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
Brodan, Detmol UA, Dowco 179, Dursban, Eradex, Lorsban, Piridane,
The EPA has established a 24-hour reentry interval for entering
crop areas treated with emulsifiable concentrate or wettable powder
formualtions of chlorpyrifos without protective clothing (40). Products
containing chlorpyrifos must bear the signal word "Warning" or
"Caution," depending on the toxicity of the formulation (46). Check
specific state regulations for local restrictions which may apply.
Chlorpyrifos is a broad spectrum insecticide, a chemical used to
kill a wide variety of insects. It was introduced in 1965 (45). While
originally used primarily to kill mosquitoes in the immature, larval
stage of development, chlorpyrifos is no longer registered for this
use. Chlorpyrifos is effective in controlling a variety of insects,
including cutworms, corn rootworms, cockroaches, grubs, flea beetles,
flies, termites, fire ants, and lice (38). It is used as an insecticide
on grain, cotton, field, fruit, nut and vegetable crops, and well as on
lawns and ornamental plants (40, 2). It is also registered for direct
use on sheep, turkey, for horse site treatment, for treatment of dog
kennels, and for domestic dwellings, farm buildings, storage bins, and
commercial establishments (40). Chlorpyrifos is available in
emulsifiable concentrate, dust, flowable, pellet, spray, granular and
wettable powder formulations (46).
Chlorpyrifos acts on pests primarily as a contact poison, with some
action as a stomach poison. It is a nonsystemic contact chemical,
meaning that it is acts only where it comes into direct contact with
plant tissues, and is not transported to other plant parts.
Chlorpyrifos is one of a class of insecticides referred to as
organophosphates. These chemicals act by interfering with the
activities of cholinesterase, an enzyme that is essential for the proper
working of the nervous systems of both humans and insects. Please refer
to the Toxicology Information Brief on cholinesterase-inhibition for a
more detailed description of this topic.
Chlorpyrifos is moderately toxic to humans (50). Poisoning from
chlorpyrifos may affect the central nervous system, the cardiovascular
system, and the respiratory system (31). It is also a skin and eye
irritant (49). While some organophosphates are readily absorbed through
the skin, studies in humans suggest that skin absorption of chlorpyrifos
is more limited (45). Skin which has come in contact with this material
should be washed immediately with soap and water and all contaminated
clothing should be removed. The acute dermal LD50 for chlorpyrifos in
male and female rats is greater than 2,000 mg/kg (53).
Three hundred and nineteen human exposure incidents were reported
by the Pesticide Incident Monitoring System (PIMS) from 1970 through
1981, most resulting from inhalation and dermal exposure. Three human
deaths were caused by chlorpyrifos and/or chlorpyrifos combined with
other active ingredients (41). Persons with respiratory ailments,
recent exposure to cholinesterase inhibitors, cholinesterase impairment,
or liver malfunction are at increased risk from exposure to
The organophosphate insecticides are cholinesterase inhibitors
which may be absorbed through all routes of exposure. When toxic
amounts are inhaled, the first effects are usually respiratory and may
include bloody or runny nose, coughing, chest discomfort, difficult or
short breath, and wheezing due to constriction or excess fluid in the
bronchial tubes. Skin contact with organophosphates may cause localized
sweating and involuntary muscle contractions. Eye contact may cause
pain, bleeding, tears, pupil constriction, and blurred vision.
Following exposure by any route, other systemic effects may begin within
a few minutes or be delayed for up to 12 hours. These may include
pallor, nausea, vomiting, diarrhea, abdominal cramps, headache,
dizziness, eye pain, blurred vision, constriction or dilation of the eye
pupils, tears, salivation, sweating, and confusion. Severe poisoning
will affect the central nervous system, producing incoordination,
slurred speech, loss of reflexes, weakness, fatigue, involuntary muscle
contractions, twitching, tremors of the tongue or eyelids, and
eventually paralysis of the body extremities and the respiratory
muscles. In severe cases there may also be involuntary defecation or
urination, psychosis, irregular heart beats, unconsciousness,
convulsions and coma. Death may be caused by respiratory failure or
cardiac arrest (39).
