E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Publication Date: 9/93
TRADE OR OTHER NAMES
Trade names include Difonate, Dy-fonate, Dyphonate, and Stauffer N
Fonofos is a soil organophosphate insecticide primarily used on
corn. It is also used on sugar cane, peanuts, tobacco, turf, and some
vegetable crops. It controls aphids, corn borer, corn rootworm, corn
wireworm, cutworms, white grubs, and some maggots.
Some or all formulations of fonofos are classified as Restricted
Use Pesticides (RUP) by the EPA. Restricted Use Pesticides may be
purchased and used only by certified applicators.
This highly toxic chemical interferes with the nervous system by
inhibiting an enzyme, cholinesterase, and is labeled with a DANGER
signal word. Symptoms of fonofos exposure may be delayed from a few
minutes to up to twelve hours after exposure. Early symptoms include
blurred vision, headache, and dizziness. Skin contact often brings
about sweating and muscle twitching. Eye contact causes tearing, pain,
and blurring. Ingestion may cause nausea, abdominal cramps, and
diarrhea (6). Deaths resulting from high exposures are often due to
The oral LD50 in male rats ranges from 6.8 to 18.5 (3) while it
ranges from 3.2 to 7.9 mg/kg in female rats (10). The dermal LD50 of
fonofos is 25 mg/kg in female rabbits, 147 mg/kg in rats, and 278 mg/kg
in guinea pigs (6).
Fonofos can be absorbed through the skin, gastrointestinal tract,
and respiratory tract. Most occupational poisonings have resulted from
absorption through the skin and by inhalation.
Cholinesterase inhibition may persist for as long as three months
after chronic exposure. Symptoms are similar to those resulting from
acute exposures. Over 21 human poisonings by fonofos have been
recorded. One woman exposed orally to a large amount of fonofos,
developed nausea, sweating, and cardiorespiratory stoppage. She also
had muscle twitching, low blood pressure and pulse rate, and pinpoint
pupils. She recovered after two months of hospitalization.
Dietary feeding of fonofos at low levels to dogs for 14 weeks
produced no effects at or below the very low level of 0.20 mg/kg (13).
A long-term reproduction test in rats showed no effects on female
reproductive ability at high doses about 2.0 mg/kg) of fonofos (9, 10).
Pregnant mice were fed very high doses of fonofos during the
sensitive period of gestation. At these levels, some abnormal bone
development and brain changes were observed in the fetuses (10).
Fonofos was not mutagenic in five microbial assays nor in a human
DNA synthesis test (10). Thus, it is unlikely to cause to cause
mutations in humans.
Male and female rats which ingested very high daily doses (relative
to the LD50) of fonofos for two years showed no cancerous effects (10).
However no carcinogen status has been officially established for
Fonofos exposure may affect the eyes, respiratory system, and
central nervous system. A fonofos product, Dyfonate, is broken down in
rat livers into several metabolites, one of which is a potent
cholinesterase inhibitor known as an oxon (5).
Fonofos and its metabolites are mostly absorbed from the stomach,
detoxified in the liver, and then excreted (4). Other than the fonofos
oxon (an anticholinesterase metabolite), fonofos' breakdown products are
less toxic than the parent compound (3).
Fate in Animals and Humans
Fonofos is quickly excreted in animals. Ninety-six hours after
rats received a single high oral dose of fonofos, three quarters of the
dose was found in the urine, a third in the feces, a small amount in
expired air, and only a trace in the tissues (4). The small amount of
residues found in storage organs and tissues was eliminated within two
to 16 days after exposure (10). In another study, rats given nearly
pure fonofos excreted almost all of it within four days (10).
Fonofos is highly toxic to birds, freshwater fish, and salt water
organisms. The metabolites of fonofos are less toxic to these
organisms than is the parent material. The LD50 for fonofos in mallard
ducks is 128 mg/kg. Its LC50 in bluegill sunfish is 0.028 mg/l, and
0.05 mg/l in trout.
Organophosphates, such as fonofos, do not bioaccumulate in the
environment or in animals (11). Although it is practically insoluble in
water, it is quickly broken down by interaction with water.
