Borax 7

Human Health and Ecological
Risk Assessment for

Borax (Sporax)
FINAL REPORT
USDA, Forest Service
Forest Health Protection

USDA Forest Service
Rosslyn Plaza Building C, Room 7129C
1601 North Kent Street
Arlington, VA 22209
February 24, 2006
Contributors
This document was originally prepared by Syracuse Environmental Research Associates, Inc.
(SERA Inc.) under USDA Purchase Order No. AG-3187-P-05-0249. The documented was
drafted by Drs. Patrick R. Durkin (SERA Inc.) and Julie Klotzbach (currently with Syracuse
Environmental Research Associates). The initial draft was reviewed externally by Drs. Rolf
Hartung and Joseph Santodonato. In addition, the initial draft document was reviewed by
USDA/Forest Service personnel: Dr. Hank Appleton, Dr. Paul Mistretta, Mr. Dave Bakke, and
Mr. Rog Siemers. The revised final report was submitted to the USDA Forest Service as SERA
TR 04-43-21/06-30-02b dated February 24, 2006.
TABLE OF CONTENTS
TABLE OF CONTENTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ii
LIST OF TABLES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
LIST OF APPENDICES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
LIST OF WORKSHEETS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
ACRONYMS, ABBREVIATIONS, AND SYMBOLS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi
COMMON UNIT CONVERSIONS AND ABBREVIATIONS . . . . . . . . . . . . . . . . . . . . . . . . viii
CONVERSION OF SCIENTIFIC NOTATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
EXECUTIVE SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . x
1. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1-1
2. PROGRAM DESCRIPTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1. OVERVIEW . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2. CHEMICAL DESCRIPTION AND COMMERCIAL FORMULATIONS . . . . .
2.3. APPLICATION METHODS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.4. MIXING AND APPLICATION RATES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.5. USE STATISTICS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2-1
2-1
2-1
2-2
2-2
2-2
3. HUMAN HEALTH RISK ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-1

3.1. HAZARD IDENTIFICATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-1
3.1.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-1
3.1.2. Mechanism of Action. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-2
3.1.3. Kinetics and Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-2
3.1.3.1. Pharmacokinetic Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-2
3.1.3.2. Dermal Absorption Rates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-3
3.1.4. Acute Oral Toxicity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-3
3.1.5. Subchronic or Chronic Systemic Toxic Effects. . . . . . . . . . . . . . . . . . . . 3-5
3.1.6. Effects on Nervous System. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-6
3.1.7. Effects on Immune System. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-7
3.1.8. Effects on Endocrine System. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-7
3.1.9. Reproductive and Teratogenic Effects. . . . . . . . . . . . . . . . . . . . . . . . . . . 3-8
3.1.10. Carcinogenicity and Mutagenicity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-9
3.1.11. Irritation and Sensitization (Effects on the Skin and Eyes). . . . . . . . . 3-10
ii
TABLE OF CONTENTS (continued)

3.1.12.
3.1.13.
3.1.14.
3.1.15.
Systemic Toxic Effects from Dermal Exposure. . . . . . . . . . . . . . . . .

Inhalation Exposure. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Inerts and Adjuvants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Impurities and Metabolites. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1.15.1 Impurities. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1.15.2 Metabolites. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1.16. Toxicologic Interactions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3-10
3-10
3-11
3-11
3-11
3-11
3-11
3.2. EXPOSURE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.2.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.2. Workers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.3. General Public. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.3.1. General Considerations and Normal Levels of Exposure . . .
3.2.3.2. Oral Exposure of Sporax Applied to Tree Stumps . . . . . . . .
3.2.3.3. Contaminated Water . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.3.3.1. Accidental Spill . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.3.3.2. Gleams Modeling . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.3.3.3. Other Modeling Efforts and Monitoring Data . . . . .
3.2.3.3.4. Concentrations of Boron in Water Used
for Risk Assessment . . . . . . . . . . . . . . . . . . . .
3.2.3.4. Background Levels of Exposure . . . . . . . . . . . . . . . . . . . . . .
3-12
3-12
3-13
3-14
3-14
3-14
3-15
3-16
3-15
3-17
3.3. DOSE-RESPONSE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.3.1. Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3.2. Chronic RfD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3.3. Acute RfD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3-21
3-21
3-21
3-22
3.4. RISK CHARACTERIZATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.4.1. Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.2. Workers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.3. General Public. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.4. Sensitive Subgroups. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.5. Connected Actions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4.6. Cumulative Effects. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3-24
3-24
3-24
3-26
3-27
3-27
3-27
3-18
3-18
4. ECOLOGICAL RISK ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4.1. HAZARD IDENTIFICATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.2. Toxicity to Terrestrial Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.2.1. Mammals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.2.2. Birds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
iii
4-1
4-1
4-1
4-2
4-2
4-3

4.1.2.3. Terrestrial Invertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.2.4. Terrestrial Plants (Macrophytes) . . . . . . . . . . . . . . . . . . . . . . .
4.1.2.5. Terrestrial Microorganisms . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3. Aquatic Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3.1. Fish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3.2. Amphibians . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3.3. Aquatic Invertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3.4. Aquatic Plants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1.3.5. Microorganisms (other than algae) . . . . . . . . . . . . . . . . . . . . .
4-4
4-4
4-5
4-5
4-5
4-6
4-6
4-7
4-7
4.2. EXPOSURE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-8

4.2.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-8
4.2.2. Terrestrial Vertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-9
4.2.2.1. Oral Exposure to Sporax Applied to Tree Stumps . . . . . . . . . . 4-9
4.2.2.2. Ingestion of Contaminated Water . . . . . . . . . . . . . . . . . . . . . 4-10
4.2.3. Terrestrial Plants. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-10
4.2.4 Other Terrestrial Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-11
4.2.5. Aquatic Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-11
4.3. DOSE-RESPONSE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2. Toxicity to Terrestrial Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2.1. Mammals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2.2. Birds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2.3. Terrestrial Invertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2.4. Terrestrial Plants and Soil Microorganisms . . . . . . . . . . . . . .
4.3.3. Aquatic Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3.1. Fish . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3.2. Aquatic Invertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3.3. Amphibians . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3.4. Aquatic Plants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3.5. Aquatic Microorganisms . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4. RISK CHARACTERIZATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.1. Overview. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2. Terrestrial Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2.1. Terrestrial Vertebrates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2.2. Terrestrial Plants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2.3. Other Terrestrial Organisms . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.3. Aquatic Organisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.3.1. Aquatic Animals . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.3.2. Aquatic Plants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.3.2. Aquatic Microorganisms Plants . . . . . . . . . . . . . . . . . . . . . . .
4-12
4-12
4-13
4-13
4-13
4-15
4-15
4-15
4-15
4-16
4-16
4-17
4-17
4-18
4-18
4-19
4-19
4-19
4-20
4-20
4-20
4-21
4-21
5. REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5-1
iv

LIST OF TABLES
Table 2-1: Selected physical and chemical properties of borax . . . . . . . . . . . . . . . . . . . . . Tables-1
Table 2-2: Summary of the Use of Borax by the Forest Service from 2000 to 2002 . . . . Tables-1
Table 3-1: Chemical and site parameters used in GLEAMS modeling for modeling
Borax as boric acid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tables-2
Table 3-2: Summary of modeled concentrations of borax and boron equivalents in
ponds at an application rate of 1 lb/acre . . . . . . . . . . . . . . . . . . . . . . . . . . Tables-3
Table 3-3: Estimated Environmental Concentrations of boron equivalents in surface water
at an application rate of 1 lb/acre of Borax . . . . . . . . . . . . . . . . . . . . . . . . Tables-4
Table 3-4: Estimated background concentrations of boron in environmental media and
normal intakes of boron relative to exposure scenarios in this
risk assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tables-5
Table 4-1: Summary of modeled concentrations of boric acid in soil . . . . . . . . . . . . . . . . Tables-6
Table 4-2: Summary of borax toxicity values used in ecological risk assessment . . . . . . Tables-7
Table 4-3: Risk Characterization for Terrestrial Plants . . . . . . . . . . . . . . . . . . . . . . . . . . . Tables-8
Table 4-4: Risk Characterization for Acute exposure of Aquatic Microorganisms . . . . . . Tables-9
NOTE: Tables are placed after Section 5, References.
LIST OF APPENDICES
Appendix 1:
Toxicity of borax and boric acid to experimental animals
Appendix 2:
Toxicity of borax and boric acid to birds
Appendix 3:
Toxicity of boric acid to terrestrial invertebrates
Appendix 4:
Toxicity of borax and boric acid to terrestrial plants
Appendix 5:
Toxicity of borax and boric acid to fish and amphibians
Appendix 6:
Toxicity of borax and boric acid to aquatic invertebrates
Appendix 7:
Toxicity of borate compounds to aquatic plants
Supplement 1:
WORKSHEETS
Borax -EXCEL Worksheets for Human Health and Ecological Risk
Assessments, SERA EXWS 05-43-30-02a, Version 4.4. Dated February
11, 2006
v
ACRONYMS, ABBREVIATIONS, AND SYMBOLS

ACGIH
a.e.
AEL
a.i.
ALS
ATSDR
B
BCF
bw
CBI
CI
cm
CNS
DAA
DAT
d.f.
ECx
EC25
EC50
ExToxNet
F
FH
FIFRA
FOIA
FQPA
g
ha
HQ
IAA
IARC
IRIS
ka
ke
kg
Ko/c
Ko/w
Kp
L
lb
LC50
LD50
American Conference of Governmental Industrial Hygienists

acid equivalents
adverse-effect level
active ingredient
acetolactate synthase
Agency for Toxic Substances and Disease Registry
boron
bioconcentration factor
body weight
confidential business information
confidence interval
centimeter
central nervous system
days after application
days after treatment
degrees of freedom
concentration causing X% inhibition of a process
concentration causing 25% inhibition of a process
concentration causing 50% inhibition of a process
Extension Toxicology Network
female
Forest Health
Federal Insecticide, Fungicide and Rodenticide Act
Freedom of Information Act
Food Quality Protection Act
gram
hectare
hazard quotient
indole-3-acetic acid
International Agency for Research on Cancer
Integrated Risk Information System
absorption coefficient
elimination coefficient
kilogram
organic carbon partition coefficient
octanol-water partition coefficient
skin permeability coefficient
liter
pound
lethal concentration, 50% kill
lethal dose, 50% kill
vi
ACRONYMS, ABBREVIATIONS, AND SYMBOLS (continued)

LOAEL
LOC
m
M
MMAD
MCS
mg/kg/day
mg B/kg/day
mL
mM
MOS
MRID
MSDS
MW
NCAP
NCI
NIOSH
NOAEL
NOEC
NOEL
NOS
NRC
NTP
OM
OPP
OPPTS
OSHA
ppm
RBC
RED
lowest-observed-adverse-effect level
level of concern
meter
male
mass median aerodynamic diameter
multiple chemical sensitivity mg
milligram
milligrams of agent per kilogram of body weight per day
milligrams of boron per kilogram of body weight per day
milliliter
millimole
margin of safety
Master Record Identification Number
material safety data sheet
molecular weight
Northwest Coalition for Alternatives to Pesticides
National Cancer Institute
National Institute for Occupational Safety and Health
no-observed-adverse-effect level
no-observed-effect concentration
no-observed-effect level
not otherwise specified
National Research Council
National Toxicology Program
organic matter
Office of Pesticide Programs
Office of Pesticide Planning and Toxic Substances
Occupational Safety and Health Administration
parts per million
red blood cells
re-registration eligibility decision
RfD
SERA
SGOT
SGPT
SRC
UF
U.S.
USDA
U.S. EPA
USGS
WCR
WHO
:
reference dose
Syracuse Environmental Research Associates
serum glutamic oxaloacetic transaminase
serum glutamic pyruvic transaminase
Syracuse Research Corporation
uncertainty factor
United States
U.S. Department of Agriculture
U.S. Environmental Protection Agency
U.S. Geological Survey
water contamination rate
World Health Organization
micron
vii
COMMON UNIT CONVERSIONS AND ABBREVIATIONS

To convert ...
acres
acres
atmospheres
centigrade
centimeters
cubic meters (m3 )
Fahrenheit
feet per second (ft/sec)
gallons (gal)
gallons per acre (gal/acre)
grams (g)
grams (g)
hectares (ha)
inches (in)
kilograms (kg)
kilograms (kg)
kilograms per hectare (hg/ha)
kilometers (km)
liters (L)
liters (L)
liters (L)
miles (mi)
miles per hour (mi/hr)
milligrams (mg)
meters (m)
ounces (oz)
ounces per acre (oz/acre)
ounces per acre (oz/acre)
ounces fluid
pounds (lb)
pounds (lb)
pounds per acre (lb/acre)
pounds per gallon (lb/gal)
square centimeters (cm2 )
square centimeters (cm2 )
square meters (m2)
yards
Into ...
hectares (ha)
square meters (m2 )
millimeters of mercury
Fahrenheit
inches
liters (L)
centigrade
miles/hour (mi/hr)
liters (L)
liters per hectare (L/ha)
ounces, (oz)
pounds, (oz)
acres
centimeters (cm)
ounces, (oz)
pounds, (lb)
miles (mi)
cubic centimeters (cm3 )
gallons (gal)
ounces, fluid (oz)
kilometers (km)
cm/sec
ounces (oz)
feet
grams (g)
grams per hectare (g/ha)
kilograms per hectare (kg/ha)
cubic centimeters (cm3 )
grams (g)
kilograms (kg)
kilograms per hectare (kg/ha)
mg/square meter (mg/m2 )
:g/square centimeter (:g/cm2 )
grams per liter (g/L)
square inches (in2 )
square meters (m2 )
square centimeters (cm2)
meters
Multiply by ...
0.4047
4,047
760
1.8 C+32
0.3937
1,000
0.556 F-17.8
0.6818
3.785
9.34
0.03527
0.002205
2.471
2.540
35.274
2.2046
0.892
0.6214
1,000
0.2642
33.814
1.609
44.70
0.000035
3.281
28.3495
70.1
0.0701
29.5735
453.6
0.4536
1.121
112.1
11.21
119.8
0.155
0.0001
10,000
0.9144
Note: All references to pounds and ounces refer to avoirdupois weights unless otherwise specified.
viii
CONVERSION OF SCIENTIFIC NOTATION

Scientific
Notation
1 @ 10-10
1 @ 10-9
1 @ 10-8
1 @ 10-7
1 @ 10-6
1 @ 10-5
1 @ 10-4
1 @ 10-3
1 @ 10-2
1 @ 10-1
1 @ 100
1 @ 101
1 @ 102
1 @ 103
1 @ 104
1 @ 105
1 @ 106
1 @ 107
1 @ 108
1 @ 109
1 @ 1010
Decimal
Equivalent
0.0000000001
0.000000001
0.00000001
0.0000001
0.000001
0.00001
0.0001
0.001
0.01
0.1
1
10
100
1,000
10,000
100,000
1,000,000
10,000,000
100,000,000
1,000,000,000
10,000,000,000
ix
Verbal
Expression
One in ten billion
One in one billion
One in one hundred million
One in ten million
One in one million
One in one hundred thousand
One in ten thousand
One in one thousand
One in one hundred
One in ten
One
Ten
One hundred
One thousand
Ten thousand
One hundred thousand
One million
Ten million
One hundred million
One billion
Ten billion
EXECUTIVE SUMMARY
OVERVIEW
The primary focus of this risk assessment is use of sodium tetraborate decahydrate to treat
annosum root disease. Sodium tetraborate decahydrate, also know as borax, is the active
ingredient and sole constituent in Sporax, the commercial formulation used by the Forest Service.
While this risk assessment nominally concerns Sporax or borax, the agent of toxicologic concern
is boron and exposures as well as toxicity information are expressed as boron equivalents in the
analysis of risk.
Unlike most other risk assessments on pesticides used by the Forest Service, the agent of
toxicologic concern in Sporax i.e., boron occurs naturally and exposures to boron are
unavoidable. Except for the most extreme exposure scenario considered in this risk assessment
i.e., the direct consumption of Sporax from a tree stump by a child the use of Sporax in Forest
Service programs will not substantially contribute to boron exposures in humans. In addition, the
use of Sporax in Forest Service programs will not typically or substantially contribute to
concentrations of boron in water or soil.
The use of Sporax in the control of annosum root disease does not present a significant risk to
humans or wildlife species under most conditions of normal use, even under the highest
application rate. Given the highly focused application method for Sporax, application of granular
product to cut tree stump surfaces, exposures considered for both the human health and
environmental risk assessments are limited to those which are expected to result in significant
exposure. Thus, the exposure scenarios evaluated in this risk assessment are as follows. For the
human health risk assessment, the exposures considered are worker exposure via spill of granular
product to the lower legs and hands, ingestion of applied Sporax by a child, and exposure via
consumption of water contaminated by an accidental spill or by run-off. For exposure of wildlife
species, the scenarios considered are the direct consumption of applied Sporax and ingestion of
contaminated water by terrestrial vertebrates, exposure of aquatic species by water contaminated
by an accidental spill or by runoff, and exposure of terrestrial plants to soil contaminated by
runoff. The most significant risk of toxicity in both humans and wildlife species results from the
direct consumption of Sporax applied to tree stumps.
For a child that consumes Sporax applied to a tree stump, hazard quotients exceed the level of
concern for small children (HQ range of 2 to 16). Based on the highest exposure value modeled
for this scenario, the estimated exposure to a child ingesting applied Sporax is less than the
lowest reported lethal dose in children by factors of about 11 to 135. For workers and the general
public, none of the other exposure scenarios considered yield hazard quotients that exceed the
level of concern. Thus, based on this analysis, there is no basis for asserting that systemic toxic
effects to workers or the general public will result from either acute or longer-term exposures,
except by direct consumption. Borax can cause eye irritation. Quantitative risk assessments for
irritation are not derived; however, from a practical perspective, eye irritation is likely to be the
only overt effect as a consequence of mishandling Sporax. This effect can be minimized or
avoided by prudent industrial hygiene practices during the handling of the compound.
x
For terrestrial species, risk associated with the application of Sporax to tree stumps appear to be
very low. Most risk quotients are range from 0.000003 to 0.005 and are below the level of
concern by factors of about 200 to over 330,000. There also does not appear to be a risk to
terrestrial plants exposed to boron through runoff of Sporax applied to tree stumps; however, this
assessment is based on relatively limited toxicity data. Since borax is used effectively in the
control of fungi and insects, adverse effects of environmental exposures to nontarget insects and
microorganisms are possible. However, given the atypical application method for Sporax,
widespread exposures are not likely.
For aquatic animals and plants, hazard quotients marginally exceed the level of concern for
amphibians for the worst-case accidental spill of 25 pounds of Sporax into a small pond (HQ,
1.3) and for the sensitive species of microorganisms for all accidental spill scenarios (HQs
ranging from about 1 to 4). None of the other exposure scenarios results in hazard quotients that
exceed the level of concern in any aquatic species. These results indicate that aquatic animals
and plants are not at risk under the exposure scenarios considered; however, an accidental spill
of large quantities of Sporax into a small pond may result in toxicity in amphibians and sensitive
species of aquatic microorganisms.
PROGRAM DESCRIPTION
The primary focus of this risk assessment is sodium tetraborate decahydrate (Sporax), also
called borax decahydrate or borax. The Forest Service uses Sporax to limit the development of
annosum root disease in conifer stands. Annosum root disease is caused by the fungus
Heterobasidion annosum, which infects cut conifer stumps following thinning or cutting
operations. Treatment of tree stumps with borax prevents annosus spores from establishing
infections in tree stumps. The commercial borate sodium salt formulation currently used by the
Forest Service is Sporax, which contains 100% sodium tetraborate decahydrate.
Sporax is applied to tree stump surfaces by dry application of the solid material. For this risk
assessment, the typical application rate for Sporax will be taken as 1 lb/acre, with a range of 0.1
lb/acre to 5 lbs/acre to reflect plausible ranges that the Forest Service may use. That is, for the
typical application rate of 1 lb/acre, given the density of stumps to be treated in a 1 acre conifer
stand, a total of 1 lb of Sporax will be applied to cut tree stumps in the 1 acre plot. For this risk
assessment, exposures are based on the typical application rate of 1 lb/acre rather than the full
range of application rates. The consequences of varying application rates within the range of 0.1
lb/acre to 5 lbs/acre are considered in the risk characterization for human health and ecological
effects. The Forest Service reported yearly application rates for borax ranging from about 0.111
lb/acre to 1.869 lbs/acre. Thus, the range of application rates calculated from actual use data
encompasses the range of application rates used for this risk assessment (0.1 lb Sporax/acre to 5
lbs Sporax/acre).
xi
HUMAN HEALTH RISK ASSESSMENT

