CHLORPYRIFOS
CASRN: 2921-88-2
For other data, click on the Table of Contents
Human Health Effects:
Human Toxicity Excerpts:
Toxic if inhaled, in contact with skin and if swallowed.
Human volunteers ingesting 0.03 mg chlorpyrifos/kg
body weight/day for three weeks did not show a statistically significant plasma
cholinesterase depression. Nine doses of 0.1 mg/kg/day caused plasma cholinesterase
depression, but no other effect. These results were confirmed in a subsequent study of
human volunteers who ingested chlorpyrifos daily
for four weeks at levels of 0.014, 0.03, and 0.1 mg/kg; significant inhibition of plasma
cholinesterase occurred only at the 0.1 mg/kg level.
OCCUPATIONAL STUDY WAS CONDUCTED ON 22 PEST CONTROL OPERATORS EXPOSED TO 8-HR LEVEL OF
27.6 MG/CU M OF DURSBAN. EFFECTS INCLUDED A
STATISTICALLY SIGNIFICANT INHIBITION OF PLASMA ACETYLCHOLINESTERASE AMONG OPERATORS AS
COMPARED TO AGE & SEX-MATCHED CONTROL GROUP.
A forty-two year old man ingested 300 mg/kg of chlorpyrifos.
The subsequent severe cholinergic syndrome lasted for 17 days with varying degrees of
severity. Thirty days after intoxication, the clinical and electrophysiologic examination
of the peripheral nervous system was normal but lymphocytic neuropathy target esterase
(NTE) was approximately 60% inhibited. On day 43, the patient began to complain of
paresthesia and leg weakness. Clinical examination, electrophysiology, and nerve biopsy
revealed signs of a peripheral neuropathy, axonal in type. Thus, measurement of
lymphocytic neuropathy esterase might be used as a clinical test to predict the
development of organophosphorus ester-induced delayed neuropathy.
Cholinesterase activity measurements for 542 California agricultural pesticide
applicators under medical supervision during the first 9 mo of 1985 were analyzed. Medical
records of applicators were used if the subject had been exposed for over 3 hr in a 30 day
period to category I and II organophosphate and carbamate pesticides. Employers of all
workers with cholinesterase activity depressions that fell to 70% or less of the workers's
plasma or RBC baselines were contacted to obtain a list of pesticides handled in the 2 wk
interval preceding the greatest reported cholinesterase activity depression. In evaluating
pesticide exposure data it was not possible to determine which of the listed pesticides
were primarily or cumulatively responsible for the noted cholinesterase activity
depressions and which pesticides were not responsible for the cholinesterase activity
depression but were coincidentally used during the same period. The pesticides associated
with plasma or RBC cholinesterase activity depression to 70% of baseline or lower are
listed. Chlorpyrifos (dursban)
usage in California for 1985 was 1,070,300 lb. Twenty-six workers, 4.8% of the sample, had
cholinesterase values at or below the California threshold value for removal from
continued exposure to cholinesterase inhibiting pesticides. Eight of these 26 workers,
31.5%, had pesticide related illnesses.
SPRAY WORKERS EXPOSED TO A 0.5% CHLORPYRIFOS
EMULSION IN FIELD TRIALS FOR MALARIA CONTROL SHOWED A MEASURABLE DECREASE IN PLASMA AND
RED BLOOD CELL CHOLINESTERASE LEVELS. IN THIS STUDY, FIVE OF SEVEN SPRAYERS SHOWED MORE
THAN 50% REDUCTION IN CHOLINESTERASE WITHIN 2 WK AFTER THE SPRAYING PROGRAM BEGAN.
All the organophosphorus insecticides have a cumulative effect by progressive
inhibition of cholinesterase ... /Organophosphorus insecticides/
The symptoms of chronic poisoning due to organophosphorus pesticides include headache,
weakness, feeling of heaviness in head, decline of memory, quick onset of fatigue,
disturbed sleep, loss of appetite, & loss of orientation. Psychic disorders,
nystagmus, trembling of the hands & other nervous system disorders can be observed in
certain cases. Sometimes neuritis, paresis & paralysis develop. /Organophosphorus
pesticides/
A woman at 34 to 35 weeks' gestation presented in acute respiratory distress with
cyanosis and tachypnea and bilateral rhonchi and crepitation. Her heart rate was 78 beats
per min and her blood pressure 120/80 mm Hg, with a fetal heart rate of 140 beats per min.
