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Ethephon

Publication Date: 9/95

TRADE OR OTHER NAMES

The active ingredient ethephon is found in a variety of commercial herbicides. Trade names for products containing ethephon include Arvest, Bromeflor, Etheverse, Flordimex, Flordimex T-Extra, Cerone, Etherel, Chipco Florel Pro and Prep (4, 10).

REGULATORY STATUS

Ethephon is a general use pesticide (GUP). Check with specific state regulations for local restrictions that may apply. Products containing ethephon carry the Signal Words "Danger," "Warning," or "Caution" depending on the product (4).

INTRODUCTION

Ethephon is a plant growth regulator. Its use varies with plant species, chemical concentration, and time of application. Ethephon regulates phases of plant growth and development by application to various growth sites (1). It is currently registered in the U.S. for use on apples, barley, blackberries, bromeliads, cantaloupes, cherries, coffee, cotton, cucumbers, grapes, guava, macadamia nuts, ornamentals, peppers, pineapples, rye, squash, sugarcane, tobacco, tomatoes, walnuts, wheat, etc. (1, 4, 5). Ethephon's mode of action acts via liberation of ethylene, which is absorbed by the plant and interferes in the growth process (1). It is also used in the acceleration of ripening of fruits and vegetables (8).

Ethephon comes in RTU (ready-to-use), emulsifiable concentrate and aqueous solution formulations (4, 10). It may also be used in combination with Terpal (with mepiquat-chloride) and Terpal C (chlormequat-chloride) (4).

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

The amount of ethephon that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The acute oral toxicity of ethephon in rats ranged from 3400 mg/kg (6) to 4229 mg/kg (2, 4, 8).

Acute animal toxicity studies in a few species show that via the oral and dermal routes, ethephon is relatively non-toxic except in hens. An acute study with rats showed an oral LD50 of 1.6 g/kg (EPA toxicity category III). An acute dermal study using rabbits showed a dermal LD50 of greater than 5 g/kg (EPA toxicity category III) (9).

In a rat study, ethephon was administered by gavage for 13 weeks to 20 rats per sex per dose level at 0, 50, 100, and 200 mg/kg/day. Plasma cholinesterase and brain cholinesterase activity were found to be different from the controls at all dose levels. However, red blood cell cholinesterase activity did not differ from the controls in either sex of any dose group (9).

The acute oral LD50 of 24% ethephon solution in propylene glycol for rats was reported to range between 3,400 mg/kg (RTECS, 1985) to 4,229 mg/kg (Hartly and Kidd, 1987) (8). The dermal LD50 for the same 24% solution for rabbits was 5,730 mg/kg. Irritation of mucous membranes in rabbits was also reported. The same study indicated that the inhalation LC50 for rats was greater than 5 mg/l of air (1, 2, 6).

EPA reported the acute oral LD50 to be 1.6 g/kg for rats; the acute dermal LD50 for rabbits to be greater than 5 g/kg; and the primary skin irritation score for rabbits to be 6.75 (corrosive) (10).

The oral LD50 for mice fed technical ethephon was 2850 mg/kg; 5,000 mg/kg for rabbits; 4,200 mg/kg for guinea pigs; and an unreported 4,200 mg/kg for mammals (6).

In a dog study, ethephon was administered in the food to 4 dogs per sex per dose level at 0, 5.0, 25.0, or 187.5 mg/kg/day for 13 weeks. Plasma cholinesterase activity was depressed in both males and females at all dose levels. Red blood cell activity was depressed in the males (at all dose levels except 5.0 mg/kg/day at 8 weeks) and at the 25.0 and 187.5 mg/kg/day dose levels in the females. Brain cholinesterase activity was significant only in females dosed at 187.5 mg/kg/day (9).

CHRONIC TOXICITY

A chronic toxicity/oncogenicity study using Swiss albino mice included 85 mice fed diets containing 0, 4.5, 45, or 150 mg/kg/day of ethephon for 78 weeks. Inhibition of plasma cholinesterase activity was significant at the 45 and 150 mg/kg/day dose levels in males and females. The No Observable Effect Level (NOEL) for plasma cholinesterase activity is 4.5 mg/kg/day for both sexes and the Lowest Effect Level (LEL) for this effect was 45 mg/kg/day for both sexes (9).