Hazard Identification The toxicity of borate compounds has been extensively studied in both
humans and laboratory animals, with most studies conducted using boric acid and borax. Boric
acid and borax have similar toxicological properties across different species. In order to facilitate
any comparisons between borax and boric acid, data are expressed in terms of the dose or
concentration of borate compound (borax or boric acid) and in terms of boron equivalents (B).
At physiologic pH, borate salts convert almost entirely to unionized boric acid; thus, boric acid
and borate salts have similar toxicologic properties. Inorganic borates are well absorbed
following oral administration, with an oral absorption of greater than 90% of the administered
dose. Borates are not readily absorbed through intact skin but is more quickly absorbed across
abraded skin. Percutaneous absorption of borax from intact human skin was shown to be very
low, with a dermal permeability coefficient of 1.810-7 cm/hr. Boron is also absorbed following
inhalation exposure to borate dust, but absorption does not appear to be complete. Borates are
distributed in body soft tissues and eliminated in the urine, primarily in the form of boric acid,
with a half-life of approximately 12 hours. Due to the excessive energy required to break the
boron-oxygen bond, borates are not metabolized by humans or animals.
Based on the results of acute exposure studies, borax is classified as moderately toxic, with an
LD50 in male rats of 4.5 g borax/kg. Clinical signs of toxicity observed following acute
exposures include depression, ataxia and convulsions. In dogs, acute exposure to borax produced
a strong dose-dependent emetic response. As expected of a compound with low percutaneous
absorption, the LD50 of borax following single dermal application is > 5 g borax/kg in rats and >2
g borax/kg in rabbits. Results of a single inhalation exposure study yield a 4-hour LC50 > 2.0 mg
borax/kg.
Results of developmental, subchronic and chronic toxicity studies show that the primary targets
for borate toxicity are the developing fetus and the male reproductive system. Regarding
developmental effects, gestational exposure of rats, mice, and rabbits to boric acid resulted in
increased fetal deaths, decreased in fetal weight, and increased fetal malformations. The types
of fetal malformations observed include anomalies of the eyes, central nervous system,
cardiovascular system, and axial skeleton in rats, short rib XIII and other skeletal anomalies
pertaining to ribs in mice, and cardiovascular malformations in rabbits. The most sensitive effect
observed following gestational exposure to boric acid is decreased body weight. No mechanisms
has been identified for the developmental effects of borates. Results of subchronic and chronic
toxicity studies show that the testis is the primary target organ for borate compounds in adult
animals. Testicular toxicity is characterized by atrophy of the testes, degeneration of the
seminiferous epithelium, and sterility. Results of reproductive studies show a dose-dependent
decrease in fertility in male rats and dogs, with dogs being slightly more sensitive than rats. At
lower exposure levels, testicular effects and infertility may be reversed, but adverse effects can
persist for at least 8 months at higher exposure levels. Results of one study in rats indicate that
borax exposure may also reduce ovulation in female rats. Although no mechanisms has been
identified for borax-induced toxicity to the male reproductive system, data are consistent with the
xii
Sertoli cell as the primary target. Borax and borate compounds do not appear to act as direct
neurotoxins or cause effects on immune system function. Studies assessing carcinogenic and
mutagenic potential show no carcinogenic or mutagenic activity for borax and other borate
compounds. Borax is not irritating to skin (Toxicity Category 4). Borax can cause severe
irritation to eyes (Toxicity Category 1). In standard mammalian studies to assay ocular irritation,
the damage persisted for the duration of the study i.e., 14 days.
Exposure Assessment Sporax is applied directly to freshly cut tree stumps. Sporax is not
applied as a liquid using backpack, broadcast or aerial spray methods and it is not applied
directly to vegetation. Therefore, many of the standard exposure scenarios that are typically
considered for Forest Service risk assessments, such as direct spray, oral exposure via ingestion
of contaminated vegetation and direct exposure from contaminated vegetation, are not applicable
for this risk assessment. The exposure scenarios used in this risk assessment are those expected
to result in potentially significant exposures considering the application method for Sporax that is
used in Forest Service programs i.e., dry application to the stumps of trees.
As with typical Forest Service risk assessments, exposure scenarios are presented for both
workers and members of the general public. For workers, accidental exposure via direct contact
of the hands and lower legs with granular Sporax during application is the only exposure scenario
considered in this risk assessment. For this scenario, exposure values range from approximately
0.000005 mg B/kg/event for the lower bound limit resulting from a 1-hour exposure to 0.0002
mg B/kg/event for the upper bound resulting from an 8-hour exposure. Other exposure scenarios
are not considered to be reasonably plausible given the atypical application method for Sporax.
For the general public, the exposure scenarios considered quantitatively in this risk assessment
are ingestion of Sporax from tree stumps by a small child and ingestion of contaminated pond
water by a child or a young woman. For ingestion of Sporax from tree stumps by a child,
exposure values range from 0.43 to 3.24 mg B/kg/event and are based on the average daily soil
consumption by a child. For ingestion of contaminated pond water, contamination of water by
both an accidental spill scenario and by runoff from the application site are considered. Acute
exposures values for a small child from ingestion of water contaminated via an accidental spill of
Sporax into a small pond range from 0.015 mg B/kg to 0.14 mg B/kg/event. To determine
exposures to pond water contaminated by runoff of Sporax applied to tree stumps, exposure
estimates are modeled by GLEAMS. For acute exposure of a child ingesting water from a pond
contaminated by runoff, values range from approximately 0.0003 to 0.01 mg B/kg/event. For
chronic exposure of adults ingesting surface waters contaminated by runoff, exposure values
range from approximately 0.00004 to 0.002 mg B/kg/day.
Dose-Response Assessment The U.S. EPA (2004) has recently derived a chronic RfD of
0.2 mg/kg/day for boron (from boric acid and borates), using the combined data of two
developmental toxicity studies in rats using decreased fetal weight as the most sensitive endpoint.
The RfD is based benchmark dose analyses identifying a 5% decrease in mean fetal body weight
compared to control as the benchmark response (BMR) level. The 95% lower bound on the dose
xiii
corresponding to the BMR, i.e., the BMDL05, of 10.3 mg B/kg/day is used as the critical dose
value to calculate the RfD. The uncertainty factor of 66, which considers both the toxicokinetic
and toxicodynamic aspects associated with interspecies and interindividual variability, was
applied to the critical dose to derive the chronic RfD of 0.2 mg B/kg/day. The U.S. EPA has not
derived an acute RfD for boron. Therefore, the chronic RfD of 0.2 mg B/kg/day will also be used
to characterize risks associated with incidents or accidents that involve an exposure period of 1
day.
Risk Characterization For exposures considered in this risk assessment, with the exception of
the accidental exposure of a child via consumption of Sporax from tree stump, all hazard
quotients are below the level of concern. For worker exposure from granular Sporax spilled on
the lower legs and hands, hazard quotients are well below the level of concern. Thus, workers do
not appear to be at risk from Sporax under typical application conditions. Because boron
compounds may be more rapidly absorbed across damaged skin, individuals with large areas of
damaged skin should avoid the application of Sporax or exercise extra caution if they do apply
Sporax or other boron-containing compounds. Borax can cause eye irritation. Quantitative risk
assessments for irritation are not derived; however, from a practical perspective, eye irritation is
likely to be the only overt effect as a consequence of mishandling Sporax. This effect can be
minimized or avoided by prudent industrial hygiene practices during the handling of the
compound.
For the general public, hazard quotients for consumption of Sporax from a tree stump by a child
range from 2 to 16 for ingestion of 50 to 400 mg of Sporax (5.67 to 45.36 mg B/day). These
estimated levels of exposure are below levels of exposure associated with nonlethal effects such
as diarrhea and vomiting by factors of about 4 to 32. Documented lethal doses are in the range
505 mg B/kg/day and 765 mg B/kg/day, factors of about 11 to 135 below the estimated levels of
exposure. Thus, while this exposure scenario raises concern in that the RfD could be
substantially exceeded in a child directly consuming Sporax from a treated stump, the most
likely adverse effects would probably be vomiting and diarrhea.
For consumption of water from a pond contaminated by Sporax due to runoff, none of the hazard
quotients exceed the level of concern, even for the highest application rate of 5 lbs Sporax/acre.
The highest hazard quotient for consumption of water contaminated by an accidental spill is 0.7,
associated with a child consuming water contaminated by the spill of 25 pounds of Sporax into a
small pond. Thus, based on this risk assessment, the only exposure scenario that appears to
present a significant potential risk is exposure by direct consumption under upper bound
conditions.
ECOLOGICAL RISK ASSESSMENT
Hazard Identification Borate salts are rapidly converted to boric acid under conditions
typically found in the environment. At physiologic pH and in most surface waters, exposure of
organisms is primarily to boric acid. Therefore, information on boric acid is reviewed as
appropriate and used as surrogate data in this risk assessment for borax. In order to facilitate any
xiv
comparisons between borax and boric acid, data are expressed in terms of the dose or
In terrestrial mammals, the primary target organ for chronic borax exposure is the testis, with
exposure resulting in decreased male fertility. In birds, acute exposure to borax is practically
non-toxic, with no significant clinical signs of toxicity at dietary concentrations up to 5000 ppm
borax (567 ppm B equivalent to 567 mg B/kg diet). Although limited data are available in birds,
it appears that longer-term dietary exposure to boron compounds results in adverse reproductive
effects in avian species. Very little information is available on the effects of boron compounds
on nontarget terrestrial invertebrates. Based on the results of a single acute topical exposure
study of honey bees (LD50 >362.58 :g boric acid/bee or 41.1 :g B/bee), boric acid is considered
essentially non-toxic. However, given that borax is used in the control of termites, ants and
house flies, toxic effects may occur in other insects.
Boron is an essential trace element for terrestrial plants. The amount of boron required to
produce optimal growth and development varies tremendously between species and even
between strains of the same species. However, excess boron can lead to the development of
phytotoxicity. In most species, there is a narrow range between the amount of boron required for
optimal growth and the amount that is phytotoxic. Standard bioassays for toxicity of boron
compounds to terrestrial plants (Tier I and Tier II seedling emergence or vegetative vigor studies)
were not identified in the available literature. While there are many studies evaluating the
phytotoxicity of boron compounds, few provide data that are useful in a quantitative assessment
of the risk of boron toxicity. Data are available for a limited number of terrestrial plants
potatoes, winter wheat, sugarbeet, poppy, oats and turnip. Based on the lowest reported NOAEC,
the most sensitive species appears to be the potato, with an NOAEC of 5 mg B/kg soil and the
most tolerant species appears to the sugarbeet, with an NOAEC of 20 mg B/kg soil. However, it
is likely that more sensitive and more tolerant species exist.
In fish and aquatic invertebrates, acute exposure to borax and boric acid appears to have a
relatively low order of toxicity. In fish, 96-hour LC50 values range from >100 mg B/L in
razorback suckers and squawfish to >1100 mg B/L in bluegill sunfish. The 48-hour LC50 values
for Daphnia magna range from 126 to 141 mg B/L. Limited information is available on chronic
exposure of fish to boric acid and borax. Chronic reproduction studies in daphnids yield an
NOAEC for reproductive effects of 6 mg B/L.
Relative to the abundant literature on the essential role of boron in terrestrial plants, very little
information is available on the effects of boron compounds on aquatic macrophytes. Short-term
exposure studies were conducted with boric acid in watermilfoil, water buttercup, and
waterweed, with similar LC50 values reported for all three plant species (watermilfoil and
waterweed: 5 mg B/L; water buttercup 10 mg B/L). In algae, the 72-hour LC50 values reported
for Scenedesmus subpicatus range from 34 mg B/L to 52 mg B/L and the 72-hour NOAEC
values range from 10 mg B/L to 24 mg B/L, with similar NOAEC values reported for
Scenedesmus quadricauda and Microcystis aeruginosa.
xv
Exposure Assessment Sporax is applied directly to the surfaces of freshly cut tree stumps.
Sporax is not applied using backpack, broadcast or aerial spray methods and it is not applied
of contaminated prey or vegetation, are not applicable for this risk assessment. The exposure
scenarios used in this risk assessment are those expected to result in substantial exposure
considering the atypical application method for Sporax. Since Sporax is not applied as a spray,
wide-spread exposure of insects is not expected; thus, an exposure assessment for insects has not
been conducted in this risk assessment. Due to a lack of toxicity data, no exposure assessment
was conducted for nontarget soil microorganisms.
For terrestrial vertebrates, two exposure scenarios are considered for this risk assessment: acute
exposure via consumption of Sporax applied to tree stumps, and acute as well as chronic
exposure via exposure to contaminated pond water. Exposure values for acute exposure via
consumption of Sporax applied to a tree stump range from 0.57 mg B/kg/event for a large
mammal to 29 mg B/kg/event for a small bird.
For contamination of water by both an accidental spill scenario and by runoff from the
application site are considered. As noted in the exposure assessment for human health, the use of
Sporax in stump treatments is not likely to have a substantial affect on concentrations of boron in
ambient water. For ingestion of contaminated water via accidental spill, acute exposure values
for a small mammal range from 0.0001 to 0.0004 mg B/kg/event. For acute exposure of a small
mammal via ingestion of water contaminated by runoff, acute exposure values range from
approximately 0.0009 to 0.014 mg B/kg/event. For chronic exposure of a small mammal by
water contaminated by runoff, exposure values range from about 0.0003 to 0.01 mg B/kg/day.
Since Sporax is not applied to vegetation, the only exposure scenario considered for terrestrial
macrophytes is exposure to boron that reaches soil via runoff. Based on the results of GLEAMS
modeling, peak concentrations of boron in soil range from 0.0026 ppm for the lowest value
associated with an application rate of 0.1 lb Sporax/acre to 2.29 ppm in soil for the highest value
associated with an application rate of 5 lbs Sporax/acre.
Exposures to aquatic organisms are based on the same information used to assess the exposure to
terrestrial species from contaminated water. For an accidental spill of Sporax into a small pond,
the central peak estimated concentration of boron in ambient water is 0.64 mg B/L (0.32 - 1.28)
mg B/L (ppm). For contamination of a small pond by runoff, the peak estimated concentration in
ambient water is 30 (6 to 100) g/L after a single application of 1 lb Sporax/acre (0.11 lb
boron/acre). For longer-term exposures, the corresponding longer term concentrations in
ambient water are estimated at about 14 (2 to 70) g/L.
Dose-Response Assessment Borate compounds are relatively non-toxic to mammals and birds.
For mammals, the toxicity values used in the ecological risk assessment are identical to those
used in the human health risk assessments: the 95% lower bound on the dose corresponding to
the BMR, i.e., the BMDL05, of 10.3 mg B/kg/day (the critical dose) for decreased fetal body
xvi
weight (Allen et al. 1996, U.S. EPA 2004) is used to assess both acute and chronic risk. For
birds, the acute NOAEL for boron is taken as 136 mg B/kg based on lack of mortality or clinical
signs of toxicity following 5-day dietary exposure of bobwhite quail to borax. For chronic
exposure of birds, the limited data available suggest that longer-term exposure to boron
compounds can cause testicular toxicity in avian species; however the available studies did not
rigorously investigate the potential for boron compounds to produce testicular toxicity.
Therefore, the mammalian critical dose of 10.3 mg B/kg/day will be used to characterize the risk
of chronic exposure to boron compounds in birds. For terrestrial invertebrates, data used to
characterize risk is from a single contact bioassay in the honey bee, with an NOAEL for mortality
of 677 mg/kg.
Although there is an abundant literature regarding the role of boron as an essential element for
terrestrial plants, standard bioassays on the effects of boron on seedling emergence and
vegetative vigor are not available. Based on the relatively limited information available, the
NOAEC of 5 mg B/kg soil for the potato will be used to characterize risk in the most sensitive
and the NOAEC of 20 mg B/kg soil will be used to assess risk in the most tolerant nontarget
plant species. However, it is likely that more sensitive and more tolerant species exist. Since
borates are effective fungicides, some nontarget soil microorganisms could be affected by
exposure to boron in soil. However, information to adequately assess risk in this class of
organisms is not available.
Toxicity values for aquatic species indicate relatively little difference between fish and aquatic
invertebrates based on acute toxicity. For fish, the acute 96-hour LC50 values are 233 mg B/L
and >1100 mg B/L for sensitive and tolerant species, respectively. For aquatic invertebrates, a
similar range in 48-hour LC50 values (133 mg B/L for sensitive species and 1376 mg B/L for
tolerant species) was observed. For chronic exposures, fish appear more sensitive than aquatic
invertebrates to boron exposure. In fish the range of NOAEC values is relatively narrow, with
the NOAEC of 0.5 ppm boron in the most sensitive species and 1.0 ppm boron in the most
tolerant species. In aquatic invertebrates, NOAEC values range from 6 mg B/L to the estimated
value of 61.8 mg B/L. To characterize the risk of acute exposure to amphibians, the NOAEC of
1.0 ppm B obtained in a single study in leopard frog larvae will be used. No studies on the
effects of chronic exposure of amphibians to boron compounds were identified in the available
literature. Based on the available data, the most sensitive algal species is the green algae
Scenedesmus subpicatus, with a 72-hour NOAEC of 10 mg B/L (Bringmann and Kuhn 1978, as
cited in ECETOC 1997) and the most tolerant species is the blue-green alga Microcystis
aeruginosa, with a 72-hour NOAEC of 20.3 mg B/L (Bringmann and Kuhn 1978, as cited in
ECETOC 1997). Although these tests are conducted for a relatively short period of time (i.e. 72
hours), these NOAEC values are applied to both acute and longer-term concentrations because of
the short life-cycle of individual algal cells. For aquatic macrophytes 21-day exposure studies
yield a range of LC50 values of 5 to10 mg B/L; these values will be used to assess acute exposure
risk to sensitive and tolerant aquatic macrophytes. For aquatic microorganisms, the NOAEC
values of 0.3 mg B/L and 291 mg B/L are used to assess the consequences of both acute and
xvii
longer-term exposures for sensitive and tolerant species of aquatic microorganisms because of
the short life-cycle of individual microorganisms.
Risk Characterization For terrestrial species, risk associated with the application of Sporax to
tree stumps appear to be very low. Most risk quotients are range from 0.000003 to 0.005 and are
below the level of concern by factors of about 200 to over 330,000. As discussed in Section
3.2.3.4, this reflects the fact that the use of Sporax in Forest Service programs will not
substantially contribute to or increase concentrations of boron in water or soil beyond those that
are associated with the normal occurrence of boron in the environment. Even in the case of
direct consumption of Sporax from a tree stump by a large mammal, the highest risk quotient is
only 1.1. The hazard quotients for other organisms consuming Sporax i.e., a small mammal, a
small bird, and a large bird range from 0.00004 to 0.08, below the level of concern by factors
of about 12 to 25,000.
There also does not appear to be a risk to terrestrial plants exposed to boron through runoff of
Sporax applied to tree stumps. Although risk to insects and soil microorganisms was not
characterized, since borax is used effectively in the control of fungi and insects, adverse effects
of environmental exposures to insects and nontarget microorganisms are possible. However,
given the atypical application method for Sporax, widespread exposures are not likely.
The exposure scenarios considered for aquatic species are for water contaminated by accidental
spill or by runoff of applied Sporax. Most aquatic animals do not appear to be at risk for any of
the exposure scenarios considered. For amphibians, the level of concern is marginally exceeded
for the accidental spill of 25 pounds of sporax into as small pond (HQ, 1.3). None of the acute or
chronic HQs for exposure via water contaminated by runoff exceed the level of concern for any
aquatic animal. These results indicate that aquatic animals are not at high risk for the exposure
scenarios considered; however, accidental spill of large quantities of Sporax into a small pond
may result in toxicity in amphibians.
For aquatic plants, the highest HQ for any exposure scenario is 0.3 associated with algae for the
accidental spill of 25 pounds of Sporax into a small pond. All other HQs for the accidental spill
scenario and for acute and longer-term exposures to water contaminated by runoff are well below
the level of concern. Thus, based on this analysis, there is no basis for asserting that effects on
aquatic macrophytes or algae are likely for either acute or longer-term exposures. Hazard
quotients for sensitive species of aquatic microorganisms exceed the level of concern for all
accidental spill scenarios, with HQs ranging from 1.1 to 4.3. For tolerant microorganisms, HQs
are well below the level of concern for the worst-case accidental spill scenario. For acute
exposure to water contaminated by runoff based on the maximum application rate of 5 lbs
Sporax/acre, all HQs are below the level of concern for both sensitive and tolerant species. The
results of this risk assessment indicate that more sensitive microorganisms may be at risk
following accidental spill of large quantities of Sporax into a small pond, but that exposure via
runoff does not present a risk to aquatic microorganisms.
xviii
1. INTRODUCTION
Boron-containing compounds, specifically boric acid and its sodium salts, have several
agricultural uses based on their algaecidal, acaricidal, fungicidal, herbicidal and insecticidal
properties. Currently the USDA uses Sporax, a commercial formulation of sodium tetraborate
decahydrate, also called borax, to limit the development of annosus root disease in conifer stands.
Since Sporax is a formulation of 100% sodium tetraborate decahydrate, the terms borax and
Sporax are used interchangeably throughout this document.
Borax (i.e., tetraborate decahydrate) will dissociate in the environment, particularly in aqueous
solutions) and the species of boron containing compounds that will exist will be dependant on the
pH of the aqueous solution. Consequently, the dose response assessments for both human health
and ecological effects are based on boron equivalents rather than borax itself. In this risk
assessment, application rates are always expressed in units of borax rather than boron. Both
exposure values and toxicity values, however, are typically given in units of boron equivalents
and are typically expressed in units such as mg B/kg/day (a dose in units of milligrams of boron
per kilogram body weight) or mg B/L (a concentration in units of milligrams of boron per liter of
water).
In 1993, the US EPA (US EPA 1993a) issued a Reregistration Eligibility Decision document
(RED) addressing eligibility for pesticides containing boric acid and its sodium salts, specifically
boric acid, sodium tetraborate decahydrate (borax decahydrate), sodium tetraborate pentahydrate
(borax pentahydrate), sodium tetraborate (anhydrous), disodium octaborate tetrahydrate,
disodium octaborate (anhydrous), and sodium metaborate. With the exception of sodium
metaborate whose chemical properties differ from the other borate sodium salts, boric acid and
its sodium salts exhibit similar chemical and toxicological properties and potency when the
exposures are expressed in boron equivalent units (US EPA 1993a, WHO 1998). Thus, except
for sodium metaborate, boric acid and it sodium salts are treated as a family of boron-containing
compounds with similar toxicological and environmental fate and transport characteristics (US
EPA 1993a). In this risk assessment, if data gaps exist for borax, information on boric acid is
used as surrogate data. In order to facilitate any comparisons between borax and boric acid, data
are expressed in terms of the dose or concentration of borate compound (borax or boric acid) and
in terms of boron equivalents (B). The conversion factors for deriving boron equivalents are
given in Table 2-1.
In water, boron compounds transform rapidly into borates, with borate speciation dependent upon
pH (ATSDR 1992, WHO 1998). Since several different borate compounds can form once the
borate salts are dissolved in water, information on the environmental fate and transport of
specific borate sodium salts is not available. Therefore, the environmental fate and transport of
borate sodium salts are best described in terms of the environmental fate and transport of boron.
Due to the large body of literature, it is not practical to provide a comprehensive review of the
primary literature on the environmental fate of boron within this risk assessment. However,
comprehensive reviews on the environmental fate and transport of boron are available (ATSDR
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1992, WHO 1998). For this risk assessment, much of the information on environmental boron is
taken from these reviews, although relevant primary literature on boron has been reviewed and
summarized as appropriate. Briefly, boron is a naturally occurring element that is widely
distributed. It is found in oceans, sedimentary rocks, coal, shale, and some soils; boron is most
commonly found in the environment in the form of borate salts (WHO 1998). Boron is released
into the environment through weathering of rocks, volcanic activity and volatilization of
seawater. Small amounts of boron are released from anthropogenic sources. Boron occurs
naturally in fruits, vegetables, and forage crops, and is an essential nutrient for many organisms.
Boron concentrations are approximately 10 mg/kg in the earths crust and 4.5 mg/L in the ocean
(WHO 1998). In fresh surface waters, boron concentrations are highly variable, but generally
range from 1 to 200 ppb (Black et al. 1993, US EPA 1993a). In soil, boron-containing
compounds dissolve in water and are transformed to borates (WHO 1998). Borate compounds
may be transported by percolation, sediment, or runoff from soil to ambient water. Borate
compounds are adsorbed to soils to varying degrees, depending on several factors, including soil
type and water pH (ATSDR 1992).
The toxicity of borax (the sole component of Sproax) has been reviewed in the Reregistration
Eligibility Decision document (RED) for boric acid and its sodium salts (US EPA 1993a).
Comprehensive reviews on the toxicity and environmental fate of boron and boron compounds
are also available (ATSDR 1992; Beyer et al. 1983; Coughlin 1996; Culver and Hubbard 1996;
Dost et al. 1996; ECETOC 1995; 1997; Fail et al. 1998; Hovatter and Ross 1995; Hubbard 1998;
Hubbard and Sullivan 1994, 1996; Moore 1997; Murray 1995; WHO 1998). In addition, risk
assessments for human and ecological effects of boric acid and boric acid salts have been
conducted by the U.S. EPA (U.S. EPA 1993b,c). These documents were obtained and reviewed
for the purpose of conducting this Forest Service risk assessment. In addition, a complete search
of the U.S. EPA files was conducted in the preparation of this risk assessment. Full text copies
of the most relevant studies [n=52] were kindly provided by the U.S. EPA Office of Pesticide
Programs. These studies, in addition to studies published in open literature, were reviewed, and
synopses of the most relevant studies are included in the appendices to this document. Given the
abundant literature on the toxicity of boron-containing compounds, a comprehensive review of
the primary literature was impractical; thus, in preparation of this risk assessment, reviews were
used to provide general information about boron-containing compounds as a class. However,
when relevant information specific to borax was available, primary studies were reviewed.
The relationship between soil boron concentration and effects on terrestrial plants is complex.
As discussed in Section 4.1.2.4, although boron is an essential nutrient for plants, the range
between beneficial and phytotoxic soil boron concentrations is often very narrow. There is an
extensive literature exploring boron requirements for plants, particularly in terrestrial crop
species. Unfortunately, much of the literature investigating the phytotoxic effects of boron in soil
does not provide the appropriate quantitative information for use in assessing risks to terrestrial
plant species; thus, the information used to assess risk of boron in soil to terrestrial plants in this
document is limited.
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Sporax is applied in granular or liquid form directly to the surfaces of freshly cut tree stumps.
Therefore, many of the standard exposure scenarios that are typically considered for Forest
Service risk assessments involving broadcast applications (e.g., direct spray, oral exposure via
ingestion of contaminated prey or vegetation) are not applicable for this risk assessment. The
exposure scenarios used in this risk assessment are those reasonably expected to result in
exposure considering the atypical application method for Sporax.
For the most part, the risk assessment methods used in this document are similar to those used in
risk assessments previously conducted for the Forest Service as well as risk assessments
conducted by other government agencies. Four chapters, including the introduction, program
description, risk assessment for human health effects, and risk assessment for ecological effects
or effects on wildlife species comprise the main body of this document. Each of the two risk
assessment chapters has four major sections, including an identification of the hazards associated
with Sporax, an assessment of potential exposure to the products, an assessment of the doseresponse relationships, and a characterization of the risks associated with plausible levels of
exposure. These sections incorporate the basic steps recommended by the National Research
Council of the National Academy of Sciences (NRC 1983) for conducting and organizing risk
assessments.
This is a technical support document, and it addresses some specialized technical areas.
Nevertheless, an effort was made to ensure that the document can be understood by individuals
who do not have specialized training in the chemical and biological sciences. Certain technical
concepts, methods, and terms common to all parts of the risk assessment are described in plain
language in a separate document (SERA 2001). The general technical terms used in this
document are defined in an environmental glossary available at www.sera-inc.com. Some of the
more complicated terms and concepts are defined, as necessary, in the text.
The information presented in the appendices and the discussions in chapters 2, 3, and 4 of the
risk assessment are intended to be detailed enough to support a review of the risk analyses;
however, they are not intended to be as detailed as the information generally presented in
Chemical Background documents or other comprehensive reviews. Almost no risk estimates
presented in this document are given as single numbers. Usually, risk is expressed as a central
estimate and a range, which is sometimes very large. Because of the need to encompass many
different types of exposure as well as the need to express the uncertainties in the assessment, this
risk assessment involves numerous calculations. Most of the calculations are relatively simple,
and the very simple calculations are included in the body of the document. Some of the
calculations, however, are cumbersome. For those calculations, worksheets are included as an
attachment to the risk assessment. The worksheets provide the detail for the estimates cited in
the body of the document. The worksheets are divided into the following sections: general data
and assumptions, chemical specific data and assumptions, exposure assessments for workers,
exposure assessments for the general public, and exposure assessments for effects on nontarget
organisms. The worksheets for Sporax are contained in an EXCEL workbook and are included
as Supplement 1 to this risk assessment. SERA (2004a) contains documentation for the use of
these worksheets.
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2. PROGRAM DESCRIPTION
2.1. OVERVIEW
The primary focus of this risk assessment is sodium tetraborate decahydrate (Sporax), also
called borax decahydrate or borax. The Forest Service uses Sporax to limit the development of
annosum root disease in conifer stands. Annosum root disease is caused by the fungus
Heterobasidion annosum, which infects cut conifer stumps following thinning or cutting
operations. Treatment of tree stumps with borax prevents annosus spores from establishing
infections in tree stumps (Wilbur-Ellis Company, No Date). The commercial borate sodium salt
formulation currently used by the Forest Service is Sporax, which contains 100% sodium
tetraborate decahydrate.
Sporax is applied to tree stump surfaces by dry application of the solid material. For this risk
assessment, the typical application rate for Sporax will be taken as 1 lb/acre, with a range of 0.1
lb/acre to 5 lbs/acre to reflect plausible ranges that the Forest Service may use. That is, for the
typical application rate of 1 lb/acre, given the density of stumps to be treated in a 1 acre conifer
stand, a total of 1 lb of Sporax will be applied to cut tree stumps in the 1 acre plot. For this risk
assessment, exposures are based on the typical application rate of 1 lb/acre rather than the full
range of application rates. The consequences of varying application rates within the range of 0.1
lb/acre to 5 lbs/acre are considered in the risk characterization for human health (Section 3.4) and
ecological effects (Section 4.4). The Forest Service reported yearly application rates for borax
ranging from 0.111 lb/acre to 1.869 lbs/acre for 2000 to 2002. Thus, the range of application
rates calculated from actual use data encompasses the range of application rates used for this risk
assessment (0.1 lb Sporax/acre to 5 lbs Sporax/acre).
2.2.
CHEMICAL DESCRIPTION AND COMMERCIAL FORMULATIONS
Sporax is registered by the Wilbur-Ellis Company as a fungicide for use in the control of
annosum root disease (Wilbur-Ellis Company, No Date,). Sporax contains 100 % sodium
tetraborate decahydrate (Na2B4O7 C10H20) and has no other active or inert ingredients.
Selected chemical and physical properties of the active ingredient in the Sporax are summarized
in Table 2-1, and the physical and chemical properties that are directly used in this risk
assessment are presented in Worksheet A02. Since borax is applied directly to the stumps of
trees and is not applied by broadcast spray, some of the environmental fate characteristics
typically included in risk assessments, such as foliar half-time, are not applicable for this risk
assessment. The environmental fate and transport of borate sodium salts is best described in
terms of boron (ATSDR 1992, WHO 1998). Additional detailed information on environmental
fate and transport of boron compounds are discussed in the exposure assessments for human
health effects (Section 3.2) as well as ecological effects (Section 4.2). Briefly, in water, boron
compounds transform rapidly into borates; no further transformation is possible.
Borates and boric acid are in pH-dependent equilibrium, with borate speciation dependent upon
pH (ATSDR 1992, WHO 1998). Below pH 7, boric acid and its sodium salts are mainly in the
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form of undissociated boric acid [B(OH)3]. Above pH 6, highly water soluble polyborate ions
such as B3O3(OH)4, B4O5(OH)42, and B5O6(OH)4, may be formed. Polyborates will occur,
however, only at high concentrations (Bodek et al. 1988; WHO 1998). At environmental
concentrations, monomeric anion species will be the most predominant form of boron
compounds. Borate compounds may be transported by percolation, sediment, or runoff from soil
to ambient water. Boron compounds dissolve in water and are transformed to borates (ATSDR
1992). Borate compounds are adsorbed to soils to varying degrees, depending on several factors,
including soil type and water pH (ATSDR 1992). Since borax is converted primarily to boric
acid in water, pertinent information on the environmental fate and transport of both boric acid
and boron are also provided in Table 2-1.
2.3.
APPLICATION METHODS
Sporax can be applied as a solid (dry application) or mixed with water for spray application. In
Forest Service programs, Sporax is applied in a dry application to the surface of freshly cut
stumps. Sufficient material is used to completely cover the surface of the stump (Wilbur-Ellis
Company, No Date). The minimum target concentration in treated stumps for the control of
Heterobasidion annosum is 300 ppm. Some applications of Sporax can lead to much higher
concentrations, on the order of 1000 to 7000 ppm (Cram 2004). Moisture from the exposed
stumps, dew or rain dissolves the product, allowing it to leach into the wood.
2.4. MIXING AND APPLICATION RATE
According to the Sporax product label, for both dry and wet applications, an application rate of 1
pound per 50 square feet of stump surface is recommended. Thus, for spray application methods,
one pound of Sporax should be mixed with enough water to spray 50 square feet of stump
surface.
For this risk assessment, the typical application rate for Sporax will be taken as 1 lb/acre, with a
range of 0.1 lb/acre to 5 lbs/acre to reflect plausible ranges that the Forest Service may use (D.
Bakke 2003, personal communication). For Forest Service applications, given the density of
stumps to be treated in conifer stands, the assumption is that Sporax will be applied at a typical
rate of 1 lb/acre. That is, given the density of stumps to be treated in a conifer stand, 1 lb of
Sporax will be applied to tree stumps in a 1 acre plot. As discussed in Section 2.5, application
rates of 0.1 lb/acre to 5 lbs/acre encompass the range of application rates used by the Forest
Service during 2000 to 2002. For this risk assessment, exposure assessments are based on the
typical application rate of 1 lb/acre rather than the full range of application rates. The
consequences of varying application rates within the range of 0.1 lb/acre to 5 lbs/acre is
considered in the risk characterization for human health (Section 3.4) and ecological effects
(Section 4.4).
2.5. USE STATISTICS
Use of Sporax by the Forest Service from 2000 to 2002 is summarized in Table 2-2. Sporax use
has been reported for Region 5 (Pacific Southwest) and Region 6 (Pacific Northwest). The
average application rate in Region 5 for 2000 to 2002 was 1.1 lbs/acre, approximately 5-fold
2-2
higher than the application rate reported for Region 6 (0.195) for 2000 to 2002. With the
exception of the application rate of 10 lbs/acre for Forest 14 in Region 5 in 2000, the application
rates reported in Table 2-2 range from 0.111 lb/acre to 1.869 lbs/acre. The application rate of 10
lbs/acre appears to be a reporting error and this application rate will not be used in Forest Service
programs.
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3. HUMAN HEALTH RISK ASSESSMENT

3.1. HAZARD IDENTIFICATION
3.1.1. Overview
The toxicity of borate compounds has been extensively studied in both humans and laboratory
animals, with most studies conducted using boric acid and borax. Boric acid and borax have
similar toxicological properties across different species (ATSDR 1992, Fail 1998, Hubbard 1998,
Hubbard and Sullivan 1996, WHO 1998). In the following sections, if data gaps exist for borax,
information on boric acid is reviewed as appropriate and used as surrogate data in this risk
assessment. In order to facilitate any comparisons between borax and boric acid, data are
expressed in terms of the dose or concentration of borate compound (borax or boric acid) and in
terms of boron equivalents (B).
At physiologic pH, borate salts convert almost entirely to unionized boric acid; thus, boric acid
and borate salts have similar toxicologic properties. Inorganic borates are well absorbed
following oral administration, with an oral absorption of greater than 90% of the administered
dose. Borates are not readily absorbed through intact skin but is more quickly absorbed across
abraded skin. Percutaneous absorption of borax from intact human skin was shown to be very
low, with a dermal permeability coefficient of 1.810-7 cm/hr. Boron is also absorbed following
inhalation exposure to borate dust, but absorption does not appear to be complete. Borates are
distributed in body soft tissues and eliminated in the urine, primarily in the form of boric acid,
with a half-life of approximately 12 hours. Due to the excessive energy required to break the
boron-oxygen bond, borates are not metabolized by humans or animals.
Based on the results of acute exposure studies, borax is classified as moderately toxic, with an
LD50 in male rats of 4.5 g borax/kg. Clinical signs of toxicity observed following acute
exposures include depression, ataxia and convulsions. In dogs, acute exposure to borax produced
a strong dose-dependent emetic response. As expected of a compound with low percutaneous
absorption, the LD50 of borax following single dermal application is > 5 g borax/kg in rats and >2
g borax/kg in rabbits. Results of a single inhalation exposure study yield a 4-hour LC50 > 2.0 mg
borax/kg.
Results of developmental, subchronic and chronic toxicity studies show that the primary targets
for borate toxicity are the developing fetus and the male reproductive system. Regarding
developmental effects, gestational exposure of rats, mice, and rabbits to boric acid resulted in
observed following gestational exposure to boric acid is decreased body weight. No mechanisms
has been identified for the developmental effects of borates. Results of subchronic and chronic
toxicity studies show that the testis is the primary target organ for borate compounds in adult
animals. Testicular toxicity is characterized by atrophy of the testes, degeneration of the
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seminiferous epithelium, and sterility. Results of reproductive studies show a dose-dependent