The mother was salivating markedly and her pupils were reduced to "pinpoint
size." An uncorrected metabolic acidosis was diagnosed. Serum and erythrocyte
acetylcholinesterase determinations were near zero. Cholinesterase inhibitor poisoning was
felt to be the likely cause of her disorders. Administration of atropine 2.4 mg iv bolus
with infusion of 0.02 mg/kg/hr lead to unacceptable fetal tachycardia. The woman had shown
increased cooperativeness and secretion control until the atropine had to be stopped. A
cesarean section was performed for delivery of a hypotonic infant with a 1 min Apgar score
of 3. The baby was mechanically ventilated for 2 days and required atropine therapy at 0.1
mg/kg/hr for 8 days. The mother required 8 days of mechanical ventilation and 11 days of
atropine therapy. In this case, the infant appeared relatively less poisoned than the
mother by a presumed organophosphate exposure. /Organophosphate poisoning/
A follow-up study of 232 people three years after a history of organophosphorus
pesticide poisoning disclosed only one person with slight residual blurring of vision that
might have been related to the earlier poisoning, though at the time of poisoning over one
third of the people had blurring, which lasted only a day or two after exposure was
discontinued. The possible exceptional case had findings suggestive of basilar artery
insufficiency, rather than effects of poisoning. /Organophosphorus pesticide poisoning/
The effects of acute intoxication by anti-cholinesterase agents are manifested by
muscarinic and nicotinic signs and symptoms and, except for compounds of extremely low
lipid solubility, by signs referable to the CNS. Local effects are due to the action of
vapors or aerosols at their site of contact with the eyes or respiratory tract, or due to
the local absorption after liquid contamination of the skin or mucous membranes, including
those of the gastrointestinal tract. Systemic effects appear within minutes after
inhalation of vapors or aerosols. In contrast, the onset of symptoms is delayed after
gastrointestinal and percutaneous absorption. The duration of effects is determined
largely by the properties of the compound: its lipid solubility, whether it must be
activated, the stability of the organophosphorus-AChE bond, and whether "aging"
of the phosphorylated enzyme has occurred. /Anticholinesterase agents/
Ocular effects include marked miosis, ocular pain, conjunctival congestion, diminished
vision, ciliary spasm, and brow ache. With acute systemic absorption, miosis may not be
evident due to sympathetic discharge in response to the hypotension. /Anticholinesterase
agents/
In addition to rhinorrhea and hyperemia of the upper respiratory tract, respiratory
effects consist of "tightness" in the chest and wheezing respiration, caused by
the combination of bronchoconstriction and increased bronchial secretion.
/Anticholinesterase agents/
Gastrointestinal symptoms occur earliest after ingestion, and include anorexia, nausea
and vomiting, abdominal cramps, and diarrhea. /Anticholinesterase agents/
With percutaneous absorption of liquid, localized sweating and muscular fasciculation
in the immediate vicinity are generally the earliest manifestations. /Anticholinesterase
agents/
... Severe intoxication is manifested by extreme salivation, involuntary defecation and
urination, sweating, lacrimation, penile erection, bradycardia, and hypotension.
/Anticholinesterase agents/
The time of death after a single acute exposure may range from less than 5 minutes to
nearly 24 hours, depending upon the dose, route, agent, and other factors. The cause of
death is primarily respiratory failure, usually accompanied by a secondary cardiovascular
component. Muscarinic, nicotinic, and central actions all contribute to respiratory
embarrassment; effects include laryngospasm, bronchoconstriction, increased
tracheobronchial and salivary secretion, compromised voluntary control of the diaphragm
and intercostal muscles, and central respiratory depression. Blood pressure may fall to
alarmingly low levels and cardiac irregularities intervene. These effects usually result
from hypoxemia; they often are reversed by assisted pulmonary ventilation.
