United States
Environmental Protection
Agency
Health Effects Support
Document for Terbacil
-------
-------
Health Effects Support Document
for
Terbacil
U.S. Environmental Protection Agency
Office of Water (43 04T)
Health and Ecological Criteria Division
Washington, DC 20460
www.epa.gov/safewater/ccl/pdf/terbacil.pdf
EPA Document Number: 822-R-08-004
January, 2008
Printed on Recycled Paper
-------
Terbacil January, 2008 iv
-------
FOREWORD
The Safe Drinking Water Act (SDWA), as amended in 1996, requires the Administrator
of the Environmental Protection Agency (EPA) to establish a list of contaminants to aid the
Agency in regulatory priority setting for the drinking water program. In addition, the SDWA
requires EPA to make regulatory determinations for no fewer than five contaminants by August
2001 and every five years thereafter. The criteria used to determine whether or not to regulate a
chemical on the Contaminant Candidate List (CCL) are the following:
The contaminant may have an adverse effect on the health of persons.
The contaminant is known to occur or there is a substantial likelihood that the
contaminant will occur in public water systems with a frequency and at levels of
public health concern.
In the sole judgment of the Administrator, regulation of such contaminant presents a
meaningful opportunity for health risk reduction for persons served by public water
systems.
The Agency's findings for all three criteria are used in making a determination to
regulate a contaminant. The Agency may determine that there is no need for regulation when a
contaminant fails to meet one of the criteria. The decision not to regulate is considered a final
Agency action and is subject to judicial review.
This document provides the health effects basis for the regulatory determination for
terbacil. In arriving at the regulatory determination, The Office of Water used the Re-
registration Eligibility Document (RED) for terbacil published by the Office of Pesticides
Programs (OPP)as well as any OPP health assessment documents that supported the RED. The
following publications from OPP were used in development of this document.
U.S. EPA (United States Environmental Protection Agency). 1998a. Reregi strati on
eligibility decision. Terbacil. EPA738-R-97-011. Washington, DC: U.S. EPA Office of
Prevention, Pesticides and Toxic Substances. Available from:
.
Information from the OPP risk assessment was supplemented with information from the
primary references for key studies where they have been published and recent studies of terbacil
identified in a literature search conducted 2004 with a focused update in 2008.
A Reference Dose (RfD) is provided as the assessment of long-term toxic effects other
than carcinogenicity. RfD determination assumes that thresholds exist for certain toxic effects,
such as cellular necrosis, significant body or organ weight changes, blood disorders, etc. It is
expressed in terms of milligrams per kilogram per day (mg/kg-day). In general, the RfD is an
estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to
Terbacil January, 2008
-------
the human population (including sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime.
The carcinogenicity assessment for terbacil includes a formal hazard identification and an
estimate of tumorigenic potency when available. Hazard identification is a weight-of-evidence
judgment of the likelihood that the agent is a human carcinogen via the oral route and of the
conditions under which the carcinogenic effects may be expressed.
Development of these hazard identification and dose-response assessments for terbacil
has followed the general guidelines for risk assessment as set forth by the National Research
Council (1983). EPA guidelines that were used in the development of this assessment may
include the following: Guidelines for the Health Risk Assessment of Chemical Mixtures (U.S.
EPA, 1986a), Guidelines for Mutagenicity Risk Assessment (U.S. EPA, 1986b), Guidelines for
Developmental Toxicity Risk Assessment (U.S. EPA, 1991), Guidelines for Reproductive Toxicity
Risk Assessment (U.S. EPA, 1996), Guidelines for Neurotoxicity Risk Assessment (U.S. EPA,
1998b), Guidelines for Carcinogen Assessment (U.S. EPA, 2005a), Recommendations for and
Documentation of Biological Values for Use in Risk Assessment (U.S. EPA, 1988), (proposed)
Interim Policy for Particle Size and Limit Concentration Issues in Inhalation Toxicity (U.S.
EPA, 1994a), Methods for Derivation of Inhalation Reference Concentrations and Application of
Inhalation Dosimetry (U.S. EPA, 1994b), Use of the Benchmark Dose Approach in Health Risk
Assessment (U.S. EPA, 1995), Science Policy Council Handbook: Peer Review (U.S. EPA,
1998c, 2000a), Science Policy Council Handbook: Risk Characterization (U.S. EPA, 2000b),
Benchmark Dose Technical Guidance Document (U.S. EPA, 2000c), Supplementary Guidance
for Conducting Health Risk Assessment of Chemical Mixtures (U.S. EPA, 2000d), and^4 Review
of the Reference Dose and Reference Concentration Processes (U.S. EPA, 2002a).
The chapter on occurrence and exposure to terbacil through potable water was developed
by the Office of Ground Water and Drinking Water. It is based primarily on first Unregulated
Contaminant Monitoring Regulation 1 (UCMR1) data collected under the SDWA. The UCMR1
data are supplemented with ambient water data, as well as data from the States, and published
papers on occurrence in drinking water.
Terbacil January, 2008 vi
-------
ACKNOWLEDGMENT
This document was prepared under the U.S. EPA contract No.68-C-02-009, Work
Assignment No. 2-54 and 3-54 with ICF Consulting, Fairfax, VA. The Lead U.S. EPA Scientist
is Octavia Conerly, Health and Ecological Criteria Division, Office of Science and Technology,
Office of Water.
Terbacil January, 2008 vii
-------
Terbacil January, 2008 viii
-------
TABLE OF CONTENTS
FOREWORD v
ACKNOWLEDGMENT vii
LIST OF TABLES xi
LIST OF FIGURES xiii
1.0 EXECUTIVE SUMMARY 1-1
2.0 IDENTITY: CHEMICAL AND PHYSICAL PROPERTIES 2-1
3.0 USES AND ENVIRONMENTAL FATE 3-1
3.1 Production and Use 3-1
3.2 Environmental Release 3-1
3.3 Environmental Fate 3-1
3.4 Summary 3-6
4.0 EXPOSURE FROM DRINKING WATER 4-1
4.1 Introduction 4-1
4.2 Ambient Occurrence 4-1
4.2.1 Data Sources and Methods 4-1
4.2.2 Results 4-3
4.3 Drinking Water Occurrence 4-4
4.3.1 Data Sources, Data Quality, and Analytical Methods 4-4
4.3.2 CCL Health Reference Level 4-5
4.3.3 Results 4-5
4.4 Summary 4-8
5.0 EXPOSURE FROM MEDIA OTHER THAN WATER 5-1
5.1 Exposure from Food 5-1
5.1.1 Concentration in Non-Fish Food Items 5-1
5.1.2 Concentrations in Fish and Shellfish 5-2
5.1.3 Intake of Terbacil from Food 5-2
5.2 Exposure from Air 5-2
5.3 Exposure from Soil 5-2
5.4 Other Residential Exposures (not drinking water related) 5-3
5.5 Occupational Exposures 5-3
5.6 Summary 5-3
6.0 HAZARD AND DOSE-RESPONSE ASSESSMENT 6-1
6.1 Characterization of Hazard 6-1
6.1.1 Synthesis and Evaluation of Major Noncancer Effects 6-1
Terbacil January, 2008 ix
-------
6.1.2 Synthesis and Evaluation of Carcinogenic Effects 6-3
6.1.3 Weight of Evidence Evaluation for Carcinogenicity 6-4
6.1.4 Potentially Sensitive Populations 6-4
6.2 Reference Dose 6-4
6.2.1 Choice of Principle Study and Critical Effect 6-5
6.2.2 Application of Uncertainty Factor(s) and Modifying Factor(s) 6-5
6.3 Carcinogen Assessment 6-5
6.4 Sensitive Population Considerations 6-5
6.5 Post Re-registration Health Effects Publications 6-5
6.6 CCL Health Reference Level 6-5
7.0 REGULATORY DETERMINATION AND CHARACTERIZATION OF RISK
FROM DRINKING WATER 7-1
7.1 Regulatory Determination for Chemicals on the CCL 7-1
7.1.1 Criteria for Regulatory Determination 7-1
7.1.2 National Drinking Water Advisory Council Recommendations 7-2
7.2 Health Effects 7-2
7.2.1 Health Criterion Conclusion 7-2
7.2.2 Hazard Characterization and Mode of Action Implications 7-3
7.2.3 Dose-Response Characterization and Implications in Risk Assessment
7-4
7.3 Occurrence in Public Water Systems 7-4
7.3.1 Occurrence Criterion Conclusion 7-5
7.3.2 Monitoring Data 7-5
7.3.3 Use and Fate Data 7-6
7.4 Risk Reduction 7-7
7.4.1 Risk Criterion Conclusion 7-7
7.4.2 Exposed Population Estimates 7-7
7.4.3 Relative Source Contribution 7-7
7.4.4 Sensitive Populations 7-8
7.5 Regulatory Determination Decision 7-8
8.0 REFERENCES 8-1
APPENDIX A: Abbreviations and Acronyms Appendix A-l
Terbacil January, 2008
-------
LIST OF TABLES
Table 2-1 Chemical and Physical Properties of Terbacil 2-2
Table 3-1 Environmental Releases (in pounds) of Terbacil in the United States, 1995-1997
3-1
Table 4-1 USGS National Synthesis Summary of NAWQA Monitoring of Terbacil in
Ambient Surface Water, 1992-2001 4-3
Table 4-2 USGS National Synthesis Summary of NAWQA Monitoring of Terbacil in
Ambient Ground Water, 1992-2001 4-4
Table 4-3 Summary UCMR1 Occurrence Statistics for Terbacil in Small Systems (Based
on Statistically Representative National Sample of Small Systems) 4-6
Table 4-4 Summary UCMR1 Occurrence Statistics for Terbacil in Large Systems (Based
on the Census of Large Systems) 4-7
Table 5-1 Estimated Environmental Concentrations on Avian and Mammalian Food Items
5-1
Table 6-1 Acute Toxicity Data for Terbacil 6-1
Terbacil January, 2008
XI
-------
Terbacil January, 2008 xii
-------
LIST OF FIGURES
Figure 2-1 Chemical Structure of Terbacil 2-1
Terbacil January, 2008 xiii
-------
Terbacil January, 2008 xiv
-------
1.0 EXECUTIVE SUMMARY
The U.S. Environmental Protection Agency (EPA) has prepared this Health Effects
Support Document for Terbacil to support a determination regarding whether to regulate terbacil
with a National Primary Drinking Water Regulation (NPDWR). The available data on
occurrence, exposure, and other risk considerations suggest that, because terbacil does not occur
in public water systems at frequencies and levels of public health concern, regulating terbacil
will not present a meaningful opportunity to reduce health risk. EPA will present a
determination and further analysis in the Federal Register Notice covering the CCL proposals.
Terbacil (Chemical Abstracts Services Registry Number 759-94-4) is an herbicide used
to selectively control many annual and some perennial weeds in crops, forestry, and feed crops.
It is an odorless, colorless to white crystalline powder. Terbacil is released primarily into the
environment through aircraft and ground equipment such as band treatment and broadcast
sprays. Terbacil is listed as a Toxic Release Inventory (TRI) chemical, with on-site releases to
surface water constituting the majority of releases.
Terbacil is applied to fields where crops are grown for weed control, and its residues can
be expected to persist and dissipate in soil by photolysis. Terbacil has not been detected in
groundwater, however, depending on the use of the herbicide and the amount of rain, this highly
mobile herbicide may reach groundwater sources. Additionally, the available data for terbacil
production, use, and environmental releases all show an increasing trend.
Data on the occurrence of terbacil in drinking water were obtained from the first
Unregulated Contaminant Monitoring Regulation (UCMR1) program. Although UCMR 1
monitoring was conducted primarily between 2001 and 2003, some results were not collected
and reported until as late as 2006. As a List 1 contaminant, terbacil was scheduled to be
monitored by all large CWSs and NTNCWSs and a statistically representative sample of small
CWSs and NTNCWSs. The data presented in this report reflect UCMR1 analytical samples
submitted and quality-checked under the regulation as of March 2006. Terbacil data were
collected and submitted by 797 small public water systems and 3,076 large public water systems.
Terbacil data were analyzed at the level of simple detections (at or above the minimum reporting
level, >MRL, or >2 |ig/L), exceedances of the health reference level (>HRL, or >90 |ig/L), and
exceedances of one-half the value of the HRL (^HRL, or >45 |ig/L). No detections of terbacil
were found in any samples, and thus there were also no exceedances of the HRL or one-half the
HRL.
There are no current studies that examine the human health effects due to terbacil
exposure. Terbacil is acutely toxic to rodents and rabbits when exposure occurs orally, dermally,
and by inhalation at high concentrations. According to oral subchronic and chronic studies, the
liver appears to be the target organ in dogs and rats. Observed hepatotoxic effects include
increased liver weights (absolute and/or relative); increased incidence of vacuolization and
hypertrophy of hepatocytes; and increased incidence in centrilobular hepatocyte hypertrophy,
biliary hyperplasia, and eosinophilic foci of cellular alteration in the liver.
Terbacil January, 2008 1-1
-------
Hepatotoxic effects also were included as critical effects observed in the principal study
for determining the RfD, which is 0.013 mg/kg/day. This principal study is a chronic toxicity
study, in which beagle dogs (4/sex/group) were administered terbacil via diet for 2 years at
concentrations of 50, 250, or 2500/10,000 ppm (equivalent to 1.25, 6.25, 62.5/250 mg/kg/day,
respectively). The no-observed-adverse-effect-level (NOAEL) was determined to be 1.25
mg/kg/day, and the lowest-observed-adverse-effect-level (LOAEL) was determined to be 6.25
mg/kg/day, based on increased thyroid to body weight ratios, slight increases in liver weights,
and elevated alkaline phosphatase levels. An uncertainty factor of 100 was used in calculating
the RfD to ensure the protection of infants and children from exposure to terbacil. A factor of 10
was used to account for interspecies differences, while another factor of 10 was used to account
for intraspecies differences.
Additionally, developmental and reproductive effects have been observed in rats and
rabbits. Developmental effects included significantly decreased number of live fetuses per litter
apparently due to fetal loss occurring before or near the time of implantation in rats (and
decreased live fetal weights in rabbits. Additionally, decreased body weight gains in 250-ppm
male offspring were observed when terbacil was administered orally over 3 generations at doses
of 0, 50, or 250 ppm (equivalent to 0, 2.5, and 12.5 mg/kg/day, respectively). These results,
however, do not suggest that offspring exhibited an increase in pre- or post-natal sensitivity to
terbacil exposure because developmental NOAELs were the same as those for maternal toxicity.
