Gerhardsson et al. (1982) measured post-mortem antimony levels in the lung tissue of workers occupationally exposed via inhalation to antimony. Levels were found to be elevated compared to a control population, even after workers had been retired for up to 20 yr, indicating a long half-life for lung clearance of antimony in humans.

Toxicokinetic studies in adult male Syrian golden hamsters given a single, intratracheal instillation of antimony trioxide (1.52 mg/kg body weight) indicate that 20% of the instilled antimony was cleared from the lung in the first 20 hr (Leffler et al. 1984). Biological half-times of about 40 hr for the initial phase and 20–40 d for the second phase were calculated for lung tissue (Leffler et al. 1984). In rats exposed to 119 mg antimony trioxide dust/m3 for 80 hr, the majority of urinary excretion occurred within the first 3 d after exposure (Gross et al. 1955a).

Following a single oral dose (200 mg antimony trioxide) of antimony trioxide to rats, 3% of the administered dose was recovered in the urine within 8 d. Only 0.15% was recovered 1 d after treatment, and 3% was recovered between d 2 and 5 post-treatment (Gross et al. 1955a). Following chronic exposure (2% antimony trioxide in the diet; 8 mo), approximately 99% of fecal excretion and the majority of urinary excretion occurred within 7 d after exposure ceased (Gross et al. 1955a). The large amount of antimony excreted in the feces soon after exposure suggests that a substantial portion of the compound is excreted without being absorbed systemically. That is consistent with the low absorption rate (1%) cited by the ICRP (ICRP 1981) (see Absorption section).

Dermatitis was reported in workers occupationally exposed to 0.4–70.7 mg antimony/m³ (Renes 1953; McCallum 1963; Potkonjak and Pavlovich 1983; White et al. 1993). Although antimony trioxide in the work environment was believed to be responsible for the dermatitis, quantitative data on dermal exposure were not available, and the workers were also exposed to other elements such as arsenic. Therefore, the causative agent for the observed dermatitis could not be positively determined.