decrease in fertility in male rats and dogs, with dogs being slightly more sensitive than rats. At
lower exposure levels, testicular effects and infertility may be reversed, but adverse effects can
persist for at least 8 months at higher exposure levels. Results of one study in rats indicate that
borax exposure may also reduce ovulation in female rats. Although no mechanisms has been
identified for borax-induced toxicity to the male reproductive system, data are consistent with the
Sertoli cell as the primary target. Borax and borate compounds do not appear to act as direct
neurotoxins or cause effects on immune system function. Studies assessing carcinogenic and
mutagenic potential show no carcinogenic or mutagenic activity for borax and other borate
compounds. Borax is not irritating to skin (Toxicity Category 4). Borax can cause severe
irritation to eyes (Toxicity Category 1). In standard mammalian studies to assay ocular irritation,
the damage persisted for the duration of the study i.e., 14 days.
3.1.2. Mechanism of Action
No mechanism of action for borax or other borate compounds has been identified. Regarding
fungicidal activity against Heterobasidion annosum, borate compounds prevent the germination
of fungal spores on newly cut stumps; however, the mechanism for this effect is unknown.
Regarding toxicity in mammals, as discussed in Sections 3.1.5 and 3.1.9, the reproductive system
is the primary target for boron toxicity, with testicular toxicity and developmental effects as the
predominant findings. No mechanisms has been proposed or identified for the developmental
effects of boron (decrease fetal weight and skeletal malformations). As discussed in Section
3.1.9 (Reproductive and Developmental Effects), borates appear to produce direct effects on
Sertoli cells rather than through alteration of hypothalamic-pituitary-testes axis function
(ECETOC 1995, Fail et al.1998). Although borates have been shown to affect the activity of
several enzymes (Beyer et al. 1983), no association has been made between alterations in
enzymatic activities and testicular toxicity. No mechanism for the phytotoxic action of borates or
the toxicity of borates in aquatic organisms has been identified.
3.1.3. Kinetics and Metabolism
3.1.3.1. Pharmacokinetic Studies The pharmacokinetics of borate compounds have
been extensively studied in both humans and laboratory animals, with several reviews available
in the published literature (ATSDR 1992, Beyer et al. 1983, ECETOC 1995, Fail et al. 1998,
Hubbard 1998, Hubbard and Sullivan 1996, Moore 1997, Murray 1995, WHO 1998). The
kinetics of borate compounds are similar in humans and animals (Hubbard 1998). Borates are
readily absorbed following oral administration and it is generally accepted that oral absorption is
greater than 90% of the administered dose (ATSDR 1992, Moore 1997, WHO 1998). Borates
are not readily absorbed through intact skin. Percutaneous absorption from intact human skin
was shown to be very low, with absorption of approximately 0.2% of the applied dose over a 24
hour period (Wester et al. 1998). Studies on the absorption of borates applied to the intact skin
of rats and rabbits show that percutaneous absorption is negligible (Murray 1995, WHO 1998).
Boron has been shown to be absorbed from abraded or damaged skin of animals (ATSDR 1992,
Hubbard 1998, Murray 1995). However, percutaneous absorption of boron across abraded
human skin was not increased compared to intact skin (Wester 1998). Boron is also absorbed
3-2
following inhalation exposures to borate dust, but absorption does not appear to be complete
(ECETOC 1995, WHO 1998). Following administration of borate compounds, boron is
distributed throughout the soft tissues of the body and does not appear to concentrate in any
particular tissue type (Moore 1997, ECETOC 1995, ). Due to the excessive energy (523 kJ/mol
needed to break the boron-oxygen bond), borates are not metabolized by humans or animals
(ECETOC 1995, Hubbard1998). However, at physiological pH borate salts convert to boric acid
(ECETOC 1995, Hubbard1998, WHO 1998). Borates are excreted almost entirely in the urine,
primarily in the form of boric acid, with a halftime of approximately 12 hours in rats and 13
hours in humans (ATSDR 1992, Hubbard 1998, Moore 1997, WHO 1998).
3.1.3.2. Dermal Absorption Rates A permeability constant (Kp) for borax has been
calculated from a dermal absorption study in human volunteers (Wester et al. 1998). In this
study a radiolabeled 10B-borax solution (5% solution) was applied over a 900 cm2 area of intact
human skin for a 24-hour period; absorption was measured based on recovery of 10B in the urine
over the14 day period following application. Results of this study show that approximately 0.2%
of the applied dose was absorbed, with a Kp of 1.810-7 cm/hr and a flux of 0.009 :g/cm2/hr.
This Kp is considerably lower than the dermal permeability coefficient estimated by U.S. EPA,
with the default assumption for inorganics of 110-3 cm/hr (U.S. EPA 1992). The value given by
U.S. EPA (1992), however, is intended to be used as a plausible upper limit for the Kp in the
absence of experimental data. The study by Wester et al. (1998) using human volunteers is
clearly preferable to the use of the EPA default value. For this risk assessment, the Kp of
1.810-7 cm/hr from the study by Wester et al. (1998) will be used for all exposure assessments
involving dermal exposures (Section 3.2.). Wester et al. (1998) due not provide information on
the variability of the Kp values among individuals. Nonetheless, Wester et al. (1998) due report
varying Kp values for boric acid, borax, and disodium octaborate tetrahydrate with and without
sodium lauryl sulfate pretreatment. The reported Kp values range from 0.910-7 to 210-7 cm/h
(Wester et al. 1998, Table 3, p. 47). In the absence of any other information, this range is used
for the bounds of the Kp value in all exposure assessments in which the Kp is used.
Since Sporax is not applied in a broadcast spray, exposure scenarios involving immersion or
prolonged contact with an aqueous solution are not considered for this risk assessment. The
dermal exposure scenario considered in this risk assessment is associated with accidental contact
of granular Sporax onto the surface of the skin. As detailed further in Section 3.2.2.2, estimates
of dermal absorption are based on Ficks first law and the water solubility of borax.
3.1.4. Acute Toxicity
Information regarding the acute oral toxicity of borax in laboratory mammals is summarized in
Appendix 1. As discussed in Section 3.1.1, if data gaps exist for borax, data obtained in studies
using boric acid will be used as surrogate data. Thus, in order to facilitate comparison between
borax and boric acid, study results are expressed in terms of both borax and boron equivalents
(B).
3-3
Boric acid and borate compounds have a low-to-moderate order of acute oral toxicity (ATSDR
1992, ECETOC 1995, Hubbard 1998, WHO 1998). Although there is an abundance of data on
the acute toxicity of borate compounds, particularly boric acid, only one study investigating the
acute oral toxicity of borax in rats and dogs was identified in the available literature (Weir and
Fisher 1972). Details of this study are provided in Appendix 1. Following administration of
single doses of borax by gavage, the acute LD50 value in male rats was 4.5 g borax/kg (0.51 g
B/kg) and in female rats was 4.98 g borax/kg (0.56 g B/kg). In this same study, the acute toxicity
of boric acid was of a similar magnitude (males rats, 0.60 g B/kg; female rats 0.71 g B/kg).
Similar signs of toxicity, including depression, ataxia and convulsion, were reported for both
borax and boric acid; however, the dose ranges used in this study and the NOAEL and LOAEL
values for these effects were not reported. Administration of single doses of borax (1.54-6.51 g
borax/kg or 0.174-0.736 g B/kg) and boric acid (1.0-3.98 g boric acid /kg or 0.175-0.697 g B/kg)
by capsule to dogs did not cause any deaths during the 14 day observation period following
dosing. However, for both borax and boric acid, a strong emetic response occurred within one
hour of administration of the test material. Therefore, since it is likely that some of the
administered dose was eliminated prior to absorption, interpretation of these results is difficult.
Based on the acute oral LD50 of 4.5 g borax/kg in rats, borax is classified as moderately toxic
(Category III), with an oral LD50 value between 500 and 5,000 mg/kg (U.S. EPA 2003).
In addition to studies on the effects of acute exposure of laboratory mammals to borate
compounds, accidental poisonings in humans provide information on the lethal dose of boric acid
(ATSDR 1992; WHO 1998). As noted by WHO (1998) in a review of the information on
poisonings in humans:
Overall, owing to the wide variability of data collected from poisoning centres,
the average dose of boric acid required to produce clinical symptoms is still
unclear but is presumably within the range of 100 mg to 55.5 g, observed by
Litovitz et al. (1988).
Note that this statement refers to clinical symptoms rather than serious adverse effects. This
range is sufficiently broad to be of little use in the assessment of potential serious adverse effects.
Assuming a 70 kg body weight, the above exposures would correspond to doses of about 1.6
mg/kg/day to 793 mg/kg/day in terms of boric acid. Using a conversion factor of 0.1748 for
boron equivalents (Table 2-1), this would correspond to a range of doses from 0.28 mg B/kg to
139 mg B/kg. As summarized in Section 3.3.2, the lower end of this range is close to the chronic
RfD of 0.2 mg B/kg/day recently derived by the U.S. EPA(2004). Thus, while the upper range of
exposure i.e., 55.5 g of boric acid may be a useful estimate of a dose that would probably be
associated with serious adverse effects, the lower range reported by WHO (1998) appears to be
an artifact of uncertainties in the exposure assessment and this lower bound is not useful for
estimating the plausibility of serious adverse effects.
The analysis presented by ATSDR (1992) provides a more useful review of a subset of
information on human exposures to boron and boron containing compounds, particularly the
3-4
study by Wong et al. (1964). This publication involves an incident in which 11 infants were
inadvertently given formula prepared with a 2.5% solution of boric acid. Five of the infants
subsequently died. Relatively good estimates of doses are available for two of the fatally
exposed infants: 505 mg boron/kg/day and 765 mg boron/kg/day. Estimates of exposure for the
other infants range from a total dose of 4,510 mg to 14,000 mg of boric acid, equivalent to 788
mg B to 2447 mg B. Sublethal effects in infants, including vomiting and diarrhea, were noted at
doses of 184 mg B/kg/day (Wong et al. 1964). Sublethal but serious signs of toxicity, including
vomiting, have also been noted in adults at doses of 241 mg/kg/day to 895 mg B/kg/day after
unsuccessful suicide attempts (Linden et al. 1986).
3.1.5. Subchronic or Chronic Systemic Toxic Effects
Several studies have been conducted on the subchronic and chronic toxicity of boric acid and
borate compounds, with most of the available data on boric acid and borax (ATSDR 1992,
Hubbard 1998, WHO 1998). The effects of short-term gestational exposure to boric acid have
been investigated in rats, mice, and rabbits (Heindel et al. 1992, 1994, Price et al. 1996a,b).
Longer-term toxicity studies (60-90 days) have assessed the subchronic and chronic toxicity of
borax in rats and dogs (Weir and Fisher 1972, Dixon et al. 1976, 1979, Lee et al. 1978). Details
for all studies are provided in Appendix 1. Results of developmental, subchronic and chronic
toxicity studies show that the developing fetus and the male reproductive system are the primary
targets for borate-induced toxicity.
Gestational exposure of rats (Heindel et al. 1992, 1994, Price et al. 1996a), mice (Heindel et al.
1992, 1994), and rabbits (Heindel et al. 1994, Price et al. 1996b) to boric acid resulted in
observed from gestational exposure to boric acid is decreased body weight, with the lowest
NOAEL of 9.6 mg B/kg/day in rats (Price et al. 1996a). Based on comparison of NOAELs for
decreased fetal weight in rats (9.6 mg B/kg/day, Price et al. 1996a) and mice (43.3 mg B/kg/day,
(Heindel et al. 1992, 1994), fetal rats appears to be more sensitive than fetal mice to boric acid
exposure. In addition to effects on the developing fetus, maternal toxicity was observed, with
decreased maternal weight or weight gain and increased kidney weight as the most commonly
observed effects (Heindel et al. 1992, 1994, Price et al. 1996a,b). In all developmental toxicity
studies, maternal toxicity was observed at higher exposure levels than fetal toxicity.
Subchronic exposure of rats and dogs to borax in food and drinking water resulted in testicular
toxicity characterized by atrophy of the testes, degeneration of the spermatogenic epithelium and
spermatogenic arrest (Dixon et al. 1976, 1979, Lee et al. 1978, Paynter 1963, Seal and Weeth
1980, Weir and Fisher 1972). Dietary exposure of rats for 90 days to borax resulted in a dosedependent atrophy of the testes and spermatogenic arrest, with an NOAEC of 175 ppm B
equivalents and an LOAEC of 525 ppm B equivalents (Weir and Fisher 1972). Complete
testicular atrophy was observed in rats exposed to 1750 ppm B. At higher dietary concentrations
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of 1750 and 5250 ppm B, decreased body weight and decreased weight of several organs,
including liver, spleen, kidneys and brain, were observed. In the 5250 ppm group, all animals
died within 6 weeks of exposure. In this same study, similar results were observed for dietary
exposure to boric acid. Testicular toxicity was also observed in rats exposed to borax in drinking
water at concentrations of 150 and 300 mg B/L (Seal and Weeth 1980). Subchronic exposure of
dogs to dietary borax resulted in testicular atrophy, including degeneration of the spermatogenic
epithelium, with an NOAEC of 175 ppm B and an LOAEC of 1750 ppm B (Weir and Fisher
1972). A decrease in thyroid size was also observed in the 1750 ppm B treatment group. Boraxinduced testicular toxicity was also observed following 90-day dietary exposure of dogs
equivalent to doses of about 270 mg/kg/day (Paynter 1963). As was observed in rats, similar
results were observed for dietary exposure of dogs to boric acid (Weir and Fisher 1972). As
discussed in Section 3.1.9, in studies designed to assess the effects of borax exposure on
reproduction in rats, exposure to dietary borax for up to 90 days resulted in toxicity to the testes
(Dixon et al. 1976, 1979, Lee et al. 1978).
In rats exposed to borax in the diet for 2 years, the NOAEC for toxicity to the testes, including
decreased testicular weight, atrophied seminiferous epithelium and decreased tubular size, was
350 ppm B (equivalent to 17.5 mg B/kg/day, according to U.S. EPA 1989), with an LOAEC of
1170 ppm B (equivalent to 58.5 mg B/kg/day, according to U.S. EPA 1989) (Weir and Fisher
1972). Other signs of toxicity noted in the 1170 ppm B treatment group included scaly tails,
hunched posture, swelling and desquamation of paws and inflamed eyes. In a similar 2-year
feeding study of borax in dogs, the NOAEC for toxicity to the testes was 350 ppm B (equivalent
to 8.8 mg B/kg/day, according to U.S. EPA 1989), with an LOAEC of 1170 ppm B (equivalent to
28 mg B/kg/day, according to U.S. EPA 1989 (Weir and Fisher 1972). Thus, based on
comparison of NOAEC and LOAEC values (expressed on a mg B/kg/day basis), dogs appear
slightly more sensitive than rats to boron-induced testicular toxicity. In the 1170 treatment
group, severe testicular atrophy and spermatogenic arrest were observed. Similar results were
observed for dogs treated with boric acid in the diet for 2-years (Weir and Fisher 1972). In boric
acid treated dogs, adverse effects on the testes were nearly completely reversed within 25 days
when dogs were removed from the boric acid diet and placed on a control diet. For both borax
and boric acid, no other adverse effects were observed at any dose level.
3.1.6. Effects on Nervous System
As discussed in Durkin and Diamond (2002), a neurotoxicant is a chemical that disrupts the
function of nerves, either by interacting with nerves directly or by interacting with supporting
cells in the nervous system. This definition of neurotoxicant distinguishes agents that act directly
on the nervous system (direct neurotoxicants) from those agents that might produce neurologic
effects that are secondary to other forms of toxicity (indirect neurotoxicants). Virtually any
chemical will cause signs of neurotoxicity in severely poisoned animals and, thus, can be
classified as an indirect neurotoxicant.
By this definition, borax may be classified as an indirect neurotoxicant. As reviewed in Section
3.1.4, acute exposure of rats to lethal doses of borax causes depression, ataxia and convulsion
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(Weir and Fisher 1972). These findings, however, do not implicate borax as a direct
neurotoxicant. No studies designed specifically to detect impairments in motor, sensory, or
cognitive functions in animals or humans exposed borax were identified. No evidence for borax
producing direct effects on the nervous system was found.
3.1.7. Effects on Immune System
Immunotoxicants are chemical agents that disrupt the function of the immune system. Two
general types of effects, suppression and enhancement, may be seen and both of these are
generally regarded as adverse. Agents that impair immune responses (immune suppression)
enhance susceptibility to infectious diseases or cancer. Enhancement or hyperreactivity can give
rise to allergy or hypersensitivity, in which the immune system of genetically predisposed
individuals inappropriately responds to chemical or biological agents (e.g., plant pollen, cat
dander, flour gluten) that pose no threat to other individuals; or the agent may give rise to
autoimmunity, in which the immune system produces antibodies to endogenous components
leading to destruction of the organ or tissue involved.
There is very little direct information on which to assess the immunotoxic potential of borax or
other borate compounds. Nonetheless, the toxicity of borax has been examined in several acute,
subchronic, and chronic bioassays. Although many of these studies did not focus on the immune
system, evidence of changes in immune function (e.g., increased susceptibility to infection
compared to controls) were not observed in any of the available long-term animal studies
(Appendix 1). Typical subchronic or chronic animal bioassays conduct morphological
assessments of the major lymphoid tissues, including bone marrow, major lymph nodes, spleen
and thymus (thymus weight is usually measured as well), and blood leukocyte counts. These
assessments can detect signs of inflammation or injury indicative of a direct toxic effect of the
chemical on the lymphoid tissue. Changes in cellularity of lymphoid tissue and blood, indicative
of a possible immune system stimulation or suppression, can also be detected (Durkin and
Diamond 2002). None of these effects have been noted in any of the longer term toxicity studies
on borax (Appendix 1). Results of a dermal challenge study show that exposure to borax did not
cause a sensitization effect (Wnorowski 1994b, Appendix 1).
3.1.8. Effects on Endocrine System
The endocrine system participates in the control of metabolism and body composition, growth
and development, reproduction, and many of the numerous physiological adjustments needed to
maintain constancy of the internal environment (homeostasis). The endocrine system consists of
endocrine glands, hormones, and hormone receptors. Endocrine glands are specialized tissues
that produce and export (secrete) hormones to the bloodstream and other tissues. The major
endocrine glands in the body include the adrenal, hypothalamus, pancreas, parathyroid, pituitary,
thyroid, ovary, and testis. Hormones are also produced in the gastrointestinal tract, kidney, liver,
and placenta. Hormones are chemicals produced in endocrine glands that bind to hormone
receptors in target tissues. Binding of a hormone to its receptor results in a process known as
postreceptor activation which gives rise to a hormone response in the target tissue, usually an
adjustment in metabolism or growth of the target tissue. Examples include the release of the
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hormone testosterone from the male testis, or estrogen from the female ovary, which act on
receptors in various tissues to stimulate growth of sexual organs and development of male and
female sexual characteristics. The target of a hormone can also be an endocrine gland, in which
case, receptor binding may stimulate or inhibit hormone production and secretion. Adverse
effects on the endocrine system can result in abnormalities in growth and development,
reproduction, body composition, homeostasis (the ability to tolerate various types of stress), and
behavior.
As discussed in Sections 3.1.5 and 3.1.9, subchronic exposure to borax results in spermatogenic
arrest and sterility in male rats and decreased ovulation in female rats (Weir and Fisher 1972). It
is most likely that the adverse effects of borax on reproductive function is due to a direct
testicular effect, rather than an effect on the hypothalamic-pituitary axis (ECETOC 1995, Fail et
al. 1998). Although time- and dose-dependent decreases in plasma luteinizing hormone (LH)
and follicle stimulating hormone (FSH) levels were reported in rats exposed to borax in the diet
(daily doses of 35 and 50 mg B/kg/day) (Lee et al. 1978), it is generally accepted that borate
compounds are not endocrine disrupters and that the reduction in plasma FSH and LH levels are
secondary to testicular toxicity (Fail et al. 1998).
In dogs exposed to dietary borax (1750 ppm B) for 90 days, a significant decrease in thyroid
weight was observed (Weir and Fisher 1972). Based on these results, borax and other boroncontaining salts may be toxic to the thyroid. However, no studies specifically designed to
investigate the effects of borax on thyroid gland function were identified in the available
literature.
3.1.9. Reproductive and Teratogenic Effects
As discussed in Section 3.1.5, effects on the male reproductive system and the developing fetus
appear to be the most sensitive endpoints in borate toxicity (i.e., the effects occurring at the
lowest doses), with the developing fetus more sensitive than the male reproductive system.
Although no studies investigating the developmental effects of borax were identified in the
available literature, given the similar toxicological profiles for borate compounds, it is likely that
gestational exposure to borax would produce similar effects to those produced by boric in the
developing fetus. As summarized in Appendix 1, gestational exposure of rats (Heindel et al.
1992, 1994, Price et al. 1996a), mice (Heindel et al. 1994), and rabbits (Heindel et al. 1992,
1994, Price et al. 1996b) to boric acid resulted in increased fetal deaths, decreased in fetal
weight, and increased fetal malformations. The types of fetal malformations observed include
anomalies of the eyes, central nervous system, cardiovascular system, and axial skeleton in rats,
short rib XIII and other skeletal anomalies pertaining to ribs in mice, and cardiovascular
malformations in rabbits. The most sensitive effect observed from gestational exposure to boric
acid is decreased body weight, with a NOAEL of 43.3 mg B/kg/day in mice and NOAELs
ranging from 9.6 (Price et al. 1996a) to <13.6 mg B/kg/day (Heindel et al. 1992, 1994) in rats.
As discussed in Section 3.3.2, the chronic RfD for boron and boron compounds was derived by
the U.S. EPA (2004) from combined data from Price et al. (1996) and Heindel et al. (1992),
using decreased fetal body weight in rats as the most sensitive effect.
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Regarding the effects of borate compounds on the reproductive system of adult animals, since the
testes is a primary target organ for boron-induced toxicity, adverse effects on male fertility are
expected outcomes of borax exposure. Several studies have been conducted to evaluate the
effects of borax exposure in rats (Dixon et al. 1976, 1979, Lee et al. 1978, Weir and Fisher
1972). Study details are provided in Appendix 1. Exposure of male rats to single doses of borax
up to 450 mg B/kg did not result in decreased fertility, as measured by the number of
spermatozoa, spermatids, spermatocytes and spermatogonia (Dixon et al. 1976). However,
dietary exposure to rats to 50 and 100 mg B/kg/day for 60 to 90 days, resulted in testicular
toxicity (as described in Section 3.1.5) and decreased fertility in male rats (Dixon et al. 1979, Lee
1978, Weir and Fisher 1972); no signs of systemic toxicity were observed at these exposure
levels. From these studies, the NOAEC for decreased reproductive function, as measured by the
number of litters produced, is approximately 25 mg B/kg/day and the LOAEC is approximately
50 mg B/kg/day. At the highest dose level assessed (approximately 100 mg B/kg/day), male rats
were completely sterile, with no litters produced (Lee et al. 1978, Weir and Fisher 1972). At the
lower dose level (approximately 50 mg B/kg/day), sterility was reversed within 5 weeks of
discontinuing borax treatment (Dixon et al. 1979). However, at the higher dose level (100 mg
B/kg/day), rats remained sterile up to 8 months after borax treatment was discontinued (Lee et al.
1978).
The reproductive effects of borax do not appear restricted to males. Results of a single study
show that dietary exposure to borax decreased ovulation in female rats (Weir and Fisher 1972).
In female rats exposed to dietary borax at a concentration of 1170 ppm B (58.5 mg B/kg/day)
for14 weeks, no litters were produced when females were mated with unexposed males.
Decreased ovarian weight was also observed. No effects on female reproduction were observed
at exposure levels of 5.9 and 17.5 mg B/kg/day. Additional information on the effects of borax
on the female reproduction system was not identified in the available literature.
The specific mechanism of borax-induced toxicity to the reproductive system has not been
identified. The induction of spermatogenic arrest in the absence of other systemic toxicity
suggests that borax produces direct effects on the testes, rather than effects on the hypothalamicpituitary-testicular axis (Fail et al. 1998). Based on histological findings showing degeneration
of the spermatogenic epithelium,(Weir and Fisher 1972), it has been proposed that the Sertoli cell
is the most likely target for borate compounds (ECETOC 1995, Fail et al. 1998, WHO 1998).
3.1.10. Carcinogenicity and Mutagenicity
The potential carcinogenicity of borax was assessed in a 2-year feeding study in rats and dogs, as
summarized in Appendix 1 (Weir and Fisher 1972). In both species, borax was negative for
carcinogenic activity. Furthermore, no borate compound has been shown to have produced
cancer in any long-term exposure study in any species (ATSDR 1992, Beyer et al. 1983, Dieter et
al. 1991, Fail et al. 1998, Hubbard 1998, WHO 1998). Based on the available data, boron (and
borate compounds) is classified by U.S. EPA as Group E chemical i.e., evidence of noncarcinogenicity in humans (U.S. EPA 1993a, p. 27).
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The mutagenic potential of borax has been tested in Salmonella typhimurium and several
cultured mammalian cell lines with and without metabolic activation; no mutagenic activity of
borax was observed (Benson et al. 1984, Landolph 1985). It is generally accepted that boron and
borate compounds are not mutagenic (ATSDR 1992, Beyer et al. 1983, ECETOC 1995, Fail et
al. 1998, Hubbard 1998, WHO 1998).
3.1.11. Irritation and Sensitization (Effects on the Skin and Eyes)
Borax was tested for irritant effects on the skin of rabbits and guinea pigs (Reagan 1985b,
Wnorowski 1994b) and the eyes of rabbits (Reagan 1985c); study details are provided in
Appendix 1. Application of 0.5 g borax to shaved skin of rabbits did not results in any dermal
irritation (Reagan 1985b). Boric acid is rated as Category III skin irritant (moderate irritant) and
anhydrous borax is rated as a Category IV skin irritant (mild irritant) (U.S. EPA 1993a, pp. 2324). Dermal challenge studies in guinea pigs show that borax does not cause skin sensitization
effects, with no skin irritation noted either pre- or post-challenge (Wnorowski 1994b). Ocular
application of 0.1 g borax in rabbits resulted in severe irritation, including irritation of the iris
and corneal opacity (Reagan 1985c). Borax is rated as a Category I (severe) eye irritant (U.S.
EPA 1993a, p. 24).
3.1.12. Systemic Toxic Effects from Dermal Exposure
Single dermal applications of borax to rats at doses up to 5 g/kg (Wnorowski 1996) and to rabbits
at doses up to 2 g/kg (Reagan 1985a) did not result in any mortality or in the development of
significant toxicity (studies detailed in Appendix 1). Thus, in rats the dermal LD50 is greater than
5 g borax/kg and in rabbits is greater than 2 g borax/kg. Based on the LD50 greater than 2 g/kg in
rabbits, borax is rated as a Category 3 compound for systemic effects resulting from dermal
exposure. These findings are consistent with the data indicating that borax has a low order of
oral toxicity.
3.1.13. Inhalation Exposure
Inhalation exposure of rats for 4 hours to 2.0 mg borax/L did not results in any mortality, placing
the 4-hour LC50 value at greater than 2.0 mg borax/L (Wnorowski 1994a). Clinical signs of
toxicity noted during the exposure period included ocular and nasal discharge, hunched posture
and hypoactivity. All symptoms resolved within 7 days of exposure.
These extremely limited data suggest that borax can induce irritant effects and perhaps systemic
toxic effects in laboratory mammals following inhalation exposure. In addition, several studies
of occupational exposure in workers show that inhalation of dust containing boron causes
irritation to the nasal mucosa and respiratory tract (Garabrant et al. 1985, Heederik et al. 1994,
Woskie et al, 1994, 1998, Hu et al. 1992). As discussed in Section 3.2.2, this finding is not
directly relevant to this risk assessment because of the implausibility of inhalation exposure to
the high concentrations of boron reported for these confined industrial facilities.
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3.1.14. Inerts and Adjuvants

As discussed in Section 2.2, the borax formulation Sporax contains 100 % sodium tetraborate
decahydrate (borax) and has no other active or inert ingredients.
3.1.15. Impurities and Metabolites
3.1.15.1. Impurities No information on the impurities of borax was identified in the
available literature. The toxicity studies reviewed in this report were conducted with technical
grade borax. Thus, if toxic impurities are present, they are likely to be encompassed by the
available toxicity studies using technical grade borax.
3.1.15.2. Metabolites As discussed in Section 3.1.3.1, due to the excessive energy (523
kJ/mol) required to break the boron-oxygen bond, borates are not metabolized by humans or
animals (ECETOC 1995, Hubbard1998). However, at physiological pH borate salts convert to
boric acid (ECETOC 1995, Hubbard1998, WHO 1998). Therefore, it is likely that most of the
administered dose of borax is converted to boric acid following absorption. Thus, the toxicity of
boric acid is encompassed in the available toxicity studies on borax.
3.1.16. Toxicologic Interactions
As discussed in Section 2, borax is used as a sole agent for the control of annosum root disease in
conifer stands. Thus, it is not expected that application of borax will be combined with other
agents. No information has been encountered on the toxicologic interactions of borax with other
agents.
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3.2.
EXPOSURE ASSESSMENT
3.2.1. Overview.
Unlike most other risk assessments on pesticides used by the Forest Service, the agent of
toxicologic concern in Sporax i.e., boron occurs naturally and exposures to boron are
unavoidable. Except for the most extreme exposure scenario considered in this risk assessment
i.e., the direct consumption of Sporax from a tree stump by a child the use of Sporax in Forest
Service programs will not substantially contribute to boron exposures in humans. In addition, the
use of Sporax in Forest Service programs will not typically or substantially contribute to
concentrations of boron in water or soil.
As discussed in Section 2.3, Sporax is applied directly to freshly cut tree stumps. Sporax is not
applied as a liquid using backpack, broadcast or aerial spray methods and it is not applied
of contaminated vegetation and direct exposure from contaminated vegetation, are not applicable
for this risk assessment. The exposure scenarios used in this risk assessment are those expected
to result in potentially significant exposures considering the application method for Sporax that is
used in Forest Service programs i.e., dry application to the stumps of trees.
As with typical Forest Service risk assessments, exposure scenarios are presented for both
workers and members of the general public. For workers, accidental exposure via direct contact
of the hands and lower legs with granular Sporax during application is the only exposure scenario
considered in this risk assessment. For this scenario, exposure values range from approximately
0.000005 mg B/kg/event for the lower bound limit resulting from a 1-hour exposure to 0.0002
mg B/kg/event for the upper bound resulting from an 8-hour exposure. Other exposure scenarios
are not considered to be reasonably plausible given the atypical application method for Sporax.
For the general public, the exposure scenarios considered quantitatively in this risk assessment
are ingestion of Sporax from tree stumps by a small child and ingestion of contaminated pond
water by a child or a young woman. For ingestion of Sporax from tree stumps by a child,
exposure values range from 0.43 to 3.24 mg B/kg/event and are based on the average daily soil
consumption by a child. For ingestion of contaminated pond water, contamination of water by
both an accidental spill scenario and by runoff from the application site are considered. Acute
exposures values for a small child from ingestion of water contaminated via an accidental spill of
Sporax into a small pond range from 0.015 mg B/kg to 0.14 mg B/kg/event. To determine
exposures to pond water contaminated by runoff of Sporax applied to tree stumps, exposure
estimates are modeled by GLEAMS. For acute exposure of a child ingesting water from a pond
contaminated by runoff, values range from approximately 0.0003 to 0.01 mg B/kg/event. For
chronic exposure of adults ingesting surface waters contaminated by runoff, exposure values
range from approximately 0.00004 to 0.002 mg B/kg/day.
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3.2.2. Workers.
Sporax is applied in granular form to the surfaces of cut tree stumps using a salt-shaker style.
Although the Forest Service uses a standard set of exposure assessments in most risk assessment
documents, the typical general exposures considered for directed foliar (backpack), boom
(hydraulic ground spray), and aerial spray as well as typical accidental exposures to a liquid are
not applicable for this risk assessment, since Sporax is not applied as a liquid. Additionally,
although there are several reports detailing local irritant effects resulting from occupational
exposures to borate dust, inhalation exposures are not considered in this risk assessment due to
the implausibility of inhalation exposures in the field reaching the high concentrations of boron
reported in confined industrial facilities (Garabrant et al. 1985; Heederik et al. 1994; Woskie et
al, 1994, 1998; Hu et al. 1992). Thus, the only exposure scenario that is considered plausible for
workers is accidental dermal exposure to the hands and lower legs of granular Sporax during
application.
For accidental exposure of workers to Sporax, dermal exposure is characterized by contamination
of the lower legs and hands. In these scenarios, it is assumed that granular Sporax powder
contaminates a given surface area of skin and that a certain amount of the powdered or granular
chemical adheres to the skin. The absorbed dose is then calculated based on Ficks first law
(U.S. EPA 1992). In most Forest Service risk assessments, this type of exposure assessment is
modeled using the concentrations of the chemical in the solution used by the worker. This
exposure assessment is somewhat atypical because borax is not in solution i.e., it is applied as a
powder. Consistent with the approach recommended by EPA (1992) for neat applications of a
compound to the skin, the concentration of borax on the surface of the skin is assumed to be
equal to the water solubility of borax (47,000 mg borax /L). In other words, the concentration of
borax in the pore water of the skin will be limited by the chemicals solubility in water. To
estimate the absorbed dose in units of mg chemical/kg body weight, the amount of absorbed
chemical is divided by body weight (kg). For this scenario, it is assumed that the contaminated
skin is effectively cleaned after 1 and 8 hours. Details of the assumptions and calculations
involved in these exposure assessments are given in Worksheet C01a for a 1-hour exposure and
Worksheet C01b for an 8-hour exposure. A summary of worker exposure assessments is
provided in Worksheet E01. Plausible levels of exposure are extremely low, ranging from
0.000013 mg B/kg/event (the lower range for a 1-hour exposure) to 0.00023 mg B/kg bw/event
(the upper bound for an 8-hour exposure). As noted in Section 3.1.3.1, higher exposures could
be anticipated in workers with serious skin damage i.e., substantial areas of abraded skin. This
factor is considered further in Section 3.4.
Borax is classified as a Category I eye irritant and may cause severe irritation upon ocular
exposure (Section 3.1.11). The available literature does not include quantitative methods for
characterizing exposure or responses associated with accidental ocular exposure; furthermore,
there appear to be no reasonable approaches to modeling this type of exposure scenario
quantitatively. Consequently, accidental exposure scenarios of this type are considered
qualitatively in the risk characterization (section 3.4).
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3.2.3. General Public.

