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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 
fetal malformations(2).


     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.

Organ Toxicity:

     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
Exposure Guidelines      
     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
World Headquarters
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 
   18(4) 709-712.


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