Some organophosphates may cause delayed symptoms beginning 1 to 4
weeks after an acute exposure which may or may not have produced
immediate symptoms. In such cases, numbness, tingling, weakness and
cramping may appear in the lower limbs and progress to incoordination
and paralysis. Improvement may occur over months or years, and in some
cases residual impairment will remain (39).
Since chlorpyrifos is absorbed through the skin, especially through
cuts and scratches, dermal contact should be avoided (40). In addition
to causing inhibition of cholinesterase, acute exposure to chlorpyrifos
may cause skin irritation. Absorption through the skin may result in
systemic intoxication, or general poisoning in a bodily system. The
severity of poisoning will determine the amount and range of symptoms
which are experienced (31).
Inhalation of chlorpyrifos may cause absorption of the insecticide
through the mucous membranes, resulting in systemic intoxication (31).
Plasma cholinesterase levels activity has been shown to be inhibited
when chlorpyrifos particles are inhaled (1).
The amount (dose) of a material that causes death in one-half
(50%) of the test population, when it is given on a short-term basis by
mouth is referred to as its oral lethal dose (LD50). The oral LD50 for
chlorpyrifos in rats is 82 to 270 milligrams per kilogram (mg/kg) (21,
41, 2). This indicates that it takes 82 to 270 mg of chlorpyrifos for
each kg of body weight to kill 50 percent of the experimental animals
tested (14, 49). The LD50 for chlorpyrifos in mice is 60 mg/kg, 1000
mg/kg in rabbits, 32 mg/kg in chickens, 500 to 504 mg/kg in guinea pigs,
and 800 mg/kg in sheep (2, 14, 17, 49). The dermal LD50 in rats is
greater than 2000 mg/kg (53), and 1000 to 2000 mg/kg in rabbits (2, 17).
The lethal concentration fifty, or LC50, is that concentration of a
chemical in air or water that kills half of the experimental animals
exposed to it for a set time period. The 4-hour inhalation LC50 for
chlorpyrifos in rats is greater than 200 mg/m3 (54).
Repeated or prolonged exposure to organophosphates may result in
the same effects as acute exposure including the delayed symptoms.
Other effects reported in workers repeatedly exposed include impaired
memory and concentration, disorientation, severe depressions,
irritability, confusion, headache, speech difficulties, delayed reaction
times, nightmares, sleepwalking and drowsiness or insomnia. An
influenza-like condition with headache, nausea, weakness, loss of
appetite, and malaise has also been reported (49).
When technical chlorpyrifos was fed to dogs at doses of 0.01, 0.03,
0.1, 1 and 3 mg/kg/day for 2 years, increased liver weight occurred at
3.0 mg/kg. Signs of cholinesterase inhibition occurred at 1 mg/kg.
Rats and mice given technical chlorpyrifos in the diet for 104 weeks
showed no adverse effects other than cholinesterase inhibition (50). An
occupational study on 22 pest control operators exposed to an 8 hour
level of 27.6 microgram per cubic meter (ug/m3) of Dursban showed
inhibition of plasma cholinesterase when compared to a control group of
the same age and sex (37). A measurable change in plasma and red blood
cell cholinesterase levels was seen in spray workers exposed to 0.5%
chlorpyrifos emulsion in field trials for malaria control. Human
volunteers who ingested 0.1 mg/kg of chlorpyrifos daily for four weeks
showed significant plasma cholinesterase inhibition (1). A low blood
cholinesterase level can sometimes persist from two to six weeks with
long-term exposure to chlorpyrifos (31).