/Anticholinesterase agents/
ACCUMULATION OF ACETYLCHOLINE IN CNS IS BELIEVED TO BE RESPONSIBLE FOR TENSION,
ANXIETY, RESTLESSNESS, INSOMNIA, HEADACHE, EMOTIONAL INSTABILITY, & NEUROSIS,
EXCESSIVE DREAMING & NIGHTMARES, APATHY, & CONFUSION ... DESCRIBED AFTER
ORGANOPHOSPHATE POISONING. /ORGANOPHOSPHATE INSECTICIDES/
Three clinical syndromes of organophosphate toxicity have been described: immediate,
intermediate (1 to 4 days), and delayed (8 to 14 days) after exposure. /Organophosphates
and related compounds/
Immediate or delayed ascending paralysis (dying back axonopathy) starting in the lower
extremities may occur. This may be confused with Guillain-Barre syndrome.
/Organophosphates and related compounds/
The usual symptoms include headache, giddiness, nervousness, blurred vision, weakness,
nausea, cramps, diarrhea, and discomfort in the chest. Signs include sweating, miosis,
tearing, salivation and other excessive respiratory tract secretion, vomiting, cyanosis,
papilledema, uncontrollable muscle twitches followed by muscular weakness, convulsions,
coma, loss of reflexes, and loss of sphincter control. The last four signs are seen only
in severe cases but do not preclude a favorable outcome if treatment is prompt and
energetic. Cardiac arrhythmias, various degrees of heart block, and cardiac arrest may
occur ... /Organic phosphorus pesticides/
Acute emphysema, pulmonary edema, pink froth in the trachea and bronchi, and
considerable congestion of the organs are found at autopsy. Slight microscopic changes may
occur in the liver and kidneys ... Petechial hemorrhages in the organs may be present,
especially if convulsions occurred during life. The findings are not diagnostic. In a few
cases in which death occurred unexpectedly after several days of survival, multiple
pericapillary and periprecapillary hemorrhages were noted in the myocardium and medulla
oblongata ... /Organic phosphorous pesticides/
... The serum cholinesterase activity of 14 men and 16 women at seven approximately
equal intervals throughout one 24 hr day was measured. The lowest average value, ... was
92% of the mean of all values at other sampling times. The next lowest value was 98.7% of
the same mean. /It was/ concluded that the small variation observed did not take the form
of a regular curve but was entirely individual without correspondence to hour. /Organic
phosphorus pesticides/
Skin, Eye and Respiratory Irritations:
May be irritating to skin and eyes.
Medical Surveillance:
Whole Blood reference Ranges: Normal - not established; Exposed - not established;
Toxic - not established. Serum or Plasma Reference Ranges: Normal - not established;
Exposed - not established; Toxic - not established. urine Reference Ranges: Normal - not
established; Exposed - not established; Toxic - not established.
Respiratory Symptom Questionnaires: Questionnaires have been published by the American
Thoracic Society (ATS) and the British Medical Research Council. These questionnaires have
been found to be useful in identification of people with chronic bronchitis, however
certain pulmonary function tests such as FEV1 (see pulmonary function test section) have
been found to be better predictors of chronic airflow obstruction.
Chest Radiography: This test is widely used for assessing pulmonary disease. Chest
radiographs have been found to be useful for detection of early lung cancer in
asymptomatic people, especially for detection of peripheral tumors such as
adenocarcinomas. However, even though OSHA mandates this test for exposure to some
toxicants such as asbestos, there are conflicting views on its efficacy in detection of
pulmonary disease.
Pulmonary Function Tests: The tests that have been found to be practical for population
monitoring include: Spirometry and expiratory flow-volume curves; Determination of lung
volumes; Diffusing capacity for carbon monoxide; Single-breath nitrogen washout;
Inhalation challenge tests; Serial measurements of peak expiratory-flow; Exercise testing.
Sputum Cytology: Sputum cytology along with chest radiographs have been the standard
procedures for detecting early lung cancer in asymptomatic patients. Sputum cytology has
been found to be useful for detection of central tumors, especially squamous carcinomas.
For this test to be effective, exfoliated respiratory mucosal cells must be present in the
expectorated specimen. Pooling of sputum collected over 2-3 days may enhance the
sensitivity of this test by increasing the yield of exfoliated cells in the specimen.
Evaluation of Peripheral Neuropathy: Nerve conduction study; Electromyography (EMG);
Quantitative sensory testing; Thermography.
Evaluation of Central Nervous System Effects: Evaluation of CNS effects can be
performed through neuropsychological assessment, which consists of a clinical interview
and administration of standardized personality and neuropsychological tests. The areas
that the neuropsychology test batteries focus on include the domains of memory and
attention; visuoperceptual, vistal scanning, visuospatial, and visual memory; and motor
speed and reaction time. There is limited data on which components of the test batteries
are best indicators of early CNS effects.
