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triadimenol (Baytan) Chemical Fact Sheet 7/89

                 EPA Pesticide Fact Sheet for Triadimenol

Name of Chemical:  beta-(4-chlorophenoxy)-alpha-(1,l-dimethyl-ethyl)-
Reason for Issuance:  New Chemical Registration
Date Issued: July 1989
Fact Sheet Number:  204

                    1. DESCRIPTION OF CHEMICAL

- Generic Name:  beta-(4-chlorophenoxy)-alpha-(1,1-dimethylethyl)-
  lH-1,2,4-triazole-1-ethanol and its metabolites c1
  ontaining chlorophenoxy and triazole moieties.
- Common Name:  triadimenol
- Trade Name:  Baytan
- EPA Shaughnessy Codes:  127201
- Chemical Abstracts Service (CAS) Number:  5219-65-3
- Year of Initial Registration:  1989
- Pesticide Type:  Fungicide
- U.S. and Foreign Producers:  Mobay Corporation


APPLICATION SITES:  Seeds of barley, corn, oats, rye, sorghum and wheat
     to control seed- and soil-borne diseases and to provide early
     season control of foliar diseases.

METHOD OF APPLICATION:  Application will be made as a waterbased slurry
     through standard slurry or mist type commercial seed treatment

TYPES OF FORMULATION:  25% dry flowable end-use product and 90%
     technical powder for formulating use.

APPLICATION RATES:  For barley, oats, rye and wheat, apply 0.25-0.5 oz.
     ai./100 lbs of seed; for sorghum, apply 0.5 oz. ai./100 lbs of
     seed; and for corn, apply 1.0 lbs of seed.


                           3. SCIENCE FINDINGS

Summary Science Statement

     Available acute toxicity studies indicate that triadimenol is in 
toxicity category II (warning) based on an acute inhalation toxicity study 
with rats.

     Chronic feeding/oncogenicity studies were conducted in both the rat 
and mouse. Clinical chemistry findings in the chronic feeding study in the 
rat suggests that the target organ for toxicity may be the liver. Although 
there was an accompaying small increase in liver weight in the females of 
the high dose group, there were no histopathologic changes in the liver in 
either sex.

     In the chronic feeding study in mice, the results of blood chemistry, 
organ weights and gross and histological examinations, again indicated the 
liver as the target organ.

     Triadimenol did not induce either genotoxic effects or chromosomal 
aberrations in a series of mutagenicity studies. In addition, no strong 
structural activity correlation to other carcinogens has been found. 
Triadimenol was also found not to be teratogenic in either the rat or 

     Environmental fate data indicates that triadimenol is stable to 
hydrolysis and appears to be stable to photolysis on the soil surface. In 
addition, based on low adsorption coefficients, triadimenol will have a low 
potential to leach in soil. However, triadimenol may have a moderate 
potential to leach in some Western soils.

     Additional studies indicate that due to the manufacturing process, 
triadimenol should have no adverse effects on non-target organisms provided 
waste is disposed of properly. An overview of the toxicity test results 
suggests that triadimenol is practically non-toxic to birds, slightly toxic 
to fish, and moderately toxic to aquatic invertebrates. It is also unlikely 
that this registration would affect endangered species because of its 
relatively low use rates, agricultural techniques which involve drill 
planting of most small grains and corn, and the low toxicity of triadimenol 
to all animals.


Acute oral toxicity in rats:
   LD50 689 mg/kg in males
        752 mg/kg in females
   Toxicity category III