Two-year feeding studies of 1 and 3 mg/kg/day of chlorpyrifos to
rats produced moderate depression of plasma and red blood cell
cholinesterase. Brain cholinesterase was decreased with the larger
dose. Cholinesterase levels recovered when the experimental feeding was
discontinued (18). Identical results occurred in a 2-year feeding study
with dogs. No long-term health effects were seen in either the dog or
rat study (1, 45). In some animal species, chlorpyrifos may produce
neurotoxicity, or harm to nerve tissue (14).
EPA has determined that chlorpyrifos does not adversely affect
reproduction (40, 50). In two studies reviewed by the EPA, no effects
were seen in the animals tested at dose levels up to 1.2 mg/kg/day (40).
No effects on reproduction occurred in a 3-generation study with rats
fed dietary doses as high as 1 mg/kg/day (1, 50). In another study in
which rats were fed 1.0 mg/kg/day for two generations, the only effect
observed was a slight increase in the number of deaths of newborn
offspring (18). Once in the bloodstream, chlorpyrifos may cross the
EPA has determined that chlorpyrifos is not teratogenic. No
teratogenic or other adverse effects to offspring were found when
pregnant rats were fed doses as high as 15 mg/kg/day for 10 days. When
pregnant mice were given doses of 1, 10 or 25 mg/kg/day for 10 days,
minor skeletal variations and a decrease in fetal length occurred at the
highest dose tested. The developmental NOEL was 10 mg/kg/day (35, 40,
50). No birth defects were seen in the offspring of male and female
rats fed 1.0 mg/kg per day during a three-generation reproduction and
fertility study (18, 1).
EPA has determined that chlorpyrifos is not mutagenic. No evidence
of mutagenicity was found in any of 4 tests reviewed by EPA (50).
Mutagenic effects were observed in fruit flies given oral concentrations
of 50 parts per billion (ppb) of chlorpyrifos for 3 days (27).
EPA has determined that chlorpyrifos is not carcinogenic. There
was no increase in the incidence of tumors when rats were fed 10
mg/kg/day for 104 weeks nor when mice were fed 2.25 mg/kg for 105 weeks
Chlorpyrifos primarily affects the nervous system through
inhibition of cholinesterase, an enzyme required for proper nerve
Fate in Humans and Animals
In humans, chlorpyrifos and its principal metabolites are
eliminated relatively rapidly following a single dose (30). It is
readily absorbed into the bloodstream through the gastrointestinal tract
if it is ingested, through the lungs if it is inhaled, or through the
skin if there is dermal exposure (40).
After a single oral dose, its half-life in the blood appears to be
about one day (29). Chlorpyrifos was found in its original form in the
blood, brain and liver of a 61-year old man who lived only one day after
accidentally eating this material (18).
Chlorpyrifos is eliminated primarily through the kidneys in urine
(38). Following oral intake of chlorpyrifos by rats, 90% was removed in
the urine and 10% was excreted in the feces (17). It is detoxified
quickly in rats, dogs and other animals (44). The major metabolite
found in rat urine after administration of a single oral dose of 0.5 or
25 mg/kg was TCP. TCP does not inhibit cholinesterase and it is not
mutagenic (50). Following intake, some chlorpyrifos becomes stored in
fat tissues. It is eventually moved out of the fat tissue and
eliminated from the body, with a half-life of about 62 hours (18, 45).
Research indicates that chlorpyrifos does not build up or persist
in body tissues. It does not have a significant bioaccumulation
potential (29). When formulated chlorpyrifos (Dursban) was fed to cows,
unchanged pesticide was found in the feces, but not in the urine or milk
(37). Chlorpyrifos was detected in the milk of cows for 4 days
following spray dipping with a 0.15% emulsion. The maximum
concentration in the milk was 0.304 ppm. This concentration was
decreased by 26 to 47% by pasteurization (45). In a rat study,
chlorpyrifos did not accumulate in any tissue except fat (26). Residues
of granular formulations of chlorpyrifos were found in salt marsh snails
immediately after they were treated with the material and for up to five
weeks after treatment. When an emulsion formulation was used, residues
were found immediately following treatment, and for up to 3 weeks
The US EPA requires precautionary language on chlorpyrifos product
labels, warning of the hazard that this insecticide poses to birds,
wildlife and aquatic organisms. It should not be applied directly to
water. Drift and runoff from treated areas may be hazardous to aquatic
organisms in adjacent aquatic sites (2, 40).
