Cases reported "Occupational Diseases"

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1/15. Successful treatments of lung injury and skin burn due to hydrofluoric acid exposure.

    Recent growth in the electronics and chemical industries has brought about a progressive increase in the use of hydrofluoric acid (HF), along with the concomitant risk of acute poisoning among HF workers. We report severe cases of inhalation exposure and skin injury which were successfully treated by administering a 5% calcium gluconate solution with a nebulizer and applying 2.5% calcium gluconate jelly, respectively. Case 1: A 52-year old worker used HF for surface treatment after welding stainless steel, and was hospitalized with rapid onset of severe dyspnea. On admission to the critical care medical center he had widespread wheezing and crackles in his lungs. Chest radiograph showed a fine diffuse veiling over both lower pulmonary fields. Severe hypocalcemia with high concentrations of F in serum and urine were disclosed. He was immediately given 5% calcium gluconate solution by intermittent positive-pressure breathing (IPPB), utilizing a nebulizer. On the 21st hospital day, chest film and CT scan did not demonstrate any abnormality. He was discharged very much improved on the 22nd hospital day. Case 2: A 35-year old worker at an electronics factory was admitted to his local hospital with severe skin burn on his face and neck after exposure to 100% HF. Treatment began with immediate copious washing with water for 20 min. calcium gluconate 2.5% gel (HF burn jelly) was applied to the area as a first-aid measure. Persistent high concentrations of serum and urinary F were disclosed for 2 weeks. After treatment with applications of HF burn jelly, he was confirmed as being completely recovered. The present cases and a review of published data suggest that an adequate method of emergency treatment for accidental HF poisoning is necessary.
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2/15. Occupational asthma due to exposure to African cherry (Makore) wood dust.

    A 35-year-old man who had been a carpenter and a cabinet worker for over 15 years, was referred to our clinic with a 4-month history of cough, chest tightness and difficulty in breathing which occurred within minutes of exposure to African cherry wood (Makore). He developed a dual asthmatic reaction on specific challenge test with an extract of African cherry wood dust. Thus, the diagnosis of occupational asthma due to exposure to African cherry wood dust was confirmed by the specific challenge test. The mechanism of asthma due to African cherry wood dust exposure is not clear.
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3/15. A case of percutaneous industrial methanol toxicity.

    methanol (CH3OH) is a chemical feedstock of increasing importance as well as a commonly used solvent. In the early 1980s methanol production was introduced at a new petrochemical complex in the Saudi port of Jubail. A case is presented of a consultant supervising tank cleaning prior to methanol loading. He wore positive pressure breathing apparatus but no protective clothing. After 2-3 hours working in the confined space of the tank, he worked on deck and continued to wear his methanol-soaked clothing which eventually dried out. Visual symptoms of acute methanol toxicity presented some 8 hours after exposure. The appropriate treatment (with ethanol provided by the ship bond) was carried out in hospital and the individual recovered completely. Most reported cases of methanol toxicity are social in origin, arising from ingestion. This particular case, though unusual, does present some interesting lessons.
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4/15. Lead exposure in outdoor firearm instructors.

    This study was conducted to determine lead exposure of firearm instructors at an outdoor firing range, while cadets were firing nonjacketed and jacketed lead ammunitions. The breathing zone air for lead exceeded the Occupational safety and health Administration standard of 50 micrograms/m3 for two instructors during firing exercises using nonjacketed bullets. The use of totally copper-jacketed bullets reduced the breathing zone lead levels by 92 percent for instructor #1 and by 96 percent for instructor #2; subsequent blood lead levels showed a significant decline in both instructors.
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5/15. Acute lead poisoning in construction workers: the failure of current protective standards.

    Construction workers who use oxyacetylene torches to cut lead-painted metal are at high risk of acute and subacute lead poisoning. Poisoning results from inhalation of submicron-diameter particles of lead fume generated in paint burning. We describe a series of 14 cases of lead poisoning in ironworkers cutting a lead-painted bridge in new york city. Peak blood lead levels ranged from 2.32 to 5.80 mumol/l (48-120 micrograms/dl). Median duration of employment was 4 wk. Two workers required chelation therapy. Personal (breathing zone) exposures to airborne lead ranged from 600 to 4,000 micrograms/m3. Construction workers are specifically exempted from the provisions of the U.S. Occupational safety and health Administration (OSHA) lead standard. The data from this study indicate that such exemption is not warranted. A need exists for improved protection of construction workers against occupational exposure to lead.
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6/15. phosgene: a practitioner's viewpoint.

