Boric Acid - PubChem PDF

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PubChem CID: 7628
Chemical Names: BORIC ACID; Orthoboric acid; Boracic acid; 10043-35-3; Borofax; Boron hydroxide More...
Molecular Formula: H3BO3 or undefined or B(OH)3 or BH3O3

Molecular Weight: 61.831 g/mol
InChI Key: KGBXLFKZBHKPEV-UHFFFAOYSA-N
Drug Information: Drug Indication Therapeutic Uses Clinical Trials FDA UNII
Safety Summary: Laboratory Chemical Safety Summary (LCSS)
Boric Acid is a weakly acidic hydrate of boric oxide with mild antiseptic, antifungal, and antiviral properties. The exact
mechanism of action of boric acid is unknown; generally cytotoxic to all cells. It is used in the treatment of yeast infections
and cold sores.
 Pharmacology from NCIt
Boric acid (H3BO3) is found in fig. Boric acid (H3BO3) is a food contaminant deriving from paper and paperboard in contact
with food. V. limited use as an antibacterial agent in cavia
 Metabolite Description from Human Metabolome Database (HMDB)
BORIC ACID is an odorless white solid. Melting point 171°C. Sinks and mixes with water. (USCG, 1999)
 Physical Description from CAMEO Chemicals
PUBCHEM  COMPOUND  BORIC ACID Modify Date: 2018-10-06; Create Date: 2004-09-16
 Contents
1 2D Structure
2 3D Status
 3 Names and Identifiers
4 Chemical and Physical Properties
5 Related Records
6 Chemical Vendors
7 Drug and Medication Information
8 Food Additives and Ingredients
9 Agrochemical Information
10 Pharmacology and Biochemistry
11 Use and Manufacturing
12 Identification
13 Safety and Hazards
14 Toxicity
15 Literature
16 Patents
17 Biomolecular Interactions and Pathways
18 Biological Test Results
19 Classification
20 Information Sources
1 2D Structure
 Search  Download  Get Image
 Magnify
 from PubChem
2 3D Status
Conformer generation is disallowed since MMFF94s unsupported element
 from PubChem
3 Names and Identifiers
3.1 Computed Descriptors
3.1.1 IUPAC Name
boric acid
 from PubChem
3.1.2 InChI
InChI=1S/BH3O3/c2-1(3)4/h2-4H
 from PubChem
3.1.3 InChI Key
KGBXLFKZBHKPEV-UHFFFAOYSA-N
 from PubChem
3.1.4 Canonical SMILES
B(O)(O)O
 from PubChem
3.2 Molecular Formula

H3BO3
 from EU Food Improvement Agents
1. BH3O3
2. B(OH)3
3. H3BO3
 from ILO-ICSC
B(OH)3
 from Wikipedia
BH3O3
 from PubChem
3.3 Other Identifiers

3.3.1 CAS
10043-35-311113-50-1
 from CAMEO Chemicals
12258-53-6
 from ChemIDplus
10043-35-3
 from ChemIDplus, DTP/NCI, DrugBank, EPA Chemicals under the TSCA, EPA DSStox, European Chemicals Agenc…
11113-50-1
 from European Chemicals Agency (ECHA)
3.3.2 EC Number
233-139-2
234-343-4
233-139-2
3.3.3 ICSC Number
0991
 from ILO-ICSC
3.3.4 NSC Number
81726
 from DTP/NCI
3.3.5 RTECS Number
ED4550000
 from The National Institute for Occupational Safety and Health (NIOSH)
3.3.6 UNII
R57ZHV85D4
 from FDA/SPL Indexing Data
3.3.7 Wikipedia
Title tetraborate
Description substance
Title boric acid
Title orthoboric acid
Description chemical compound
 from Wikipedia
3.4 Synonyms
3.4.1 MeSH Entry Terms
1. boric acid
2. boron oxide hydroxide
3. orthoboric acid
 from MeSH
3.4.2 Depositor-Supplied Synonyms
1. BORIC ACID 11. Trihydroxyborone 21. Trihydroxyborane 31. Borsaure [German]

2. Orthoboric acid 12. Flea Prufe 22. Acidum boricum 32. Collyrium Eye Wash
3. Boracic acid 13. Super Flea Eliminator 23. Dr.'s 1 Flea Terminator DT 33. Dr.'s 1 Flea Terminator D
4. 10043-35-3 14. Orthoboric acid (B(OH)3) 24. Boric acid (VAN) 34. NCI-C56417
5. Borofax 15. Orthoborsaeure 25. Bluboro 35. Caswell No. 109
6. Boron hydroxide 16. Boric acid (BH3O3) 26. Optibor 36. B(OH)3
7. Boron trihydroxide 17. Borsaeure 27. component of Aci-Jel 37. trihydroxidoboron
8. Three Elephant 18. Borsaure 28. Dr.'s 1 Flea Terminator DFPBO 38. Kjel-sorb
9. Boric acid (H3BO3) 19. Tetraborate 29. Orthboric Acid 39. Ant flip
10. Basilit B 20. 11113-50-1 30. Dr.'s 1 Flea Terminator DF 40. Homberg's salt
 from PubChem
4 Chemical and Physical Properties
4.1 Computed Properties
Property Name Property Value
Molecular Weight 61.831 g/mol
Hydrogen Bond Donor Count 3
Hydrogen Bond Acceptor Count 3
Rotatable Bond Count 0
Complexity 8
AAADcQIAMAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA
AAAAAAAAAAAIAAAACAAAAAAAAAAAAAAAAAAAAAAA
CACTVS Substructure Key Fingerprint
AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA
AAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAAA==
Topological Polar Surface Area 60.7 A^2
Monoisotopic Mass 62.018 g/mol
Exact Mass 62.018 g/mol
Compound Is Canonicalized true
Formal Charge 0
Heavy Atom Count 4
Defined Atom Stereocenter Count 0
Undefined Atom Stereocenter Count 0
Defined Bond Stereocenter Count 0
Undefined Bond Stereocenter Count 0
Isotope Atom Count 0
Covalently-Bonded Unit Count 1
 from PubChem
4.2 Experimental Properties
4.2.1 Physical Description
BORIC ACID is an odorless white solid. Melting point 171°C. Sinks and mixes with water. (USCG, 1999)
1. CBI
2. DryPowder
3. Liquid
4. OtherSolid, Liquid
5. Withheld
 from EPA Chemicals under the TSCA
Colourless, odourless, transparent crystals or white granules or powder; slightly unctuous to the touch; occurs in nature as
the mineral sassolite
Solid
 from Human Metabolome Database (HMDB)
ODOURLESS COLOURLESS CRYSTALS OR WHITE POWDER.

 from ILO-ICSC
Odorless white solid.

 from OSHA Occupational Chemical DB
4.2.2 Color
Colorless, transparent crystals or white granules or powder

O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Whitehouse Station, NJ: Merck and Co., Inc.,
2006., p. 218
 from HSDB
Colorless triclinic crystals

2006., p. 4-53
 from HSDB
White waxy triclinic solid plates

Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V3: 521
 from HSDB
4.2.3 Odor
Odorless
2006., p. 218
 from HSDB
4.2.4 Taste
Faintly bitter
Krieger, R. (ed.). Handbook of Pesticide Toxicology. Volume 2, 2nd ed. 2001. Academic Press, San Diego, California., p. 1413
 from HSDB
4.2.5 Boiling Point
572° F at 760 mm Hg (decomposes) (NTP, 1992)

300
MSDS
 from DrugBank
572°F
4.2.6 Melting Point
340° F (NTP, 1992)

169
MSDS
 from DrugBank
170.9 deg C
Haynes, W.M. (ed.) CRC Handbook of Chemistry and Physics. 91st ed. Boca Raton, FL: CRC Press Inc., 2010-2011, p. 4-53
 from HSDB
171 °C
171°C
 from OSHA Chemical Sampling Information
340°F
4.2.7 Solubility
10 to 50 mg/mL at 66° F (NTP, 1992)

Water Solubility
Soluble in hot water, partially soluble in cold water
MSDS
 from DrugBank
Solubility: in glycerol 17.5% at 25 deg C; ethylene glycol 18.5% at 25 deg C; in methanol 173.9 g/L at 25 deg C; in ethanol
94.4 g/L at 25 deg C; in acetone 0.6% at 25 deg C; ethyl acetate 1.5% at 25 deg C
Schubert D; Kirk-Othmer Encyclopedia of Chemical Technology. (1999-2011). New York, NY: John Wiley & Sons; Boron Oxides, Boric
Acid, and Borates. Online Posting Date: 15 April 2011
 from HSDB
Water solubility: 2.52% at 0 deg C; 3.49% at 10 deg C; 4.72% at 20 deg C; 6.23% at 30 deg C; 8.08% at 40 deg C; 10.27% at
50 deg C; 12.97% at 60 deg C; 15.75% at 70 deg C; 19.10% at 80 deg C; 23.27% at 90 deg C; 27.53% at 100 deg C
 from HSDB
Solubility in water is increased by hydrochloric acid

2006., p. 218
 from HSDB
In water, 5.0X10+4 mg/L at 25 deg C

Abstract: PubMed
Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187 (1990)
 from HSDB
50 mg/mL at 25 °C
Solubility in water, g/100ml at 20°C: 5.6

 from ILO-ICSC
4.2.8 Density
1.435 at 68° F (USCG, 1999)

1.5 g/cu cm
Haynes, W.M. (ed.) CRC Handbook of Chemistry and Physics. 91st ed. Boca Raton, FL: CRC Press Inc., 2010-2011, p. 4-53
 from HSDB
Relative density (water = 1): 1.5

 from ILO-ICSC
1.435
4.2.9 Vapor Pressure
1.6X10-6 mm Hg at 25 deg C (2.136X10-4 Pa); log P (in Pa) = 26.83 - 9094/T where T is deg K
Pankajavalli R et al; J Nuclear Materials 362: 128-131 (2007)
 from HSDB
Vapour Pressure
Vapour pressure at 20°C: negligible
 from ILO-ICSC
4.2.10 LogP
log Kow = 0.175

WHO; Environmental Health Criteria 204, Boron. World Health Org (1998). Available from, as of Oct 4, 2011:
http://www.inchem.org/documents/ehc/ehc/ehc204.htm
 from HSDB
0.18
-1.09
 from ILO-ICSC
4.2.11 Stability
Stable in air.
Osol, A. (ed.). Remington's Pharmaceutical Sciences. 16th ed. Easton, Pennsylvania: Mack Publishing Co., 1980., p. 1257
 from HSDB
...Stable up to 100 deg C

 from HSDB
4.2.12 Decomposition
Boric acid decomposes in heat above 100 deg C forming boric anhydride and water.
Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2002. 4th ed.Vol 1 A-H Norwich, NY: Noyes Publications,
2002., p. 356
 from HSDB
171°C
 from ILO-ICSC
4.2.13 pH
3,8-4,8 (3,3 % aqueous solution)

pH = 5.1 (0.1 Molar)

2006., p. 218
 from HSDB
4.2.14 Dissociation Constants
Ka = 5.80X10-10 at 25 deg C (pKa = 9.24)

 from HSDB
4.3 Crystal Structures
Crystal Structures: 1 of 1 (CCDC Number)
CCDC Number 214361
Crystal Structure Data DOI:10.5517/cc761wb
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Thumbnail (Generated by
CCDC using JSmol)
Associated Article DOI:10.1107/S0108270103009685
 from The Cambridge Structural Database
4.4 Spectral Properties

Index of refraction: 1.337, 1.461, 1.462
Weast, R.C. (ed.) Handbook of Chemistry and Physics. 69th ed. Boca Raton, FL: CRC Press Inc., 1988-1989., p. B-77
 from HSDB
4.4.1 Infrared Spectra
Infrared Spectra: 1 of 5 (FTIR Spectra)
Technique KBr WAFER
Source of Sample Mallinckrodt Inc., St. Louis, Missouri
Copyright Copyright © 1980, 1981-2018 Bio-Rad Laboratories, Inc. All Rights Reserved.
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 from SpectraBase
Technique KBr WAFER
Source of Sample EASTMAN ORGANIC CHEMICALS, ROCHESTER, NEW YORK
Catalog Number P1064 (PRACTICAL GRADE)
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Technique KBr WAFER
Source of Sample J. T. Baker Chemical Company
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View All 5 Infrared Spectra
4.4.2 1D NMR Spectra
1D NMR Spectra: 1 of 2 (11B NMR Spectra)
Copyright © 2016 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights
Copyright
Reserved.
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Thumbnail
1D NMR Spectra: 2 of 2 (17O NMR Spectra)
Copyright © 2016 W. Robien, Inst. of Org. Chem., Univ. of Vienna. All Rights
Copyright
Reserved.
1D NMR Spectra: 2 of 2 (17O NMR Spectra)
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4.4.3 Mass Spectrometry
4.4.3.1 GC-MS
GC-MS Spectrum 25381 - GC-MS Ei Predicted by CFMID-EI, energy0

GC-MS: 1 of 1 (GC-MS Fields)
NIST Number 158012
Library Main library
Total Peaks 24
m/z Top Peak 45
m/z 2nd Highest 62
m/z 3rd Highest 44
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 from NIST
4.4.3.2 MS-MS
1. MS-MS Spectrum 92154 - 10V Positive Predicted by CFM-ID
4. MS-MS Spectrum 155724 - 10V Negative Predicted by CFM-ID
4.4.4 Other Spectra
Other Spectra: 1 of 2 (Raman Spectra)
Instrument Name Bio-Rad FTS 175C with Raman accessory
Technique FT-Raman
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Instrument Name Bio-Rad FTS 175C with Raman accessory
Technique FT-Raman
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5 Related Records
CLICK TO LOAD...
 from NCBI
5.1 Related Compounds with Annotation
CLICK TO LOAD...
 from PubChem
5.2 Related Compounds
Same Connectivity 4 records
Mixtures, Components, and

1391 records
Neutralized Forms
Similar Compounds 16 records
 from PubChem
5.3 Substances
5.3.1 Related Substances
All 2669 records
Same 199 records

Mixture 2470 records
 from PubChem
5.3.2 Substances by Category
CLICK TO LOAD...
 from PubChem
5.4 Entrez Crosslinks
PubMed 20 records
Protein Structures 24 records
Taxonomy 4 records
Gene 62 records
 from PubChem
6 Chemical Vendors
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 from PubChem
7 Drug and Medication Information
7.1 Drug Indication

No FDA- or EMA-approved therapeutic indications on its own.
 from DrugBank
7.2 Clinical Trials
 Download
1 to 4 of 4
Record ID Title Status Phase
NCT00799214 BASIC (Boric Acid, Alternate Solution for Intravaginal Colonization) Study Completed 3
Effectiveness of 3% Boric Acid in 70% Alcohol Versus 1% Clotrimazole Solution

NCT01547221 Completed
in Otomycosis Patients
Unknown
NCT02517957 Xia Shi Surgical Treatment for Eczema Multi-center Clinical Research 2
status
NCT02738515 Boric Acid in Degree 2 Furcation Defect Completed 3
 from ClinicalTrials.gov
7.3 Therapeutic Uses

/Former use:/ The substance is included in rectal suppositories for hemorrhoids ...
Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New
York: Macmillan Publishing Co., Inc. 1980., p. 971
 from HSDB
Aqueous solutions of boric acid are used topically for ophthalmic irrigation to cleanse, refresh, and soothe irritated eyes.
Aqueous solutions of boric acid also are used for removal of loose foreign material, air pollutants (e.g., smog, pollen), or
chlorinated water.
American Society of Health-System Pharmacists 2011; Drug Information 2011. Bethesda, MD. 2011
 from HSDB
Boric acid, borates and perborates have been used as mild antiseptics or bacteriostats in eyewashes, mouthwashes, burn
dressings, and diaper rash powders; however, the effectiveness of boric acid has largely been discredited.
Seiler, H.G., H. Sigel and A. Sigel (eds.). Handbook on the Toxicity of Inorganic Compounds. New York, NY: Marcel Dekker, Inc. 1988., p.
131
 from HSDB
MEDICATION (VET): Antibacterial and antifungal. Used chiefly in aqueous solutions or powders for external use.
2006., p. 218
 from HSDB
A double-blind comparison was made of the use of 14 daily intravaginal gelatin capsules containing 600 mg of boric acid
powder versus the use of identical capsules containing 100,000 U nystatin diluted to volume with cornstarch for the
treatment of vulvovaginal candidiasis albicans. Cure rates for boric acid were 92% at 7 to 10 days after treatment and 72%
at 30 days, whereas the nystatin cure rates were 64% at 7 to 10 days and 50% at 30 days. The speed of alleviation of signs
and symptoms was similar for the two drugs. There were no untoward side effects, and cervical cytologic features were
not affected.
Abstract: PubMed
Van Slyke KK et al; Am J Obstet Gynecol 141 (2): 145-8 (1981)
 from HSDB
7.4 Drug Warning

... The chronic use of boric acid in rectal suppositories and in vaginal deodorants carries the risk of intoxication.
 from HSDB
Borax and boric acid used in powders and ointments have resulted in serious poisonings and death.
135
 from HSDB
An outbreak of an illness in a newborn nursery consisting of vomiting, diarrhea, dehydration, and exfoliative dermatitis
was mistakenly thought to be due to an infectious agent because Staphylococcus aureus was cultured from the nose,
throat, and feces in two patients. The clinical picture was similar to Ritter's disease. However, because S. aureus was not
found in other hospital cultures, boric acid toxicity was subsequently considered. It was discovered as a contaminant of
the infant formula. Three infants died.
Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1323
 from HSDB
Boric acid enhanced action of hypnotics, but devoid of activity itself.

Abstract: PubMed
Pham Huu Chanh et al; Agressologie 15 (1): 61-72 (1974)
 from HSDB
Patients using boric acid ophthalmic solutions should be advised to consult a physician if ocular pain or visual changes
occur, they experience continued ocular redness or irritation, or the condition worsens or persists. Patients with open
wounds in or near the eyes should be advised to seek immediate medical treatment.
 from HSDB
7.5 Minimum/Potential Fatal Human Dose

The fatal dose /in humans/ is thought to be 2000-3000 mg for infants, 5000-6000 mg for children, and 15,000-20,000 mg
for adults.
 from HSDB
8 Food Additives and Ingredients
8.1 Food Additive Classes
JECFA Functional Classes

Food Additives: PRESERVATIVE
 from FAO/WHO Food Additive Evaluations (JECFA)
8.2 Evaluations of the Joint FAO/WHO Expert Committee on Food Additives - JECFA
Evaluations of the Joint FAO/WHO Expert Committee on Food Additives - JECFA: 1 of 1 (JECFA Chemical)
Chemical Name BORIC ACID
ADI NO ADI ALLOCATED
Evaluation Year 1961
Report NMRS 31/TRS 228-JECFA 6/37

9 Agrochemical Information
9.1 Agrochemical Category

Insecticide
 from EPA Office of Pesticide Programs, EU Pesticides Database
9.2 EU Pesticides Data
EU Pesticides Data: 1 of 1 (EU Pesticides Substance)
Substance boric acid
Status Not Approved
 from EU Pesticides Database

10 Pharmacology and Biochemistry
10.1 Pharmacology
Boric acid exhibits minimal bacteriostatic and antifungal activities [L2140]. Boric acid is likely to mediate antifungal actions
at high concentrations over prolonged exposures [A32457].
 from DrugBank
Boric Acid is a weakly acidic hydrate of boric oxide with mild antiseptic, antifungal, and antiviral properties. The exact
mechanism of action of boric acid is unknown; generally cytotoxic to all cells. It is used in the treatment of yeast infections
and cold sores.
 from NCIt
10.2 MeSH Pharmacological Classification
Insecticides
Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as
disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics.
See a list of PubChem compounds matching this category.
 from MeSH
10.3 ATC Code