Additionally, the NOAEL for systemic (parental) toxicity was set at a lower concentration than
the NOAEL for reproductive toxicity, indicating that the reproductive system is less sensitive
than other organ systems to the effects of terbacil.
Two oral studies examined the carcinogenic effects of terbacil. Both studies conclude
that oral administration of terbacil did not show evidence of increased tumor incidence in the
treated animals when compared to the controls. Consequently, terbacil is classified as not likely
to be carcinogenic to humans because animal evidence failed to demonstrate a carcinogenic
effect in at least two well-designed and well-conducted studies in two appropriate animal species
(U.S. EPA, 2005a). Additionally, terbacil is not mutagenic. Terbacil was tested and found
negative in a chromosomal aberration study in rat bone marrow cells, found negative in a gene
mutation assay (with and without S9 activation), and found negative for DNA synthesis when
tested up to cytotoxic levels in rats.
When considered in its totality, the data on the occurrence of terbacil in public potable
water systems indicate that a positive regulatory determination to regulate this compound in
drinking water is not justified at this time. Although terbacil's physicochemical properties and
increasing use causes some concern, it does not occur widely in drinking water systems.
Terbacil does not occur in potable water systems at levels of concern, and regulation would not
provide a meaningful opportunity to reduce risk for the population.
Terbacil January, 2008 1-2
-------
2.0 IDENTITY: CHEMICAL AND PHYSICAL PROPERTIES
Terbacil is an odorless, colorless to white crystalline powder, herbicide (HSDB, 2004).
Terbacil is noncorrosive and stable to hydrolysis (Ahrens, 1994). It is stable at its melting point
temperature and in aqueous alkaline media at room temperature (Tomlin, 1997).
Figure 2-1 Chemical Structure of Terbacil
Source: Chemfinder (2004)
The chemical structure of terbacil is shown above (Figure 2-1). Its physical and chemical
properties, and other reference information are listed in Table 2-1.
The chemical name for terbacil is 3-tert-butyl-5-chloro-6-methyluracil or 5-chloro-3-(l,
l-dimethylethyl)-6-methyl-2,4(lH, 3H)-pyrimidinedione (U.S. EPA, 1998a). Terbacil also is
referred to as Sinbarฎ, Geonter, Herbicide 732, Compound 732, Dupont 732, and experimental
herbicide 732 (U.S. EPA, 1998a, 2000c). Ninety-five percent of technical grade terbacil is the
pure active compound. Terbacil is available in wettable powder form consisting of 80% active
ingredient; Krovar, a combination of terbacil and Hyvar X (Spencer, 1982); and in mixtures with
diuron (Farm Chemicals Handbook 1993), MPCA, Huron, diuron, and linuron, or with linuron
and monolinuron (Tomlin, 1997).
Terbacil January, 2008
2-1
-------
Table 2-1 Chemical and Physical Properties of Terbacil
Property
Chemical Abstracts Registry
(CAS) No.
EPA Pesticide Chemical Code
Synonyms
Registered Trade Name(s)
Chemical Formula
Molecular Weight
Physical State (25ฐC)
Boiling Point
Melting Point
Density (25ฐC)
Vapor Pressure (29.5ฐC)
Partition Coefficients:
Log Kow
LogKoc
Solubility in:
Water (25ฐC)
Other Solvents
Information
5902-51-2
OPP Code: 012701
Geonter, Dupont Herbicide 732
Sinbarฎ
C9H13C1N2O2
216.65
White crystals
~
175-177ฐC
1.34 g/mL
4.8 x 10'7 mmHg
1.89
9.00
710mg/L
dimethylformamide (337 g/kg at
25ฐC), cyclohexanone (220 g/kg at
25ฐC), methyl isobutyl ketone (121
g/kg at 25ฐC), butyl acetate (88 g/kg
at 25ฐC), xylene (65 g/kg at 25ฐC)
and is very soluble in strong aqueous
alkalis; it is sparingly soluble in
mineral oils aliphatic hydrocarbons
Source(s): U.S. EPA (1989a); Hansch et al. (1995); Wauchope et al. (1991);
U.S. EPA (1998a); Tomlin (1997)
Terbacil January, 2008
2-2
-------
3.0 USES AND ENVIRONMENTAL FATE
This section summarizes information derived from cited secondary references pertaining
to the production, use, environmental release, and environmental fate of terbacil.
3.1 Production and Use
Terbacil is a herbicide used to selectively control many annual and some perennial weeds
(Tomlin, 1997) in crops (e.g., apples, mint, sugarcane, asparagus, blackberries, boysenberries,
dewberries, loganberries, raspberries, youngberries, strawberries, and peaches), forestry (e.g.,
cottonwood), and feed crops (e.g., alfalfa, sainfoin, and forage) (U.S. EPA, 1998a). The
chemical in the form of 80% (20% a.i.) wettable powder (WP; EPA Reg. No. 352-317) is
manufactured from an unregistered Technical Grade Active Ingredient (TGAI) (95% a.i) by E.I.
du Pont de Nemours and Company, Inc. (U.S. EPA, 1998a). The estimated use of terbacil during
1992 was recorded as 285,000 Ibs (USGS, 1992). Terbacil can be applied by aircraft and ground
equipment such as band treatment and broadcast sprays (U.S. EPA, 1998a). The maximum
application rates range from 0.120 to 1.45 kg a.i./acre (U.S. EPA, 1998a). Lower rates generally
are used on coarse textured soils and higher rates on fine textured soils (U.S. EPA, 1998a).
Annual usage data between 1987 and 1995 show that terbacil was used to treat
approximately 401,000 acres of crop land and 4,000 acres of non-crop land (i.e., fallow, forest
trees, and ornamentals). These uses accounted for an annual application of approximately
100,000 and 4,000 kg of terbacil a.i., respectfully (U.S. EPA, 1998a).
3.2 Environmental Release
Terbacil is listed as a Toxic Release Inventory (TRI) chemical. TRI data for terbacil (see
Table 3-1) are reported for the years 1995 to 1997. During that three-year period, all reported
releases were on-site releases to surface water. These releases were all in Texas (U.S. EPA,
2004a) and showed an increase in surface water discharge over the years.
Table 3-1 Environmental Releases (in pounds) of Terbacil in the United States, 1995-
1997
Year
1997
1996
1995
On-Site Releases
Air Emissions
0
0
0
Surface Water
Discharges
10,318
3,835
4.608
Underground
Injection
0
0
0
Releases
to Land
0
0
0
Off-Site
Releases
0
0
0
Total On- &
Off-site
Releases
10,318
3,835
4.608
Source: U.S. EPA (2004a)
3.3 Environmental Fate
Terbacil dissipation in soil appears to depend on microbial-mediated degradation,
photodegradation in water, and movement into ground and surface waters. Terbacil has a low
sorption affinity to soil (Kad=0.39 to 1.3 mL/g; Koc=44 to 61 mL/g) and relatively high solubility
Terbacil January, 2008
3-1
-------
in water (710 mg/L); therefore, it is expected to be mobile in soil. The current data on terbacil
and its degradation products indicate that it is persistent and potentially mobile in terrestrial
environments (U.S. EPA, 1998a). Terbacil has a low vapor pressure (4.8 x 10"7 mmHg at
29.5ฐC) and Henry's Law constant (1.9 x 10"9 atm m3/mole); therefore, is not expected to occur
in large concentrations in the air.
Degradation
Terbacil is resistant to abiotic hydrolysis and slowly degrades through photolysis in
water. Terbacil was stable for up to 6 weeks at pH of 5, 7, and 9 in the dark and in buffered
solutions at 25ฐC at pH of 4-10 (U.S. EPA, 1998a). Photosensitizers such as riboflavin, rose
bengal, and methylene blue enhance the process of photodegradation. Under natural sunlight,
radiolabeled terbacil had a first-order photodegradation half-life (t1/2) of 29 days in standard
reference water (no further descriptions of water quality were presented), 37 days in river water
(Brandywine River), 54 days in river water (Brandywine River) with suspended sediment, and
3.25 days in reference water with riboflavin (Rhodes, 1975). In the same laboratory, when
exposed to ultraviolet (UV) rays, the radiolabeled terbacil displayed photodegradation half-lives
of 44 days in standard reference water, 82.91 days in river water, and 4.8 days in reference water
with a riboflavin sensitizer (U.S. EPA, 1998a). After 4 weeks of irradiation of terbacil at 5 ppm
in distilled water with a pH of 6.2 with UV light of 300 to 400 nm, approximately 16% was
photodegraded (Davidson et al., 1978). Major photodegradation products were
5-chloro-6-methyluracil, 3-tert-butyl-6-methyluracil, and
6-chloro-2,3-dihydro-3,3,7-trimethyl-5Hoxazolo (3,2-a)-pyrimidine-5-one.
In non-buffered aqueous solutions of pH 3.4 to 9.2, radiolabeled terbacil at 700 g/mL
under natural sunlight with photosensitizers, a first-order photodegradation reaction was
observed with the half-life being less than 2 hours (Acher, 1981). However, at 250 ppm, terbacil
was photolytically stable in non-buffered aqueous solutions irradiated with a mercury vapor
lamp at 25ฐC. The dyes, rose bengal and methylene blue, were effective photosensitizers in
alkaline non-buffered aqueous solutions with a pH above 6.6. Humic acid was not an effective
sensitizer in aqueous solutions. Major photodegradation products were
3-tert-butyl-5-hydroxyhydantoin (Compound II), 3-tert-butyl-5-hydroxyhydantoin (Compound
III), and
5-chloro-6-methyl-(3',5')-5'-chloro-6'-methyl-5',6'-dihydro-6',2-anhydro-3'-tert-butyluracil
(Compound VI), and an unidentified product (Compound V). Compound II does not appear to
be a photodegradate because it was detected in dark controls. In the dark, radiolabeled terbacil
was stable in buffer solutions of pH between 4 and 10 for greater than 6 weeks (U.S. EPA,
1998a).
Degradation of terbacil in aerobic and anaerobic soil is slow. Terbacil degradation was
dependant on first-order degradation kinetics (U.S. EPA, 1998a). In soil, terbacil is stable to
abiotic hydrolysis and if it is not in contact with direct sunlight; photolysis is the only
degradation pathway with a half-life of 122 days (U.S. EPA, 1998a). Irradiated and dark
treatment of terbacil yielded the degradation product 5-chloro-6-methyluracil.
Terbacil January, 2008 3-2
-------
Terbacil in silt loam continuously irradiated with fluorescent sun lamps and black lights
for an 8 week period, displayed a first-order degradation half-life of 46 days (Rhodes, 1975).
The photodegradation rate appears to be dramatically enhanced by the presence of the
photosensitizers, riboflavin and methylene blue. The major transformation product was CO2 and
minor transformation products were t-butylurea and 3-tert-butyl-6-methyluracil (U.S. EPA,
1998a). In nonsterile soils incubated in a greenhouse, terbacil was found to have a half-life of 2
to 3 months (Rhodes, 1975). Furthermore, 90 percent of 2 ppm terbacil remained after a 90-day
incubation period in sterile and nonsterile soil, and 0.8 to 1.5 percent of the applied 14C was later
found in CO2 molecules from nonsterile soil, while 0.01 percent was in the CO2 from sterile soil
(U.S. EPA, 1982). Only trace amounts of radiolabeled terbacil applied at 2.88 ppm were
degraded to radiolabeled carbon dioxide after 145 days when metabolized by microbes in a dark
anaerobic environment (Rhodes, 1975).
Radiolabeled terbacil at 9.3 jig/g in sandy loam soil was found to have a first-order
half-life of 653 days after 12 months in the dark (U.S. EPA, 1998a). Another study found that
terbacil at 100 g had a half-life of 720 days in sandy loam soils (Marsh and Davis, 1978). When
2.1 ppm terbacil is applied to anaerobic silt loam and sandy soil, after 60 days at 20ฐC less than 5
percent of the chemical degraded (U.S. EPA, 1982). A study performed in 1970 illustrated that 8
ppm of terbacil had a half-life of approximately 5 months in aerobic loam soil (Zimdahl et al.,
1970). Eight ppm of terbacil had a 5-month half-life in aerobic loam soil at 32ฐC, and 2 ppm of
terbacil had a 2 to 3 month half-life in aerobic silt loam and sandy loam soils (U.S. EPA, 1982).
In terms of biodegradation, 20% of 100 ppm terbacil biodegraded after 32 weeks in aerobic
sandy loam soil at 23ฐC (U.S. EPA, 1982). Terbacil, at 4.5 Ibs. a.i./A, had a half-life of 32.5
days when incubated in silt loam soil irradiated with UV light for 12 hr/d for 6.5 weeks (Rhodes
et al., 1969). When 2.88 ppm radiolabeled terbacil was applied on sandy loam soil 28%
degraded to 14CO2 (Wolf, 1973; Wolf, 1974; Wolf and Martin, 1974).
In the atmosphere, photochemically-produced hydroxyl radicals degrade vapor-phase
terbacil with a half-life for this degradation of 51 hrs. Wet and dry deposition removes
particulate-phase terbacil from the atmosphere and redistributes it into terrestrial or aquatic
systems (HSDB, 2004).
Environmental Media Transport and Distribution
A model of gas/particle partitioning of semivolatile organic compounds in the
atmosphere (Bidleman, 1988) portrays that terbacil may exist in the vapor and particulate phases
in the ambient atmosphere due to its 4.7 x 10"7 mm Hg vapor pressure. Volatilization is not
expected to be a major route of dissipation for terbacil because of its low vapor pressure and low
Henry's Law constant of 1.9 x 10'9 atm nrVmole (U.S. EPA, 1998a).
Terbacil is usually applied by aircraft and orchard airblasts, which is a potential risk to
nontarget aquatic organisms. The Spray Drift Task Force (SDTF) completed and submitted a
series of studies intended to characterize spray droplet drift potential to the EPA's Office of
Pesticide Prevention Agency, which had not yet been evaluated by time the RED document was
published in 1998. Previous data indicate, however, that off-target drift rates are 1% of the
Terbacil January, 2008 3-3
-------
applied spray volume from ground applications and 5% from aerial and orchard airblast
applications at 100 feet downwind (U.S. EPA, 1998a).
With regard to terbacil in soil, studies show that terbacil does not adsorb to suspended
solids and sediment and has a high/very high mobility due to its Koc values that range from 41 to
85 (U.S. EPA, 1998a; Kenaga, 1980; Rao and Davidson, 1982). Terbacil was negligibly
adsorbed to soils ranging in texture from sand to clay (Davidson et al., 1978; Liu et al., 1971;
Rao and Davidson, 1979). Studies indicated that 54% of terbacil was adsorbed to muck soil,
which is 36% organic matter (Liu et al., 1977).