Effects on Birds
Chlorpyrifos is moderately to very highly toxic to birds (50). Its
oral LD50 in pheasants is 8.41 mg/kg, 112 mg/kg in mallard ducks, 21.0
mg/kg in house sparrows, and 32 mg/kg in chickens (17, 37, 50). The
LD50 for a granular product (15G) in bobwhite quail is 108 mg/kg (50).
Two one-generation reproductive studies resulted in NOELs of 125
ppm (the highest dose tested) for bobwhite quail and 25 ppm for mallard
ducks. At 125 ppm, mallards laid significantly fewer eggs (50).
There was no evidence of changes in weight gain, or in the number,
weight and quality of eggs produced by hens fed dietary levels of 50
parts per million (ppm), or about 5.12 mg/kg, of chlorpyrifos (18).
Bird deaths have not been observed in repeated mosquito control efforts
Effects on Aquatic Organisms
Chlorpyrifos is very highly toxic to freshwater fish, aquatic
invertebrates and estuarine and marine organisms (50). Cholinesterase
inhibition was observed in acute toxicity tests of fish exposed to very
low concentrations of this insecticide (29). Precautions and
restrictions are being imposed by EPA to decrease potential hazards
(40). Application of concentrations as low as 0.01 pounds of active
ingredient per acre may cause fish and aquatic invertebrate deaths (50).
Chlorpyrifos accumulates in the tissues of aquatic organisms.
Studies involving continuous exposure of fish during the embryomic
through fry stages have shown BCF values of 58 to 5100 (52).
Chlorpyrifos toxicity to fish may be related to water temperature.
Its 96-hour LC50 varied in rainbow trout from 7.1 micrograms per liter
(ug/l) to 51 ug/l at three different temperatures (34). The 24-hour
LC50 for chlorpyrifos in goldfish is 180 ug/l, and less than 1,000 ug/l
in mosquito fish (46). The 96-hour LC50 for chlorpyrifos in mature
rainbow trout is 9 ug/l, 98 ug/l in lake trout, 806 ug/l in goldfish, 10
ug/l in bluegill, and 331.7 ug/l in fathead minnow (38).
Due to its high acute toxicity and its persistence in sediments,
chlorpyrifos may represent a hazard to sea bottom dwellers (34).
Smaller organisms appear to be more sensitive than larger ones (38).
When fathead minnows were exposed to Dursban for a 200-day period
during which they reproduced, the first generation of offspring had
decreased survival and growth, as well as a significant number of
deformities. This occurred at approximately 2.68 microgram per liter
(ug/l) exposure for a 30 day-period (37).
Effects on Other Animals (Nontarget Species)
Aquatic and general agricultural uses of chlorpyrifos may be
extremely poisonous to wildlife and honeybees (40, 17). Treated areas
should not be used for grazing, nor should the chemical be used when
bees are actively collecting pollen or nectar (2, 25, 36). Studies
indicate that with continuous exposure over time, chlorpyrifos may
accumulate to toxic levels in test animals (36).
While one study did not detect any negative effect to nontarget
insects when chlorpyrifos was applied to rice fields at 0.01 to 0.02
kilogram per hectare (kg/ha), another study reported that practically
all nontarget insects died after a similar application (15).
Chlorpyrifos is moderately persistent, but relatively immobile in
the environment (50). Chlorpyrifos may bioconcentrate at very low
levels in ecological systems (BCF = 2.50 to 3.54) (48).