There appeared to be a dose-related decrease in red blood cell cholinesterase activity in females. There was significant depression in RBC cholinesterase activity at the 45 and 150 mg/kg/day dose levels, while females in the 4.5 mg/kg/day dose groups exhibited depression in RBC cholinesterase activity at 52 weeks and 78 weeks, which was not considered statistically significant. Because of the apparent dose-related decrease in RBC cholinesterase activity in females in the 4.5 mg/kg/day dose group, the NOEL for this effect in females is considered to be below 4.5 mg/kg/day, the lowest dose tested (9).

RBC cholinesterase activity was nominally decreased in males at the mid- and high-dose groups.

Brain cholinesterase activity was not different from control values at any dose level in males or females.

In two-year feeding studies, rats receiving greater than or equal to 12,500 mg/kg diet showed no ill-effect except at top dose levels toward the end of the trial (2). The highest dose without adverse effects reported in rats was 375 mg/kg/day for 90 days (1).

Reproductive Effects

A developmental toxicity study was conducted on New Zealand white rabbits. The doses tested were 50, 100, or 150 mg/kg. The teratogenic NOEL was greater than 50 mg/kg/day (LDT or lowest dose tested). The number of litters at termination of the study were insufficient to determine teratogenic effects at the 100 and 150 mg/kg/day levels. The embryotoxic NOEL was 50 mg/kg/day (LDT); an increased average number of resorptions occurred. The maternal toxic NOEL was 100 mg/kg, while the maternal LEL was 250 mg/kg (HDT or highest dose tested); decreased body weight, food consumption and increased mortality occurred at this dose level. The fetal toxic NOEL was reported to be 50 mg/kg/day. The fetotoxic LEL was 100 mg/kg/day, at which decreased fetal viability was reported (7).

In another study, doses of 0, 200, 750, and 1,500 ppm of 39% ethephon were tested in a multigeneration rat reproduction study. The NOEL was reported to be greater than 1500 ppm (highest dose tested) (7).

Teratogenic Effects

The NOEL for rat teratogenic effects is 600 mg/kg/day, while in the rabbit, the NOEL was reported to be 50 mg/kg/day based on fetal resorptions at higher dose levels tested (7, 10).

Mutagenic Effects

Ethephon studies in Salmonella typhimurium indicated no mutagenic effect up to 1,000 micrograms/100 microliters, without enzyme activation (10).

Carcinogenic Effects

A carcinogenicity study was conducted in mice using 70.6-72.1% ethephon. The doses were administered in feed at 0, 15.5, 156 or 1630 mg/kg/day to CD-1 mice for 78 weeks. No dose-related evidence of carcinogenicity/oncogenicity was reported (7).

Organ Toxicity

No information currently available.

Fate in Humans and Animals

No information currently available.

ECOLOGICAL EFFECTS

Effects on Birds

Data indicate that technical-grade ethephon is slightly toxic on an acute oral basis to bobwhite quail, and slightly toxic on a subacute dietary basis to bobwhite quail and mallard ducks. The acute oral LC50 in bobwhite quail is from 596 to 804 mg/kg. The acute oral LC50 is 3,750 ppm for mallard ducks and greater than 2,160 ppm in bobwhite quail. The average acute oral toxicity for formulated products is greater than 10,000 ppm in bobwhite quail, or practically non-toxic (9, 10). Another source reported the oral LD50 for bobwhite quail to be 1,000 mg/kg (2).

The chronic toxicity LC50 for birds was reported to be 804 mg/kg for quail and 3,750 ppm for ducks (4); and the LC50 (8 days) for mallard ducks was greater than 10,000 mg/kg diet.

Effects on Aquatic Organisms

Laboratory and field studies indicate that ethephon is slightly toxic to fish. Studies indicated LC50 values for fish of 170 mg/l for rainbow trout; and 180 mg/l for bluegill sunfish. Also, a 96-hour LC50 for rainbow trout ranged from 254 mg/l to 350 mg/l and for bluegill sunfish 222 mg/l to 300 mg/l (Worthing and Hance, 1991) (1, 2, 10).

Effects on Other Animals (Nontarget species)

Two studies using ethephon were conducted in humans. In the first study, some symptoms characteristic of anticholinesterase activity were observed. Five humans of each sex were dosed with ethephon at an average dose level of 1.8 mg/kg/day. Subjects receiving the test compound reported the following symptoms and/or signs; sudden onset of diarrhea or an urgency of bowel movements, stomach cramps or gas and increased urgency or frequency of urination, and either an increase or decrease in appetite. None of the control subjects had complaints similar to the test group. Plasma CHE and RBC CHE activities were similar to or higher than initial values in test subjects (9).