Field dissipation studies indicate that terbacil, at 5 Ibs a.i./A, is persistent and mobile
under actual use conditions. Field dissipation half-lives in Delaware, Illinois, and California
ranged from 204 to 252 days (U.S. EPA, 1998a). These field dissipation studies showed that
terbacil's persistence in the soil is dependant on application rate, soil type, and rainfall. In the
field, terbacil residues persisted in soil for up to 16 months following a single application.
Residues were found at the maximum depths sampled, i.e., 3 to 43 inches (Gardiner, No date a,b;
Gardiner et al., 1969; Isom et al., 1969; Isom et al., 1970; Liu et al., 1977; Mansell et al., 1977;
Mansell et al., 1979; Morrow and McCarty, 1976; Rahman, 1977; Rhodes, 1975). Multiple
applications of terbacil demonstrated persistence for 1 to more than 2 years following the final
application of the herbicide (Skroch et al., 1971; Tucker and Phillips, 1970; Benson, 1973;
Doughty, 1978).
Laboratory soil mobility studies demonstrated that terbacil and its minor transformation
products can leach through a 30 cm column of silt loam and sand loam soil when eluted with 20
inches of 0.01 M CaCl2 (U.S. EPA, 1998a). Terbacil was predominately detected in the elution
samples. In another study, 4 to 64% of radioactive terbacil (2 Ibs/A), as well as an unidentified
radioactive product was leached through 18 inches of packed soil columns of sandy loam and silt
loam when eluted with 20 inches of water (Rhodes, 1975). Terbacil residues were eluted with 10
to 20 cm of water to a depth of 27.5 to 30 cm in packed 30 cm soil columns of sandy orchard soil
(Marriage et al., 1977). A fourth study utilized fine sand (30 cm column) and approximately 73
to 90% of applied radioactivity was leached when eluted with 15.5 to 20 inches of 0.01 M
CaSO4.
Terbacil applied as spray at 5 Ibs a.i./A had a first order half-life of 212 days on silt loam,
204 days on silty clay soil, and 252 days on a sandy loam soil (U.S. EPA, 1998a). Terbacil
residues of less than 0.09 jig of terbacil/g of soil were detected at a maximum soil depth of 45 to
50 cm (U.S. EPA, 1998a). In some field studies, the transformation product,
3-t-butyl-5-chloro-6-hydroxymethyluracil, had a maximum concentration of 0.14 jig of terbacil/g
of soil at 15 days. The transformation product,
6-chloro-2,3-dihydro-7-(hydroxymethyl)3,3-dimethyl-5H-oxazolo[3,2-a]pyrimidin-5-one, had a
maximum concentration of 0.07 jig of terbacil/g of soil at 60 days post-treatment (U.S. EPA,
1998a).
In a microplot field dissipation study, radiolabeled terbacil at 2 Ibs a.i./A had a half-life
of 1 to 2 months when incubated in the field for 4 months with a cumulative rainfall of 18.33
Terbacil January, 2008 3-4
-------
inches (Rhodes, 1975). Terbacil was detected in the 12 to 15 inch soil segment. Terbacil
applied at 4 Ibs a.i./A had an estimated half-life of 131 days when incubated for 52 weeks in silt
loam (Gardiner et al., 1969). Residues were detected through the lysimeter at 5 weeks post-
treatment.
Terbacil applied at 1.6 Ibs a.i./A on orchard soil was detected 1 year post-treatment using
oats, beans, and cucumbers as phytotoxicity indicators at a maximum depth of 18 to 24 inches
(Benson, 1973). Terbacil applied at 2.24 kg/ha/year for 4 consecutive years caused phytotoxic
effects on oats and beans 2 year post-treatment on acidic clay loam soil (Doughty, 1978). A
phytotoxic amount of terbacil residues were not detected on a high organic matter, acidic, silt
loam on which 4.48 kg/ha of terbacil was applied for 4 consecutive years (U.S. EPA, 1998a).
Other studies indicate that phytotoxic levels of terbacil residues were detected 7 to 13 months
post-treatment in clay loam soil (Liu et al., 1977; Isom et al., 1969; Isom et al., 1970). Terbacil
applied on the soil surface or incorporated at rates of 2.24 and 4.48 kg/ha for 3 consecutive years
degraded with a half-life of approximately 157 days on peach orchard sandy soil (Skroch et al.,
1971). Terbacil was detected at maximum soil depths of 15 to 30 cm soil following the second
and third year applications (U.S. EPA, 1998a).
Terbacil is persistent and mobile in soils, which are conditions favorable for it to
dissipate into groundwater (U.S. EPA, 1989a). Based on the environmental fate data, terbacil
exceeds the mobility and persistence triggers for the proposed Restricted Use Classification for
ground water concerns. The Groundwater Ubiquity Score (GUS) for terbacil is 5.32 in the best
case scenario (scores above 2.8 indicate relatively high leaching potential) (U.S. EPA, 1998a).
Currently, there are insufficient terbacil detections in ground water to warrant a Restricted Use
classification. The lack of detections of terbacil in ground water may be associated with its
limited geographical use. Terbacil has relatively low total environmental loading relative to
other herbicides. Testing for terbacil has been conducted in areas where the herbicide was not
used. In addition to this, the limit of detection for terbacil is 5 to 100 times higher than those of
other herbicides (U.S. EPA, 1998a).
PATRIOT (Pesticide Assessment Tool for Rating Investigations of Transport) modeling,
can do a comparative leaching assessment of terbacil, relative to a conservative tracer, and can
predict the amount of potential leaching in soils. The modeling predicted that approximately 40
to 75% of the terbacil mass applied could leach to shallow ground water (4.5 feet) (U.S. EPA,
1998a). Annual leaching may be highly variable depending on the rainfall. Since terbacil is
persistent in soil, it will most likely accumulate in soil and the total mass reaching ground water
in a particular year may exceed the total mass applied in a given year. The mass of terbacil
estimated to leach to ground water for each year ranged from 0 to 125% of the annual application
(U.S. EPA, 1998a). Terbacil is only used on minor crops; therefore, the impact on groundwater
is expected to be limited to very localized, site specific soil/hydrological conditions. According
to the PATRIOT model, based on the use pattern and site conditions, mint and sugarcane
production areas are predicted to be vulnerable groundwater areas for terbacil. Terbacil could
reach the shallow groundwater at high concentrations (U.S. EPA, 1998a).
Terbacil January, 2008 3-5
-------
A groundwater screening model, Screening Concentrations in Ground Water (SCI-GRO)
predicted that terbacil could potentially contaminate shallow groundwater near specific use sites
at low levels. This is due to its use on limited areas of minor crops with relatively low
environmental loading (U.S. EPA, 1998a).
Tier 1 GENEEC (Generic Expected Environmental Concentration) modeling indicates
that terbacil may reach surface waters at concentrations between 19 and 154 g/L. Another
surface water simulation device, PRZM-EXAMS EECs, suggests that terbacil may accumulate in
static surface waters from long-term use, and that surface water runoff may be an important route
of dissipation, while the STORET database suggests that terbacil does not accumulate in surface
waters (U.S. EPA, 1998a). More research is required in this area.
Bioaccumulation
The BCF (the bioconcentration factor) of terbacil is estimated to be 16, which indicates
that bioconcentration of terbacil in aquatic organisms is unlikely (HSDB, 2004). Its log Kow
(Hansch, 1995) and regression-derived equation (Meylan, 1999) also point to a low
bioconcentration of terbacil in aquatic organisms. In a study with a 4-week exposure period,
0.01 and 1.00 |ig/mL of radiolabeled terbacil was accumulated, respectively, at concentrations of
0.11 and 7.9 jig of terbacil/g of tissue in viscera, 0.02 and 1.8 jig of terbacil/g of tissue in head,
0.07 and 4.4 jig of terbacil/g of tissue in the livers, and 0.02 and 1.7 jig of terbacil/g of tissue in
edible tissue of bluegill sunfish (U.S. EPA, 1998a). After 3 days of depuration, radioactive
terbacil residues were below the detection limit of 0.01 jig of terbacil/g of tissue in all fish
tissues (U.S. EPA, 1998a). A metabolism study, which used 65x feeding level of terbacil,
indicated that there is no likelihood of finite residues in poultry (U.S. EPA, 1998a). Terbacil
residues in ruminant commodities showed no likelihood of finite residues (U.S. EPA, 1998a).
3.4 Summary
In summary, terbacil is applied to fields where crops are grown for weed control, and its
residues can be expected to persist and dissipate in soil by photolysis. Terbacil has not been
detected in groundwater, however, depending on the use of the herbicide and the amount of rain,
this highly mobile herbicide may reach groundwater sources. Finally, terbacil is applied to fields
but is not expected to remain in the atmosphere.
Terbacil January, 2008 3-6
-------
4.0 EXPOSURE FROM DRINKING WATER
4.1 Introduction
EPA used data from several sources to evaluate the potential for occurrence of terbacil in
Public Water Systems (PWSs). The primary source of drinking water occurrence data for
terbacil was the first Unregulated Contaminant Monitoring Regulation (UCMR1) program. The
Agency also evaluated ambient water quality data from the United States Geological Survey
(USGS).
4.2 Ambient Occurrence
4.2.1 Data Sources and Methods
USGS instituted the National Water Quality Assessment (NAWQA) program in 1991 to
examine ambient water quality status and trends in the United States. NAWQA is designed to
apply nationally consistent methods to provide a consistent basis for comparisons among study
basins across the country and over time. These occurrence assessments serve to facilitate
interpretation of natural and anthropogenic factors affecting national water quality. For more
detailed information on the NAWQA program design and implementation, please refer to Leahy
and Thompson (1994) and Hamilton and colleagues (2004).
Study Unit Monitoring
The NAWQA program conducts monitoring and water quality assessments in significant
watersheds and aquifers referred to as "study units." NAWQA's sampling approach is not
"statistically" designed (i.e., it does not involve random sampling), but it provides a
representative view of the nation's waters in its coverage and scope. Together, the 51 study units
monitored between 1991 and 2001 include the aquifers and watersheds that supply more than
60% of the nation's drinking water and water used for agriculture and industry (NRC, 2002).
NAWQA monitors the occurrence of chemicals such as pesticides, nutrients, volatile organic
compounds (VOCs), trace elements, and radionuclides, and the condition of aquatic habitats and
fish, insects, and algal communities (Hamilton et al., 2004).
Monitoring of study units occurs in stages. Between 1991 and 2001, approximately one-
third of the study units at a time were studied intensively for a period of three to five years,
alternating with a period of less intensive research and monitoring that lasted between five and
seven years. Thus, all participating study units rotated through intensive assessment in a ten-
year cycle (Leahy and Thompson, 1994). The first ten-year cycle was called "Cycle 1."
Summary reports are available for the 51 study units that underwent intensive monitoring in
Cycle 1 (USGS, 2001). Cycle 2 monitoring is scheduled to proceed in 42 study units from 2002
to 2012 (Hamilton et al., 2004).
Terbacil January, 2008 4-1
-------
Pesticide National Synthesis
Through a series of National Synthesis efforts, the USGS NAWQA program is preparing
comprehensive analyses of data on topics of particular concern. These data are aggregated from
the individual study units and other sources to provide a national overview.
The Pesticide National Synthesis began in 1991. Results from the most recent USGS
Pesticide National Synthesis analysis, based on complete Cycle 1 (1991-2001) data from
NAWQA study units, are posted on the NAWQA Pesticide National Synthesis website (Martin
et al., 2003; Kolpin and Martin, 2003; Nowell, 2003; Nowell and Capel, 2003). USGS considers
these results to be provisional. Data for surface water, ground water, bed sediment, and biota are
presented separately, and results in each category are subdivided by land use category. Land use
categories include agricultural, urban, mixed (deeper aquifers of regional extent in the case of
ground water), and undeveloped. The National Synthesis analysis for pesticides is a first step
toward the USGS goal of describing the occurrence of pesticides in relation to different land use
and land management patterns, and developing a deeper understanding of the relationship
between spatial occurrence of contaminants and their fate, transport, persistence, and mobility
characteristics.
The surface water summary data presented by USGS in the Pesticide National Synthesis
(Martin et al., 2003) only include stream data. Sampling data from a single one-year period,
generally the year with the most complete data, were used to represent each stream site. Sites
with few data or significant gaps were excluded from the analysis. NAWQA stream sites were
sampled repeatedly throughout the year to capture and characterize seasonal and hydrologic
variability. In the National Synthesis analysis, the data were time-weighted to provide an
estimate of the annual frequency of detection and occurrence at a given concentration.
The USGS Pesticide National Synthesis only analyzed ground water data from wells;
data from springs and agricultural tile drains were not included. The sampling regimen used for
wells was different than that for surface water. In the National Synthesis analysis (Kolpin and
Martin, 2003), USGS uses a single sample to represent each well, generally the earliest sample
with complete data for the full suite of analytes.
NAWQA monitored bed sediment and fish tissue at sites considered likely to be
contaminated and sites that represent various land uses within each Study Unit. Most sites were
sampled once in each medium. In the case of sites sampled more than once, a single sample was
chosen to represent the site in the Pesticide National Synthesis analysis (Nowell, 2003). In the
case of multiple bed sediment samples, the earliest one with complete data for key analytes was
used to represent the site. In the case of multiple tissue samples, the earliest sample from the
first year of sampling that came from the most commonly sampled type offish in the Study Unit
was selected.
As part of the National Pesticide Synthesis, USGS also analyzed the occurrence of select
semivolatile organic compounds (SVOCs) in bed sediment at sites considered likely to be
contaminated and sites that represent various land uses within each Study Unit (Nowell and
Terbacil January, 2008 4-2
-------
Capel, 2003). Most sites were sampled only once. When multiple samples were taken, the
earliest one was used to represent the site in the analysis.
Over the course of Cycle 1 (1991-2001), NAWQA analytical methods may have been
improved or changed. Hence, reporting levels (RLs) varied over time for some compounds. In
the summary tables, the highest RL for each analyte is presented for general perspective. In the
ground water, bed sediment, and tissue data analyses, the method of calculating concentration
percentiles sometimes varied depending on how much of the data was censored at particular
levels by the laboratory (i.e., because of the relatively large number of non-detections in these
media).
4.2.2 Results
Under the NAWQA program, USGS monitored terbacil between 1992 and 2001 in
representative watersheds and aquifers across the country. Reporting limits varied but did not
exceed 0.034 |ig/L. All concentrations determined for terbacil are estimated concentrations.