Evaluation of Cranial Neuropathies: Evaluation of cranial nerve damage, as evidenced by
symptoms such as loss of balance, visual function, smell, taste, or sensation on the face,
can be accomplished through a physical examination focusing on tests such as: Smell
assessment ... Vision assessment ... Facial and Trigerminal Nerve assessment ...
Vestibular assesssment ... Hearing assessment.
Workers handling & applying pesticides must undergo an annual medical examination
at the beginning of each agricultural season. Contraindications /meaning further clinical
evaluations/ for work with /organophosphorus pesticides/ are organic diseases of the
central nervous system, mental disorders & epilepsy, pronounced endocrine &
vegetative disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory
diseases, cardiovascular diseases & circulatory disorders, gastrointestinal diseases
(peptic ulcer), gastroenterocolitis, diseases of liver & kidneys, eye diseases
(chronic conjunctivitis & keratitis). The blood cholinesterase activity must be
determined before work starts. In the event of prolonged work periods, this activity
should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase
activity of 25% or more must be transferred to other work where they are not exposed to
organophosphorus pesticides until this activity is completely restored. Persons with
initial signs of indisposition should /be protected from exposure from/ pesticides.
/Organophosphorus pesticides/
... Surveillance of workers could be carried out through measurement of blood or
urinary levels of the cmpd to which they are exposed, or through measurement of a
metabolite. /Organic phosphorus pesticides/
Populations at Special Risk:
Young persons under 18 yr, expectant or nursing mothers, /alcoholics/, or persons for
whom work with toxic chemicals is contraindicated on account of their state of health /are
at elevated risk from the toxic effects of organophosphorus pesticides. Those individuals
with/ organic diseases of the CNS, mental disorders & epilepsy, pronounced endocrine
& vegetative disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory
diseases, cardiovascular diseases and circulatory disorders, gastrointestinal diseases
(peptic ulcer), gastroenterocolitis, diseases of the liver & kidneys, eye diseases
(chronic conjunctivitis and keratitis) /are at elevated risk from exposure/.
/Organophosphorus pesticides/
Those individuals who are exposed to organophosphorus pesticides with pre-existing/
organic diseases of the central nervous system, mental disorders & epilepsy,
pronounced endocrine & vegetative disorders, pulmonary tuberculosis, bronchial asthma,
chronic respiratory diseases, cardiovascular diseases & circulatory disorders,
gastrointestinal diseases (peptic ulcer), gastroenterocolitis, diseases of liver &
kidneys, eye diseases (chronic conjunctivitis & keratitis) /are at elevated risk from
exposure/. The blood cholinesterase activity must be determined before work starts. In the
event of prolonged work periods, this activity should be determined at intervals of 3-4
days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be
transferred to other work where they are not exposed to organophosphorus pesticides until
this activity is completely restored. Persons with initial signs of indisposition should
cease work with pesticides. /Organophosphorus pesticides/
Probable Routes of Human Exposure:
Those involved in the manufacture, formulation, and application of this pesticide /are
at risk of exposure/.
An occupational study of pest control operators in Texas using chlorpyrifos
determined a mean air concentration of 7540 ng/cu m during an eight hour work shift with a
maximum concn of 27600 ng/cu m measured(1). Airborne levels of chlorpyrifos
in a test room (simulating a typical American home) containing pest control strips
(gradual release) ranged from 100 to 230 ng/cu m over a 30 day period after
application(2). Airborne average concentration of chlorpyrifos
in dormitory rooms receiving spray applications to cracks and crevices were 100, 1100,
1100, 800 and 300 ng/cu m before treatment, immediately after treatment, one day after,
two days after and three days after treatment, respectively(3). Airborne concentration in
rooms receiving either spray or aerosol application of chlorpyrifos
to cracks and crevices ranged from 2700 ng/cu m immediately after application to 50 ng/cu
m three days later(4). Mean levels of 220, 126 and 96 ng/cu m were detected in storage
rooms, offices and vehicles, respectively, of commercial pest control operators(5).