Acute dermal toxicity in rats:
   LD50 >5000 mg/kg
   Toxicity category III

Acute inhalation toxicity in rats
   LC50 >1.56 mg/L
   Toxicity category III

Primary eye irritation in rabbit:
   Slight irritation

Primary dermal irritation in rabbit:
   Toxicity category IV

Dermal sensitization in guinea pigs:
   core minimum; no effect

Chronic studies:  Triadimenol has been evaluated in the following

Rodent Feeding/Oncogenicity

     1. A 2-year feeding/oncogenicity study with rats using dietary 
concentrations of 0, 125, 500, and 2000 parts per million (ppm) equivalent 
to 0, 6.25, 25.0, and 100 mg/kg bwt/day in males and females. Clinical 
chemistry findings suggest that the target organ for toxicity may be the 
liver. The levels of SGOT and SGPT enzymes were consistently higher at 2000 
ppm in males and females when compared to controls, and some increase in 
these two parameters was also observed at 500 ppm. Although there was an 
accompanying small increase in liver weight in 2000 ppm females, there were 
no accompanying increases in histopathologic changes of the liver in either 
sex. There were only marginal effects seen on other clinical chemistry 
parameters, and no effect of test compound on clinically observed signs of 
toxicity, food consumption, hematologic, or urinalysis parameters. The 
systemic NOEL (no-observed effect level) is 125 ppm (6.25 mg/kg/day for 
males and females) based on the increase in liver enzymes (SGOT and SGPT). 
The systemic LEL (lowest effect level) was 500 ppm (25 mg/kg/day for males 
and for females).

     2. A 2-year chronic feeding/oncogenicity study in mice using dietary 
concentrations of 0, 125, 500, and 2000 ppm (equivalent to doses of 0, 18, 
72, and 285 mg/kg/day for males and females). The results of blood 
chemistry, organ weights, and gross and histological examinations indicated 
the liver to be the target organ. There were time- and dose-related 
increases in SAP (serum alkaline phosphatase), SGOT and SGPT activities in 
both male and female animals receiving 500 and 2,000 ppm of the test 

     In addition, increased incidence of enlarged livers, hyperplastic 
nodules and increased liver weights in both male and female animals 
receiving 2,000 ppm of test material were detected at necropsy. Female 
animals receiving 2000 ppm exhibited a significant increase in the 
incidences of liver adenomas only, a compound-related oncoqenic effect. In 
males, there were no differences in the incidences of these lesions in 
treated and control males, and the incidences of liver adenomas were 
similar to those observed in historical controls.

     Based on this evidence the Agency classified triadimenol as a Category 
C (possible human carcinogen) in accordance with the EPA Guidelines for 
Carcinogen Risk Assessment (September 24, 1986, 51 FR 33992). This 
evaluation was confirmed by the Agency's Scientific Advisory Panel on 
December 15, 1987. However, it was also concluded that this evidence of 
carcinogenicity did not warrant a low dose extrapolation of risks since the 
tumors were only benign, were observed in only one sex, and only at the 
highest dose tested. Moreover, the chemical was negative in the genotoxic 
assay battery.

     Based on blood chemistry findings, the systemic NOEL and the LEL are 
125 ppm and 500 ppm respectively (equivalent to 18 and 72 mg/kg/day for 
males and females).

     3. A 3-month rat feeding study using doses of 0, 150, and 600 ppm 
(equivalent to 0, 7.5, and 30 mg/kg bwt/day for males and females) 
demonstrated a decrease in body weight, decrease in hematocrit values, 
eosinophil count and medium cell hemoglobin and increase in the high dose 
group and dose-related increase in liver weight. The NOEL is 150 ppm and 
the LEL is 600 ppm.

Non-Rodent Feeding Study

     1. A 2-year male and female dog feeding study using doses of 0, 150, 
600 and 2400 ppm (equivalent to 0, 3.75, 15, and 60 mg/kg bwt/day for males 
and females). The NOEL is 150 ppm based on changes in enzyme levels 
(equivalent to 3.75 mg/kg bwt/day for males and females). The LEL is 600 
ppm. Although there were significant decreases in mean body weights in 
males receiving 150 and 2400 ppm and in females receiving 600 and 2400 ppm, 
the biological significance of these changes could not be assessed. There 
were noted increases in alkaline phosphatase N-demethylase, and cytochrome 
P-450 in males receiving 2400 ppm and significant increases in N-
demethylase in females receiving 600 and 2400 ppm and in cytochrome P-450 
in females receiving 2400 ppm when compared to controls.