Results for surface water and ground water are presented in Tables 4-1 and 4-2. Terbacil was
not monitored in bed sediment or biota.
Table 4-1 USGS National Synthesis Summary of NAWQA Monitoring of Terbacil in
Ambient Surface Water, 1992-2001
Land Use Type
Agricultural
Mixed
Undeveloped
Urban
No. of Samples
(and No. of
Sites)
1,858 (77)
996 (46)
60(4)
896 (33)
Detection
Frequency
4.52%
1.82%
1.40%
1.98%
50th Percentile
(Median)
Concentration
-------
Table 4-2 USGS National Synthesis Summary of NAWQA Monitoring of Terbacil in
Ambient Ground Water, 1992-2001
Land Use Type
Agricultural
Mixed (Major
Aquifer)
Undeveloped
Urban
No. of Wells
1,438
2,708
67
830
Detection
Frequency
0.76%
0.26%
0.0%
1.20%
50th Percentile
(Median)
Concentration
-------
year, six-month interval monitoring schedule for ground water systems. Although UCMR1
monitoring was conducted primarily between 2001 and 2003, some results were not collected
and reported until as late as 2006.
The objective of the UCMR1 sampling approach for small systems was to collect
contaminant occurrence data from a statistically selected, nationally representative sample of
small systems. The small system sample was stratified and population-weighted, and included
some other sampling adjustments such as allocating a selection of at least two systems from each
State. With contaminant monitoring data from all large PWSs and a statistical, nationally
representative sample of small PWSs, the UCMR1 List 1 Assessment Monitoring program
provides a contaminant occurrence data set suitable for national drinking water estimates.
4.3.2 CCL Health Reference Level
To evaluate the systems and populations exposed to terbacil through PWSs, the
monitoring data were analyzed against the Minimum Reporting Level (MRL) and a benchmark
value for health that is termed the Health Reference Level (HRL). Two different approaches
were used to derive the HRL, one for chemicals that cause cancer and exhibit a linear response to
dose and the other applies to noncarcinogens and carcinogens evaluated using a non-linear
approach.
The RfD for terbacil is 0.013 mg/kg/day based on a chronic toxicity feeding study with
beagle dogs where critical effects included increased relative thyroid weights, increased liver
weights, and elevated liver enzymes (Wazeter et al., 1967a). Additional detail concerning the
RfD can be found in section 6.2. The Agency established the HRL for terbacil using the RfD
and a 20 percent relative source contribution as follows:
HRL = [(0.013 mg/kg/day x 70 kg)/2 L/day] x 20% = 0.091 mg/L (or 90 |lg/L using the
round number)
4.3.3 Results
As a List 1 contaminant, terbacil was scheduled to be monitored by all large CWSs and
NTNCWSs and a statistically representative sample of small CWSs and NTNCWSs. The data
presented in this report reflect UCMR1 analytical samples submitted and quality-checked under
the regulation as of March 2006. Terbacil data were collected and submitted by 797 (99.6
percent) of the 800 small systems selected for the small system sample and 3,076 (99.2 percent)
of the 3,100 large systems defined as eligible for the UCMR1 large system census. Terbacil data
have been analyzed at the level of simple detections (at or above the minimum reporting level,
>MRL, or >2 |ig/L), exceedances of the health reference level (>HRL, or >90 |ig/L), and
exceedances of one-half the value of the HRL (>/^HRL, or >45 |ig/L).
Results of the analysis are presented in Tables 4-3 and 4-4. No detections of terbacil
were found in any samples and, thus, there also were no exceedances of the HRL or one-half the
HRL.
Terbacil January, 2008 4-5
-------
Table 4-3 Summary UCMR1 Occurrence Statistics for Terbacil in Small Systems
(Based on Statistically Representative National Sample of Small Systems)
Frequency Factors
Total Number of Samples
Percent of Samples with Detections
99th Percentile Concentration (all samples)
Health Reference Level (HRL)
Minimum Reporting Level (MRL)
Maximum Concentration of Detections
99th Percentile Concentration of Detections
Median Concentration of Detections
Total Number of PWSs
Number of GW PWSs
Number of SW PWSs
Total Population
Population of GW PWSs
Population of SW PWSs
Occurrence by System
PWSs (GW & SW) with Detections (> MRL)
PWSs (GW & SW) > 1/2 HRL
PWSs (GW & SW) > HRL
Occurrence by Population Served
Population Served by PWSs with Detections
Population Served by PWSs > 1/2 HRL
Population Served by PWSs > HRL
UCMR Data -
Small Systems
3,251
0.00%
^HRL, or PWSs > HRL = PWSs with at
least one sampling result greater than or equal to the MRL, exceeding the HHRL benchmark, or exceeding the HRL benchmark, respectively;
Population Served by PWSs with detections, by PWSs >'/2HRL, or by PWSs >HRL = population served by PWSs with at least one sampling
result greater than or equal to the MRL, exceeding the '/2HRL benchmark, or exceeding the HRL benchmark, respectively
Notes:
-Small systems are those that serve 10,000 persons or fewer.
-Only results at or above the MRL were reported as detections. Concentrations below the MRL are considered non-detects.
-Due to differences between the ratio of GW and SW systems with monitoring results and the national ratio, extrapolated GW and SW figures
might not add up to extrapolated totals.
Terbacil January, 2008
4-6
-------
Table 4-4 Summary UCMR1 Occurrence Statistics for Terbacil in Large Systems
(Based on the Census of Large Systems)
Frequency Factors
Total Number of Samples
Percent of Samples with Detections
99th Percentile Concentration (all samples)
Health Reference Level (HRL)
Minimum Reporting Level (MRL)
Maximum Concentration of Detections
99 Percentile Concentration of Detections
Median Concentration of Detections
Total Number of PWSs
Number of GW PWSs
Number of SW PWSs
Total Population
Population of GW PWSs
Population of SW PWSs
Occurrence by System
PWSs (GW & SW) with Detections (> MRL)
PWSs (GW & SW) > 1/2 HRL
PWSs (GW & SW) > HRL
Occurrence by Population Served
Population Served by PWSs with Detections
Population Served by PWSs > 1/2 HRL
Population Served by PWSs > HRL
UCMR Data -
Large Systems
30,549
0.00%
ViHRL, and PWSs > HRL = PWSs with at
least one sampling result greater than or equal to the MRL, exceeding the '/2HRL benchmark, or exceeding the HRL benchmark; Population
Served by PWSs with detections, by PWSs >'/2HRL, and by PWSs >HRL = population served by PWSs with at least one sampling result greater
than or equal to the MRL, exceeding the ViHRL benchmark, or exceeding the HRL benchmark.
Notes:
-Large systems are those that serve more than 10,000 persons.
-Only results at or above the MRL were reported as detections. Concentrations below the MRL are considered non-detects.
Terbacil January, 2008
4-7
-------
4.4 Summary
Under the NAWQA program, USGS monitored terbacil between 1992 and 2001 in
representative watersheds and aquifers across the country. The 95th percentile concentrations in
surface and ground water were less than the reporting limit in all land use settings. Terbacil was
detected more frequently in ambient surface water than in ambient ground water in all land use
settings (1.40% vs. 0% of samples from undeveloped areas; 1.82% vs. 0.26% of samples from
mixed land use settings; 1.98% vs. 1.20% of urban samples; and 4.52% vs. 0.76% of agriculture
samples).
For UCMR1, terbacil was scheduled to be monitored by all large CWSs and NTNCWSs
and a statistically representative sample of small CWSs and NTNCWSs. The data that were
available in March of 2006 were analyzed at the level of simple detections (at or above the
minimum reporting level, >MRL, or 9 |ig/L), exceedances of the health reference level (>HRL,
or >90 |ig/L), and exceedances of one-half the value of the HRL (>/^HRL, or >45 |ig/L). No
detections of terbacil were found in any samples and, thus, there were also no exceedances of the
HRL or one-half the HRL.
Terbacil January, 2008 4-8
-------
5.0 EXPOSURE FROM MEDIA OTHER THAN WATER
This section summarizes human population exposures to terbacil from food, air, and soil.
The primary purpose is to estimate average daily intakes of terbacil by members of the general
public. When exposure data on sub-populations were located, such as occupationally exposed
persons, these data were summarized and included in this section.
5.1 Exposure from Food
Terbacil is used to control broad leaf non-essential plants in food and feed crop areas
such as apples, mint, sugarcane, asparagus, berries, peach, alfalfa, and sainfoin. Terbacil is
believed to be persistent in the environment; therefore, the general population may be exposed to
terbacil through diet.
5.1.1 Concentration in Non-Fish Food Items
The U.S. EPA (1998a) evaluated the estimated environmental concentrations (EECs) of
terbacil on avian or mammalian food items immediately following a direct single application at 1
Ib a.i./A in nongranular form (e.g., liquid or dust). The table below presents the predicted
maximum and mean residues on these products.
Table 5-1 Estimated Environmental Concentrations on Avian and Mammalian Food
Items
Food Items
Short grass
Tall grass
Broadleaf/forage plants, and
small insects
Fruits, pods, seeds, and large
insects
EEC (ppm)
Predicted Maximum Residue*
240
110
135
15
EEC (ppm)
Predicted Mean Residue*
85
36
45
7
*U.S. EPA1998a
In 1977, Cessna measured terbacil residue in highbush and lowbush blueberries that were
treated with only terbacil as well as those that were treated with a combination of herbicides.
The maximum residue measured was 2.0 ppb where the limit of detection was 1.0 ppb based on a
25 g sample and recoveries were in the order of 90%.
Cessna (1991) conducted a 2-year study on terbacil residues extracted from asparagus
spears from established agricultural sites in British Columbia and Ontario following pre-
emergence and early post-emergence applications at 0.6, 1.1, and 2.2 kg/ha. At one site,
maximum residues in the pre-emergence samples were found to be 14ฑ3 |ig/kg for the 2.2 kg/ha
application rate, whereas maximum residues in the early post-emergence samples for the 2.2
kg/ha application rate were 493ฑ250 |ig/kg at a second site. Recoveries of terbacil from fortified
Terbacil January, 2008
5-1
-------
asparagus tissue were 96ฑ19%, 87.2ฑ11.9% and 83.3ฑ7.8% at 10, 50, and 100 |ig/kg,
respectively.
The New Jersey Department of Environmental Protection reported in 2004 that 0.010
Hg/g of terbacil was detected in the squash grown in the State (NJFMEP, 2004).
Maier-Bode et al.(1970) reviewed the presence of terbacil residues, along with other
herbicides in cultivated crops in Germany. They determined that when terbacil was used as
indicated by the directions, the chemical did not leave any measurable residues at harvest time.
5.1.2 Concentrations in Fish and Shellfish
EPA's Registration Eligibility Decision (RED) for Terbacil (1998a) noted that terbacil
bioaccumulated (<8 |ig/g) in bluegill sunfish tissues under static conditions of 0.01 and 1.00
|ig/mL, but declined below the detection limit (<0.01 |ig/g) within 3 days of depuration. It was
thus concluded that terbacil did not bioaccumulate in fish tissues.
5.1.3 Intake of Terbacil from Food
Data on dietary concentrations from food were not located in the available literature.
Consequently, calculating the intake of terbacil from food is not possible. However, pesticide
tolerance values have been established for terbacil in a variety of fruits, including berries, and
asparagus (U.S. EPA, 2006). Accordingly, some exposure through ingestion of these foods is
possible. Terbacil does not bioaccumulate in fish; therefore, it is anticipated that there would
typically be no chronic exposure to terbacil via fish consumption.
5.2 Exposure from Air
Terbacil is used as an herbicide. Although terbacil does not readily volatilize due to its
low vapor pressure and low Henry's Law constant, when in the atmosphere, terbacil may exist in
the vapor and particulate phase (HSDB, 2004). Terbacil may enter the atmosphere as a result of
being sprayed onto fields where crops are grown for weed control. Data on concentrations of
terbacil in air were not located in the available literature; consequently, the intake of terbacil
from air cannot be calculated.
5.3 Exposure from Soil
The half-life of terbacil in a variety of soils suggests that terbacil, its degradates, or both
can persist in treated areas for many months after treatment (Chapter 3). However, results of
terbacil monitoring in ambient soils were not identified in the published literature. Because
terbacil use is not wide spread, exposure from soils in nontreated areas is unlikely.
Terbacil January, 2008 5-2
-------
5.4 Other Residential Exposures (not drinking water related)
No data were identified for residential exposures to terbacil.
5.5 Occupational Exposures
An occupational exposure assessment is required for an active ingredient if (1) certain
toxicological criteria are triggered and (2) there is potential exposure to handlers during use or to
persons entering treated sites after application is complete. The Toxicity Endpoint Selection
Committee found that neither dermal nor inhalation toxicity criteria were triggered for terbacil
(U.S. EPA, 1998a). Although terbacil is present in certain manufacturing settings, normal
control measures usually limit the amount of worker exposure. Industrial employees, such as
railroad workers, and agricultural workers are exposed to the wettable powders and aqueous
emulsions (Clayton and Clayton, 1993-1994). In occupational settings where terbacil is
produced or used, inhalation of dusts and sprays along with skin contact with dusts, emulsions,
and sprays are the two main routes of exposure (Clayton and Clayton, 1993-1994). Data on
concentrations of terbacil in the work environment were not located in the available literature.
5.6 Summary
There is currently no substantial data documenting the concentration and estimated intake
values of terbacil from media other than water.
Terbacil January, 2008 5-3
-------
Terbacil January, 2008 5-4
-------
6.0 HAZARD AND DOSE-RESPONSE ASSESSMENT
6.1 Characterization of Hazard
6.1.1 Synthesis and Evaluation of Major Noncancer Effects
Information regarding the noncancerous and cancerous effects of terbacil were identified
primarily from the EPA re-registration eligibility decision on terbacil (U.S. EPA, 1998a). A
recent literature search did not result in the identification of any newly published material.
Consequently, the studies discussed below are those reported in the re-registration document and
are noted as secondary sources. There were no epidemiological, case, or other studies in humans
identified. Experimental studies in animals and in vitro systems characterize the major effects
that are attributable to terbacil exposure.
Terbacil is toxic to rodents and rabbits when exposed orally, dermal, and by inhalation at
high concentrations. Table 6-1 summarizes the acute toxicity tests and results for terbacil. As
depicted in the table, rats exhibited an oral LD50 of > 5000 mg/kg/day when exposed to terbacil
80% wettable powder (Haskell Laboratories, 1965a,b). Additionally, terbacil causes mild ocular
irritation in rabbits; however, it does not cause dermal sensitization in guinea pigs.