Airborne levels found after spraying cracks and crevices in food-preparation serving areas
were 20-1488 ng/cu m immediately after spraying and 4-361 ng/cu m 24 hours later(5). Five
occupants of an office demonstrated organophosphate intoxication after chloropyrifos
application(6).
NIOSH (NOES Survey 1981-1983) has statistically estimated that 10,493 workers (588 of
these are female) are potentially exposed to chlorpyrifos
in the US(1). The NOES Survey does not include farm workers who may be exposed to chlorpyrifos through its application as an
insecticide. Occupational exposure to chlorpyrifos
may occur through inhalation and dermal contact with this compound at workplaces where chlorpyrifos is produced or used(SRC). The general
population may be exposed to chlorpyrifos via
inhalation of ambient air and ingestion of food products that contain this compound(SRC).
Body Burden:
A urinary metabolite (3,5,6-trichloro-2-pyridinol) of chlorpyrifos
was detected in the urine of 5.8% of 6990 samples collected from the general population
(persons 12-74 years old) during 1976-1980(1). The mean concentration of urinary chlorpyrifos metabolites found in the urine of pest
control operators in Texas was 5.6-8.3 ug/8 hours(2).
Average Daily Intake:
AIR INTAKE: Insufficient data. WATER INTAKE: Insufficient data. FOOD INTAKE: Based on
the FDA's Total Diet Study of food composites collected between Oct 1979 and Sept 1980,
the FDA has estimated the average daily food intake of chlorpyrifos
to be 0.04 ug(1).
The AVDI of chlorpyrifos estimated for
farmworkers was reported as 2.9X10-6 to 2.1X10-4 mg/kg/day(1). The AVDI for children
residing in farmworkers homes was 1.95X10-5 to 4.7X10-5 mg/kg/day(1). The AVDI of chlorpyrifos from 1986-1991 was estimated as 0.0147
ug/kg/day (6-11 months old), 0.0138 ug/kg/day (2 years old), 0.0038 ug/kg/day (14-16 years
old female), 0.006 ug/kg/day (14-16 years old male), 0.0038 ug/kg/day (25-30 years old
female), 0.0038 ug/kg/day (25-30 years old male), 0.0041 ug/kg/day (60-65 years old
female) and 0.0040 (60-65 years old male)(2). The AVDI of chlorpyrifos
from 1984-1986 was estimated as 0.0125 ug/kg/day (6-11 months old), 0.0172 ug/kg/day (2
years old), 0.0044 ug/kg/day (14-16 years old female), 0.006 ug/kg/day (14-16 years old
male), 0.0045 ug/kg/day (25-30 years old female), 0.0039 ug/kg/day (25-30 years old male),
0.0047 ug/kg/day (60-65 years old female) and 0.0046 (60-65 years old male)(3). Based on
data from 78,882 adult females and 38,075 adult males in 1990, the mean AVDI of chlorpyrifos in the US was reported as 0.8 ug/day(4).
Emergency Medical Treatment:
Emergency Medical Treatment:
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of Micromedex' copyrights and is strictly prohibited. The following Overview, *** CHLORPYRIFOS ***, is relevant for this HSDB record chemical. |
| Life Support: |
o This overview assumes that basic life support measures
have been instituted.
|
| Clinical Effects: |
SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
o Chlorpyrifos appears to be one of the safer
organophosphates. Exposures characteristically cause
selective depression of plasma, but not red blood cell,
cholinesterase activity.
o ONSET - Symptoms may be DELAYED BY SEVERAL HOURS after
an acute exposure because chlorpyrifos requires
metabolic activation to the more toxic oxon form.
o EFFECTS -
1. All of the effects of organophosphates may not be
documented for chlorpyrifos, but could potentially
occur in individual cases if doses are sufficient.
2. MUSCARINIC (PARASYMPATHETIC) EFFECTS may include
bradycardia, bronchospasm, bronchorrhea, salivation,
lacrimation, diaphoresis, vomiting, diarrhea, and
miosis.
3. NICOTINIC (SYMPATHETIC AND MOTOR) EFFECTS may include
tachycardia, hypertension, fasciculations, muscle
cramps, weakness, and RESPIRATORY PARALYSIS.
4. CENTRAL EFFECTS may include CNS depression, agitation,
confusion, psychosis, delirium, coma, and seizures.
