820K88118 August, 1987
DINOSEB
Health Advisory
Office of Drinking Water
U.S. Environmental Protection Agency
DRAFT
I. INTRODUCTION
The Health Advisory (HA) Program, sponsored by the Office of Drinking
Water (ODW), provides information on the health effects, analytical method-
ology and treatment technology that would be useful in dealing with the
contamination of drinking water. Health Advisories describe nonregulatory
concentrations of drinking water contaminants at which adverse health effects
would not be anticipated to occur over specific exposure durations. Health
Advisories contain a margin of safety to protect sensitive members o£ the
population.
Health Advisories serve as informal technical guidance to assist Federal,
State and local officials responsible for protecting public health when
emergency spills or contamination situations occur. They are not to be
construed as legally enforceable Federal standards. The HAs are subject to
change as new information becomes available.
Health Advisories are developed for one-day, ten-day, longer-term
(approximately 7 years, or 10% of an individual's lifetime) and lifetime
exposures based on data describing noncarcinogenic end points of toxicity.
Health Advisories do not quantitatively incorporate any potential carcinogenic
risk from such exposure. For those substances that are known or probable
human carcinogens, according to the Agency classification scheme (Group A or
B), Lifetime HAs are not recommended. The chemical concentration values for
Group A or B carcinogens are correlated with carcinogenic risk estimates by
employing a cancer potency (unit risk) value together with assumptions for
lifetime exposure and the consumption of drinking water. The cancer unit
risk is usually derived from the linear multistage model with 95% upper
confidence limits. This provides a low-dose estimate of cancer risk to
humans that is considered unlikely to pose a carcinogenic risk in excess
of the stated values. Excess cancer risk estimates may also be calculated
using the One-hit, Weibull, Logit or Probit models. There is no current
understanding of the biological mechanisms involved in cancer to suggest that
any one of these models is able to predict risk more accurately than another.
Because each model is based on differing assumptions, the estimates that are
derived can differ by several orders of magnitude.
-------
Dinoseb
August, 1987
-2-
II. GENERAL INFORMATION AND PROPERTIES
CAS No. 88-85-7
Structural Formula
2-sec-butyl-4,6-dinitrophenol
Synonyms
Uses
DNBP, dinitro, dinoseb (BSI, ISO, WSSA); dinosebe (Prance); Basanite
(BASF Wyandotte); Caldon, Chemox General, Chemox PE, Chemsect DNBP,
DN-289 (product discontinued), Dinitro, Dinitro-3, Dinitro General,
Dynamite (Drexel Chemical); Elgetol 318, Gebutox, Hel-Fire (Helena);
Kiloseb, Nitropone C, Premerge 3(Agway), Sinox General (FMC Corp.);
Subitex, Unicrop DNBP, Vertac Dinitro Weed Killer 5, Vertac General
Heed Killer, Vertac Selective Weed Killer (Meister, 1984).
0 Dinoseb is used as a herbicide, desiccant and dormant fruit spray
(Meister, 1984).
C10H12N2°5
240
Dark amber crystals
32CC
1.2647 (45°C)
(262eC) 100 mmHg
0.05 g/100 ml
Properties (WSSA, 1983)
Chemical Formula
Molecular Weight
Physical State (room temp.)
Boiling Point
Melting Point
Density (°C)
Vapor Pressure
Specific Gravity
Water Solubility
Log Octanol/Water Partition
Coefficient
Taste Threshold
Odor Threshold
Conversion Factor.
Occurrence
Dinoseb has been found in 1 of 79 surface water samples analyzed and
in 21 of 819 ground water samples (STORET, 1987). Samples were
collected at 70 surface water locations and 814 ground water locations.
-------
Dinoseb August, 1987
-3-
and dinoseb was found in California, Georgia and Ohio. The 85th
percentile of all non-zero samples was 1 ug/L in surface water and
10 ug/L in ground water sources. The maximum concentration found in
surface water was 1 ug/L and in ground water it was 100 ug/L.
0 Dinoseb has been found in New York ground water; typical positives
were 1 to 5 ppb (Cohen et al., 1986).
Environmental Pate
0 Dinoseb was stable to hydrolysis at pH 5, 7, and 9 at 25"C over a
period of 30 days (Dzialo, 1984).