Table 6-1 Acute Toxicity Data for Terbacil
Test3
Oral LD50
Inhalation LC50
Dermal LD50
Eye Irritation
Dermal Sensitization
%AI
80.0
97.8
80.0
96.1
96.1
Species
Rats
Rats
Rabbits
Rabbits
Guinea Pigs
Result
> 5000 mg/kg/day
> 4.4 mg/L
> 5000 mg/kg/day
Mild conjunctiva! irritant
up to 72 hours
Not a dermal sensitizer
Reference
Haskell Laboratories, 1965a,b
Burgess et al., 1982
Haskell Laboratories, 1965a,b
Hood, 1966
Henry, 1986
a Exposure scenarios for the acute oral toxicity studies were not provided in detail in U.S. EPA (1998a).
Only one oral subchronic study was identified, in which many of the details regarding the
exposure scenario and study conduct are not available. According to the information provided,
rats were exposed to terbacil (% a.i. not reported) for a 90-day feeding period. An NOAEL of
100 ppm (equivalent to 5 mg/kg/day) and LOAEL of 500 ppm (equivalent to 25 mg/kg/day)
were established based on increased absolute and relative liver weights, vacuolization, and
hypertrophy of hepatocytes (Haskell Laboratories, 1965c; Wazeter et al., 1964).
One subchronic dermal toxicity study was reported in the EPA re-registration eligibility
decision on terbacil. In the study, terbacil (80% a.i.) was applied to prepared skin at 5000
mg/kg/day, 5 hours/day, 5 days/week, over 21 days to male and female rabbits (Hood, 1966).
There was no systemic toxicity observed; mild scaling and staining were reported at the test
sites.
Terbacil January, 2008
6-1
-------
Several chronic toxicity studies have been conducted. As in the oral subchronic study,
two chronic studies also resulted in liver toxicity. Terbacil (80% a.i.) was administered via diet
to beagle dogs (4/sex/group) for 2 years at concentrations of 50, 250, or 2500/10,000 ppm
(equivalent to 1.25, 6.25, and 62.5/250 mg/kg/day, respectively). It was not reported (within the
Reregi strati on Eligibility Decision for Terbacil; U.S. EPA, 1998a) when the increase in the
maximum dose level occurred. An NOAEL of 50 ppm (equivalent to 1.25 mg/kg/day) and an
LOAEL of 250 ppm (equivalent to 6.25 mg/kg/day) were established based on increased thyroid
to body weight ratios, slight increases in liver weights, and elevated alkaline phosphatase levels.
Relative liver weights also were increased at 2500 and 10,000 ppm in dogs that were sacrificed
at both 1 and 2 years (Wazeter et al., 1967a).
In another chronic toxicity study (Malek, 1993), terbacil (97.4% a.i.) was administered
via diet to male and female Sprague-Dawley rats (Crl:CD BR) for two years. Administered
concentrations were 0, 25, 1500, or 7500 ppm (approximately equivalent to 0, 0.9, 58, and 308
mg/kg/day for males, respectively; 0, 1.4, 83, and 484 mg/kg/day for females, respectively).
According to the study design, an interim sacrifice (10 animals/sex/dose) occurred 12 months
into the study. Excessive mortality was observed in the control and low-dose groups, and the
study was terminated at 23 months. No treatment-related clinical signs of toxicity were reported.
Treatment-related effects of the study included significantly decreased body weight
(7500-ppm males and females; 1500-ppm females) and body weight gain (7500-ppm males and
females; 1500-ppm females), and increased serum cholesterol levels (significant at 7500 ppm for
males and females; marginal increase at 1500 ppm for females). Hepatotoxic effects included
significantly increased mean liver to body weight ratios (7500-ppm males and females; 1500-
ppm females) and significantly increased mean liver weight (7500-ppm males). These increases
were accompanied by an increase in centrilobular hepatocyte hypertrophy (7500-ppm males and
females; 1500-ppm females), biliary hyperplasia (7500-ppm females), and eosinophilic folic of
cellular alteration in the liver. Eosinophilic folic of cellular alteration in the liver was observed
in treated males and females with a significant trend; however, this finding is considered of
equivocal importance because it was not accompanied by hypertrophic or hyperplastic changes
or hepatocellular tumors). There was no evidence of increased tumor incidence in the treated
animals when compared to the controls. Although excess mortality was observed in the control
and low-dose groups, a systemic NOAEL of 25 ppm (equivalent to 0.9 mg/kg/day for males and
1.4 mg/kg/day for females) and LOAEL of 1500 ppm (equivalent to 56 mg/kg/day for males and
83 mg/kg/day for females) based on the liver effects and decreased body weight gain in females
was established (Malek, 1993).
The excessive mortality in the study conducted by Malek (1993), raises concerns to the
overall quality and conduct of the study. However, both studies showed evidence of liver
toxicity and set NOAEL and LOAEL values based on liver effects and increased liver weights.
This evidence supports the theory that the target organ for terbacil is the liver.
Two developmental studies regarding terbacil were identified. In a study conducted by
Haskell Laboratories (1980), terbacil (% a.i. not reported) was administered via diet to female
rats at concentrations of 0, 250, 1250 or 5000 ppm (equivalent to 0, 12.5, 62.5, and 250
Terbacil January, 2008 6-2
-------
mg/kg/day, respectively) from gestation days (gd) 6 through 15. A developmental NOAEL of
250 ppm (12.5 mg/kg/day) and an LOAEL of 1250 ppm (62.5 mg/kg/day) were established,
based on a significantly decreased number of live fetuses per litter apparently due to fetal loss
occurring before or near the time of implantation. The maternal NOAEL was determined to be
250 ppm (12.5 mg/kg/day), and the LOAEL, based on decreased body weight, was determined to
be 1250 ppm (62.5 mg/kg/day).
Terbacil (% a.i. not reported) also was administered via gavage to rabbits at
concentrations of 0, 30, 200, or 600 mg/kg/day on gd 7 through 19. The maternal NOAEL was
200 mg/kg/day and the maternal LOAEL was 600 mg/kg/day, based on maternal deaths (5 died
and 2 were sacrificed in extremis). The developmental NOAEL was 200 mg/kg/day and the
LOAEL was 600 mg/kg/day, based on decreased live fetal weights (Solomon, 1984).
One reproductive study regarding terbacil was identified. Terbacil (% a.i. not reported)
was administered via diet to male and female rats at concentrations of 0, 50, or 250 ppm
(equivalent to 0, 2.5, and 12.5 mg/kg/day, respectively) over 3 generations. The first litter of
each generation was discarded, while the second litter was bred to produce the next generation.
A systemic NOAEL of <50 ppm (2.5 mg/kg/day) and an LOAEL of 250 ppm were established
based on decreased body weight gains in 250 ppm male offspring. This effect was not
considered to be a reproductive effect because the decreased weight gain appeared at late periods
in the study and not in the early development of the offspring. No reproductive effects were
observed and, therefore, the reproductive NOAEL was >250 ppm (12.5 mg/kg/day) (Wazeter,
1967b).
Lastly, technical terbacil (96.1% a.i.) was tested and found negative for clastogenicity in
a chromosomal aberration study in rat bone marrow cells, at doses up to 500 mg/kg (Cortina,
1984). It also was negative in a CHO (HGPRT) (Chinese hamster ovary
cell/hypoxanthine-guanine phosphoribosyl-transferase) gene mutation assay when tested up to
cytotoxic levels, with and without S9 activation (cytotoxicity > 3.0 mM without activation; >
2.75 mM with activation) (Haskell Laboratories, 1984). Technical terbacil (% a.i. not reported)
also was negative for unscheduled DNA synthesis when tested up to cytotoxic levels (5 mM) in
the rat.
6.1.2 Synthesis and Evaluation of Carcinogenic Effects
Information regarding the noncancerous and cancerous effects of terbacil were identified
primarily from the EPA re-registration eligibility decision on terbacil (U.S. EPA, 1998a). A
recent literature search did not result in the identification of any newly published material.
Consequently, the studies discussed below are those reported in the re-registration document and
are noted as secondary sources. There were no epidemiological, case, or other studies in humans
identified. Experimental studies in animals and in vitro systems characterize the major effects
that are attributable to terbacil exposure
Two oral studies examined the carcinogenic effects of terbacil. Both studies conclude
that oral administration of terbacil did not show evidence of increased tumor incidence in the
treated animals when compared to the controls.
Terbacil January, 2008 6-3
-------
In the 2-year dietary study in rats by Malek (1993) (details provided above), there was no
evidence of carcinogenicity reported. Goldenthal et al. (1981) administered terbacil (% a.i. not
reported) via diet to male and female mice in a 2-year oncogenicity study at doses of 0, 50, 1250,
or 5000/7500 ppm (equivalent to 7, 179, and 714/1071 mg/kg/day). The increase in the
maximum dose level occurred after week 54. A systemic NOAEL of 50 ppm is based on the
LOAEL of 1250 ppm, which resulted in mild hypertrophy of the centrilobular hepatocytes, and
decreased pituitary weights in males. Pituitary weights also were decreased in high-dose
females. Additionally, there was an increased incidence lung neoplasms (adenomas and
adenocarcinomas) in all treated male mice. The increases were within the range of similar
tumors observed in historical control mice, and therefore not considered to be treatment related.
Administration of terbacil did not significantly increase the incidence of any proliferative
hepatocellular carcinomas, single/multiple adenomas, foci of cellular alteration, or combined
hepatocellular adenomas and carcinomas in either sex
6.1.3 Weight of Evidence Evaluation for Carcinogenicity
Terbacil is classified as not likely to be carcinogenic to humans (U.S. EPA, 2005a). This
is because animal evidence failed to demonstrate a carcinogenic effect in at least two
well-designed and well-conducted studies in two appropriate animal species (U.S. EPA, 2005a).
6.1.4 Potentially Sensitive Populations
There were no potentially sensitive populations identified. Data do not suggest increased
pre- or post-natal sensitivity of children and infants to terbacil exposure because developmental
NOAELs were the same as those for maternal toxicity. Additionally, the NOAEL for systemic
(parental) toxicity was set at a lower concentration than the NOAEL for reproductive toxicity,
indicating that the reproductive system is less sensitive to terbacil.
6.2 Reference Dose
The reference dose (RfD) is an estimate of the daily oral exposure to the human
population that is likely to be without appreciable risk of deleterious effects over a lifetime. The
RfD is derived from the NOAEL in the critical or most sensitive study, which is then divided by
a variable uncertainty factor as follows:
RfD = 1.25 mg/kg/day/100 = -0.013 mg/kg/day
where 1.25 is the NOAEL from the critical study (Wazeter et al., 1967a) and 100 is the
uncertainty factor.
Terbacil January, 2008 6-4
-------
6.2.1 Choice of Principle Study and Critical Effect
The principal study for determining the RfD is a chronic toxicity study, in which beagle
dogs (4/sex/group) were administered terbacil via diet for 2 years at concentrations of 50, 250, or
2500/10,000 ppm (equivalent to 1.25, 6.25, 62.5/250 mg/kg/day, respectively) (Wazeter et al.,
1967a). The NOAEL was determined to be 1.25 mg/kg/day and the LOAEL was determined to
be 6.25 mg/kg/day, based on increased thyroid to body weight ratios, slight increases in liver
weights, and elevated alkaline phosphatase levels.
6.2.2 Application of Uncertainty Factor(s) and Modifying Factor(s)
An uncertainty factor of 100 is used in calculating the RfD to ensure the protection of
infants and children from exposure to terbacil. A factor of 10 is used to account for interspecies
differences, while another factor of 10 is used to account for intraspecies differences.
6.3 Carcinogen Assessment
Terbacil is classified as not likely to be carcinogenic to humans (U.S.
EPA, 1998a) according to the 1996 draft of the Agency's revised procedures for carcinogen risk
assessment. This classification remains appropriate under the final 2005 guidelines.
Accordingly, there is no need for a quantitative assessment of cancer risk.
6.4 Sensitive Population Considerations
The available literature does not suggest any increased pre- or post-natal sensitivity of
children and infants to terbacil (see Section 6.1.5), nor any indication of gender sensitivity.
Therefore, there are no special considerations needed for a sensitive population
6.5 Post Re-registration Health Effects Publications
There were no post re-registration health effects publications identified.
6.6 CCL Health Reference Level
The CCL health reference level is 0.091 mg/L. EPA derived the HRL using an RfD
approach as follows: HRL = (RfD x?0 kg)/2 L/day x RSC, where:
RfD = An estimate (with uncertainty spanning perhaps an order of magnitude) of a daily
oral exposure (mg/kg/day) to the human population (including sensitive subgroups) that
is likely to be without an appreciable risk of deleterious effects during a lifetime. It can
be derived from an NOAEL, LOAEL, or BMD, with uncertainty factors generally
applied to reflect limitations of the data used;
70 kg = The assumed body weight of an adult;
2 L = The assumed daily water consumption of an adult;
Terbacil January, 2008 6-5
-------
RSC = The relative source contribution, or the level of exposure believed to result
from drinking water when compared to other sources (e.g., air), and is assumed to
be 20% unless noted otherwise.
Therefore, the HRL = 0.013 mg/kg/dav x 70kg x 0.20 = 0.091 mg/L
2L/day
A discussion of the HRL as a benchmark for evaluating occurrence using monitoring data from
public water systems is found in Section 4.3.2.
Terbacil January, 2008 6-6
-------
7.0 REGULATORY DETERMINATION AND CHARACTERIZATION OF RISK
FROM DRINKING WATER
7.1 Regulatory Determination for Chemicals on the CCL
The Safe Drinking Water Act (SDWA), as amended in 1996, required the Environmental
Protection Agency (EPA) to establish a list of contaminants to aid the Agency in regulatory
priority setting for the drinking water program. EPA published a draft of the first Contaminant
Candidate List (CCL) on October 6, 1997 (62 Federal Register [FR] 52193, U.S. EPA, 1997).
After review of and response to comments, the final CCL was published on March 2, 1998 (63
FR 10273, U.S. EPA, 1998d).
On July 18, 2003 EPA announced final Regulatory Determinations for one microbe and 8
chemicals (68 FR 42897, U.S. EPA, 2003a) after proposing those determinations on June 3, 2002
(67 FR 36222, U.S. EPA, 2002b). The remaining 40 chemicals and ten microbial agents from
the first CCL became CCL 2 and were published in the Federal Register on April 2, 2004 (69 FR
17406, U.S. EPA 2004b) and finalized on February 24, 2005 (70 FR 9071, U.S. EPA, 2005b).