Breakdown of Chemical in Soil and Groundwater
Chlorpyrifos adsorbs strongly to soil particles and it is not
readily soluble in water (47, 52). It is therefore immobile in soils
and unlikely to leach or to contaminate groundwater (32, 50, 52). It is
not mobile in sandy loam and loamy sand soils (41). TCP, the principle
metabolite of chlorpyrifos, adsorbs weakly to soil particles and appears
to be moderately mobile and persistent in soils. EPA has required
additional testing to determine the environmental fate of TCP (50).
In aerobic soils, the soil half-life of chlorpyrifos was from 11 to
141 days in seven soils ranging in texture from loamy sand to clay and
with soil pHs from 5.4 to 7.4. Chlorpyrifos was less persistent in the
soils with a higher pH. Soil half-life was not affected by soil texture
or organic matter content. In anaerobic soils, the half-life was 15
days in loam and 58 days in clay soil (50). Adsorbed chlorpyrifos is
subject to degradation by UV light, chemical hydrolysis and by soil
microbes. When treated on moist soils, the volatility half-life of
chlorpyrifos was 45-163 hours, with 62-89% of the applied chlorpyrifos
remaining on the soil after 36 hours. In another study, 2.6 and 9.3% of
the chlorpyrifos applied to sand or silt loom soil remained after 30
days (52). The half-life of chlorpyrifos in soil, or the time that it
takes for half of the insecticide to be broken down, is usually between
60 and 120 days, but can range from 2 weeks to over 1 year, depending on
the soil type, climate and other conditions (17, 40, 48).
Breakdown of Chemical in Water
The current label for this material states that it is not to be
applied directly to bodies of water. In open waters, the concentration
and persistence of chlorpyrifos will vary depending on the type of
formulation. For example, immediately after entering open waters,
emulsifiable concentrates and wettable powders tend to produce a large
increase in chlorpyrifos concentrates in water. As the pesticide
adheres, or (adsorbs) to sediments and suspended organic matter,
however, concentrations rapidly decline. Granules and controlled-
release formulations do not produce as rapid an increase in the
concentration of insecticide in the water, but the resulting
concentration persists longer (38). Slow desorption from sediments can
also maintain low (ppb) residual concentrations of chlorpyrifos in open
waters for long periods of time (48).
Chlorpyrifos enters freshwater and saltwater ecosystems primarily
as spray drift. It is also carried on eroded soil particles from
treated areas (38). If soil with adsorbed chlorpyrifos is carried by
runoff, surface water may be contaminated (32).
In water, chlorpyrifos readily adsorbs to suspended sediment and
bottom materials. Volatilization is probably the primary route of loss
of chlorpyrifos from water. Volatility half-lives of 3.5 and 20 days
have been estimated for pond water (52). The photolysis half-life of
chlorpyrifos is 3 to 4 weeks during midsummer in the U.S., but
photodegradation of chlorpyrifos is not expected to be significant in
deep waters, during winter, or in waters which sunlight can not
penetrate (48). Its change into other natural forms (biotransformation)
is slow (34). Research suggests that this insecticide is unstable in
water, and the rate at which it is hydrolyzed increases with
temperature, decreasing by 2.5 to 3-fold with each 10 degrees C drop in
temperature. The rate of hydrolysis is constant in acidic to neutral
waters, but increases in alkaline waters. In water at pH 7.0 and 25
degrees C, it had a half-life of 35 to 78 days (48). The half-life of
chlorpyrifos in water of an unknown pH was about 80-100 days (37).
Breakdown of Chemical in Vegetation
Chlorpyrifos may be toxic to some plants, such as head lettuce
(23). Residues remain on plant surfaces for approximately 10-14 days
(36, 16). Data indicate that this insecticide and/or its soil
metabolites, can accumulate in certain crops (41).
