determining sensory-neural hearing status in occupationally Pb-exposed adults.
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9/116. Three patients with lead poisoning following use of a Chinese herbal pill.

    We report on three patients with lead poisoning following use of the Chinese herbal pill Bao ning dan, prepared by the same traditional Chinese medicine practitioner. The patients had varying degrees of exposure to Bao ning dan and different clinical manifestations. Blood lead concentrations did not correlate with clinical severity. Two patients received chelating therapy and blood lead concentrations subsequently rapidly decreased. One patient was managed conservatively and end-organ complications resolved gradually. With increasing use of traditional Chinese medicines, related adverse reactions are expected to become increasingly common. Practitioners of western medicine should remain alert to this possibility. A comprehensive drug review, including the use of herbal medicines, should form a routine part of medical history taking.
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keywords = exposure
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10/116. lead poisoning: case studies.

    Early clinical features of lead toxicity are non-specific and an occupational history is particularly valuable. Lead in the body comprises 2% in the blood (t1/2 35 days) and 95% in bone and dentine (t1/2 20-30 years). Blood lead may remain elevated for years after cessation from long exposure, due to redistribution from bone. Blood lead concentration is the most widely used marker for inorganic lead exposure. zinc protoporphyrin (ZPP) concentration in blood usefully reflects lead exposure over the prior 3 months. Symptomatic patients with blood lead concentration >2.4 micromol l-1 (50 microg dl-1) or in any event >3.8 micromol l-1 (80 microg dl-1) should receive sodium calciumedetate i.v., followed by succimer by mouth for 19 days. Asymptomatic patients with blood lead concentration >2.4 micromol l-1 (50 microg dl-1) may be treated with succimer alone. sodium calciumedetate should be given with dimercaprol to treat lead encephalopathy.
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