S - Sensory organs
S02 - Otologicals
S02A - Antiinfectives
S02AA - Antiinfectives
S02AA03 - Boric acid
 from WHO ATC
10.4 Absorption, Distribution and Excretion
Absorption
Boric acid is well absorbed from the gastrointestinal tract, open wounds, and serous cavities but displays limited
absorption in intact skin [L2140]. Following intraperitoneal injection in mice, the peak concentration was reached in about
1.0-1.5 hr in the brain whereas the value was 0.5 hr in other tissues [L2140].
 from DrugBank
Route of Elimination
Regardless the route of administration, boric acid predominantly undergoes rapid renal excretion of >90% of total
administered dose as unchanged form. Small amounts are also excreted into sweat, saliva, and feces. Following
administration as ointment, urinary excretion of boric acid accounted for only 1% of the administered dose [L2140].
 from DrugBank
Volume of Distribution
Volume of distribution ranges from 0.17 to 0.5 L/kg in humans, where large amounts of boric acid are localized in brain,
liver, and kidney [L2140].
 from DrugBank
Clearance
A case report of acute boric acid poisoning following oral ingestion of 21 g of boric acid presents the total body clearance
of 0.99 L/h before hemodialysis [A32450].
 from DrugBank
Boric acid is readily absorbed from GI tract, serous cavities, and abraded or inflamed skin. It does not penetrate intact skin.
Approximately 50% of given dose is excreted within 24 hr. During chronic administration, plateau in urinary excretion is
reached only after 2 wk. ... Large amounts of boric acid are localized in brain, liver, and kidney. ... Intracytoplasmic
inclusions in pancreas /have been noted/ in fatal cases. /Boric acid/
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975.,
p. 995
 from HSDB
In animals, boric acid has been shown to be readily absorbed from the GI tract. Among the species studied were rats,
rabbits, sheep, and cattle.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V3 p.535
 from HSDB
... Boric acid (5%) was applied topically to 10-15% of the body surface of rabbits with an occlusive dressing for 1.5 hr per
day for 4 consecutive days. Minimal amounts of boric acid were absorbed across intact skin and slightly abraded skin of
rabbits as measured by excretion of B in urine. Absorption was greater in rabbits with more seriously damaged skin.
 from HSDB
In rats given boric acid in an ointment, urinary excretion accounted for only 1% of the administered dose. However, boric
acid applied to the skin of rats in an aqueous jelly was absorbed, with 23% of the administered dose appearing in the
urine.
 from HSDB
With repeated applications of the powder to abraded or inflamed skin, sufficient amount ... is or /may be/ absorbed to
cause acute poisoning, especially in infants. Lethal amount can be absorbed from wound cavities irrigated with boric acid
solution.
 from HSDB
By studies in adult volunteers who were heavily exposed to 5% solution or to 10% boric acid ointment, they showed by
analysis of the urine that no detectable boron was absorbed from the intact skin.
 from HSDB
Following intraperitoneal injection /in mice/, a peak concentration was reached in about 1.0-1.5 hr in the brain and in
about 0.5 hr in other tissues. The concentration of borate in the tissues were directly proportional to dosage over the
range 18-700 mg/kg.
 from HSDB
/In human, boric acid has a/ volume of distribution of 0.17 to 0.5 L/kg.
 from HSDB
Boric acid distributes evenly throughout the body fluids. The most complete study of boron distribution was conducted in
male F-344 rats (30/dose group) fed a control diet (<20 mg boron/kg) or a diet containing 9000 mg boric acid/kg
(approximately 68 mg boron/kg body weight per day) for up to 7 days. Six animals/ group were killed at 1, 2, 3, 4, and 7
days after the start of exposure. Boron levels were determined in all major tissues and organs. The authors reported that
boron concentrations were comparable in all tissues examined, including plasma, liver, kidney, muscle, colon, brain, testis,
epididymis, seminal vesicles, prostate, and adrenals. Most of the tissues appeared to reach steady-state boron levels (12-
30 mg boron/kg tissue) by 3-4 days; these levels were 3- to 20-fold above controls. Adipose tissue accumulated only 20%
as much boron as other tissues (3.78 mg/kg tissue). Bone boron levels (47.4 mg/kg tissue) indicated greater accumulation
in bone than in other tissues; in addition, bone boron levels continued to increase throughout the 7 days. The higher
affinity of boron for bone is indicative of a second kinetic component in which a small percentage of the boron absorbed
may be sequestered. Elimination kinetics from bone also differ from those from soft tissue and body fluids. Accumulation
of boron in bone has also been observed in humans and other animal species.
WHO; Environmental Health Criteria 204: Boron p.55 (1998). Available from, as of May 12, 2005:
http://www.inchem.org/pages/ehc.html
 from HSDB
Male Fischer-344 rats were exposed to boric acid at 3000-9000 mg/kg in the diet for up to 9 weeks. Urinary boron was
elevated (450-600 ug boron/mg creatinine) 24 hr after the end of dosing. By 3-4 days post-treatment, urinary boron in all
groups had returned to average control levels (8.97 +/- 1.95 ug boron/mg creatinine for days 1, 7, and 14 post-
treatment). Elimination of boron from bone followed a different time-course from elimination from serum or soft tissues.
F-344 rats consuming boric acid in the diet for 9 weeks (approx. 1.4-6.8 mg boron/kg body weight per day) showed dose-
related elevation of bone boron, which declined very gradually during the post-treatment period. Bone boron levels
remained elevated above controls in all exposed groups at 32 weeks post-treatment. ...
 from HSDB
Clearance of boron compounds is similar in humans and animals. Elimination of /boric acid/ from the blood is largely by
excretion of >90% of the administered dose via the urine, regardless of the route of administration. Excretion is relatively
rapid, occurring over a period of a few to several days, with a half-life of elimination of 24 hr or less.
 from HSDB
Boric acid is predominantly eliminated unchanged by the kidney. Small amounts are also excreted into sweat, saliva, and
feces. Boric acid is concentrated in the brain and liver.
Goldfrank, L.R. (ed). Goldfrank's Toxicologic Emergencies. 7th Edition McGraw-Hill New York, New York 2002., p. 1289
 from HSDB
Eight male volunteers aged 22-28 years were infused intravenously with boric acid in sterile water (21 mg/mL) over 20
minutes. Urinary excretion of boron was 98.7% of the dose in 120 hours after treatment. This indicated nearly complete
excretion of boron with no tendency for tissue accumulation. None of the volunteers registered any discomfort following
iv infusion of boric acid solution.
Jansen JA et al; Arch Toxicol 55: 64-7 (1984) as cited in USEPA; Health Advisory for Boron (Draft) p.6 (1988)
 from HSDB
Using an in vitro technique it has been demonstrated that water emulsifying and hydrophobic ointments containing boric
acid liberate only minute amounts (1-6%) within 24 hr compared with the nearly total liberation from a jelly. When an
amount of boric acid containing ointment is swallowed, the absorption is only slightly delayed compared with a similar
intake when dissolved in water, and in both cases nearly total excretion is found in the urine within 96 hr. ...
Abstract: PubMed
Schou JS et al; Arch Toxicol Suppl 7: 232-5 (1984)
 from HSDB
Six male volunteers aged 30-58 years received single oral doses of boric acid. Three volunteers ingested 750 mg boric
acid dissolved in 100 mL of water. Three other volunteers swallowed 24.95 g to 49.6 g of commercial water-emulsifying
ointment containing 2.97% (wt/wt) boric acid The accumulated mean 96 hour excretion was 93.9% of the dose after
ingestion of the solution and 92.4% after ingestion of the ointment. The initial urinary excretion rate was generally lower
after ingestion of the ointment than after ingestion of solution. More than 50% of the ingested dose was excreted within
the first 24 hr post-ingestion. No adverse health effects were reported for any of the individuals following a single
ingestion of about 1.8 mg boron/kg during the 96 hour observation period.
Jansen JA et al; Food Chem Toxicol 22: 49-53 (1984) as cited in USEPA; Health Advisory for Boron (Draft) p.6 (1988)
 from HSDB
10 students who drank spa water containing 102 mg boron excreted 92% of the boron in the urine within a 4-day period.
 from HSDB
Eight young adult males infused with 600 mg of boric acid excreted 98.7% of the dose in 120 hours; the total clearance
was 54.6 54.6 mL/min/1.73 sq m.
 from HSDB
Boric acid is rapidly distributed throughout the body water in both animals and humans. The only tissue that appears to
accumulate boron significantly above blood levels is bone. ... In rats fed boric acid in the chow, boron was reported in
bone at levels four times those in blood; all other tissues were not significantly different than blood. Adipose tissue
contained 20% of the level found in rat blood.
 from HSDB
...The back of the hand of volunteers /was exposed/ to a 5% aqueous solution of boric acid... and measured urinary boron
concentrations to determine the extent of absorption, the flux, and the permeability constants (Kp) for intact skin.
Following exposure to boric acid, 0.23% of the applied dose was excreted, flux was calculated as 0.01 ug/sq cm/hr and Kp
was 1.9x10-7 cm/hr. ...
NAS, Commission of Life Sciences; Toxicological Risks of Selected Flame-Retardant Chemicals p.152 (2000). Available from, as of May 19,
2005: http://www.nap.edu/books/0309070473/html/
 from HSDB
No absorption of boric acid (measured as boron in the blood) occurred 1-9 days after a single topical application of boric
acid in an anhydrous, water-emulsifying ointment. However, blood boron concentrations were increased within 2-6 hr
after application of the same amount of boric acid in a water-based jelly, indicating that the vehicle in which boric acid is
applied to the skin affects absorption.
NAS, Commission of Life Sciences; Toxicological Risks of Selected Flame-Retardant Chemicals p.152 (2000). Available from, as of May 19,
2005: http://www.nap.edu/books/0309070473/html/
 from HSDB
... The in-vivo effects of /boric acid/ were assessed in rats fed 9,000 parts per million (ppm) BA for up to 7 days. ... Steady
state boron levels in tissues were observed after 3 to 4 days of exposure and no selective accumulation in either the brain
or the testis was noted at this time. ...
Ku W Chapin R; Environmental Health Perspectives 102 (7): 99-105 (1994)
 from HSDB
Timed-mated Sprague-Dawley rats (28 to 32/group) were exposed to boric acid (BA) in the diet from Gestational Day (GD)
0 to 20. Dietary concentrations of added BA (0%, 0.025%, 0.050%, 0.075%, 0.100%, or 0.200%) yielded average daily
intakes equivalent to 0, 3, 6, 10, 13, or 25 mg boron/kg body weight/day. Dams and their fetuses were evaluated for
evidence of maternal or developmental toxicity, as reported previously. At termination on GD 20, ... inductively coupled
plasma optical emission spectrometry. Increasing dietary concentrations of BA were positively associated with whole
blood boron concentrations in confirmed pregnant rats, specifically 0.229 +/- 0.143, 0.564 +/- 0.211, 0.975 +/- 0.261, 1.27
+/- 0.298, 1.53 +/- 0.546, or 2.82 +/- 0.987 ug boron/g whole blood (mean +/- SD) for the control through high-dose
groups. Maternal blood boron concentrations were positively correlated with indices of maternal dietary intake of boron
and with embryo/fetal toxicity observed at 0.100% and 0.200% BA in the diet reported previously. Thus, blood boron
concentrations of 1.27 +/- 0.298 and 1.53 +/- 0.546 ug boron/g were associated with the no-observed-adverse-effect
level (10 mg boron/kg/day) and lowest-observed-adverse-effect level (13 mg boron/kg/day) for developmental toxicity
reported previously.
Price C et al; Toxicol 11 (6): 833-842 (1997)
 from HSDB
/Investigators/ exposed adult male mallard ducks to a dietary concentration of 1600 mg boron/kg for up to 48 days.
Equilibrium levels were reached between days 2 and 15. Boron concentrations were highest in the blood, followed by the
brain and liver. Boron was rapidly eliminated, with few detectable residues after 1 day on a "clean diet." The presence of
arsenic (300 mg/kg) in the diet slowed the accumulation of boron.
 from HSDB
Pharmacokinetic data indicate that boron, usually administered as boric acid, is absorbed rapidly and virtually completely
from the gastrointestinal tract, as evidenced by recovery of >90% of the dose in urine. /Boric acid/
WHO; Environmental Health Criteria Document No. 204 (1998): Boron (7740-42-8) p.53. Available from, as of July 22, 2005:
 from HSDB
10.5 Metabolism/Metabolites
Metabolism
No metabolic pathways reported.
 from DrugBank
Metabolism of inorganic borates by biological systems is not feasible owing to the excessive energy (523 kJ/mol) required
to break the boron-oxygen bond. Inorganic borates, in low concentrations, convert to boric acid at physiological pH in the
aqueous layer overlying mucosal surfaces prior to absorption. This is supported by the evidence in both human and
animal studies, where more than 90% of the administered dose of borate is excreted as boric acid. There is evidence in
both in vitro and in vivo systems that boric acid has an affinity for cis-hydroxyl groups, and this may be the mechanism
that explains the biological effects of boric acid. However, this attachment is known to be reversible and concentration
dependent, responding to clearance mechanisms.
 from HSDB
10.6 Biological Half-Life
According to human cases of poisoning, the elimination half-life of boric acid ranges from 13 to 24 hours [A32450,
L2140].
 from DrugBank
The kinetics of elimination of boron have been evaluated in human volunteers given boric acid via the intravenous and
oral routes. The half-life for elimination was the same by either route in these studies and was approximately 21 hr.
 from HSDB
A mean half-life of 13.4 hours (range, 4 to 28 hours) was reported in nine human cases of poisoning /with boric acid/.
 from HSDB
In humans, the reported excretion half-life is between 13 and 21 hr.

 from HSDB
The elimination half-life reported for rats is 4.6 hr.

 from HSDB
... Excretion is relatively rapid, occurring over a period of a few to several days, with a half-life of elimination of 24 hr or
less.
 from HSDB
10.7 Mechanism of Action

Information regarding the mechanism of action of boric acid in mediating its antibacterial or antifungal actions is limited.
Boric acid inhibits biofilm formation and hyphal transformation of _Candida albicans_, which are critical virulence factors
[A32457]. In addition, arrest of fungal growth was observed with the treatment of boric acid [A32457].
 from DrugBank
Boric acid and its derivatives have been shown to promote riboflavinuria in both animals and man. Boric acid complexes
with the polyhydroxyl ribitol side chain of riboflavin and greatly increases its water solubility.
Abstract: PubMed
Pinto JT, Rivlin S; Drug Nutr Interact 5 (3): 143-51 (1987)
 from HSDB
10.8 Human Metabolite Information
10.8.1 Metabolite Description
Description
Boric acid (H3BO3) is found in fig. Boric acid (H3BO3) is a food contaminant deriving from paper and paperboard in
contact with food. V. limited use as an antibacterial agent in cavia
10.8.2 Cellular Locations
CytoplasmExtracellular
11 Use and Manufacturing
11.1 Uses
EPA Safer Chemical Functional Use Classes

Enzymes and Enzyme Stabilizers
 from EPA Safer Choice
Food additives
Agrochemical Category
Insecticide
 from EU Pesticides Database
JECFA Functional Classes

Food Additives: PRESERVATIVE
11.1.1 Industry Uses
1. Adsorbents and absorbents 11. Laboratory chemicals

2. Agricultural chemicals (non-pesticidal) 12. Not known or reasonably ascertainable
3. CBI 13. Oxidizing/reducing agents
4. Catalyst 14. Paint additives and coating additives not described by other catego
5. Corrosion inhibitors and anti-scaling agents 15. Plating agents and surface treating agents
6. Flame retardants 16. Processing aids, specific to petroleum production
7. Fuels and fuel additives 17. Solvents (which become part of product formulation or mixture)
8. Functional fluids (closed systems)
9. Intermediates
10. Internal Panels & Linings
11.1.2 Consumer Uses
1. Agricultural products (non-pesticidal) 11. Glass Products

2. Automotive care products 12. Laboratory Use
3. Building/construction materials - wood and engineered wood products 13. Metal products not covered elsewhere
4. Building/construction materials not covered elsewhere 14. Not known or reasonably ascertainable
5. CBI 15. Paints and coatings
6. Catalyst 16. Photographic supplies, film, and photo c
7. Electrical and electronic products 17. Plastic and rubber products not covered
8. Fabric, textile, and leather products not covered elsewhere 18. Used in product(s) which are used in a v
9. Fuels and related products
10. General Distributor Sales
11.2 Methods of Manufacturing

Boric acid is manufactured industrially from borate minerals and brines. Alkali and alkaline-earth metal borates, such as
borax, kernite, colemanite, ascharite, ulexite, or hydroboracite, react with strong mineral acids to form boric acid. In the
United States boric acid is made primarily from sodium borate minerals, whereas in Europe it is made from colemanite
imported from Turkey.
Smith RA; Ullmann's Encyclopedia of Industrial Chemistry 7th ed. (1999-2011). NY, NY: John Wiley & Sons; Boric Oxide, Boric Acid, and
Borates. Online Posting Date: June 15, 2000
 from HSDB
(1) By adding hydrochloric or sulfuric acid to a solution of borax and crystallizing. (2) From weak borax brines, by
extraction with a kerosine solution of chelating agent such as 2-ethyl-1,3-hexanediol, or other polyols. Borates are
stripped from the chelate by sulfuric acid
Lewis, R.J. Sr.; Hawley's Condensed Chemical Dictionary 15th Edition. John Wiley & Sons, Inc. New York, NY 2007., p. 174
 from HSDB
Boric acid is produced mainly from sodium- or calcium-containing borate ores. The mined ore is crushed and ground
before being reacted with sulfuric acid in the presence of a hot aqueous recycled liquor containing some boric acid. The
resultant slurry contains insoluble gangue and either calcium or sodium sulfate by-product. After separation of unwanted
insoluble gangue, recovery of the boric acid product is similar to that for borax.
WHO; Environmental Health Criteria Document No. 204 (1998): Boron (7740-42-8) p. 18. Available from, as of October 17, 2011:
 from HSDB
Crushed kernite ore is reacted with sulfuric acid in recycled weak liquor (contains low concentration of borates) at 100 deg
C. Coarse gangue is separated by rake classifiers and fine particles are settled in a thickener. The boric acid strong liquor
(high borate concentration) is nearly saturated with sodium sulfate. Complete solubility of sodium sulfate is maintained
throughout the process by careful control of pH and temperature. The strong liquor is filtered at 98 deg C and boric acid
crystallized in two stages using continuous evaporative crystallizers. The temperature is dropped to 70 deg C in the first
stage and to 35 deg C in the second. Crystals are filtered and washed with progressively weaker liquor in a countercurrent
fashion. The final product is dried in rotary driers and screened for packaging.
Smith RA; Ullmann's Encyclopedia of Industrial Chemistry 7th ed. (1999-2011). NY, NY: John Wiley & Sons; Boric Oxide, Boric Acid, and
Borates. Online Posting Date: June 15, 2000
 from HSDB
11.3 Impurities
The principal impurities in technical grade boric acid are the by-product sulfate (0.1%) and various minor metallic
impurities present in the borate ore /technical grade/
Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V4: 76
(1978)
 from HSDB
11.4 Formulations/Preparations
Technical, 99.9%; CP; USP
 from HSDB
Three grades of granular and powdered boric acid are manufactured in the United States. ... technical grade, NF grade ...
/and/ special quality grade
Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V4: 76
(1978)
 from HSDB
Single Active Ingredient Products: Wettable powder 99.0%; Dust 99.0%, 64.0%, and 65.0%; Liquid Concentrate 26.3%;
Ready-to-Use Paste 50.0%; Pelleted/Tableted 40.0%; Bait Tube 53.3%.
USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document - Boric acid and its Sodium Salts. February 1994.
Available from, as of May 16, 2005: http://www.epa.gov/pesticides/reregistration/status.htm
 from HSDB
Harris Famous Roach Tablets (P.F. Harris Manufacturing Co., LLC), Boric acid 40%.
Purdue University; National Pesticide Information Retrieval System, Boric acid (10043-35-3), PC Code: 11001. Available from, as of
October 14, 2011 http://npirspublic.ceris.purdue.edu/ppis/
 from HSDB
Harris Famous Roach Powder (P.F. Harris Manufacturing Co., LLC), Boric acid 99%.
 from HSDB
Bonide No Escape Liquid Bait Ant Killer (Bonide Products, Inc.), Boric acid 5.4%.
 from HSDB
Bonide Roach Powder with Boric Acid (Bonide Products, Inc.), Boric acid 98%.
 from HSDB
Eaton's Answer Boric Acid Insecticidal Dust (Eaton JT & Co., Inc), Boric acid 99%.
 from HSDB
Dexol Predator Roach Powder with Boric Acid (Value Gardens Supply, LLC), Boric acid 99%.
 from HSDB
Roach Kil Commercial (FMC Corp. Agricultural Products Group), Boric acid 99%.
 from HSDB
Drax Ant Kill Gel (FMC Corp. Agricultural Products Group), Boric acid 5%.
 from HSDB
Drax Ant Kil-PF (FMC Corp. Agricultural Products Group), Boric acid 5%.
 from HSDB
Aerosol Boric Acid (FMC Corp. Agricultural Products Group), Boric acid 20%.
 from HSDB
Drax Roach Assault SWT (FMC Corp. Agricultural Products Group), Boric acid 50%.
 from HSDB
Drax Liquid Ant Killer II SWT (FMC Corp. Agricultural Products Group), Boric acid 1%.
 from HSDB
Drax Granular Bait with Boric Acid & Nylar (FMC Corp. Agricultural Products Group), Boric acid 1%, Pyriproxyfen 0.25%.
 from HSDB
Drax Bait Station (FMC Corp. Agricultural Products Group), Boric acid 5%.
 from HSDB
Drax - PF Bait Station (FMC Corp. Agricultural Products Group), Boric acid 5%.
 from HSDB
Whitmire PT 240 Perma-dust Insecticide (Whitmire Micro-Gen Research Laboratories, Inc.), Boric acid 35.5%.
 from HSDB
TC 273 (Whitmire Micro-Gen Research Laboratories, Inc.), Boric acid 5%.

 from HSDB
Whitmire PT 240D Perma-Dust (Whitmire Micro-Gen Research Laboratories, Inc.), Boric acid 99%.
 from HSDB
Safecide Brand IC (Intervet Inc.), Boric acid 99%.

 from HSDB
Enoz Roach Away Boric Acid (Willert Home Products), Boric acid 99%.
 from HSDB
Boric Acid Manufacturing Grade (U.S. Borax Inc.), Boric acid 100%.
 from HSDB
Optibor Guard (U.S. Borax Inc.), Boric acid 100%.

 from HSDB
20 Mule Team Boratrol and 20 Mule Team Sectrol (U.S. Borax Inc.), Boric acid 99%.
 from HSDB
Eco2000-GR (EcoLab Inc.), Boric acid 54%.

 from HSDB
Eco 2000-XP Freshbait (EcoLab Inc.), Boric acid 43.4%.

 from HSDB
Firepro (Osmose Inc.), Boric acid 25%, Boron sodium oxide (B4Na2O7), pentahydrate 45%.
 from HSDB
Pic Ant Control Systems (Pic Corporation), Boric acid 4%, Borax (B4Na2O7.10H2O) 5%.
 from HSDB
Pic Boric Acid Roach Killer Gel (Pic Corporation), Boric acid 33.3%.
 from HSDB
Pic Ant Killing Systems (Pic Corporation), Boric acid 4%, Borax (B4Na2O7.10H2O) 5%.
 from HSDB
Pic Ant Killer Bait (Pic Corporation), Boric acid 4%, Borax (B4Na2O7.10H2O) 5%.
 from HSDB
Pic Boric Acid Roach Killer II (Pic Corporation), Boric acid 99%.
 from HSDB
Roach Destroyer (Bacon Products Company, Inc.), Boric acid 99%.

 from HSDB
Raid Roach Gel Baits (S.C. Johnson & Son Inc.), Boric acid 2%.
 from HSDB
Protexall "Ant-Kil" (Protexall Products Inc.), Boric acid 6%.

 from HSDB
Alco Sta-gon Insecticidal Dust (Amvac Chemical Corporation), Boric acid 99%.
 from HSDB
Vertagreen Boric Acid Insecticide Powder (United Industries Corp.), Boric acid 99%.
 from HSDB
Black Jack Boric Acid Powder Roach Killer (Safeguard Chemical Corporation), Boric acid 100%.
 from HSDB
R Value's Roach Kil (Waterbury Companies Inc.), Boric acid 99%.

 from HSDB
Drax Roach D-Stroy Mix (Waterbury Companies Inc.), Boric acid 50%.
 from HSDB
Drax Roach Assault PGF (Waterbury Companies Inc.), Boric acid 50%.
 from HSDB
Borid Barrier with Boric Acid (Waterbury Companies Inc.), Boric acid 52%.
 from HSDB
Drax Liquid Ant Killer - SWT (Waterbury Companies Inc.), Boric acid 0.5%.
 from HSDB
Drax Liquid Ant Killer with Nylar and Boric Acid (Waterbury Companies Inc.), Boric acid 0.5%, Pyriproxyfen 0.25%.
 from HSDB
Drax Ant Kill Gel RBA (Waterbury Companies Inc.), Boric acid 0.5%.
 from HSDB
Drax Ant Kil Gel 2X RBA (Waterbury Companies Inc.), Boric acid 1%.
 from HSDB
Drax Granular Bait with Boric Acid (Waterbury Companies Inc.), Boric acid 1%.
 from HSDB
Drax 2X Granular Bait with Boric Acid (Waterbury Companies Inc.), Boric acid 2%.
 from HSDB
Drax 2X Granular Bait with Boric Acid & Nylar (Waterbury Companies Inc.), Boric acid 2%, Pyriproxyfen 0.25%.
 from HSDB
Country Vet Roach Kil (Waterbury Companies Inc.), Boric acid 99%.
 from HSDB
Roach Prufe (Copper Brite, Inc.), Boric acid 98%.

 from HSDB
Powder Roach Killer (Athea Laboratories Inc.), Boric acid 99%.

 from HSDB
Boric Acid Granular Technical (Drexel Chemical Co.), Boric acid 100%.
 from HSDB
Boric Acid (Drexel Chemical Co.), Boric acid 100%.

 from HSDB
Drexel Borexel (Drexel Chemical Co.), Boric acid 5%.

 from HSDB
Drexel Roach Powder (Drexel Chemical Co.), Boric acid 100%.

 from HSDB
Orlik Insect Powder (Phaeton Corporation), Boric acid 100%.

 from HSDB
Enforcer Roach Ridd (Zep Commercial Sales & Service), Boric acid 99%.
 from HSDB
Zone Defense (In-Cide Technologies, Inc.), Boric acid 64%.

 from HSDB
Incide Pest Control Insulation (In-Cide Technologies, Inc.), Boric acid 14.72%.
 from HSDB
Chem-Tox Pro! Roach Kill Powder (CTX-Cenol, Inc.), Boric acid 99%.
 from HSDB
Best Brand Roach & Ant Bait Gel (Chem-Tech, Limited), Boric acid 51%.
 from HSDB
Seabright Roach Bait (Seabright Enterprises Limited), Boric acid 51.24%.

 from HSDB
Woodstream Boric Acid Powder Formula #1 (Woodsteam Corporation), Boric acid 40%, German cockroach pheromone
0.005%.
 from HSDB
Catchmaster Roach Killing Powder (with Boric Acid) (AP&G Co., Inc.), Boric acid 99%.
 from HSDB
Agro Roach Tablets (Agro Products and Pet Supply, Inc.), Boric acid 40%.
 from HSDB
Zap-a-roach Boric Acid Roach Killer (HBC Chemical, Inc.), Boric acid 100%.
 from HSDB
Ant Gel Bait (Control Solutions, Inc.), Boric acid 5%.

 from HSDB
Stapleton's Magnetic Roach Food M.R.F. 2000 - Paste Formula (Blue Diamond Exterminating & MFG Co., Inc.), Boric acid
33.3%.
 from HSDB
Pro-Joe-S Bait/Gel Formula 15 (Blue Diamond Exterminating & MFG Co., Inc.), Boric acid 15%.
 from HSDB
Pro-Joe-S Bait/Formula 4.5 (Blue Diamond Exterminating & MFG Co., Inc.), Boric acid 4.5%.
 from HSDB
Buddies Puddy (Buddies Puddy Co.), Boric acid 50%.

 from HSDB
Rx for Fleas Plus (Rx for Fleas, Inc.), Boric acid 64%.
 from HSDB
Timbertreat ICA-20 (Kop-Coat, Inc.), Boric acid 20%.

 from HSDB
Best Brand Roach & Ant Bait Gel (Hacco, Inc.), Boric acid 51%.
 from HSDB
Dricon Fire Retardant (Arch Wood Protection, Inc.), Boric acid 26.3%.
 from HSDB
Arch BA (Arch Wood Protection, Inc.), Boric acid 100%.

 from HSDB
Echols Roach Tablets (Kittrich Corporation), Boric acid 40%.

 from HSDB
Goodbye Roaches (Kittrich Corporation), Boric acid 99%.

 from HSDB
Redzone Bait (Nisus Corporation), Boric acid 5%.

 from HSDB
Ant-fix (Nisus Corporation), Boric acid 5.8%.

 from HSDB
Three Elephant Boric Acid Granular Technical (Searles Valley Minerals, Inc.), Boric acid 100%.
 from HSDB
Fleago the Magic Crystal (Evergreen Pet Supply, Inc.), Boric acid 99%.
 from HSDB
Fleago Stoppers Carpet Powder (Flea Stoppers), Boric acid 100%.

 from HSDB
Boric Acid Technical Grade (National Boraxx Corporation), Boric acid 100%.
 from HSDB
Darkling Beetle Control (National Boraxx Corporation), Boric acid 100%.

 from HSDB
First Defense Premise Treatment (Synergy Labs), Boric acid 100%.

 from HSDB
Flea Maxx (Protechnology Inc.), Boric acid 65%.

 from HSDB
Bugg-less (Bugless Inc.), Boric acid 66%.

 from HSDB
Advantage 1000 (Advantage 1000), Boric acid 54.17%.

 from HSDB
Dekko Silverfish Paks (Dekko Manufacturing, LLC), Boric acid 20%.

 from HSDB
NAC 20 (Grow More, Inc.), Boric acid 100%.

 from HSDB
Protectol CX Type A (Dr. Wolman GMBH), Boric acid 5%, Copper carbonate, basic 16.3%, Copper, bis[1-cyclohexyl-1,2-
di(hydroxy-.kappa.O)diazeniumato(2-)] 3.5%.
 from HSDB
Sinesto PFB (Dr. Wolman GMBH), Boric acid 9%, Fenpropimorph 5.4%, Propiconazole 2.7%.
 from HSDB
Diffusit SP (Dr. Wolman GMBH), Boric acid 63%.

 from HSDB
Diffusit SP 124 (Dr. Wolman GMBH), Boric acid 34%, Boron sodium oxide (B4Na2O7), pentahydrate 27.7%.
 from HSDB
Cobra Rod (Genics, Inc.), Boric acid 4.7%, Boron sodium oxide (B8Na2O13) 90.6%, Copper hydroxide 2.9%.
 from HSDB
Cobra Crush MDT (Genics, Inc.), Boric acid 7.9%, Boron sodium oxide (B8Na2O13), tetrahydrate 80.5%, Copper hydroxide
8.8%.
 from HSDB
Genics Cub (Genics, Inc.), Boric acid .89%, Boron sodium oxide (B8Na2O13), tetrahydrate 9.1%, Copper hydroxide 0.99%.
 from HSDB
Genics Gel Wrap (Genics, Inc.), Boric acid .85%, Boron sodium oxide (B8Na2O13), tetrahydrate 8.65%, Copper hydroxide
0.94%.
 from HSDB
T*A*P (Cellulose Technologies Group, Inc.), Boric acid 12.5%.

 from HSDB
Intice Granular Bait (Rockwell Laboratories, Limited), Boric acid 5%.

 from HSDB
Boractin Insecticide Powder (Rockwell Laboratories, Limited), Boric acid 99%.

 from HSDB
Intice Roach Bait (Rockwell Laboratories, Limited), Boric acid 30%.

 from HSDB
Green Zone (TM) Granular Bait (Rockwell Laboratories, Limited), Boric acid 10%.
 from HSDB
Boric Acid FG (American Borate Co.), Boric acid 100%.