0 With natural sunlight on a California sandy loam soil, dinoseb had a
half-life of 14 hours; with artificial light, it had a half-life of
30 hours, indicating that dinoseb is subject to photolytic degradation
{Dinoseb Task Force, 1985a).
0 In water with natural sunlight, dinoseb had a half-life of 14-18
days; with artificial light, it had a half-life of 42-58 days (Dinoseb
Task Force, 1985b).
0 With soil TLC plates, dinoseb was intermediate to very mobile in a
silt loam, sand, sandy loam and silty clay loam (Dinoseb Task Force,
1985c).
0 Soil adsorption studies gave a K
-------
Dinoseb August, 1987
acid)-4,6-diaminophenol, 2-(2-butyric acid)-4,6-dinitrophenol, 2-sec-
butyl-4-nitro-6-aminophenol, 2-sec-butyl-4-acetamido-6-nitrophenol and
2-(3-butyric acid)-4,6-dinitrophenol (Ernst and Bar, 1964; Froslie and
Karlog, 1970; Bandal and Casida, 1972).
Excretion
In mice, dinoseb is excreted in both urine (20%) and feces (30%)
following oral administration (specific means of administration not
specified) (Gibson and Rao, 1973).
IV. HEALTH EFFECTS
Humans
Short-term Exposure
0 While minimal data are available concerning human toxicity, at least
one death has been attributed to an accidental exposure of a farm worker
to sprayed dinoseb and dinitro-ortho-cresol (Heyndrickx et al., 1964).
Long-term Exposure
0 No information was found in the available literature on the long-term
health effects of dinoseb in humans.
Animals
Short-term Exposure
• In rats and mice, the acute oral LD5Q of dinoseb ranges from 20 to
40 mg/kg (Bough et al., 1965).
Dermal/Ocular Effects
0 In rats, the acute dermal toxicity of dinoseb ranges from 67 to
134 mg/kg (Noakes and Sanderson, 1969).
0 No information was found in the available literature on the dermal
or ocular effects of dinoseb in animals.
Long-term Exposure
e Hall et al. (1978) reported the results (abstract only) of a feeding
study in male and female rats. Eight groups of rats, each group
composed of 14 males and 14 females, were exposed to levels of 0, 50,
100, 150, 200, 300, 400 or 500 ppm of dinoseb (80% pure) in the diet
for 153 days, respectively. Assuming that 1 ppm in the diet of rats
is equivalent to 0.05 mg/kg/day (Lehman, 1959), these levels correspond
to 0, 2.5, 5.0, 7.5, 10.0, 15.0, 20.0 and 25.0 mg/kg/day. Mortality
was observed at 300 ppm (15 mg/kg/day) and above, and growth was
depressed at all dose levels. The LOAEL for this study was identified
as 50 ppm (2.5 mg/kg/day), the lowest dose tested.
-------
Dinoseb August, 1987
-5-
0 In a 6-month dietary study by Spencer et al. (1948), groups of male
rats were exposed to dinoseb (99% pure) at levels of 0 (30 animals),
1.35, 2.7, 5.4 (20 animals) and 13.5 mg/kg/day (10 animals). Based
on increased mortality at the highest dose and an increase in liver
weight at intermediate doses, the NOAEL for dinoseb was identified as
2.7 mg/kg/day.
0 In a study submitted to EPA in support of the registration of dinoseb
(Hazleton, 1977), four groups of rats (60/sex/dose) were exposed to
dinoseb (purity not specified) in their diets for periods up to two
years at dose levels of 0, 1, 3 and 10 mg/kg/day, respectively.
Although no evidence of dose-related changes in histopathology,
hematology, blood chemistry or certain other parameters were observed,
a dose-related decrease in mean thyroid weight was observed in all
treated males. The LOAEL in this study was identified as 1 mg/kg/day.
