Abstract

The experiments recorded in this paper were designed to investigate the effects of the inhalation of nickel carbonyl by rats and rabbits, and to study in detail the distribution of nickel in the body, the development of pathological lesions, and the in fluence of the therapeutic agent 2-3 dimercapto propanol (BAL) on these changes. The study was made because occasional cases of accidental poison ing in man by mixtures of nickel carbonyl and carbon monoxide occur in the production of nickel by the Mond process, which entails the formation and subsequent decomposition by heat of gaseous nickel carbonyl. When the process was first developed in this country, accidental exposure to nickel carbonyl led to some fatalities and from time to time fatal accidents have been reported in other countries. No fatal accidents have occurred in Great Britain during the past 40 years, but accidental exposure due to leaks and other technical faults in the factory sometimes leads to severe and protracted illness in workmen. The toxic material, nickel carbonyl, is a clear volatile liquid, boiling at 43 ?C. Its vapour rapidly decomposes in the presence of moisture to give metallic nickel and carbon monoxide ; in the presence of carbon dioxide the nickel is deposited as the suboxide. Some of the earlier writers con sidered that the toxic action of nickel carbonyl was due to the carbon monoxide that it liberated, but this view was effectively refuted by Armit (1907, 1908) who has made the only significant con tribution to the experimental study of nickel carbonyl poisoning. Armit pointed out that nickel carbonyl had a higher toxicity than could be accounted for by its carbon monoxide moiety, and that a dose of nickel carbonyl sufficient to kill a rabbit would liberate so little carbon monoxide that only 5% of the animal's haemoglobin could be converted to carboxy-haemoglobin. In addition to the considerable pathological changes in the lung,

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