 from HSDB
JT Eaton Answer the Liquid Bait System with Activator (Baker's & 18 Corporation), Boric acid 1%.
 from HSDB
Impralit KDS (Rutgers Organics GMBH), Boric acid 8%, Copper carbonate, basic 12.47%, Boric acid (H3BO3), polymer with
N-decyl-1-decanamine, oxirane and 1,2-propanediol 5.96%.
 from HSDB
Antmasters Complete Gel Bait (Bugguys.com LLC), Boric acid 5%.

 from HSDB
Borathor Granular Scatter Bait (Ensystex II, Inc.), Boric acid 5%.
 from HSDB
Green Dragon Insect Bait (Green Dragon Pest Solutions), Boric acid 40%.
 from HSDB
Papa Richter's Roach Rider (Papa Richter's Roach Ridder), Boric acid 27%.
 from HSDB
Kill Fleas Dead (Kill Fleas Dead), Boric acid 100%.

 from HSDB
Ophthalmic: Solution, Collyrium for Fresh Eyes Eye Wash (Bausch & Lomb).
 from HSDB
Bulk: Powder.
 from HSDB
11.5 Consumption
Textile-grade glass fibers, 35%; borosilicate glasses, 20%; fire retardants, 15%; enamels, fruits and glazes, 7%; metallurgy,
5%; adhesives, 3%; miscellaneous, 15% (1984)
CHEMICAL PRODUCTS SYNOPSIS: Boric Acid, 1984
 from HSDB
Boron oxide & boric acid combined: 20% is used in textile glass fibers; 19% as a flux in enamels, frits, & glazes; 9% in
glasses; 1% as a herbicide; 51% in misc applications, including use as a catalyst in oxidation of hydrocarbons, as a
conditioning agent, & in manufacture of other boron compounds (1969)
SRI
 from HSDB
11.6 U.S. Production

(1972) 6.17X10+10 G
SRI
 from HSDB
(1975) 6.81X10+10 G
SRI
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(1984) 1.26X10+11 g (est)

CHEMICAL PRODUCTS SYNOPSIS: Boric Acid, 1984
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Production volumes for non-confidential chemicals reported under the Inventory Update Rule.
Year Production Range (pounds)
1986 No Reports
1990 No Reports
1994 >1 million - 10 million
1998 >1 million - 10 million
2002 >500 thousand - 1 million
US EPA; Non-confidential Production Volume Information Submitted by Companies for Chemicals Under the 1986-2002 Inventory
Update Rule (IUR). Boric acid (10043-35-3). Available from, as of October 11, 2011: http://www.epa.gov/oppt/iur/tools/data/2002-
vol.html
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Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Boric acid.
Aggregated National Production Volume: 100 to < 500 million pounds.
US EPA; Non-Confidential 2006 Inventory Update Reporting. National Chemical Information. Boric acid (10043-35-3). Available from, as
of October 11, 2011: http://cfpub.epa.gov/iursearch/index.cfm?s=chem&err=t
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11.7 U.S. Imports

(1984) 7.03x10+9 g
BUREAU OF THE CENSUS. U.S. IMPORTS FOR CONSUMPTION AND GENERAL IMPORTS 1984 p.1-345
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(1986) 12.28x10+6 lb
BUREAU OF THE CENSUS. US IMPORTS FOR CONSUMPTION AND GENERAL IMPORTS 1986 P. 1-511
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(1985) 10 short tons

BUREAU OF MINES. MINERAL COMMODITY SUMMARIES 1989 P.28
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(1986) 6 short tons

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(1987) 2 short tons

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(2000) 39 thousand metric tons

USGS; Mineral Commodity Summaries, Boron (2005). Available from, as of June 1, 2005: http://minerals.usgs.gov/minerals/pubs/mcs/
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(2004) 52 thousand metric tons (estimated)

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Cadmium: Salient Import Statistics for the United States:

2006 2007 2008 2009 2010 (estimated)
Imports for consumption: metal only 179 315 153 117 210
Imports for consumption: metal, alloys, scrap 180 316 197 122 215
USGS; Mineral Commodity Summaries 2011. Cadmium. Available from, as of July 21, 2011:
http://minerals.usgs.gov/minerals/pubs/mcs/2011/mcs2011.pdf
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11.8 U.S. Exports

(1972) 1.72X10+11 G (PLUS SODIUM BORATES)
SRI
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(1975) 1.91X10+10 G
SRI
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(1984) 3.63X10+10 g
BUREAU OF THE CENSUS. U.S. EXPORTS, SCHEDULE E, 1984 p.2-88
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(1987) 5.95X10+4 content ton

BUREAU OF THE CENSUS. U. S. EXPORTS, SCHEDULE E, DECEMBER 1987, P.2-93
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(2004) 43 thousand metric tons (estimated)

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12 Identification
12.1 Analytic Laboratory Methods

Method: AOAC 952.15, Boric Acid in Deodorants and Antiperspirants; Ion exchange method; Analyte: boric acid; Matrix:
deodorants and antiperspirants; Detection Limit: not provided.
Horwitz W, ed.; Official Methods of Analysis of AOAC International 17th ed. (2003). CD-ROM, AOAC International, Gaithersburg, MD
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Method: AOAC 969.26, Boric Acid in Caviar; Spectrophotometric method; Analyte: boric acid; Matrix: caviar; Detection
Limit: not provided.
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Method: AOAC 970.34, Boric Acid in Food; Titrimetric method; Analyte: boric acid; Matrix: deodorants and antiperspirants;
Detection Limit: not provided.
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Method: AOAC 972.19, Boric Acid in Food; Atomic absorption spectrophotometric method ; Analyte: boric acid; Matrix:
food; Detection Limit: not provided.
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Method: AOAC 975.26, Boric Acid in Food; Emission spectroscopic method; Analyte: boric acid; Matrix: food; Detection
Limit: not provided.
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An automated fluorometric method is described for measuring boron in compounds such as boric acid, borax, & sodium
perborate in water & sewage effluents.
Afgahan BK et al; Water Res 6 (12): 1475 (1972)
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12.2 Clinical Laboratory Methods

Boric acid is determined by ashing tissues in an alkaline medium at 600 deg C, dissolving in hydrochloric acid,
centrifuging, mixing part of the supernatant with carminic acid in sulfuric acid and measuring the color at 575 nm after 1
hr.
Kobylecka K, Sadlik J; Krim Forensisch Wiss 41: 77-9 (1980)
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12.3 OSHA Chemical Sampling

Boric Acid
13 Safety and Hazards
13.1 Hazards Identification
13.1.1 GHS Classification
Signal: Danger
GHS Hazard Statements
Aggregated GHS information provided by 1514 companies from 38 notifications to the ECHA C&L Inventory.
Reported as not meeting GHS hazard criteria by 1 of 1514 companies. For more detailed information, please visit ECHA
C&L website
Of the 37 notification(s) provided by 1513 of 1514 companies with hazard statement code(s):
H360 (99.93%): May damage fertility or the unborn child [Danger Reproductive toxicity]
Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in
parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with
percentage values above 10% are shown.
Precautionary Statement Codes

P201, P202, P281, P308+P313, P405, and P501
(The corresponding statement to each P-code can be found here.)
View all (6) GHS Classification entries
13.1.2 EPA Safer Chemical
Orthoboric acid - Yellow triangle - The chemical has met Safer Choice Criteria for its functional ingredient-class, but has
some hazard profile issues. Specifically, a chemical with this code is not associated with a low level of hazard concern for
all human health and environmental endpoints. (See Safer Choice Criteria). While it is a best-in-class chemical and among
the safest available for a particular function, the function fulfilled by the chemical should be considered an area for safer
chemistry innovation.
13.1.3 Health Hazard
Although no adverse effects have been reported from inhaling boric acid dust, it is absorbed through mucous
membranes. Ingestion of 5 grams or more may irritate gastrointestinal tract and affect central nervous system. Contact
with dust or aqueous solutions may irritate eyes; no chronic effects have been recognized, but continued contact should
be avoided. Dust and solutions are absorbed through burns and open wounds but not through unbroken skin. (USCG,
1999)
13.1.4 Fire Hazard
Literature sources indicate that this compound is nonflammable. (NTP, 1992)

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.
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13.1.5 Fire Potential
Not flammable
U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government
Printing Office, 1984-5.
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13.1.6 Skin, Eye, and Respiratory Irritations
Irritant to skin in dry form.

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Boric acid ... produced mild eye irritation in the Draize test in rabbits.
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Boric acid irritates the eyes, skin, and the respiratory tract. ...
2002., p. 356
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Products containing 0.4% and 2.4% boric acid were moderately irritating and practically nonirritating /to the skin/,
respectively.
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13.2 Safety and Hazard Properties
13.2.1 Chemical Dangers
Decomposes above 100°C . This produces water and irritant boric anhydride. The solution in water is a weak acid. Attacks
metals. This produces hydrogen. This generates fire and explosion hazard.
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13.3 First Aid Measures
13.3.1 First Aid
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline
solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments,
oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim
after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood
affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas
thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be
prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area;
take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth,
throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory
protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA)
should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.
INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to
dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a
hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that
the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE
VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)
13.3.2 Inhalation First Aid
Fresh air, rest.

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13.3.3 Skin First Aid
Rinse and then wash skin with water and soap.

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13.3.4 Eye First Aid
Rinse with plenty of water (remove contact lenses if easily possible).

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13.3.5 Ingestion First Aid
Rinse mouth. Do NOT induce vomiting. Refer immediately for medical attention.
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13.4 Fire Fighting Measures
13.4.1 Fire Fighting
Fire Extinguishing Agents: Water fog. (USCG, 1999)

In case of fire in the surroundings, use appropriate extinguishing media.

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13.5 Accidental Release Measures
13.5.1 Spillage Disposal
Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled
substance into covered containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of
water.
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13.5.2 Disposal Methods
SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for
occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use
or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air
quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental
and public health regulations.
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13.5.3 Other Preventative Measures
SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental
effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the
substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of
the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing
of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the
usual eye protection equipment should be worn even when contact lenses are in place.
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Containers of boric acid should bear an autoclavable poison label.

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Avoid depositing product onto exposed food and feed processing, preparation and serving surfaces, or introducing
material into air. Do not apply when food processing facility is in operation. Any product visible after application must be
brushed into cracks and crevices, or removed. Place product in areas that are inaccessible to children and pets.
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13.6 Handling and Storage
13.6.1 Nonfire Spill Response
SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then
transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any
remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual
disposal. Wash all contaminated surfaces with a strong soap and water solution. Do not reenter the contaminated area
until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE
PRECAUTIONS: You should store this material under ambient temperatures. (NTP, 1992)
13.6.2 Safe Storage
Separated from strong bases.

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13.6.3 Storage Conditions
Preserve in well-closed containers.

USP Convention. The United States Pharmacopeia 21st Revision/The National Formulary 16th ed. Rockville, MD: United States
Pharmacopeial Convention, Inc., Jan. 1, 1985 (plus Supplements 1-6)., p. 1537
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13.7 Exposure Control and Personal Protection
13.7.1 Threshold Limit Values
8 hr Time Weighted Avg (TWA): 2 mg/cu m (inhalable fraction); 15 min Short Term Exposure Limit (STEL): 6 mg/cu m
(inhalable fraction). /Borate compounds, inorganic/
American Conference of Governmental Industrial Hygienists; 2011 Threshold Limit Values for Chemical Substances and Physical Agents
and Biological Exposure Indices . Cincinnati, OH 2011, p. 14
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A4; Not classifiable as a human carcinogen. /Borate compounds, inorganic/

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(inhalable fraction): 2 mg/m3, as TWA; 6 mg/m3 as STEL; A4 (not classifiable as a human carcinogen).
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(inhalable fraction): 10 mg/m3; peak limitation category: I(1); pregnancy risk group: B
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13.7.2 Other Occupational Permissible Levels
Limit for livestock is 5 ug/ml boron in water. /Boron/

135
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0.5 mg/l maximum (USSR) /Boron in drinking water/

136
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13.7.3 Inhalation Risk
Evaporation at 20°C is negligible; a harmful concentration of airborne particles can, however, be reached quickly ,
especially if powdered.
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13.7.4 Effects of Short Term Exposure
The substance is irritating to the respiratory tract. May cause mechanical irritation to the eyes. The substance may cause
effects on the central nervous system and kidneys. This may result in impaired functions.
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13.7.5 Effects of Long Term Exposure
Repeated or prolonged contact with skin may cause dermatitis. The substance may have effects on the testes. Animal
tests show that this substance possibly causes toxicity to human reproduction or development.
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13.7.6 Allowable Tolerances
An exemption from the requirement of a tolerance is established for residues of the pesticidal chemical boric acid and its
salts, borax (sodium borate decahydrate), disodium octaborate tetrahydrate, boric oxide (boric anhydride), sodium borate
and sodium metaborate, in or on raw agricultural commodities when used as an active ingredient in insecticides,
herbicides, or fungicides preharvest or postharvest in accordance with good agricultural practices.
40 CFR 180.1121 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from,
as of October 9, 2011: http://www.ecfr.gov
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Residues of boric acid are exempted from the requirement of a tolerance when used in accordance with good agricultural
practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only. Use:
sequestrant. Limit: none.
40 CFR 180.920 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as
of October 9, 2011: http://www.ecfr.gov
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13.7.7 Exposure Prevention
PREVENT DISPERSION OF DUST! STRICT HYGIENE!

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13.7.8 Inhalation Prevention
Use local exhaust or breathing protection.

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13.7.9 Skin Prevention
Protective gloves. Protective clothing.

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13.7.10 Eye Prevention
Wear safety spectacles or eye protection in combination with breathing protection.

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13.7.11 Ingestion Prevention
Do not eat, drink, or smoke during work.

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13.7.12 Protective Equipment and Clothing
Chemical goggles; chemical resistant gloves and clothing. (USCG, 1999)

13.8 Stability and Reactivity
13.8.1 Air and Water Reactions
Water soluble.
13.8.2 Reactive Group
Acids, Weak
13.8.3 Reactivity Profile
BORIC ACID is a very weak acid. Incompatible with alkali carbonates and hydroxides. During an attempt to make triacetyl
borate, a mixture of boric acid and acetic anhydride exploded when heated to 58-60°C [Chem. Eng. News 51:(34) 1973].
Reacts violently with the strong reducing agent potassium metal.
13.8.4 Reactivities and Incompatibilities
During an attempt to make triacetyl borate, a mixture of boric acid and acetic anhydride exploded when heated to 58-60
deg C.
National Fire Protection Association; Fire Protection Guide to Hazardous Materials. 14TH Edition, Quincy, MA 2010, p. 491-31
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A mixture of potassium and /boric acid/ ... may explode on impact ...
National Fire Protection Association; Fire Protection Guide to Hazardous Materials. 14TH Edition, Quincy, MA 2010, p. 491-154
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Incompatible /with/ alkali carbonates and hydroxides.

O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. 13th Edition, Whitehouse Station, NJ: Merck
and Co., Inc., 2001., p. 223
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13.9 Transport Information
13.9.1 EC Classification
R: 60-61; S: 53-45; Symbol: T

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13.10 Regulatory Information
13.10.1 Federal Drinking Water Guidelines
EPA 600 ug/L /Boron/

USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee (FSTRAC). Summary of State and Federal Drinking Water
Standards and Guidelines (11/93) To Present
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13.10.2 State Drinking Water Guidelines
(CA) CALIFORNIA 1000 ug/L /Boron/

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(NH) NEW HAMPSHIRE 630 ug/L /Boron/

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(ME) MAINE 1,400 ug/L /Boron/

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(MN) MINNESOTA 1,000 ug/L /Boron/

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(WI) WISCONSIN 960 ug/L /Boron/

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13.10.3 FIFRA Requirements
Residues of boric acid are exempted from the requirement of a tolerance when used in accordance with good agricultural
practice as inert (or occasionally active) ingredients in pesticide formulations applied to growing crops only. Use:
sequestrant. Limit: none.
40 CFR 180.920 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as
 from HSDB
An exemption from the requirement of a tolerance is established for residues of the pesticidal chemical boric acid and its
salts, borax (sodium borate decahydrate), disodium octaborate tetrahydrate, boric oxide (boric anhydride), sodium borate
and sodium metaborate, in or on raw agricultural commodities when used as an active ingredient in insecticides,
herbicides, or fungicides preharvest or postharvest in accordance with good agricultural practices.
40 CFR 180.1121 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from,
as of October 9, 2011: http://www.ecfr.gov
 from HSDB
Based on the reviews of the generic data for the active ingredients of boric acid and its sodium salts, the Agency has
sufficient information on the health effects of boric acid and its sodium salts and their potential for causing adverse
effects in fish and wildlife and the environment. Therefore, the Agency concludes that products containing boric acid and
its sodium salts for all uses are eligible for reregistration. The Agency has determined that boric acid and its sodium salts,
labeled and used as specified in the RED document, will not pose unreasonable risks or adverse effects to humans or the
environment.
USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document - Boric Acid. Available from, as of October 9, 2011:
http://www.epa.gov/pesticides/reregistration/status.htm
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As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their continued use. Under this pesticide reregistration
program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November
1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey
standards, such as those described in the Food Quality Protection Act of 1996. Borax is found on List A, which contains
most food use pesticides and consists of the 194 chemical cases (or 350 individual active ingredients) for which EPA
issued registration standards prior to FIFRA '88. Case No: 0024; Pesticide type: insecticide, fungicide herbicide;
Registration Standard Date: 11/01/85; Case Status: RED Approved 9/93; OPP has made a decision that some/all uses of
the pesticide are eligible for reregistration, as reflected in a Reregistration Eligibility Decision (RED) document .; Active
ingredient (AI): boric acid; Data Call-in (DCI) Date(s): 2/16/94; AI Status: OPP has completed a Reregistration Eligibility
Decision (RED) for the case/AI.
United States Environmental Protection Agency/ Prevention, Pesticides and Toxic Substances; Status of Pesticides in Registration,
Reregistration, and Special Review. (1998) EPA 738-R-98-002, p. 91
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13.10.4 FDA Requirements
Boric acid is an indirect food additive for use only as a component of adhesives.
21 CFR 175.105 (USFDA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as
 from HSDB
Drug products containing certain active ingredients offered over-the-counter (OTC) for certain uses. A number of active
ingredients have been present in OTC drug products for various uses, as described below. However, based on evidence
currently available, there are inadequate data to establish general recognition of the safety and effectiveness of these
ingredients for the specified uses: boric acid is included in topical acne drug products; dandruff/seborrheic
dermatitis/psoriasis drug products; skin protectant drug products; astringent drug products; fever blister and cold sore
treatment drug products; insect bite and sting drug products; poison ivy, poison oak, poison sumac drug products;
ophthalmic anti-infective drug products; diaper rash drug products; and antiseptic drug products.
21 CFR 310.545 (USFDA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as
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14 Toxicity
14.1 Toxicological Information
14.1.1 NIOSH Toxicity Data
 Download
1 to 5 of 159 View More
Measurement System Route/Organism Dose Effect Date
Skin and Eye 15 mg/3D- October

skin /human mild
Irritation intermittent 2015
17000
ppm/24H (-
mutation in October
Mutation Data /Escherichia coli enzymatic
microorganisms 2015
activation
step)
Reproductive: Paternal effects:

Spermatogenesis (including
9600 genetic material, sperm
Reproductive October
inhalation/rat µg/m3/4H morphology, motility, and count)
Effects 2015
(16W male)
Reproductive: Paternal effects:
Testes, epididymis, sperm duct
Reproductive: Effects on embryo

or fetus: Fetotoxicity (except
1000 death, e.g., stunted fetus)
Reproductive October
intraperitoneal/mouse mg/kg (8D
Effects 2015
pregnant) Reproductive: Specific
developmental abnormalities:
Musculoskeletal system
Reproductive: Effects on fertility:

Post- implantation mortality (e.g.,
dead and/or resorbed implants
750 mg/kg
Reproductive per total number of implants) October
oral/rat (10D
Effects 2015
pregnant)
Reproductive: Specific
developmental abnormalities:
Musculoskeletal system
 from The National Institute for Occupational Safety and Health (NIOSH)
14.1.2 Carcinogen
Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans

USEPA Office of Pesticide Programs, Health Effects Division, Science Information Management Branch: "Chemicals Evaluated for
Carcinogenic Potential" (April 2006)
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A4; Not classifiable as a human carcinogen. /Borate compounds, inorganic/

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TLV-A4
14.1.3 Health Effects
Irritation-Eyes, Nose, Throat, Skin---Mild (HE16); Acute toxicity (CNS, kidney) (HE4); Potential developmental and
reproductive hazards (HE5).
Health Effect Code(s)

HE16, HE4, HE5
14.1.4 Exposure Routes
The substance can be absorbed into the body by inhalation of dust and by ingestion.
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14.1.5 Symptoms
Irritation of eyes, skin, respiratory tract; cough, sore throat; skin rash; kidney damage, diminished urinary output;
metabolic acidosis; Acute ingestion: Abdominal pain, nausea, vomiting, diarrhea; neurologic symptoms (headache,
tremulousness, irritability, delirium, seizures); skin redness on palms, soles and buttocks followed by peeling.
14.1.6 Inhalation Symptoms
Cough. Sore throat.

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14.1.7 Skin Symptoms
No acute symptoms expected.

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14.1.8 Eye Symptoms

Redness. Pain.
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14.1.9 Ingestion Symptoms
Nausea. Vomiting. Diarrhoea. Abdominal pain. Skin rash. Headache. Drowsiness. Convulsions.
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14.1.10 Target Organs
Eyes, skin, respiratory system, kidneys, CNS (In animals: testes)

14.1.11 Interactions
... Genetic effects of boric acid and borax (2.5, 5 and 10 microm) on cultures with and without TiO(2) addition. No
significant increase in /sister-chromatid exchanges/ (SCE) and micronuclei frequencies were observed at all concentrations
of boron compounds. However, TiO(2)-induced SCE and micronuclei could be reduced significantly by the presence of
boric acid and borax. In conclusion, this study indicated for the first time that boric acid and borax led to an increased
resistance of DNA to damage induced by TiO(2).
Abstract: PubMed
Turkez H; J Appl Toxicol. 28 (5): 658-64 (2008)
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Boric acid enhanced action of hypnotics, but devoid of activity itself.