3.2.3.1. General Considerations Under normal conditions of application, members of the
general public should not be exposed to substantial levels of Sporax as a result of Forest Service
activities. Nonetheless, any number of exposure scenarios can be constructed for the general
public. As discussed in the exposure assessment for workers (Section 3.2.2), the atypical
application method for Sporax limits the number of exposure scenarios for the general public that
can be reasonably expected to occur. Therefore, typical exposures involving spray of a chemical
to vegetation, such as dermal contact with contaminated vegetation and the consumption of
contaminated fruit, are not applicable to this risk assessment. Exposure scenarios based on oral
exposures from consumption of contaminated fish are not considered since borate compounds do
not bioaccumulate in fish (Ohlendorf et al.1986; Klasing and Pilch 1988).
Two types of exposure scenarios, ingestion of Sporax from a tree stump by a child and ingestion
of contaminated water, are considered the most likely exposure for the general public. For
ingestion of Sporax from a tree stump, only acute exposure is considered. Exposure scenarios
developed for the general public for contaminated water include acute exposure and longer-term
or chronic exposure. The scenarios developed for this risk assessment should tend to overestimate exposures in general. The exposure scenarios developed for the general public are
summarized in Worksheet E03. As with the worker exposure scenarios, details of the
assumptions and calculations involved in these exposure assessments are given in the worksheets
that accompany this risk assessment (Worksheets D01D04). The remainder of this section
focuses on a qualitative description of the rationale for and quality of the data supporting each of
the assessments.
Boron is a naturally occurring element and a normal constituent in environmental media (e.g.,
water, soil, and air) as well as plants and animals, including humans. While exposures to Sporax
used in Forest Service programs may be limited, this risk assessment also considers background
levels of exposure to boron and the relative contribution of Sporax to other sources of exposure
to boron compounds (Section 3.2.3.4) as well as the potential cumulative effects of these
exposures (Section 3.4.6).
3.2.3.2. Oral Exposure of Sporax Applied to Tree Stumps Although Sporax is not applied in
residential areas, it is applied in campgrounds used by members of the general public. For this
risk assessment, an acute exposure scenario is used in which a child ingests Sporax applied to
tree stumps. There is no information in the available literature to estimate the amount of Sporax
that a child could be predicted to consume in one day. The estimated amount of Sporax that a
child may consume in one day is based on the amount of soil that an average child may ingest per
day. According to the EPA Exposure Factors Handbook (U.S. EPA 1996), the mean amount of
soil that a child consumes per day is estimated to be 100 mg soil/day, with an upper bound
estimate of 400 mg soil/day.
For this risk assessment, the amount of Sporax consumed from tree stumps in a single day is
taken as the range of 50 (an estimated lower bound) to 400 mg Sporax/day (5.67 to 45.36 mg
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B/day). A central estimate for Sporax consumption is taken as 100 mg Sporax/day (11.34 mg
B/day). To yield an estimated dose in units of mg chemical/kg body weight, these exposure
numbers are divided by body weight (kg). Details for the calculations involved in this exposure
scenario are given in the worksheets that accompany this risk assessment (Worksheet D01). The
estimated doses range from about 0.4 mg B/kg bw/event to 3.2 mg B/kg bw/event. It should be
emphasized that this exposure estimate is highly uncertain and not based on empirical data for
consumption of any borate compound; thus exposures via this scenario may be under- or
overestimated.
3.2.3.3. Contaminated Water The borax application method considered in this risk assessment
application to tree stumps has a limited potential to contaminate water. Nonetheless, after
application of tree stumps, rainfall and consequent runoff could lead to contamination of standing
water or streams. In addition, accidental spills of the Sporax formulation into a small body of
water are possible. Exposure assessments for both of these scenarios are presented in the
following subsections.
3.2.3.3.1. Accidental Spill The accidental spill scenario assumes that a young child
consumes contaminated water shortly after an accidental spill into a small pond. The specifics of
this scenario, which are given in Worksheet D02, are based on the spill of Sporax into a small
pond. The amount of Sporax spilled ranges from 6.25 to 25 lbs (0.7 to 2.8 pounds of boron
equivalents), with a central estimate of 12.5 lbs (1.42 pounds of boron equivalents). Because this
scenario is based on the assumption that exposure occurs shortly after the spill, no dissipation of
Sporax is considered. This scenario is dominated by variability and uncertainty and the specific
assumptions used may overestimate or underestimate exposure. The actual concentrations in the
water would depend on the actual amount of compound spilled, the size of the water body into
which it is spilled, the time at which water consumption occurs relative to the time of the spill,
and the amount of contaminated water that is consumed.
Based on the spill scenario used in this risk assessment, the concentration of boron in a small
pond is estimated to range from about 0.3 to 1.3 mg B/L with a central estimate of approximately
0.6 mg B/L. As discussed in Section 3.2.3.4., these are within the range of naturally occurring
concentrations of boron in water. Based on plausible ranges of water consumption (U.S.
EPA/ORD 1996), the estimated doses for the child are estimated at about 0.015 to 0.14 mg
B/kg/event, with a central estimate of approximately 0.05 mg B/kg/event (Worksheet D02). This
is intended to be an extreme accidental exposure scenario. The purpose of this scenario is simply
to suggest the intensity of measures that would be appropriate in response to a relatively large
spill of Sporax into a relatively small body of water.
3.2.3.3.2. Gleams Modeling Modeling of concentrations in stream water conducted for
this risk assessment are based on GLEAMS (Groundwater Loading Effects of Agricultural
Management Systems) modeling. GLEAMS is a root zone model that can be used to examine
the fate of chemicals in various types of soils under different meteorological and hydrogeological
conditions (Knisel and Davis 2000). As with many environmental fate and transport models, the
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input and output files for GLEAMS can be complex. The general application of the GLEAMS
model and the use of the output from this model to estimate concentrations in ambient water are
detailed in SERA (2004b).
GLEAMS is typically applied to and validated with organic compounds for which adsorption and
desorption to soil are the predominant factors affecting transport in soil. Borax and related
compounds are inorganics and the modeling of such compounds using GLEAMS may be viewed
as tenuous. Nonetheless, boron interactions with soil will be governed by adsorption/desorption
processes analogous to those of many organic weak acids rather than precipitation and
dissolution processes (Bodek et al. 1990; Tanji 1998).
Environmental transport models for inorganics, however, are not available. In addition, as
reviewed by U.S. EPA (1993b), borax will rapidly convert to boric acid, which has a pKa of
9.14. Thus, at neutral pH, the proportion of boric acid that will be non-ionized (protonated) is
greater than 0.99 and the behavior of boric acid in soil may approximate that of a neutral organic
compound. Another complication in modeling the movement of boron involves interactions with
minerals in soils which can substantially impact transport (Tanji 1990).
For the current risk assessment, the application site was assumed to consist of a 10 hectare area
that drained directly into a small pond or stream. The chemical-specific values as well as the
details of the pond and stream scenarios used in the GLEAMS modeling are summarized in
Table 3-1. All simulations were conducted at an application rate of 1 lb borax/acre. Because
borax rapidly converts to boric acid (U.S. EPA 1993a,b), the Kow of boric acid was used as an
input parameter for GLEAMS. As discussed below, the concentrations of borax were converted
to boron equivalents because boron equivalents are the basis for the dose-response assessments
of both human health effects (Section 3.3) and ecological effects (Section 4.3).
The GLEAMS modeling yielded estimates of loss of the compound in runoff, sediment and
percolation that were used to calculate concentrations in a stream and pond adjacent to a treated
plot, as detailed in Section 6.4 of SERA (2004b). Over annual rainfall rates of 5 to 250 inches
per year, the concentrations modeled in a small stream were less than 0.00001 ppb (g/L). These
very low modeled concentrations were the result of the amount of runoff water required to
transport boric acid to the stream as well as the base flow rate of the stream (i.e., 710,000 L/day
as specified in Table 3-1 and discussed in Section 6.4. of SERA 2004b). This runoff water and
base flow diluted the concentration of boric acid to very low and essentially negligible values.
Higher concentrations were modeled in a small pond (Table 3-2). This is in some respects an
artifact of the pond model. As detailed in SERA 2004b (Section 6.4), a variable volume pond
model is used but no overflow or drainage from the pond is considered. Thus, boron is
transported to the pond and is diluted only by the volume of water in the pond as well as rainfall
and runoff. The upper portion of Table 3-2 gives the concentration as borax at an application
rate of 1 lb/acre. The bottom portion of Table 3-2 gives the concentration in water as boron
equivalents i.e., g of boron per liter of water.
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For regions with annual rainfall rates of 15 inches or more, the modeled peak concentrations in
ponds expressed as boron equivalents range from about 6 g/L (clay at 250 inches of rainfall per
year) to about 100 g/L (sand or loam at an annual rainfall rate of 15 inches per year). Because
degradation is assumed to be negligible i.e., elemental boron will not be transmuted the
longer term concentrations are only somewhat less than the peak concentrations. It will be noted
in Table 3-2 that the concentrations of boron in water are inversely related to rainfall rate. This
occurs because borax may be transported off site once the amount of rainfall reaches the
minimum necessary for runoff. Because of the high water solubility of borax (as boric acid),
relatively small amounts of water can transport a large amount of borax. As the amount of water
increases, the primary effect is dilution of borax rather than an increase in the amount of borax in
runoff. Thus, the expected concentrations of borax in a small pond increase as the rainfall rate
decreases.
3.2.3.3.3. Other Modeling Efforts and Monitoring Data Detailed modeling efforts for
borax or related compounds have not been encountered. As summarized in Table 3-3, the U.S.
EPA (1993b) conducted a very simple modeling exercise for boric acid assuming that a
proportion of 0.05 of the applied boric acid contaminates a six foot deep pond, similar to the
pond used in the GLEAMS analysis (see Table 3-1). Based on this assumption, the U.S. EPA
(1993b) estimated a concentration of boric acid in water of 30.5 ppb as boric acid, equivalent to
5.2 ppb as boron (Table 3-3). While the U.S. EPA (1993b) does not provide a detailed rationale
for the runoff assumption, this is a standard value used by U.S. EPA in screening level
assessments. The concentration of 5.2 ppb as boron is at the lower range of the peak values
estimated from GLEAMS.
Very little monitoring data on boron have been encountered in the literature and no monitoring
studies associated with the type of applications used by the Forest Service are available.
Available monitoring data on boron concentrations in U.S. surface waters are summarized in
Table 3-3. Normal ambient concentrations of boron in water are highly variable, ranging from 1
ppb (U.S. EPA 1993b) to 750 ppb (Black et al. 1993). As discussed further in Section 3.2.3.4,
some areas may have much higher concentrations of boron in water i.e., up to 5 ppm. The
upper range of typical concentrations, 750 ppb, exceeds the upper range of concentrations (100
ppb) that are modeled using GLEAMS by a factor of 7.5 Thus, in areas that have naturally low
levels of boron in water (i.e, about 1 ppb), the use of boron in Forest Service programs could
have a substantial impact on local concentrations of boron in standing bodies of water such as
small ponds. Likewise, in areas with a naturally high level of boron in water (i.e., about 750
ppb), the use of boron in Forest Service programs would have little impact on boron
concentrations in surface waters.
Monitoring data in soils after applications of Sporax to tree stumps have been compiled by Dost
et al. (1996). These data are relevant to the assessment of exposures in ambient water because
they offer another means of comparing the concentrations of boron in soil modeled using
GLEAMS to actual concentrations found in the field after applications that are comparable to
those used in Forest Service programs. As summarized in Dost et al. (1996, Appendix A, Tables
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1 to 4), concentrations of boron in soil after stump treatments ranged from about 0.1 to 2 mg
B/kg soil (0.1 to 2 ppm boron). As discussed further in Section 4.2.3 and detailed in Table 4-1,
peak concentrations of boron in soil modeled by GLEAMS are about 0.3 ppm to 0.5 ppm, very
near the geometric mean (0.44 ppm) of the range reported by Dost et al. (1996).
3.2.3.3.4. Concentrations of Boron in Water Used for Risk Assessment The peak and
longer term average concentrations of boron in ponds, summarized in Table 3-3, are used in this
risk assessment as water contamination rates i.e., concentrations in water in units of mg/L or
ppm that are expected at an application rate of 1 lb borax/acre. By comparison to the lower
concentrations used by U.S. EPA (1993b), these values appear to be conservative i.e., they may
somewhat overestimate likely concentrations. As noted in Section 3.2.3.4.2, however, there are
substantial uncertainties in the application of GLEAMS to an inorganic compound. This as well
as the lack of monitoring data for applications of borax similar to those conducted by the Forest
Service adds uncertainty to this risk assessment.
3.2.3.4. Background Levels of Exposure Boron is a naturally occurring element and is
relatively abundant in water, foods, and soil. In general, the exposure of humans to boron is
attributable primarily to the consumption of food and, to a lesser extent, the consumption of
water containing boron compounds (ATSDR 1992; WHO 1998). The normal background
exposure to boron has a substantial impact on the current risk assessment in terms of determining
whether the use of Sporax in Forest Service programs will have a significant effect on normal
levels of exposure to boron and whether exposures associated with the use of Sporax could
combine with background exposures to cause otherwise unanticipated effects. A summary of
typical background exposures to boron and a comparison to levels of exposure to boron from
Forest Service uses is given in Table 3-4 and discussed in this section. As discussion of the
potential toxicologic significance of these increased exposures is given in Section 3.4.6.
In terms of consumption by humans, food is the predominant source of exposure to boron
(ATSDR 1992; WHO 1998). Levels of boron in food items vary substantially. The review by
WHO (1998) provides an extensive summary of boron levels in various environmental media:
aquatic animals (3-11 ppm), aquatic vegetation (26-382 ppm), and most terrestrial vegetation
(2.3-94.7 ppm). Much higher concentrations of boron may occur in fruit as well as some forms
of vegetation i.e., boron levels in different consumables may range from 1 ppm in lemons to
over 300 ppm in red cabbage ( U.S. EPA (1993a, pp. 27-28). Because of the high concentrations
of naturally occurring boron in foods and the relatively low toxicity of boron compounds, the
U.S. EPA (1993a) has determined that boric acid and the salts of boric acid are exempted from
tolerances on raw agricultural commodities.
Based on an assessment of all sources of exposure (i.e., food, water, air, consumer products),
ATSDR (1992, p. 55) has estimated that humans typically consume boron at levels of about 10 to
25 mg/day. Assuming a standard 70 kg body weight, this corresponds to daily doses of about
0.14 to 0.36 mg/kg/day. WHO (1998) does not provide a single estimate of total daily boron
intake but the figures provided by WHO (1998) for various sources of exposure suggest a total
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average intake of about 5.5 mg/day, somewhat below the lower range of the estimate given by
ATSDR (1992).
An alternative approach to estimating normal daily exposures to boron can be based on a
consideration of the pharmacokinetics of boron and typical body burdens of boron. The typical
body burden of boron in humans is estimated at less than 0.02 grams or 20 mg (ICRP 1975, p.
294). Assuming a 70 kg body weight, this is equivalent to about 0.286 mg/kg bw. Using the
plateau principle (e.g., Goldstein et al. 1974), the body burden can be related to daily dose as:
XInf = X0 / (1- e-ke t*))

where XInf is the body burden after an infinite exposure/steady state, X0 is the body burden after
an initial dose, ke is the first-order elimination rate, t* is the fixed interval between dosing. As
summarized in Section 3.1.3.1, the halftime in humans is about 13 hours or 0.54 days. This
corresponds to a first-order elimination rate of about 1.3 days-1 [ln(2)/0.54 days]. Taking t* as
one day and using 0.286 mg/kg bw as an upper bound on body burden, X0 can be calculated by
rearrangement of the above equation as a surrogate for daily intake of about 0.21 mg/kg/day [X0
= 0.286 mg/kg bw (1-e-1.3)] or about 14.7 mg/day for a 70 kg man. This is within the range of
intake estimated by ATSDR (1992) i.e., 0.14 to 0.36 mg/kg/day.
Based on the exposure scenarios derived for this risk assessment, the use of Sporax in Forest
Service programs would not typically contribute to background levels of exposure. As
summarized in Table 3-4, the plausible non-accidental routes of exposure are associated with the
consumption of contaminated water. The estimated doses are 0.002 (0.0003-0.011) mg/kg
bw/day based on peak exposures and 0.0004 (0.00004-0.0024) mg/kg bw/day based on longerterm exposures. These are below typical levels of exposure by factors of about 13 [the lower
range of background exposure {0.14 mg/kg/day} divided by the peak acute exposure {0.011
mg/kg bw} for a one day period] to a factor of 9000 [the upper range of background exposure
{0.36 mg/kg/day} divided by the lower range of longer-term exposure {0.00004 mg/kg bw}].
Taking 0.25 mg/kg/day as the central estimate of normal background exposures (i.e., the mean of
the range given by ATSDR 1992) and using the central estimates associated with the application
of Sporax i.e., an acute dose of 0.002 mg/kg and a longer term does of 0.0004 mg/kg/day, the
typical exposure is above those associated with normal background exposures by a factor of 125
for acute exposure and 625 for chronic exposure.
These exposure factors simply reflect the differences in normal concentrations of boron in water
and concentrations of boron in water that could be added by the use of Sporax in Forest Service
programs. Actual levels of exposure to background concentrations of boron will be variable due
in large part to different distributions of boron in different regions and in different materials. The
average concentration of boron in the earths crust is about 10 ppm. Boron is occurs primarily in
sedimentary rock and sediment and is released to soil and water by weathering (WHO 1998).
Because of differences in the distribution of boron in the earths crust, there are substantial
3-19
differences in the concentrations of boron in soil and water in different regions. The average
concentration of boron in drinking water is in the range of 0.1 and 0.3 mg boron/L (WHO 1998).
In the United States, the average concentration of boron in water is about 0.1 mg/L but the range
of concentrations is vary large: about 0.001 mg/L to 5 mg/L (ATSDR 1992, p. 54). As noted in
Table 3-4, these concentrations are less than the concentrations that would be expected in water
after applications of Sporax.
Concentrations in soil are similarly variable, with a mean concentration in the U.S. of about 26
ppm with an upper bound of about 300 ppm (ATSDR 1992, p. 54). These concentrations,
however, are far in excess of the concentrations that would be added to soil as a result of Sporax
applications based either on GLEAMS modeling or the monitoring data presented by Dost et al.
(1996).
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3.3. DOSE-RESPONSE ASSESSMENT

3.3.1. Overview
The U.S. EPA (2004) has recently derived a chronic RfD of 0.2 mg/kg/day for boron (from boric
acid and borates), using the combined data of two developmental toxicity studies in rats using
decreased fetal weight as the most sensitive endpoint (Price et al. 1996a, Heindel et al. 1992).
The RfD is based on a benchmark dose analyses identifying a 5% decrease in mean fetal body
weight compared to control as the benchmark response (BMR) level (Allen et al. 1996). The
95% lower bound on the dose corresponding to the BMR, i.e., the BMDL05, of 10.3 mg B/kg/day
is used as the critical dose value to calculate the RfD. The uncertainty factor of 66, which
considers both the toxicokinetic and toxicodynamic aspects associated with interspecies and
interindividual variability, was applied to the critical dose to derive the chronic RfD of 0.2 mg
B/kg/day. The U.S. EPA has not derived an acute RfD for boron. Therefore, the chronic RfD of
0.2 mg B/kg/day will also be used to characterize risks associated with incidents or accidents that
involve an exposure period of 1 day.
3.3.2. Chronic RfD
The U.S. EPA recently derived an agency-wide chronic RfD for boron (from boric acid and
borates) of 0.2 mg B/kg/day (U.S. EPA 2004), as currently listed at the U.S. EPA web site for
RfDs http://www.epa.gov/ngispgm3/iris/. For this risk assessment, the chronic RfD value of 0.2
mg/kg/day is used directly for consistency with the U.S. EPA. As discussed in Section 3.1.9,
results of several studies demonstrate developmental effects following gestational exposure to
boron compounds (decreased fetal weight, increased fetal death, and increase in fetal
malformations). Specific developmental effects observed include a dose-dependent decreases in
fetal body weight and fetal malformations (primarily skeletal and central nervous system). Based
on an analysis of the data from developmental studies, the Institute for Evaluating Health Risks
(Moore 1997) concluded that decreased fetal body weight occurred at the same or lower boron
doses than skeletal malformations; thus, U.S. EPA (2004) has used decreased fetal weight as the
most sensitive effect of boron exposure. Although the previous RfD for boron and borates of
0.08 mg B/kg/day was based on the slightly lower NOAEL or critical dose of 8.8 mg B/kg/day
for testicular toxicity in dogs (Weir and Fisher 1972, U.S. EPA 1989), due to limitations of the
dogs studies (small number of animals per treatment group, NOAEL and LOAEL values
obtained at different time points), the U.S. EPA (2004) considers results of the developmental
studies in rats (Price et al. 1996a, Heindel et al. 1992) to be a more appropriate basis for the oral
RfD.
The chronic RfD for boron and boron compounds was derived by the U.S. EPA (2004) from
combined data of two developmental toxicity studies in rats using decreased fetal weight as the
most sensitive endpoint (Price et al. 1996a, Heindel et al. 1992). In the Heindel et al. (1992)
study, time-mated rats were fed diets containing 1, 0.1, 0.2, or 0.4% boric acid (equivalent to
approximately 0, 13.6, 28.5, or 57.7 mg B/kg/day) on gestational days 0-20, or 0.8% boric acid
(equivalent to approximately 94.2 mg B/kg/day) on gestational days 6-20. A dose-dependent
decrease in fetal weight was observed, with mean fetal weights significantly decreased compared
to control in all boron-treatment groups. The LOAEL for decreased fetal weight was defined as
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0.1% dietary boric acid (13.6 mg B/kg/day), the lowest dietary concentration tested; a NOAEL
was not established. In the Price et al. (1996a) study, time-mated rats were exposed to dietary
boric acid at concentrations of 0, 0.025, 0.050, 0.075, 0.10, or 0.20% (equivalent to
approximately 19, 36, 76, and 143 mg B/kg/day) on gestational days 0-20. Decreases in fetal
body weights were observed in the 0.10 and 0.20% boric acid treatment groups, with a NOAEL
of 0.075% dietary boric acid (equivalent to approximately 9.6 mg B/kgday) and a LOAEL of
0.10% dietary boric acid (equivalent to approximately 13.3 mg B/kg/day).
The RfD for boron is based on results of benchmark dose analyses conducted by Allen et al.
(1996) using the combined Heindel et al. (1992) and Price et al. (1996a) data. Allen et al.
identified a 5% decrease in mean fetal body weight compared to control as the benchmark
response (BMR) level. The 95% lower bound on the dose corresponding to the BMR, i.e., the
BMDL05, is used as the critical dose value to calculate the RfD. Allen et al. (1996) defined the
BMDL05 as 10.3 mg B/kg/day, a value very close to the NOAEL of 9.6 mg B/kg/day reported by
Price et al. (1996). The critical dose (the BMDL05 of 10.3 mg B/kg/day) is then divided by an
uncertainty factor of 66 to derive the chronic RfD of 0.2 mg B/kg/day. The uncertainty factor
consists of animal-to-human (UFA) and sensitive-human (UFH) uncertainty factors, both of which
are divided into toxicokinetic and toxicodynamic adjustment factors. The total uncertainty factor
is the product of four adjustment factors, which were assigned the following values for boron:
AFAK interspecies toxicokinetic adjustment factor (value 3.3, based on differences in kinetic
parameters between pregnant rats and pregnant women); AKAD interspecies toxicodynamic
adjustment factor (default value 3.16); AFHK interindividual toxicokinetic adjustment factor
(value 2, based on interindividual differences in kinetic parameters among pregnant women);
AFHD interindividual toxicodynamic adjustment factor (default value 3.16). Thus, the total
uncertainty factor is calculated as 66 [3.3 3.16 2 3.16 ].
3.3.3. Acute RfD
The U.S. EPA has not derived an acute/single dose RfD for boron compounds. As discussed in
Section 3.3.2, decreased fetal weight is considered the most sensitive endpoint resulting from
gestational exposure to dietary boron (Heindel et al. 1992, Price et al. 1996a). Although the
exposure duration in these studies was actually quite short (20 days), results were used to derive
the oral (chronic) RfD, based on a critical dose of 10.3 mg B/kg/day. As summarized in Section
3.1.5 and 3.1.9, results of reproductive toxicity studies identify testicular toxicity as the most
sensitive endpoint for longer-term exposures, with an NOAEL of 8.8 mg/kg/day in dogs (Weir
and Fisher 1972). However, given the concerns raised by U.S. EPA (2004) regarding the dog
study, coupled with the shorter exposure duration used in the developmental studies in rats,
assessing acute risk based on the results of the gestational studies in rats appears more
appropriate than using results of the longer-term toxicity studies in dogs. Thus, the RfD of 0.2
mg B/kg/day derived by EPA (2004) for chronic exposure will also be used to characterize risks
associated to incidents or accidents that involve an exposure period of 1 day.
As detailed in Section 3.4 (Risk Characterization), some of the accidental exposures to boron that
are considered in this risk assessment exceed the RfD of 0.2 mg B/kg/day by a very large margin.
3-22
In order to better assess the potential consequences of such exposures, the approximate lethal
doses to infants of 505 mg boron/kg/day and 765 mg boron/kg/day as well as the non-lethal dose
in infants of 184 mg B/kg/day (Wong et al. 1964) and the non-lethal doses of 241 mg/kg/day to
895 mg B/kg/day in adults (Linden et al. 1986) are used. These estimates are discussed in
Section 3.1.4.
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3.4. RISK CHARACTERIZATION

3.4.1. Overview
For exposures considered in this risk assessment, with the exception of the accidental exposure
of a child via consumption of Sporax from tree stump, all hazard quotients are below the level of
concern. For worker exposure from granular Sporax spilled on the lower legs and hands, hazard
quotients are well below the level of concern. Thus, workers do not appear to be at risk from
Sporax under typical application conditions. Because boron compounds may be more rapidly
absorbed across damaged skin, individuals with large areas of damaged skin should avoid the
application of Sporax or exercise extra caution if they do apply Sporax or other boron-containing
compounds. Borax can cause eye irritation. Quantitative risk assessments for irritation are not
derived; however, from a practical perspective, eye irritation is likely to be the only overt effect
as a consequence of mishandling Sporax. This effect can be minimized or avoided by prudent
industrial hygiene practices during the handling of the compound.
For the general public, hazard quotients for consumption of Sporax from a tree stump by a child
range from 2 to 16 for ingestion of 50 to 400 mg of Sporax (5.67 to 45.36 mg B/day). These
estimated levels of exposure are below levels of exposure associated with nonlethal effects such
as diarrhea and vomiting by factors of about 4 [184 45.36] to 32 [184 5.67]. Documented
lethal doses are in the range 505 mg B/kg/day and 765 mg B/kg/day, factors of about 11 to 135
below the estimated levels of exposure. Thus, while this exposure scenario raises concern in that
the RfD could be substantially exceeded in a child directly consuming Sporax from a treated
stump, the most likely adverse effects would probably be vomiting and diarrhea.
For consumption of water from a pond contaminated by Sporax due to runoff, none of the hazard
quotients exceed the level of concern, even for the highest application rate of 5 lbs Sporax/acre.
The highest hazard quotient for consumption of water contaminated by an accidental spill is 0.7,
associated with a child consuming water contaminated by the spill of 25 pounds of Sporax into a
small pond. Thus, based on this risk assessment, the only exposure scenario that appears to
present a significant potential risk is exposure by direct consumption under upper bound
conditions.
3.4.2. Workers
A quantitative summary of the risk characterization for workers is presented in Worksheets E02a,
E02b and E02c (Supplement 1). Risk is characterized as the estimated dose divided by the RfD.
This ratio is referred to as the hazard quotient (HQ). An HQ of one or less indicates that the
estimated exposure is less than the toxicity value; when this is the case, there is no basis for
asserting that adverse effects are plausible. Estimated exposures are summarized in Worksheet
E01. For acute accidental/incidental exposures, the acute RfD of 0.2 mg B/kg/day is used. As
noted in Section 3.3.3, the U.S. EPA (2004) has not derived an acute RfD for boron and the
chronic RfD derived by U.S. EPA (2004) is used in this risk assessment as a surrogate acute RfD.
As discussed in Section 3.2.2, the only exposure scenario considered in this risk assessment is
accidental spill of granular Sporax to the skin of the lower legs and hands during application.
3-24
Since the exposure scenarios is not dependant on application rate i.e., it is an incident that
could occur while applying Sporax at any application rate the hazard quotients given in
Worksheets E02a, E02b and E02c are the same and range from 0.00003 to 0.001. These hazard
quotients are below a level of concern by factors of 1000 to about 33,300. The highest hazard
quotient is 0.001, associated with an 8-hour dermal exposure of granular Sporax spilled on the
lower legs and hands. Thus, based on the available information and under the foreseeable
conditions of application, there is no route of exposure or scenario suggesting that workers will
be at any substantial risk from acute exposures to Sporax.
As noted in Section 3.1.3.1, rates of dermal absorption could be much higher in individuals with
large areas of abraded or otherwise damage skin. This is not considered quantitatively because
the impact of damaged skin would be highly dependent on the surface area of skin that was
damaged. In addition, it does not seem likely that individuals with large areas of seriously
damaged skin would be involved in the types of physical activities associated with the
application of Sporax. Nonetheless, the increased dermal absorption of boron compounds in
individuals with damaged skin suggests that workers will seriously damaged skin should either
not be involved in the application of Sporax or that these individuals should employ extra
measures to ensure that Sporax does not come into contact with damaged skin.
As also discussed in Section 3.1.3.1, borates are rapidly excreted in humans, with a halftime of
about 13 hours. Using the plateau principle (Section 3.2.3.4), the increase in body burden after
an infinite period of time (XInf) relative to the body burden after a single dose (X0) can be
calculated as:
XInf/X0 = 1 / (1- e-ke t*))
where t* is the interval between exposures and ke is the first-order rate of elimination. Using a
halftime of 13 hours (0.54 days, ke=1.27 days-1) and a one day exposure interval, the increase in
body burden would be a factor of about 1.4. Based on this factor, the highest hazard quotient of
0.001 for a single event would correspond to a chronic hazard quotient of no greater than 0.0014
for any longer term exposure. Thus, even if workers were to repeatedly spill granular Sporax on
the lower legs and hands every day, the hazard quotient associated with longer term exposures
would be far below the level of concern.
Borax can cause eye irritation (section 3.1.11). Quantitative risk assessments for irritation are
not derived; however, from a practical perspective, eye irritation is likely to be the only overt
effect as a consequence of mishandling Sporax. This effect can be minimized or avoided by
prudent industrial hygiene practices during the handling of the compound. The Sporax label
requires eye protection during application.
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3.4.3. General Public

