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Pulmonary edema and hemorrhage are well unkown results of exposure of animals to toxic doses of ozone( 1-5). Experiments on dogs by Kabins ct d ( 6 ) suggest that Shydroxytryptamiiie (5-HT) may have a role in formation of lung edema. Since 5-HT is present in the lungs of rats in appreciable amounts ( 7 3 ) . this investigation was undertaken to study the effects of ozone induced pulmonary edema on the lung 5-HT content.Materials and mcthods. Male albino Wktar rats (325-375 g) were placed in wire cages 20 x 28 k: 20 cm high set upon a hardware cloth shelf within an exposure chamber. constructed of galvanized sheet steel, 76 y 76 >< 79 cni high. Air. passed through a Barnebey-Cheney Model 8CF air filter was admitted a t the top, directed throughout the chamber by baffles, and pumped from the chamber at each of the bottom corners. Air was changed once every minute. Ozone. produced from tank oxygen in a 12,000 volt discharge ozonizer of the type employed by Quilligan at al.(O), was mixed with the filtered air before entering the chamber. Air samples were taken from a point just above the animals every 30 minutes during an experiment. and ozone content was determined by the neutral buffered 1 % potassium iodide method of Byers and Saltzman ( lo), liberated iodine being measured photometrically at 352 mp in a Beckman DU Spectrophotometer. Ozone concentration was maintained at 6 parts per million (p.p.m.) by volume, and exposure time was 4 hours in all experiments. Control animals were handled in the Sitme manner except that addition of ozone to the chamber was omitted. Each group consisted of 11 animals. After exposure, these animals were

The older literature contains many reports on the deleterious effects of chronic nicotine poisoning, describing retardation of g r o~t h , l -~ tolerance development,6-12 interference with reproduction,2,"J4 enlargement or injury of the adrenals,2J5-20 atrophy of the gonads,2J7,21 changes in other endocrine organ^,^^^^^ and production of arterial d i s e a~e .~~-~~ Because most of the reports were based upon poorly controlled experiments or on too small a number of animals, my associates and I initiated a systematic reinvestigation of the chronic effects of nicotine, employing littermate or other closely related controls. Test animals received subconvulsive doses of nicotine dissolved in 0.9 per cent saline, and controls were injected with the same volumes of saline. Experiments extended over intervals of three months to a year. Thus was demonstrated a species difference with respect to g r o~t h ,~~,~~ a decrease in fertility of female rats but not of male rats,35 but without gross or histological evidence of organ injury, and the development of drug tolerance of the chronically poisoned animals.36

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