CNS effects may be slowly reversible or irreversible.
o INHALATION EXPOSURE -
1. MILD EXPOSURE to organophosphate vapors produces a
rapid onset of local irritant symptoms, followed by
systemic symptoms if exposed to significant
concentrations. Eye, nose, and throat irritation,
miosis, blurred vision, eye pain, and rhinorrhea may
be noted. Local respiratory symptoms include dyspnea,
coughing, chest tightness, and wheezing.
2. MODERATE-SEVERE EXPOSURE - With prolonged exposure,
systemic symptoms can include all those listed above,
affecting muscarinic, nicotinic, and CNS sites.
o ROUTES OF EXPOSURE - Organophosphates are efficiently
absorbed across the lung, mucous membranes (including
the gut), and skin. The occurrence of poisoning
depends upon inherent toxicity, dosage, rate of
absorption, rate of organophosphate metabolic
breakdown, and prior exposure to other cholinesterase
inhibitors.
o IMPURITIES/DILUENTS - Impurities in the formulated
pesticide and improper application can greatly enhance
the toxic hazard. The hydrocarbon diluent may
contribute to the overall picture of toxicity:
0.2.1.2 CHRONIC EXPOSURE
o Daily exposure to concentrations that are insufficient
to produce symptoms following a single exposure may
result in the onset of symptoms. Continued daily
exposure may be followed by increasingly severe
effects.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Mydriasis may occur in severe poisonings. Opsoclonus
has occurred rarely.
o Excessive salivation commonly occurs.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Hypotension, bradycardia and chest pain may occur.
Arrhythmias and conduction defects may occur in severe
poisonings.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Dyspnea, rales, bronchorrhea, or tachypnea may be
noted. Pulmonary edema may occur in severe cases.
o Bronchospasm may occur in previously sensitized
asthmatics or as a muscarinic effect.
o Acute respiratory insufficiency is the main cause of
death in acute poisonings.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Headache, dizziness, muscle spasms and profound
weakness are common. Seizures may be more common in
children.
o Delayed neurotoxicity occurred in the standard hen
assay, but the effects were reversible. There is one
case in the clinical literature of delayed peripheral
neurotoxicity in an acute overdose. Chlorpyrifos did
not induce delayed neurotoxicity in mice.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Vomiting, diarrhea, fecal incontinence and abdominal
pain may occur.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Increased urinary frequency or, in severe cases,
urinary incontinence has occurred.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis has occurred in several severe
poisonings.
HEMATOLOGIC
0.2.13.1 ACUTE EXPOSURE
o Alteration in prothrombin time and/or tendency to
bleeding may occur.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Irritation and slight burns may occur.
o Sweating is a consistent but not universal sign.
o Dermal sensitization may occur.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Hyperglycemia can occur in severe organophosphate
poisoning.
METABOLISM
0.2.17.1 ACUTE EXPOSURE
o Chlorpyrifos characteristically causes selective
depression of plasma cholinesterase.
PSYCHIATRIC
0.2.18.1 ACUTE EXPOSURE
o Decreased vigilance, hallucinations, defects in
expressive language and cognitive function, impaired
memory, depression, anxiety or irritability and
psychosis have been reported, more commonly in persons
having other clinical signs of organophosphate
poisoning.
REPRODUCTIVE HAZARDS
o It was not teratogenic and had no other effects on
fertility in rats.
o It has been detected in cow's milk.
o Sporadic reports of human birth defects related to
organophosphates have not been fully verified.
CARCINOGENICITY
0.2.21.2 HUMAN OVERVIEW
o Chlorpyrifos has not been carcinogenic in chronic
studies on rats and mice.
o The widely used organophosphates are thought not to be
carcinogenic; however, some controversy exists in this
area.
GENOTOXICITY
o Chlorpyrifos was inactive for inducing mutations in
microbial assays. It did not induce sister chromatid
exchanges. Mixed results have been obtained for DNA
repair.
OTHER
0.2.23.1 ACUTE EXPOSURE
o Delayed toxicity can occur from acute exposure to
highly lipophilic organophosphates.
|
| Laboratory: |
o Determine plasma and red blood cell cholinesterase
activities. While there may be poor correlation between
cholinesterase values and clinical effects, depression in
excess of 50% activity is generally associated with severe
symptoms. Correlation between cholinesterase levels and
clinical effects in milder poisonings may be poor.
|
| Treatment Overview: |
SUMMARY EXPOSURE
o Suction oral secretions as required until atropinization
is achieved.
o Atropinization should rapidly be performed, concurrently
with decontamination measures.
o Pralidoxime (Protopam, 2-PAM) should be administered to
seriously ill organophosphate-poisoned patients.