A quantitative summary of the risk characterization for members of the general public is
presented in Worksheets E04a, E04b, E04c for the range of application rates considered in this
risk assessment. As with the risk characterization for workers, risk is expressed quantitatively as
the hazard quotient using the oral RfD of 0.2 mg B/kg for acute and chronic exposures (Section
3.3) . With the exception of the direct consumption of Sporax applied to a tree stump by a small
child, none of the hazard quotients exceed the level of concern.
For a child ingesting Sporax from a tree stump, hazard quotients range from 2 to 16, with a
central estimate of 4. As discussed in Section 3.2.3.2, the estimated amount of Sporax that a
child may consume in one day is based on the range for the amount of soil that may be consumed
by children i.e., 50 to 400 mg/day (5.67 to 45.36 mg B/day) (U.S. EPA 1996) and this may not
reflect the amount of Sporax that a child might consume in a single event. Since the exposure
estimate is highly uncertain and not based on empirical data for borate consumption, risk for this
exposure scenario may be underestimated or overestimated. As discussed in Section 3.1.4,
relatively good estimates of lethal and sublethal doses in children are available (ATSDR
1992;Wong et al. 1964). Documented lethal doses are in the range 505 mg B/kg/day and 765
mg B/kg/day, factors of about 11 [505 45.36] to 135 [765 5.67] below the estimated levels of
exposure from ingesting borax from a treated stump. A nonlethal dose in children is about 184
mg B/kg/day and this dose is associated with gastrointestinal effects such as vomiting and
diarrhea. The estimated levels of exposure for a child ingesting borax from a treated stump are
below this nonlethal level by factors of about 4 [184 45.36] to 32 [184 5.67]. Thus, while this
exposure scenario raises concern in that the RfD is substantially exceeded, the most likely
adverse effects would probably be vomiting and diarrhea.
Hazard quotients for a small child consuming water contaminated by an accidental spill of borax
into a small pond range from 0.07 to 0.7. For this worst-case scenario, the spill of a 25 pounds of
Sporax, the hazard quotient is below the level of concern. The exposures for the accidental spill
scenario are based on amounts of borax ranging from 6.25 to 25 pounds. Since risk is linearly
related to the amount of the chemical that is spilled into a pond, for spills of larger amounts,
hazard quotients could exceed the level of concern.
For exposure via consumption of water contaminated by runoff, the range of application rates
considered is 0.1 lb Sporax/acre to 5 lbs Sporax/acre (0.01 to 0.57 lb B/acre), with a typical rate
of 1 lb Sporax/acre (0.11 lb B/acre). Hazard quotients for acute exposure of a child and chronic
exposure of an adult male to water contaminated by runoff are below the level of concern for all
application rates considered. The highest hazard quotient of 0.3 is associated with the upper
bound for acute exposure of a child. Thus, even at the highest application rate, there does not
appear to be a risk associated with acute or chronic exposure to water contaminated by runoff.
The number of other exposure scenarios could be considered. For example, deer may consume
Sporax from a tree trunk. A hunter consuming meat from a deer that previously consumed
Sporax might then be exposed to a greater than normal amount of boron. This type of exposure
3-26
scenario for a deer is considered in Section 4.2. As detailed in Worksheet F01, the maximum
dose for a deer is estimated at 11.5 mg B/kg bw. As detailed in Section 3.2.3.4, however, this
concentration (equivalent to 11.5 ppm boron) is in the range of normal concentrations of boron in
most terrestrial vegetation (2.3-94.7 ppm) and near the lower end of range of boron in many food
commodities (1 to 300 ppm). Thus, the consumption of deer is not considered quantitatively.
Like most other exposure scenarios covered in this risk assessment, all but the most extreme
exposure scenarios associated with the use of Sporax in Forest Service programs simply do not
lead to a substantial increase in normal exposures to boron (e.g., Table 3-4).
3.4.4. Sensitive Subgroups
As discussed in Section 3.1.5, the primary targets for boron toxicity are the developing fetus and
the testes. Thus, exposure of pregnant women to borate compounds places the developing fetus
at risk. Since the oral (chronic) RfD for boron and borates is based on effects (decreased fetal
weight) in the developing fetus, risk to this subgroup is assessed throughout this document.
Regarding other sensitive subgroups, males with underlying testicular dysfunction could be at
increased risk for boron-induced testicular toxicity. However, no data are available to quantify
this risk.
3.4.5. Connected Actions
Sporax is not applied in combination with other products or additives. In addition, no data are
available regarding the effects of boron compounds applied in conjunction with other chemicals.
Thus, an assessment of toxicological effects of borax mixed with other chemicals cannot be
made.
3.4.6. Cumulative Effects
As noted above, chronic exposure to borax is considered for the exposure scenario of an adult
consuming surface water contaminated by runoff. Based on the limited analysis in this risk
assessment, as discussed above and summarized in Worksheet E04c, there is no indication that
repeated exposures will exceed the threshold for toxicity.
As detailed in Section 3.2.3.4, Sporax is unusual for a pesticide in that the toxicologic agent of
concern i.e., boron is a naturally occurring compound. Boron is a normal consistent of the
earths crust, all environmental media, as well as all forms of life including humans. Based on
estimates of normal background exposures supported by pharmacokinetic analysis, typical
exposures to boron are about 0.14 to 0.36 mg/kg/day. Based on central estimates of exposures to
boron associated with the application of Sporax in Forest Service programs, non-accidental
exposures are below normal background concentrations by factors of about the typical exposure
is above those associated with normal background exposures by a factor of 125 for acute
exposure and 625 for chronic exposure. Considering the variability of the estimates of both
normal background exposures and estimates of exposure associated with the application of
Sporax, Sporax applications lead to exposures that are below those associated with normal
background exposures by factors of 13 to 9000 (Section 3.2.3.4). Thus, under foreseeable and
typical conditions, applications of Sporax in Forest Service programs will not lead to any
3-27
substantial increase in exposure. This is not the case for accidental exposures. For these
scenarios, the application of Sporax could approach normal background exposures in the case of
an accidental spill and could substantially exceed normal background exposures in the case of a
child consuming borax from a treated stump.
In considering the added exposure to boron associated with the application of Sporax,
consideration of the design of the toxicity studies in important. The toxicity studies used to
characterize risk quantitatively were all conducted based on the addition of boric acid to the diet
(e.g., Heindel et al. 1992, 1994, Price et al. 1996a,b). The total exposure of the animals to boron,
the agent of concern, involved both the added boric acid as well as background concentrations of
boron. Similarly , the reports of human exposures to borax that are used qualitatively modify the
risk characterization (i.e., Linden et al. 1986; Wong et al. 1964) also involved exposures to boric
acid and background concentrations of borax.
The significance of this is evident in a simple comparison of the chronic RfD of 0.2 mg B/kg/day
(Section 3.3) to normal background levels of exposure i.e., 0.14 to 0.36 mg/kg/day (Section
3.2.3.4). Mathematically, these numbers could be used to derive risk quotients of 0.7 to 1.8.
Interpreting these risk quotients in a manner to suggest that humans are typically exposed to
hazardous or nearly hazardous levels of boron would be a misinterpretation. Many naturally
occurring substances such as oxygen and carbon dioxide can be toxic and some of the
mechanisms of action e.g., oxidative damage to tissue and binding of carbon dioxide to
hemoglobin are normal processes in living organisms that cannot be avoided. A more
appropriate interpretation of the RfD would be that increase exposure to boron by the amount of
the RfD would reach a level of concern. This is the interpretation given in the current risk
assessment and is consistent with approach taken by U.S. EPA (1993a) in waiving tolerances for
boric acid and the salts of boric acid in agricultural commodities.
3-28
4. ECOLOGICAL RISK ASSESSMENT

4.1. HAZARD IDENTIFICATION
4.1.1. Overview.
As discussed in Section 2, borate salts are rapidly converted to boric acid under conditions
typically found in the environment. At physiologic pH and in most surface waters, exposure of
organisms is primarily to boric acid. Therefore, information on boric acid is reviewed as
appropriate and used as surrogate data in this risk assessment for borax. In order to facilitate any
comparisons between borax and boric acid, data are expressed in terms of the dose or
As discussed in Section 3.1, in terrestrial mammals, the primary target organ for chronic borax
exposure is the testis, with exposure resulting in decreased male fertility. In birds, acute
exposure to borax is practically non-toxic, with no significant clinical signs of toxicity at dietary
concentrations up to 5000 ppm borax (567 ppm B equivalent to 567 mg B/kg diet). Although
limited data are available in birds, it appears that longer-term dietary exposure to boron
compounds results in adverse reproductive effects in avian species. Very little information is
available on the effects of boron compounds on nontarget terrestrial invertebrates. Based on the
results of a single acute topical exposure study of honey bees (LD50 >362.58 :g boric acid/bee or
41.1 :g B/bee), boric acid is considered essentially non-toxic. However, given that borax is used
in the control of termites, ants and house flies, toxic effects may occur in other insects.
Boron is an essential trace element for terrestrial plants. The amount of boron required to
produce optimal growth and development varies tremendously between species and even
between strains of the same species. However, excess boron can lead to the development of
phytotoxicity. In most species, there is a narrow range between the amount of boron required for
optimal growth and the amount that is phytotoxic. Standard bioassays for toxicity of boron
compounds to terrestrial plants (Tier I and Tier II seedling emergence or vegetative vigor studies)
were not identified in the available literature. While there are many studies evaluating the
phytotoxicity of boron compounds, few provide data that are useful in a quantitative assessment
of the risk of boron toxicity. Data are available for a limited number of terrestrial plants
potatoes, winter wheat, sugarbeet, poppy, oats and turnip. Based on the lowest reported NOAEC,
the most sensitive species appears to be the potato, with an NOAEC of 5 mg B/kg soil and the
most tolerant species appears to the sugarbeet, with an NOAEC of 20 mg B/kg soil. However, it
is likely that more sensitive and more tolerant species exist.
In fish and aquatic invertebrates, acute exposure to borax and boric acid appears to have a
relatively low order of toxicity. In fish, 96-hour LC50 values range from >100 mg B/L in
razorback suckers and squawfish to >1100 mg B/L in bluegill sunfish. The 48-hour LC50 values
for Daphnia magna range from 126 to 141 mg B/L. Limited information is available on chronic
exposure of fish to boric acid and borax. Chronic reproduction studies in daphnids yield an
NOAEC for reproductive effects of 6 mg B/L.
4-1
Relative to the abundant literature on the essential role of boron in terrestrial plants, very little
information is available on the effects of boron compounds on aquatic macrophytes. Short-term
exposure studies were conducted with boric acid in watermilfoil, water buttercup, and
waterweed, with similar LC50 values reported for all three plant species (watermilfoil and
waterweed: 5 mg B/L; water buttercup 10 mg B/L). In algae, the 72-hour LC50 values reported
for Scenedesmus subpicatus range from 34 mg B/L to 52 mg B/L and the 72-hour NOAEC
values range from 10 mg B/L to 24 mg B/L, with similar NOAEC values reported for
Scenedesmus quadricauda and Microcystis aeruginosa.
4.1.2. Toxicity to Terrestrial Organisms.
4.1.2.1. Mammals As summarized in the human health risk assessment (see Section 3.1), the
mode of action of borax and other borate salts in mammals is not well understood. There are
several standard toxicity studies in experimental mammals that were conducted as part of the
registration process. Results of studies in laboratory mammals are summarized in Section 3.1,
with additional information provided in Appendix 1. Based on the results of acute exposure
studies, borax is classified as moderately toxic, with an LD50 in male rats of 4.5 g borax/kg (Weir
and Fisher 1972). Clinical signs of toxicity observed following acute exposures include
depression, ataxia and convulsions. In dogs, acute exposure to borax produced a strong dosedependent emetic response (Weir and Fisher 1972). As expected of a compound with a low
dermal absorption rate, the LD50 of borax following single dermal application is > 5 g/kg in rats
(Wnorowski 1996a) and > 2 g/kg in rabbits (Reagan 1985a). Results of a single inhalation
exposure study yielded a 4-hour LC50 > 2.0 mg/L (Wnorowski 1994a).
Results of developmental, subchronic and chronic toxicity studies show that the developing fetus
and the male reproductive system are the primary targets for borate-induced toxicity (Sections
3.1.5 and 3.1.9). Gestational exposure of rats, mice, and rabbits to boric acid resulted in
observed from gestational exposure to boric acid is decreased body weight. Regarding testicular
toxicity, results of subchronic and chronic dietary exposure studies in adult rats and dogs show
that testicular toxicity is characterized by dose-dependent atrophy of the testes, degeneration of
the seminiferous epithelium, and sterility (Weir and Fisher 1972, Dixon et al. 1976, 1979, Lee et
al. 1978). At lower exposure levels, testicular effects and infertility may be reversed (Dixon et
al. 1979), but adverse effects can persist for at least 8 months at higher exposure levels (Lee et al.
1978).
As discussed in Section 3.3.3, the U.S. EPA (2004) has recently derived an oral (chronic) RfD of
0.2 mg/kg/day for boron (boron and borates only), using the combined data of two developmental
toxicity studies in rats using decreased fetal weight as the most sensitive endpoint (Price et al.
1996a, Heindel et al. 1992). The RfD is based on a benchmark dose analyses identifying a 5%
decrease in mean fetal body weight compared to control as the benchmark response (BMR) level
4-2
(Allen et al. 1996). The 95% lower bound on the dose corresponding to the BMR, i.e., the
BMDL05, of 10.3 mg B/kg/day is used as the critical dose value to calculate the RfD. The
uncertainty factor of 66, which considers both the toxicokinetic and toxicodynamic aspects
associated with interspecies and interindividual variability, was applied to the critical dose to
derive the chronic RfD of 0.2 mg B/kg/day. Based on a review of the studies considered by the
U.S. EPA, the selection of this study seems reasonable and appropriate. The U.S. EPA has not
derived an acute RfD for boron. Therefore, the chronic RfD of 0.2 mg B/kg/day will also be used
to characterize risks associated to incidents or accidents that involve an exposure period of 1 day.
Additional details on these developmental studies are provided in Sections 3.1.5, 3.1.9, and 3.3.2
and in Appendix 1.
Two internal Forest Service documents provide information on the effects of borax in field
settings - one study on the attractant effects of borax applied to tree stumps and a veterinarians
report on the death of a cow in a borax-treated area. In a field study conducted by the Forest
Service, the attractant effects of borax applied to freshly cut Douglas fir stumps were evaluated
(Campbell et al., no date). Deer were introduced to a 2.5 acre pen with freshly cut tree stumps
that were either untreated or had been treated with 1 oz (28.4 g borax) of borax. Deer appeared
equally attracted to both control stumps and borax-treated stumps, exhibiting sniffing and licking
behavior. There was no apparent attractant effect of borax-treated stumps and there were no
obvious signs of toxicity to deer that did eat borax from the stumps. The amount of borax that
deer licked from the stumps was not quantified. Dost (1994) summarizes an incident involving
the death of a cow in an area that had been treated with borax. Although Dost (1994) concluded
that it was unlikely that the cow had died due to the ingestion of borax, this opinion appears to be
formulated largely on the basis of the literature reviewed by Dost (1994) on the toxicity of borax
and on the environmental circumstances encountered. As the cow was found at least 10 days
after death, Dost (1994) also noted that pathological or chemical examinations of the carcass
were not possible.
4.1.2.2. Birds Limited information is available on the acute and chronic effects of borax and
other boron-containing salts in avian species. In standard test species, acute single and acute
dietary exposure studies have been conducted on borax and boric acid (Fink et al. 1982a, Reinart
and Fletcher 1977, U.S. EPA 1993b); results are summarized in Appendix 2. Based on the LD50
of >2510 mg borax/kg (equivalent to >284 mg B/kg) in bobwhite quail, exposure to a single oral
dose of borax is considered to be practically non-toxic to avian species (Fink et al. 1982a). A
similar low level of toxicity was also observed following 5-day dietary exposures of bobwhite
quail to borax, with an LC50 value >5000 ppm dietary borax (>567 ppm B) (Reinhart and
Fletcher 1977). In these two studies, no clinical signs of toxicity were observed. Similarly, 5day dietary exposures of bobwhite quail and mallard ducks to boric acid yielded LC50 values
>5000 ppm boric acid (equivalent to 874 ppm B), indicating that boric acid is also practically
non-toxic to avian species (U.S. EPA 1993b). Since LD50 and LC50 values obtained in these
studies were greater than the highest dose tested, it is difficult to draw conclusions regarding the
toxicity of borax relative to boric acid. However, based on the limited results available, birds
appear to exhibit similar sensitivity to borax and boric acid in acute exposures.
4-3
No chronic exposure studies (21-week exposure studies) on borax or boric acid using standard
test avian species were identified. The only avian reproduction study on borax identified in the
available literature is a 28-day dietary exposure study in broiler chickens (Rossi et al. 1993).
Results of this study show decreased hatchability in offspring of chickens exposed to 250 ppm B.
In male chickens exposed to borax (250 ppm B), an increase in the number of damaged
spermatozoa was observed (p = 0.051) (Rossi et al. 1993). Only one concentration of borax was
tested in this study; thus, the NOAEL is <250 ppm B and the LOAEL is 250 ppm B. A single
avian reproduction study in mallard ducks exposed to dietary boric acid for 6 weeks reported
decreased hatching, post-hatching growth and survival in the 1000 ppm B treatment group
(NOAEL = 300 ppm B; LOAEL = 1000 ppm B) (Smith and Anders 1989). There was no effect
of treatment on adult survival or egg fertility and no evidence of male reproductive toxicity was
observed (NOAEL >1000 ppm B). Details of these studies are provided in Appendix 2.
4.1.2.3. Terrestrial Invertebrates Very little information is available on the effects of borate
compounds in nontarget terrestrial invertebrates. No studies on the acute or chronic effects of
borax in nontarget terrestrial invertebrates were identified in the available literature. Results of a
single study on the effects of acute topical exposure of honey bees to boric acid show that boric
acid is essentially non-toxic to honey bees (Atkins 1987, U.S. EPA 1993b). No mortality was
observed in honey bees exposed to 363 :g boric acid/bee (equivalent to about 63 :g B/bee).
Results of efficacy studies show that borax is effective for the control of various insect pests,
including termites (Grace and Abdallay 1990, Grace and Yamamoto 1994, Toyoshima et al.
1997), ants (Klotz et al. 2000) and the house fly (Hogsette and Koehlet 1992). Based on its
effective use as an insecticide, it is likely that borax may have adverse effects on other insects.
However, data on the effects of boric acid and boric acid salts on nontarget insects are not
available in the literature.
4.1.2.4. Terrestrial Plants (Macrophytes) Boron is an essential trace element for terrestrial
plants. The amount of boron required to produce optimal growth and development varies
tremendously between species and even between strains of the same species ( ECETOC 1997,
Jamjod and Rerkasem 1999, Moore 1997, Tanji 1990, WHO 1998). Symptoms of boron
deficiency include cessation of root and leaf growth, leaf, stem and root tip necrosis, reduced
germination, and death (WHO 1998). Use of fertilizers containing boron can improve plant
vigor and increase crop yield for plants grown in boron-deficient soils (ECETOC 1997).
However, excess boron can lead to adverse effects in plants including chlorosis of leaves, leaf
necrosis and decreased germination (ECETOC 1997, WHO 1998). In most plant species, there is
a narrow range between the amount of boron required for optimal growth and the amount that is
phytotoxic (ECETOC 1997, Moore 1997, WHO 1998). According to the product label for
Sporax (Wilbur-Ellis Company, no date), borax spilled or applied to crops may retard plant
growth or kill plants. The label does not specify which plants species are at greatest risk for
borax-induced phytotoxicity.
4-4
Standard bioassays for toxicity of boron compounds to terrestrial plants (Tier I and Tier II
seedling emergence or vegetative vigor studies) were not identified in the CBI literature. While
there are many studies evaluating the phytotoxicity of boron compounds, few provide data that
are useful in a quantitative assessment of the risk of boron toxicity; much of the available data is
from studies focused primarily on the correlation between boron toxicity and boron accumulation
in plant leaves. The studies providing adequate data to allow for a quantitative assessment of
risk are summarized in Appendix 4. Data are available for a limited number of terrestrial plants
potatoes, winter wheat, sugarbeet (Kluge 1990, as cited in ECETOC 1997), poppy (Sopova et
al. 1981),oats and turnip (Stanley and Tapp 1982, as cited in Windeatt et al. 1991). All studies
summarized in Appendix 4 follow similar protocols: seeds are planted in boron-containing soil
(added as borax or boric acid). Phytotoxicity and plant development are assessed at a later time
point in the study. However, it is difficult to compare results of these studies since toxicity
endpoints vary between studies (in some studies the toxicity endpoints are reported as the EC50
and in others as the NOAEC) and standard toxicity bioassay protocols were not followed. Based
on the lowest reported NOAEC, the most sensitive species appears to be the potato, with an
NOAEC of 5 mg B/kg soil (Kluge 1990, as cited in ECETOC 1997) and the most tolerant species
appears to be the sugarbeet with an NOAEC of 20 mg B/kg soil (Kluge 1990, as cited in
ECETOC 1997). However, it is likely that more sensitive and more tolerant species exist.
4.1.2.5. Terrestrial Microorganisms Very little information is available on the effects of boric
acid or borax on nontarget terrestrial microorganisms. There is no evidence to suggest that boron
is an essential nutrient for soil microorganisms (WHO 1998). An in vitro study of soil treated
with borax (concentrations not specified) showed that borax treatment had no effect on total soil
counts of actinomyces, fungi, protozoa and bacteria involved in nitrification (Smith et al. 1946).
Borax is effective in the control of various wood-rotting fungi, including Heterobasidion
annosum (Findlay 1953, 1960, Graham 1970). Although inadequate data are available to provide
an assessment of the effects of borax in nontarget microorganisms, given the effectiveness of
borax in the control of annosum root disease, it is likely that borax will have effects on nontarget
microorganisms.
4.1.3. Aquatic Organisms.
4.1.3.1. Fish Information on the toxicity of boron to fish is summarized in Appendix 5.
Standard bioassays on the acute toxicity of borax in fish were not identified in the CBI literature.
As discussed in Section 2, since borax is converted to boric acid in water, studies on boric acid
can be used to supplement the limited information available on the effects of acute borax
exposure in fish. Acute exposure studies on borax have been conducted in rainbow trout
(Alabaster 1969, as cited in Hovatter and Ross 1995) and western mosquito fish (Wallen et al.
1957, as cited in Hovatter and Ross 1995). Based on the 48-hour LC50 values obtained in these
studies, rainbow trout (LC50 = 387 mg B/L) appear more sensitive than mosquito fish (LC50 = 930
mg B/L) to acute exposure to borax. More information is available on acute exposure of fish to
boric acid, with data available in bluegill sunfish, rainbow trout (LaLievre 1988, as cited in U.S.
EPA 1993b), Colorado squawfish, razorback sucker, bonytail (Hamilton 1995) and young salmon
fry (Hamilton and Buhl 1990). Based on the available acute LC50 values for borax and boric
4-5
acid, razorback suckers in the fry stage appear to be the most sensitive species to acute boron
exposure (96-hour LC50 of 233 mg B/L from Hamilton 1995) and rainbow trout appear to be the
most tolerant species (96-hour LC50 >1100 mg B/L from U.S. EPA 1993b). Based on these
values and the classification scheme typically used by the U.S. EPA (U.S. EPA/EFED 2001),
these compounds are classified as practically nontoxic to fish.
Longer-term toxicity studies on borax were conducted using rainbow trout, channel catfish, and
goldfish. Data from these studies were reported in a single publication from the open literature
(Birge and Black 1977) and are summarized in Appendix 5. No standard chronic exposure
studies on borax or boric acid were identified in the CBI literature. Results of the Birge and
Black (1977) study show a similar degree of sensitivity for the three species tested. The lowest
estimated NOAEC (for mortality) of 0.5 ppm B was reported for goldfish and the highest
estimated NOAEC (for mortality) of 1.0 ppm B was reported for rainbow trout and channel
catfish. Since different exposure times were used for each of the three species tested (up to 28
days for trout, 9 days for catfish, and 7 days for goldfish), it is difficult to identify a most
sensitive and most tolerant species for longer-term exposure.
4.1.3.2. AmphibiansVery little information is available on the effects of borax to amphibians.
A single study in larval leopard frogs exposed to borax for 7.5 days reports an LC50 of 47 ppm B,
with an estimated NOAEC (for mortality) of 1.0 ppm B and an estimated LOAEC (for mortality)
of 5.0 ppm B (Birge and Black 1977). Thus, toxicity of borax to leopard frogs appears to be
relatively low. Results of a study in wood frog, Jefferson salamander, spotted salamander, and
American toad show that boron concentrations of 50 and 100 mg B/L caused a dose-related
decrease in proportion of eggs hatching in American toad, while hatching was unaffected in the
other three species (Laposata and Dunson 1998). In this same study, a dose-dependent increase
in proportion of deformed larvae was observed in wood frog, Jefferson salamander, and spotted
salamander (not assessed in American toad). Details of these studies are provided in
Appendix 5.
4.1.3.3. Aquatic Invertebrates No standard bioassays of the acute and chronic toxicity of borax
or boric acid to aquatic invertebrates were identified in the CBI literature. Acute toxicity studies
on borax and boric acid have been conducted in Daphnia magna, with results reported in the
published literature (Appendix 6). Results of 48-hour exposure studies show similar LC50 values
for borax (48-hour LC50 = 141 mg B/L, Maier and Knight 1991) and boric acid (48-hour LC50 =
133 mg B/L, Gersich 1984; 48-hour LC50 = 126 mg B/L, Lewis and Valentine 1981). The larval
freshwater midge Chironomus decorus (a benthic organism) appears to be more tolerant than
daphnids to acute boron exposure, with a 48-hour LC50 value of 1376 mg B/L (Maier and Knight
1991).
Two 21-day exposure studies in daphnids were conducted with boric acid, with results reported
in the published literature; similar results were reported for both studies (Appendix 6). The
lowest 21-day LC50 value reported for exposure of daphnids to boric acid is 52.2 mg B/L
4-6
(Gersich 1984). The lowest NOAEC value reported for reproductive parameters is 6 mg B/L with
a LOAEC for reproductive parameters of 13 mg B/L (Lewis and Valentine 1981).
4.1.3.4. Aquatic Plants No studies on the effects of borax in aquatic macrophytes were
identified in the available literature. Short-term exposure studies were conducted with boric acid
in watermilfoil, water buttercup, and waterweed (Nobel 1981, as cited in WHO 1998). Similar
LC50 values were reported for all three plant species (watermilfoil and waterweed: 5 mg B/L;
water buttercup 10 mg B/L). A chronic exposure study of boric acid in common reed
(Phragmites australis) reports a 2-3 month NOAEC of 8 mg B/L and a 2-year NOAEC of 4 mg
B/L (Bergmann et al. 1995, as cited in ECETOC 1997 and WHO 1998).
The effects of boron exposure in algae have been reviewed by ECETOC (1997) and WHO
(1998). The 72-hour LC50 values reported for Scenedesmus subpicatus range from 34 mg B/L to
53 mg B/L and the 72-hour NOAEC values range from 10 mg B/L to 24 mg B/L. Similar
NOAEC values were reported for Scenedesmus quadricauda and Microcystis aeruginosa. Based
on the information presented in the ECETOC 1997 and WHO 1998 reviews, the algal species
tested show a similar degree of sensitivity to the toxic effects of boron. Based on the information
presented in these reviews, it is not possible to determine the chemical species of boron used in
these studies because exposures were reported in terms of boron equivalents.
4.1.3.5. Aquatic Microorganisms (Other than algae)
The effects of boron exposure to aquatic microorganisms (other than algae) was recently
reviewed by WHO (1998). Data are reported in several species, with 72-hour NOAEC values
ranging from 0.3 mg B/L in Entosiphon sulfacum, a flagellate (Bringmann and Kuhn 1980, as
cited in WHO 1998), to 291 mg B/L in Pseudomonas putida (Schoberl and Huber 1988, as cited
in WHO 1998).
4-7
4.2. EXPOSURE ASSESSMENT

4.2.1. Overview
As discussed in Section 3.2, Sporax is applied directly to the surfaces of freshly cut tree stumps.
Sporax is not applied using backpack, broadcast or aerial spray methods and it is not applied
of contaminated prey or vegetation, are not applicable for this risk assessment. The exposure
scenarios used in this risk assessment are those expected to result in substantial exposure
considering the atypical application method for Sporax. Since Sporax is not applied as a spray,
wide-spread exposure of insects is not expected; thus, an exposure assessment for insects has not
been conducted in this risk assessment. Due to a lack of toxicity data, no exposure assessment
was conducted for nontarget soil microorganisms.
For terrestrial vertebrates, two exposure scenarios are considered for this risk assessment: acute
exposure via consumption of Sporax applied to tree stumps, and acute as well as chronic
exposure via exposure to contaminated pond water. Exposure values for acute exposure via
consumption of Sporax applied to a tree stump range from 0.57 mg B/kg/event for a large
mammal to 29 mg B/kg/event for a small bird.
For contamination of water by both an accidental spill scenario and by runoff from the
application site are considered. As noted in the exposure assessment for human health, the use of
Sporax in stump treatments is not likely to have a substantial affect on concentrations of boron in
ambient water. For ingestion of contaminated water via accidental spill, acute exposure values
for a small mammal range from 0.0001 to 0.0004 mg B/kg/event. For acute exposure of a small
mammal via ingestion of water contaminated by runoff, acute exposure values range from
approximately 0.0009 to 0.014 mg B/kg/event. For chronic exposure of a small mammal by
water contaminated by runoff, exposure values range from about 0.0003 to 0.01 mg B/kg/day.
Since Sporax is not applied to vegetation, the only exposure scenario considered for terrestrial
macrophytes is exposure to boron that reaches soil via runoff. Based on the results of GLEAMS
modeling, peak concentrations of boron in soil range from 0.0026 ppm for the lowest value
associated with an application rate of 0.1 lb Sporax/acre to 2.29 ppm in soil for the highest value
associated with an application rate of 5 lbs Sporax/acre.
Exposures to aquatic organisms are based on the same information used to assess the exposure to
terrestrial species from contaminated water. For an accidental spill of Sporax into a small pond,
the central peak estimated concentration of boron in ambient water is 0.64 mg B/L (0.32 - 1.28)
mg B/L (ppm). For contamination of a small pond by runoff, the peak estimated concentration in
ambient water is 30 (6 to 100) g/L after a single application of 1 lb Sporax/acre (0.11 lb
boron/acre). For longer-term exposures, the corresponding longer term concentrations in
ambient water are estimated at about 14 (2 to 70) g/L.
4-8
4.2.2. Terrestrial Vertebrates