EPA proposed Regulatory Determinations for 11 chemicals from CCL2 on May 1, 2007
(72FR 24016) (U.S. EPA, 2007). Determinations for all 11 chemicals were negative based on a
lack of national occurrence at levels of health concern. The Agency is given the freedom to
determine that there is no need for a regulation if a chemical on the CCL fails to meet one of
three criteria established by the SDWA and described in section 7.1.1. After review of public
comments and submitted data, the negative determinations for the 11 contaminants have been
retained. Each contaminant will be considered in the development of future CCLs if there are
changes in health effects and/or occurrence.
7.1.1 Criteria for Regulatory Determination
These are the three criteria used to determine whether or not to regulate a chemical on the
CCL:
The contaminant may have an adverse effect on the health of persons.
The contaminant is known to occur or there is a substantial likelihood that the
contaminant will occur in public water systems with a frequency and at levels of
public health concern.
In the sole judgment of the Administrator, regulation of such contaminant presents a
meaningful opportunity for health risk reduction for persons served by public water
systems.
The findings for all criteria are used in making a determination to regulate a contaminant.
As required by the SDWA, a decision to regulate commits the EPA to publication of a Maximum
Contaminant Level Goal (MCLG) and promulgation of a National Primary Drinking Water
Regulation (NPDWR) for that contaminant. The Agency may determine that there is no need for
a regulation when a contaminant fails to meet one of the criteria. A decision not to regulate is
Terbacil January, 2008 7-1
-------
considered a final Agency action and is subject to judicial review. The Agency can choose to
publish a Health Advisory (a nonregulatory action) or other guidance for any contaminant on the
CCL independent of the regulatory determination.
7.1.2 National Drinking Water Advisory Council Recommendations
In March 2000, the EPA convened a Working Group under the National Drinking Water
Advisory Council (NDWAC) to help develop an approach for making regulatory determinations.
The Working Group developed a protocol for analyzing and presenting the available scientific
data and recommended methods to identify and document the rationale supporting a regulatory
determination decision. The NDWAC Working Group report was presented to and accepted by
the entire NDWAC in July 2000.
Because of the intrinsic difference between microbial and chemical contaminants, the
Working Group developed separate but similar protocols for microorganisms and chemicals.
The approach for chemicals was based on an assessment of the impact of acute, chronic, and
lifetime exposures, as well as a risk assessment that includes evaluation of occurrence, fate, and
dose-response. The NDWAC protocol for chemicals is a semi-quantitative tool for addressing
each of the three CCL criteria. The NDWAC requested that the Agency use good judgment in
balancing the many factors that need to be considered in making a regulatory determination.
The EPA modified the semi-quantitative NDWAC suggestions for evaluating chemicals
against the regulatory determination criteria and applied them in decision-making. The
quantitative and qualitative factors for terbacil that were considered for each of the three criteria
are presented in the sections that follow.
7.2 Health Effects
The first criterion asks if the contaminant may have an adverse effect on the health of
persons. Because all chemicals have adverse effects at some level of exposure, the challenge is
to define the dose at which adverse health effects are likely to occur, and estimate a dose at
which adverse health effects are either not likely to occur (threshold toxicant), or have a low
probability for occurrence (non-threshold toxicant). The key elements that must be considered in
evaluating the first criterion are the mode of action, the critical effect(s), the dose-response for
critical effect(s), the reference dose (RfD) for threshold effects, and the slope factor for
nonthreshold effects.
A full description of the health effects information and dose-response assessment
associated with exposure to terbacil is presented in Chapter 6 of this document and summarized
below in Sections 7.2.2 and 7.2.3.
7.2.1 Health Criterion Conclusion
There are no current studies that examine the human health effects due to terbacil
exposure. According to dog and rat studies, the liver appears to be the target organ in oral
subchronic and chronic studies. Observed hepatotoxic effects include increased liver weights
Terbacil January, 2008 7-2
-------
(absolute and/or relative) (Haskell Laboratories, 1965c; Malek, 1993; Wazeter et al., 1964;
Wazeter et al., 1967a); increased incidence of vacuolization and hypertrophy of hepatocytes
(Haskell Laboratories, 1965c; Wazeter et al., 1964); and increased incidence in centrilobular
hepatocyte hypertrophy, biliary hyperplasia, and eosinophilic foci of cellular alteration in the
liver (Malek, 1993). Additionally, terbacil is acutely toxic to rodents and rabbits when exposure
occurs orally, dermally, and by inhalation at high concentrations; terbacil was negative in assays
of mutagenicity.
The RfD, which was verified by EPA (1989b), is -0.013 mg/kg/day. This value was
calculated using an NOAEL of 1.25 mg/kg/day (Wazeter et al., 1967a) that was divided by a
100-fold uncertainty factor, which accounted for inter- and intraspecies differences. The critical
effect associated with the RfD is increased thyroid to body weight ratios, slight increases in liver
weights, and elevated alkaline phosphatase levels.
Based on these considerations, the evaluation of the first criterion for terbacil is positive;
terbacil may have an adverse effect on human health.
7.2.2 Hazard Characterization and Mode of Action Implications
Terbacil is acutely toxic to rodents and rabbits when exposure occurs orally, dermally,
and by inhalation at high concentrations. Rats exhibited an oral LD50 of > 5000 mg/kg/day when
exposed to 80% terbacil as a wettable powder (Haskell Laboratories, 1965a,b). Additionally,
terbacil causes mild ocular irritation in rabbits; however, it does not cause dermal sensitization in
guinea pigs.
The liver appears to be the target organ for terbacil, with oral subchronic and chronic
studies in dogs and rats showing hepatotoxic effects. Observed hepatotoxic effects include
increased liver weights (absolute and/or relative) (Haskell Laboratories, 1965c; Malek, 1993;
Wazeter et al., 1964; Wazeter et al., 1967a); increased incidence of vacuolization and
hypertrophy of hepatocytes (Haskell Laboratories, 1965c; Wazeter et al., 1964); and increased
incidence in centrilobular hepatocyte hypertrophy, biliary hyperplasia, and eosinophilic foci of
cellular alteration in the liver (Malek, 1993).
Additionally, developmental and reproductive effects have been observed in rats and
rabbits. Developmental effects included significantly decreased number of live fetuses per litter
apparently due to fetal loss occurring before or near the time of implantation in rats (Haskell
Laboratories, 1980) and decreased live fetal weights in rabbits (Solomon, 1984). Additionally,
decreased body weight gains in 250-ppm male offspring were observed when terbacil was
administered orally over 3 generations at doses of 0, 50, or 250 ppm (equivalent to 0, 2.5, and
12.5 mg/kg/day, respectively). These results, however, do not suggest that offspring exhibited
an increase in pre- or post-natal sensitivity to terbacil exposure because developmental NOAELs
were the same as those for maternal toxicity. Additionally, the NOAEL for systemic (parental)
toxicity was set at a lower concentration than the NOAEL for reproductive toxicity, indicating
that the reproductive system is less sensitive to terbacil than other organ systems.
Terbacil January, 2008 7-3
-------
7.2.3 Dose-Response Characterization and Implications in Risk Assessment
The RfD, which was verified by EPA (1989b), is -0.013 mg/kg/day. This value was
calculated using an NOAEL of 1.25 mg/kg/day (Wazeter et al., 1967a) that was divided by a
100-fold uncertainty factor accounting for inter- and intraspecies differences. The critical effect
associated with the RfD is increased thyroid to body weight ratios, slight increases in liver
weights, and elevated alkaline phosphatase levels.
Terbacil is not genotoxic. Terbacil was tested and found negative in a chromosomal
aberration study in rat bone marrow cells, found negative in a gene mutation assay (with and
without S9 activation), and did not induce unscheduled DNA synthesis when tested up to
cytotoxic levels in rats (Cortina, 1984; Haskell Laboratories, 1984). Terbacil is classified as not
likely to be carcinogenic to humans because animal evidence failed to demonstrate a
carcinogenic effect in at least two well-designed and well-conducted studies in two appropriate
animal species (U.S. EPA, 2005a).
The health reference level (HRL) for terbacil is established by using its RfD (0.013
mg/kg/day), and applying a lifetime Health Advisory methodology with a 20% relative source
contribution. The HRL is calculated to be 0.091 mg/L or 90 |ig/L when using the round number.
7.3 Occurrence in Public Water Systems
The second criterion asks if the contaminant is known to occur or if there is a substantial
likelihood that the contaminant will occur in public water systems with a frequency and at levels
of public health concern. In order to address this question the following information was
considered:
Monitoring data from public water systems
Ambient water concentrations and releases to the environment
Environmental fate
Data on the occurrence of terbacil in public drinking water systems were the most
important determinants in evaluating the second criterion. EPA looked at the total number of
systems that reported detections of terbacil, as well as those that reported concentrations of
terbacil above an estimated drinking-water HRL. For noncarcinogens, the estimated HRL level
was calculated from the RfD assuming that 20% of the total exposure would come from
drinking. For carcinogens, the HRL was the 10"6 risk level (i.e, the probability of one excess
tumor in a population of a million people). The HRLs are benchmark values that were used in
evaluating the occurrence data while the risk assessments for the contaminants were being
developed.
The available monitoring data, including indications of whether or not the contaminant is
a national or a regional problem, are included in Chapter 4 of this document and summarized
below. Additional information on production, use, and fate are found in Chapters 2 and 3.
Terbacil January, 2008 7-4
-------
7.3.1 Occurrence Criterion Conclusion
The available data for terbacil production, use, and environmental releases all show an
increasing trend. However, monitoring data show no detections of terbacil in any of the large
(i.e., serving more than 10,000 people) community water systems (CWSs), large non-transient
non-community water systems (NTNCWSs), or the statistically representative national sample of
800 small (i.e., serving 10,000 people or fewer) CWSs and NTNCWSs.
The physicochemical properties of terbacil suggest that terbacil appears to be persistent
(i.e., does not break down easily) in terrestrial areas and may reach groundwater sources due to
its mobility in water. Because of these physicochemical properties, coupled with the increasing
use of terbacil, there is some concern regarding terbacil exposure.
Based its physicochemical properties and increasing use, it is unclear whether terbacil
will occur in public water systems at frequencies or concentration levels that are of public health
concern. Thus, the evaluation for the second criterion is equivocal.
7.3.2 Monitoring Data
Under the National Water-Quality Assessment (NAWQA) program, U.S. Geological
Survey (USGS) monitored terbacil between 1992 and 2001 in representative watersheds and
aquifers across the country. Terbacil was not monitored in bed sediment or biota. Reporting
limits varied but did not exceed 0.034 |ig/L. In surface water, terbacil was detected at the
following frequencies in samples: 1.40% in undeveloped land settings; 1.82% in mixed land-use
settings; 1.98% in urban settings; and 4.52% in agricultural settings. The 95th percentile
concentrations were less than the reporting limit in all settings. The highest maximum
concentration, estimated at 0.540 |ig/L, occurred in an agricultural land-use setting (Martin et al.,
2003).
In ground water, terbacil detection frequencies were as follows: 0.0% in undeveloped
settings; 0.26% in mixed land-use (major aquifer) settings; 0.76% in agricultural settings; and
1.20% in urban land-use settings. The 95th percentile concentrations were less than the reporting
limit in all settings. The highest concentration, 0.891 |ig/L, was in a mixed land-use (major
aquifer) setting (Kolpin and Martin, 2003).
Additionally, the first Unregulated Contaminant Monitoring Regulation (UCMR1)
collected information on the national occurrence of select emerging contaminants in drinking
water. EPA designed the UCMR1 data collection with three parts (or tiers), primarily based on
the availability of analytical methods. Terbacil belonged to the first tier, List 1. As a List 1
contaminant, EPA requires all large PWSs (systems serving more than 10,000 people), plus a
statistically representative national sample of 800 small PWSs (systems serving 10,000 people or
fewer) to conduct Assessment Monitoring, with the exception of transient non-community
systems and systems that purchase 100% of their water.
Approximately one-third of the participating small systems were scheduled to monitor for
these contaminants during each calendar year from 2001 through 2003. Large systems could
Terbacil January, 2008 7-5
-------
conduct one year of monitoring anytime during the 2001-2003 UCMR1 period. EPA specified a
quarterly monitoring schedule for surface water systems and a twice-a-year, six-month interval
monitoring schedule for ground water systems. Although UCMR1 monitoring was conducted
primarily between 2001 and 2003, some results were not collected until as late as 2006.
The data presented in this report reflect UCMR1 analytical samples submitted and
quality-checked under the regulation as of March 2006. Terbacil data were collected and
submitted by 797 (99.6 percent) of the 800 small systems selected for the small system sample
and 3,076 (99.2 percent) of the 3,100 large systems defined as eligible for the UCMR1 large
system census. Terbacil data have been analyzed at the level of simple detections (at or above
the minimum reporting level, >MRL, or >2 |ig/L), exceedances of the health reference level
(>HRL, or >90 |ig/L), and exceedances of one-half the value of the HRL (>!/2HRL, or >45 |ig/L).
No detections of terbacil were found in any samples, and thus there were also no exceedances of
the HRL or one-half the HRL.
7.3.3 Use and Fate Data
Terbacil is an herbicide used to selectively control many annual and some perennial
weeds (Tomlin, 1997) in crops (e.g., apples, mint, sugarcane, asparagus, blackberries,
boysenberries, dewberries, loganberries, raspberries, youngberries, strawberries, and peaches),
forestry (e.g., cottonwood), and feed crops (e.g., alfalfa, sainfoin, and forage) (U.S. EPA, 1998a).
The chemical in the form of 80% (20% a.i.) wettable powder (WP; EPA Reg. No. 352-317) is
manufactured from an unregistered Technical Grade Active Ingredient (TGAI) (95% a.i) by E.I.
du Pont de Nemours and Company, Inc. (U.S. EPA, 1998a).
Although there was an increase in the use of terbacil during the 1990s, recent monitoring
data indicate that there were no detections of terbacil in any of the finished water samples, and
thus no exceedances of the HRL or one-half the HRL.
Although terbacil has not been detected in finished water samples to date, fate data
indicate that depending on the use of the herbicide and the amount of rain, the compound may
infiltrate groundwater sources. This is due to terbacil's low sorption affinity to soil (Kad=0.39 to
1.3 mL/g; Koc=44 to 61 mL/g) and relatively high solubility in water (710 mg/L). Additionally,
terbacil appears to be persistent (i.e., does not break down easily) in terrestrial environments.
The low vapor pressure (4.8 x 10"7 mmHg at 29.5ฐC) and Henry's Law constants (1.9 x 10"9 atm
m3/mole), suggest that terbacil is not likely to volatilize into the air to a significant extent.