Reproductive Effects
0 In a reproduction study by Linder et al. (1982), four groups of ten
male rats each were exposed to dinoseb (97% pure) in the diet at
levels of 0, 3.8, 9.1 or 15.6 mg/kg/day over an 11-week period,
respectively. In addition, a group of five animals was exposed to
22.2 mg/kg/day. The fertility index was reduced to 0 at 22.2 mg/kg
and to 10% at 15.6 mg/kg/day; in neither case did the fertility index
improve in 104 to 112 days following treatment. A variety of other
effects were seen at levels of 9.1 mg/kg/day and higher, including
decreased weight of the seminal vesicles, decreased sperm count and
an increased incidence of abnormal sperm. The NOAEL for dinoseb in
this study was 3.8 mg/kg/day based on a decrease in sperm count and
other effects at higher levels.
0 In a 2-generation rat reproduction study (Irvine, 1981), four groups
of rats (25/sex/dose) were exposed to 0, 1, 3, and 10 mg/kg/day of
dinoseb in the diet for 29 weeks. Although no reproductive effects
were observed in this study per se, a decrease in pup body weight was
observed at day 21 post-parturition for all dose levels. Thus, based
on a compound-related depression in pup body weight at all dose
levels, the LOAEL in this study was 1 mg/kg/day.
Developmental Effects
0 Although dinoseb has been reported to be teratogenic (e.g., oligodactyly,
imperforate anus, hydrocephalus, etc.) when administered to mice
intraperitoneally (Gibson, 1973), it was not teratogenic when admini-
stered orally to mice (Gibson, 1973; Gibson and Rao, 1973) or rats
(Spencer and Sing, 1982).
0 Dinoseb (95% pure), administered to pregnant rats in the diet on
days 6 through 15 of gestation, produced a marked reduction in fetal
survival at doses of 9.2 mg/kg/day and above but not at doses of
6.9 mg/kg/day (NOAEL) and below (Spencer and Sing, 1982).
-------
Dinoseb August, 1987
-6-
0 Dinoseb (purity not specified) was without effect in a study in which
pregnant mice were orally exposed to a single dose of 15 mg/kg/day
(Chernoff and Kavlock, 1983).
0 In a developmental toxicity study by Research and Consulting Company
(1986), four groups of 16 Chinchilla rabbits were exposed to dinoseb
(98% pure) by oral gavage at levels of 0, 1, 3 or 10 mg/kg/day from
day 6 to 18 of gestation. At the highest dose level dinoseb produced
a statistically significant increase in malformations and/or anomalies
when compared to the controls, with external, internal (body cavities
and cephalic viscera) and skeletal defects being observed in 11/16
litters examined. Neural tube defects, the major developmental toxic
effect, included dyscrania associated with hydrocephaly, scoliosis,
kyphosis, malformed or fused caudal and sacral vertebrae and
encephalocele. The NOAEL for dinoseb in this study was identified as
3.0 mg/kg/day, based on the occurrence of neural tube defects at the
highest dose level.
0 In a study by the Dinoseb Task Force (1986), developmental toxicity
was observed in Wistar/Han rats. Groups of 25 rats received dinoseb
(purity 96.1%) by gavage at levels of 0, 1, 3 or 10 mg/kg/day from
day 6 to 15 of gestation. Developmental toxicity was observed at the
high dose as evidenced by a slight depression in fetal body weight,
increased incidence of absence of skeletal ossification for a number
of sites and an increase in the number of supernumerary ribs. Slight
to moderate decreases in body weight gain and food consumption was
observed in dams at the intermediate- and high-dose levels. Based on
the occurrence of developmental effects at the highest dose level, a
NOAEL of 3.0 mg/kg/day was identified.
Mutagenicity
0 With the exception of an increase in DNA damage in bacteria (waters,
et al., 1982), dinoseb was not mutagenic in a number of organisms
including Salmonella typhimurium, Escherichia coli, Saccharomyces
cerevisiae, Drosophila melanogaster or Bacillus subtilis (Simmon
et al., 1977; Waters et al., 1982; Moriyta et al., 1983).
Carcinogenicity
0 No evidence of a carcinogenic response was observed in a 2-year
chronic feeding study in which dinoseb was administered to rats at
levels as high as 10 mg/kg/day (Hazleton, 1977).
V. QUANTIFICATION OF TOXICOLOGICAL EFFECTS
Health Advisories (HAs) are generally determined for one-day, ten-day,
longer-term (approximately 7 years) and lifetime exposures if adequate data
are available that identify a sensitive noncarcinogenic end point of toxicity.