    Clinical experience with five patients exposed to phosgene is described. The treatment of phosgene poisoning was focused upon the presenting problem, pulmonary edema. Arterial hypoxemia was treated with a face mask with 10 cm CPAP with the FiO2 adjusted as needed or with a volume ventilator with controlled ventilation. ventilation was controlled to reduce the work of breathing. Metabolic acidosis was treated with NaCHO3 to produce a normal pH. A vigorous program of diuresis was used to treat the pulmonary edema. Lasix was administered to produce a negative fluid balance while maintaining a good urinary output. The negative fluid balance correlated well with reduced oxygen requirements.
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7/15. Occupational asthma due to formaldehyde.

    Bronchial provocation studies on 15 workers occupationally exposed to formaldehyde are described. The results show that formaldehyde exposure can cause asthmatic reactions, and suggest that these are sometimes due to hypersensitivity and sometimes to a direct irritant effect. Three workers had classical occupational asthma caused by formaldehyde fumes, which was likely to be due to hypersensitivity, with late asthmatic reactions following formaldehyde exposure. Six workers developed immediate asthmatic reactions, which were likely to be due to a direct irritant effect as the reactions were shorter in duration than those seen after soluble allergen exposure and were closely related to histamine reactivity. The breathing zone concentrations of formaldehyde required to elicit these irritant reactions (mean 4.8 mg/m3) were higher than those encountered in buildings recently insulated with urea formaldehyde foam, but within levels sometimes found in industry.
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8/15. Pleural mesothelioma after a short interval from first exposure in the wine filter industry.

    Pleural mesotheliomas are usually reported after a long interval has passed since first exposure to asbestos. We, however, describe a case observed after a latent period of only 7.5 years in a worker exposed in a factory manufacturing auxiliary products for wine treatment, including chrysotile asbestos filters. The exposure to asbestos lasted 3-4 months per year, during which airborne fiber concentrations ranged from 1 to 4 ff/cc in the patient's workplace. Due to the characteristics of the manufacturing process, the asbestos fibers were very thin in diameter. The patient also suffered from nasal breathing impairment. An examination of the literature showed that asbestos-related mesotheliomas have been reported, albeit rarely, after less than 10 years from onset of exposure. Therefore, it is believed that this case should be related to past exposure to asbestos.
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9/15. Combined alveolitis and asthma due to hexamethylene diisocyanate (HDI), with demonstration of crossed respiratory and immunologic reactivities to diphenylmethane diisocyanate (MDI).

    A worker exposed intermittently to hexamethylene diisocyanate (HDI) developed episodes of dyspnea, wheezing, and fever on working days. Complete lung function tests performed when the subject was asymptomatic were normal except for increased airway responsiveness to histamine, which significantly improved after a 3 wk period off work. At that time, specific inhalation challenges with HDI were carried out. After being exposed for 5 min, the subject developed general malaise, cough, fever, and leukocytosis, together with a mixed restrictive and obstructive breathing defect. We demonstrated a subsequent increase in airway hyperexcitability, which lasted for 2 mo. The subject was also challenged with diphenylmethane diisocyanate (MDI) for 15 min. A late obstructive reaction was documented. Increased levels of specific IgG antibodies against HDI-human serum albumin (HSA) and MDI-HSA were demonstrated.
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10/15. Occupational hypersensitivity pneumonitis after exposure to diphenylmethane diisocyanate.

    A foundry worker developed dyspnea and a restrictive breathing defect after being exposed to diphenylmethane diisocyanate (MD) at work. His symptoms and lung function impairment subsided a few weeks after he left work. Specific inhalation challenges with the offending agent induced general malaise together with a significant increase in body temperature and leukocyte count as well as a significant decrease in forced vital capacity and transfer factor. Total antibody activity to a MDI human serum albumin (MDI-HSA) conjugate was detected by ammonium sulfate precipitation. Specific IgG antibodies were demonstrated by the enzyme-linked immunoabsorbent (ELISA) technique. Thus, it was found that MDI exposure can cause hypersensitivity pneumonitis and induce the production of specific antibodies.
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