Abstract: PubMed
Pham Huu Chanh et al; Agressologie 15 (1): 61-72 (1974)
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The usefulness of N-acetylcysteine (NAC) as a chelating agent was studied for ... boric acid. Mature Sprague-Dawley rats
were intoxicated; urinary excretion rates of intoxicant and total urine volume were determined during treatment. N-
acetylcysteine proved to be the most effective agent at increasing the excretion of boron and was also able to reverse the
oliguria associated with this chemical.
Abstract: PubMed
Banner W JR et al; Toxicol Appl Pharmacol 83 (1): 142-47 (1986)
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... Previous results have shown that exposure of pregnant rats on GD10 to either hyperthermia (42C) or boric acid (BA)
specifically targets segmentation patterns. Exposure to hyperthermia increased the prevalence of fused and/or reduced
numbers of vertebrae and ribs, primarily in the thoracic area. BA (500-1000 mg/kg, single oral dose) resulted in a
significant increase in segmentation defects similar to those seen after hyperthermia, with a greater incidence in lumbar
defects. In this study, we focused on the interaction of these two agents and their effects on axial skeletal development.
Pregnant rats were treated on GD10 as follows: Anesthesia with Nembutal (30 mg/kg), followed by oral dosing with either
water or BA (500 mg/kg) and immersion in a water bath at 37C (30 min) or 42C (rectal temp maintained at 42C for 5 min).
After delivery, pups were evaluated on postnatal day (PND) 1 and 3 for number, sex, and weight. No differences were seen
in litter size, pup survival, or pup weight in any of the groups. On PND3, pups were examined and processed for skeletal
staining with alizarin red and alcian blue. Preliminary data indicate an increase in skeletal alterations with BA+37C (47%),
water+42C (75%), or BA+42C (67%), as compared to water+37C controls (0%). Alterations included defects in ribs and
vertebrae and a decrease in the number of presacral vertebrae. Because the incidence of segmentation defects in the
water+42C group was high, any interaction between BA and hyperthermia might have been obscured...
Harrouk W et al; Teratology 63 (6): 276 (2001)
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14.1.12 Toxicity Summary
Toxicity
Acute oral LD50 is 2660 mg/kg in rat [MSDS]. Individuals are likely to be exposed to boric acid from industrial
manufacturing or processing. Local tissue injury from boric acid exposure is likely due to caustic effects. Systemic effects
from boric acid poisoning usually occur from multiple exposures over a period of days and involve gastrointestinal,
dermal, CNS, and renal manifestations. Gastrointestinal toxicity include persistent nausea, vomiting, diarrhea, epigastric
pain, hematemesis, and blue-green discoloration of the feces and vomit [L2140]. Following the onset of GI symptoms, a
characteristic intense generalized erythroderma follows [L2140]. Management of mild to moderate toxicity should be
supportive. In case of severe toxicity, dialysis may be required in addition to supportive treatment.
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14.1.13 Antidote and Emergency Treatment
The diagnoses of boric acid poisoning can be confirmed with the measurement of blood or serum boric acid levels
(nL=1.4 nmol/mL), but this test is not routinely available. Treatment of boric acid toxicity is mainly supportive. Activated
charcoal is not recommended because of its relatively poor adsorptive capacity for boric acid. In cases of massive oral
overdose or renal failure, hemodialysis, or perhaps exchange transfusion in infants, may be helpful in shortening the half-
life of boric acid.
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In acute poisonings, if a large amount has been ingested and the patient is seen within one hour of exposure,
gastrointestinal decontamination should be considered ... .It is important to keep in mind that vomiting and diarrhea are
common, and severe poisoning may be associated with seizures. Therefore induction of emesis by syrup of ipecac is
probably contraindicated in these exposures. Catharsis is not indicated if diarrhea is present. /Boric acid and Borates/
U.S. Environmental Protection Agency/Office of Prevention, Pesticides, and Toxic Substances. Reigart, J.R., Roberts, J.R. Recognition and
Management of Pesticide Poisonings. 5th ed. 1999. EPA Document No. EPA 735-R-98-003, and available in electronic format at:
http://www.epa.gov/pesticides/safety/healthcare , p. 77
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If ingestion of borate has been massive (several grams), or has extended over several days, administer intravenous
glucose and electrolyte solutions to sustain urinary excretion of borate. Monitor fluid balance and serum electrolytes
(including bicarbonate capacity) regularly. Monitor cardiac status by ECG. Test the urine for proteins and cells to detect
renal injury, and monitor serum concentration of borate. Metabolic acidosis may be treated with sodium bicarbonate. If
shock develops, it may be necessary to infuse plasma or whole blood. Administer oxygen continuously. If oliguria (less
than 25 to 30 mL urine per hour) occurs, intravenous fluids must be slowed or stopped to avoid overloading the
circulation. Such patients should be referred to a center capable of providing intensive care for critically ill patients. /Boric
acid and Borates/
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If renal failure occurs, hemodialysis may be necessary to maintain fluid balance and normal extracellular fluid composition.
Hemodialysis has had limited success in enhancing clearance of borates. Peritoneal dialysis has been performed in borate
poisoning and is felt to be as effective as, and safer than, exchange transfusion in removing borate. No large study has
been done, but it is still used somewhat less frequently than hemodialysis. /Boric acid and Borates/
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Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial
respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR
as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs,
lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent
aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Boron and Related
Compounds/
Currance, P.L. Clements, B., Bronstein, A.C. (Eds).; Emergency Care For Hazardous Materials Exposure. 3Rd edition, Elsevier Mosby, St.
Louis, MO 2005, p. 473
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Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary.
Aggressive airway management may be necessary. Watch for signs of respiratory insufficiency and assist ventilations if
necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if
necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water.
Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth
and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not
drool. Administer activated charcoal ... . Cover skin burns with dry sterile dressing after decontamination ... . /Boron and
Related Compounds/
Louis, MO 2005, p. 473-4
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Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious,
has severe pulmonary edema, or is in severe respiratory distress. Early intubation at the first sign of upper airway
obstruction may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial.
Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV
administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of
hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if
patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to
assist eye irrigation ... . /Boron and Related Compounds/
Louis, MO 2005, p. 474
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Emergency and supportive measures: Maintain an open airway and assist ventilation if necessary. Treat coma, seizures,
hypotension, and renal failure if they occur.
OLSON, K.R. (Ed). Poisoning and Drug Overdose, Sixth Edition. McGraw-Hill, New York, NY 2012, p. 147
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Decontamination: Activated charcoal is not very effective. consider gastric lavage for very large ingestions.
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Enhanced elimination: Hemodialysis is effective and is indicated after massive ingestions and for supportive care of renal
failure. Peritoneal dialysis has not proved effective in enhancing elimination in infants.
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14.1.14 Medical Surveillance
No specific considerations are needed for boric acid or borates except for general health and liver and kidney function.
/Boric acid and borates/
2002., p. 356
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14.1.15 Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ ... Collected boron exposure/dose measures in workplace inhalable dust, dietary
food/fluids, blood, semen, and urine from boron workers and two comparison worker groups (n=192) over three months
and determined correlations between boron and semen parameters (total sperm count, sperm concentration, motility,
morphology, DNA breakage, apoptosis and aneuploidy). Blood boron averaged 499.2 ppb for boron workers, 96.1 and
47.9 ppb for workers from high and low environmental boron areas (p<0.0001). Boron concentrated in seminal fluid. No
significant correlations were found between blood or urine boron and adverse semen parameters. Exposures did not
reach those causing adverse effects published in animal toxicology work but exceeded those previously published for
boron occupational groups.
Abstract: PubMed
Robbins WA et al; Reprod Toxicol. 29 (2): 184-90 (2010)
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/HUMAN EXPOSURE STUDIES/ ... The present study was conducted to investigate the reproductive effects of boron
exposure in workers employed in boric acid production plant in Bandirma, Turkey. In order to characterize the external
and internal boron exposures, boron was determined in biological samples (blood, urine, semen), in workplace air, in
food, and in water sources. Unfavorable effects of boron exposure on the reproductive toxicity indicators (concentration,
motility, morphology of the sperm cells and blood levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH),
and total testosterone) were not observed. The mean calculated daily boron exposure (DBE) of the highly exposed group
was 14.45 +/- 6.57 (3.32-35.62) mg/day. These human exposures represent worst-case exposure conditions to boric
acid/borates in Turkey. These exposure levels are considerably lower than exposures, which have previously led to
reproductive effects in experimental animals. ...
Abstract: PubMed
Duydu Y et al; Arch Toxicol. 85 (6): 589-600 (2011)
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/HUMAN EXPOSURE STUDIES/ /Investigators/ determined the prevalence of respiratory and eye irritation in a group of
113 workers exposed to boric acid and boric oxide at an average concentration of 4.1 mg/cu m (range,1.2 -8.5 mg/cu m).
The exposed employees and 214 control workers who had never been exposed to boric acid or boric oxide and who had
only low or minimal exposure to borax were interviewed regarding eye and respiratory tract irritation, nose bleeds, and
other respiratory symptoms. Reports of eye irritation; dryness of mouth, nose or throat; and sore throat and productive
cough were significantly more common in exposed workers.
American Conference of Governmental Industrial Hygienists. Documentation of Threshold Limit Values for Chemical Substances and
Physical Agents and Biological Exposure Indices for 2001. Cincinnati, OH. 2001., p. 1
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/HUMAN EXPOSURE STUDIES/ Limited data were located regarding reproductive effects in humans after inhalation
exposure to boron. One study reported ... occupational exposure (10 years or greater) to boron aerosols (22-80 mg/cu m)
in males engaged in the production of boric acids. The study group was small, consisting of 28 men. Low sperm counts,
reduced sperm motility and elevated fructose content of seminal fluids were observed.
DHHS/ATSDR; Toxicological Profile for Boron (PB/93/110674/AS) (July 1992). Available from, as of April 25, 2005:
http://www.atsdr.cdc.gov/toxpro2.html
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/HUMAN EXPOSURE STUDIES/ Newborn infants who ingested 4.5-14 g boric acid /have exhibited/ central nervous system
involvement manifested by headache, tremors, restlessness, and convulsions followed by weakness and coma.
Histological examination ... revealed congestion and edema of brain and meninges with perivascular hemorrhage and
intravascular thrombosis at a dose greater than or equal to 505 mg boron/kg/day.
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/SIGNS AND SYMPTOMS/ Boric acid irritates the eyes, skin, and the respiratory tract. High exposure may cause effects on
the gastrointestinal tract, liver and kidneys. ... May affect the nervous system. Serious overexposure can cause seizures,
unconsciousness, and death.
2002., p. 356
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/SIGNS AND SYMPTOMS/ Chronic boron toxicity ... usually is seen in children who have been treated in the past with a
boric acid preparation for diaper rash. Cutaneous findings develop regardless of the route of poisoning. Alopecia has
been reported after chronic exposure in adults. Hypothermia and hyperthermia may occur.
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/SIGNS AND SYMPTOMS/ Application of boric acid powder for diaper rash /produced/ severe erythema of the skin,
gastrointestinal symptoms and deaths in infants.
Goldbloom RB, Goldbloom A; J Pediat 43: 631-43 (1953) as cited in Baselt RC; Biological Monitoring Methods for Industrial Chemicals p.
50 (1980)
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/SIGNS AND SYMPTOMS/ Two retrospective studies on boric acid ingestions suggest that a single acute ingestion of boric
acid is generally quite benign. In these studies, 79-88% of patients remained asymptomatic. Symptoms, when present,
primarily consist of GI irritative symptoms, such as nausea and vomiting. None of the 1184 patients in these two studies
manifested the generalized erythroderma so commonly described in previous reports. CNS manifestations of acute
overdose were infrequent and limited to occasional lethargy and headache. Renal toxicity did not occur following single
acute ingestions. Several reports suggest, however, that significant toxicity from massive acute ingestion of boric acid can
occur.
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/SIGNS AND SYMPTOMS/ Dermatologic effects are more common after chronic or subacute exposures. Skin changes may
develop after boric acid ingestion or application of boric acid powder. Erythema and desquamation occurs in 1 to 2 days.
Exfoliation that is generalized or localized to the hands, feet or face may occur and has been termed the boiled lobster
syndrome. Erythema may be prominent on the buttocks and scrotum.
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/SIGNS AND SYMPTOMS/ /Boric acid poisoning/ usually begins about 8 hr after ingestion. Signs include vomiting,
diarrhea, rapidly progressing prostration, tremors, meningismus, and convulsions. An erythematous eruption of the skin
that may progress to exfoliative dermatitis is characteristic. The eruption tends to be prominent on the palms, soles, and
buttocks. Death may occur in less than a day or after as much as a week. In very severe cases, onset may be within an
hour and death within 4 hr.
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/SIGNS AND SYMPTOMS/ ...From reports on the use of borates to treat epilepsy where doses between 1,000 mg/day of
boric acid to 25 g/day of boric tartrate were administered chronically, toxicity was expressed as dermatitis, alopecia,
anorexia, and indigestion.
NAS, Food and Nutrition Board; Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron,
Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc p.514 (2000). Available from, as of May 19, 2005:
http://www.nap.edu/books/0309072794/html/
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/SIGNS AND SYMPTOMS/ Central nervous system effects include hyperexcitability, irritability, restlessness, opisthotonus,
tremor, convulsions, delirium, coma, weakness, lethargy, headaches, excitement, and CNS depression.
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/SIGNS AND SYMPTOMS/ Classic boric acid poisoning, ... usually involves multiple exposures over a period of days.
Gastrointestinal, dermal, CNS, and renal manifestations predominate. The initial symptoms- nausea, vomiting, diarrhea,
and occasionally crampy abdominal pain- may be confused with an acute gastroenteritis. At times, the emesis and
diarrhea are greenish blue. Following the onset of GI symptoms, the majority of patients develop a characteristic intense
generalized erythroderma. This rash, described as producing a "boiled lobster" appearance, may appear indistinguishable
from toxic epidermal necrolysis or staphylococcal scalded skin syndrome in the neonate. The rash may be especially
noticeable on the palms, soles, and buttocks. Typically, extensive desquamation takes place within 1-2 days. At times,
prominent mucous membrane involvement of the oral cavity and conjunctivae is also apparent. At about the time of the
development of the erythroderma, patient, particularly young infants, may develop prominent signs of CNS irritability,
resembling meningeal irritation. Seizures, delirium, and coma can occur. Renal injury is common, a result of the renal
elimination of this compound and prerenal azotemia from GI losses. Other complications of boric acid poisoning include
hepatic injury, hyperthermia, and cardiovascular collapse. The abandonment of boric acid as an irrigant and particularly its
removal from the nursery setting have led to a marked decrease in the incidence of significant boric acid poisoning.
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/SIGNS AND SYMPTOMS/ Renal effects include renal tubular damage, oliguria, and elevated serum creatinine. Hepatic
effects are rare, but elevated transaminases and jaundice have been reported. Cardiovascular effects include tachycardia
and hypotension. Death results from cardiovascular collapse in severe poisonings.
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/SIGNS AND SYMPTOMS/ Gastrointestinal effects include persistent nausea, vomiting, and diarrhea in children that lead
to acute dehydration and shock. Nausea, vomiting, and diarrhea and epigastric pain, hematemesis, and blue-green
discoloration of the feces and vomit characterize adult boron intoxication.
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/SIGNS AND SYMPTOMS/ Boric acid poisoning begins with nausea, vomiting and diarrhea, regardless of route of
administration. The body temperature falls, and erythematous rash... develops. This is followed by desquamation, not only
in areas of rash but also of mucous membranes. ...Headache, restlessness, and weakness... renal injury... Death results from
circulatory collapse and shock usually within 5 days.
Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975.,
p. 994
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/CASE REPORTS/ ... An 18-month-old child ... died following the accidental ingestion of a boric acid-containing,
commercially available roach pesticide product.
Abstract: PubMed
Hamilton RA, Wolf BC; J Forensic Sci. 52 (3): 706-8 (2007)
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/CASE REPORTS/ ... Because the patient's symptoms were similar to those caused by boric acid and slightly similar to
those caused by sulfite, the concentrations of boric acid and sulfite (as sulfur dioxide) in the patient's vomitus and in
shrimp collected from bait stores and markets were analyzed. The concentration of boric acid was 36.8 to 37.1 mg/g in
the patient's vomitus, 1.4 to 3.8 mg/g in shrimp meats obtained from bait stores, and not detectable (less than 0.001
mg/g) in shrimp meat obtained from commercial markets. No significant differences in sulfur dioxide concentrations
(0.067 to 0.088 mg/g) were found in patient's vomitus and the shrimp meat from both bait stores and commercial
markets. A fragment of the cytochrome b gene (approximately 406 bp) was amplified by PCR using a pair of primers
(UCYTB151F and UCYTB270R) from shrimp meat of two species and the vomitus. The vomited shrimp was identified as
Parapenaeus fissuroides on the basis of gene sequencing and restriction fragment length polymorphism patterns after
treatment with endonuclease Alu I. Based on the patient's symptoms and analytical data, ... boric acid at toxic levels had
been illegally added to the bait shrimp P. fissuroides.
Abstract: PubMed
Huang KM et al; J Food Prot. 73 (12): 2250-5 (2010)
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/CASE REPORTS/ A 45-year-old man dissolved boric acid crystals in water and ingested it in a suicide attempt. He
developed nausea, vomiting and green diarrhea. He presented to the hospital 2 days after ingestion with lethargy,
dehydration, hypotension, renal failure, metabolic acidosis, and generalized erythematous rash. Despite treatment with
intravenous fluids and vasopressors, he developed atrial fibrillation, then pulseless electrical activity, and died 17 hours
after admission. His whole blood boric acid concentration was 420 mg/L 52 hours after ingestion.
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/CASE REPORTS/ Four cases of nonfatal ingestion of boric acid were reported after two subjects (adult females) ingested
298 g of a 99% boric acid containing insecticide and 80 g of boric acid in a fungicide, respectively (presumably 1.0 and
0.28 g B/kg, respectively, for a 50 kg body weight). Ingested doses for the two other subjects were not fully specified. All
four subjects recovered, and the two adults presented no systemic symptoms following release from the hospital.
Linden CH et al; Clin Toxicol 24: 269-79 (1986) as cited in USEPA; Health Advisory for Boron (Draft) p.6 (1988)
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/CASE REPORTS/ Eleven infants accidentally ingested boric acid in their formula; from 2-4.5 g of the compound was
ingested by six of the survivors, who developed serum borate levels of 20-150 mg/L, while the five infants who ingested
larger amounts (4.5-14 g) exhibited levels of 200-1600 mg/L and died within 3 days.
Wong LC et al; Can Med Assoc J 90: 1018-23 (1964) as cited in Baselt RC; Biological Monitoring Methods for Industrial Chemicals p. 50-1
(1980)
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/CASE REPORTS/ An outbreak of an illness in a newborn nursery consisting of vomiting, diarrhea, dehydration, and
exfoliative dermatitis was mistakenly thought to be due to an infectious agent because Staphylococcus aureus was
cultured from the nose, throat, and feces in two patients. The clinical picture was similar to Ritter's disease. However,
because S. aureus was not found in other hospital cultures, boric acid toxicity was subsequently considered. It was
discovered as a contaminant of the infant formula. Three infants died.
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/CASE REPORTS/ A transplacental distribution of boric acid in a human was reported when a 34-wk pregnant female
accidentally swallowed 70 g of boric acid (approximately 245 mg B/kg, 50 kg body weight). A fetus delivered 2 hours later
by cesarean section died shortly afterward from cardiovascular failure.
Grella PB et al; Acta Anaesthesiol 27: 745-8 (1976) as cited in USEPA; Health Advisory for Boron (Draft) p.5 (1988)
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/CASE REPORTS/ A mixture containing 3 g of boric acid and 300 mg of cinchocaine chloride prescribed due to painful
dental protrusion was accidentally ingested by a 12 month old girl. She developed violent vomiting and coughing.
Irritability, tremor, seizures and a delirious reaction. She was treated with diazepam, intubated, sedated and ventilated.
Her diuresis was stimulated with furosemide and fluid. Within the first 24 hr she was treated with hemodialysis twice on
femoral catheters. Her renal function was unaffected. In two days she fully recovered. The maximum measured levels of
boric acid and cinchocaine chloride approximately 6 hr after ingestion were 26 ug/mL and 71 ng/mL respectively. ... The
total body clearance of boric acid increased correspondingly from 21 mL/min to 41 and 34 mL/min during the two
hemodialyses.
Abstract: PubMed
Egfjord M et al; Hum Toxicol 7 (2): 175-8 (1988)
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/CASE REPORTS/ A 77-year-old man ingested 30 g of boric acid powder with water for hiccups. He developed vomiting,
diarrhea, and generalized erythema, renal failure, and hypotension within 24 hours. His serum boric acid level was 37.7
mg/L 30 hours post-ingestion. He developed refractory hypotension despite hemodialysis, charcoal hemoperfusion, fluid
resuscitation and vasopressor, and died 63 hours post-ingestion.
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/CASE REPORTS/ Long-term chronic exposure to boric acid results in alopecia in adults and seizures in children. A 32 yr
old woman who chronically ingested mouthwash containing boric acid over a 7 month period developed progressive hair
loss.
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/CASE REPORTS/ A case where 28 g (70 mg C/kg) of boric acid was mistakenly administered by subcutaneous infusion to
an adult patient in postoperative recovery exhibited severe cutaneous manifestations but recovered with only the
maintenance of fluid balance and promotion of diuresis.
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/CASE REPORTS/ When through error a 42-year-old patient received an iv infusion of about 15,000 mg of boric acid as a
2.5% solution with 10% dextrose, she showed slight flushing, slight nausea, one episode of vomiting, and no further
trouble. A total of 14,650 mg of boric acid was recovered from the urine.
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/CASE REPORTS/ An 82-year-old woman with senile dementia ate a homemade boric acid ball by mistake that was used
to eliminate cockroaches. She was treated in a hospital, but died 8 days after the ingestion. One of the remaining balls
weighed 24 g and contained 12 g of boric acid. The concentrations of boric acid in serum and urine samples which were
collected 3 days after the ingestion were 400 and 4,416 mug/mL, respectively. In addition, those in blood and gastric
content collected at autopsy were 20 and 48 mug/mL, respectively.
Miyazaki T et al; Res Pract Forensic Med 35 (0): 173-176 (1992)
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/CASE REPORTS/ ... A 26-year-old female who attempted suicide by consuming a large quantity of boric acid. She was
brought to the hospital in a state of clouded consciousness, fever and erythema 14 h after ingestion. 3.25 L of intravenous
fluid and 100 mg of furosemide were administered over a period of 4 h in the intensive care unit and the serum and
urinary concentrations of boric acid measured. The elimination rate of boric acid obtained with diuresis was similar to that
obtained with hemodialysis on a previous occasion when the same patient attempted suicide with boric acid. The patient
showed only temporary emesis and diarrhea along with erythema, and was moved to the general ward 4 h after
admission. Although in the general ward the patient's fever persisted and nausea, vomiting and headache often recurred,
possibly because of an insufficient dose of furosemide, the patient's condition steadily improved over the 64 h after
admission. ...
Abstract: PubMed
Teshima D et al; J Clin Pharm Ther 26 (5): 387-390 (2001)
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/EPIDEMIOLOGY STUDIES/ An ecological study assessed boron exposure from drinking-water and fertility among
residents in two geographical regions in Turkey. Region I comprised 2368 residents, whereas Region II comprised 2319
residents. Boron levels in drinking-water were noticeably higher in Region I (range 2.05-29 mgL) than in Region II (range
0.03-0.40 mg/L). Ever-married residents from each region who could provide reproductive histories for three generations
of family members represented the study sample-- i.e. 159 probands (6.7% of population) in Region I and 154 (6.7%) in
Region II. The percentages of married couples with one or more live births (>90%) were comparable for the two regions,
regardless of generation assessed. The overall percentage of couples with unresolved infertility or those without children
across three generations was comparable for the two regions (i.e. 6.0% and 4.6%, respectively). Secondary sex ratios (ratio
of male to female live births) appeared to be different for the two regions. Region I had a ratio below 1 (0.89), suggesting
an excess of female births; Region II had a ratio slightly above 1 (1.04), suggesting a slight excess of male births. Statistical
significance was not formally evaluated in any of the above analyses. The results of this descriptive study suggest that
fertility, as measured by the ability to produce a live birth, is not adversely affected for residents of this geographical area
with high levels of boron in their drinking-water and soil. The observed reversal of the secondary sex ratio for Region I
requires careful interpretation, as no attention was given to factors reported to alter sex ratios (e.g. advancing parental
age, elective abortion rates, and multiple births).
WHO; Environmental Health Criteria Document 204: Boron p.100 (1998). Available from, as of May 12, 2005:
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/EPIDEMIOLOGY STUDIES/ There have been some epidemiology studies in Turkey comparing family birth rates in boron
rich areas with those in lower-boron areas. Some village drinking waters are reported with boron levels as high as 29 ppm
B. No evidence of reproductive toxicity was found in this population.
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/SURVEILLANCE/ The medical literature reporting 109 cases of acute toxicity caused by boric acid was reviewed in 1953... .