The HAs for noncarcinogenic toxicants are derived using the following formula;
HA * (NOAEL or LOAEL) x (BW) = mg/L ( ug/L)
(UF) x ( L/day)
-------
-6a-
ATTENTION
I. BACKGROUND
Over approximately the last 18 months, HEB/ODW has been
developing a Health Advisory (HA) for the herbicide Dinoseb.
Among other toxic endpoints, the Dinoseb HA notes that there is
a positive rabbit oral teratology study with a NOAEL of 3 mg/kg/day-
the basis of the proposed Ten-day HA value.
Subsequent to the latest HEB revision of the Dinoseb HA, a
rabbit dermal teratology study and certain other studies became
available. Both the rabbit dermal teratology study and the -
other studies are currently under Agency review. However, the
rabbit dermal teratology is positive with a NOAEL of 1 mg/kg/day.
In addition, the same toxic effect, neural tube defects, was
observed in both the oral and dermal teratology studies.
II. ISSUE
While no final decision concerning Dinoseb can be made until
all available data have undergone Agency review, the dermal
teratology raises certain issues of concern to ODW. Specifically:
0 Exposure to both the embryo and fetus is determined by the
mother's exposure. Thus, in the case of a teratogen, woman of
child bearing age are the group of principal interest.
0 In the case of an adult - i.e. woman of child bearing age - the
HA values are based on the consumption of 2 liters of water per
day by a 70-kg adult.
° Considerably more water is used to bathe (roughly 100 L/day)
than is ingested (2 L/dayJT
0 Toxic amounts of Dinoseb can be readily absorbed dermally - i.e.,
the dermal NOAEL of 1 mg/kg/day is less than the oral NOAEL of
3 mg/kg/day.
0 Since bathing and other practices involve dermal exposure to
drinking water contaminants, it is at least possible that the
dermal absorption of Dinoseb may result in significant exposure.
Until the issue of the dermal absorption of Dinoseb is
resolved, ODW believes the following procedure should be used to
allow for the positive dermal teratology study.
-------
-6b-
III. RESOLUTION OF ISSUE
A. Interim
Until such time as detailed data concerning the dermal
absorption of Dinoseb are available, it is suggested that, on an
interim basis, an HA value of 3.5 ug/L be used to evaluate all
exposure situations (e.g. One-day, Ten-day etc.) where significant
dermal exposure may be involved. This conclusion is based on
the following analysis which suggests that a level of 3.5 ug
Dinoseb/L will offer adequate protection against both the oral
and dermal teratogenic potential of Dinoseb:
Oral and dermal HA
Where:
1 mg/kg/day
70 kg
100
102 L/day
(1 mg/kg/day)(70 kg)
(100)(102 L/day)
0.007 mg/L (7 ug/L)
tentative NOAEL in rabbit dermal teratogenic
study.
assumed body weight of a woman of child
bearing age.
uncertainty factor, chosen in accordance with
NAS/ODW guidelines for use with a NOAEL from
an animal study.
possible volume of water from which all
Dinoseb is either absorbed dermally (100 L)
or ingested (2 L). While this value is
possibly overly conservative, it provides
an interim worst case until such time as
Dinoseb dermal absorption studies (in
progress) are available.
Normally, ODW uses a Relative Source Contribution (RSC) factor
of 20% when the actual RSC is unknown. However, since it is at
least possible that the RSC may be of some magnitude (due to
dermal absorption), ODW has determined that it is appropriate to
use an RSC of 50% in this case. Using an RSC of 50%, ODW recommends
that an HA value of 3.5 ug/L (7.0 ug/L x 50%) not be exceeded.
B. Final
Any final conclusion must await the results of ongoing
Dinoseb dermal absorption studies.
-------
Dinoseb August, 1987
-7-
where:
NOAEL or LOAEL * No- or Lowest-Observed-Adverse-Effect-Level
in mg/Jcg bw/day.
BW - assumed body weight of a child (10 kg) or
an adult (70 kg).
UF « uncertainty factor (10, 100 or 1,000), in
accordance with NAS/ODW guidelines.
L/day = assumed daily water consumption of a child
(1 L/day) or an adult (2 L/day).
