MSDS

SECTION 9 - PHYSICAL AND CHEMICAL PROPERTIES
Appearance: White, odorless powder Boiling Point: Not Applicable
Vapor Pressure: Negligible @ 20ºC Flash Point: None
Solubility in Water: 9.5% @ 20ºC; 32.0% @ 50ºC; pH: 8.3 (3.0% solution); 7.6
(10.0% solution) @ 23ºC
Formula Weight: 412.52
SECTION 10 - STABILITY AND REACTIVITY
General: Disodium Octaborate Tetrahydrate is a stable product.
Incompatible Materials and Conditions to Avoid:
Reaction with strong reducing agents such as metal
hydrides or alkali metals will generate hydrogen gas which could create an explosive hazard.
Hazardous Decomposition: None
SECTION 11 - TOXICOLOGICAL INFORMATION
Ingestion (acute oral toxicity): Low acute oral toxicity; LD
50
of Disodium Octaborate Tetrahydrate in rats is
2500 mg/kg of body weight.
Skin (acute dermal toxicity):
Low acute dermal toxicity; LD
50
of Disodium Octaborate Tetrahydrate in rabbits
is greater than
2000 mg/kg of body weight. Disodium Octaborate Tetrahydrate is not absorbed through
intact skin.
Primary Skin Irritation Index:
0.5, Disodium Octaborate Tetrahydrate is non-corrosive
Eye:
Draize test in rabbits produced mild eye irritation effects. Many years of occupational exposure history
reflects no indication of human eye injury from exposure to Disodium Octaborate Tetrahydrate.
NOTE: Disodium Octaborate Tetrahydrate is chemically and toxicologically related to boric acid; the
majority of the borate chronic toxicology studies were conducted using boric acid. Disodium Octaborate
Tetrahydrate is converted to boric acid in biological systems. The boric acid data discussed in this section
can be converted to Disodium Octaborate Tetrahydrate equivalent data by dividing by a factor of 1.1992.
Inhalation: Human epidemiological studies show no increase in pulmonary disease in occupational
populations with chronic exposures to boric acid dust and sodium borate dust.
Carcinogenicity: A Technical Report issued by the National Toxicology Program showed "no evidence of
carcinogenicity" from a full 2-year bioassay on boric acid in mice at feed doses of 2500 and 5000 ppm in the
diet. No mutagenic activity was observed for boric acid in a recent battery of four short-term mutagenicity
assays.
Reproductive / Developmental Toxicity: Animal studies indicate Boric Acid reduces or inhibits sperm
production, causes testicular atrophy, and, when given to pregnant animals during gestation, may cause
developmental changes. These feed studies were conducted under chronic exposure conditions leading to
doses many times in excess of those that could occur through inhalation of dust in occupational settings.
Reproductive Toxicity (Fertility): Dietary boric acid levels of 6,700 ppm in chronic feeding studies in rats
and dogs
produced testicular atrophy, while dogs and rats receiving 2000 ppm did not develop testicular
changes (
1
Weir, Fisher, 1972). In chronic feeding studies of mice on diets containing 5000 ppm (550
mg/kg/d) boric acid, testicular atrophy was present while mice fed 2500 ppm (275 mg/kg/d) boric acid
showed no significant increase in testicular atrophy (
2
NTP, 1987). In another boric acid chronic study, in
mice given 4500 ppm (636 mg/kg/d), degeneration of seminiferous tubules was present together with a
reduction of germ cells, while at 1000 ppm (152 mg/kg/d) no effect was seen (
3
Fail et al., 1991). In a
reproduction study on rats, 2000 ppm of dietary boric acid had no adverse effect on lactation, litter size,
weight and appearance (
1
Weir, Fisher, 1972). In a continuous breeding study in mice there was reduction in
fertility rates for males receiving 4500 ppm (636 mg/kg/d) boric acid, but not for females receiving 4500 ppm
boric acid (
3
Fail et al., 1991)
Developmental Toxicity:
Boric acid at dietary levels of 1000 ppm (78 mg/kg/d) administered to pregnant
female rats throughout gestation caused a slight reduction in fetal weight, but was considered to be close
to the LOAEL. Doses of 2000 ppm (163 mg/kg/d) and above caused fetal malformations and maternal
toxicity. In mice the no effect level for fetal weight reduction and maternal toxicity was 1000 ppm (248
mg/kg/d) boric acid. Fetal weight loss was noted at dietary boric acid levels of 2000 ppm (452 mg/kg/d) and
above. Malformations (agenesis or shortening of the thirteenth rib) were seen at 4000 ppm (1003 mg/kg/d),
(
4
Heindel et al., 1992).
1
(Weir, R.J. and Fisher, R.S., Toxicol. Appl. Pharmacol., 23:351-364 (1974))
2
(National Toxicology Program (NTP)-Technical Report Series No. TR324, NIH Publication NO. 88-2580
(1987),PB88-213475/XAB)
3
(Fail et al., Fund. Appl. Toxicol. 17, 225-239 (1991))