In this series 35% were children less than 1 year of age; their mortality rate was 70%. The mortality rate of the entire series
was 55%. Of the 80 cases for which information is available, 73% had GI disturbances, 67% had CNS effects, and 76% had
cutaneous lesions.
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/SURVEILLANCE/ ... /From/ 782 cases of boric acid ingestion reported by the National Capital Poison Center and Maryland
Poison Center between 1981 and 1985. All except two cases were acute ingestions; 88.3% were asymptomatic. Among the
remaining 11.7%, frequent symptoms included vomiting, abdominal pain, and diarrhea; less frequent findings included
lethargy, headache, lightheadedness, and rash. Among the children less than 6 years of age, 21 ingested more than the
estimated lethal dose of 15 g, all without severe manifestations of toxicity or life-threatening symptoms. In this series only
minimal toxicity was seen at serum levels of less than or equal to 640 mg/mL.
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/SURVEILLANCE/ ... The correlation of prostate cancer incidence and mortality with groundwater boron and selenium
concentrations; and the impact of boron on prostate cancer cell proliferation during co-treatment with alternative chemo-
preventative agents, along with boron pre-treatment effects on cell sensitivity to ionizing radiation /was determined/. For
regression analysis, data on prostate cancer incidence and mortality were obtained from the Texas Cancer Registry, while
groundwater boron and selenium concentrations were derived from the Texas Water Development Board. Cultured DU-
145 prostate cancer cells were used to assess the impact of boric acid on cell proliferation when applied in combination
with selenomethionine and genistein, or preceding radiation exposure. Groundwater boron levels correlated with a
decrease in prostate cancer incidence (R = 0.6) and mortality (R = 0.6) in state planning regions, whereas selenium did not
(R = 0.1; R = 0.2). Growth inhibition was greater during combined treatments of boric acid and selenomethionine, or boric
acid and genistein, versus singular treatments. 8-day boric acid pre-exposure enhanced the toxicity of ionizing radiation
treatment, while dose-dependently decreasing the expression of anti-apoptotic protein Bcl-2. Increased groundwater
boron concentrations, across the state of Texas, correlate with reduced risk of prostate cancer incidence and mortality.
Also, boric acid improves the anti-proliferative effectiveness of chemo-preventative agents, selenomethionine and
genistein, while enhancing ionizing radiation cell kill.
Abstract: PubMed
Barranco WT et al; Cancer Causes Control. 18 (1): 71-7 (2007)
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/BIOMONITORING/ Urinary excretion levels can also be useful indicators of elevated total body burden of boron.
Concentrations of boron in the normal population range from ... 0.004 to 0.66 mg/100 mL. In one infant, the urine
contained 13.9 mg boron/L as borax or 1.38 mg boron/mL of boric acid following ingestion of a borax and honey mixture
over a period of 12 weeks.
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/BIOMONITORING/ Normal dietary concentrations of boron in the blood of humans range from 0 to 1.25 pg/mL in
children and infants. Boron blood levels (reported as borate) of 20-150 ug/mL have been associated with adverse systemic
effects in infants who ingested boric acid in infant formula. Boron concentrations, expressed as borate, reported in fatal
cases vary from 200 to 1,600 ug/mL in infants. In adults, a serum boron level (as boric acid) of 2,320 ug/mL was not
associated with significant toxicity.
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/ALTERNATIVE and IN VITRO TESTS/ ... Proliferation assay of MCF-7 human breast cancer cells ... was conducted in this
study. ... Boric acid could not ... stimulate the proliferation of MCF-7 human breast cancer cells. ...
Abstract: PubMed
Wang Y et al; Biol Trace Elem Res. 121 (2): 160-70 (2008)
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/OTHER TOXICITY INFORMATION/ Life-threatening toxicity resulted from the repetitive topical application of boric acid
for the treatment of diaper rash or the use of infant formulas unintentionally contaminated with boric acid. Fatality rates
greater than 50% were reported in some series.
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/OTHER TOXICITY INFORMATION/ Individuals who have accidentally consumed boric acid or one of its derivatives excrete
high levels of riboflavin within the first 24 to 48 hours following ingestion. The administration of certain agents, either
therapeutic or toxic, which enhance urinary riboflavin excretion may be of particular concern for high-risk patients who
are already nutritionally compromised because of illness or disease.
Abstract: PubMed
Pinto JT, Rivlin S; Drug Nutr Interact 5 (3): 143-51 (1987)
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/OTHER TOXICITY INFORMATION/ An outbreak of an illness in a newborn nursery consisting of vomiting, diarrhea,
dehydration, and exfoliative dermatitis was mistakenly thought to be due to an infectious agent because Staphylococcus
aureus was cultured from the nose, throat, and feces in two patients. The clinical picture was similar to Ritter's disease.
However, because S. aureus was not found in other hospital cultures, boric acid toxicity was subsequently considered. It
was discovered as a contaminant of the infant formula. Three infants died.
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/OTHER TOXICITY INFORMATION/ Borax and boric acid used in powders and ointments have resulted in serious
poisonings and death.
135
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/OTHER TOXICITY INFORMATION/ The fatal dose /in humans/ is thought to be 2000-3000 mg for infants, 5000-6000 mg
for children, and 15,000-20,000 mg for adults.
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14.1.16 Non-Human Toxicity Excerpts
/LABORATORY ANIMALS: Acute Exposure/ /In an acute inhalation toxicity study, rats were exposed to about 2.03 mg/L
boric acid for 4 hr./... No deaths occured. Animal observations were limited due to the accumulation of test material on
the walls of the exposure chamber. During the first 30 minutes of exposure, ocular discharge, hypoactivity and hunched
posture were noted. Ocular discharge and or nasal discharge persisted in most animals after removal from the chamber.
Animals recovered by day seven.
European Chemicals Bureau; IUCLID Dataset, Boric acid (10043-35-3) (2000 CD-ROM edition). Available from, as of May 18, 2005:
http://esis.jrc.ec.europa.eu/
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/LABORATORY ANIMALS: Acute Exposure/ Symptoms /in rats and mice during studies to determine the LD50/ include
signs of CNS depression, ataxia and convulsions.
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/LABORATORY ANIMALS: Acute Exposure/ 100 mg boric acid was applied to one eye of each of six rabbits. The eyes were
rinsed after 24 hours. Changes /were noted/ in coloration and texture of the eye and blistered appearance to conjunctiva.
Classified in US Category III (40 CFR 156) "Corneal involvement or irritation clearing in 7 days or less."
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/LABORATORY ANIMALS: Acute Exposure/ The prelethal symptoms in /rats and mice exposed sc during LD50 studies/...
were depression and ataxia (occasionally convulsions), fall in body temperature, violet-red color of the skin and mucous
membrane.
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/LABORATORY ANIMALS: Acute Exposure/ Six guinea pigs with clipped depilated intact abdomens and six with clipped
depilated abraded backs were treated with 5 mL 10% w/w boric acid in water on a cellulose pad. Boric acid was reported
as a moderate irritant at both 24 and 72 hr with the abraded skin being less sensitive than intact skin. The exposure
period is uncertain, but probably 72 hours.
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/LABORATORY ANIMALS: Acute Exposure/ Boric acid applied as 10% w/w in water, 5 mL on cellulose pads to six rabbits
with intact skin and six rabbits with abraded skin. Boric acid reported as mild irritant after 24 and 72 hr with abraded skin
being more sensitive than intact skin.
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/LABORATORY ANIMALS: Acute Exposure/ Boric acid ... produced mild eye irritation in the Draize test in rabbits.
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ ... Exposure /of rats to boric acid (BA)/ for 28 days did not
induce significant changes in tissue flavins. Significant decreases in serum inorganic phosphorus and creatinine were
observed. Leydig cells from rats exposed to BA and challenged with human chorionic gonadotropin (hCG) in-vitro did not
demonstrate increased basal or hCG stimulated testosterone production. A significant decrease in follicle stimulating
hormone induced intracellular cyclic-adenosine-monophosphate (cAMP) accumulation was seen in Sertoli cell enriched
cultures exposed to 10 mM BA in-vitro. Plasminogen activator activity in cultured seminiferous tubule segments was
unaffected by BA but BA treatment did induce significant decreases in media lactate and pyruvate concentrations and
cellular cAMP levels in Sertoli cell cocultures. BA also decreased the synthetic activity of DNA in cocultures without
affecting RNA activity and decreased the leptotene spermatocyte/Sertoli cell ratio in stage IX tubules in rats treated with
9,000ppm BA for 3 weeks in-vivo. The authors conclude that these data suggest that the mechanisms underlying the BA
induced inhibition of sperm release may be an effect on the DNA synthetic activity of mitotic and meiotic germ cells as
well as on energy metabolism in Sertoli cells and germ cells.
Ku W Chapin R; Environmental Health Perspectives 102 (7): 99-105 (1994)
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ A total of 96 male albino Sprague-Dawley rats were used in
this study. Seventy-two rats were selected for the experimental group and 24 rats constituted the control group.
Experimental group rats were divided into three groups for exposure to three different doses of orally administered boric
acid (100, 275, 400 mg/kg/day). Kidney tissues were removed at the 10th, 30th, and 45th day after sacrificing the rats.
Kidney weights, kidney boron concentration and histopathological changes were determined. In the experimental group,
a significant accumulation of boron in kidney tissue was seen, but there was a significant drop in boron concentration on
the 45th day compared with the 30th day. Histopathological degenerative changes were observed especially in the
proximal tubule cells, that were dose and time dependent.
Abstract: PubMed
Sabuncuoglu BT et al; Clin Toxicol (Phila). 44 (3): 249-53 (2006)
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Boric acid ... was fed to Beagle dogs for 90 days. In the 90-
day boric acid study (weight-normalized doses of 0, 0.44, 4.4, or 44 mg of boron per kg of body weight per day; five
animals per sex per dose), testis weight was significantly lower than controls in the middle and upper dose groups
(reduced by 25% and 40%, respectively). Although testicular microscopic structure was not detectably abnormal in the
controls and middle dose group, four of five dogs in the high-dose group had complete atrophy, and the remaining high-
dose dog had one-third of tubules showing some abnormality.
WHO; Boron in Drinking-water: Background document for development of WHO Guidelines for Drinking-water Quality
(WHO/SDE/WSH/03.04/54). Available from, as of May 9, 2005: http://www.who.int/water_sanitation_health/dwq/boron.pdf
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Growth of rats was inhibited when their drinking water
contained boric acid a concentration of 2500 ppm, resulting in a dosage of about 325 mg/kg/day; growth was unaffected
at a concentration of 1000 ppm (about 130 mg/kg/day).
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In a 13 week study, mice were exposed to boric acid in the
diet at concentrations sufficient to produce doses of approximately 0, 200, 400, 800, 1600, or 3200 mg/kg per day.
Increased mortality was noted at the two highest doses. At 800 mg/kg of boric acid per day, testicular effects
(degeneration and atrophy of the seminiferous tubules) were observed. At all doses, extramedullary hematopoiesis of the
spleen of minimal to mild degree was seen.
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In a 90-day study in rats (10 per sex per dose) receiving 0,
2.6, 8.8, 26, 88, or 260 mg of boron per kg of body weight per day in the diet as boric acid ... , all animals at the highest
dose died within 3-6 weeks. In animals receiving 88 mg of boron per kg of body weight per day, body weights in males
and females were reduced; absolute organ weights, including the liver, spleen, kidneys, brain, adrenals, and ovaries, were
also significantly decreased in this group. Organ-to-body-weight ratios for the adrenals and kidneys were significantly
increased, but relative weights of the liver and ovaries were decreased. A pronounced reduction in testicular weights in
males in the 88 mg of boron per kg of body weight per day group was also observed.
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/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Survival was also reduced in mice following intermediate-
duration /(15-364 days)/ exposure. Males (10%) died after exposure to a dose of 288 mg boron/kg/day (as boric acid) in
the diet, while 80% of males and 60% of females died at 577 mg boron/kg/day. Hyperkeratosis and/or acanthosis in the
stomach and extramedullary hematopoiesis of the spleen in both sexes were observed at the highest dose tested (577 mg
boron/kg/day).
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a 2 year, study, rats were administered doses of boric
acid or borax in the diet at doses equivalent to approximately 0, 33, 100, or 333 mg/kg of boric acid per day. Animals
receiving the high dose exhibited coarse hair, scaly tails, hunched posture, swollen and desquamated pads of the paws,
abnormally long toenails, shrunken scrotum, inflamed eyelids, and bloody eye discharge. Hematocrit and hemoglobin
levels were significantly lower than in controls. Testicular weight (absolute and relative) was significantly reduced at the
high dose, and the relative weights of the brain and thyroid gland were significantly increased compared to controls. No
significant effects were observed at the lower dose levels.
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a 2 yr study in mice, boric acid in the diet provided
doses of 0, 275, and 550 mg/kg of boric acid per day. The high dose was associated with a significant decrease in body
weight in both males and females. In males, increased mortality and testicular histopathologic effects were observed at
the high dose.
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In animals chronic poisoning has shown itself only in
inhibition of growth when boric acid was given /at a concentration/ of 0.25% in drinking water. There were no ... lesions at
autopsy and no changes in peripheral blood.
Browning, E. Toxicity of Industrial Metals. 2nd ed. New York: Appleton-Century-Crofts, 1969., p. 92
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In rats, high boron levels at 1750 and 5250 ppm of borax
and boric acid administered orally caused growth suppression, decreased food utilization efficiency, degeneration of
gonads, and skin desquamation on the paws and tails. Both compounds could be tolerated by rats and dogs at 350 ppm
for 2 yr. Rats fed either borax or boric acid at 1170 ppm were sterile, and testicular degeneration was observed in both
rats and dogs fed this dosage. Both compounds at 350 ppm had no adverse effect on fertility, lactation, litter size, weight,
and appearance.
Abstract: PubMed
Weir RJ, Fisher RS; Toxicol Appl Pharmacol 23 (3): 351-64 (1972)
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ In a life-time bioassay in which male and female B6C3Fl
mice consumed 48 mg boron/kg/day or 96 mg boron/kg/day as boric acid in the diet, there was no evidence of
carcinogenicity.
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/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ A 2 yr chronic feeding/oncogenicity study using boric acid
was conducted with B6C3F1 mice. The compound was administered in the diet at levels of 0, 2500 or 5000 ppm
(approximately 0, 450, or 1150 mg/kg/day). No clinical signs of toxicity were observed during the course of the study.
Testicular pathology was present at the highest dose tested and consisted of testicular atrophy and interstitial cell
hyperplasia. Other pathological findings included a dose related increase (at both levels) in the incidence of splenic
lymphoid depletion in male mice that was believed to be associated with stress and a dose related increase in the
incidence of pulmonary hemorrhage that was of unknown biological significance. The compound was not found to be
carcinogenic at the levels tested. A NOEL for systemic toxicity was not determined; the LOEL for systemic toxicity was 2500
ppm (approximately 450 mg/kg/day based on the pathological findings.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... Six-week-old female Sprague-Dawley rats were fed
diets containing 2.0 (/recommended daily intake/ for pregnant rats), 1.0 (marginal) or 0.176 (low) mg folate/kg diet for
five weeks, then bred with chow-fed males. Sperm-positive females were fed their respective diets through pregnancy,
during which groups were exposed to at least two dosages and a vehicle control of Tomudex (a folate analog),
dichloroacetic acid (DCA, drinking water contaminant), ethylenethiourea (ETU, fungicide breakdown product), 5-
fluorouracil (5-FU, chemotherapeutic), or boric acid (BA, insecticide). Dosing regimens were based on previous studies and
varied, but the highest dosages were teratogenic. Dams were killed on gestation day 21 for teratologic evaluations. ... ETU
and BA were teratogenic at the dosages tested, but the incidence of terata was not affected by maternal folate intake.
However, the observed increase in prenatal mortality with decreasing maternal dietary folate may have masked effects on
the incidence of terata. ...
Abstract: PubMed
Rogers JM et al; Birth Defects Res A Clin Mol Teratol 73 (5): 314 (2005)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ ... Dams were treated on gestational day 10 with boric
acid (BA) (0, 250, or 500 mg/kg) and hyperthermia (37, 41, or 42 degrees C) and allowed to deliver their pups. ... Litters
were evaluated on postnatal days (PND) 1 and 3 for number, gender, and weight of pups. On PND3, pups were examined
externally and viscerally, and double-stained for skeletal evaluation. A dose-dependent, statistically significant increase in
fetal skeletal defects was seen on PND 3 with BA or hyperthermia alone with even greater effects when given in
combination. Defects included rib and vertebral fusions, split vertebral centra in the thoracic and lumbar areas, and a
decrease in the total number of ribs and vertebrae. The increased incidence of skeletal defects resulting from combined
exposure to hyperthermia and BA was additive for segmentation defects and synergistic for the reduction in numbers of
vertebrae.
Abstract: PubMed
Harrouk WA et al; Birth Defects Res B Dev Reprod Toxicol. 74 (3): 268-76 (2005)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Crl:CD-1 (ICR) VAF/PlusT outbred albino Swiss mice
were dosed with boric acid in diet at 0, 0.1, 0.2, or 0.4% on days 0-17 /post coital/. No maternal NOEL was identified, due
to dose-related increases in "renal tubule dilatation/regeneration". No developmental NOEL was found, since "pale
spleen" was increased, dose-related, in all groups. For both maternal and developmental toxicity, 0.1% in diet appeared to
be near to a no-effect level. The study is considered to indicate a "possible adverse effect", since there were increased
resorptions at 0.4% and above, and fetal body weight decrements, and some skeletal malformations at 0.2% and above.
California Environmental Protection Agency/Department of Pesticide Regulation; Toxicology Data Review Summaries. Available as of
May 6, 2005. http://www.cdpr.ca.gov/docs/risk/toxsums/toxsumlist.htm
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The developmental toxicity of boric acid was evaluated
in rats fed estimated daily doses of 0, 78, 165, and 330 mg/kg, of boric acid in the diet on gestation days 0-20. To limit
prenatal mortality, an additional group of rats was fed boric acid at an estimated daily dose of 536 mg/kg of boric acid on
gestation days 6-15 only. Maternal toxicity was observed at 165, 330, and 536 mg/kg of boric acid per day as
demonstrated by increased relative liver and kidney weights... . The NOAEL for maternal toxicity was 78 mg/kg/day.
Prenatal mortality was increased among rats at 330 and 536 mg/kg of boric acid per day. Average fetal body weight was
reduced at all dose levels, ranging from a 6% decrease at the lowest dose to about 50% decrease at the highest dose. The
incidence of fetal malformations was increased at doses of greater than or equal to 165 mg/kg/day; the most frequently
observed malformations were enlarged ventricles of the brain and agenesis or shortening of the 13th rib. An increase in
enlarged ventricles of the brain was observed among fetal rats of dams administered 330 and 536 mg/kg of boric acid per
day. Skeletal variations were noted to occur with a lower incidence than controls at 78 and 165 mg/kg of boric acid per
day, primarily to a reduction in the incidence of full or rudimentary first lumbar malformations. In contrast, the incidence
of variations was increased above control levels at 330 mg/kg per day primarily because of an increase of another skeletal
variation: wavy rib(s). The lowest dose tested, 78 mg/kg of boric acid per day, was considered... to be the LOAEL rather
than the NOAEL for developmental toxicity in rats because of the 6% decrease in fetal body weight.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ To assess whether or not male reproductive toxicity
can be evaluated in a 2-week administration study, boric acid was administered daily by oral gavage to male Jcl:Wistar
rats at dosage levels of 0, 300 and 500 mg/kg for 2 and 4 weeks, and the results obtained with the two different treatment
schedules were compared. After a 2-week administration, decreased testis weights were observed in the 500 mg/kg
group. Histopathologically, exfoliation of round spermatids, retention of step 19 spermatids and increased numbers of
residual body-like structures in the seminiferous tubules and cell debris in the cranial epididymal ducts were observed in
the 300 and 500 mg/kg groups. Distorted cytoplasmic lobes of step 19 spermatids, debris in the seminiferous tubules and
focal atrophy of the seminiferous tubules with multinucleated giant cells formation and necrosis of spermatocytes were
also observed in the 500 mg/kg group. After a 4-week administration, testis and epididymis weights were decreased in
the 300 and 500 mg/kg groups. Histopathological changes in the 300 mg/kg group were similar to those found in the 300
and 500 mg/kg groups after a 2-week administration. Diffuse atrophy of the seminiferous tubules was additionally
observed in the 500 mg/kg group.
Abstract: PubMed
Fukuda R et al; J Toxicol Sci 25: 233-239
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Male rats exposed to lower doses of boric acid for
shorter time periods exhibit reversible inhibition of spermiation (sperm release in the tubules). These early effects have
been observed in rats at a daily dose of 217 mg/kg of boric acid for 14 days. At a lower dose of 149 mg/kg of boric acid
per day, similar reversible effects on spermiation were noted after 28 days of exposure. Higher doses of boric acid in rats
have been associated with testicular atrophy, reduced spermatogenesis, and infertility. A single oral dose of 500 mg/kg of
boric acid per day was reported to affect spermiation in rats. Inhibition of spermiation was the earliest reproductive effect
produced by boric acid, appearing by day 7 in rats receiving the substance in the diet at a dose level of approximately 350
mg/kg of boric acid per day.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Sprague-Dawley rats were exposed to boric acid in the
diet on gestation days 1-20. In phase I (teratology evaluation), approximately 30 dams/group were terminated, and
examinations were performed on gestation day 20. In phase II (postnatal evaluation), additional dams (approximately
30/group) were allowed to deliver and rear their litters until postnatal day 21. No evidence of developmental toxicity was
observed in this study (phase I and II) in the offspring of rats fed diets delivering a dose of 55 mg/kg/day of boric acid or
less from gestation days 0-20. At approximately 75 mg/kg of boric acid/day, reduced fetal body weight and
morphological changes in the fetal skeleton (specifically an increased incidence of short rib XIII and wavy rib) were
observed on gestation day 20 (phase I). None of these effects were observed at a comparable dose in the postnatal
period (phase II) of the study; pup body weight recovered by postnatal day 0. At the highest daily dose (approximately
145 mg/kg of boric acid), the same effects observed at 75 mg/kg/day were more pronounced (phase I); in addition, a
slight (but not statistically significant) decrease in the incidence of extra rib on lumbar 1 was observed. None of these
effects was discerned postnatally at the highest daily dose (approximately 145 mg/kg of boric acid) with the exception of
an increase in short rib XIII. There was little evidence of maternal toxicity at any of the doses tested. Thus, the NOAELs for
developmental toxicity in the prenatal and postnatal phases of this study (phases I and II) were 55 and 75 mg of boric acid
per day, respectively.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Mice were given 0, 245, 450, or 1000 mg/kg of boric
acid per day on gestation days 0-20 in the diet. Maternal toxicity was observed at all dose levels. Signs of development
toxicity included decreased fetal body weight at the middle and increased resorptions, malformations, and skeletal
variations as well as decreased fetal weight, at the high dose. The NOAEL for developmental mice was 245 mg/kg of boric
acid per day.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In rabbits administered daily doses 0, 63, 125, or 250
mg/kg of boric acid by gavage on gestation days 6-19, developmental effects were seen at the highest dose only,
including an increase incidence of resorptions and malformations. No evidence of developmental toxicity was observed at
lower doses. The NOAEL for maternal and developmental toxicity was 125 mg/kg of boric acid per day.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Sperm morphological examination, computer-assisted
sperm analysis (CASA) and histopathologic examination of the testis and epididymis were performed for male rats treated
orally with boric acid for 3 weeks at dosage levels of 50, 150 and 500 mg/kg/day, and treated males were mated with
untreated females. None of the males treated with 500 mg/kg/day could impregnate untreated females. The fertility index
showed a tendency to decrease in males treated with 150 mg/kg/day. At necropsy, the pre-implantation loss rate in
females mated with males treated with 150 mg/kg/day was higher than the control values. Upon epididymal sperm
analysis using the CASA system, all parameters including the number of sperm and sperm motions were found to be
affected in males treated with 500 mg/kg/day, and the number of sperm, percent motile, velocities and amplitude of
lateral head displacement (ALH) were affected in males treated with 150 mg/kg/day. Upon sperm morphological
examination, head and tail abnormalities were observed in males treated with 150 and 500 mg/kg/day. In the
histopathological examination, atrophy of the seminiferous tubules and multinucleated giant cells in the testes were
observed in males treated with 500 mg/kg/day.
Abstract: PubMed
Yoshizaki H et al; Journal of Toxicological Sciences 24 (3): 199-208 (1999)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Rats were fed boric acid in their feed at 3000, 4500,
6000, and 9000 ppm for up to 9 weeks. Rats were sacrificed weekly and examined for multiple end points including serum
and tissue boron levels, testis histology, weight and sperm count. Inhibited spermiation was separated from atrophy
based on dose, with inhibited spermiation observed at 3000- to 4500-ppm levels and atrophy at 6000 to 9000 ppm.
Inhibited spermiation was reversible and atrophy was not.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a continuous breeding study of boric acid in mice,
testicular effects (testicular atrophy, decreased sperm count, reduced motility, and abnormal sperm morphology) were
observed in a dose-related manner. Fertility was partially and completely impaired in mice at doses of approximately 630
and 1260 mg/kg of boric acid per day, respectively. The NOAEL was considered to be 154 mg/kg of boric acid per day;
this dose had no effect on fertility, but appeared to cause a slight decrease in motility of epididymal sperm.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ /In/ a mouse study utilizing the continuous breeding
protocol..., doses of 0, 1000, 4500, and 9000 ppm boric acid in the feed were utilized. No litters were obtained at 9000
ppm. All measured parameters, including fertility and litter size, were reduced at 4500 ppm. There were no differences
from the controls noted for the 1000 ppm group during the 14 week continuous breeding period. The final litters from
the 1000 ppm and control groups were allowed to mature and breed an F2 litter. A decrease in the adjusted body weight
of the F2 was reported. In addition, a crossover mating trial was carried out which established the male as the affected
sex.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ In a 2 generation reproduction study conducted in

