Boric acid, widely used in manufacturing, cosmetics and pharmaceuticals, was tested for developmental toxicity in timed-mated CD-1 mice. BORA (0, 0.1, 0.2 or 0.4% in feed) was administered from gestational day 0 to 17 with average intakes of 248, 452 or 1003 mg/kg/day . Dams exposed to 0.4% BORA exhibited decreased weight gain during treatment (gestation) compared to controls, even though food and water consumption were not reduced. Gestational weight gain corrected for gravid uterine weight was not affected. High-dose BORA caused increased water consumption during late gestation (gd 15-17) and increased relative kidney weight. A dose-related incidence of renal tubule dilatation/regeneration was observed in 0/10, 2/10, 8/10 and 10/10 randomly selected dams in the control through high-dose groups.
Reduction of fetal body weight was dose-dependent (94%, 89% and 66% of controls), but statistically significant only at 0.2 and 0.4% BORA. The high-dose group had an increased percentage of resorptions (19% vs. 6% for controls) and malformed fetuses/litter (9% vs. 3% for controls). The most apparent treatment-related morphological changes involved deficient rib development at the thoracic-lumbar junction, i.e., an increased incidence of short rib XIII (a malformation) and a decreased incidence of rudimentary or full rib(s) at Lumbar I (an anatomical variation).
In summary, maternal renal toxicity was observed at all BORA exposures. The low exposure (0.1%) approached the maternal no-observed adverse effect level with mild renal lesions in only 2 of 10 females. The no-observed-adverse-effect-level for developmental toxicity of BORA was 0.1%.