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Abstract for TER89027

Developmental Toxicity of Boric Acid in Sprague Dawley Rats

CASRN: 10043-35-3
Chemical Formula: H3BO3
Molecular Weight: 61.8317
Report Date: May 1, 1990

Abstract

The following abstract presents results of a study conducted by a contract laboratory for the National Toxicology Program. The findings may not have been peer reviewed and were not evaluated in accordance with the levels of evidence criteria established by NTP in March 2009. For more information, see the Explanation of Levels of Evidence for Developmental Toxicity. The findings and conclusions for this study should not be construed to represent the views of NTP or the U.S. Government.

Boric acid is used as an insecticide and constituent of commercial products, including topically applied medicinals and cosmetics. In this study, developmental toxicity was evaluated in timed-mated Sprague-Dawley-derived (CD) rats exposed to boric acid in feed at concentrations of 0.1%, 0.2% or 0.4% on gestational days 0 to 20 (n=29/group); exposure to 0.8% dietary boric acid (n=14) was restricted to the period of major organogenesis (gd 6 to 15) in order to limit early embryolethality.

Average daily intake of boric acid was 78, 163, 330 and 539 mg/kg/day , respectively. Exposure to 0.2% and 0.4% resulted in increased maternal food intake for gd 12 to 20; water intake was increased on gd 18, to 20 at 0.4%. Food intake was decreased during treatment at 0.8% with a rebound increase on gd 15 to 18; water intake was decreased on gd 6 to 9. Other effects summarized across all dose levels included increased relative maternal liver and kidney wts. at greater than or equal to 0.2%, decreased gravid uterine weight at greater than or equal to 0.4%, decreased wt. gain during treatment and gestation at greater than or equal to 0.4%, and increased corrected body wt. gain only at 0.4%. Microscopic evaluation of maternal kidneys (10 dams/group) did not provide any definitive evidence for treatment-related renal pathology.

Average fetal body wt./litter was reduced at all doses. Prenatal mortality was increased only at 0.8%. The incidence of fetal malformations was significantly increased at greater than or equal to 0.2% dietary boric acid (2, 3, 8, 50 and 73% malformed fetuses/litter in the control through high-dose groups). The most frequently observed malformations were enlarged lateral ventricles of the brain, and agenesis or shortening of rib XIII. As an associated finding, the incidence of Lumbar I rib(s), a common variation in the CD rat, was reduced following boric acid treatment.

In conclusion, the no observed adverse effect level for maternal toxicity was 0.1% dietary boric acid and the lowest observed adverse effect level was 0.2%. Embryo/fetal toxicity occurred in all treatment groups (greater than or equal to 0.1%).