The main route of human exposure to ammonia is inhalatory. It is also absorbed by ingestion. Data are not available on absorption of low concentrations of ammonia through the skin, while it is probably absorbed percutaneously at concentration high enough to cause skin injury. In male volunteers exposed to 350 mg/m3 (500 ppm) ammonia for 30 min, initial ammonia retention was around 75%, and it decreased progressively until at steady state it was 23% (range 4-30%). The level of expired ammonia increased gradually to a peak between the 21st and 29th min of exposure, with cyclic variation in respiratory minute volume. The expired air ammonia at equilibrium ranged 350-400 ppm, and the time to attain equilibrium ranged 10-27 min. At the end of the exposure, the ammonia level of expired air fell precipitously, reaching the pregassing level in 3-8 min (Silverman et al.,1949). Ammonia is normally present in all tissues, and it constitutes a dynamic pool throughout which absorbed ammonia is distributed. The distribution is pH dependent, since NH3 diffuses more easily than NH4+. Once absorbed, ammonia is converted to the ammonium ion as hydroxide and as salts, especially as carbonates. The ammonium salts are rapidly converted to urea. Urea is excreted by mammals, which may also secrete ammonia directly into the urine. Thus, excretion of ammonia is primarily via the kidneys, but a not insignificant amount is passed through the sweat glands. Ammonia may also be excreted through expired air. Ammonia was reported mutagenic in in vitro studies at toxic levels (E.coli), and it may affect mutagenic responses to other agents. Mutagenic effects were also described on Drosophila, which were minimal or achieved only at toxic levels. There is no evidence that ammonia is mutagenic in mammals. The carcinogenity studies are inconclusive. The available data does not support that ammonia is carcinogenic. In a study concerning the effect of various ammonia concentrations in enclosed atmosphere on human adrenocortical system, the most pronounced changes in 20 young healthy subjects were observed at 5 mg/m3. However, it is impossible to take into account this study (by Kalandarov et al.,1984), available only as abstract in which no further information were reported concerning the "changes" observed in adrenocortical system at ammonia/air levels of 5 mg/m3. In unaccustomed subjects, clear indications of irritation of the skin, eyes and upper respiratory tract were reported with exposure to 50-55 ppm for periods of between "several" or 10 minutes and 6 hours. However signs of slight irritation to skin and eye were reported in subjects exposed to ammonia concentrations of 25-30 ppm for exposure time ranging 10 minutes - 2 hours . In an inhalation study (Alpatov & Mikhailov, 1963; Alpatov, 1964), the threshold concentration for effects on respiration, skin electric potential, and electroencephalogram was found to be 22 mg/m3 (31 ppm). Conclusion and proposal for an occupational exposure limit: The evaluation of the found information allows to consider the actual level of 17 mg/m3 (25 ppm) as border-line value. It seems reasonable to suggest to keep the exposure limit at 14 mg/m3 (20 ppm). If a STEL value will be considered necessary, the found effects indicate a level of 22 mg/m3 (32 ppm) as reasonable.