4.2.2.1. Oral Exposure to Sporax Applied to Tree Stumps Very little information is available
to estimate the amount of Sporax that deer, other mammals, or birds are likely to consume.
Thus, exposures developed for this scenario are highly uncertain.
A field study conducted by the Forest Service on the attractant effects of Sporax applied to tree
stumps (Campbell et al., no date) reports that deer will lick borax applied to the surface of tree
stumps. Because deer also licked the surface of untreated control stumps, it is not clear that
Sporax is an attractant for deer. Nonetheless, the study by Campbell et al. (no date) suggests that
the consumption of Sporax from treated stumps is a plausible exposure scenario for deer and may
be plausible for other species as well.
For large mammals such as a deer, exposure is based on the underlying assumption that a deer
might consume all of the Sporax applied to a tree stump that is 1 foot in diameter. Based on the
application rate for Sporax of 1 lb/50 ft2 of stump area and the application area of a 1 foot
diameter stump of 0.7854 ft2 [Br2 = (3.1416) (0.5 ft)2 = 0.7854 ft2], the amount of Sporax applied
to a 1 foot diameter stump is 0.0157 pounds [1 lb/50 ft2 0.7854 ft2 = 0.0157 lb] or 7.12 grams
of Sporax or 807 mg boron equivalents [7.12 g 1000 mg/g 0.1134]. As with the exposure
assessments for small mammals and birds, the central estimate of the proportion of the Sporax
that is consumed from the stump will be taken as 0.3 with a range of 0.05 to 1.0. Thus, the
consumption in units of boron equivalents is 242 mg [807 mg 0.3] with a range of 40 mg [807
mg 0.05] to 807 mg. This exposure scenario is detailed in Worksheet F01.
While the direct consumption of Sporax by a large mammal such as a deer seems plausible,
direct consumption by a large bird (such as a goose or heron) seems implausible. Large birds
such as heron or geese will typically consume either vegetation or fish (U.S. EPA/ORD 1993).
Nonetheless, a similar scenario is developed for a Canada goose with a body weight of 4 kg. The
amount of boron that might be consumed is reduced in proportion to the body weight of the
goose relative to the deer i.e., 4/70 or about 0.057. Thus, the consumption in units of boron
equivalents is estimated at 13.7 mg [242 mg 0.057] with a range of 2.3 mg [40 mg 0.057] to
46 mg [807 mg 0.057]. This exposure scenario is detailed in Worksheet F02.
For smaller species, it seems less plausible that the animal would consume all of the Sporax on a
treated stump. The body weights that are used in most Forest Service risk assessments are
adopted from U.S. EPA/ORD (1993) and range from 10 grams for a small bird and 20 grams for
a small mammal (SERA 2001). As noted above, the amount of Sporax on a stump with a 1 foot
diameter would be approximately 7 grams. Based on allometric relationships given in U.S.
EPA/ORD (1993), the daily food consumption for small mammals and birds will typically be
equivalent to about 10% to 20% of their body, depending on the caloric value of the food source.
Consuming 7 grams of Sporax would be equivalent to 35% to 70% of the body weight of a small
mammal and bird, respectively.
4-9
As an alternative to assuming complete consumption for small mammals and birds, the
assumption is made that the amount of Sporax that might be consumed from the surface of a
treated stump will range from 0.05 to 0.2 of the body weight of the animal, with a central
estimate of 0.1. These values for Sporax are adjusted downward by a factor of 0.1134 to convert
the consumption of Sporax to boron equivalents (Table 2-1). Thus, rounding to 2 significant
figures, the proportion of the body weights used to estimate boron consumption is 0.011 with a
range of 0.0056 to 0.023. The scenarios for a small mammal and small bird are given in
worksheets F03 and F04, respectively.
4.2.2.2. Ingestion of Contaminated Water As discussed in the human health exposure
assessment (Section 3.2.3.3), the borax application considered in this risk assessment
application of granular product to tree stumps has a limited potential to contaminate water.
Nonetheless, after application to tree stumps, rainfall and consequent runoff could lead to
contamination of standing water or streams. In addition, accidental spills of the Sporax
formulation into a small body of water are possible.
The accidental spill scenario parallels that used in the human health risk assessment (3.2.3.4.1).
The amount of Sporax spilled ranges from 6.25 to 25 lbs (0.7 to 2.8 pounds of boron
equivalents), with a central estimate of 12.5 lbs (1.42 pounds of boron equivalents). This
exposure scenario is detailed in Worksheet F05 for a small mammal.
For non-accidental exposures, estimated concentrations of boron in water are identical to those
used in the human health risk assessment (Worksheet B06). The only major differences involve
the weight of the animal and the amount of water consumed. There are well-established
relationships between body weight and water consumption across a wide range of mammalian
species (e.g., U.S. EPA 1989). Unlike the human health risk assessment, estimates of the
variability of water consumption are not available. Thus, the only factor affecting the variability
of the ingested dose estimates is the concentration of the boron in water. The acute and chronic
scenarios for non-accidental exposures are given in Worksheets F06 and F07, respectively.
4.2.3. Terrestrial Plants
Since Sporax is not applied to vegetation and is not applied as a liquid, exposure scenarios that
are typically included in Forest Service risk assessment documents for terrestrial macrophytes,
such as exposure by direct spray or spray drift, are not applicable to this risk assessment. The
only exposure scenario considered for plants is exposure to boron in soil.
The available toxicity data on boron in terrestrial plants are expressed in units of soil
concentration i.e., mg boron/kg soil which is equivalent to parts per million (ppm)
concentrations in soil. The GLEAMS modeling discussed in Section 3.2.3.4.2 provides
estimates of concentration in soil as well as estimates of off-site movement (runoff, sediment,
and percolation). Based on the GLEAMS modeling, concentrations in clay, loam, and sand over
a wide range of rainfall rates are summarized in Table 4-1. As indicated in this table, peak soil
concentrations in the range of about 0.46 ppm boron are likely in arid loam at an application rate
4-10
of 1 lb Sporax/acre (0.11 lb boron/acre). As rainfall rate increases, maximum soil concentrations

are substantially reduced for each soil type because of losses from soil through percolation. The
potential consequences of such exposures are discussed in Section 4.4 (Risk Characterization).
Based on monitoring data, which show that normal boron concentrations range from 10 to 30
ppm, it is not expected that runoff from application of Sporax to tree stumps will contribute
significantly to boron soil concentrations.
4.2.4 Other Terrestrial Organisms
Borax is a fungicide and it is anticipated that at least some soil microorganisms will be exposed
to borax and could be adversely affected. However, due to a lack of quantitative toxicity data
applicable to soil exposures, the risks cannot be quantitatively characterized. Thus, no exposure
assessment is conducted for soil microorganisms in this risk assessment. Acute toxicity data are
available for honey bees. However, since Sporax is applied only to cut tree stumps and is not
applied by broadcast spray, it is unlikely that there will be wide-spread exposure to insects.
Thus, an exposure assessment for insects is not conducted as part of this risk assessment.
Exposure of individual insects that are on the treated stump surface at the time of treatment may
result in toxicity to a susceptible insect species.
4.2.5. Aquatic Organisms
The potential for effects on aquatic species is based on estimated concentrations of borax (as
boron equivalent) in water that are identical to those used in the human health risk assessment.
For this risk assessment, contamination of water is considered for two scenarios accidental spill
of a bag of Sporax (containing an amount ranging from 6.25 to 25 pounds Sporax) into a small
pond and contamination of pond water and contamination of a small pond by runoff. For an
accidental spill of Sporax into a small pond, the peak estimated concentration of boron in
ambient water is 0.64 mg B/L (0.32 - 1.28) mg B/L (ppm). Details of this calculation are
provided in Worksheet F05. As summarized in Table 3-3, for contamination of a small pond by
runoff, the peak estimated concentration of boron in ambient water is 30 (6 to 100) g boron/L
after a single application of 1 lb Sporax/acre (0.11 lb boron/acre). For longer-term exposures, the
corresponding longer term concentrations in ambient water are estimated at about 14 (2 to 70) g
boron/L.
4-11
4.3. DOSE-RESPONSE ASSESSMENT

4.3.1. Overview
The specific toxicity values used in this risk assessment are summarized in Table 4-2, and the
derivation of each of these values is discussed in the various subsections of this dose-response
assessment. The first column in Table 4-2 specifies the organism to which the toxicity value
applies. The available toxicity data support separate dose-response assessments in ten classes of
organisms: terrestrial mammals, birds, nontarget terrestrial invertebrates, terrestrial macrophytes,
fish, aquatic invertebrates, amphibians, aquatic macrophytes, algae, and aquatic microorganisms.
Different units of exposure are used for different groups of organisms depending on how
exposures are likely to occur and how the available toxicity data are expressed.
Borate compounds are relatively non-toxic to mammals and birds. For mammals, the toxicity
values used in the ecological risk assessment are identical to those used in the human health risk
assessments: the 95% lower bound on the dose corresponding to the BMR, i.e., the BMDL05, of
10.3 mg B/kg/day (the critical dose) for decreased fetal body weight (Allen et al. 1996, U.S. EPA
2004) is used to assess both acute and chronic risk. For birds, the acute NOAEL for boron is
taken as 136 mg B/kg based on lack of mortality or clinical signs of toxicity following 5-day
dietary exposure of bobwhite quail to borax. For chronic exposure of birds, the limited data
available suggest that longer-term exposure to boron compounds can cause testicular toxicity in
avian species; however the available studies did not rigorously investigate the potential for boron
compounds to produce testicular toxicity. Therefore, the mammalian critical dose of 10.3 mg
B/kg/day will be used to characterize the risk of chronic exposure to boron compounds in birds.
For terrestrial invertebrates, data used to characterize risk is from a single contact bioassay in the
honey bee, with an NOAEL for mortality of 677 mg/kg.
Although there is an abundant literature regarding the role of boron as an essential element for
terrestrial plants, standard bioassays on the effects of boron on seedling emergence and
vegetative vigor are not available. Based on the relatively limited information available, the
NOAEC of 5 mg B/kg soil for the potato will be used to characterize risk in the most sensitive
and the NOAEC of 20 mg B/kg soil will be used to assess risk in the most tolerant nontarget
plant species. However, it is likely that more sensitive and more tolerant species exist. Since
borates are effective fungicides, some nontarget soil microorganisms could be affected by
exposure to boron in soil. However, information to adequately assess risk in this class of
organisms is not available.
Toxicity values for aquatic species indicate relatively little difference between fish and aquatic
invertebrates based on acute toxicity. For fish, the acute 96-hour LC50 values are 233 mg B/L
and >1100 mg B/L for sensitive and tolerant species, respectively. For aquatic invertebrates, a
similar range in 48-hour LC50 values (133 mg B/L for sensitive species and 1376 mg B/L for
tolerant species) was observed. For chronic exposures, fish appear more sensitive than aquatic
invertebrates to boron exposure. In fish the range of NOAEC values is relatively narrow, with
the NOAEC of 0.5 ppm boron in the most sensitive species and 1.0 ppm boron in the most
tolerant species. In aquatic invertebrates, NOAEC values range from 6 mg B/L to the estimated
4-12
value of 61.8 mg B/L. To characterize the risk of acute exposure to amphibians, the NOAEC of
1.0 ppm B obtained in a single study in leopard frog larvae will be used. No studies on the
effects of chronic exposure of amphibians to boron compounds were identified in the available
literature. Based on the available data, the most sensitive algal species is the green algae
Scenedesmus subpicatus, with a 72-hour NOAEC of 10 mg B/L (Bringmann and Kuhn 1978, as
cited in ECETOC 1997) and the most tolerant species is the blue-green alga Microcystis
aeruginosa, with a 72-hour NOAEC of 20.3 mg B/L (Bringmann and Kuhn 1978, as cited in
ECETOC 1997). Although these tests are conducted for a relatively short period of time (i.e. 72
hours), these NOAEC values are applied to both acute and longer-term concentrations because of
the short life-cycle of individual algal cells. For aquatic macrophytes 21-day exposure studies
yield a range of LC50 values of 5 to10 mg B/L; these values will be used to assess acute exposure
risk to sensitive and tolerant aquatic macrophytes. For aquatic microorganisms, the NOAEC
longer-term exposures for sensitive and tolerant species of aquatic microorganisms because of
the short life-cycle of individual microorganisms.
4.3.2. Toxicity to Terrestrial Organisms
4.3.2.1. Mammals As summarized in the dose-response assessment for the human health risk
assessment (Section 3.3), the most sensitive effect in experimental animals is decreased body
weight in the developing fetus. The critical dose used to derive the oral (chronic) RfD for boron
and borates is the 95% lower bound on the dose corresponding to the BMR, i.e., the BMDL05, of
10.3 mg B/kg/day (the critical dose) for decreased fetal body weight (Allen et al. 1996, U.S. EPA
2004). The NOEC of 10.3 mg B/kg/day will be use in the ecological risk assessment to
characterize risks associated with longer-term exposures of mammalian wildlife species to borax.
As discussed in Section 3.3.3, the U.S. EPA has not derived an acute/single dose RfD for boron
compounds. Decreased fetal weight is considered the most sensitive endpoint resulting from
gestational exposure to dietary boron (Heindel et al. 1992, Price et al. 1996a). Although the
exposure duration in these studies was actually quite short (20 days), results were used to derive
the oral (chronic) RfD, based on a critical dose of 10.3 mg B/kg/day. As summarized in Section
3.1.5 and 3.1.9, results of reproductive toxicity studies identify testicular toxicity as the most
sensitive endpoint for longer-term exposures, with an NOAEL of 8.8 mg/kg/day in dogs (Weir
and Fisher 1972). However, given the concerns raised by U.S. EPA (2004) regarding the dog
study (Section 3.3.2), coupled with the shorter exposure duration used in the developmental
studies in rats, assessing acute risk based on the results of the gestational studies in rats appears
more appropriate than using results of the longer-term toxicity studies in dogs. Thus, the critical
dose of 10.3 mg B/kg/day used for longer-term exposures will also be used to characterize risks
to mammals associated to incidents or accidents that involve an exposure period of 1 day.
4.3.2.2. Birds Compared to the many studies conducted in laboratory mammals, there is very
little information available on the effects of acute and chronic exposure of avian species to boron
compounds. As detailed in Appendix 2, results of an acute (5-day) dietary exposure of bobwhite
quail yield an LC50 value >5000 ppm borax (equivalent to >567 ppm B), indicating that acute
4-13
exposure to borax has a low order of toxicity in avian species (Reinart and Fletcher 1977). No
clinical signs of toxicity were observed in birds exposed to dietary concentrations up to 5000
ppm borax. Thus, the NOAEL for acute exposure of birds is taken as 567 ppm B in the diet (136
mg B/kg/day). Conversion of dietary concentrations of boron to a daily dose of boron was made
by multiplying the average fractional weight of food consumption per bird (0.24) by the
concentration of boron in food (567 ppm B). The average fractional weight of food consumption
of 0.24 was determined by dividing the average food consumption/bird/day (10.4 g/bird/day) by
the average body weight (43 g). Both the average food consumption/bird/day and the average
body weight were reported by the authors. Thus, acute (1-day) exposures to avian species will be
based on the acute NOAEL of 136 mg B/kg/day from the 5-day dietary borax exposure study in
young bobwhite quail (Reinart and Fletcher 1977).
Standard bioassays of the reproductive effects of boron compounds in birds were not identified in
the available literature. A 6-week exposure study of boric acid in mallard ducks yielded an
NOAEL of 300 ppm B (60 mg B/kg/day) and an LOAEL of 1000 ppm boron (200 mg B/kg/day)
for decreased hatching and post-hatching growth and survival (Smith and Anders 1989).
Conversion of dietary concentrations of boron to a daily dose of boron was made by multiplying
the average fractional weight of food consumption per bird (0.20) by the concentration of boron
in food (300 and 1000 ppm B). The average fractional weight of food consumption of 0.20 was
determined by dividing the average food consumption/bird/day (209 g/bird/day) by the average
body weight (1,056 g). Both the food consumption/bird/day and the average body weight were
reported by the authors. A 28-day dietary exposure study of borax in broiler chickens reports a
LOAEL of 250 ppm B (6.5 mg B/kg/day) for decreased hatchability and damage to spermatozoal
cells, indicating that exposure to boron can cause developmental and testicular toxicity in birds
(Rossi et al. 1993); however, only one exposure level was tested in this study. Conversion of
dietary concentrations of boron to a daily dose of boron was made by multiplying the average
fractional weight of food consumption per bird (0.026) by the concentration of boron in food
(250 ppm B). The average fractional weight of food consumption of 0.026 was determined by
dividing the average food consumption/bird/day (146 g/bird/day) by the average body weight
(5,667 g). Both the food consumption/bird/day and the average body weight were reported by the
authors. In this study, only one dietary concentration (250 ppm B) was evaluated; no other boron
concentrations were tested.
Based on the limited data available, it appears that birds are susceptible to boron-induced
developmental and testicular toxicity. Data from the Rossi et al. (1993) study are of limited
usefulness since only one exposure level was assessed. In the Smith and Anders (1989) study,
decreased hatchability was observed at the 200 mg B/kg/day dose, with the NOAEL of 60 mg
B/kg/day. The results of these studies indicate that exposure to boron compounds can adversely
affect reproductive function in birds. However, since neither of these studies rigorously assessed
the potential of boron to produce developmental or testicular effects in birds or followed standard
bird reproduction bioassay protocols, the critical dose of 10.3 mg B/kg/day for developmental
effects in rats used to derive the oral (chronic) RfD will be used to assess risk of chronic
exposure to boron in birds.
4-14
4.3.2.3. Terrestrial Invertebrates As detailed in Appendix 3, a single study on the acute topical
exposure of boric acid in honey bees reports an LD50 >362.58 :g boric acid/bee (63.38 :g B/bee)
(Atkins 1987). Since no mortality occurred at this exposure level, 63.38 :g B/bee is taken as the
NOAEL for mortality in this study. Using a body weight of 0.093 g for the honey bee
(USDA/APHIS 1993), this value corresponds to a dose of 677 mg B/kg [0.063 mg/0.000093 kg].
This type of toxicity value, however, is used to assess the consequences of broadcast
applications. Because Sporax is not applied by this method, no quantitative risk characterization
for insects is developed.
4.3.2.4. Terrestrial Plants and Microorganisms As reviewed in Section 4.1.2.4, boron is an
essential trace element for terrestrial plants. The amount of boron required to produce optimal
growth and development varies tremendously between species and even between strains of the
same species. However, excess boron can lead to phytotoxicity. In most species, there is a
narrow range between the amount of boron required for optimal growth and the amount that is
phytotoxic. Standard bioassays for toxicity of boron compounds to terrestrial plants (Tier I and
Tier II seedling emergence or vegetative vigor studies) were not identified in the literature. Due
to the limited data available, coupled with the narrow dose range between beneficial and
phytotoxic effects, it is difficult to identify a most sensitive and a most tolerant plant species.
Based on results of studies published in the open literature (detailed in Appendix 4), the most
sensitive species appears to be the potato, with an NOAEC of 5 mg B/kg soil (Kluge 1990, as
cited in ECETOC 1997) and the most tolerant species appears to be the sugarbeet with an
NOAEC of 20 mg B/kg soil (Kluge 1990, as cited in ECETOC 1997). These values will be used
to characterize risk to nontarget terrestrial plants. However, it is likely that more sensitive and
more tolerant species exist.
Based on the effective use of borax in the control of various wood-rotting fungi, including
Heterobasidion annosum, it is likely that borax could adversely affect nontarget microorganisms.
However, no standard toxicity studies have been encountered that could be used to quantify risk
to soil microorganisms. Consequently, no dose-response assessment can be conducted for this
group of organisms.
4.3.3.1. Fish The acute bioassays on fish summarized in Appendix 5 provide estimates of
exposure which might be associated with acute effects in fish. Acute 96-hour LC50 values for
boric acid range from >100 mg B/L in large juvenile razorback sucker fish (Hamilton 1995) and
233 mg B/L in swimup razorback sucker fish (Hamilton 1995) to >1100 mg B/L in rainbow trout
(LaLievre 1988, as cited in U.S. EPA 1993b). Based on the available acute exposure data on
borax and boric acid, razorback sucker fry (96-hour LC50 233 mg B/L ) appear to be the most
sensitive aquatic organisms and rainbow trout (96-hour LC50 >1100 mg B/L) appear to be the
most tolerant aquatic species. The LC50 of >100 mg B/L in juvenile razorback sucker fish is not
considered as a endpoint to assess risk, since no mortality occurred at the highest exposure level;
thus an LC50 could not be estimated from the available data. For this risk assessment the 96-hour
LC50 of 233 mg B/L will be used to assess the risk of acute exposure to boron in the most
4-15
sensitive species and the 96-hour LC50 >1100 mg B/L will be used to assess acute exposure of the
most tolerant species.
Standard chronic exposure studies on the effects of borax or boric acid in fish were not identified
in the literature; all of the available data are from a single study on the effects of borax on
rainbow trout, channel catfish, and goldfish (Birge and Black 1977). Results of this study show a
similar degree of sensitivity for the three species tested. The lowest estimated NOAEC (for
mortality) of 0.5 mg B/L was reported for goldfish and the highest estimated NOAEC (for
mortality) of 1.0 mg B/L was reported for rainbow trout and channel catfish. NOAEC values
were estimated based on tabular results reported in the study. Since different exposure times
were used for each of the three species tested (up to 28 days for trout, 9 days for catfish, and 7
days for goldfish), it is difficult to identify a most sensitive and a most tolerant species for
longer-term exposure. To assess the risk of longer-term exposures of fish to boron, the NOAEC
of 0.5 mg B/L in goldfish will be used to represent the most sensitive species and the NOAEC of
1.0 mg B/L in rainbow trout and channel catfish will be used to represent the most tolerant
species.
4.3.3.2. Aquatic Invertebrates As detailed in Appendix 6, acute toxicity studies on boron using
borax and boric acid have been conducted in aquatic invertebrates. Based on the 48-hour LC50
value, Daphnia magna appears to be the most sensitive species (48-hour LC50 133 mg B/L)
(Gersich 1984), and Chironomas decorus, a midge, is the most tolerant species (48-hour LC50
1376 mg B/L) (Maier and Knight 1991). These values will be used to assess risk of acute boron
exposure in sensitive and tolerant aquatic invertebrates.
For chronic exposure studies on boron, data are only available in daphnids. The lowest NOAEC
reported for daphnids is 6 mg B/L for decreased brood size in organisms exposed to boric acid
(Lewis and Valentine 1981). Although no chronic exposure data are available in a more tolerant
species, a NOAEC for tolerant species can be derived based on the relative acute toxicity of
daphnids and midges. Based on comparisons of the 48-hour LC50 values for daphnids (133 mg
B/L) and midges (1376 mg B/L), midges are more tolerant to boron toxicity by a factor of 10.3
[1376 133 = 10.3]. Thus, to calculate a surrogate NOAEC in midges, the daphnid NOAEC of
6 mg B/L is multiplied by 10.3, yielding a value of 61.8 mg B/L. To characterize the risk of
chronic exposure to boron compounds, the NOAEC of 6 mg B/L will be used for the most
sensitive species and the surrogate NOAEC of 61.8 mg B/L will be used for the most tolerant
species.
4.3.3.3 Amphibians Exposure of leopard frog larvae to borax for 7.5 days yielded an LC50
value of 47 ppm boron and estimated NOAEC and LOAEC for mortality of 1.0 and 5.0 ppm B,
respectively (Birge and Black 1977). To assess the risk of acute exposure to amphibians, the
NOAEC of 1.0 ppm B will be used. No studies on the effects of chronic exposure of amphibians
to boron compounds were identified in the available literature.
4-16
4.3.3.4 Aquatic Plants The relevant data on the toxicity of boron compounds to aquatic plants
are summarized in Appendix 7. Based on the available data, the most sensitive algal species is
the green alga Scenedesmus subpicatus, with a 72-hour NOAEC of 10 mg B/L (Bringmann and
Kuhn 1978, as cited in ECETOC 1997) and the most tolerant species is the blue-green alga
Microcystis aeruginosa, with a 72-hour NOAEC of 20.3 mg B/L (Bringmann and Kuhn 1978, as
cited in ECETOC 1997). Although these tests are conducted for a relatively short period of time
(i.e. 72 hours), these NOAEC values are applied to both acute and longer-term concentrations
because of the short life-cycle of individual algal cells.
For aquatic macrophytes, results of a 21-day exposure study on the effect of boric acid in
watermilfoil, water buttercup and waterweed show that these three species have a similar level of
sensitivity to boron in terms of decreases in photosynthesis (Nobel 1981, as cited in WHO 1998).
However, the 21-day EC50 of water buttercup (10 mg B/L) is 2-fold higher than the 21-day EC50
value reported for watermilfoil and waterweed. Thus, to assess acute exposure risk of boron
exposure to aquatic macrophytes, the value of 5 mg B/L will be used to represent sensitive
species and the value of 10 mg B/L will be used to represent tolerant species. Results of a 2-year
study on the common reed yielded an NOAEC of 4 mg B/L (Bergmann et al. 1995, as cited in
ECETOC 1997). Due to the lack of long-term exposure data in other plant species, a sensitive
and tolerant species cannot be identified to characterize the chronic risks in aquatic macrophytes
exposed to boron. Thus, the value of 4 mg B/L will be used to assess risk for both sensitive and
tolerant aquatic plant species.
4.3.3.5. Aquatic Microorganisms As reviewed in Section 4.1.3.5, for aquatic microorganisms,
the 72-hour NOAEC values range from 0.3 mg B/L in Entosiphon sulfacum, a flagellate
(Bringmann and Kuhn 1980, as cited in WHO 1998), to 291 mg B/L in Pseudomonas putida
(Schoberl and Huber 1988, as cited in WHO 1998). For this risk assessment, these NOAEC
longer-term exposures for sensitive and tolerant species of aquatic microorganisms.
4-17
4.4 Risk Characterization

4.4.1 Overview
For terrestrial species, risk associated with the application of Sporax to tree stumps appear to be
very low. Most risk quotients are range from 0.000003 to 0.005 and are below the level of
concern by factors of about 200 to over 330,000. As discussed in Section 3.2.3.4, this reflects the
fact that the use of Sporax in Forest Service programs will not substantially contribute to or
increase concentrations of boron in water or soil beyond those that are associated with the normal
occurrence of boron in the environment. Even in the case of direct consumption of Sporax from
a tree stump by a large mammal, the highest risk quotient is only 1.1. The hazard quotients for
other organisms consuming Sporax i.e., a small mammal, a small bird, and a large bird range
from 0.00004 to 0.08, below the level of concern by factors of about 12 to 25,000.
There also does not appear to be a risk to terrestrial plants exposed to boron through runoff of
Sporax applied to tree stumps. Although risk to insects and soil microorganisms was not
characterized, since borax is used effectively in the control of fungi and insects, adverse effects
of environmental exposures to insects and nontarget microorganisms are possible. However,
given the atypical application method for Sporax, widespread exposures are not likely.
The exposure scenarios considered for aquatic species are for water contaminated by accidental
spill or by runoff of applied Sporax. Most aquatic animals do not appear to be at risk for any of
the exposure scenarios considered. For amphibians, the level of concern is marginally exceeded
for the accidental spill of 25 pounds of sporax into as small pond (HQ, 1.3). None of the acute or
chronic HQs for exposure via water contaminated by runoff exceed the level of concern for any
aquatic animal. These results indicate that aquatic animals are not at high risk for the exposure
scenarios considered; however, accidental spill of large quantities of Sporax into a small pond
may result in toxicity in amphibians.
For aquatic plants, the highest HQ for any exposure scenario is 0.3 associated with algae for the
accidental spill of 25 pounds of Sporax into a small pond. All other HQs for the accidental spill
scenario and for acute and longer-term exposures to water contaminated by runoff are well below
the level of concern. Thus, based on this analysis, there is no basis for asserting that effects on
aquatic macrophytes or algae are likely for either acute or longer-term exposures. Hazard
quotients for sensitive species of aquatic microorganisms exceed the level of concern for all
accidental spill scenarios, with HQs ranging from 1.1 to 4.3. For tolerant microorganisms, HQs
are well below the level of concern for the worst-case accidental spill scenario. For acute
4-18
4.4.2 Terrestrial Organisms

4.4.2.1. Terrestrial Vertebrates The quantitative risk characterization for mammals and birds
is summarized in Worksheets G02a G02c. As with the human health risk assessment, risk is
characterized as the estimated dose divided by the toxicity value. This ratio is referred to as the
hazard quotient (HQ). A HQ of one or less indicates that the estimated exposure is less than the
toxicity value; when this is the case, there is no basis for asserting that adverse effects are
plausible. Exposure values are summarized in Worksheet G01. For exposure via consumption
of water contaminated by runoff, the application rate range used is 0.1 lb Sporax/acre to 5 lbs
Sporax/acre, with the typical application rate taken as 1 lb Sporax/acre. Toxicity values are
displayed in the last column of Worksheets G02a G02c and are also summarized in Table 4-2.
As discussed in Section 4.2.2 for terrestrial vertebrates, the exposure scenarios considered in this
risk assessment are the direct consumption of Sporax applied to tree stumps (acute exposure),
consumption of water contaminated by an accidental spill (acute exposure), and acute and
chronic exposure by consumption of water contaminated by runoff. With the exception of direct
consumption of Sporax applied to tree stumps, none of the exposure scenarios are associated
with hazard quotients that exceed the level of concern.
For the direct consumption scenario, there appears to be very little risk to either mammals or
birds. The only HQ to exceed a level of concern is the upper bound of the HQ for the direct
consumption of Sporax from a treated stump by a large mammal such as deer. The exceedence,
however, is minor with an HQ of 1.1. As noted in Worksheet G01, this HQ is associated with a
dose of about 11.5 mg/kg bw, which is only marginally above the NOAEL of 10.3 mg/kg bw. As
discussed in Section 4.1.2.1, Sporax applied to tree stumps does not appear to have attractant
effects for deer and no clinical signs of toxicity were observed in deer allowed free access to
Sporax-treated stumps (Campbell et al., no date). The hazard quotients for other organisms
i.e., a small mammal, a small bird, and a large bird range from 0.00004 to 0.08, below the level
of concern by factors of about 12 to 25,000.
Risk associated with other exposure scenarios are very low. As shown in worksheets G02a
G02c, risk of exposure via the longer term consumption of contaminated water is characterized
for a small mammal. These risk quotients are very low, ranging from 0.000003 to 0.005 and are
below the level of concern by factors of about 200 to over 330,000. As discussed in Section
3.2.3.4, this reflects the fact that the use of Sporax in Forest Service programs will not
substantially contribute to or increase concentrations of boron in water or soil beyond those that
are associated with the normal occurrence of boron in the environment.
4.4.2.2. Terrestrial Plants A quantitative summary of the risk characterization for exposure of
terrestrial plants to boron in soil via runoff is presented in Table 4-3. Exposure estimates for
terrestrial plants are taken from GLEAMS modeling (Table 4-1) and are summarized in Table 43. Toxicity values, summarized in Table 4-3, are based on NOAEC values for the most sensitive
and most tolerant species (Section 4.3.2.4).
4-19
None of the HQ values derived for terrestrial plants exceeds the level of concern. The highest
HQ is 0.46 associated with exposure of the most sensitive species for the application rate of 5 lbs
Sporax/acre and the peak soil concentration in clay with 5 inches of rainfall per year. For these
same conditions, the HQ for the most tolerant species (sugarbeet) is 0.11. All other HQ values
associated with lower application rates do not approach the level of concern. Based on this
analysis, nontarget terrestrial plants do not appear to be at risk from exposure to borax at the
maximum application rate used by the Forest Service. However, this risk assessment is based on
data from relatively few terrestrial plant species. It is possible that more sensitive species exist
and may be at risk for boron-induced toxicity.
4.4.2.3 Other Terrestrial Organisms As discussed in Section 4.2.1, exposure assessments were
not conducted for insects and soil microorganisms. Thus, risk of exposure of these organisms
cannot be characterized quantitatively. Since borax is used effectively in the control of fungi and
insects, adverse effects of environmental exposures to insects and nontarget microorganisms is
possible. However, given the atypical application method for Sporax, widespread exposures are
not likely.
4.4.3.1. Aquatic Animals The quantitative risk characterization for aquatic animals is
summarized in Worksheets G03a G03c. Exposure values are the same as those to assess risk
of exposure to contaminated water in the human health risk assessment (Worksheet E04). As
with the human health risk characterization, risk is characterized as the estimated dose divided by
the toxicity value. For exposure via consumption of water contaminated by runoff, the
application rate range used is 0.1 lb Sporax/acre to 5 lbs Sporax/acre, with the typical application
rate taken as 1 lb Sporax/acre. Exposures values for an accidental spill are based on spill of 6.25
to 25 lbs Sporax, with a central value of 12.5 lbs Sporax, into a small pond. Acute and chronic
toxicity values are displayed in the last column of Worksheets G02a G02c and are also
summarized in Table 4-2.
With the exception of amphibians, all HQs associated with exposure of aquatic animals to water
contaminated by an accidental spill are well below the level of concern. For worst-case scenario
of the spill of 25 pounds of Sporax into a small pond, the HQ for amphibians of 1.3 only
marginally exceeds the level of concern; HQs for spill of 6.25 and 12.5 pounds of Sporax are
below the level of concern. Based on the results of this analysis, if large amounts of borax
accidentally contaminate surface waters, amphibians may be at risk. However, for all other
aquatic animals, there is no indication that adverse effects will occur.
Hazard quotients for acute and chronic exposure of aquatic animals to water contaminated by
runoff are all below the level of concern, even at the maximum application rate of 5 lbs
Sporax/acre. The HQs for acute exposure range from 0.0000004 in aquatic invertebrates for the
lower bound estimate associated with an application rate of 0.1 lb Sporax/acre to 0.5 in
amphibians for the upper bound estimate associated with an application rate of 5 lbs Sporax/acre.
For longer-term exposure, HQs range from 0.000003 in aquatic invertebrates for the lower bound
4-20
estimate associated with an application rate of 0.1 lb Sporax/acre to 0.7 in fish for the upper
bound estimate associate with an application rate of 5 lbs Sporax/acre. Thus, there is no basis for
asserting that effects on nontarget aquatic species are likely for either acute or longer-term
exposures.
4.4.3.2. Aquatic Plants Exposure scenarios for aquatic plants are the same as those conducted
for aquatic animals. The quantitative risk characterization for aquatic plant species includes
assessments for macrophytes and algae (Worksheets G03a G03c). Exposure values are the
same as those used to assess risk of exposure to contaminated water in the human health risk
assessment (Worksheet E04). Acute and chronic toxicity values are displayed in the last column
of Worksheets G02a G02c and are also summarized in Table 4-2.
The highest HQ for any exposure scenario is 0.3 associated with algae for the accidental spill of
25 pounds of Sporax into a small pond. All other HQs for the accidental spill scenario and for
acute and longer-term exposures to water contaminated by runoff are well below the level of
concern. Thus, based on this analysis, there is no basis for asserting that effects on aquatic
macrophytes or algae are likely for either acute or longer-term exposures.
4.4.3.2. Aquatic Microorganisms Exposure scenarios for aquatic microorganisms are the same
as those conducted for aquatic animals. The quantitative risk characterization for aquatic
microorganisms is summarized in Table 4-4. Exposure values are the same as those used to
assess risk of exposure to contaminated water for aquatic animals (Worksheet G03a for
accidental exposure and Worksheet G03c for exposure via runoff using the maximum application
rate). Toxicity values are displayed in the last column of Table 4-4.
Hazard quotients for the most sensitive species of microorganisms exceed the level of concern
for all accidental spill scenarios, with HQs ranging from 1.1 to 4.3. For tolerant microorganisms,
HQs are well below the level of concern, ranging from approximately 0.001 to 0.004. For acute
4-21
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5-19
Table 2-1. Selected physical and chemical properties of boron compounds