In the second human study, 10 humans of each sex were administered ethephon at 0.5 mg/kg/day for 16 days, followed by a 2-week recovery period. Dose related effects occurred in plasma cholinesterase activity, but not in red blood cell cholinesterase activity. The effect was reversible within 15 days. When the control group and test groups were compared, the decreased plasma cholinesterase activity was statistically significant. No dose-related effects were seen in hematology, blood chemistry, or urine analysis. Based on this study, the NOEL for plasma cholinesterase inhibition in humans is less than 0.5 mg/kg/day (9).

Ethephon usage has resulted in four cases of skin injury (irritation) reported from 1980 through 1986 in California due to exposure to field residues (9).

Ethephon is considered relatively non-toxic to honeybees (1, 9).

ENVIRONMENTAL FATE

Breakdown of Chemical in Soil and Groundwater

Ethephon was found to have low to moderate mobility in soils ranging in texture from loamy sand to peat and silt loam based on soil thin layer chromatography tests. Therefore, the potential for contamination of groundwater appears to be low to moderate (9).

In soil, rapid degradation to phosphoric acid, ethylene, and chloride ions was reported (Hartley and Kidd, 1987) (1, 8).

Breakdown of Chemical in Surface Water

No information currently available.

Breakdown of Chemical in Vegetation

In plants, ethephon rapidly degrades to phosphate, ethylene, and chloride (1, 9). Ethephon and the ethylene gas it produces are the major metabolites in plants (9).

Residues of monochloroacetic acid may be found in ethephon-treated commodities. Monochloroacetic acid is a potential degradation product of an impurity in ethephon, monochloroethyl ester of (2-chloroethyl)-phosphonic acid (9).

PHYSICAL PROPERTIES AND GUIDELINES

Physical Properties:

CAS No.: 16672-87-0
Chemical name: 2-chloroethylphosphonic acid (IUPAC, CA) (1)
Chemical Class/Use: organic phosphorus compound/plant growth regulator
Specific gravity: 1.58 (2, 6)
Solubility in water: readily soluble in water
Solubility in other solvents: readily soluble in methanol, ethanol, isopropanol, acetone, ether and other polar organic solvents. Slightly soluble in non-polar solvents such as benzene and toluene (1)
Melting point: 74-75 degrees C (165-167 degrees F) (1, 2, 6, 8)
Flammability: nonflammable (8)
Vapor pressure: <10 to the minus 7 mbar at 20 degrees C (1); 7.5 x 10 to the minus 5 mmHg at 20 degrees C (8)
Koc: 0.29 (calculated) (8)

BASIC MANUFACTURER

Rhone-Poulenc
P.O. Box 12014
2 T.W. Alexander Drive
Research Triangle Park, NC 27709

Review by Basic Manufacturer:

Comments solicited: October, 1994
Comments received:

REFERENCES

  1. The Agrochemicals Handbook. 1983. The Royal Society of Chemistry, The University, Nottingham, England.
  2. Worthing, C. R. (ed.). 1983. The Pesticide Manual: A World Compendium. Seventh edition. Published by The British Crop Protection Council.
  3. Herbicide Handbook of the Weed Science Society of America. Sixth edition. 1989. Champaign, IL.
  4. Farm Chemicals Handbook. 1994. Meister Publishing Co. Willoughby, OH.
  5. Thomson, W. T. 1992. Agricultural Chemicals. Book II: Herbicides. Thomson Publications, Fresno, CA.
  6. OHS Database. August, 1993. MSDS for Ethephon. MDL Information Systems Inc., San Leandro, CA.
  7. U.S. Environmental Protection Agency. 1992. Office of Pesticides. TOX Oneliners -- ethephon. September, 1992.
  8. Montgomery, J. H. 1993. Agrochemicals Desk Reference: Environmental Data. Lewis Publishers. Chelsea, MI.
  9. U.S. Environmental Protection Agency. September, 1988. Guidance for the Reregistration of Pesticide Products Containing Ethephon as the Active Ingredient. US EPA, Office of Pesticide Programs, Registration Div., Washington, DC.
  10. U.S. Environmental Protection Agency. September 29, 1988. Pesticide Fact Sheet Number 176: Ethephon. US EPA, Office of Pesticide Programs, Registration Div., Washington, DC.