mice, boric acid was administered throughout the study in the diet at levels of 0, 1000, 4500, or 9000 ppm (0, 150, 675, or
1350 mg/kg). The NOEL for parental and reproductive toxicity was 1000 ppm (150 mg/kg). The parental LOEL was 4500
ppm based on decreases in organ weights in both sexes. The reproductive LOEL was also 4500 ppm based on decreased
fertility and decreased pup weight. At this dose, the average number of days between litters increased after the second
litter and the number of dams producing litters decreased significantly. At the highest dose tested, no litters were
produced and the males in this group had a decrease in sperm concentration and motility when compared to controls.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Two rat studies were conducted to elucidate the ...
observation of enlarged lateral ventricles of the brain at the two highest doses, 330 and 539 mg boric acid/kg/day. The
first study was carried out at 0.8. 1.6, and 2.4% boric acid in the diet during gestation days 14-17 and showed that this
was not a sensitive period for boric acid-induced ventricular enlargement. The second study incorporated boric acid in the
feed at 0.4, 0.5, 0.6, and 0.8% during gestation days 6-15... . After adjusting for body weight effects, there was no
significant dose-related enlarged lateral ventricles, either incidence or severity. Hydrocephaly was reported to be
significant in the 0.8% group (2% in controls and 15% in the highest dose).
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Developmental toxicity and teratogenicity of boric acid
in rabbits were investigated at doses of 0, 11, 22, or 44 mg of boron/kg bw/day, given by gavage. Frank developmental
effects in rabbits exposed to 44 mg of boron/kg bw/day included a high rate of prenatal mortality, an increased number
of pregnant females with no live fetuses, and fewer live fetuses per live litter on day 30. At the high dose, malformed live
fetuses per litter increased significantly, primarily because of the incidence of fetuses with cardiovascular defects, the most
prevalent of which was interventricular septal defect. Skeletal variations observed were extra rib on lumbar 1 and
misaligned sternebra. The NOAEL for maternal and developmental effects was 22 mg of boron/kg bw/day.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Crl:CD BR VAF/Plus Sprague-Dawley rats were dosed
with boric acid in diet at 0, 62.5, 125, or 250 mg/kg/day throughout the 20-day gestation period (29 dams/group). Groups
of 14 dams were fed 0 or 250 mg/kg boric acid in diets on days 6-15 in a parallel study. Maternal NOEL = 62.5 (slight
increases in kidney weight). The developmental NOEL = was not established (dose related, statistically significant
decreases in mean fetal weight were noted in all groups: also, "shortened rib XIII" and wavy ribs were dose-related at all
dose levels). A "possible adverse effect" was indicated by a variety of effects, generally at higher doses, in the absence of
marked maternal toxicity. These developmental effects included sharply increased resorptions (250 mg/kg group), late
fetal deaths (250 mg/kg group), fetal weights reduced by about 1/3 to 1/2 (125 and 250 mg/kg groups, respectively),
gross malformations: short, curly tail (250 mg/kg group), anophthalmia or microphthalmia (250 mg/kg group); soft tissue
malformations: enlarged lateral ventricles (125 and 250 mg/kg groups), displaced eyes (250 mg/kg group), various defects
of heart and great vessels (250 mg/kg group); skeletal malformations: agenesis of rib XIII (125 and 250 mg/kg groups,
related to "shortened rib XIII" noted above), fused ribs (250 mg/kg group), cleft sternum (62.5, 125 and 250 mg/kg
groups). A number of variations, many of which were ossification delays, were common in the 125 and 250 mg/kg groups.
Maternal NOEL = 125 mg/kg/day (modest reduction in body weight corresponding to modest reduction in food intake).
250 mg/kg/day dose characteristically had vaginal bleeding over about a 10-day period after cessation of dosing. Three
250 mg/kg/day does aborted (vs. none in other groups): a possible treatment effect. Developmental NOEL = 62.5
mg/kg/day (agenesis of gall bladder at 125 and 250 mg/kg/day). Main findings at 250 mg/kg/day were resorptions (90%
of implants), with cardiovascular malformations in remaining conceptuses (enlarged aorta, interventricular septal defects,
pulmonary artery and aorta both arising from right ventricle).
California Environmental Protection Agency/Department of Pesticide Regulation; Toxicology Data Review Summaries. Available from:
http://www.cdpr.ca.gov/docs/toxsums/toxsumlist.htm on Boric acid and related inorganic Borates as of May 6, 2005.
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The majority of toxicological studies have been
reported on boric acid (H3BO3) or disodium tetraborate, known as borax (Na2B4O7.10H2O). The inorganic borates
display low acute toxicity orally, dermally or by inhalation. They are either not irritant or mild skin and eye irritants. They
are not skin sensitisers, nor are they mutagenic or carcinogenic. In sub acute and chronic studies of boric acid in rats, mice
and dogs, the target organ is the testis. Effects on reproductive organs in females were seen, but at higher doses than in
males. Effects on fertility were also seen in rats in a three-generation study and in mice in a continuous breeding study.
The testicular effects observed include reduction in sperm count, inhibition of spermiation and testicular atrophy. Reversal
of inhibition of spermiation and reduced sperm count in rats was seen after removal of treatment at 38 mgB/kg bw/day
(equivalent to 217 mg/kg bw/day boric acid). Minimal inhibition of spermiation was observed at 26 mgB/kg bw/day. A
dose of 17 mgB/kg bw/day in male rats (equivalent to 97 mg/kg bw/day boric acid) was the no-observed-adverse-effect-
level. Developmental toxicity has also been demonstrated in mice, rats and rabbits, with rats the most sensitive species.
Administration of a wide range of doses of boric acid to pregnant rats for the whole of gestation has shown that at doses
of 330 mg/kg bw/day (equivalent to 58 mgB/kg bw/day) and above, there is a high resorption rate and retardation of
fetal development. At a lower dose of 28 mgB/kg bw/day, the only effects observed were reduced foetal weight and short
13th rib and wavy rib. These effects disappear if the pups are allowed to be delivered and reared to weaning. ...
Hubbard S Sullivan F; Journal of Trace Elements in Experimental Medicine 8 (2): 133 (1995)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ /Boric acid/ was administered to timed-mated
Sprague-Dawley-derived rats (60/group) in the diet at added concentrations of 0, 0.025, 0.050, 0.075, 0.100 or 0.200%
from gestational day (gd) 0 to 20. On gd 20, half the dams were terminated (n = 27-30 pregnant/group); the remaining
dams delivered their litters (n = 25-29/group), and pup growth and viability were monitored until scheduled termination
on postnatal day (pnd) 21. The dams sacrificed on gd 20 (pnd 21) ingested average doses of 0(0), 19(19), 36(37), 55(56),
76(74) or 143(145) mg BA/kg/day. Maternal clinical signs, body weight, and food and water intake were measured at
regular intervals during gestation and lactation. At termination, maternal liver and right kidney were weighed, and live
offspring (fetuses on gd 20 or pups on pnd 21) were weighed, sexed and examined for morphological anomalies
(external, visceral, skeletal). Maternal effects were minimal even at 0.200% BA (increased relative kidney weight). Prenatal
and postnatal viability of the offspring were not affected. Fetal body weight was reduced (94 and 88% of controls) at
0.100% and 0.200% BA, but recovery was complete by the time of natural delivery (avg. gd 22). The incidence of short rib
XIII was increased on gd 20 at greater than or equal to 0.100% BA, but only at 0.200% on pnd 21. The incidence of wavy
rib was increased on gd 20 at greater than or equal to 0.100% BA, but not on pnd 21, confirming the reversibility of this
skeletal variation. A slight (not statistically significant) decrease in extra lumbar ribs was observed at 0.200% BA on gd 20.
Extra lumbar ribs were not found in any pups, including controls, on pnd 21. Thus, a NOAEL was clearly established for
developmental toxicity in the rat: 0.075% BA (55 mg/kg/day) at gd 20 and 0.100% BA (74 mg/kg/day) at pnd 21.
Price C et al; J Am Coll Toxicol 14 (2): 173 (1995)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Prenatal exposure to boric acid (BA) has been shown
to cause shortening or agenesis of the 13th rib, as well as reduced incidences of supernumerary ribs, in multiple
laboratory species. /The authors/ sought to more fully characterize the morphological changes in the axial skeleton
caused by BA. Sprague-Dawley rats were treated by gavage with 500 mg/kg b.i.d on gestation days (GD) 5-9, 6-9, or 6-10
(GD 0 = plug day). Distilled water was used as the vehicle; animals received 10 mL/kg/dose. Control animals received
similar volumes of vehicle on GD 5-10. Progeny were delivered by cesarean section on GD 21 and were subsequently
stained with alizarin red S for skeletal examination. Major malformations involving the axial skeleton included
exencephaly, agnathia, cleft palate, sternoschisis, rachischisis, scoliosis, and a variety of bone fusions. Examples of
abnormal synostosis observed were atlas-exoccipital, scapula-vertebra, and right-left mandible fusions, as well as
intercostal and intervertebral fusions. Rib and vertebral duplications and agenesis were also noted. No 14th (i.e., lumbar)
ribs were noted in the group treated on GD 6-10. Shortening or agenesis of the 13th thoracic rib was seen in all BA-
treated groups, with greatest frequencies in the GD 5-9 and 6-10 exposure groups. Although the incidence of cervical ribs
was significant only for the group treated on GD 6-9, other axial abnormalities anterior to T3 (thoracic vertebra #3) were
most frequently observed in the group treated on GD 5-9. Interestingly, examination of vertebral morphology revealed
normal or increased, not fewer, numbers of vertebrae in the posterior thoracic region; however, less than the normal
complement of vertebrae was seen in the cervical, T1-2, and T3-10 regions. Malformed or misshapen ribs or vertebrae
predominantly occurred anterior to T7. These findings indicate that the reduction of the number of ribs was not due to a
homeotic shift in the posterior thoracic region, but, rather in the anterior half of the rib field.
Narotsky M et al; Teratology 51 (3): 192 (1995)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Adult male rats were dosed orally on day 0 with
/water/ or 2000 mg/kg of boric acid and killed on posttreatment day 2, 14, 28, and 57, or dosed with 0, 250, 500, 1000, or
2000 mg/kg of boric acid and killed on posttreatment day 14. At day 14, atypical structures that appeared to be enlarged
irregular cytoplasmic lobes of Step 19 spermatids were observed in Stage VIII seminiferous tubules of rats dosed with
1000 and 2000 mg/kg. Abnormal retention of Step 19 spermatids and residual bodies was also observed in Stage IX-XIII
tubules of these rats. The retained spermatids and residual bodies were seen in both the luminal and basal regions of the
epithelium. A substantial increase in the testicular sperm head count occurred in animals dosed with 2000 mg/kg.
Abnormal caput epididymal sperm morphology /(the sperm head appeared slightly distorted or swollen)/ and reduced
caput epididymal sperm reserves were observed at 1000 mg/kg and higher. Serum LH, FSH, TSH, and prolactin values
were not affected at any dosage. At day 28, rats dosed with 2000 mg/kg exhibited continued retention of Step 19
spermatids into Stage X, abnormal caput and cauda sperm morphology, and decreased percentages of motile cauda
spermatozoa with reduced straight-line swimming velocities. By day 57 substantial recovery was apparent; some retention
of Step 19 spermatids into Stage X tubules was still present in two out of six rats but the sperm parameters were
comparable to controls. The study indicated that acute oral exposure to boric acid adversely affected spermiation and
sperm quality in the adult male rat. At the dosages used the effects appeared reversible. The no-effect level was 500
mg/kg.
Linder R et al; Toxicol Environ Health 31 (2): 133-146 (1990)
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/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Rat testicular cell culture systems were studied
following in-vitro exposure to boric-acid (BA). Sertoli cells and germ cells from Fischer-344-rats were isolated and
cocultured. Leydig cells and tubule segments from different stages of the seminiferous cycle from Fischer-344-rats were
isolated and cultured. ... There was no observed effect of BA on the steroidogenic function of isolated Leydig cells. This
finding supported the theory of a central nervous system mediated rather than a direct hormone effect. An evaluation was
made of both Sertoli cell cAMP accumulation in Sertoli/germ cell cocultures and the stage specific secretion of BA activity
in cultured seminiferous tubules after in-vitro BA exposure. Inhibited spermiation was not shown to be due to BA effects
on either process. A study of BA effects in Sertoli-germ cell cocultures examined morphology/germ cell attachment;
Sertoli cell energy metabolism; and DNA synthesis. The most sensitive in-vitro endpoint was DNA synthesis of
mitotic/meiotic germ cells, with energy metabolism in Sertoli or germ cells affected to a lesser extent. A decrease was
noted in the early germ cell/Sertoli cell ratio prior to atrophy in a reevaluation of testis sections from rats exposed to BA.
Abstract: PubMed
Ku W et al; Reproductive Toxicology 7 (4): 321-331 (1993)
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/GENOTOXICITY/ ... Genetic effects of boric acid and borax (2.5, 5 and 10 microm) on cultures with and without TiO(2)
addition. No significant increase in /sister-chromatid exchanges/ (SCE) and micronuclei frequencies were observed at all
concentrations of boron compounds. However, TiO(2)-induced SCE and micronuclei could be reduced significantly by the
presence of boric acid and borax.
Abstract: PubMed
Turkez H; J Appl Toxicol. 28 (5): 658-64 (2008)
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/GENOTOXICITY/ Technical boric acid, 99.7%; tested with Chinese hamster ovary cells with and without S9 from Aroclor
1254 induced male Sprague-Dawley rat liver; incubated without S9 for 8-10 hours at 0 (DMSO), 500, 1000, 1500 or 2000
ug/mL followed by 2-3 hours with colcemid; with S9 at 1000, 1600, 2000 or 2500 ug/mL, for 2 hours followed by an
additional 8-10 hr incubation including 2-3 with colcemid; harvested by mitotic shake-off; scored 100 cells per
concentration; positive controls of mitomycin C (-S9) and cyclophosphamide (+S9); no evidence of an adverse genotoxic
effect...
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/GENOTOXICITY/ Boric acid, 99.7% technical grade; tested with mouse lymphoma cells with and without S9 from Fischer
344 male rats, induced with Aroclor 1254; incubated for 4 hours with boric acid followed by a 48 hour expression time;
concentrations of 0 (vehicle not stated), 1000, 1800, 2600, 3400, 4200 or 5000 ug/mL without S9 and 0, 1000, 2000, 3000,
4000 or 5000 ug/mL with S9; /No adverse effect indicated/.
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/GENOTOXICITY/ Salmonella strains TA 1535, TA 1537, TA 1538, TA 98 and TA 100 were exposed to boric acid in the plate
incorporation assay without S9 or with 4% or 10% Aroclor 1254-induced male rat liver activation. Concentrations were 0,
10, 50, 100, 500, 1000 or 2500 ug/plate. Two assays with triplicate plates in each. No evidence of cytotoxicity at any
concentration. Limit of solubility in water given as 50 mg/mL. No increase in revertants. Negative for an adverse effect.
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/GENOTOXICITY/ Boric acid, granular technical, >99% purity, was tested with primary hepatocytes from male F-344 rats,
three cultures per concentration for 19 hours. Unscheduled DNA synthesis was measured by autoradiography.
Concentrations in the first trial were 0 (medium), 10, 100, 250, 500, 1000 or 5000 ug/mL. In the second trial,
concentrations were 0, 5, 10, 50, 100, 250, 500, 1000, 2500, 3800 or 5000 ug/mL. Thirty cells per slide for a total of 90 were
scored per concentration. Examination of the data for the 3 slides per concentration suggests a possible adverse effect
with an increase in the nuclear grains but especially in the % in repair.
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/GENOTOXICITY/ The genotoxic potential of boric acid in Escherichia coli PQ37 was assessed ... using SOS chromotest.
Boric acid induced beta-galactosidase synthesis on the tester bacteria both /in/ the presence and absence of S9 activation
mixture. ...
Abstract: PubMed
Odunola O; East AFr Med J 74 (8): 499-502 (1997)
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/GENOTOXICITY/ ... /Results from a test of the genotox potentials of boric acid in the presence of aflatoxin in B1 in E. coli
PQ37 using the SOS chromotest/ boric acid may not interfere with nor block the epoxidation of aflatoxin B1. It may
however interact with the epoxide thereby inhibiting its activity. Boric acid may be a genotoxin and could possibly act as a
syngenotoxic and/or a cogenotoxic agent.
Abstract: PubMed
Odunola O ; East AFr Med J 74 (8): 499-502 (1997)
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/GENOTOXICITY/ The mutagenicity of borax and boric acid was examined in Salmonella typhimurium strains TA 98 and TA
100 by the preincubation method. No mutagenic activity of borax or boric acid was observed with or without S-9 rat liver
enzymes. Experiments also were conducted to investigate the enhancement or inhibition of benzo(a)pyrene mutagenicity
by the 2 compounds. Neither borax nor boric acid had any effect on the response of Salmonella typhimurium test to
benzo(a)pyrene.
Benson WH et al; Environ Toxicol Chem 3 (2): 209-14 (1984)
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/ALTERNATIVE and IN VITRO TESTS/ .../Researchers/ determined the estrogen-like effect of boric acid. ... Uterotrophic
assay, measure assay of the estradiol (E2), proliferation assay of mucous membrane cells, and assay of estrogen receptor
were conducted in this study. Boric acid could increase the weight of uterus of ovariectomized SD rats and the height of
epithelium cells of mucous membrane, enhance the expression of the proliferating cell nucleus antigen, and reduce the
density of estrogen receptors. Boric acid could not affect the level of estradiol in serum. ...
Abstract: PubMed
Wang Y et al; Biol Trace Elem Res. 121 (2): 160-70 (2008)
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/ALTERNATIVE and IN VITRO TESTS/ The most sensitive in vitro effect involved a reduction of DNA synthesis of
mitotic/meiotic germ cells, and next was an effect on energy metabolism in Sertoli or germ cells.
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/ALTERNATIVE and IN VITRO TESTS/ ... Boric acid, the dominant form of boron in plasma, inhibits the proliferation of
prostate cancer cell lines, DU-145 and LNCaP, in a dose-dependent manner. Non-tumorigenic prostate cell lines, PWR-1E
and RWPE-1, and the cancer line PC-3 were also inhibited, but required concentrations higher than observed human
blood levels. Studies using DU-145 cells showed that boric acid induced a cell death-independent proliferative inhibition,
with little effect on cell cycle stage distribution and mitochondrial function.
Abstract: PubMed
Barranco W Eckhert C; Cancer Lett 216 (1): 21-29
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/OTHER TOXICITY INFORMATION/ ... Boric acid (BA) inhibits NAD+ and NADP+ as well as mechanically induced release of
stored Ca2+ in growing DU-145 prostate cancer cells. Cell proliferation was inhibited by 30% at 100 uM, 60% at 250 uM,
and 97% at 1,000 uM BA. NAD+-induced Ca2+ transients were partly inhibited at 250 uM BA and completely at 1,000 uM
BA, whereas both NADP+ and mechanically induced transients were inhibited by 1,000 uM BA. Expression of CD38
protein increased in proportion to BA exposure (0-1,000 uM). In vitro mass spectrometry analysis showed that BA formed
adducts with the CD38 products and Ca2+ channel agonists cyclic adenosine diphosphate ribose (cADPR) and nicotinic
acid adenine dinucleotide phosphate (NAADP). Vesicles positive for the Ca2+ fluorophore fluo-3 acetoxymethyl ester
accumulated in cells exposed to 250 and 1,000 uM BA. ....
Abstract: PubMed
Barranco WT et al; Cell Biol Toxicol. 25 (4): 309-20 (2009)
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/OTHER TOXICITY INFORMATION/ Twenty-six cows died after accidental exposure to boron fertilizer. Cows developed
diarrhea, weakness, ataxia, signs of depression, and died, usually within a few hours. Seizure-like behavior was noticed in
two cows, and two were suspected of aborting. High boron concentrations in tissues from affected cows confirmed
ingestion of an appreciable amount of boron fertilizer. In an attempt to confirm the diagnosis of boron poisoning, boron
fertilizer was administered to goats. A kid goat given 3.6 g of fertilizer/kg of body weight developed clinical signs similar
to those seen in the cattle. Boron compounds such as boric acid have been considered generally nontoxic, and reports of
livestock toxicosis are uncommon. This case report suggests that these compounds may be palatable under certain
circumstances leading to ingestion of toxic quantities.
Abstract: PubMed
Sisk DB et al; J Am Vet Med Assoc 193 (8): 943-5 (1988)
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/OTHER TOXICITY INFORMATION/ /In rat/ symptoms of toxicity were CNS depression ataxia, convulsion, and death.
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14.1.17 Non-Human Toxicity Values
LD50 Mouse iv 1780 mg/kg bw

