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Propylamine (Cas-No. 107-10-8) is a colourless liquid with a molecular weight of 59.1 g/mol and a vapour pressure of 330 hPa (20°C). It is miscible in all proportions in water and the log Po/w is 0.28.


Evidence for systemic availability of Propylamine comes from the acute toxicity(oral, dermal, inhalation).

In an acute oral study the LD50 in rats was calculated as ca. 370 mg/kg body weight (BASF AG, 1978). Main clinical signs observed were dyspnoea, apathy, irregular respiration, staggering, spastic gait, piloerection. At necropsy, acute dilatation and congestion of the heart, slight acute lug distensions, strong diffuse erythema in the glandular stomach, strong erythema of the intestinal mucosa with and bloody diarrhetic content were observed.

Dermal toxicity studys with rabbits, the acute dermal toxicity was 398 mg/kg bw (Smyth et al, 1962).

In an acute inhalation toxicity study (BASF AG, 1978) the LC50 was calculated as 6.32 mg/L air. Main clinical signs observed were watery to reddish eye and nose discharge, corrosions at nose and eyes, clouded cornea, salivation, dyspnoea, apathy, crouched position, rough and sticky coat, tremor and staggering walk. At necropsy, acute dilatation and congestion of the heart, infarctoic congestion of the lung partially accompanied by lung edema, effusion of blood in the thorax, mucosal bleeding in the cranial region, swelling of the anogenital region (except rectum) and cachexia were noted.

In a further study with mist the calculated LC50 was 2310 ppm for 8 h of exposure. (Hine et al. 1991; reliability score: 2). There were no gross tissue changes in any group, but microscopically, central pallor of the liver and tubular degeneration of the kidney were seen. In spite of the rapid death of all rats, there was central degeneration of the liver and focal lymphocytic infiltration of the heart at the highest dose group (3200 ppm).

In an older repeated inhalation study a NOAEC could not be identified (Hine et al., 1960). Based on the information from the acute toxicity studies Propylamine seems to be available via the inhalative, oral and dermal route of exposure. However, the corrosive effects appear to be the primary effect. Thus, a local effect is the primary effect.

Groups of Sprague-Dawley rats were made acidotic or alkaloic before the treatment. A solution of NH4Cl or NaHCO3 (1000 mg/kg bw) respectively was administered by stomach tube at 2 h or 12 h and at zero time in relation to the start of the excretion studies.

Urinary excretion of n-propylamine was examined after intraperitoneal injection (100 mg /kg bw). The rats were placed in metabolic cages and urine was collected for three consecutive periods; 0-4 h, 4-8 h and 8-12 h after each injection. The excretion of n-propylamine, after the appropriate injections was significantly higher in the acidoic than in the alkaloic rats (Bourke et al. 1972).