     2. A 6-month dog feeding study using doses of 0, 10, 30, and 100 ppm 
(equivalent to 0, 0.25, 0.75, 2.5 mg/kg bwt/day for males and females). The 
NOEL was demonstrated at doses up to 100 ppm, the highest dose level 

     3. A 3-month dog feeding study using doses of 0, 150, 600 and 2400 ppm 
(equivalent to 0, 3.75, 15, and 60 mg/kg bwt/day for males and females). 
Weight gain in all male groups and in the highest dose female group was 
significantly less than the control. Alkaline phosphatase in males and 
females showed a dose-related negative trend. There was no gross 
pathological changes. Effects at 600 ppm included an increase in serum 
cholesterol level in males. Although the NOEL appeared to be less than 150 
ppm based on reduced body weight and decreased alkaline phosphatase in 
males, the Agency has concluded that effects below 600 ppm in the 2-year 
dog study were not biologically significant and the longer-term study 
supercedes the 90-day dog study. Therefore, the NOEL remains at 150 ppm.


     1. A rabbit teratology study with a NOEL for maternal toxicity of 8 
mg/kg. The maternal LEL was 40 mg/kg based on decreased body weight gains 
and food consumption. The developmental NOEL and LEL were 40 mg/kg and 200 
mg/kg respectively. This study has to be resubmitted with all the findings 
statistically analyzed on a per litter and per fetus basis in order to be 
upgraded from its current classification as core supplementary.

     2. A rat teratology study using dose levels 0, 30, 60, and 120 
mg/kg/day was determined to be core supplementary because the NOEL for 
developmental toxicity (supernumerary ribs) was not definitively 
established. The NOEL and LOEL for maternal toxicity for this study are 30 
and 60 mg/kg/day, respectively, based on decreases in maternal body weight, 
body weight gain, and food consumption at 60 and 120 mg/kg/day. 
Furthermore, increased embryolethality (embryotoxicity) was only observed 
at the highest dose level tested (120 mg/kg/day). This study must be 
repeated to clearly define a NOEL for developmental toxicity.

     The above rat study indicated that triadimenol caused a dose-
dependent, statistically significant increase in the incidence of 
rudimentary supernumerary ribs. Although the effect at the low dose level 
was not statistically significant, it was considered to be treatment 
related because of the dose-related trend.

     The biological significance of the manifestation of supernumerary ribs 
is subject to scientific debate, especially if the ribs are not fully 
developed (rudimentary). Nonetheless, the margin of safety (MOS) for this 
effect must be taken into consideration. The MOS is the ratio between the 
NOEL for the effect and the acute exposure in mg/kg/day. A NOEL for 
developmental toxicity could not be defined in the rat teratology study but 
it is unlikely to be far below the threshold (LEL) of 30 mg/kg/day observed 
in the current study.

     Based on worker exposure information and an estimation of the NOEL at 
about 15 mg/kg/day for developmental toxicity (rudimentary supernumerary 
ribs in rats) and assuming a maximum dermal penetration of about 10%, a 
margin of safety was calculated to be >100 for factory workers involved in 
seed treatments using a closed system. Because of possible developmental 
toxicity and the lack of a well defined NOEL for this effect, the product 
label must include a recommendation for the use of protective clothing by 
factory workers involved in the treatment of seeds and for farm workers 
handling the treated seed.


     A rat multigeneration reproduction study using doses of 0, 20, 100, 
and 500 ppm (equivalent to 0, 1, 5, and 25 mg/kg bwt/day for males and 
females) indicated that the NOEL and LOEL for both parental and pup 
toxicity are 100 and 500 ppm, respectively, based on significant body 
weight and organ weight changes. The NOEL for reproductive toxicity is 500 
ppm, highest dose level tested.


     A reverse mutation assay (AMES), a dominant lethal test in mice, DNA 
damage/repair, unscheduled DNA synthesis, in vitro and in vivo (rat) 
cytogenic assays, and a forward mutation in mice, all of which were 
negative for mutagenic effects.

                          5. ENVIRONMENTAL FATE

Hydrolysis:  STABLE. Triadimenol in sterile aqueous buffer solutions
             showed no apparent degradation at either temperature or pH
             tested. Recovery was 97% greater after 32 days of

Soil Surface Photolysis:  STABLE. Triadimenol appears to be stable to
             photolysis on the soil surface. Studies indicate that
             triadimenol photodegrades with a half-life of 36 hours in
             distilled water and 17 hours in a photo-sensitized
             (acetone) solution.