Information is limited on chlorpyrifos toxicity to freshwater
plants, although algal blooms frequently follow its field application
PHYSICAL PROPERTIES AND GUIDELINES
Technical chlorpyrifos is an amber to white crystalline solid with
a mild sulfur (mercaptan) odor (18, 2, 50). Volatile components or
contaminants, such as diethyl sulfide and diethyl disulfide, are partly
responsible for the offensive odor of the technical grade of
chlorpyrifos (37). Chlorpyrifos may undergo violent decomposition at
temperatures above 130 degrees C (266 degrees F), causing a build-up of
heat and pressure that may lead to violent rupture of containers.
Thermal decomposition of chlorpyrifos may release toxic or hazardous
gases (49, 50).
Chlorpyrifos is corrosive to copper and brass (17). It is
compatible with most fungus-killing chemicals (fungicides) and other
insecticides (16). Chlorpyrifos is stable in neutral or acidic aqueous
solutions. Non-aqueous solutions of chlorpyrifos can be stored
indefinitely under appropriate storage conditions. It is, however,
unstable under alkaline conditions (18, 41).
Technical-grade chlorpyrifos has generally been found to be more
toxic than an equal amount of active ingredient in a formulated product.
The effects of inert ingredients can not, therefore, be ignored (38).
Avoid eye and skin contact with chlorpyrifos as well as inhalation of
its vapors, dusts, or sprays (17). A pesticide face mask (respirator)
is recommended (2). Chlorpyrifos should not be used near water (17).
Persons who work with organophosphate materials for long periods of
time should have frequent blood tests of their cholinesterase levels.
If the cholinesterase level falls below a critical point, no further
exposure should be allowed until it returns to normal (51).
Protective clothing must be worn when handling chlorpyrifos.
Before removing gloves, wash them with soap and water. Always wash
hands, face and arms with soap and water before smoking, eating or
After work, remove all work clothes and shoes. Shower with soap
and water. Wear only clean clothes when leaving the job. Wash
contaminated clothing and equipment with soap and water after each use.
Keep contaminated work clothes separate from regular laundry.
|OSHA TWA (skin) ||0.2 mg/m3 (49)
|ACGIH TWA (skin) ||0.2 mg/m3 (49)
|TLV/TWA: ||0.2 mg/m3. Occupational intake at 0.028 mg/kg/day is considered safe (1, 18)
|NOEL: ||0.10 mg/kg/day (rats); 0.03 mg/kg/day(dogs)(18); 100 ug/kg/day (human, rat, dog) (29)
|ADI: ||0.003 mg/kg/day based on a human cholinesterase study with a NOEL of 0.03 mg/kg/day and a 10-fold safety factor (40, 50)
|STEL: ||For skin = 0.6 mg/m3 (1)
|CAS #: ||2921-88-2
|Specific gravity: ||1.398 at 43 degrees C (49)
|H2O solubility: ||low; 2 ppm at 35 degrees C (29, 18, 23); 2 ppm water at 2 degrees C (44)
|Solubility in other solvents: ||In benzene 790, acetone 650, chloroform 630, carbon disulfide 590, diethyl ether 510, xylene 645, methylene chloride 714, isooctane 79, methanol 45 (all in g/100 g at 25 degrees C) (17)
|Melting Point: ||41.5 to 44 degrees C (106 to 108 degrees F) (52)
|Flash point: ||greater than 200 degrees F (54).
|Vapor pressure: ||1.87 x 10 to the minus 5 power mm Hg at 25 degrees C (35b)
|Kow: ||66,000 at 23 degrees C (29)
- log Kow = 4.7 (35a); 3.06, 5.11 (22); 4.82 (42)
|Koc: ||6070 g/ml (47); 7,000-25,000 ml/g (52)
|Kd: ||pc = 128,000 (20); 13,490 (32)
|Chemical Class/Use: ||Organophosphate insecticide
9002 Purdue Rd.
Indianapolis, IN 46268-1189
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received: November, 1992
American Conference of Governmental Industrial Hygienists, Inc.
1986. Documentation of the threshold limit values and biological
exposure indices. Fifth edition. Cincinnati, OH: Publications Office,
Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Cornell University. 1987. 1988 New York State pesticide
recommendations. Forty-ninth annual pest control conference. Nov. 9,
10, 11. Ithaca, NY.