European Chemicals Bureau; IUCLID Dataset for Boric Acid (10043-35-3), p.26 (2000 CD-ROM edition). Available from, as of October 3,
2011: http://esis.jrc.ec.europa.eu/
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LD50 Mouse sc 2070 mg/kg bw

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LC50 Rat inhalation >0.16 mg/L 4hr
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LD50 Rat oral 3000-4000 mg/kg bw

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LD50 Rat oral 2660 mg/kg

Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ.
2004., p. 536
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LD50 Rat sc 1400 mg/kg

2004., p. 536
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LD50 Rat iv 1330 mg/kg

2004., p. 536
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LD50 Mouse oral 3450 mg/kg

2004., p. 536
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LD50 Mouse sc 1740 mg/kg

2004., p. 536
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LD50 Mouse iv 1240 mg/kg

2004., p. 536
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LD50 Dog oral 2000 mg/kg

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LD50 Rabbit dermal >2000 mg/kg bw

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LC50 Rat inhalation >2 mg/cu m/4 hr

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LD50 Guinea pig sc 1200 mg/kg bw

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LD50 Chicken (1 day old) oral 2.95 g/kg

Abstract: PubMed
Sander J et al; Avian Dis 35 (4): 745-749 (1991)
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14.1.18 Ecotoxicity Values
LC50; Species: Oncorhynchus mykiss (Rainbow trout); Concentration: 100 ppm for 96 hr (soft water); exposure was
initiated subsequent to fertilization and maintained through 4 days posthatching /Conditions of bioassay not specified in
source examined/
Birge WJ, Black JA; Sensitivity of Vertebrate Embryos to Boron Compounds p. 1-77 (1977) NTIS# PB-267085
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LC50; Species: Oncorhynchus mykiss (Rainbow trout); Concentration: 79 ppm for 96 hr (hard water); exposure was initiated
subsequent to fertilization and maintained through 4 days posthatching /Conditions of bioassay not specified in source
examined/
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LC50; Species: Ictalurus punctatus (Channel catfish); Concentration: 155 ppm for 96 hr (soft water); exposure was initiated
examined/
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LC50; Species: Ictalurus punctatus (Channel catfish); Concentration: 22 ppm for 96 hr (hard water); exposure was initiated
examined/
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LC50; Species: Ictalurus punctatus (Channel catfish); Conditions: flow through; Concentration: 1.26 g/L for 5 days; 0.89 g/L
for 9 days
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LC50; Species: Carassius auratus (Goldfish); Concentration: 46 ppm for 96 hr (soft water); exposure was initiated
examined/
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LC50; Species: Carassius auratus (Goldfish); Concentration: 75 ppm for 96 hr (hard water); exposure was initiated
examined/
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LC50; Species: Carassius auratus (Goldfish); Conditions: flow through; Concentration: 1.02 g/L for 3 days; 0.26 g/Lfor 7 days
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LC50; Species: Daphnia magna (Water flea); Conditions: static bioassay; Concentration: 133 (115-153) mg/L for 48 hr
Gersich FM; Environ Toxicol Chem 3 (1): 89-94 (1984)
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LC50; Species: Anas platyrhynchos (Mallard duck) 1 day old dietary >5620 ppm for 8 days
USEPA, Office of Pesticide Programs; Pesticide Ecotoxicity Database (2000) on Boric acid (10043-35-3). Available from, as of May 13,
2005: http://cfpub.epa.gov/ecotox/quick_query.htm
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LC50; Species: Colinus virginianus (Northern bobwhite) 1 day old dietary >5620 ppm for 8 days
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LD50; Species: Colinus virginianus (Northern bobwhite) oral >2510 mg/kg/14 days
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LD50; Species: Apis mellifera (Honey bee) worker topical >362.58 ug/bee for 48 hr
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LC50; Species: Catostomus latipinnis (Flannelmouth sucker); Conditions: static; Concentration: 1000 mg/L for 24 hr (95%
confidence interval: 746-3510 mg/L) /technical product/
Hamilton SJ, Buhl KJ; Ecotoxicol Environ Saf 38 (3): 296-308 (1997). ECOTOX database on Boric acid (10043-35-3). Available from, as of
May 13, 2005: http://cfpub.epa.gov/ecotox/quick_query.htm
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EC50; Species: Ceriodaphnia dubia (Water flea); Conditions: static; Concentration: 180.6 g/L for 24 hr (95% confidence
interval: 101.1-232.2 g/L); Effect: intoxication, immobilization /technical product/
Hickey CW; N.Z. J Mar Freshwater Res 23 (1): 131-137 (1989). ECOTOX database on Boric acid (10043-35-3). Available from, as of May
13, 2005: http://cfpub.epa.gov/ecotox/quick_query.htm
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EC50; Species: Ceriodaphnia pulchella (Water flea); Conditions; static; Concentration: 101.2 g/L for 24 hr (95% confidence
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EC50; Species: Daphnia carinata (Water flea); Conditions: static; Concentration: 267.7 g/L for 24 hr (95% confidence
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EC50; Species: Daphnia magna (Water flea); Conditions: static; Concentration: 319.8 g/L for 24 hr (95% confidence interval:
264.3-496.7 g/L); Effect: intoxication, immobilization /technical product/
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LC50; Species: Elodea canadensis (Waterweed); Conditions: static; Concentration: 5 mg B/L for 28 days
WHO; Environ Health Criteria 204: Boron p.111-2 (1998) Available from, as of May 13, 2005:
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LC50; Species: Myriophyllum alterniflorum (Watermilfoil); Conditions: static; Concentration: 5 mg B/L for 28 days
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LC50; Species: Ranunculus penicillatus (Buttercup); Conditions: static; Concentration: 10 mg B/L for 28 days
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LC50; Species: Gambusia affinis (Western mosquitofish); Conditions: static; Concentration: 18,000 ppm for 24 hr
Wallen IE et al; Sewage Ind Wastes 29 (6): 695-711 (1957). ECOTOX database on Boric acid (10043-35-3). Available from, as of May 13,
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LC50; Species: Lepomis macrochirus (Bluegill); Conditions: static; Concentration: >1021 ppm for 96 hr /formulated
product/
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LC50; Species: Oncorhynchus kisutch (Coho salmon); Conditions: static; Concentration: >10 mg/L for 24 hr /technical
product/
Hamilton SJ, Buhl KJ; Arch Environ Contam Toxicol 19 (3): 366-373 (1990). ECOTOX database on Boric acid (10043-35-3). Available
from, as of May 13, 2005: http://cfpub.epa.gov/ecotox/quick_query.htm
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LC50; Species: Oncorhynchus kisutch (Coho salmon); Conditions: static; Concentration: 447 mg/L for 96 hr (95%
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LC50; Species: Oncorhynchus tshawytscha (Chinook salmon); Conditions: static; Concentration: >1 g/L for 24 hr /technical
product/
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EC50; Species: Simocephalus vetulus (Water flea); Conditions: static; Concentration: 123.4 g/L for 24 hr (95% confidence
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EC50; Species: Spriostomum ambiguum (Protozoa); Conditions: static, 25 deg C, total hardness 2.8 mg CaCO3, pH 7.4
+/-0.2; Concentration: 752 ppm for 24 hr; Effect: deformations
Abstract: PubMed
Nalecz-Jawecki G, Sawicki J; Arch Environ Contam Toxicol 34 (1): 1-5 (1998)
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EC50; Species: Spriostomum ambiguum (Protozoa); Conditions: static, 25 deg C, total hardness 2.8 mg CaCO3, pH 7.4
+/-0.2; Concentration: 364 ppm for 48 hr; Effect: deformations
Abstract: PubMed
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LC50; Species: Spriostomum ambiguum (Protozoa); Conditions: static, 25 deg C, total hardness 2.8 mg CaCO3, pH 7.4
+/-0.2; Concentration: 5825 ppm for 24 hr
Abstract: PubMed
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LC50; Species: Spriostomum ambiguum (Protozoa); Conditions: static, 25 deg C, total hardness 2.8 mg CaCO3, pH 7.4
+/-0.2; Concentration: 4871 ppm for 48 hr
Abstract: PubMed
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LC50; Species: Ptychocheilus lucius (Colorado squawfish) swimup fry 17-31 day; Conditions: static, 25 +/-1 deg C, pH 7.0-
8.5; Concentration: 279 mg/L as boron for 96 hr
EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans.
Triisopropylborate (TIPB). Available from, as of May 17, 2005: http://www.epa.gov/hpv/pubs/hpvrstp.htm
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LC50; Species: Ptychocheilus lucius (Colorado squawfish) juvenile 99-115 day; Condtions: static, 25 +/-1 deg C, pH 7.0-8.5;
Concentration: >100 mg/L as boron for 96 hr
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LC50; Species: Ptychocheilus lucius (Colorado squawfish) juvenile 193-207 day; Conditions: static, 25 +/-1 deg C, pH 7.0-
8.5; Concentration: 527 mg/L as boron for 96 hr
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LC50; Species: Xyrauchen texanus (Razorback sucker) swimup fry 10-17 day; Conditions: static, 25 +/-1 deg C, pH 7.0-8.5;
Concentration: 233 mg/L as boron for 96 hr
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LC50; Species: Xyrauchen texanus (Razorback sucker) juvenile 133-139 day; Conditions: static, 25 +/-1 deg C, pH 7.0-8.5;
Concentration: 279 mg/L as boron for 96 hr
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LC50; Species: Xyrauchen texanus (Razorback sucker) juvenile 176-178 day; Conditions: static, 25 +/-1 deg C, pH 7.0-8.5;
Concentration: >100 mg/L as boron for 96 hr
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LC50; Species: Gila elegans (Bonytail) swimup fry 11-18 day; Conditions: static, 25 +/-1 deg C, pH 7.0-8.5; Concentration:
280 mg/L as boron for 96 hr
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LC50; Species: Gila elegans (Bonytail) juvenile 138-145 day; Condtions: static, 25 +/-1 deg C, pH 7.0-8.5; Concentration:
>100 mg/L as boron for 96 hr
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LC50; Species: Gila elegans (Bonytail) juvenile 220-234 day; Conditions: static, 25 +/-1 deg C, pH 7.0-8.5; Concentration:
553 mg/L as boron for 96 hr
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LC50; Species: Daphnia magna; Conditions: static renewal procedure, with batchwise replacement of test and control
solutions at regular intervals (Monday, Wednesday, and Friday), 20 +/- 1 deg C, pH 8.1 +/- 0.1, conductivity was 290 +/-
31 umhos/cm, hardness was 148 +/- 7 mg/L as CaCO3, and alkalinity was 58 +/- 5 mg/L as CaCO3; Concentration: 52.2
mg/L for 21 days, as boron (95% confidence interval, 42.6-66.7 mg/L)
 from HSDB
14.1.19 National Toxicology Program Reports
Toxicology and carcinogenesis studies were conducted by feeding technical grade boric acid (99.7% pure) to groups of
male and female B6C3F1 mice for 2 yr. ... Diets containing boric acid /were fed/ at concentrations of 0, 2,500, or 5,000
ppm to groups of 50 male or 50 female mice. ... Under the conditions of these 2 yr feed studies, there was no evidence of
carcinogenicity of boric acid at doses of 2,500 or 5,000 ppm for male or female B6C3F1 mice. ... The decrease in survival of
dosed male mice may have reduced the sensitivity of this study.
Toxicology & Carcinogenesis Studies of Boric Acid in F344/N Rats and B6C3F1 Mice (Feed Studies) p.3 Technical Report Series No. 324
(1987) NIH Publication No. 88-2580 U.S. Department of Health and Human Services, National Toxicology Program, National Institute of
Environmental Health Sciences, Research Triangle Park, NC 27709
 from HSDB
The potential reproductive toxicity of boric acid (BA) in CD- l (Swiss) mice was evaluated using the Reproductive
Assessment by Continuous Breeding (RACB) Protocol. Male and female Swiss (CD-l) mice were exposed to BA at
concentrations of 0, 1000, 4500, or 9000 ppm in the feed; this produced estimated consumption levels of approximately
152, 636, and 1262 mg/kg bw. During 14 wks of cohabitation with continuous access to a BA-containing diet, no litters of
dead or live pups were produced by 9000 ppm cohabited pairs. Among the litters born to pairs fed BA at 4500 ppm, live
litter size and pup body weight were significantly reduced in comparison to controls. All aspects of fertility were
unaffected at 1000 ppm BA. A crossover mating trial (Task 3) at the end of the continuous cohabitation phase, using the
middle dose group, confirmed the male as the affected sex, with observed fertility rates of: 0 ppm male x 0 ppm female,
74%; 4500 ppm male x 0 ppm female, 5%; and 0 ppm male x 4500 ppm female, 65%. The mating index was 79%, 30% and
70% for the same groups. Additionally, adjusted body weights, for pups born from the mating of control male x 4500
ppm female, were significantly decreased from controls (P<O.Ol), indicating that the female and/or pup are also affected
by BA. At sacrifice, after 27 wks of BA exposure, the F0 males fed 9000 ppm BA had significantly lower body weight and
reproductive organ weights (testes, combined caput and corpus epididymis and cauda epididymis) and significantly fewer
spermatozoa in the cauda epididymis. Males fed 4500 ppm BA also had significantly lower testes, epididymis, prostate
weight and fewer spermatozoa in the cauda epididymis. Organ weights were unaffected at 1000 ppm BA for the F0 males.
The germinal epithelium of F0 males in the 9000 ppm group was atrophied and consisted mostly of Sertoli cells with
occasional spermatogonia. The 4500 ppm group had fewer spermatids than in the controls; multinucleate giant cells were
observed. Sperm concentration/mg cauda was dramatically reduced in 9000 ppm males (2.8+/-1.7 x 10+3) compared to
controls (519+/-36 x 10+3). Motility was difficult to quantify due to extremely low sperm concentrations. In 4500 ppm
males, both sperm concentration (146.9+/-26.5 x 10+3)and sperm motility (53.3+/- 8.2%) were lower than in controls
(519+/-36 x 10+3 sperm with 78.1+/-3.0% motility). Males fed 1000 ppm BA had normal sperm concentrations with
reduced motility (69.0+/-4.5%). At necropsy, F0 female body weight was significantly decreased in the high dose group.
The F0 females in the 4500 ppm group had significantly decreased kidney/adrenals and liver weights. The F1 mice
exposed to dietary BA (0 and 1000 ppm), beginning at conception, had normal fertility. The adjusted mean body weight
of F2 pups was decreased. However, the number of live pups/litter, the proportion of pups born alive, sex of pups born
alive, and unadjusted weights of pups born alive, were not significantly changed by BA exposure. At necropsy, F1 males
had normal reproductive organ weights and sperm motility. However, BA treatment decreased sperm concentrations in F1
males (585.6+/-32.5 x 10+3 in controls vs. 442.6+/-51.2 x 10+3). Female F1 mice had significantly greater uterus and
kidney/adrenal weights than controls. This study confirms that BA is a reproductive toxicant in mice, primarily through an
effect in the male. The 1000 ppm dose approached a No Observed Adverse Effects Level (NOAEL) for the adult
reproductive system, as well as for the developing reproductive system.
Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program;
Reproductive Toxicity of Boric Acid (CAS No. 10043-35-3) in CD-1 Swiss Mice, NTP Study No. RACB88034 (April 1990) Available from, as
of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847F35A-0850-D1E7-B02ED4DDD150F990
 from HSDB
... In this study, developmental toxicity was evaluated in timed-mated Sprague-Dawley-derived rats exposed to boric acid
in feed at concentrations of 0.1%, 0.2% or 0.4% on gestational days (gd) 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. ... 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 NOAEL for maternal toxicity was 0.1% dietary boric
acid and the LOAEL was 0.2%. Embryo/fetal toxicity occurred in all treatment groups (greater than or equal to 0.1%).
Developmental Toxicity of Boric Acid (CAS No. 10043-35-3) in Sprague-Dawley Rats, NTP Study No. TER89027 (May 1, 1990) Available
from, as of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-C685-88B4D7EAC975BD44
 from HSDB
... In the present study, boric acid (0, 0.8, 1.6 or 2.4% in the diet) was provided to timed-mated female /Sprague-Dawley
derived/ rats from gd 14 to 17. During the treatment period, the vehicle control group was fed undosed diet ad libitum,
and a pair-fed control group was provided with the median amount of food consumed (g of food/kg of body wt/day) by
the 2.4% boric acid group. During the remainder of the study, dams and pups had ad libitum access to undosed diet,
except during the second week of lactation (Phase I) when food consumption exceeded the available supply of food
during one measurement period. Thus, dam and pup data collected on pnd 14, 21 and 26 may have been compromised
due to this temporary shortage of food. ... Maternal body weight on gd 20 (both phases), maternal weight gain for the
gestational period as a whole (gd 0 to 20, both phases), gravid uterine weight (Phase II) and corrected maternal weight
gain on gd 20 (Phase II) were not affected by boric acid exposure or by pair feeding. Maternal relative liver weight was
increased on gd 20 (Phase II) by 1.6 and 2.4% boric acid, but not by pair feeding. This effect on relative liver weight was
not present on pnd 21. No changes were noted for maternal relative kidney weight on gd 20 or pnd 21 in either the boric
acid or pair-fed groups relative to the vehicle (ad libitum) control group. ... Fetal body weight was significantly reduced in
the low, mid, and high dose boric acid groups on gd 20 (82%, 68% and 69% of control weight, respectively). By pnd 21,
recovery from body weight deficits was complete for the low dose group (104% of control weight). Persistent body weight
deficits were observed at the mid dose (83% of control weight; biologically relevant but not statistically significant) and at
the high dose (75% of control weight: statistically significantly). Prenatal mortality was not affected on gd 20 (Phase II),
but cumulative post-implantation mortality through pnd 21 was increased at the high dose (34%, 44%, 33% and 72% for
the vehicle control through high-dose boric acid groups, respectively). The incidence of treatment-related mortality was
most pronounced during the early postnatal period (pnd 0 to 4) as follows: 2%, 8%, 27% and 44% of pups per litter in the
vehicle control through high-dose boric acid groups, respectively. No treatment-related effects were noted for the
incidence of craniofacial, palatal or CNS structural defects. ... These results indicate that boric acid can reduce fetal body
weight to 69% of control weight on gd 20 without a concomitant increase in the incidence of ventricular enlargement.
However, this study did not answer the question of whether boric acid could induce more severe weight reductions
without concomitant ventricular enlargement, or whether there is a sensitive period earlier in gestation for induction of
ventricular enlargement in the absence of fetal body weight effects. Preliminary evidence is provided that exposure to
boric acid (1.6% or 2.4% on gd 14 to 17) may alter brain weights (total and/or regional), but such effects were not found
at 0.8% boric acid. Boric acid-induced developmental toxicity in this study occurred independently of maternal food
intake and body weight deficits, since the pair-fed control group did not differ from the ad libitum control group for any
developmental measure in this study.
Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program; Boric Acid
(CAS No. 10043-35-3) CNS Developmental Toxicity Studies in Sprague-Dawley CD Rats Exposed on Gestation Days 14-17, NTP Study
No. TER90123 (October, 1994) Available from, as of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-
C685-88B4D7EAC975BD44
 from HSDB
... The present study was designed to determine (1) whether the induction of ventricular enlargement could be
experimentally repeated following exposure to boric acid on gestational days 6 to 15, (2) whether the incidence would
exhibit a dose-response relationship at exposure concentrations of 0.4% to 0.8% boric acid in the diet, and (3) whether
the incidence and severity of ventricular enlargement would change during postnatal life. Thus, in the present study,
/boric acid/ BORA (0.4%, 0.5%, 0.6% or 0.8% in the diet) was provided to timed-mated CD rats (42-76/group) from
gestational days 6 to 15. ... After treatment ended, maternal food and water intake increased in all boric acid-exposed
groups (gestational days 15 to 20). Maternal relative liver weight was increased at 0.8% boric acid on gestational days 20,
and decreased at greater than or equal to 0.6% boric acid on postnatal day 21. Relative kidney weight was increased at
greater than or equal to 0.5% boric acid on gestational day 20, with no treatment- related effects on postnatal day 21.
Post implantation mortality (i.e., resorption, late fetal death and postnatal death) was increased at greater than or equal to
0.6% BORA on gestational days 20 (4%, 4%, 5%, 9% and 25% for control through high-dose groups), and at all BORA
exposures by postnatal day 21 (9%,17%, 30%, 64% and 97%). ... Offspring body weight was decreased in all boric acid-
exposed groups on gestational day 20 (79%, 70%, 62% and 51 % of control weight for the low- to high-dose groups) and
on postnatal day 0 (94%, 87%, 76% and 66% of control weight). ... Craniofacial (external) malformations were observed in
28% of high-dose fetuses on gestational day 20 and 17% of high-dose pups on postnatal day 21, as compared to 0% for
controls at both ages. ... Anophthalmia and microphthalmia were the most frequently observed craniofacial
malformations. Examination of head sections revealed a high background incidence of minimal ventricular enlargement
(ELV) on gestational day 20 (77% of control fetuses), with a dramatic decrease in ELV by postnatal day 21 (2% of control
pups). On gestational day 20, ELV incidence was increased at 0.4%-0.6% boric acid (92-95%), but not in the 0.8% group
(80%), and no treatment-related effects were observed on postnatal day 21. ...Exposure to 0.4-0.8% boric acid (gestational
days 6 to 15) in this study was also associated with dose-related intrauterine growth retardation. Complete recovery from
growth deficits was observed prior to the end of lactation at 0.4-0.6% boric acid, but not at 0.8% boric acid. The LOAEL for
post implantation mortality ... was 0.4% boric acid in this study when postnatal mortality was taken into consideration.
After adjusting for fetal body weight by covariate analysis, the incidence of ELV showed no significant dose-response
relationship, but the incidence of hydrocephaly was increased at all doses. These results support the interpretation that
boric acid exposure during organogenesis adversely affects CNS development in the rat independent of its effect upon
fetal growth. The LOAEL for adverse CNS effects in this study was 0.4% boric acid in the diet...
Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program; CNS
Developmental Toxicity of Boric Acid (CAS No. 10043-35-3) in Sprague-Dawley CD Rats Exposed on Gestation Days 6-15, NTP Study
No. TER93138 (October, 1994) Available from, as of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-
C685-88B4D7EAC975BD44
 from HSDB
Boric acid (BORA), ... 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 (NOAEL) with mild renal lesions in only 2 of 10
females. The NOAEL for developmental toxicity of BORA was 0.1%.
Department of Health & Human Services/National Institute of Environmental Health Sciences, National Toxicology Program; Final
Report on the Developmental Toxicity of Boric Acid (CAS No. 10043-35-3) in CD-1 Swiss Mice, NTP Study No. TER89028 (August 11,
1989) Available from, as of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-C685-88B4D7EAC975BD44
 from HSDB
Artificially-inseminated New Zealand White (NZW) rabbits (30 per group) were exposed to 0, 62.5, 125 or 250 mg/kg/day
boric acid. Aqueous solutions were delivered by gavage in a volume of 5 mL/kg on gestational days (gd) 6-19. At study
termination (gestational days 30), the uterus was examined to determine pregnancy status (18-23 pregnancies/group),
and to evaluate the number of resorptions, and dead or live fetuses. ... Pregnant does exhibited no overt symptoms
attributable to boric acid toxicity, except that vaginal bleeding was noted at 250 mg/kg/day (2-11 does/day on
gestational days 19-30). All high-dose does with this symptom had no live fetuses on gestational days 30. ... Relative
maternal kidney weight was increased at 250 mg/kg/day , but absolute kidney weight was not affected. Microscopic
evaluation of maternal kidney sections did not indicate any pathology associated with boric acid exposure. Thus, 250
mg/kg/day was the "Lowest Observed Adverse Effect Level" (LOAEL) for pregnant does, and 125 mg/kg/day was the
maternal "No Observed Adverse Effect Leve1" (NOAEL). No definitive evidence of developmental toxicity was observed
following exposure of pregnant does to either 62.5 or 125 mg/kg/day boric acid during the period of major
organogenesis (gestational days 6-19). At 250 mg/kg/day , developmental toxicity included a high rate of prenatal
mortality (90% of implants/litter were resorbed vs. 6% for controls). Prenatal mortality was also expressed as an increased
proportion of pregnant females with no live fetuses (73% vs 0% of controls) and as a reduction in the number of live
fetuses/live litter on gestational days 30 (2.3/litter vs. 8.8 for controls). The incidence of malformed live fetuses/litter was
also increased at 250 mg/kg/day (81% vs. 26% for controls), primarily due to the incidence of fetuses with cardiovascular
defects (72% vs. 3% for controls). The most prevalent cardiovascular malformation was interventricular septal defect which
was observed in 57% (8/14) of high dose fetuses as compared to 0.6% (1/159) of fetuses in the control group. At 250
mg/kg/day , the average fetal body weight/litter was 92% of the average control weight, but this difference did not reach
statistical significance. Thus, 250 mg/kg/day was the LOAEL for developmental toxicity and 125 mg/kg/day was the
NOAEL. In summary, decreased food intake and vaginal bleeding associated with pregnancy loss were the only clear
manifestations of toxicity in does exposed to 250 mg/kg/day boric acid on gestational days 6-19. The same dose was
associated with severe developmental toxicity, i.e. 90% prenatal mortality/litter and 81% malformed fetuses/litter. No
definitive maternal or developmental effects were observed at 62.5 or 125 mg/kg/day.
Developmental Toxicity of Boric Acid (CAS No. 10043-35-3) in New Zealand White Rabbits, NTP Study No. TER90003 (November 1991)
Available from, as of August 14, 2002: http://ntp.niehs.nih.gov/index.cfm?objectid=0847FF31-90CC-C685-88B4D7EAC975BD44
 from HSDB
14.1.20 TSCA Test Submissions
Boric acid (CAS No. 10043-35-3) was evaluated for developmental toxicity in artificially inseminated New Zealand White
rabbits. A 5 ml aqueous solution of 0, 62.5, 125, or 250 mg/kg/day was orally administered to 30 females per group on
days 6-19 of gestation. Two early, non-treatment related mortalities were recorded, one each in the 62.5 mg/kg/day
group and the 125 mg/kg/day group. Does from the 250 mg/kg/day group exhibited vaginal bleeding with associated
pregnancy loss. This group also showed decreased food consumption, body weight, weight change during treatment, and
gravid uterine weight relative to controls. No clinical signs of toxicity were seen in the other groups. Evidence of
developmental toxicity at 250 mg/kg/day included a 90% average rate of resorption compared to 6% for controls, and
complete prenatal loss (73% compared to 0% for controls). No maternal toxicity or developmental effects were noted for
groups receiving 62.5 or 125 mg/kg/day. The incidence of late fetal deaths was low for all groups relative to controls and
showed no relationship to dose. The overall incidence of external fetal changes was statistically significantly increased in
litters from the 250 mg/kg/day group, but a dose-response relationship for individual changes was not shown. Changes in
the cardio-vascular system observed in fetuses from the high dose group (250 mg/kg/day) occurred with statistically
significant frequency and included interventricular septal defects, enlarged aorta, papillary muscle malformations, and the
pulmonary artery and the aorta arising from the right ventricle. External fetal changes at 62.5 and 125 mg/kg/day were
comparable to controls. The incidence of skeletal changes was comparable for all groups.
U.S. Borax & Chemical Corp.; Developmental Toxicity of Boric Acid in New Zealand White Rabbits (10/28/05); EPA Doc. No. 8EHQ-1092-
2002; Fiche No. OTS0535248
 from HSDB
14.1.21 Protein Binding
No protein binding reported.

 from DrugBank
14.2 Ecological Information
14.2.1 EPA Ecotoxicity
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1 to 5 of 43 View More
Record ID Pesticide Type Organism Dose Type Toxicity
4415 Insecticide Mallard duck LC50 > 5620 PPM
4416 Insecticide Bobwhite quail LC50 > 5620 PPM
4417 Insecticide Bluegill sunfish LC50 1021 PPM
4418 Insecticide Rainbow trout LC50 > 1100 PPM
4419 Insecticide Honey bee LD50 > 362.58 UGB
 from EPA Office of Pesticide Programs
14.2.2 Environmental Fate/Exposure Summary
Boric acid is found in nature as the mineral sassolite and is the predominant form of boron in natural waters. Atmospheric
emissions of boric acid in particulate and vapor form occur as a result of volatilization of boric acid from the sea and
volcanic activity; seawater evaporation is the biggest contribution in air. Boric acid's production and use in a wide variety
of consumer and commercial products and applications may result in its release to the environment through various
waste streams. It's use as a crosslinking agent and friction reducer in hydraulic fracturing fluids and its use as an active
registered pesticide will result in its direct release to the environment. Atmospheric emissions of boric acid occur as a
result of mining operations, glass and ceramics manufacturing, the application of agricultural chemicals, and coal-fired
power plants. If released to air, a vapor pressure of 1.6X10-6 mm Hg at 25 deg C indicates boric acid will exist in both the
vapor and particulate phases in the atmosphere. Vapor-phase boric acid will be degraded in the atmosphere by reaction
with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be about 38 days.
Particulate-phase boric acid will be removed from the atmosphere by wet or dry deposition. If released to soil, the pKa of
boric acid, 9.24 at 25 deg, indicates this compound will exist primarily in the undissociated form at an environmental pH
range between pH 5 and pH 9, although the anion form will partially exist in alkaline soils(SRC). Adsorption of boron in
soils depends on pH, organic content and types of clay and minerals in the soil. At acidic pH, boron exists in solutions in
the form of undissociated boric acid; at alkaline pH, presence of borate ion occurs, which reaches maximum adsorption at
pH 8.5-9. Field studies have observed boron to leach readily in soil; undissociated boric acid is transported in soil with
little adsorption. Volatilization of boric acid from moist soil surfaces is not expected to be an important fate process given
an estimated Henry's Law constant of 2.6X10-12 atm-cu m/mole, based upon its vapor pressure, 1.6X10-6 mm Hg, and
water solubility, 5X10+4 mg/L. Boric acid is not expected to volatilize from dry soil surfaces based upon its vapor pressure.
No biotransformation processes have been reported for boron compounds, including boric acid. If released into water,
boric acid is not expected to adsorb to suspended solids and sediment based upon its observed leaching in soil.
Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated
Henry's Law constant. However, evaporation of seawater itself is reported to be the biggest environmental contribution of
boric acid to air. Occupational exposures to boron compounds (including boric acid) occurs through inhalation of dusts
and dermal absorption. The general population is exposed to boric acid in various cosmetic products, including make-up,
skin and hair care preparations, deodorants, moisturizing creams, breath fresheners, and shaving creams. (SRC)
 from HSDB
14.2.3 Natural Occurring Sources
Boric acid is found in nature as the mineral sassolite and is also the predominant form of boron in natural waters and an
important form in biological systems(1). Atmospheric emissions of borates and boric acid in particulate (<1-45 um in size)
or vapor form occur as a result of volatilization of boric acid from the sea and volcanic activity(2); seawater evaporation is
the biggest contribution to boron in air(2).
(1) Schubert D; Kirk-Othmer Encyclopedia of Chemical Technology. (1999-2011). New York, NY: John Wiley & Sons; Boron Oxides, Boric
Acid, and Borates. Online Posting Date: 15 April 2011. (2) WHO; Environmental Health Criteria 204, Boron. World Health Org (1998)
Available from, as of Oct 4, 2011: http://www.inchem.org/documents/ehc/ehc/ehc204.htm
 from HSDB
14.2.4 Artificial Sources
Boric acid's production and use in a wide variety of consumer and commercial products and applications(1) may result in
its release to the environment through various waste streams(SRC). Boric acid's use as a crosslinking agent and friction
reducer in hydraulic fracturing fluids(2,3) and its use as an active registered pesticide(4) will result in its direct release to
the environment(SRC). Atmospheric emissions of boric acid in particulate and vapor form occur as a result of mining
operations, glass and ceramics manufacturing, the application of agricultural chemicals, and coal-fired power plants(1).
(1) WHO; Environmental Health Criteria Document No. 204 (1998): Boron (7740-42-8). Available from, as of Oct 4, 2011:
http://www.inchem.org/pages/ehc.html (2) US EPA; Draft Plan to Study the Potential Impacts of Hydraulic Fracturing on Drinking Water
Resources. EPA/600/D-11/001. February 2001. Washington, DC: US Environ Prot Agency. Available from, as of Sept 19, 2011:
http://www.epa.gov/research (3) FracFocus Chemical Disclosure Registry; Ground Water Protection Council and the Interstate Oil and
Gas Compact Commission. Available from, as of Sept 16, 2011: http://fracfocus.org/chemical-use/what-chemicals-are-used (4) U.S.
Environmental Protection Agency/Office of Pesticide Program's Chemical Ingredients Database on Boric Acid (10043-35-3). Available
from, as of Oct 5, 2011: http://npirspublic.ceris.purdue.edu/ppis/
 from HSDB
14.2.5 Environmental Fate
TERRESTRIAL FATE: The pKa of boric acid is 9.24 at 25 deg C(1), indicating that this compound will exist primarily in the
undissociated form at an environmental pH range between pH 5 and pH 9, although the anion form will partially exist in
alkaline soils(SRC). Adsorption of boron in soils depends on pH, organic content and types of clay and minerals in the
soil(1). At acidic pH, boron exists in solutions in the form of undissociated boric acid; at alkaline pH, presence of borate
ion occurs, which reaches maximum adsorption at pH 8.5-9(2). Field studies have observed boron to leach readily in
soil(1); undissociated boric acid is transported in soil with little adsorption(2). Volatilization of boric acid from moist soil
surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.6X10-12 atm-
cu m/mole(SRC), based upon its vapor pressure, 1.6X10-6 mm Hg(3), and water solubility, 5X10+4 mg/L(4). Boric acid is
not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure. No biotransformation processes have
been reported for boron compounds, including boric acid(2).
Acid, and Borates. Online Posting Date: 15 April 2011 (2) WHO; Environmental Health Criteria Document No. 204 (1998): Boron (7740-
42-8). Available from, as of Oct 4, 2011: http://www.inchem.org/pages/ehc.html (3) Pankajavalli R et al; J Nuclear Materials 362: 128-
131 (2007) (4) Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187 (1990)
 from HSDB
AQUATIC FATE: The pKa of boric acid is 9.24 at 25 deg C(1), indicating that this compound will exist primarily in the
undissociated form at an environmental pH range between 5 and 9, although the anion form will partially exist in alkaline
waters(SRC). Boric acid leaches readily in soils(2) which indicates adsorption to suspended solids and sediment in water
will not be an important fate process(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated
Henry's Law constant of 2.6X10-12 atm-cu m/mole(SRC), derived from its vapor pressure, 1.6X10-6 mm Hg(4), and water
solubility, 5X10+4 mg/L(5). However, evaporation of seawater itself is reported to be the biggest environmental
contribution of boric acid to air(2). No biotransformation processes have been reported for boron compounds, including
boric acid(2).
Acid, and Borates. Online Posting Date: 15 April 2011 (2) WHO; Environmental Health Criteria Document No. 204 (1998): Boron (7740-
42-8). Available from, as of Oct 4, 2011: http://www.inchem.org/pages/ehc.html (3) Lyman WJ et al; Handbook of Chemical Property
Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990) (4) Pankajavalli R et al; J Nuclear Materials 362: 128-
131 (2007) (5) Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187 (1990)
 from HSDB
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), boric acid, which has a vapor pressure of 1.6X10-6 mm Hg at 25 deg C(2), will exist in both the vapor and
particulate phases in the ambient atmosphere. One monitoring study found that approximately 90% of boric acid in the
atmosphere is in gaseous form and 10% in particulate form(3). Vapor-phase boric acid is degraded in the atmosphere by
reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be
about 38 days(SRC), calculated from its rate constant of 4.2X10-13 cu cm/molecule-sec at 25 deg C(SRC) that was derived
using a structure estimation method(4). Particulate-phase boric acid may be removed from the air by wet or dry
deposition(SRC).
(1) Bidleman TF; Environ Sci Technol 22: 361-367 (1988) (2) Pankajavalli R et al; J Nuclear Materials 362: 128-131 (2007) (3) Anderson
DL et al; Atmos Environ 28: 1401-1410 (1994) (4) Meylan WM, Howard PH; Chemosphere 26: 2293-99 (1993)
 from HSDB
14.2.6 Biodegredation
No biotransformation processes have been reported for boron compounds(1). Boric acid has been shown to be a mild
antiseptic agent with bacteriostatic action(2). A concentration beyond 10 mg/L produces toxicity to activated sludge
cultures(3).
(1) WHO; Environmental Health Criteria 204, Boron. World Health Org (1998) Available from, as of Oct 4, 2011:
http://www.inchem.org/documents/ehc/ehc/ehc204.htm (2) Waggott A; Water Res 3: 749-65 (1969) (3) Banerji SK; pp. 1118-1127 in
Proc. of the 24th Ind. Waste Conf. Univ. Ext. Series No. 135 P1118FF (1969)
 from HSDB
14.2.7 Abiotic Degredation
In aqueous solution, boron is normally present as boric acid and borate ions, with the dominant form of inorganic boron
as undissociated boric acid in natural aqueous systems(1). In aqueous solution, boric acid acts as an electron acceptor
(Lewis acid), accepting hydroxide from water to form (B(OH)4)- ion(1). In concentrated solutions (>0.1 M boric acid)
polymeric species are formed(1,2). Photodegradation of boric acid is not a relevant environmental fate process(3).
(1) Choi W, Chen KY; Environ Sci Tech 13: 189-96 (1979) (2) ATSDR; Toxicological Profile for Boron and Compounds. Atlanta, GA:
Agency for Toxic Substances and Disease Registry (1992) Available from, as of Apr 18, 2005: http://www.atsdr.cdc.gov/ (3) US EPA;
EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program. Summary of existing data, proposed
test plan and rationale for cobalt borate neodecanoate complexes (68457-13-6). September, 2005. 201-16042A. Available from, as of
Dec 9, 2005: http://www.epa.gov/chemrtk/metalcarb/c14172rt7.pdf
 from HSDB
The rate constant for the vapor-phase reaction of boric acid with photochemically-produced hydroxyl radicals has been
estimated as 4.2X10-13 cu cm/molecule-sec at 25 deg C(SRC) using a structure estimation method. This corresponds to
an atmospheric half-life of about 38 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1).
(1) Meylan WM, Howard PH; Chemosphere 26: 2293-99 (1993)
 from HSDB
14.2.8 Bioconcentration
Highly water soluble materials are unlikely to bioaccumulate to any significant degree, and borate species are all present
essentially as undissociated boric acid at neutral pH(1). The octanol/water partition coefficient for boric acid has been
measured as 0.175(1), indicating low bioaccumulation potential(1). Boron did not bioaccumulate in 47-day and 21-day
exposure tests using oysters and sockeye salmon respectively(1).
 from HSDB
14.2.9 Soil Adsorption/Mobility
Boric acid adsorption to illite (three-layered clay consisting of two outer layers of hydrated SiO2 and a central layer of
hydrated Al2O3) and kaolinite (alternate layers of SiO2 and Al2O3) clays, as well as activated sludge was studied. The
compound was added to 100 mL flasks corresponding to a boron concentration range of zero to 256 mg/L. It was
observed that kaollinite adsorbed about 40 times (Kd = 0.199 (Freundlich adsorption coefficient)) more boric acid than
illinite (Kd = 0.005) at pH 7; five times as much boric acid adsorbed to activated sludge (Kd = 0.025) as to illinite at pH
7(1). Boron adsorption is influenced by the distribution of boron species (H3BO3; B(OH)4(-)) as well as pH, the type and/or
composition of the solution matrix, and surface properties(2). The pKa of boric acid is 9.24(3), indicating that this
compound will exist primarily in the undissociated form in the environment, but partially in the anion form in alkaline
soils(SRC). However, boric acid is a Lewis acid and therefore behaves as an electron acceptor, rather than a proton
donor(3).
(1) Banerji SK; pp. 1118-1127 in Proc. of the 24th Ind. Waste Conf. Univ. Ext. Series No. 135 P1118FF (1969) (2) Choi W, Chen KY;
Environ Sci Technol 13: 189-96 (1979) (3) Schubert D; Kirk-Othmer Encyclopedia of Chemical Technology. (1999-2011). New York, NY:
John Wiley & Sons; Boron Oxides, Boric Acid, and Borates. Online Posting Date: 15 April 2011
 from HSDB
Adsorption of boron in soils depends on pH, organic content and types of clay and minerals in the soil(1). At acidic pH,
boron exists in solutions in the form of undissociated boric acid; at alkaline pH, presence of borate ion occurs, which
reaches maximum adsorption at pH 8.5-9(1). Field studies have observed boron to leach readily in soil(1).
 from HSDB
14.2.10 Volatilization from Water/Soil