Obidoxime may alternatively be used. Pyridostigmine
bromide may afford some protection from organophosphates
used in chemical warfare.
o If induction of paralysis with muscle relaxing agents is
required for intubation, succinylcholine should be
avoided because of potential prolonged duration of
paralysis secondary to pseudocholinesterase inhibition
by the organophosphate.
o Respiratory stimulants should NOT be used for acute
poisonings in general because they are contraindicated
in cases of bronchospasm, neuromuscular block and
seizures.
ORAL EXPOSURE
o Inducing emesis is CONTRAINDICATED because of possible
respiratory depression and seizures.
o GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1. CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
o ACTIVATED CHARCOAL: Administer charcoal as slurry (240
mL water/30 g charcoal). Usual dose: 25 to 100 g in
adults/adolescents, 25 to 50 g in children (1 to 12
years), and 1 g/kg in infants less than 1 year old.
o Suction oral secretions until atropinization.
o ATROPINE THERAPY - If symptomatic, administer IV
atropine until atropinization is achieved. Adult - 2 to
5 mg every 10 to 15 minutes; Child - 0.05 mg/kg every 10
to 15 minutes. Atropinization may be required for hours
to days depending on severity.
o PRALIDOXIME (Protopam, 2-PAM): Treat moderate to severe
poisoning (fasciculations, muscle weakness, respiratory
depression, coma, seizures) with 2-PAM in addition to
atropine; most effective if given within 48 hours, but
has had efficacy up to 6 days. May require
administration for several days.
1. INITIAL DOSE: ADULT: 1 to 2 g in 100 to 150 ml 0.9%
saline IV over 30 min. CHILD: 20 to 50 mg/kg as a 5%
solution IV over 30 min.
2. Repeat these doses in 1 hour and then every 6 to 12
hours if muscle weakness or fasciculations persist, or
begin continuous infusion.
3. CONTINUOUS INFUSION: Administer as a 2.5% solution in
0.9% saline. ADULT: 500 mg/hour. CHILD: 9 to 19
mg/kg/hour.
o CONTRAINDICATIONS - Succinylcholine and other
cholinergic agents.
o SEIZURES: Administer a benzodiazepine IV; DIAZEPAM
(ADULT: 5 to 10 mg, repeat every 10 to 15 min as
needed. CHILD: 0.2 to 0.5 mg/kg, repeat every 5 min
as needed) or LORAZEPAM (ADULT: 4 to 8 mg; CHILD: 0.05
to 0.1 mg/kg).
1. Consider phenobarbital if seizures recur after diazepam
30 mg (adults) or 10 mg (children > 5 years).
2. Monitor for hypotension, dysrhythmias, respiratory
depression, and need for endotracheal intubation.
Evaluate for hypoglycemia, electrolyte disturbances,
hypoxia.
o PULMONARY EDEMA (NONCARDIOGENIC): Maintain ventilation
and oxygenation and evaluate with frequent arterial
blood gas or pulse oximetry monitoring. Early use of
PEEP and mechanical ventilation may be needed.
o HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid,
place in Trendelenburg position. If hypotension
persists, administer dopamine (5 to 20 mcg/kg/min) or
norepinephrine (0.1 to 0.2 mcg/kg/min), titrate to
desired response.
INHALATION EXPOSURE
o INHALATION: Move patient to fresh air. Monitor for
respiratory distress. If cough or difficulty breathing
develops, evaluate for respiratory tract irritation,
bronchitis, or pneumonitis. Administer oxygen and
assist ventilation as required. Treat bronchospasm with
beta2 agonist and corticosteroid aerosols.
o If respiratory tract irritation or respiratory
depression is evident, monitor arterial blood gases,
chest x-ray, and pulmonary function tests.
o Carefully observe patients with inhalation exposure for
the development of any systemic signs or symptoms and
administer symptomatic treatment as necessary.
o Suction oral secretions until atropinization.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
o CONTRAINDICATIONS - Succinylcholine and other
cholinergic agents are contraindicated.