Dow Chemical Company. 1986 (May). Farm and ranch chemicals
specimen label book.
Federal Register. 48 FR 39454. Aug. 31, 1983. U.S. Government
Printing Office. Washington, DC.
_____. 48 Federal Register 6894. Feb. 16, 1983. U.S. Government
Printing Office. Washington, DC.
_____. 47 Federal Register 30479 July 14, 1982. U.S. Government
Printing Office. Washington, DC.
_____. 47 Federal Register 25961. June 16, 1982. U.S. Government
Printing Office. Washington, DC.
_____. 47 Federal Register 19336. May 5, 1982. U.S. Government
Printing Office. Washington, DC.
_____. 47 Federal Register 19321. May 5, 1982. U.S. Government
Printing Office. Washington, DC.
_____. 47 Federal Register 13526. Mar. 31, 1982. U.S.
Government Printing Office. Washington, DC.
_____. 46 Federal Register 48197. Oct. 1, 1981. U.S. Government
Printing Office. Washington, DC.
_____. 46 Federal Register 31008. June 12, 1981. U.S.
Government Printing Office. Washington, DC.
Gosselin, R. E., et al. 1984. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD: Williams and Wilkins.
Guenzi, W. D. ed. 1974. Pesticides in soil and water. Madison,
WI: Soil Science Society of America, Inc.
Harding, W. C. 1979. Pesticide profiles. Part one:
Insecticides and miticides. Bulletin 267. Cooperative Extension
Service. University of Maryland.
Hartley, D. and H. Kidd, eds. 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
Hayes, W. J. 1982. Pesticides studied in man. Baltimore, MD:
Williams and Wilkins.
Kenaga, E. 1980. Predicted bioconcentration factors and soil
sorption coefficients of pesticides and other chemicals. Ecotox. Envir.
Khan, M. A. Q., ed. 1977. Pesticides in aquatic environments.
NY: Plenum Press.
Leo, A. 1978. Report on the calculation of octanol/water log P
values for structures in the USEPA files. Claremont, CA.
Li, F. 1982. Technical data submitted in support of the San Luis
drain report of waste discharge. File report. Branch of Scientific
Resources, USBR Department of Interior. (Contract #2-0-20-X0221).
McEwen, F. L. and G. R. Stephenson. 1979. The use and
significance of pesticides in the environment. NY: John Wiley and
Menzie, C. M. 1980. Metabolism of pesticides. Update III. U.
S. Department of the Interior. Fish and Wildlife Service. Special
Scientific Report. Wildlife No. 232. Washington, DC: U. S. Government
Morse, R. A. 1987. Bee poisoning. In 1988 New York State
pesticide recommendations. Forty-ninth annual pest control conference.
Nov. 9, 10, 11. Cornell University, Ithaca, NY.
National Academy of Sciences. 1982. Possible long-term health
effects of short-term exposure to chemical agents. Volume 1. Anti-
cholinesterases and anticholinergics. Washington, D.C.: National
National Institute for Occupational Safety and Health (NIOSH).
1981-1986. Registry of toxic effects of chemical substances (RTECS).
Cincinnati, OH: NIOSH
New Jersey Department of Health. 1986. Hazardous Substance Fact
Sheet: Chlorpyrifos. Trenton, NJ.
New York State Department of Environmental Conservation. 1986
(Feb.). Draft Environmental Impact Statement on Amendments to 6 NYCRR
Part 326 Relating to the restriction of the pesticides aldrin,
chlordane, chlorpyrifos, dieldrin and heptachlor. Division of Lands and
Forests. Bureau of Pesticides. Albany, NY.
Nolan, R. J. et al. 1984. Chlorpyrifos: Pharmacokinetics in
human volunteers. Toxicol. Appl. Pharmacol. 73: 8-15.