Fonofos is toxic to bees (13).
Fonofos is rapidly metabolized in plant tissues to non-toxic
compounds which, when ingested by an animal, are readily excreted (8).
Moderately persistent, fonofos has a soil half-life of a few months
in general (7). On a silty clay loam, the half-life was 82 days after a
high level of application, while at lower application rates, the half-
life was 46 days (2). It can be transported in runoff primarily in
sediment. It is immobile in sandy loam and silt loam soils, but is
mobile in quartz sand. Soil microbes, such as fungi, rapidly degrade
Fonofos resists soil leaching, and has been detected only rarely in
ground water and then at very low levels. Fonofos has been detected in
California groundwater at 0.01 to 0.03 ppb, and in Iowa groundwater at
0.1 ppb (10).
The compound is not readily absorbed by plant foliage and it is not
translocated throughout plants (13).
PHYSICAL PROPERTIES AND GUIDELINES
Fonofos is a relatively non-reactive insecticide. This
organophosphate is a yellow liquid with a disagreeable, sulfurous odor.
Its molecular weight is 246.32. Its chemical name is O-ethyl-S-phenyl
|NOEL: ||0.2 mg/kg/day (10)
|ADI: ||0.002 mg/kg/day (10)
|TLV: ||0.1 mg/m3 (air); 100 ug/m3(skin) (1)
|Drinking water |
|Drinking Water Equivalent Level (DWEL): 0.07 ug/L (10)
|CAS #: ||944-22-9
|Solubility in water: ||almost insoluble (12)
|Solubility in solvents: ||miscible in organic solvents like kerosene, xylene, and isobutyl methyl ketone.
|Melting point: ||32 degrees C at 0.3 mm Hg (9).
|Boiling point: ||130 degrees C at .1 mm Hg (3).
|Vapor pressure: ||2.1 x 10 to the minus 4 power mm Hg at 25 degrees C (3)
Zeneca Ag Products
Wilmington, Delaware 19897
Review by Basic Manufacturer:
Comments solicited: November, 1992
American Conference of Governmental Industrial Hygienists.
Threshold Limit Values for Chemical Substances. 1984-85.
Ahmad, N., Walgenbach, D.D. and Sutter, G.R. 1979. Bull.
Environm. Contam. Toxicol. 23, 423-429.
Hayes, W.J. 1982. Pesticides Studied in Man. pp. 425-427.
Williams & Wilkins.
Hoffman, L.J., Ford, I.M., and Menn, J.J. 1971. Dyfonate
metabolism studies. I. Absorption, distribution, and excretion of
Dyfonate in rats. Pesticide Biochem. and Physiol. 1: 349-355.
McBain, J.B., Yamamoto, I., and Casida, J.E. 1971. Mechanism of
Activation and deactivation of dyfonate by rat liver microsomes. Life
Sci. 10: 947-954. Pergamon Press.
Occupational Health Services Inc. Material Safety Data Sheet:
Fonofos. 4/10/87. OHS. NY.
Rao, P.S.C. and Davidson, J.M. 1980. Estimation of pesticide
retention and transformation parameters required in nonpoint source
pollution models. In Environmental Impact of Nonpoint Source
Pollution. Overcash, M.R. and Davidson, J.M., eds. Ann Arbor Science.
Stauffer Chemical's Product Safety Information Booklet. 1986.
Fonofos. pp. 22-27.
U.S. Environmental Protection Agency. "Chemical Fact Sheet for
Fonofos." Fact Sheet No. 36. 30 September 1984.
U.S. Environmental Protection Agency. Office of Drinking Water.
"Fonofos Health Advisory." Draft Report. August 1987.
Wagner, S.L. 1983. Clinical Toxicology of Agricultural
Chemicals. Noyes Data Corp. Park Ridge, NJ.
Windholz, M. et al., eds. 1983. Fonofos. p. 604. The Merck
Index. 10th edition. Merck & Co. Inc.
ACGIH. 1992. Documentation of the Threshold Limit Values and
Biological Exposure Indices, 6th edition. American Conference of
Governmental and Industrial Hygienists, Inc. Cincinnati, OH.
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