Aerobic Soil Metabolism:  STABLE. Studies indicate that triadimenol has
             an estimated aerobic half-life of 8 to 9 months.
             Triadimenol reached a maximum level of 68% of that applied
             at 14C in 71 days and declined slightly to 45.2% by day
             238. Consequently, the anaerobic half-life is considerably
             greater than 8-9 months.

Adsorption/Desorption:  Because of its low adsorption coefficients,
             triadimenol is shown to have a low to moderate potential to
             bind to soil particles. Studies indicate that the
             adsorption coefficient, k, for triadimenol ranged from 2.37
             to 5.26. The k values for desorption ranged from 1.49 in a
             silty clay soil (0.49 ppm) to 9.12 in a loam soil (9.57
             ppm). Consequently, there is no correlation between
             adsorption and soil organic matter content. The highest
             degree of adsorption was observed with the loam soil,
             intermediate in organic matter content.

     Environmental fate data requirements have been satisfied with the 
exception of a field dissipation study. The company will be required to 
submit results of this study by July 1990.

                      6. ECOLOGICAL CHARACTERISTICS

     Studies submitted show that this chemical is practically non-toxic to 
birds, slightly toxic to fish and moderately toxic to aquatic 
invertebrates. It is unlikely that the seed treatment use of triadimenol 
will affect any terrestrial or aquatic animals. Chronic effects are 
unlikely due to the low use rates and because the seed treatment use 
requires incorporation of seeds into the soil. For the above reasons it is 
also unlikely that this use will affect any endangered species.

                          7. BENEFITS

     This chemical has been shown to be environmentally safe, is used at 
low rates and has a broad biological spectrum. Triadimenol controls seed-, 
soil-, and wind-borne pathogens of wheat, barley, oats, rye, corn and 
sorghum. Crops may be grazed 40 days after seeding. The chemical improves 
winter survival and drought tolerance of cereals, lowers the inoculum 
levels for overwintering foliar diseases and may eliminate the need for 
early season foliar sprays.

                        8. TOLERANCE ASSESSMENT:

     Tolerances are established for the fungicide triadimenol and its 
butanediol metabolite (calculated as triadimenol) in or on the following 
commodities:  2.5 ppm for green forage of barley, oats, rye and wheat; 0.1 
ppm for straw of barley, oats, rye and wheat; 0.05 ppm for grains of 
barley, oats, rye and wheat, corn fodder, fresh corn (including sweet), 
corn forage, corn grain, and green forage of sorghum; and 0.01 ppm for 
sorghum grain and sorghum fodder. Tolerances are established for the 
fungicide triadimenol and its metabolites containing the chlorophenoxy 
moiety (calculated as triadimenol) in or on the following commodities: 0.1 
ppm for fat, meat and meat by-products of cattle, goats, hogs, horses, and 
sheep; and 1.01 ppm for eggs, milk, and fat, meat and meat by-products of 

     Where tolerances are established for residues of both 1-(4-
(triadimefon) and triadimenol, including its butanediol metabolite, in or 
on the same raw agricultural commodity and its products thereof, the total 
amount of such residues shall not yield more residue than that permitted by 
the higher of the two tolerances. The nature of the residue is adequately 
understood and the Agency concluded that the pesticide is useful for the 
purposes for which tolerances are sought and that the establishment of the 
tolerances will protect the public health.

                      9. SUMMARY OF MAJOR DATA GAPS:

     The Agency concurs with conditional registration of this chemical for 
use as a seed treatment fungicide pending submission of a field dissipation 
study by July 1990.

                         10. CONTACT PERSON AT EPA

Susan T. Lewis,
Acting Product Manager (PM) 21,
Registration Division (H-7505C),
Environmental Protection Agency,
401 M St., SW.,
Washington, DC  20460

Office location and telephone number:
Rm. 227, CM#2,
1921 Jefferson Davis Highway,
Arlington, VA  22202
(703) 557-1900

DISCLAIMER: The information in this Pesticide Fact Sheet is a summary only 
and is not to be used to satisfy data requirements for pesticide 
registration and reregistration.