The Henry's Law constant for boric acid is estimated as 2.6X10-12 atm-cu m/mole(SRC) derived from its vapor pressure,
1.6X10-6 mm Hg(1), and water solubility, 5X10+4 mg/L(2). This Henry's Law constant indicates that boric acid is expected
to be essentially nonvolatile from water surfaces(3). Boric acid is not expected to volatilize from dry soil surfaces based
upon its vapor pressure(SRC).
(1) Pankajavalli R et al; J Nuclear Materials 362: 128-131 (2007) (2) Shiu WY et al; Rev Environ Contam Toxicol 116: 15-187 (1990) (3)
Lyman WJ et al; Handbook of Chemical Property Estimation Methods. Washington, DC: Amer Chem Soc pp. 15-1 to 15-29 (1990)
 from HSDB
14.2.11 Water Concentrations
DRINKING WATER: The concentration of boron in tap water ranges from 7 ppb to 0.2 ppm(1).
(1) Choi W, Chen KY; Environ Sci Technol 13: 189-96 (1979)
 from HSDB
SURFACE WATER: A worldwide average concentration of boron in fresh river water is reported to be 13 ppb(1).
 from HSDB
SEAWATER: A worldwide average concentration of boron in seawater is reported to be about 5 mg/L(1).

 from HSDB
14.2.12 Atmospheric Concentrations
SOURCE DOMINATED: A mean boric acid/boric oxide dust concentration of 4.1 mg/cu m has been reported in a boric acid
manufacturing plant(1).
 from HSDB
RURAL/REMOTE: Atmospheric concentrations of boron were measured at continental, coastal, and remote marine sites(1);
mean particulate boron concentrations ranged from 1.8 to 12.2 ng/cu m, from 2.4 to 3.7 ng/cu m, and from <0.5 to 2.8
ng/cu m for the three types of site, respectively; mean gaseous boron concentrations ranged from <0.5 to 20.7 ng/cu m,
from 3.5 to 82.8 ng/cu m, and from 0.6 to 25 ng/cu m, respectively(1).
 from HSDB
14.2.13 Probable Routes of Human Exposure
According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in
the industrial manufacturing, processing, and use of boric acid is 100 to 999; the data may be greatly underestimated(1).
(1) US EPA; Inventory Update Reporting (IUR). Non-confidential 2006 IUR Records by Chemical, including Manufacturing, Processing and
Use Information. Washington, DC: U.S. Environmental Protection Agency. Available from, as of Sept 9, 2011:
http://cfpub.epa.gov/iursearch/index.cfm
 from HSDB
NIOSH (NOES Survey 1981-1983) has statistically estimated that 489,668 workers (211,838 of these are female) are
potentially exposed to boric acid in the US(1). Occupational exposures to boron compounds (including boric acid) occurs
through inhalation of dusts and dermal absorption(2). A mean boric acid/boric oxide dust concentration of 4.1 mg/cu m
has been reported in a boric acid manufacturing plant(2). The general population may be exposed to boric acid through
use of various consumer products containing this compound(SRC). Sodium borate and boric acid are used in various
cosmetic products, including make-up, skin and hair care preparations, deodorants, moisturizing creams, breath
fresheners, and shaving creams; concentrations may be up to 5%(2).
(1) NIOSH; International Safety Cards. Boric acid. CAS No. 10043-35-5 Available from, as of April 19, 2005:
http//www.cdc.gov/niosh/ipcs/nicstart.html (2) WHO; Environmental Health Criteria 204, Boron. World Health Org (1998). Available
from, as of Oct 4, 2011: http://www.inchem.org/documents/ehc/ehc/ehc204.htm
 from HSDB
The products registered for use which contain boric acid as the active ingredient are applied in aquatic, outdoor and
indoor sites (i.e., commercial, industrial, domestic dwellings, food handling establishments, sewage systems, wood
protection treatment to buildings, etc). Depending on the use site, boric acid may be applied using a spreader, fixed-wing
aircraft, knife/spatula, airblower, power duster, squeeze applicator, or aerosol can. Based on the use patterns, the potential
for dermal and inhalation exposure exists, (i.e., exposure to persons applying the products, exposure to humans
reentering the treated areas, etc)(1).
(1) USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document - Boric acid and its Sodium Salts p.28 (February
1994) Available from, as of December 9, 2005. http://www.epa.gov/pesticides/reregistration/status.htm
 from HSDB
14.2.14 Body Burdens
In serum (children): Conventional reference range: < 7 mg/L; international recommended reference range: < 119 umol/L
/From table, borate/
Tietz, N.W. (ed.). Clinical Guide to Laboratory Tests. Philadelphia, PA: W.B. Saunders Co., 1983., p. 88
 from HSDB
In serum (male adult): Conventional reference range: < 2 mg/L; international recommended reference range: < 34 umol/L
/From table, borate/
 from HSDB
In serum (toxic concn): Conventional reference range: > 20 mg/L; international recommended reference range: > 340
umol/L /From table, borate/
 from HSDB
15 Literature
15.1 Depositor Provided PubMed Citations
CLICK TO LOAD...
 from PubChem
15.2 NLM Curated PubMed Citations
CLICK TO LOAD...
 from PubChem
15.3 General References
General Reference
Iavazzo C, Gkegkes ID, Zarkada IM, Falagas ME: Boric acid for recurrent vulvovaginal candidiasis: the clinical evidence. J
Womens Health (Larchmt). 2011 Aug;20(8):1245-55. doi: 10.1089/jwh.2010.2708. Epub 2011 Jul 20.
Abstract: PubMed
 from DrugBank
General Reference
Teshima D, Morishita K, Ueda Y, Futagami K, Higuchi S, Komoda T, Nanishi F, Taniyama T, Yoshitake J, Aoyama T: Clinical
management of boric acid ingestion: pharmacokinetic assessment of efficacy of hemodialysis for treatment of acute boric
acid poisoning. J Pharmacobiodyn. 1992 Jun;15(6):287-94.
Abstract: PubMed
 from DrugBank
General Reference
De Seta F, Schmidt M, Vu B, Essmann M, Larsen B: Antifungal mechanisms supporting boric acid therapy of Candida
vaginitis. J Antimicrob Chemother. 2009 Feb;63(2):325-36. doi: 10.1093/jac/dkn486. Epub 2008 Dec 4.
Abstract: PubMed
 from DrugBank
General Reference
BORIC ACID - National Library of Medicine HSDB Database- Toxnet - NIH
 from DrugBank
General Reference
Boric Acid - National Toxicology Program - NIH
 from DrugBank
15.4 Metabolite References
 Download
1 to 1 of 1
PMID Reference
Yannai, Shmuel. (2004) Dictionary of food compounds

with CD-ROM: Additives, flavors, and ingredients. Boca
Raton: Chapman & Hall/CRC.
15.5 Springer Nature References
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 from Springer Nature
15.6 Chemical Co-Occurrences in Literature
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View More Chemical-Chemical Co-Occurrences and Evidence for Boric Acid
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15.7 Chemical-Disease Co-Occurrences in Literature
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View More Chemical-Disease Co-Occurrences and Evidence for Boric Acid
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15.8 Chemical-Gene Co-Occurrences in Literature
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 from PubChem
16 Patents
16.1 Depositor-Supplied Patent Identifiers
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 from PubChem
17 Biomolecular Interactions and Pathways
17.1 Protein Bound 3-D Structures
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 from PDB
View 24 proteins in NCBI Structure

 from PubChem
18 Biological Test Results
18.1 BioAssay Results
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 from PubChem
19 Classification
19.1 Ontologies
19.1.1 MeSH Tree
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 from MeSH
19.1.2 ChEBI Ontology
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 from ChEBI
19.1.3 KEGG: Drug
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 from KEGG
19.1.4 KEGG: ATC
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19.1.5 KEGG: JP15
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19.1.6 KEGG: Risk Category of Japanese OTC Drugs
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19.1.7 KEGG: OTC drugs
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19.1.8 KEGG: Additive
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19.1.9 KEGG: Animal Drugs
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19.1.10 WHO ATC Classification System

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 from WHO ATC
19.1.11 WIPO IPC
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 from WIPO
19.1.12 EPA Safer Choice
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19.1.13 ChemIDplus
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 from ChemIDplus
19.1.14 CAMEO Chemicals
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19.1.15 ChEMBL Target Tree
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 from ChEMBL
20 Information Sources
1. CAMEO Chemicals /source/CAMEO Chemicals
BORIC ACID
https://cameochemicals.noaa.gov/chemical/8334 https://cameochemicals.noaa.gov/chemical/8334
CAMEO Chemical Reactivity Classification
https://cameochemicals.noaa.gov/browse/react https://cameochemicals.noaa.gov/browse/react
2. ChemIDplus /source/ChemIDplus
Tetraborate
https://chem.nlm.nih.gov/chemidplus/sid/0012258536 https://chem.nlm.nih.gov/chemidplus/sid/0012258536
Boric acid [JAN:NF]
https://chem.nlm.nih.gov/chemidplus/sid/0010043353 https://chem.nlm.nih.gov/chemidplus/sid/0010043353
ChemIDplus Chemical Information Classification
https://chem.sis.nlm.nih.gov/chemidplus/chemidheavy.jsp https://chem.sis.nlm.nih.gov/chemidplus/chemidheavy.jsp
3. DTP/NCI /source/DTP/NCI
BORIC ACID
https://dtp.cancer.gov/dtpstandard/servlet/dwindex?searchtype=NSC&outputformat=html&searchlist=81726
https://dtp.cancer.gov/dtpstandard/servlet/dwindex?searchtype=NSC&outputformat=html&searchlist=81726
4. DrugBank /source/DrugBank
Boric acid
http://www.drugbank.ca/drugs/DB11326 http://www.drugbank.ca/drugs/DB11326
5. EPA Chemicals under the TSCA /source/EPA Chemicals under the TSCA
Boric acid (H3BO3)
http://www.epa.gov/chemical-data-reporting http://www.epa.gov/chemical-data-reporting
6. EPA DSStox /source/EPA DSStox

Boric acid
https://comptox.epa.gov/dashboard/dsstoxdb/results?search=DTXSID1020194 https://comptox.epa.gov/dashboard/dsstoxdb/results?
search=DTXSID1020194
7. European Chemicals Agency (ECHA) /source/European Chemicals Agency (ECHA)

Boric acid
https://echa.europa.eu/substance-information/-/substanceinfo/100.031.209 https://echa.europa.eu/substance-
information/-/substanceinfo/100.031.209
Boric acid
https://echa.europa.eu/substance-information/-/substanceinfo/100.030.114 https://echa.europa.eu/substance-
information/-/substanceinfo/100.030.114
Boric acid
https://echa.europa.eu/information-on-chemicals/cl-inventory-database/-/discli/details/78377 https://echa.europa.eu/information-
on-chemicals/cl-inventory-database/-/discli/details/78377
Boric acid
Boric acid
8. Human Metabolome Database (HMDB) /source/Human Metabolome Database (HMDB)

Boric acid (H3BO3)
http://www.hmdb.ca/metabolites/HMDB0035731 http://www.hmdb.ca/metabolites/HMDB0035731
9. ILO-ICSC /source/ILO-ICSC
BORIC ACID
http://www.ilo.org/dyn/icsc/showcard.display?p_version=2&p_card_id=0991 http://www.ilo.org/dyn/icsc/showcard.display?
p_version=2&p_card_id=0991
10. OSHA Occupational Chemical DB /source/OSHA Occupational Chemical DB

BORIC ACID
http://www.osha.gov/chemicaldata/chemResult.html?RecNo=906 http://www.osha.gov/chemicaldata/chemResult.html?RecNo=906
11. EU Food Improvement Agents /source/EU Food Improvement Agents

BORIC ACID
http://eur-lex.europa.eu/legal-content/EN/ALL/?uri=CELEX%3A32012R0231 http://eur-lex.europa.eu/legal-content/EN/ALL/?
uri=CELEX%3A32012R0231
12. ChEBI /source/ChEBI

Boric acid
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:33118 http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:33118
ChEBI Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
http://www.ebi.ac.uk/chebi/userManualForward.do#ChEBI%20Ontology
13. NCIt /source/NCIt

Boric Acid
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C47416
https://ncit.nci.nih.gov/ncitbrowser/ConceptReport.jsp?dictionary=NCI_Thesaurus&ns=NCI_Thesaurus&code=C47416
14. HSDB /source/HSDB

BORIC ACID
https://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+10043-35-3 https://toxnet.nlm.nih.gov/cgi-
bin/sis/search/r?dbs+hsdb:@term+@rn+@rel+10043-35-3
15. OSHA Chemical Sampling Information /source/OSHA Chemical Sampling Information

Boric Acid
https://www.osha.gov/dts/chemicalsampling/data/CH_221430.html
https://www.osha.gov/dts/chemicalsampling/data/CH_221430.html
16. ClinicalTrials.gov /source/ClinicalTrials.gov

Boric acid
https://clinicaltrials.gov/ https://clinicaltrials.gov/
17. EPA Office of Pesticide Programs /source/EPA Office of Pesticide Programs

The EPA OPP Pesticide Ecotoxicity Database, updated by the Ecological Fate and Effects Division of the EPA Office of Pesticide
Programs, contains all EPA reviewed ecotoxicity endpoints for pesticides registered or previously registered in the U.S. Toxicity data.
Read more. http://www.ipmcenters.org/Ecotox/index.cfm
http://www.ipmcenters.org/Ecotox/index.cfm http://www.ipmcenters.org/Ecotox/index.cfm
18. EU Pesticides Database /source/EU Pesticides Database

Boric acid
http://ec.europa.eu/food/plant/pesticides/eu-pesticides-database/public/?
event=activesubstance.detail&language=EN&selectedID=1039 http://ec.europa.eu/food/plant/pesticides/eu-pesticides-
database/public/?event=activesubstance.detail&language=EN&selectedID=1039
19. EPA Safer Choice /source/EPA Safer Choice

Orthoboric acid
https://www.epa.gov/saferchoice/safer-ingredients https://www.epa.gov/saferchoice/safer-ingredients
EPA Safer Chemical Ingredients Classification
https://www.epa.gov/saferchoice https://www.epa.gov/saferchoice
20. FAO/WHO Food Additive Evaluations (JECFA) /source/FAO/WHO Food Additive Evaluations
(JECFA)
BORIC ACID
http://apps.who.int/food-additives-contaminants-jecfa-database/chemical.aspx?chemID=1110 http://apps.who.int/food-additives-
contaminants-jecfa-database/chemical.aspx?chemID=1110
21. Wikipedia /source/Wikipedia

orthoboric acid
https://en.wikipedia.org/wiki/Boric_acid https://en.wikipedia.org/wiki/Boric_acid
tetraborate
https://www.wikidata.org/wiki/Q27077623 https://www.wikidata.org/wiki/Q27077623
22. Hazardous Chemical Information System (HCIS), Safe Work Australia /source/Hazardous Chemical
Information System (HCIS), Safe Work Australia
boric acid
http://hcis.safeworkaustralia.gov.au/HazardousChemical/Details?chemicalID=622
23. NITE-CMC /source/NITE-CMC

Boric acid
http://www.safe.nite.go.jp/english/ghs/13-mhlw-2047e.html http://www.safe.nite.go.jp/english/ghs/13-mhlw-2047e.html
24. Safe Work Australia - HCIS /source/Safe Work Australia - HCIS

boric acid
25. FDA/SPL Indexing Data /source/FDA/SPL Indexing Data

R57ZHV85D4
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/
https://www.fda.gov/ForIndustry/DataStandards/SubstanceRegistrationSystem-UniqueIngredientIdentifierUNII/
26. NIST /source/NIST

Boric acid
http://www.nist.gov/srd/nist1a.cfm http://www.nist.gov/srd/nist1a.cfm
27. PDB /source/PDB

The Protein Data Bank (PDB) is a crystallographic database for the three-dimensional structural data of large biological molecules,
such as proteins and nucleic acids
http://www.rcsb.org/ligand/BO3 http://www.rcsb.org/ligand/BO3
28. SpectraBase /source/SpectraBase

https://spectrabase.com/spectrum/CAm364A0h4Y https://spectrabase.com/spectrum/CAm364A0h4Y
https://spectrabase.com/spectrum/3Su1jap05kG https://spectrabase.com/spectrum/3Su1jap05kG
https://spectrabase.com/spectrum/LpYjIGzBVPT https://spectrabase.com/spectrum/LpYjIGzBVPT
https://spectrabase.com/spectrum/59Ki4te2IA6 https://spectrabase.com/spectrum/59Ki4te2IA6
https://spectrabase.com/spectrum/DPisNt3tfM9 https://spectrabase.com/spectrum/DPisNt3tfM9
https://spectrabase.com/spectrum/3mEmRkeuaM4 https://spectrabase.com/spectrum/3mEmRkeuaM4
https://spectrabase.com/spectrum/Im8D7wwnQls https://spectrabase.com/spectrum/Im8D7wwnQls
https://spectrabase.com/spectrum/BrLfIGCdgvQ https://spectrabase.com/spectrum/BrLfIGCdgvQ
https://spectrabase.com/spectrum/4ki21gdjRzz https://spectrabase.com/spectrum/4ki21gdjRzz
29. Springer Nature /source/Springer Nature

Literature references related to scientific contents from Springer Nature journals and books. Read more ... https://link.springer.com/
30. The Cambridge Structural Database /source/The Cambridge Structural Database

The Cambridge Structural Database provides access to 3D structures of molecules determined experimentally using diffraction
techniques.
http://www.ccdc.cam.ac.uk/pages/Home.aspx http://www.ccdc.cam.ac.uk/pages/Home.aspx
31. The National Institute for Occupational Safety and Health (NIOSH) /source/The National Institute
for Occupational Safety and Health (NIOSH)
Boric acid
https://www.cdc.gov/niosh-rtecs/ED456D70.html https://www.cdc.gov/niosh-rtecs/ED456D70.html
32. WHO ATC /source/WHO ATC

https://www.whocc.no/atc/ https://www.whocc.no/atc/
ATC Code
https://www.whocc.no/atc_ddd_index/ https://www.whocc.no/atc_ddd_index/
33. PubChem
Data deposited in or computed by PubChem
https://pubchem.ncbi.nlm.nih.gov https://pubchem.ncbi.nlm.nih.gov
34. MeSH /source/MeSH

boric acid
https://www.ncbi.nlm.nih.gov/mesh/67032688 https://www.ncbi.nlm.nih.gov/mesh/67032688
MeSH Tree
http://www.nlm.nih.gov/mesh/meshhome.html http://www.nlm.nih.gov/mesh/meshhome.html
Insecticides
https://www.ncbi.nlm.nih.gov/mesh/68007306 https://www.ncbi.nlm.nih.gov/mesh/68007306
35. KEGG /source/KEGG

Therapeutic category of drugs in Japan
http://www.genome.jp/kegg-bin/get_htext?br08301.keg http://www.genome.jp/kegg-bin/get_htext?br08301.keg
Anatomical Therapeutic Chemical (ATC) classification
Drugs listed in the Japanese Pharmacopoeia
Risk category of Japanese OTC drugs
Classification of Japanese OTC drugs
Animal drugs in Japan
Pharmaceutical additives in Japan
36. WIPO /source/WIPO

International Patent Classification
http://www.wipo.int/classifications/ipc/ http://www.wipo.int/classifications/ipc/
37. ChEMBL /source/ChEMBL

Target Tree
https://www.ebi.ac.uk/chembl/target/browser https://www.ebi.ac.uk/chembl/target/browser
38. NCBI
LinkOut is a service that allows one to link directly from NCBI databases to a wide range of information and services beyond NCBI
systems.
https://www.ncbi.nlm.nih.gov/projects/linkout https://www.ncbi.nlm.nih.gov/projects/linkout

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Boric Acid  Cite this Record

PubChem CID: 7628

Molecular Formula: H3BO3 or undefined or B(OH)3 or BH3O3

Safety Summary: Laboratory Chemical Safety Summary (LCSS)

 3 Names and Identifiers

4 Chemical and Physical Properties

7 Drug and Medication Information

8 Food Additives and Ingredients

10 Pharmacology and Biochemistry

11 Use and Manufacturing

13 Safety and Hazards

17 Biomolecular Interactions and Pathways

18 Biological Test Results

3.1 Computed Descriptors

3.1.1 IUPAC Name

3.1.3 InChI Key

3.1.4 Canonical SMILES

3.2 Molecular Formula

3.3 Other Identifiers

3.3.3 ICSC Number

3.3.4 NSC Number

3.3.5 RTECS Number

Title boric acid

Title orthoboric acid

Description chemical compound

3.4.1 MeSH Entry Terms

3.4.2 Depositor-Supplied Synonyms

1. BORIC ACID 11. Trihydroxyborone 21. Trihydroxyborane 31. Borsaure [German]

4.1 Computed Properties

Property Name Property Value

Molecular Weight 61.831 g/mol

Hydrogen Bond Donor Count 3

Hydrogen Bond Acceptor Count 3

Rotatable Bond Count 0

Topological Polar Surface Area 60.7 A^2

Monoisotopic Mass 62.018 g/mol

Exact Mass 62.018 g/mol

Compound Is Canonicalized true

Heavy Atom Count 4

Defined Atom Stereocenter Count 0

Undefined Atom Stereocenter Count 0

Defined Bond Stereocenter Count 0

Undefined Bond Stereocenter Count 0

Isotope Atom Count 0

Covalently-Bonded Unit Count 1

4.2 Experimental Properties

4.2.1 Physical Description

 from EPA Chemicals under the TSCA

ODOURLESS COLOURLESS CRYSTALS OR WHITE POWDER.

Odorless white solid.

Colorless, transparent crystals or white granules or powder

Colorless triclinic crystals

White waxy triclinic solid plates

572° F at 760 mm Hg (decomposes) (NTP, 1992)

4.2.6 Melting Point

340° F (NTP, 1992)

10 to 50 mg/mL at 66° F (NTP, 1992)