Boron
Boric Acid
Sodium Tetraborate
Decahydrate
Appearance, ambient
black or brown solid
white crystalline powder (1)
white crystalline solid (2)
Bioconcentration factor
NA
NA
NA
% Boron
100
17.48
(4)
(3)
CAS number
7440-42-8
Commercial
formulations
NA
NA
Empirical Formula
H 3BO 3
EPA Registration
Number
NA
NA
K o/w
no data
Molecular weight
10.81
pH
NA
(3)
10043-35-3
11.34
(1)
1303-96-4 (2)
Sporax
(1)
Na 2B 4O 7 C10H 20
(1)
2935-501 (2)
Kow = 0.175
(3)
(3)
61.83
(1)
NA
(1)
381.37
5.1 (1% solution) at 20 BC
(1,4)
9.24 (1% solution) at 20 BC
(1)
(1)
Soil half-time (days)
NA
NA
NA
Soil sorption, K o/c
NA
NA
Specific Gravity
NA
1.5128 at 20 BC
Synonyms
none
NA
(1)
NA
boracid; orthoboric acid
(1)
borax; sodium borate

decahydrate; borax decahydrate
(1)
Vapor pressure
-4
1.5610-4 atm at 20
B
C (4)
<10 torr at 20 C
Volatility
NA
NA
W ater half-time (days)
NA
NA
W ater solubility (mg/L)
insoluble
(3,4)
(1)
NA
(1)
4.72% at 20 C ; 63.5
g/L at 25 BC (3)
; 64.5 g/L at 30
B
C (4)
US EPA 1993a (RED)

W ilbur Ellis 2002 (MSDS).
(3)
W HO 1998
(2)
ATSDR 1993
NA = not available
(4)
Tables-1
(1)
NA
B
(1)
<10 -6 torr
4.70 g/100mL at20 BC (1); 20.1

g/L at 0 BC (4); 5.92g/100 g
at20 BC (1,4)
Table 2-2. Summary of the Use of Sporax by the Forest Service from 2000 to 2002
(Source: http://www.fs.fed.us/foresthealth/pesticide/reports.shtml )
Year
Region
Forest
Lbs Applied
Acres Treated
Lbs/Acre
200022000
5
5
5
14
5965 21450
5480 54109
0.46102..034872958
2000
5
7
15
20
0.750
2000
5
11
585
2234
0.262
2000
5
12
125
460
0.272
2000
5
13
200.5
417
0.481
2000
5
13
27
58
0.466
2000
5
14
8380
838
10.000
2000
5
15
10
40
0.250
2000
5
17
8573.5
4675
1.834
2000
5
6
5125.5
4469
1.147
2000
5
9
830
2353
0.353
30091.5
21603
1.393
Region 5 Total/Average:
2000
6
14
217
1074
0.202
217
1074
0.202
2001
5
1
5
10
0.500
2001
5
4
563
1870
0.301
2001
5
5
43
370
0.116
2001
5
6
2515
4472
0.562
2001
5
9
4815
4938
0.975
2001
5
11
663
2168
0.306
2001
5
12
125
380
0.329
2001
5
15
10
10
1.000
2001
5
17
3417
2185
1.564
2001
5
19
30
111
0.270
12186
16514
0.738
2001
6
1
80
259
0.309
2001
6
14
125
258
0.485
205
517
0.397
2002
5
1
10
20
0.500
2002
5
11
698
2333
0.299
2002
5
17
5274
2822
1.869
2002
5
19
58
210
0.276
2002
5
4
555
1700
0.326
2002
5
5
1012
2441
0.415
2002
5
6
9327.5
5837
1.598
2002
5
9
190
483
0.393
17124.5
15846
1.081
2002
6
14
145
1302
0.111
145
1302
0.111
Summary for Region 5 All Years
59402
53963
1.100
Summary for Region 6 All Years
567
2893
0.195
Summary for Both Regions All
59969
56856
1.054
Tables-2
Table 3-1: Chemical and site parameters used in GLEAMS modeling for modeling Borax as
boric acid.
Chemical Specific Parameters
Parameter
Clay
Loam
Sand
Comment/
Reference
Halftimes (days)
Aquatic Sediment
Note 1
Foliar
10000
Note 1
Soil
10000
Note 1
Note 1
Kow
0.175
Note 2
Ko/c, mL/g
0.11
Note 3
Water
K d, mL/g
0.0033
0.0165
0.00033
Note 4
W ater Solubility, mg/L
47,200
Note 5
Foliar wash-off fraction
Note 6
Fraction applied to foliage
Note 6
Note 1
Borax is modeled using chemical and physical properties of boric acid. The results of the modeling is
given as boron equivalents. The assumption is made that no degradation occurs in terms of boron.
GLEAMS requires a finite halftime for vegetation and soil. A value of 10,000 days (about 27 year) is
used to set the degradation rate to a negligible value over the 4-year course of the model run.
Note 2
This the Kow cited by US EPA (1993a, p.19) for boric acid. Borax is modeled using the chemical and
physical properties of boric acid and the results are converted to boron equivalents. See text for
discussion.
Note 3
The Koc is estimated from the relationship given by W inegardner (1996):

log Koc = log Kow - 0.21
log Koc = log 0.175 - 0.21 = -0.97
Koc = 10 -0.97 = 0.11
Note 4
Based on the general relationship: Kd = Koc OC using OC values of 0.003 for sand, 0.015 for loam,
and 0.030 for clay (SERA 2004b).
Note 5
This the water solubility given for boric acid by US EPA (1993a, p.19) as 47.2 g/L at 20C.
Note 6
Borax is not applied to leaf surfaces. Thus, foliar washoff for modeling is set to 1.0 and fraction
applied to foliage is set to 0. These are necessary for the adaptation of GLEAMS to borax. See text
for discussion.
Site Parameters
(see SERA 2004, TD 2004-02.04a dated February 8, 2004 for details)
Pond
1 hectare pond, 2 meters deep, with a 0.01 sediment fraction. 10 hectare square field (1093' by
1093') with a root zone of 12 inches.
Stream
Base flow rate of 710,000 L/day with a flow velocity of 0.08 m/second or 6912 meters/day.
Stream width of 2 meters (about 6.6 feet'). 10 hectare square field (1093' by 1093') with a root
zone of 12 inches.
Tables-3
Table 3-2: Summary of modeled concentrations of borax and boron equivalents in ponds (all
units are g/L or ppb) at an application rate of 1 lb/acre.
Annual
Rainfall
(inches)
Rainfall
per
Event
(inches)
1
5
0.14
10
0.28
15
0.42
20
0.56
25
0.69
50
1.39
100
2.78
150
4.17
200
5.56
250
6.94
Conversion factor
2
:
5
10
15
20
25
50
100
150
200
250
0.14
0.28
0.42
0.56
0.69
1.39
2.78
4.17
5.56
6.94
Clay
Average
0.00
0.00
415.29
292.51
224.32
107.37
53.68
35.83
26.90
21.56
0.1134
0
0
47.09
33.17
25.44
12.18
6.09
4.06
3.05
2.44
Loam
Maximum
Average
Maximum
Sand
Average
Maximum
Concentration per lb/acre applied (from GLEAMS)

0.00
0.00
0.00
0.00
0.00
0.00
0.00
0.00
0.00
0.00
718.04
556.07
882.67
613.40
909.47
395.81
356.14
447.00
376.44
454.87
272.70
265.08
300.25
276.60
333.17
149.67
124.05
258.80
127.15
303.64
105.99
62.71
229.98
63.98
272.22
80.25
42.62
206.02
43.54
245.19
64.19
32.47
185.87
33.21
233.04
53.64
26.30
166.78
26.93
223.98
lbs/acre as boron equivalents
Concentration at above application rate
0
0
0
0
0
0
0
0
81.43
63.06
100.09
69.56
44.88
40.39
50.69
42.69
30.92
30.06
34.05
31.37
16.97
14.07
29.35
14.42
12.02
7.11
26.08
7.26
9.10
4.83
23.36
4.94
7.28
3.68
21.08
3.77
6.08
2.98
18.91
3.05
0
0
103.13
51.58
37.78
34.43
30.87
27.80
26.43
25.40
Rain is assumed to occur at the same rate every 10th day i.e., 36 rainfall events per year.
2
The molecular weight of Borax is 381.37 g/mole and borax contains 4 atoms of boron
(atomic weight of 10.81). Thus, the conversion factor is approximately 0.1134
(410.81/381.37).
Tables-4
Table 3-3: Estimated Environmental Concentrations (g/L or ppb) of boron equivalents in

surface water at an application rate of 1 lb/acre of Borax.
Scenario
Peak
Long-Term Average
GLEAMS, Stream
<0.00001
<0.00001
GLEAMS, Pond 1
30 (6 to 100)
14 (2 to 70)
OTHER MODELING
U.S. EPA/OPP 1993b,
Appendix 1
30.5 ppb as boric acid at

1 lb boric acid/acre
[equivalent to 5.2 ppb
boron 2]
N/A
MONITORING STUDIES
Water
U.S. EPA/OPP 1993b
Normal ambient concentrations of boron in fresh water are

in the range of 1 to 100 ppb.
Moore 1997
Average ambient concentrations in U.S. surface waters

typically range from 100 to 200 ppb
Black et al. 1993
Ambient boron concentration in natural Lake waters ranged

from 0.023 ppm to 0.75 ppm. Waters were collected from
Tennessee (0.023 ppm), Wyoming (0.75 ppm) and Indiana
(0.19 ppm).
Other
No monitoring data on concentration of boron in water

associated with stump treatment applications has been
encountered.
Soil
WHO 1998, Moore 1997
Boron generally occurs in soils at concentrations ranging

from 10 to 30 mg/kg, depending on such factors as soil type,
amount of rainfall, and irrigation type
Water contamination rates concentrations in units of mg boron/L expected at an application

rate of 1 lb borax/acre. These values are converted to units of mg/L (ppm) and are entered into
Worksheet A04 for borax. This rate is adjusted to the program application rate in all
worksheets involving exposure to contaminated water.
2
MW of boric acid = 61.84. Atomic weight of boron = 10.81. Conversion factor = 0.17
[10.81 61.84 = 0.17480]
Tables-5
Table 3-4: Estimated background concentrations of boron in environmental media and normal
intakes of boron relative to exposure scenarios in this risk assessment.
Media/
Exposure
Total intake
Water
Soil
Normal
Background 1
0.14-0.36 mg
B/kg bw/day
0.1 (0.001 - 5)
mg/L
26-300 mg/kg
soil
Sporax Scenarios in
this risk assessment
Comment
0.85 (0.4-3.2) mg/kg bw
Direct consumption from tree

stump [WS D01]
0.05 (0.015-0.14) mg/kg

bw/ day
Water, accidental spill [WS

D02]
0.002 (0.0003-0.011)
mg/kg bw/day
Water, acute ambient [WS

D03]
0.0004 (0.00004-0.0024)
mg/kg bw/day
Water, chronic ambient [WS

D03]
0.03 (0.006-0.1) mg/L
Expected concentration based

on GLEAM modeling [WS
D03]
0.6 (0.3-1.3) mg/L
Accidental spill [WS D02]
0.3 ppm - 0.5 mg/kg soil
Peak based on GLEAMS

modeling (Table 4-1)
0.1 to 2 mg/kg soil
Monitored levels after stump

treatment (Dost et al. 1996)
See Section 3.2.3.1.
Tables-6
Table 4-1: Summary of modeled concentrations of boric acid in soil (all units are mg/kg or
ppm)
Annual
Rainfall
(inches)
Rainfall
per Event
(inches)1
Clay
Average
Loam
Maximum
Average
Maximum
Sand
Average
Maximum
Concentration per lb/acre applied (from GLEAMS)

5
0.14
1.11265 2.39208
2.05470 4.03529
1.13548 2.49736
10
0.28
1.00287 2.30443
0.94758 2.25804
0.87079 2.05700
15
0.42
0.30745 0.94675
0.15204 0.66760
0.09484 0.48669
20
0.56
0.18238 0.76443
0.07705 0.52685
0.04786 0.39754
25
0.69
0.13582 0.68811
0.05145 0.45302
0.03185 0.34213
50
1.39
0.07530 0.57113
0.01972 0.28814
0.01238 0.23125
100
2.78
0.05323 0.52866
0.00961 0.23125
0.00587 0.23125
150
4.17
0.04852 0.52249
0.00708 0.23125
0.00402 0.23125
200
5.56
0.04692 0.51431
0.00594 0.23125
0.00315 0.23125
250
6.94
0.04594 0.50891
0.00529 0.23125
0.00264 0.23125
lbs/acre as boron equivalents
Application rate: 0.1134
Concentration as boron equivalents at above application rate
5
0.14
0.12617
0.27126
0.233
0.4576
0.12876
0.2832
10
0.28
0.11373
0.26132
0.10746
0.25606
0.0987
0.23326
15
0.42
0.0349
0.10736
0.0172
0.0757
0.0108
0.0552
20
0.56
0.0207
0.0867
0.009
0.0597
0.005
0.0451
25
0.69
0.0154
0.078
0.006
0.0514
0.004
0.0388
50
1.39
0.009
0.0648
0.002
0.0327
0.001
0.0262
100
2.78
0.006
0.06
0.001
0.0262
0
0.0262
150
4.17
0.006
0.0593
0
0.0262
0
0.0262
200
5.56
0.005
0.0583
0
0.0262
0
0.0262
250
6.94
0.005
0.0577
0
0.0262
0
0.0262
1
Rain is assumed to occur at the same rate every 10th day i.e., 36 rainfall events per year.
Tables-7
Table 4-2: Summary of borax toxicity values used in ecological risk assessment 1
Organism
Endpoint
Toxicity Value
Reference, Species
acute (rats)
NOAEL
10.3 mg B/kg/day
Allen et al. 1996, U.S. EPA 2004
chronic (rats)
NOAEL
10.3 mg B/kg/day
Allen et al. 1996, U.S. EPA 2004
acute (bobwhite quail)
NOAEL
136 mg B/kg/day
Reinart and Fletcher 1977
NOAEL
10.3 mg B/kg/day
see Section 4.3.2.2.
NOAEL
677 mg B/kg
Atkins 1987, as cited in U.S. EPA

1993b
sensitive
(potato)
NOAEC
5 mg B/kg soil
Kluge 1990, as cited in ECETOC 1997
tolerant
(sugarbeet)
NOAEC
20 mg B/kg soil
Kluge 1990, as cited in ECETOC 1997
sensitive
(razorback sucker
swimup fry )
96-hour LC 50
233 ppm B
Hamilton 1995
tolerant
(rainbow trout)
96-hour LC 50
>1100 ppm B
LaLievre 1988, as cited in U.S. EPA

1993b
sensitive
(goldfish)
NOAEC
0.5 ppm B
Birge and Black 1977
tolerant
(rainbow trout and
channel catfish )
NOAEC
1.0 ppm B
Terrestrial Species
mammals
birds
chronic (rats)
terrestrial invertebrates - honey bee

acute
terrestrial plants
acute
Aquatic Species
fish
cute
chronic
Tables-8
aquatic invertebrates
acute
sensitive
(Daphnia magna )
48-hour LC 50
133 ppm B
Gerisch 1984
tolerant
(Chironomas decorus)
48-hour LC 50
1376 ppm B
Maier and Knight 1991
sensitive
(Daphnia magna)
NOAEC
6 ppm B
Lewis and Valentine 1981
sensitive
(Chironomas decorus)
NOAEC
61.8 ppm B
surrogate value derived from acute

exposure data 3
NOAEC
1.0 ppm B
sensitive
(watermilfoil
and waterweed)
21-day EC 50 for
photosynthesis
5 ppm B
Nobel 1981, as cited in W HO 1998
tolerant
(water buttercup)
21-day EC 50 for
photosynthesis
10 ppm B
Nobel 1981, as cited in W HO 1998
chronic
(common reed)
NOAEC
4 ppm B
Bergmann et al. 1995, as cited in

ECETOC 1997
sensitive
(Scenedesmus subpicatus)
72-hour
NOAEC
10 ppm B
Bringmann and Kuhn 1978, as cited in

ECETOC 1997
tolerant
(Microcystis aeruginosa)
72-hour
NOAEC
20.3 ppm B

ECETOC 1997
sensitive
(Entosiphon sulfacum)
72-hour
NOAEC
0.3 ppm B

W HO 1998
tolerant
(Pseudomonas putida)
72-hour
NOAEC
291 ppm B
Schoberl and Huber 1988, as cited in

W HO 1998
chronic
amphibians
acute
(leopard frog)
aquatic macrophytes
acute
algae
aquatic microorganisms
See Sections 3.3 and 4.3 for discussion on the selection of toxicity values
See Section 4.3.3.2 for discussion of the selection of this toxicity value
3
Surrogate chronic NOAEC derived due to lack of chronic toxicity data in a tolerant species. See Section 4.3.3.2
for details regarding derivation of this surrogate value.
2
Tables-9
Table 4-3: Risk Characterization for Terrestrial Plants

Application Rate
(lb Sporax/acre)
0.1
Lower Exposure
Estimate
(ppm B) 1
Lower HQ
Upper Exposure
Estimate
(ppm B) 2
Upper HQ
Toxicity Value
(ppm B) 3
Sensitive
(potato)
0.00262
5.2e-04
0.04576
9.2e-03
Tolerant
(sugarbeet)
0.00262
1.3e-04
0.04576
2.3e-03
20
Sensitive
(potato)
0.0262
5.2e-03
0.4576
9.2e-02
Tolerant
(sugarbeet)
0.0262
1.3e-03
0.4576
2.3e-02
20
Sensitive
(potato)
0.1310
2.6e-02
2.2880
0.46
Tolerant
(sugarbeet)
0.1310
6.6e-03
2.2880
0.11
20
1.0
5.0
1 This value is the lowest peak soil concentration of boron based on GLEAMS modeling. The lowest exposure
estimate is associated with annual rainfalls of 100 inches or more in loam and 50 inches or more in sand. See
Table 4-3.
2 This value is the highest peak soil concentration of boron based on GLEAMS modeling. The highest exposure
estimate is associated with the maximum value in clay for an annual rainfall of 5 inches. See Table 4-3.
3 See Section 4.3.2.4
4 Table 4-3 gives the GLEAMS modeling soil concentrations for an application rate of 1 lb Sporax/acre. To
calculate soil concentrations for the application rate of 0.1 lb Sporax/acre, soil concentrations were multiplied by
0.1.
5 Table 4-3 gives the GLEAMS modeling soil concentrations for an application rate of 1 lb Sporax/acre. To
calculate soil concentrations for the application rate of 5 lb Sporax/acre, soil concentrations were multiplied by 5.
Tables-10
Table 4-4: Risk Characterization for Acute exposure of Aquatic Microorganisms

Species
Central
Exposure
Estimate
(ppm B)
Accidental Spill Scenario
Central
HQ
Lower
Exposure
Estimate
(ppm B)
Lower
HQ
Upper
Exposure
Estimate
(ppm B)
Upper
HQ
Toxicity Value
(ppm B) 1
Sensitive
0.6418
2.1
0.3209
1.1
1.2837
4.3
0.3
Tolerant
0.6418
2.2e-03
0.3209
1.1e-03
1.2837
4.4e-03
291
Short-term peak exposure from run-off
Sensitive
0.03
1.0e-01
0.006
2.0e-02
0.1
3.3e-01
0.3
Tolerant
0.03
1.0e-04
0.006
2.1e-05
0.1
3.4e-04
291
1 See Section 4.2.2.5.

2 See W orksheet D02. For exposure values, central estimate is based on spill of 12.5 pounds of Sporax, lower
estimate based on spill of 6.24 pounds of Sporax, and upper estimate based on spill of 25 pounds of Sporax.
3 Exposure values for an application rate of 5 lb Sporax/acre. See W orksheet G03c
Tables-11
APPENDICES
Appendix 1:
Toxicity of borax and boric acid to experimental animals
Appendix 2:
Toxicity of borax and boric acid to birds
Appendix 3:
Toxicity of boric acid to terrestrial invertebrates
Appendix 4:
Toxicity of borax and boric acid to terrestrial plants
Appendix 5:
Toxicity of borax and boric acid to fish and amphibians
Appendix 6:
Toxicity of borax and boric acid to aquatic invertebrates
Appendix 7:
Toxicity of borate compounds to aquatic plants
Appendix 1: Toxicity of borax to experimental mammals

Animal
Dose/Exposure
Response
Reference
single doses of borax

and boric acid
administered in
aqueous solutions by
gavage. Dose range
not reported
Borax
SD (males): LD50 = 4.50 g/kg (0.51 g
B/kg) (CL 4.14-5.01)
SD (females): LD50 = 4.98 g/kg (0.56 g
B/kg) (CL 4.31-5.76)
LE (males): LD50 = 6.08 g/kg (0.69 g
B/kg) (CL 3.54-10.4)
Weir and
Fisher 1972
ORAL
Acute Oral
rats,
SpragueDawley
(SD) and
LongEvans
(LE)
Boric acid
SD (males): LD50 = 3.450 g/kg (0.60 g
B/kg) (CL .295-4.04)
SD (females): LD50 = 4.08 g/kg (0.71 g
B/kg) (CL 3.64-4.56)
LE (males): LD50 = estimate 3.16 g/kg
(0.55 g B/kg)
Signs of toxicity similar for both borax
and boric acid: depressions, ataxia,
convulsions, death.
dogs
oral administration of
borax (1.54-6.51 g
borax/kg or 0.1740.736 g B/kg) and
boric acid (1.0-3.98 g
boric acid/kg or 0.1750.697 g B/kg) by
capsule, followed by
14 day observation
period
for both borax and boric acid,

no deaths during 14-day observation
period for all at doses tested. Except at
lowest doses, administration of test
compounds produced strong doserelated emetic response within 1 hour of
dosing
Subchronic Oral
Appendix 1-1
Weir and
Fisher 1972

Animal
Dose/Exposure
Response
Reference
rats
1 g/kg borax and

boric acid for 1-3
weeks administered by
gavage. Rats were
sacrificed when clinical
signs of toxicity were
observed.
In borax treated rats, decrease in body

weight after 1 week of treatment. After
3 weeks, clinical signs of toxicity (not
specified) were observed.
Dani et al.
1971
90-day dietary
exposure of dogs to
borax at
concentrations of 0,
0.0154%, 0.154%, and
1.54% B
No treatment-related effect for any

blood or urine values in males. In
females, decreased hematocrit and
hemoglobin in the 1.54% treatment
group
dogs
According to U.S. EPA

1993c, daily doses are Males: 0, 3, 35, and
268 mg borax/kg/day;
Females: 0, 2, 22, and
192 mg borax/kg/day
Analysis of liver tissue shows

significant inhibition of DNA synthesis.
Paynter
1963
MRID
406923-07
In the 1.54% treatment group, decrease

testicular weights, testicular atrophy,
and alterations in the seminiferous
tubules.
For males NOAEL = 35 mg borax/kg/day (3.97
mg B/kg/day
LOAEL = 268 mg borax/kg/day (33.80
mg B/kg/day)
For females NOAEL = 22 mg borax/kg/day (2.50
mg B/kg/day
LOAEL = 192 mg borax/kg/day (21.78
mg B/kg/day)
rats
70-day to borax in
exposure in drinking
water at concentrations
of 0, 150 and 300 mg
B/L
Compared to controls, rats in the 150

and 300 mg B/L treatment groups had
decreased body weights. Weights of
seminal vesicle and testes decreased in
both borax treatment groups. Inhibition
of spermatogenesis in both treatment
groups.
NOAEL <150 mg B/L in drinking water
(authors did not calculate mg B/kg/day)
Appendix 1-2
Seal and
Weeth 1980

Animal
Dose/Exposure
Response
Reference
rats,
SpragueDawley
90 day dietary
exposure to borax and
boric acid at
concentrations in food
ranging of 52.5, 175,
525, 1750, and 5250
ppm boron equivalents
borax: No signs of toxicity up to

concentrations of 525 ppm. At 1750
and 5250 ppm, signs of toxicity
included rapid respiration, inflamed
eyes, swollen paws and desquamated
skin. All rats in 5250 group died within
3-6 wks of treatment. Food
consumption and body wt decreased for
males at 1750 and 5250 ppm and for
females at 5250 ppm. At lower doses,
some organ weights were increased
compared to controls. For males in the
1750 group, decrease in weights of
testes, liver, spleen, kidneys and brain.
In females, in the 1750 ppm group,
decrease in wts of liver, spleen and
ovaries. Gross pathology of dead
animals from the 5250 ppm group
showed congestion of liver and kidneys,
bright red lungs, swollen appearance of
brain, small testes and thickened
pancreas. Microscopic pathology
showed dose-related atrophy of testes,
with complete atrophy in the 1750 ppm
group. 4 males in the 525 ppm group
showed partial atrophy of testes and
spermatogenic arrest (NOAEC = 175
ppm).
boric acid: No signs of toxicity up to
concentrations of 525 ppm. At 1750
and 5250 ppm, signs of toxicity
included rapid respiration, inflamed
eyes, swollen paws and desquamated
skin. All rats in 5250 group died within
3-6 wks of treatment. Food
consumption and body wt decreased for
males and females at 1750 and 5250
ppm.
Weir and
Fisher 1972
Appendix 1-3

Animal
Dose/Exposure
Response
Reference
dogs
(5M/5F)
90 day dietary
exposure to borax and
boric acid at
concentrations in food
of 17.5, 175 and 1750
ppm boron equivalents
Borax
With one exception (1 dog in 1750
borax group died of severe diarrhea), no
signs of toxicity were observed in any
treatment group. Hematology,
biochemistry and urinalysis parameters
normal except for decreased packed cell
volume and hemoglobin in the 1750
ppm borax group.
Weir and
Fisher 1972
Testes and thyroid size significantly

decreased in 1750 ppm group. Severe
testicular atrophy, complete
degeneration of spermatogenic
epithelium in 1750 ppm group
Boric acid
Observations similar to borax
Chronic Oral
Appendix 1-4

Animal
Dose/Exposure
Response
Reference
rats
(SpragueDawley)
2-year dietary exposure

to borax and boric
acid at concentrations
in food of 117, 350 and
1170 ppm boron
equivalents
For both borax and boric acid for the

117 and 350 ppm exposure groups, no
effects of treatment were observed
(NOAEC = 350 ppm boron
equivalents). In the 1170 ppm groups
clinical signs of toxicity included coarse
hairs, scaly tails, hunched posture,
swelling and desquamation of the pads
of paws, shrunken scrotum in males,
and inflamed eyes with bloody
discharge. Lower packed cell volume
and hemoglobin in 1170 ppm group. In
the 1170 ppm group, atrophy of testes
observed, including decreased testes
weight, atrophied seminiferous
epithelium and decreased tubular size
(LOAEC for testes effects = 1170 ppm
boron equivalents).
Weir and
Fisher 1972

1989, these doses are
equivalent to 5.9, 17.5,
and 58.5 mg B/kg/day
No evidence of carcinogenesis in any

treatment group.
Appendix 1-5

Animal
Dose/Exposure
Response
Reference
dogs (4M
and 4 F
per dose
group)
2-year dietary exposure

to borax and boric
acid at concentrations
in food of 58, 117 and
350 ppm boron
equivalents. An
additional group
received 38-week
exposure to 1170 ppm
(boron equivalents)
borax or boric acid
No clinical signs of toxicity in any

treatment group. No change in body
weight, gross pathology, or
hematological or biochemical
parameters in any group. No testicular
changes in any treatment group
[NOAEC = 350 ppm boron
equivalents (8.8 mg B/kg/day)].
Weir and
Fisher 1972

1989, the 350 ppm
concentration is
equivalent to a daily
dose of 8.8 mg
B/kg/day and the 1170
ppm concentration is
equivalent to 28 mg
B/kg/day
Exposure to 1170 ppm produced

testicular atrophy in both borax and
boric acid groups [LOAEC for testes
effects = 1170 ppm boron equivalents
(28 mg B/kg/day)]. Severe testicular
atrophy was observed, with
spermatogenic arrest observed in 2 dogs
sacrificed at 26 weeks. Microscopic
examination revealed atrophy of the
seminiferous epithelium of the tubules.
Changes appear reversible - when dogs
were placed back on control diet for 25
days from the boric acid group,
testicular changes returned to control or
nearly control levels.
No other adverse effects were observed
in any treatment group.
treatment group.
Appendix 1-6

Animal
Dose/Exposure
Response
Reference
dogs
(beagles)
(8M/8F);
8 dogs
(4M/4F)
in each
treatment
group
1.03% sodium
tetraborate decahydrate
in diet (100% a.i.
borax) for 38 weeks.
Control group
included. 25-day
recovery period
following 38-week
treatment period.
No difference in treatment groups for

weight or general appearance. No
differences for hematology,
biochemistry or urinalysis.
Wier 1967
MRID
00005620
Average daily dose of

test material was
approximately 378 mg
borax/kg/day (43 mg
boron equivalents
/kg/day). Averages
calculated from weekly
compound
consumption and boron
equivalents
consumption for each
dog (displayed in Table
1 of fiche)
In borax-treated males, testicular

atrophy, with microscopic pathology
revealing spermatogenic arrest at the
spermatocyte stage, progressing to
complete atrophy of the seminiferous
epithelium. No change in reproductive
organs of female dogs.
appears to
be same
results as
reported in
Weir and
Fisher 1972
No tissue accumulation of boron

observed.
treatment group.
Reproduction Studies
rats,
males,
SpragueDawley
single doses of borax