One-day Health Advisory
No information was found in the available literature that was suitable
for determination of the One-day HA value. It is therefore recommended that
the Ten-day HA value for a 10-kg child (0.3 mg/L, calculated below) be used
as a conservative estimate of the One-day HA value.
Ten-day Health Advisory
The rabbit developmental toxicity. study (Research and Consulting Co.,
1986) in which dinoseb produced neural tube defects at doses greater than 3
mg/kg/day (NOAEL) was selected as the basis for determination of the Ten-day
HA. While it is reasonable to base a Ten-day HA for the adult on a positive
developmental toxicity study, there is some question as to whether it is
appropriate to base the Ten-day HA for a 10-kg child on a such a study.
However, since this study is of appropriate duration and since the fetus may
be more sensitive than a 10-kg child, it was judged that, while it may be
overly conservative, it is reasonable to base the Ten-day HA for a 10-kg
child on such a study.
Using a NOAEL of 3.0 mg/kg/day, the Ten-day HA for a 10-kg child is
calculated as follows:
Ten-day HA = (3.0 mg/kg/day) (10 kg) = 0.3 mg/L (300 ug/L)
(100) (1 L/day)
where:
3.0 mg/kg/day = NOAEL, based on the absence of teratogenic effects
in rabbits.
10 kg = assumed body weight of a child.
100 = uncertainty factor; chosen in accordance with NAS/ODW
guidelines for use with a NOAEL from an animal study.
1 L/day = assumed daily water consumption of a child.
-------
Dinoseb August, 1987
-8-
Longer-term Health Advisory
The Hall et al. (1978) 153-day dietary dinoseb study in rats was
originally selected to serve as the basis for determination of the Longer-
term HA (decreased growth was observed at all exposure levels with a LOAEL of
2.5 mg/kg/day). Subsequently, however, a 2-generation reproduction study in
rats (Irvine, 1981) was identified with a LOAEL of 1 mg/kg/day (based on a
decrease in pup body weight at all dose levels). Since a reproduction study
is of appropriate duration, the Irvine ( 1 981 ) study has been selected to serve
as the basis for determination of the Longer-term HA.
Using a LOAEL of 1 mg/kg/day, the Longer-term HA for a 1 0-kg child is
calculated as follows:
Longer-term HA - (1'° mg/kg/day) (10 kg) „ 0.010 mg/L (10 ug/L)
(1,000) (1 L/day)
where:
1.0 mg/kg/day * LOAEL, based on decreased pup body weight.
1 0 kg « assumed body weight of a child .
1,000 » uncertainty factor; chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
1 L/day » assumed daily water consumption of a child.
The Longer-term HA for a 70-kg adult is calculated as follows:
Longer-term HA = (UO ^Ag/day) (70 kg) . Oi035 /L (35 /L)
(1,000) (2 L/day)
where:
1.0 mg/kg/day = LOAEL, based on decreased pup body weight.
70 kg » assumed body weight of an adult.
1,000 » uncertainty factor? chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
2 L/day » assumed daily water consumption of an adult.
Lifetime Health Advisory
The Lifetime HA represents that portion of an individual's total exposure
that is attributed to drinking water and is considered protective of noncar-
cinogenic adverse health effects over a lifetime exposure. The Lifetime HA
is derived in a three-step process. Step 1 determines the Reference Dose
(RfD), formerly called the Acceptable Daily Intake (ADI). The RfD is an esti-
mate of a daily exposure to the human population that is likely to be without
appreciable risk of deleterious effects over a lifetime, and is derived from
-------
Dinoseb' *-••"•• •--- August, 1987
-9-
the NOAEL (or LOAEL), identified from a chronic (or subchronic) study, divided
by an uncertainty factor(s). From the RfD, a Drinking Water Equivalent Level
(OWEL) can be determined (Step 2). A DWEL is a medium-specific (i.e., drinking
water) lifetime exposure level, assuming 100% exposure from that medium, at
which adverse, noncarcinogenic health effects would not be" expected to occur.