Occupational Health Services, Inc. 1986. Material safety data
sheet on chlorpyrifos. Secaucus, N.J: OHS, Inc.
Rao, P. S. C., et al. 1983 (Sept.). Pesticides and their
behavior in soil and water. Florida Cooperative Extension Service.
Institute of Food and Agricultural Sciences, University of Florida.
Soil science fact sheet adapted from: Herbicide injury, symptoms and
diagnosis, Skroch and Sheets, eds. 1981 (Dec.). North Carolina
Agricultural Extension Service. AG-85.
Sax, N. I. 1982. Dangerous properties of industrial materials
Schimmel, S.C. et al. 1983 (Jan.-Feb.). Acute toxicity,
bioconcentration, and persistence of AC 222, 705, Benthiocarb,
Chlorpyrifos, Fenvalerate, Methyl Parathion, and Permethrin in the
estuarine environment. In Journal of Agricultural and Food Chemistry.
The American Chemical Society.
Shepard, T. H. 1986. Catalog of teratogenic agents. Fifth
edition. Baltimore, MD: The Johns Hopkins University Press.
Thomson, W.T. 1982. 1982. Insecticides, acaricides and
ovicides. Agricultural Chemicals, Book I. Fresno, CA: Thomson
TOXNET. 1975-1986. National library of medicine's toxicology
data network. Hazardous Substances Databank (HSDB). Public Health
Service. National Institute of Health, U.S. Department of Health and
Human Services. Bethesda, MD: NLM.
U.S. Environmental Protection Agency. 1986 (Sept.). Ambient
water quality criteria for chlorpyrifos-1986. Office of Water
Regulations and Standards. Criteria and Standards Division.
_____. 1984 (Dec.). User's manual for the pesticide root zone
model (PRZM). Release 1. Athens, GA: Environmental Research
_____. 1984 (Sept.). Chemical fact sheet for chlorpyrifos. Fact
sheet no. 37. Washington, DC.
_____. 1984 (Sept.) Guidance for reregistration of pesticides
containing chlorpyrifos as the active ingredient. Case #0100. Office
of Pesticide Programs. Washington, DC.
Vieth, et al. 1979. Measuring and estimating the
bioconcentration factor of chemicals in fish. J. Fish Res. Board Can.
Woodard, R. 1985. Project report. Interagency delta health
aspects monitoring program. California Department of Water Resources
Worthing, C. R., ed. 1983. The pesticide manual: A world
compendium. Croyden, England: The British Crop Protection Council.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
U. S. Department of Agriculture, Soil Conservation Service. 1990
(Nov.). SCS/ARS/CES Pesticide properties Database: Version 2.0
(Summary). USDA - Soil Conservation Service, Syracuse, NY.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis
Publishers, Chelsea, MI.
Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for
Chlorpyrifos. OHS Inc., Secaucus, NJ.
US Environmental Protection Agency. June, 1989. Registration
Standard (Second Round Review) for the Reregistration of Pesticide
Products Containing Chlorpyrifos. Office of Pesticide Programs, US EPA,
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Racke, K.D. 1992. The environmental fate of chlorpyrifos. Rev.
Environ. Contam. Toxicol. 131:.
The Dow Chemical Company. 1986 (June 30). Summary of acute
dermal toxicity study on chlorpyrifos in Fischer 344 rats. Dow
Chemical, Indianapolis, IN.
Dow Elanco. 1992 (Nov. 20). Material Saety Data Sheet: Dursban
Insecticidal Chemical-Unflaked. Dow Elanco, Indianapolis, IN.
- 35a. Smith, C. N. 1981. Partition coefficients (Log Kow) for
- selected chemicals. In U.S. EPA, 1984. User's manual for the pesticide
- root zone model (PRZM). Release 1. Athens, GA: Environmental Research
- 35b. Stecher, P. G., ed. 1960. The Merck index. Seventh edition.
- Rahway, NJ: Merck and Company, Inc.