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8.  Renal damage from industrial arsine poisoning 
Uldall, P. R., Khan, H. A., Ennis, J. E., McCallum, R. I., and Grimson, T. A. (1970).Brit. J. industr. Med.,27, 372-377. Renal damage from industrial arsine poisoning. An incident is reported in which three men were accidentally poisoned by arsine (As H3) in an industrial chemical plant. Two mildly affected individuals recovered quickly-without treatment but the third, who was severely poisoned, developed oliguric renal failure. Though this patient recovered after repeated peritoneal dialysis he was left with a legacy of chronic renal insufficiency and hypertension. This severe case drew attention to a previous incident in the same factory involving three other men, the cause of which had not hitherto been suspected.
The previous reports of arsine-induced renal failure treated by dialysis have been reviewed and certain common features are apparent. Dangerous uraemia may persist long after the onset of the diuretic phase. Dialysis provides a high chance for recovery in what was previously a universally fatal condition, but permanent renal interstitial damage is a likely sequel. There are strong reasons for the prompt use of exchange transfusion in the severely affected patient with oliguria.
Mild arsine poisoning unaccompanied by oliguria may remain unrecognized and should therefore be considered in the differential diagnosis of any patient presenting with haematuria or jaundice, particularly if his occupation brings him in contact with acids and metals.
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PMCID: PMC1069430  PMID: 5488698
17.  Chronic Pulmonary Berylliosis in a Female Chemist 
A chronic progressive granulomatous disease of the lungs is described in a female chemist who worked for about two years with a beryllium compound in the manufacture of fluorescent lighting tubes. The level of beryllium in the laboratory atmosphere was found to be 2·7 μg. per cu.m. and in other parts of the factory up to 39·1 μg. per cu.m. were recorded. Symptoms began about two years after she left this work and she died three years later. A diagnosis of chronic pulmonary berylliosis was made, and confirmation was obtained by lung biopsy when early in the course of the disease a large cyst attached to the right middle lobe was removed by thoracotomy. Tests of lung function showed that there was a low arterial saturation at rest and a normal Pco2 in spite of marked hyperventilation. Both elastance and resistance of the lungs were greater than normal and total work of breathing was six times the normal. Pregnancy was associated with relief of symptoms which persisted for some months after a normal birth. Death occurred about seven years after exposure to beryllium ceased. At necropsy beryllium was detected in the lungs chemically and demonstrated in histological sections by special stains. Microscopic examination of the lung showed conchoidal bodies and doubly refractile crystals and the pathogenesis of these lesions is discussed. It is suggested that there is a sensitivity reaction to beryllium, which is probably combined with protein to form an antigen, and that the breakdown of necrotic foci provokes a further reaction in the lung with the repeated appearance of fresh lesions.
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PMCID: PMC1038106  PMID: 13773748

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