The DWEL is derived from the multiplication of the RfD by the assumed body
weight of an adult and divided by the assumed daily water consumption of an
adult. The Lifetime HA is determined in Step 3 by factoring in other sources
of exposure, the relative source contribution (RSC). The RSC from drinking
water is based on actual exposure data or, if data are not available, a
value of 20% is assumed for synthetic organic chemicals and a value of 10%
is assumed for inorganic chemicals. If the contaminant is classified as a
Group A or B carcinogen, according to the Agency's classification scheme of
carcinogenic potential (U.S. EPA, 1986), then caution should be exercised in
assessing the risks associated with lifetime exposure to this chemical.
The 2-year dietary rat study by Hazelton (1977) was selected to
serve as the basis for determination of the Lifetime HA. In this study, a
compound-related decrease in mean thyroid weights was observed in all males
(LOAEL « 1 mg/kg/day) treated with dinoseb (purity not specified).
Using a LOAEL of 1 mg/kg/day, the Lifetime HA for a 70 kg adult is
calculated as follows:
Step 1: Determination of the Reference Dose (RfD)
RfD = (1 mg/kg/day) , 00001 nig/kg/day
(1,000)
where:
1 mg/kg/day = LOAEL, based on decreased thyroid weight in male rats
exposed to dinoseb via the diet for up to two years.
1,000 = uncertainty factor; chosen in accordance with NAS/ODW
guidelines for use with a LOAEL from an animal study.
Step 2: Determination of the Drinking Water Equivalent Level (DWEL)
DWEL = (0.001 mg/kg/day) (70 kg) = 0>035 /L
(2 L/day)
where:
0.001 mg/kg/day = RfD.
70 kg = assumed body weight of an adult.
2 L/day = assumed daily water consumption of an adult.
Step 3: Determination of the Lifetime Health Advisory
Lifetime HA = (0.035 mg/L) (20%) = 0.007 mg/L (7 ug/L)
-------
Dinoseb August, 1987
-10-
where:
0.035 mg/L » DWEL.
20% = assumed relative source contribution from water.
Evaluation of Carcinogenic Potential
0 No evidence of carcinogenic!ty was found in a 2-year dietary study
in which dinoseb was administered to rats at levels as high as 10
mg/kg/day (Hazleton Labs, 1977).
0 The International Agency for Research on Cancer has not evaluated the
carcinogenic potential of dinoseb.
0 Applying the criteria described in EPA's guidelines for assessment
of carcinogenic risk (U.S. EPA, 1986), dinoseb is classified in
Group D: not classified. This group is for agents with indadequate
human and animal evidence of carcinogenicity.
VI. OTHER CRITERIA, GUIDANCE AND STANDARDS
0 Tolerances have been established for dinoseb (40 CFR 180.281) at
0.1 ppm on a wide variety of agricultural commodities.
0 The EPA RfD Workgroup approved a 0.001 mg/kg/day RfD for dinoseb.
The EPA RfD Workgroup is an EPA wide group whose function is to
ensure that consistent RfD values are used throughout the EPA.
VII. ANALYTICAL METHODS
0 Analysis of dinoseb is by a gas chromatographic (GC) method applicable
to the determination of certain chlorinated acid pesticides in water
samples (U.S. EPA, 1985). In this method, approximately 1 liter of
sample is acidified. The compounds are extracted with ethyl ether
using a separatory funnel. The derivatives are hydrolyzed with
potassium hydroxide, and extraneous organic material is removed by
a solvent wash. After acidification, the acids are extracted and
converted to their methyl esters using diazomethane as the derivatizing
agent. Excess reagent is removed, and the esters are determined by
electron capture GC. The method detection limit has been estimated
at 0.07 ug/L for dinoseb.
VIII. TREATMENT TECHNOLOGIES
0 The treatment technologies which will remove dinoseb from water include
activated carbon and ion exchange. No data were found for the removal
of dinoseb from drinking water by conventional treatment or by aeration.
However, limited data suggest that aeration would not be effective in
the removal of dinoseb from drinking water (ESE, 1984).
-------
Dinoseb August, 1987
-11-
Becker and Wilson (1978) reported on the treatment of a contaminated
lake water with three activated carbon columns operated in series.