The BCF (the bioconcentration factor) of terbacil is estimated to be 16, which indicates
that bioconcentration of terbacil in aquatic organisms is unlikely (HSDB, 2004). Its log Kow
(Hansch, 1995) and regression-derived equation (Meylan, 1999) also point to a low estimated
bioconcentration of terbacil in aquatic organisms.
Because of its physicochemical properties and increasing use, there is some concern
regarding terbacil exposure.
Terbacil January, 2008 7-6
-------
7.4 Risk Reduction
The third criterion asks if, in the sole judgment of the Administrator, regulation presents
a meaningful opportunity for health risk reduction for persons served by public water systems.
In evaluating this criterion, EPA looked at the total exposed population, as well as the population
exposed to levels above the estimated HRL. Estimates of the populations exposed and the levels
to which they are exposed were derived from the monitoring results. These estimates are
included in Chapter 4 of this document and summarized in section 7.4.2 below.
In order to evaluate risk from exposure through drinking water, EPA considered the net
environmental exposure in comparison to the exposure through drinking water. For example, if
exposure to a contaminant occurs primarily through ambient air, regulation of emissions to air
provides a more meaningful opportunity for EPA to reduce risk than does regulation of the
contaminant in drinking water. In making the regulatory determination, the available
information on exposure through drinking water (Chapter 4) and information on exposure
through other media (Chapter 5) were used to estimate the fraction that drinking water
contributes to the total exposure. The EPA findings are discussed in Section 7.4.3 below.
In making its regulatory determination, EPA also evaluated effects on potentially
sensitive populations, including the fetus, infants and children. Sensitive population
considerations are included in section 7.4.4.
7.4.1 Risk Criterion Conclusion
The presence of terbacil in water is rare. To date, there have been no detections of
terbacil in any of the analyzed samples. Consequently, there also have been no exceedances of
the HRL or one-half of the HRL. Thus, the evaluation of the third criterion is negative.
7.4.2 Exposed Population Estimates
Terbacil was scheduled to be monitored in all large (i.e., serving more than 10,000
people) community water systems (CWSs) and large non-transient non-community water
systems (NTNCWSs), plus a statistically representative national sample of 800 small (i.e.,
serving 10,000 people or fewer) CWSs and NTNCWSs. As of March 2006, there have been no
detections of terbacil in any of the samples. Therefore, it appears that the general population is
not exposed to terbacil through water consumption or use.
7.4.3 Relative Source Contribution
Relative source contribution analysis compares the magnitude of exposure expected via
drinking water to the magnitude of exposure from intake of terbacil in other media, such as food,
air, and soil. In situations where terbacil occurs in drinking water, the water is likely to be the
major source of exposure. There are no national data for the intake of terbacil in foods, air, or
soil. Recent residue measurements on foods indicate that 0.010 jig/g of terbacil was detected in
the squash grown in New Jersey (NJFMEP, 2004). Additionally, Cessna (1991) conducted a two
year study on terbacil residues extracted from asparagus spears from established agricultural
Terbacil January, 2008 7-7
-------
sites in British Columbia and Ontario following pre-emergence and early post-emergence
applications at 0.6, 1.1, and 2.2 kg/ha (hectare). At one site, maximum residues in the pre-
emergence samples were found to be 14ฑ3 |ig/kg for the 2.2 kg/ha application rate, whereas
maximum residues in the early post-emergence samples for the 2.2 kg/ha application rate were
493ฑ250 |ig/kg at a second site. Recoveries of terbacil from fortified asparagus tissue were
96ฑ19%, 87.2ฑ11.9% and 83.3ฑ7.8% at 10, 50, and 100 |ig/kg, respectively. Concentrations of
terbacil in air and soil have not been reported. However, these exposure routes should be
considered when analyzing the relative source contribution. This is because terbacil may exist in
the vapor and particulate phase (HSDB, 2004) as a result of being sprayed onto fields where
crops are grown for weed control. Additionally, terbacil is believed to be persistent (i.e., does
not break down easily) and mobile in soil depending on the application rate, soil type, and
rainfall. Due to the lack of national data for the intake of terbacil in foods, air, or soil, an RSC
value other than the default value of 20% is not needed.
7.4.4 Sensitive Populations
There were no potentially sensitive populations identified. Data do not suggest increased
pre- or post-natal sensitivity of children and infants to terbacil exposure because developmental
NOAELs were the same as those for maternal toxicity. Additionally, the NOAEL for systemic
(parental) toxicity was set at a lower concentration than the NOAEL for reproductive toxicity,
indicating that the reproductive system is less sensitive to terbacil than are other systems.
7.5 Regulatory Determination Decision
As stated in Section 7.1.1, a positive finding for all three criteria is required in order to
make a determination to regulate a contaminant. In the case of terbacil, the criterion on health
effects is positive and the criterion on occurrence is equivocal. Terbacil may have an adverse
effect on human health. Although monitoring is not yet complete, data available as recently as
March 2006 have been analyzed and indicate that there were no detections of terbacil in any of
the water samples analyzed. As a result, no exceedances of the HRL or one-half the HRL were
reported. However, because of its physicochemical properties and increasing use, there is some
concern with terbacil exposure. Nevertheless, because a positive finding was not met for all
three criteria, a determination to regulate terbacil is not appropriate.
Terbacil January, 2008 7-8
-------
8.0 REFERENCES
Acher, AJ. 1982. The fate of organic pollutants in frozen waters: sunlight photodecomposition
of uracil herbicides in frozen aqueous solutions. Water Res. 16:405 (as cited in HSDB, 2004).
Ahrens, W. 1994. Herbicide Handbook of the Weed Science Society of America. 7th ed.
Champaign, IL: Weed Sci. Soc. Amer. p. 278 (as cited in HSDB, 2004).
Benson, N.R. 1973. Efficacy, leaching and persistence of herbicides in apple orchards. Bulletin
No. 863. Washington State University, College of Agriculture Research Center (as cited in U.S.
EPA, 1989a).
Bidleman, T.F. 1988. Atmospheric processes. Environ. Science & Technol. 22:361-367 (as cited
in HSDB, 2004).
Burgess, B., R. Ferenz, and M. Koechert. 1982. Inhalation median lethal concentration (LC50):
[IND-732-38]: Haskell Laboratory Report No. 351-82. 50 [unpublished study]. Submitted by E.I.
du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Cessna, AJ. 1977. Determination of terbacil in blueberries [letter]. J. Agric. Food Chem. 25:432-
434.
Cessna, AJ. 1991. The determination of the herbicide terbacil in asparagus spears by gas
chromatography. Can. J. Plant Sci. 71:915-921.
Chemfmder.com. 2004. CambridgeSoft Corporation. Available from:
.
Clayton, G.D. and F.E. Clayton (eds.) 1993-1994. Patty's Industrial Hygiene and Toxicology.
Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc.
p.3381 (as cited in HSDB, 2004).
Cortina, T. 1984. In vivo bone marrow chromosome study in rats: H# 14,673: Final Report:
Project No. 201-695 [unpublished study]. Prepared by Hazleton Laboratories America, Inc. (as
cited in U.S. EPA, 1998a).
Davidson J.M., P.S.C. Rao, L.T. Ou, et al. 1978. Adsorption, movement, and biological
degradation of high concentrations of selected herbicides in soils. In: Land Disposal of
Hazardous Wastes. EPA 600/9-78-016. U.S. Environmental Protection Agency, Office of
Research and Development, pp. 233-244 (as cited in U.S. EPA, 1989a).
Doughty, C.C. 1978. Terbacil phytotoxicity and quackgrass (Agropyron Repens). Control in
highbush blueberries (Vaccinium Corymbosum). Weed Sci. 26:448-492 (as cited in U.S. EPA,
1989a).
Terbacil January, 2008 8-1
-------
Farm Chemicals Handbook 1993. Willoughby, OH: Meister Publishing Co. p. C-335 (as cited in
HSDB, 2004).
Gardiner, J.A. No date a. Examination of 14C-terbacil-treated soil for the possible presence of 5-
chlorouracil [unpublished study]. Submitted by E.I. du Pont de Nemours and Company, Inc. (as
cited in U.S. EPA, 1989a)1.
Gardiner, J.A. No date b. Exposure of 2-14C-labeled terbacil to field conditions, Supplement I
[unpublished study]. Submitted by E.I. du Pont de Nemours and Company, Inc. (as cited in U.S.
EPA, 1989a)1.
Gardiner, J.A., R.C. Rhodes, J.B. Adams, et al. 1969. Synthesis and studies with 2-14C-labeled
bromacil and terbacil. J. Agric. Food Chem. 17:980-986 (as cited in U.S. EPA, 1989a).
Goldenthal, E., S. Homan, and W. Richter. 1981. 2-Year feeding study in mice: [Terbacil]:
125-027 [unpublished study]. Prepared by International Research and Development Corp.
Submitted by E.I. du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Hamilton, P.A., T.L. Miller, and D.N. Myers. 2004. Water Quality in the Nation's Streams and
Aquifers: Overview of Selected Findings, 1991-2001. USGS Circular 1265. Available from:
. Link to document from:
.
Hansch, C., A. Leo, and D. Hoekman. 1995. Exploring QSAR - Hydrophobic, Electronic, and
Steric Constants. Washington, DC: American Chemical Society, p. 61 (as cited in HSDB, 2004).
Haskell Laboratories. 1965a. 14-Day rat feeding study. Wilmington, Delaware: E.I. du Pont de
Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Haskell Laboratories. 1965b. 3-Week rabbit dermal toxicity study. Wilmington, Delware: E.I. du
Pont de Nemours & Co., Inc (as cited in U.S. EPA, 1998a).
Haskell Laboratories. 1965c. Rat 90-day feeding study in rats. Wilmington, Delaware: E.I. du
Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Haskell Laboratories. 1980. Rat oral teratology with terbacil. Wilmington, Delaware: E.I. du
Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Haskell Laboratories. 1984. CHO (HGPRT) gene mutation assay with terbacil. Wilmington,
Delaware: E.I. du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Confidential Business Information submitted to the Office of Pesticide Programs.
Terbacil January, 2008 8-2
-------
Henry, J. 1986. Skin sensitization test of terbacil (IND-732-53) in guinea pigs for EPA Pesticide
Registration: Revised : Rept. No. 600-85: MR No. 4581-277 [unpublished study]. Prepared by
Dupont Haskell Laboratory (as cited in U.S. EPA, 1998a).
Hood, D. 1966. 15-Exposure skin absorption studies with 3-tert-butyl-5- chloro-6-methyluracil:
Report No. 33-66 [unpublished study]. Submitted by E.I. du Pont de Nemours & Co., Inc. (as
cited in U.S. EPA, 1998a).
HSDB (Hazardous Substances Data Bank). 2004. Terbacil. Available from:
.
Isom, W.H. et al. 1969. Persistence (sic) of herbicides in irrigated soils [unpublished study].
Prepared by Sandoz-Wander, Inc. Submitted by American Carbonyl, Inc.(as cited in U.S. EPA,
1989a)2.
Isom, W.H., H.P. Ford, M.P. Lavalleye, et al. 1970. Persistence (sic) of herbicides in irrigated
soils. Proc. Ann. Calif. Weed Conf. 22:58-63 (as cited in U.S. EPA, 1989a).
Kenaga, E.E. 1980. Predicted bioconcentration factors and soil sorption coefficients of pesticides
and other chemicals. Ecotox. Environ. Safety 4:26-38 (as cited in HSDB, 2004).
Kolpin, D.W. and J.D. Martin. 2003. Pesticides in ground water: summary statistics; preliminary
results from Cycle I of the National Water Quality Assessment Program (NAWQA), 1992-2001.
Available from: . Link to
document from: .
Leahy, P.P. and T.H. Thompson. 1994. The National Water-Quality Assessment Program. U.S.
Geological Survey Open-File Report 94-70. p.4. Available from:
.
Liu, L.C., H. Cubes-Viade, and F.K.S. Koo. 1971. Adsorption of atrazine and terbacil by soils. J.
Agric. Univ. Puerto Rico 55:451-460 (as cited in U.S. EPA, 1989a).
Liu, L.C., H.R. Cibes-Viade, and J. Gonzalez-Ibanez. 1977. Persistence of several herbicides in a
soil cropped to sugarcane. J. Agric. Univ. Puerto Rico 55:147-152 (as cited in U.S. EPA, 1998a).
Maier-Bode H.Z. Jr. 1970. Herbicide residues in crop products [article in German].
Pflanzenkrankh. Pflanzenschtz. Suppl. 5:71-6.
Malek, D. 1993. Combined chronic toxicity/oncogenicity study with DPX-D732-66 (terbacil)
Two year feeding study in rats: Lab Project Number: 9027-001: 453-93: 18260 [unpublished
study]. Prepared by E. I. du Pont de Nemours and Co. (as cited in U.S. EPA, 1998a).
Confidential Business Information submitted to the Office of Pesticide Programs.
Terbacil January, 2008 8-3
-------
Mansell, R.S. et al. 1977. Fertilizer and pesticide movement from citrus groves in Florida
flatwood soils. Report No. EPA 600/2-77-177. Athens, GA: U.S. Environmental Protection
Agency, Environmental Research Laboratory. Available from: NTIS, Springfield, VA, PB-272
889 (as cited in U.S. EPA, 1989a).
Mansell, R.S., W.B. Wheeler, D.V. Calvert, et al. 1979. Terbacil movement in drainage waters
from a citrus grove in a Florida flatwood soil. Proc. Sci. Soc. Florida 37:176-179 (as cited in
HSDB 2004; U.S. EPA, 1989a).
Marriage, P.B., S.U. Khan, and WJ. Saidak. 1977. Persistence and movement of terbacil in
peach orchard soil after repeated annual applications. Weed Res. 17:219-225 (as cited in U.S.
EPA, 1989a).
Marsh, J.A.P. and Davies, H.A. 1978. The effect of herbicides on respiration and transformation
of nitrogen in two soils. III. Lenacil, terbacil, chlorithiamid and 2,4,5-T. Weed Res. 18:57-62 (as
cited in U.S. EPA, 1989a).
Martin, J.D., C.G. Crawford, and SJ. Larson. 2003. Pesticides in streams: summary statistics;
preliminary results from Cycle I of the National Water Quality Assessment Program (NAWQA),
1992-2001. Available from: .
Link to document from: .
Meylan W.M., P.H. Howard, R.S. Boethling, et al. 1999. Improved method for estimating
bioconcentration/bioaccumulation factor from octanol/water partition coefficient. Environ.
Toxicol. Chem. 18:664-72 (as cited in HSDB, 2004).
