It therefore seemed clear that, whatever illness was produced in the animals exposed to fresh paint, they were not suffering from absorption of lead, but of some other compound of which the paint was made. Various constituents of the paint were therefore tried—namely, the metallic bases, lead or zinc, and linseed-oil, with turpentine and lead acetate mixed with turpentine. The animal exposed to the turpentine alone very rapidly showed signs of disease—salivation, a tendency to diarrhœa, strabismus, but the latter only after a two-hour exposure, whilst the quantity of turpentine present in the cage air did not exceed 10 milligrammes per litre.
The animal exposed to turpentine and lead acetate exhibited few symptoms, but the same in kind as the animal exposed to turpentine alone. The linseed-oil animal showed no signs of disease whatever. The animals exposed to the metallic bases of the paint—namely, zinc oxide or white lead—showed no signs of poisoning as long as the compound itself was not thrown into the air in the form of dust; but when lead dust was present in the air the animal rapidly showed the ordinary signs of lead poisoning. The animal exposed to zinc oxide dust showed very little sign of discomfort, but by prolonged exposure early kidney disease was produced, and signs of chronic inflammation were detectable in the lung.
It is interesting to note in this connection that Lehmann[7] describes symptoms produced in cats when exposed to the vapour of turpentine. The animals which I exposed to turpentine vapour exhibited the same symptoms as those described by Lehmann. He gave no result of the histological inquiry of the animals so exposed, but in no case, apparently, was the animal killed after exposure. In my animals exposed to the vapour of turpentine very definite disease of the kidney was produced, the inflammation tending rather to the tubular than the interstitial variety of nephritis. The tubules were found blocked with débris, their contour irregular and destroyed, and their substance pale and almost hyaline; whilst areas of cloudy swelling, together with small hæmorrhages, were to be found scattered about the kidney. The heart muscle was flabby, and the heart tending to dilatation; whilst microscopically hæmorrhages could be found throughout the organ of a minute capillary nature, and passing between and disturbing the muscle bundles.
No changes of any sort were found in the tissues of the animals exposed to the emanations given off from white lead paste. By analyses these emanations were found to contain no lead, but traces of aldehyde, formic acid, and CO2. It follows, therefore, that the effect of turpentine when inhaled by the painter must be to act as a contributory cause of lead poisoning, and it is interesting in this connection to recall the fact noted on [p. 38], that Garrod has described gout as occurring constantly among painters. The statement already quoted, that gout is not common among workers in white lead factories, where the exposure to lead is very much greater than among painters, points to turpentine as the cause of the increased incidence of gout among house-painters rather than lead absorption. The importance of dust containing lead as a source of illness and lead poisoning in painters must not be minimized, as in sand-papering, etc. (see [p. 137]). The importance of lead dust inhaled in this way is perfectly understood. It is, however, highly probable that the combined action of the turpentine with the lead accounts for the fact that headache is a common symptom of early disease in painters, which is not the case among white-lead workers.
REFERENCES.
[1] Goadby, K. W.: Journal of Hygiene, vol. ix., No. 1, 1909.
[2] Goadby, K. W., and Goodbody: The Lancet, vol. ii., p. 988, 1909.
[3] Goadby, K. W.: Report of the Committee on Lead, etc., in Potteries, vol. iii., p. 478, 1910.
[4] Moore: Private communication.
[5] Armit: Journal of Hygiene, vol. viii., No. 5, 1908.