The columns processed about 2 million gallons of lake water and
achieved a 99.98 percent removal of dinoseb. Weber and Gould (1966)
performed successful isotherm tests using Columbia LC carbon, which
is coconut based, and reported the following Langmuirian equilibrium
constants:
Q = 444 mg dinojseb per g of carbon
1/b - 1.39 mg/L
Though the Langmuir equation provides a good fit over a broad
concentration range, greater adsorption would probably be achieved at
lower concentrations (less than 100 ug/L) than predicted by using
these constants.
Weber (1972) has classified dinoseb as an acidic pesticide; and such
compounds have been readily adsorbed in large amounts by ion exchange
resins. Harris and Warren (1964) studied the adsorption of dinoseb
from aqueous solution by anion exchanger (Amberlite* IRA-400) and a
cation exchanger (Amberlite* IR-200). The anion exchanger adsorbed
dinoseb to less than detectable limits in solution.
-------
Dinoseb August, 1987
-12-
IX. REFERENCES
Bandal, S.K., and J.E. Casida. 1972. Metabolism and photoalteration of
2-sec-butyl-4,6-dinitrophenol (DNBP herbicide) and its isopropyl carbonate
derivative (dinobuton acaricide). J. Agr. Food Chem. 20:1235-1245.
Becker, D.L. and Wilson, S.C. 1978. The use of activated carbon for the
treatment of pesticides and pestididal wastes. In Carbon Adsorption
Handbook (D.H. Cheremisinoff and F. Ellerbusch, Eds.}. Ann Arbor Science
Publishers, Ann Arbor, MI.
Bough, R.G., E.E. Cliffe and B. Lessel. 1965. Comparative toxicity and blood
level studies on binapacryl and DNBP. Toxicol. Appl. Pharmacol. 7:353-360.
CFR. 1985. Code of Federal Regulations. 40 CFR 180.281. July 1, 1985.
Chernoff, N., and R.J. Kavlock. 1983. A teratology test system which
utilizes postnatal growth and viability in the mouse. Environ. Sci. Res.
27s417-427.
Cohen, S.Z., C. Eiden and M.N. Lorber. 1986. Monitoring ground water for
pesticides in the USA. In American Chemical Society Symposium Series
titled Evaluation of 'Pesticides in Ground Water (in press).
Dinoseb Task Force. 1985a. Photodegradation of dinoseb on soil. Prepared
by Hazleton Laboratories America, Inc. Report No. 6015-191 (Tab 3),
July 19, 1985.
Dinoseb Task Force. 1985b. Photodegradation of dinoseb in water. Prepared
by Hazleton Laboratories America, Inc. Report No. 6015-190 (Tab 4),
July 19, 1985.
Dinoseb Task Force. 1985c. Determination of the mobility of dinoseb in
selected soils by soil TLC. Prepared by Hazleton Laboratories America,
Inc. Report No. 6015-192 (Tab 1). July 19, 1985.
Dinoseb Task Force. 1985d. The adsorption/desorption of dinoseb on repre-
sentative agricultural soils. Prepared by Hazleton Laboratories America,
Inc. Report No. 6015-193 (Tab 2), July 19, 1985.
Dinoseb Task Force. 1986. Probe embryotoxicity study with dinoseb technical
grade in Wistar rats. Prepared by Research and Consulting Company.
Project No. 045281. April 22, 1986.
Dzialo, D. 1984. Hydrolysis of dinosebs Project No. 84239. Unpublished
study prepared by Uniroyal Inc.
Environmental Science and Engineering (ESE). 1984. Review of treatability
data for removal of twenty-five synthetic organic chemicals from drinking
water. U.S. Environmental Protection Agency, Office of Drinking Water,
Washington, DC.
Ernst, W., and F. Bar. 1964. Die umwandlung des 2,4-dinitro-6-sec-butylphenols
and seiner ester im tierischen organismus. Arzenimittel Forschung 14:81-84.
-------
Oinoseb August, 1987
-13-
Froslie, A., and O. Karlog. 1970. Ruminal metabolism of DNOC and DNBP. Acta
Vet. Scand. 11:31-43.
Gibson, J.E. 1973. Teratology studies in mice with 2-sec-butyl-4,6-dinitro-
phenol (dinoseb). Fd. Cosmet. Toxicol. 11:31-43.
Gibson, J.E, and K.S. Rao. 1973. Disposition of 2-sec-butyl-4,6-dinitrophenol
(dinoseb) in pregnant mice. Food Cosmet. Toxicol. 11:45-52.