(45, 1590, and 450 mg
B/kg)
No effects on male fertility for any dose

tested (measured as % fertile by
assessing spermatozoa, spermatids,
spermatocytes and spermatogonia).
Appendix 1-7
Dixon et al.
1976

Animal
Dose/Exposure
Response
rats,
males,
SpragueDawley
exposure to borax in
drinking water for 30,
60, and 90 days.
Concentrations in
drinking water 0, 0.3, 1
and 6 mg/L.
At all borax exposure levels, seminal

Dixon et al.
vesicle weight was significantly
1976
decreased compared to controls after 30
and 90 days of exposure, but not after
60-day exposure (table 5, p. 66 of
paper). However, authors state that
treatment with borax had no affect on
body weight, or weight of testis,
prostate or seminal vesicles. According
to U.S. EPA 1989, NOAEL is 0.426 mg
B/kg/day (HDT).

equivalent to 0.02,
0.072, and 0.426
mg/kg/day).
Reference
Plasma levels of FSH and LH

unaffected by treatment
In forced breeding, no effect in fertility
at any dose level
rats,
SpragueDawley
90-day dietary
diet at concentrations
of 0, 500, 1000, and
2000 ppm boron
equivalents.
equivalent to 25, 50,
and 100 mg B/kg/day).
No effects noted at the 500 ppm

exposure level.
At concentrations of 1000 and 2000
ppm, decreased weights of liver and
testes. Testicular atrophy, decrease in
seminiferous tubular diameter, and
marked reduction in spermatocytes and
spermatogenic cells. Decreased fertility
(as measured by percentage of pregnant
females). At 1000 ppm, most effects
reversible within 5 weeks of
discontinuation of treatment. At 2000
ppm, sterility was not reversed after 5
weeks. No dose-related decrease in
litter size or fetal death, indicating that
effects of boron were due to germinal
aplasia, and not a dominant lethal effect.
NOAEL = 25 mg B/kg/day
LOAEL = 50 mg B/kg/day
Appendix 1-8
Dixon et al.
1979

Animal
Dose/Exposure
Response
Reference
rats
boric acid in feed (0,

0.1, 0.2, or 0.4%)
throughout gestation
(days 0-20) or 0.8% pm
gestational days 6-15.
Equivalent to daily
doses of 0, 78, 163,
330, and 539 mg
BA/kg/day (0, 13.6,
28.5, 57.7, and 94.3 mg
B/kg/day).
For maternal toxicity: no effect noted in

the 13.6 mg B/kg/day. At doses of 28.5
mg B/kg/day and higher, increased liver
and kidney weight. At doses of 57.7 mg
B/kg/day and greater, altered food
and/or water intake. For highest dose
only, decreased weight gain.
Heindel et
al. 1992,
1994
boric acid (BA) in

feed (0, 0.1, 0.2, or
0.4%) throughout
gestation (days 0-17).
Equivalent to daily
doses of 248, 452, and
1003 mg BA/kg/day (0,
43.3, 79.0, 175 mg
B/kg/day).
For maternal toxicity: mild renal

lesions, increased kidney wt, decreased
wt gain for all boron treatment groups.
mice
For fetal toxicity:

Increased fetal deaths (NOAEL 57.7 mg
B/kg/day; LOAEL 94.3 mg B/kg/day)
decreased fetal body weight (NOAEL
< 13.6 mg B/kg/day; LOAEL13.6 mg
B/kg/day)
increase in fetal malformations
(anomalies of the eyes, CNS,
cardiovascular system, and axial
skeleton) (NOAEL 13.6 mg B/kg/day;
LOAEL 28.5 mg B/kg/day).
For fetal toxicity:

Increased fetal deaths (NOAEL 79
mg B/kg/day; LOAEL 175 mg
B/kg/day)
decreased fetal body weight (NOAEL
43.3 mg B/kg/day; LOAEL 79mg
B/kg/day)
increase in fetal malformations (short
rib XIII and other skeletal anomalies
pertaining to ribs) (NOAEL 79 mg
B/kg/day; LOAEL 175 mg B/kg/day)
Appendix 1-9
Heindel et
al. 1992,
1994

Animal
Dose/Exposure
Response
Reference
rabbits
oral exposure (gavage)

to boric acid (BA) 0,
62.5, 125, or 250 mg
BA/kg/day (0, 10.9,
21.8, or 43.7 mg
B/kg/day) on
gestational days 6-19.
For maternal toxicity: At highest

exposure level only, decreased food
consumption and vaginal bleeding
associated with pregnancy loss.
Heindel et
al. 1994
dietary exposure to
dietary boric acid at 0,
0.025, 0.050, 0.075,
0.1, or 0.2% in feed on
gestational days 0-20
(approximately
equivalent to 18.6,
36.2, 55.1, 75.9, and
142.9 mg BA/kg/day or
3.3, 6.3, 9.6, 13.3, and
25 mg B/kg/day)
For maternal toxicity: No maternal

deaths or signs of toxicity in any boron
treatment group. Only effect was
Increased kidney wt in 0.2% group.
NOAEL = 13.3 mg B/k/day.
LOAEL = 25 mg B./kg /day
rats
For fetal toxicity:

Increased fetal deaths (NOAEL 21.8 mg
B/kg/day; LOAEL 43.7 mg B/kg/day)
cardiovascular malformations (NOAEL
21.8 mg B/kg/day; LOAEL 43.7 mg
B/kg/day)
For fetal toxicity: Fetal viability

unaffected. Fetal weight significantly
decreased in 0.1 (94% of control) and
0.2% (88% of control) groups.
Increased wavy rib in 0.1 and 0.25
groups. Rib malformation reversed by
post-natal day 21. For developmental
toxicity (skeletal malformations and
reduced fetal weight):
NOAEL = 9.6 mg B/kg/day
LOAEL = 13.7 mg B/kg/day
Appendix 1-10
Price et al.
1996a

Animal
Dose/Exposure
Response
Reference
rabbits
oral exposure (gavage)

to boric acid (62.6,
125, or 250 mg boric
acid/day) on gestational
days 6-19. Doses
equivalent to 10.9,
21.8, or 43.7 mg
B/kg/day.
For maternal toxicity: In 21.8 and 43.7

mg B/kg/day groups, decreased body wt
and wt gain, decreased gravid uterus wt,
decrease number of ovarian corpus
lutea. In 43.7 mg B/kg/day group,
increase in kidney wt, but no treatmentrelated renal pathology observed.
Price et al.
1996b
For fetal toxicity: In 43.7 mg B/kg/day

group, increased fetal resorptions (90%
for B, 6% for control, reduction in litter
size, and increase in malformed fetuses
(cardiovascular malformation of
interventricular septal defect). Slight
decreased in fetal wt, but not
statistically significant.
For developmental toxicity:
NOAEL = 21.8 mg B/kg/day
LOAEL = 43.7 mg B/kg/day
Appendix 1-11

Animal
Dose/Exposure
Response
Reference
rats, male
feed at concentrations
of 0, 500, 1000, and
2000 ppm boron
equivalents for 30 and
60 days.
No adverse effects observed in the 500

ppm exposure group for either 30- or
60-day exposure.
Lee et al.
1978

equivalent to 25, 50,
and 100 mg/kg/day).
In the 1000 and 2000 ppm groups, doserelated testicular atrophy, with complete
depletion of germ cells within 60 days
of exposure in the 2000 ppm group. In
both groups, decrease in seminiferous
tubular diameter and accumulation of
testicular boron. Reduction in activities
of enzymes that are markers of postmeiotic germ cell activity. Time- and
dose-dependent increases in plasma FS
and LH, but normal plasma
concentrations of testosterone.
Serial mating studies show decreased
fertility without change in copulatory
behavior. Dose-dependent decrease in
fertility. No litters produced in the 2000
ppm group. In the 2000 ppm group,
infertility persisted for 8 months
following the cessation of treatment.
No other clinical signs of systemic
toxicity were observed in any treatment
group.
For male reproductive effects NOAEL = 25 mg B/kg/day
LOAEL - 50 mg B/kg/day
Appendix 1-12

Animal
Dose/Exposure
Response
Reference
rats
(albino)
Reproduction study.
Rats exposed to borax
(sodium tetraborate
decahydrate) at
0.103, 0.308, and
1.030% in diet.
Exposure period was
for 3 generations,
through the weaning of
the second litter of the
3rd generation.
No effects on reproduction in 0.103 and

0.308% groups compared to control.
Wier 1966
MRID
00005623
Average daily dose of

test material were
approximately 70, 200
and 700 mg
borax/kg/day (8, 24,
and 80 mg boron
equivalents/kg/day).
Averages calculated
from weekly
compound
consumption and boron
equivalents
consumption for each
treatment group
(displayed in Tables 6
and 7 of fiche)
Mating of animals in the 1.03% test

group was discontinued due to failure to
produce litters.. Microscopic evaluation
of males showed lack of viable sperm
and grossly atrophied testes in all males
of this group. Evidence of decreased
ovulation noted in females of this group.
When females of this group were mated
with control males, no litters were
produced. Possible causes could be
adverse effects on ovum, implantation,
or gestation after implantation.
In 1.03% test group, decreased body
weight gain.
No alterations in behavior in any test
group.
For male reproductive effects:
NOAEL = 24 mg B/kg/day
LOAEL = 80 mg B/kg/day
Appendix 1-13
appears to
be same
data as
presented in
Weir and
Fisher 1972
and Weir
and Crews
1972
(MRID
406923-11)

Animal
Dose/Exposure
Response
Reference
rats
Borax and boric acid

in diet at
350, and1170 ppm
(boron equivalents) for
14 weeks prior to
mating. Diets
continued through 3
generations
No effects on reproduction (fertility

index, lacation index or live birth index)
in the 117 or 350 ppm diets for either
borzx or boric acid. NOAEC for
reproductive effects = 350 ppm (17.5
mg B/kg/day)
Weir and
Fisher 1972

equivalent to 5.9, 17.5,
and 58.5 mg B/kg/day
In the 1170 ppm group for both borax

and boric acid, no litters were produced.
Mating of treated females with
untreated males was not successful.
Microscopic examination showed lack
of viable sperm and atrophied testes in
males. Evidence of decreased ovulation
in females. LOAEC for reproductive
effects = 1170 ppm (58.5 mg
B/kg/day)
DERMAL
rabbits
(10 White
New
Zealand)
Acute dermal toxicity

test of borax (sodium
tetraborate
decahydrate) (purity
not reported). Single
dose of test substance
applied to clipped skin
at 2.0 g/kg and
occluded. Test
substance removed
after 2 hours. Animals
observed for 15 days
after application.
No mortalities.
LD50 >2.0 g/kg
Clinical observations: anorexia,
decreased activity, diarrhea, soft stools,
and nasal discharge.
Gross pathological examination
revealed no significant findings.
No control group.
Appendix 1-14
Reagan
1985a
MRID
43553200

Animal
Dose/Exposure
Response
Reference
rabbits
(White
New
Zealand)
Primary dermal
irritation study of
borax (sodium
tetraborate
decahydrate) (purity
not reported). Single
dose of 0.5 g applied to
shaved skin and
occluded. Animals
observed for 28, 52,
and 76 hours after
application.
No irritation noted. Mean primary

irritation score = 0.
Reagan
1985b
MRID
43553203
guinea
pigs (10)
Dermal sensitization
test for borax (sodium
tetraborate
decahydrate) (98%
pure) repeated
exposure to once
weekly for 3 weeks,
followed by challenge
test. Concentrations
tested: 25%, 50%, 75%
and 95%.
Challenge test revealed no sensitizing

effect.
Wnorowski
1994b
MRID
34500802
Acute dermal toxicity

study of borax (sodium
tetraborate
decahydrate) (100%
pure). Single dermal
application of 5000
mg/kg to shaved skin
and occluded for 24
hours. Animals
after exposure.
No mortalities.
rats
(5M/5F)
No irritation noted at any test site.
LD50 > 5000 mg/kg.

On days 1 and 2 after application,
dermal irritation was noted in all
animals. Irregular breathing in one male.
On necropsy, red lungs were noted in all
animals.
No control group.
EYES
Appendix 1-15
Wnorowski
1996
MRID
44048603

Animal
Dose/Exposure
Response
Reference
rabbits (6
White
New
Zealand)
0.1g borax (sodium

tetraborate
decahydrate) instilled
in one eye of each
rabbit. Material was
not washed out.
Animals observed for
72 hours posttreatment.
Severe irritation observed, including

irritation of the iris, corneal opacity and
conjunctival redness, chemosis, and
discharge.
Reagan
1985c
MRID
43553202
Appendix 1-16

Animal
Dose/Exposure
Response
Reference
No mortalities. 4-hour LC50 > 2.03

mg/L.
Wnorowski
1994a
MRID
43500801
INHALATION
rats
(5M/5F)
4- hour inhalation
exposure to 2.0 mg/L
borax (sodium
tetraborate
decahydrate) for 14
days. Measured
concentration = 2.03
mg/L. Animals
after exposure.
During 1st hour of exposure, ocular

discharge, hypoactivity and hunched
posture were observed. After removal
from chamber, ocular discharge
persisted and 2/10 rats had nasal
discharge. All symptoms resolved by
day 7 after exposure.
No significant finding on gross
pathological exam.
Appendix 1-17
Appendix 2: Toxicity of borax and boric acid to birds

Species
Nature of
Exposure
Exposure
Time
single oral doses

(0, 398, 631, 1000,
1590, and 2510
mg/kg) of borax
(sodium
tetraborate
decahyrate, 100%
a.i.) administered
by gavage
single oral
dose. Birds
observed for
14 days after
dosing
Effects
Reference
Single Dose
Bobwhite
quail (age: 5
months
LD50 > 2510 mg borax/kg

(equivalent to > 284 mg
B/kg).
Fink et al.
1982a,
MRID
001000657
One mortality in the 2510

mg/kg group. No
mortalities in any other
treatment group.
No behavioral changes in
any treatment group.
Slight loss of body weight
during the first 3 days after
treatment in the 1590 and
2510 mg/kg treatment
groups.
Acute Dietary
Bobwhite
quail (10-15
days old)
dietary exposure
to borax (sodium
tetraborate
decahyrate (100%
a.i.) at
concentrations of
0, 312.5, 625,
1250, 2500, 5000
ppm.
Average body
weight: 43 g
average food:
consumption: 10.4
g/bird/day
5-day dietary
exposure.
Birds
observed for
total of 8
days.
LC50 > 5000 ppm borax

(equivalent to >567 ppm
B)
One mortality (10%) in the
5000 ppm treatment group.
10% and 20 % mortality
observed in 2/4 control
groups.
No abnormal behavior
observed in any group. No
change in mean body
weight in treatment groups
compared to controls.
Appendix 2-1
Reinart
and
Fletcher
1977
MRID
00149195
Appendix 2: Toxicity of borax and boric acid to birds

Species
Nature of
Exposure
Exposure
Time
Effects
Reference
Hatchlings
decrease in hatching, posthatching growth and
survival following
exposure to 1000 ppm.
Smith and
Anders
1989
Reproduction Studies
mallard
ducks
dietary exposure
to boric acid in
feed at
concentrations of
0, 30, 300 and
1000 ppm B.
3 weeks of
treatment
prior to
mating.
Treatment
continued
through 21days after
ducklings
hatched.
NOAEL = 300 ppm B

LOAEL = 1000 ppm B
Adults
No effect of treatment on
adult survival or egg
fertility
NOAEL >1000 ppm
broiler
chickens
dietary exposure
borax, 0 and 250
ppm B
equivalents.
Average weight of
male birds = 5,667
g
Average food
consumption
g/bird/day = 146
g/bird/day
Females
were
exposed for
28 days,
during which
egg
production
was
recorded.
Males were
exposed for
28 days
In exposed females mated

with unexposed males, no
effect on body weight, egg
production, or fertility.
Hatchability was
significantly decreased (to
approximately 75% of
control value) in borzx
group.
In exposed males, increase
in number of damaged
spermatozoal cells in
boron-treated birds
(approached statistical
significance p<0.051)
Appendix 2-2
Rossi et al.
1993
Appendix 3: Toxicity of boric acid to terrestrial invertebrates

Species
honey bee
Exposure
Effects
acute topical
exposure to boric
acid (362.58
:g/bee)
No mortality.
LD50 >362.58 :g boric
acid/bee (or 41.1 :g B/bee)
Boric acid is rated as
essentially non-toxic
Appendix 3 - 1
Reference
Atkins 1987
MRID
402692-01
Appendix 4: Toxicity of borax and boric acid to terrestrial plants

Species
potatoes, winter
wheat, and
sugarbeet
Exposure
Effects
boron (added as
boric acid) in soil.
Concentration
range not specified.
Greenhouse study to determine

the threshold soil concentrations
of boron for producing
phytotoxicity. Soil types were
described as light and heavy
soils.
Reference
Kluge 1990,
as cited in
ECETOC
1997
In light soils:, the NOEAC for

phytotoxic effects:
potatoes: 5.0 - 7.5 mg B/kg soil
winter wheat: 9 - 13 mg B/kg soil
sugarbeet: 20 - 35 mg B/kg soil
Higher values observed in
heavy soils
poppy (Papaver
somniferum)
borax at
concentrations of 1
to 32 ppm B in soil
NOEAC = 8 ppm B
LOAEC = 16 ppm B
Sopova et al.
1981
Signs of phytotoxicity included

decline in plant development,
yellow leaves, late flowering, and
reduction of mitotic frequency in
root tip cells.
Oat and turnip
borax added to soil

at concentrations of
1, 10, 100 and 1000
mg/kg dry soil
(added prior to
planting)
Greenhouse study.
EC50 values (based on fresh
weight of 21-day old plants)
Oats: 310 mg borax /kg soil (35.2
mg B/kg soil)
turnip: 115 mg borax /kg soil
(13.0 mg B/kg soil)
NOAEC values not reported
Appendix 4 - 1
Stanley and
Tapp 1982, as
cited in
Windeatt et
al. 1991
Appendix 5: Toxicity of borax and boric acid to fish and amphibians

Species
Nature of
Exposure
Exposure
Time
Effects
Reference
FISH
Acute
rainbow trout
Borax,
concentration
range not
reported
24- and
48-hour
exposure
24-hr LC50 = 602.0 mg B/L

48-hr LC50 = 387.0 mg B/L
Alabaster
1969, as cited
in Hovatter
and Ross 1995
Bluegill
sunfish
acute toxicity
test of boric acid
96-hour
96-hour LC50 >1021 ppm

B/L
LaLievre 1998
MRID
40594602, as
cited in U.S.
EPA 1993b
rainbow trout
acute toxicity
test of boric acid
96-hour
96-hour LC50 >1100 ppm

B/L
LaLievre 1998
MRID
40594602, as
cited in U.S.
EPA 1993b
Colorado
squawfish,
razorback
sucker, and
bonytail (all
endangered
fish collected
from the
Green River,
Utah
acute toxicity
test with boric
acid
96-hour
exposure
all values expressed as mg

B/L
Hamilton 1995
Colorado squawfish
96-hr LC50 for
swimup fry = 279
small juvenile > 100
larger juvenile = 527
razorback sucker
96-hr LC50 for
swimup fry = 233
small juvenile = 279
larger juvenile > 100
bonytail
96-hr LC50 for
swimup fry = 280
small juvenile = 552
larger juvenile = 337
Appendix 5 -1

Species
Nature of
Exposure
Young
salmon fry
(Chinook and
Coho)
static acute
toxicity test for
boron in water boric acid
Exposure
Time
up to 96
hour
exposure
Effects
Chinook Salmon
24-hr LC50 >1000 mg B/L
96-hr LC50 = 600 mg B/L
Reference
Hamilton and
Buhl 1990
For eyed egg and alevin,

24- and 96 hr LC50 >1000
mg B/L
Coho Salmon
24-hr LC50 >1000 mg B/L
96-hr LC50 = 447 mg B/L
Western
mosquitofish
borax,
concentration
range not
reported
24-, 48-,
and 96hour
exposure
24-hr LC50 =1361 mg B/L

48-hr LC50 = 930 mg B/L
96-hr LC50 = 408 mg B/L
Appendix 5 -2
Wallen et al,.
1957, as cited
in Hovatter
and Ross 1995

Species
Nature of
Exposure
Exposure
Time
Effects
Reference
Longer Term
Rainbow trout Exposure from
before
fertilization to 4
days post-hatch,
in hard and soft
water.
Borax
concentrations:
0.001 to 300
ppm boron
up to 28
days
All numbers expressed as

boron equivalents
Authors note that no
consistent effect of water
hardness no boron toxicty
was observed.
The following LCx values
represent the combined
response for embryonic
mortality, embryogenic
teratogenesis and posthatch
mortality.
Borax
LC1 in soft water (CaCl2 50
ppm) = 0.07 ppm B
LC50 in soft water (CaCl2
50 ppm) = 27 ppm B
LC1 in hard water (CaCl2
200 ppm) = 0.07 ppm B
LC50 in hard water (CaCl2
200 ppm) = 54 ppm B
NOAEC (% mortality) =
1.0 ppm Boron
LOAEC (% mortality) =
10.0 ppm boron
(NOAECs and LOAECs
estimated based on tabular
results. No statistics were
performed in this study)
Appendix 5 -3
Birge and
Black 1977

Species
channel
catfish
Nature of
Exposure
Exposure to
0.001 to 300
ppm B (as
borax) from
before
fertilization to 4
days post-hatch.
Exposure
Time
9 days
Effects
LC50 = 71 Boron ppm
Reference
Birge and
Black 1977
1.0 ppm Boron
5.0 ppm boron
(NOAECs and LOAECs
Goldfish
Exposure to
0.001 to 300
ppm B (as
borax) from
before
fertilization to 4
days post-hatch.
7 days
LC50 = 59 Boron ppm
Birge and
Black 1977
0.5 ppm Boron
1.0 ppm boron
(NOAECs and LOAECs
Field/Mesocosm Bioconcentration Studies

Western
mosquito fish
(Gambusia
affinis)
Field study.
Fish collected
from various
waters in
California.
Surface water
boron
concentrations
ranged from 7.420 mg B/L
Chronic
exposure.
Field
study.
Bioconcentration factors
ranged from 0.08 to 0.2.
No evidence of
bioconcentration
Appendix 5 -4
Ohlendorf et
al.1986, as
cited in
ECETOC
Working
Group 1997

Nature of
Exposure
Exposure
Time
Bluegill
sunfish
(Lepomis
macrochirus)
Field study.
Fish collected
from waters in
the San Joaquin
Valley, CA,
Surface water
boron
concentrations
ranged from 1.13.1 mg B/L
Chronic
exposure.
Field
study.
No evidence of
bioconcentration
Klasing and
Pilch 1988, as
cited in
ECETOC
Working
Group 1997
Common carp
(Cyprinus
carpio)
Field study.
Fish collected
from waters in
the San Joaquin
Valley, CA,
Surface water
boron
concentrations
ranged from 1.13.1 mg B/L
Chronic
exposure.
Field
study.
No evidence of
bioconcentration
Klasing and
Pilch 1988, as
cited in
ECETOC
Working
Group 1997
Species
Effects
Reference
AMPHIBIANS
Leopard Frog
Exposure to
0.001 to 300
ppm B (as
borax) from
before
fertilization to 4
days post-hatch
(7.5 days)
7.5 days
LC50 = 47 ppm Boron

1.0 ppm Boron
5.0 ppm boron
(NOAECs and LOAECs
Appendix 5 -5
Birge and
Black 1977

Species
Wood Frog
Nature of
Exposure
eggs exposed to
borax (0, 50, or
100 mg/L) until
hatch
Exposure
Time
13-23
days
Effects
Dose-dependent increase
in proportion of deformed
larvae (crescent shaped
bodies).
Reference
Lapsota and
Dunson 1998
No effect of boron
exposure on proportion of
eggs hatching.
Jefferson
Salamander
eggs exposed to
borax (0, 50, or
100 mg/L) until
hatch
17-35
days
larvae (crescent shaped
bodies).
Lapsota and
Dunson 1998
No effect of boron
eggs hatching.
Spotted
Salamander
eggs exposed to
borax (0, 50, or
100 mg/L) until
hatch
38-44
days
larvae (swollen thoracic
region and enlarged,
shortened gills).
Lapsota and
Dunson 1998
No effect of boron
eggs hatching.
American
toad
eggs exposed to
borax (0, 50, or
100 mg/L) until
hatch
15-23
days
Dose-related decrease in
proportion of eggs
hatching in boron
treatment groups.
Appendix 5 -6
Lapsota and
Dunson 1998
Appendix 6: Toxicity of borax and boric acid to aquatic invertebrates

Species
Effectsa
Exposure Time
Reference
Acute
Daphnia magna
48-hour exposure
to borax
48-hr LC50 = 141 mg B/L
Maier and
Knight 1991
Chironomas
decorus (a
freshwater benthic
invertebrate)
48-hour and 96hour exposure to

borax
48-hr LC50 = 1376 mg B/L
Maier and
Knight 1991
96-hour NOAEC (for decreased

growth) 10 mg B/L
96-hour LOAEC (for decreased
growth) 20 mg B/L
No 96-hour LC50 reported
Daphia magna
24-hour exposure
to borax.
Concentration
range not reported
24-hr LC50 = 73 mg B/L
Bringmann
and Kuhn
1977, as cited
in Hovatter
and Ross 1995
Daphia magna
48-hour exposure
to boric acid.
Concentration
range not reported
48-hr LC50 = 133.0 mg B/L
Gersich 1984,
Daphia magna
48-hour exposure
to boric acid.
Concentration
range not reported
48-hr LC50 = 226.0 mg B/L
Lewis and
Valentine
1981
Longer Term
Appendix 6 - 1
Appendix 6: Toxicity of borax and boric acid to aquatic invertebrates

Species
Daphia magna
Effectsa
Exposure Time
21-day exposure
to boric acid, 6106 mg B/L
21-day LC50 = 53.2 mg B/L

(based on adult mortality)
Reference
Lewis and
Valentine
1981
NOEAC (decreased length) = 27

mg B/L
LOAEC (decreased length) = 53
mg B/L
NOEAC (decreased brood size)

= 6 mg B/L
LOAEC (decreased brood size)
= 13 mg B/L
Daphnia magna
21-day exposure
to boric acid at
concentrations
ranging from 6.359.3 mg B/L
21-day LC50 = 52.2 mg B/L

(based on adult mortality)
NOAEC (for reproductive
parameters) = 6.4 mg B/L
LOAEC (for reproductive
parameters) = 13.6 mg B/L
Appendix 6 - 2
Gerisch 1984
Appendix 7: Toxicity of borate compounds to aquatic plants

Species
Effects a
Exposure
Reference
ALGAE
green algae
(Scenedesmus
quadricauda)
72-hour exposure
(borate compound
not specified)
72-hour EC3 = 16 mg B/L
Bringmann
and Kuhn
1978, as cited
in ECETOC
Working
Group 1997
blue-green
algae
(Microcytsis
aeruginosa)
72-hour exposure
(borate compound
not specified)
72-hour EC3 = 20.3 mg B/L
Bringmann
and Kuhn
1978, as cited
in ECETOC
Working
Group 1997
green algae
(Scenedesmus
subpicatus)
72-hour exposure
(borate compound
not specified)

72-hour EC100 = 100 mg B/L
Guhl 1992, as
cited in
ECETOC
Working
Group 1997
green algae
(Scenedesmus
subpicatus)
72-hour exposure
(borate compound
not specified)

Kopf and
Wilk 1995, as
cited in
ECETOC
Working
Group 1997
MACROPHYTES
Short-term Exposure
watermilfoil
21-day exposure to
boric acid at
1, 2, 10 mg B/L
21-day EC50 for decreased

photosynthesis = 5 mg B/L
Nobel 1981,
as cited in
WHO 1998
water buttercup
21-day exposure to
boric acid at
1, 2, 10 mg B/L

photosynthesis = 10 mg B/L
Nobel 1981,
as cited in
WHO 1998
Appendix 7 - 1
Appendix 7: Toxicity of borate compounds to aquatic plants

Species
waterweed
Exposure
Effects a
Reference
21-day exposure to
boric acid at
1, 2, 5, 10 and 250
mg B/L

photosynthesis= 5 mg B/L
Nobel 1981,
as cited in
WHO 1998
NOAEC (2-3 months) for

visual damage to that plant =
8 mg B/L
Bergmann et
al. 1995, as
cited in
ECETOC
Working
Group 1997
and WHO
1998
Long-term Exposure
Common reed
(Phragmites
australis)
boric acid in
concentrations of 1.
0.5, 1.0, 2.0, 4.0,
8.0, 16.0 mg B/L for
2-3 months or 2
years
NOAEC (2 years) for visible

damage to the plant = 4 mg
B/L
A pot study water concentrations

maintained the
indicated
concentrations
Appendix 7 - 2

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Human Health and Ecological

Risk Assessment for

Forest Health Protection

February 24, 2006

3. HUMAN HEALTH RISK ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3-1

TABLE OF CONTENTS (continued)

Systemic Toxic Effects from Dermal Exposure. . . . . . . . . . . . . . . . .

3.2. EXPOSURE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.3. DOSE-RESPONSE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

3.4. RISK CHARACTERIZATION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4. ECOLOGICAL RISK ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

TABLE OF CONTENTS (continued)

4.2. EXPOSURE ASSESSMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4-8

TABLE OF CONTENTS (continued)

Toxicity of borax and boric acid to experimental animals

Toxicity of borax and boric acid to birds

Toxicity of boric acid to terrestrial invertebrates

Toxicity of borax and boric acid to terrestrial plants

Toxicity of borax and boric acid to fish and amphibians

Toxicity of borax and boric acid to aquatic invertebrates

Toxicity of borate compounds to aquatic plants

ACRONYMS, ABBREVIATIONS, AND SYMBOLS

American Conference of Governmental Industrial Hygienists

ACRONYMS, ABBREVIATIONS, AND SYMBOLS (continued)

COMMON UNIT CONVERSIONS AND ABBREVIATIONS

CONVERSION OF SCIENTIFIC NOTATION

HUMAN HEALTH RISK ASSESSMENT

3. HUMAN HEALTH RISK ASSESSMENT

seminiferous epithelium, and sterility. Results of reproductive studies show a dose-dependent

3.1.14. Inerts and Adjuvants

3.2.3. General Public.

XInf = X0 / (1- e-ke t*))

3.3. DOSE-RESPONSE ASSESSMENT

3.4. RISK CHARACTERIZATION

3.4.3. General Public

4. ECOLOGICAL RISK ASSESSMENT

4.2. EXPOSURE ASSESSMENT

4.2.2. Terrestrial Vertebrates

of 1 lb Sporax/acre (0.11 lb boron/acre). As rainfall rate increases, maximum soil concentrations

4.3. DOSE-RESPONSE ASSESSMENT

4.4 Risk Characterization

4.4.2 Terrestrial Organisms

Jamjod S; Rerkasem B. 1999. Genotypic variation in response of barley to boron deficiency.

U.S. EPA 1993c. United States Environmental Protection Agency/Office of Prevention,

Table 2-1. Selected physical and chemical properties of boron compounds

black or brown solid

white crystalline powder (1)

white crystalline solid (2)

5.1 (1% solution) at 20 BC

9.24 (1% solution) at 20 BC

Soil half-time (days)

Soil sorption, K o/c

boracid; orthoboric acid

borax; sodium borate

W ater half-time (days)

W ater solubility (mg/L)

US EPA 1993a (RED)