carboxin (Vitavax) Research Report
Carboxin is a systemic carboxanilide fungicide. Carboxin is used as
a seed treatment for control of smut, rot, and blight on corn and wheat.
It is very often used in combination with other fungicides such as
thiram or captan.
One study reported a rat oral LD50 of 430 mg/kg(4). Since chronic
studies were successfully completed at doses higher than this, the LD50
of 3820 mg/kg which was reported in another study seems more
reasonable(5), and is consistent with the oral LD50 of 3550 mg/kg in
Rabbits dosed fifteen times dermally at 1500 or 3000 mg/kg for
three weeks had no irritation but did have skin staining(2). The rat
dermal LD50 was 1050 mg/kg according to the above mentioned study with
the low oral toxicity, however, in other work dermal LD50 in rabbits was
greater than 8000 mg/kg(7). The inhalation LC50 for rats was greater
than 20 mg/l/hour.
A 28-day study with rats fed up to 311 mg/kg indicated a LOAEL of
5.5 mg/kg/day based on fluid accumulation in the liver(2). In another
rat study the LOAEL of 30 mg/kg/day was based on renal changes. These
animals were fed up to 1000 mg/kg for 90 days(2). A two-year rat study
with levels up to 30 mg/kg had no compound-related effects in terms of
physical appearance, behavior, hematology, blood chemistry, or
urinalysis(2). However, there were changes in organ weights for which
the NOAEL was 10 mg/kg.
Mice had a NOAEL of 8 mg/kg/day for males and 9 mg/kg/day for
females based on hepatic effects observed in an 84-week study. Diets
were up to 912 mg/kg/day(2). Beagle dogs had a NOAEL at the highest dose
tested, 15 mg/kg for two years(2). Carboxin has an unusually broad range
between the maximum tolerated dose and the NOAEL.
A three-generation study with rats had no treatment related effects
on reproductive performance at levels from 5 to 30 mg/kg/day. However,
at the highest dose, there was moderate growth suppression in the
nursing pups; the NOAEL was 10 mg/kg(2).
At the highest dose tested, 40 mg/kg on days 6 through 15, there
were no teratogenic effects in rats(2). Rabbits treated with up to 750
mg/kg on days 6 through 27 of gestation had increased abortions but no
Carboxin was found to be negative in several Ames tests, both with
and without activation. In an unscheduled DNA synthesis assay using
primary rat hepatocytes there was an increase in the nuclear
A two-year study with rats fed up to 30 mg/kg/day showed no
evidence of increased tumor frequency based on both gross and
histological examination(2). Another two-year study at levels up to 3000
ppm (approximately 180 mg/kg/day), had similar results(5).
Mice fed up to 5000 ppm (912 mg/kg) for 84 weeks had no apparent
compound-related increase in tumor incidence. Although the males had 34%
incidence of pulmonary adenomas, historical data indicates that
incidence up to 31.1% can be expected from untreated Charles River CD-l
mice(2), and the difference is not significant.
In an adolescent human, ingestion of treated seeds resulted in
headache and vomiting within one hour, with the patient recovering
quickly after being administered an emetic.
Fate in Humans and Animals:
Rats excreted 88 to 99% of a carboxin dose, mostly in 24 hours,
with 42 - 89% in urine and 10 - 45% in feces(5). Rabbits excreted 85% in
the urine and 10% in the feces. These findings would indicate incomplete
absorption from the gut, especially in rats(2). The main metabolite
found was carboxin sulfoxide for which the rat oral LD50 is 2000 mg/kg.
Carboxin sulfoxide is sold as a pesticide called oxycarboxin(5).
Only trace amounts of carboxin were found in rat tissues 48 hours
after dosing(2). In milk cows fed up to 5 ppm for 10 days, 8 ppm
appeared in the milk after a few days with less than 2% in tissues at
sacrifice. The greatest amounts were in the kidney and liver which was
also what was found in a rat study(5).
The oral LD50 in chickens is 24 grams/kg(1). In chronic exposure of
5.5 months at levels of 0.01 to 0.4 LD50, changes were noted in the
digestive tract, cardiovascular system and blood(3).
The 96-hour LC50 for rainbow trout was greater than 0.1 mg/l(1).
Juvenile crayfish in a similar test had a 217 mg/l LC50(3).
Carboxin is rapidly degraded to carboxin sulfoxide in soil. After
seven days, 95% of the parent was gone and the sulfoxide represented 31
to 45% of the amount applied. Minor products formed were carboxin
sulfone, hydroxy carboxin and C02. Carboxin does not readily absorb to
soil (adsorption coefficient less than one). Both parent and sulfoxide
are very mobile and could possibly leach to groundwater(2).
In water, carboxin oxidizes to the sulfoxide and sulfone within
seven days(2). This happens both under ultraviolet light and in the
Although the distribution pattern of the parent and sulfoxide
metabolite vary, carboxin is systemic in all species of plants
studied(5). Plants grown from treated seed had no carboxin present six
weeks after emergence. The carboxin sulfoxide found in plants can be
either from the soil or oxidation within the plant.
Common name carboxin
CAS # 5234-68-4 5,6-dihydro-2-mtehyl-N-phenyl-1,4-oxathiin-3-
Chemical class/use carboxanilide/ fungicide
Solubility in water 170 mg/l at 25 degrees C
Solubility in solvents acetone 600 g/kg, benzene 150 g/kg,
methanol 210 g/kg
Melting Point 93 - 95 degrees C
Vapor Pressure less than 1 mm Hg at 20 degrees C
Absorption Coefficient less than 1
rats 10 mg/kg/day; multiple effects; 2 yrs
HA 0.7 mg/l (ppm) (lifetime)
ADI 0.1 mg/kg/day (ppm) (EPA)
LEL 0.052 oz/cubic feet
Uniroyal Telephone: 203/573-2000
Crop Protection Div
Middlebury, CT 06749 Emergency: 203/723-3670
1. National Library of Medicine (1987). Hazardous Substances Databank.
TOXNET, Medlars Management Section, Bethesda, MD.
2. U. S. Environmental Protection Agency (1987). Health Advisory, Office
of Drinking Water.
3. U. S. Environmental Protection Agency (1968-81). Pesticide Abstracts,
Office of Pesticides and Toxic Substances, Management Support
Division, 79-0210, 81-3526.
4. National Institute for Occupational Safety and Health (1983
Supplement) Registry of Toxic Effects of Chemical Substances, U. S.
Dept of Health and Human Services, Public Health Service, Centers for
Disease Control, Cincinnati, OH.
5. Food and Drug Administration (1986). The FDA Surveillance Index.
Bureau of Foods, Dept of Commerce, National Technical Information
Service, Springfield, VA.
6. Occupational Health Services, Inc. (1988). Hazardline, New York, NY.
7. Hartley, D., and H. Kidd, Editors (1986). The Agrochemicals Handbook.
The Royal Society of Chemistry, The University, Nottingham, England.
8. Chin, Wei-Tsung, G. M. Stone and A. E. Smith (1970).Metabolism of
Carboxin (Vitavax) by Barley and Wheat Plants. J. Agric Food Chem
DISCLAIMER: The information in this profile does not in any way replace
or supersede the information on the pesticide product label/ing or other
regulatory requirements. Please refer to the pesticide product