Morrow, L.A. and M.K. McCarty. 1976. Selectivity and soil persistence of certain herbicides
used on perennial forage grasses. J. Environ. Qual. 5:462-465 (as cited in U.S. EPA, 1989a).
NJFMEP (New Jersey Department of Environmental Protection, Food Monitoring & Evaluation
Program). 2004. Comprehensive Report. 2004. Available from:
.
Nowell, L. 2003. Organochlorine pesticides and PCBS in bed sediment and aquatic biota from
United States Rivers and streams: summary statistics; preliminary results of the National Water
Quality Assessment Program (NAWQA), 1992-2001. Available from:
.
Nowell, L. and P. Capel. 2003. Semivolatile organic compounds (SVOC) in Bed sediment from
United States rivers and streams: summary statistics; preliminary results of the National Water
Quality Assessment Program (NAWQA), 1992-2001. Available from:
.
NRC (National Research Council). 1983. Risk Assessment in the Federal Government:
Managing the Process. Washington, DC: National Academy Press.
Terbacil January, 2008 8-4
-------
NCR (National Research Council). 2002. Opportunities to Improve the U.S. Geological Survey
National Water Quality Assessment Program. National Academy Press, p. 238. Available on-line
at: http://www.nap.edu/catalog/10267.html.
Rahman, A. 1977. Persistence of terbacil and trifluralin under different soil and climatic
conditions. Weed Res. 17:145-152 (as cited in U.S. EPA, 1989a).
Rao, P.S.C. and J.M. Davidson. 1979. Adsorption and movement of selected pesticides at high
concentrations in soils. Water Res. 13:375-380 (as cited in U.S. EPA, 1989a).
Rao, P.S.C. and J.M. Davidson. 1982. Retention and transformation of selected pesticides and
phosphorus in soil-water systems. U.S. EPA-600/S3-82-060(as cited in HSDB, 2004).
Rhodes, R.C. 1969? Four week residue studies with 2-14C-terbacil and bluegill sunfish
[unpublished study]. Prepared in cooperation with Cannon Laboratories, Inc. Submitted by E.I.
du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1989a)3
Rhodes, R.C. 1975. Biodegradation studies with 2-14C-terbacil in water and soil [unpublished
study]. Prepared in cooperation with University of Delaware, College of Agricultural Sciences.
Submitted by E.I. du Pont de Nemours and Company, Inc. (as cited in U.S. EPA, 1989a)4.
Skroch, W.A., TJ. Sheets, and J.W. Smith. 1971. Herbicides effectiveness, soil residues, and
phytotoxicity to peach trees. Weed Sci. 19:257-260 (as cited in U.S. EPA, 1998a).
Solomon, H. 1984. Embryo-Fetal toxicity and teratogenicity study of terbacil by gavage in the
rabbit: Medical Research Project No. 4512-001: Haskell Report No. 528-83 [unpublished study].
Prepared by E.I. du Pont de Nemours & Co., Inc., Haskell Laboratory for Toxicology and
Industrial Medicine, (as cited in U.S. EPA, 1998a).
Spencer, E.Y. 1982. Guide to the Chemicals Used in Crop Protection. 7th ed. Publication 1093.
Research Institute, Agriculture Canada, Ottawa, Canada: Information Canada, p. 541 (as cited in
HSDB, 2004).
Tomlin, C.D.S. (ed.). 1997. The Pesticide Manual 11th ed. The British Crop Protection Council.
pp. 1163-1165 (as cited in HSDB, 2004).
Tucker, D.P. and R.L. Phillips. 1970. Movement and degradation of herbicides in Florida citrus
soil. Citrus Ind. 51:11-13 (as cited in U.S. EPA, 1989a).
Confidential Business Information submitted to the Office of Pesticide Programs. There is a question mark
after the date in the U.S. EPA, 1989a document.
4Confidential Business Information submitted to the Office of Pesticide Programs.
Terbacil January, 2008 8-5
-------
U.S. EPA (United States Environmental Protection Agency). 1982. Pesticides Pollution and
Control Terbacil-Registration Standard. Washington, DC: Off Pest Programs U.S. EPA/540/RS-
82/013.
U.S. EPA (United States Environmental Protection Agency). 1986a. Guidelines for the health
risk assessment of chemical mixtures. Fed. Reg. 51:34014-34025.
U.S. EPA (United States Environmental Protection Agency). 1986b. Guidelines for mutagenicity
risk assessment. Fed. Reg. 51:34006-34012.
U.S. EPA (United States Environmental Protection Agency). 1988. Recommendations for and
documentation of biological values for use in risk assessment. EPA 600/6-87/008. Available
from: National Technical Information Service, Springfield, VA; PB88-179874/AS.
U.S. EPA (United States Environmental Protection Agency). 1989a. Terbacil. In: Drinking
Water Health Advisories: Pesticides. Chelsea, MI: Lewis Publishers, Inc. p. 743.
U.S. EPA (United States Environmental Protection Agency). 1989b. Integrated Risk Information
System. Available from: .
U.S. EPA (United States Environmental Protection Agency). 1991. Guidelines for
developmental toxicity risk assessment. Fed. Reg. 56:63798-63826.
U.S. EPA (United States Environmental Protection Agency). 1994a. Interim policy for particle
size and limit concentration issues in inhalation toxicity studies. Fed. Reg. 59:53799.
U.S. EPA (United States Environmental Protection Agency). 1994b. Methods for derivation of
inhalation reference concentrations and application of inhalation dosimetry. EPA/600/8-90/066F.
Available from: National Technical Information Service, Springfield, VA; PB2000-500023, and
.
U.S. EPA (United States Environmental Protection Agency). 1995. Use of the benchmark dose
approach in health risk assessment. U.S. Environmental Protection Agency. EPA/630/R-94/007.
Available from: National Technical Information Service (NTIS) , Springfield, VA; PB95-
213765, and .
U.S. EPA (United States Environmental Protection Agency). 1996. Guidelines for reproductive
toxicity risk assessment. Fed. Reg. 61:56274-56322.
U.S. EPA (United States Environmental Protection Agency). 1997. Announcement of the Draft
Drinking Water Contaminant Candidate List. Fed. Reg. 62:52193-52219.
U.S. EPA (United States Environmental Protection Agency). 1998a. Reregi strati on eligibility
decision. Terbacil. EPA738-R-97-011. Washington, DC: U.S. EPA Office of Prevention,
Pesticides and Toxic Substances. Available from:
.
Terbacil January, 2008 8-6
-------
U.S. EPA (United States Environmental Protection Agency). 1998b. Guidelines for neurotoxicity
risk assessment. Fed. Reg. 63:26926-26954.
U.S. EPA (United States Environmental Protection Agency). 1998c. Science policy council
handbook: peer review. Prepared by the Office of Science Policy, Office of Research and
Development, Washington, DC. EPA 100-B-98-001. Available from: National Technical
Information Service, Springfield, VA; PB98-140726, and
.
U.S. EPA (United States Environmental Protection Agency) 1998d. Announcement of the Draft
Drinking Water Contaminant Candidate List. Fed. Reg. 63:10273-10287.
U.S. EPA (United States Environmental Protection Agency). 2000a. Science policy council
handbook: peer review. 2nd edition. Prepared by the Office of Science Policy, Office of
Research and Development, Washington, DC. EPA 100-B-OO-OOl. Available from:
.
U.S. EPA (United States Environmental Protection Agency). 2000b. Science policy council
handbook: risk characterization. Prepared by the Office of Science Policy, Office of Research
and Development, Washington, DC. EPA 100-B-00-002. Available from:
.
U.S. EPA (United States Environmental Protection Agency). 2000c. Benchmark dose technical
guidance document [external review draft]. EPA/630/R-00/001. Available from:
.
U.S. EPA (United States Environmental Protection Agency). 2000d. Supplemental guidance for
conducting for health risk assessment of chemical mixtures. EPA/630/R-00/002. Available from:
http://www.epa.gov/iris/backgr-d.htm.
U.S. EPA (United States Environmental Protection Agency). 2002a. A review of the reference
dose and reference concentration processes. Risk Assessment Forum, Washington, DC;
EPA/630/P-02/0002F. Available from: .
U.S. EPA (United States Environmental Protection Agency). 2002b.Announcement of
preliminary regulatory determinations for priority contaminants on the drinking water. Fed. Reg.
67(106):38222-38244.
U.S. EPA (United States Environmental Protection Agency). 2003a. Announcement of
regulatory determinations for priority contaminants on the Drinking Water Contaminant
Candidate List. Fed. Reg. 68:42897-42906.
U.S. EPA (United States Environmental Protection Agency). 2004a. TRI Explorer: Trends.
Search for terbacil. Available from: .
Terbacil January, 2008 8-7
-------
U.S. EPA (United States Environmental Protection Agency). 2004b. Drinking Water
Contaminant Candidate List 2; Notice. Fed. Reg. 69:17406-17415.
U.S. EPA (United States Environmental Protection Agency). 2005a. Guidelines for carcinogen
risk assessment. Risk Assessment Forum, Washington, DC; EPA/630/P-03/001B. Available
from: .
U.S. EPA (United States Environmental Protection Agency). 2005b. Drinking Water
Contaminant Candidate List 2; Final Notice. Fed. Reg. 70:9071-9077.
U.S. EPA (United States Environmental Protection Agency). 2006. Terbacil: pesticide tolerance.
Fed. Reg. 71(104):30811-30818.
USGS (United States Geological Survey). 1992. Pesticide 1992 Annual Use Map (Terbacil).
Nation Water Quality Assessment, Pesticide Synthesis Project, US Geological Survey. Available
from: (as cited in HSDB, 2004).
U.S. EPA(United States Environmental Protection Agency). 2007. Drinking Water: Regulatory
Determinations Regarding Contaminants on the Second Drinking Water Contaminant Candidate
List - Preliminary Determinations: Proposed Rule Fed. Reg. 72(83):24016-24058.
USGS (United States Geological Survey). 2001. Summary publications from 51 NAWQA study
units sampled in 1991-2001. Available from: .
Wauchope R.D. Buttler TM, Hornsby AG, et al. 1991. The SCS/ARS/CES pesticide properties
database for environmental decision-making. Rev. Environ. Contam. Toxicol. 123:1-36 (as cited
in HSDB, 2004).
Wazeter, F.X., R.H. Buller, and R.G. Geil. 1964. Ninety-day feeding study in the rat: IRDC No.
125-004 [unpublished study]. Prepared by International Research and Development Corp.
Submitted by E.I. du Pont de Nemours & Co. (as cited in U.S. EPA, 1998a).
Wazeter, F.X., R.H. Buller, and R.G. Geil. 1967a. Two-year feeding study in the dog: IRDC No.
125-011 [unpublished study]. Prepared by International Research and Development Corp.
Submitted by E.I. du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Wazeter, F.X. R.H. Buller, and R.G. Geil. 1967b. Three-generation reproduction study in the rat:
IRDC No. 125-012 [unpublished study]. Prepared by International Research and Development
Corp. Submitted by E.I. du Pont de Nemours & Co., Inc. (as cited in U.S. EPA, 1998a).
Wolf, D.C. 1973. Degradation of bromacil, terbacil, 2,4-D and atrazine in soil and pure culture
and their effect on microbial activity. Ph.D. Dissertation. University of California, Riverside (as
cited in U.S. EPA, 1989).
Terbacil January, 2008
-------
Wolf, D.C. 1974. Degradation of bromacil, terbacil, 2,4-d and atrazine in soil and pure culture
and their effect on microbial activity. Dissertation Abstracts International B. 34(10):4783-4784
(as cited in U.S. EPA, 1989).
Wolf, D.C. and J.P. Martin. 1974. Microbial degradation of 2-Carbon-14-bromacil and terbacil.
Proc Soil Sci Soc Am 38:921-925 (as cited in HSDB, 2004; U.S. EPA, 1989).
Zimdhal, R.L., V.H. Freed, M.L. Montgomery, et al. 1970. The degradation of triazine and uracil
herbicides in soil. Weed Res. 10:18-26 (as cited in U.S. EPA, 1989).
Terbacil January, 2008 8-9
-------
Terbacil January, 2008 8-10
-------
APPENDIX A: Abbreviations and Acronyms
A
a.i.
atm
BCF
BMD
CAS
CCL
CHO (HGPRT)
cm
cws
EEC
EPA
FR
GENEEC
GUS
ha
Hg
hr
HRL
HSDB
Kads
kg
Koc
Kow
L
Ib
LOAEL
m
MCLG
mg
mL
mm
mM
MRL
NAWQA
NCOD
NDWAC
NJFMEP
NOAEL
NPDWR
NTNCWS
OPP
acre
active ingredient
atmosphere
bioaccumulation factor
benchmark dose
Chemical Abstracts Registry
Contaminant Candidate List
Chinese hamster ovary cell/hypoxanthine-guanine
phosphoribosyl-transferase
centimeter
community water system
estimated environmental concentration
Environmental Protection Agency
Federal Register
Generic Expected Environmental Concentration
Groundwater Ubiquity Score
hectare
mercury
hour
health reference level
Hazardous Substances Database
adsorption coefficient
kilogram
organic carbon partitioning coefficient
octanol-water partition coefficient
liter
pound
lowest-observed-adverse-effect-level
meter
Maximum Contaminant Level Goal
milligram
milliliter
millimeter
millimolar
minimum reporting level
National Water Quality Assessment
National Drinking Water Contaminant Occurrence Database
National Drinking Water Advisory Council
New Jersey Department of Environmental Protection, Food Monitoring &
Evaluation Program
no-observed-adverse-effect-level
National Primary Drinking Water Regulation
non-transient non-community water system
Office of Pesticides Programs
Terbacil January, 2008
Appendix A-l
-------
PATRIOT
PBPK
ppm
PWS
QAPP
RED
RfD
RL
RSC
SCI-GRO
SDTF
SDWA
SVOCs
tl/2
UCMR1
Hg
U.S. EPA
USGS
UV
TRI
VOC
WP
Pesticide Assessment Tool for Rating Investigations of Transport
physiologically-based pharmacokinetic
parts per million
Public Water Systems
Quality Assurance Project Plan
Re-registration Eligibility Document
reference dose
reporting level
relative source contribution
Screening Concentrations In Ground Water
Spray Drift Task Force
Safe Drinking Water Act
select semivolatile organic compounds
half-life
Unregulated Contaminant Monitoring Regulation 1
microgram
United States Environmental Protection Agency
United States Geological Service
ultraviolet
Toxic Release Inventory
volatile organic compound
wettable powder
Terbacil January, 2008
Appendix A-2
------- |