Hall, L., R. Linder, T. Scotti, R. Bruce, R. Moseman, T. Heidersheit, D. Hinkle,
T. Edgerton, S. Chaney, J. Goldstein, M. Gage, J. Farmer, L. Bennett,
J. Stevens, W. Durham and A. Curley. 1978. Subchronic and reproductive
toxicity of dinoseb. Toxicol. Appl. Pharmacol. 45:235-236. (abstract
only)
Harris, C.I. and G.F. Warren. 1964. Adsorption and desorption of herbicides
by soil. Weeds, 12:120.
Hazleton.* 1977. Hazleton Labs. 104-Week dietary study in rats. Dinoseb DNBP.
Final Report. Unpublished study. MRID 00211
Heyndrickx, A., R. Maes and F. Tyberghein. 1964. Fatal intoxication by man
due to dinitro-ortho-cresol (DNOC) and dinitro butylphenol (DNBP). Mededel
Lanbovwhoge School Opzoekingstaa Staa Gent 29:1189-1197.
Irvine, L.F.H.* 1981. 3-Generation reproduction study; Hazelton Laboratories
Europe, Ltd.
Lehman, A. J. 1959. Appraisal of the safety of chemicals in foods, drugs
and cosmetics. Assoc. Food Drug Off. U.S., Q. Bull.
Linder, R.E., T.M. Scotti, D.J. Svendsgaard, W.K. McElroy and A. Curley.
Testicular effects of dinoseb in rats. Arch. Environ. Toxicol.
11:475-485.
Meister, R., ed. 1984. Farm Chemicals Handbook. Willoughby, OH: Meister
Publishing Co.
Moriya, M., T. Ohta, T. Watanabe', K. Kato and Y. Shirasu. 1983. Further
mutagenicity studies on pesticides in bacterial reversion assay systems.
Mut. Res. 116:185-216.
Noakes, D.N., and D.M. Sanderson. 1969. A method for determining the dermal
toxicity of pesticides. Brit. J. Ind. Med. 26:59-64.
Research and Consulting Company. 1986. Embryotoxicity study with dinoseb
technical grade in the rabbit (oral administration). Unpublished study.
Simmon, V.F., A.D. Mitchell and T.A. Jorgenson. 1977. , Evaluation of selected
pesticides as chemical mutagens in vitro and in vivo studies. Research
Triangle Park, NC: U.S. Environmental Protection Agency, EPA 600/1-77-028.
-------
Dinoseb August, 1987
-14-
Spencer, F. and L.T. Sing. 1982. Reproductive toxicity in pseudopregnant
, and pregnant rats following postimplantational exposure: Effects of the
herbicide dinoseb. Pestic. Biochem. Physiol. 18:150-157.
Spencer, H.C., V.K. Rowe, E.M. Adams and D.D. Irish. 1948. Toxicological
studies' on laboratory animals of certain alkyldinitrophenols used in
agriculture. J. Ind. Hyg. Toxicol. 30:10-25.
STORET. 1987.
U.S. EPA. 1985. U.S. EPA Method 615 - Chlorinated Phenoxy Acids. 50 FR
50701, October 4, 1985.
U.S. EPA. 1986. U.S. Environmental Protection Agency. Guidelines for
carcinogen risk assessment. Fed. Reg. 51(185):33992-34003. September 24.
Waters, M.D., S. Shahbeg, S. Sandhu et al. 1982. Study of pesticide
genotoxicity. -Basic Life Sci. 21:275-326.
Weber, J.B. 1972. Interaction of organic pesticides with particulate matter
in aquatic and soil systems. In Advances in Chemistry Series 111 (R.F.
Gould, Ed.). American Chemical Society, Washington, DC.
Weber, W.J.,Jr. and J.P. Gould. 1966. Sorption of organic pesticides from
aqueous solution. In Advances in Chemistry Series 60 (R.F. Gould,
Ed.). American Chemical Society, Washington, DC.
WSSA. 1983. Weed Science Society of America. Herbicide handbook, 5th edition.
Champaign, IL.
Confidential Business Information submitted to the Office of Pesticide
Programs.
------- |