EYE EXPOSURE
o DECONTAMINATION: Irrigate exposed eyes with copious
amounts of tepid water for at least 15 minutes. If
irritation, pain, swelling, lacrimation, or photophobia
persist, the patient should be seen in a health care
facility.
o Patients symptomatic following exposure should be
observed in a controlled setting until all signs and
symptoms have fully resolved.
o Suction oral secretions until atropinization.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
o CONTRAINDICATIONS - Succinylcholine and other
cholinergic agents are contraindicated.
DERMAL EXPOSURE
o Systemic effects can occur from dermal exposure to
organophosphates.
o Remove contaminated clothing and jewelry; wash skin,
hair and nails vigorously with repeated soap washings.
Leather absorbs pesticides; all contaminated leather
should be discarded. Rescue personnel and bystanders
should avoid direct contact with contaminated skin,
clothing, or other objects.
o Treatment should include recommendations listed in the
ORAL EXPOSURE section when appropriate.
o Some chemicals can produce systemic poisoning by
absorption through intact skin. Carefully observe
patients with dermal exposure for the development of any
systemic signs or symptoms and administer symptomatic
treatment as necessary.
o CONTRAINDICATIONS - Succinylcholine and other
cholinergic agents are contraindicated.
|
| Range of Toxicity: |
o Oral doses of 0.03 mg/kg/day had no detectible effect.
Depression of plasma pseudocholinesterase of up to 70
percent has been accompanied by only mild symptoms.
|
Antidote and Emergency Treatment:
Basic treatment: Establish a patent airway. Suction if necessary. Aggressive airway
control may be needed. Watch for signs of respiratory insufficiency and assist
ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min.
Monitor for pulmonary edema and treat if necessary ... Monitor for shock and treat if
necessary ... Anticipate seizures and treat if necessary ... For eye contamination, flush
eyes immediately with water. Irrigate each eye continuously with normal saline during
transport ... Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to
200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does
not drool. Administer activated charcoal ... /Organophosphates and related compounds/
Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control
in the patient who is unconscious or has severe pulmonary edema. Positive pressure
ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac
rhythm and treat arrhythmias if necessary ... Start an IV with D5W /SRP: "To keep
open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present.
Administer atropine. Correct hypoxia before giving atropine ... Administer pralidoxime
chloride (2 PAM). USE UNDER DIRECT PHYSICIAN ORDERS ONLY ... Treat seizures with adequate
atropinization and correction of hypoxia. Rarely is diazepam necessary ... For hypotension
with signs of hypovolemia, administer fluid cautiously and consider vasopressors for
hypotension with a normal fluid volume. Watch for signs of fluid overload (refer to shock
protocol in Section Three). Use proparacaine hydrochloride to assist eye irrigation ...
/Organophosphates and related compounds/
A comatose patient who is diaphoretic, has pinpoint pupils and the odor of an
insecticide on clothing or breath, and is noted to have muscle fasciculations represents
the classic presentation of organophosphate poisoning. ... Specific steps in management
include the following. 1. Decontamination. ... 2 Airway. Establish an airway if necessary.
... 3. Respiratory Status. Respiratory distress, in fact, is commonly found in these
patients from multiple causes. ... 4. Cardiac Monitoring. ... 5. Cholinesterase Level. ...
6. Pralidoxime. Pralidoxime is the treatment of choice for organophosphate poisoning and
should be used for nearly all patients with clinically significant orgnophosphate
poisoning, particularly whose patients with muscular fasciculations and weakness. ... 7.
Atropine. Atropine is the physiologic antidote for organophosphate poisoning. A trial dose
of atropine should be instituted on clinical ground when one suspects organophosphate
intoxication. /Organophosphate poisoning/
1. INSURE THAT A CLEAR AIRWAY EXISTS BY ASPIRATION OF SECRETIONS IF NECESSARY. ADMIN
OXYGEN BY MECHANICALLY ASSISTED PULMONARY VENTILATION IF RESPIRATION IS DEPRESSED. IMPROVE
TISSUE OXYGENATION AS MUCH AS POSSIBLE BEFORE ADMIN ATROPINE TO MINIMIZE RISK OF
VENTRICULAR FIBRILLATION. IN SEVERE POISONINGS, IT MAY BE NECESSARY TO SUPPORT PULMONARY
VENTILATION MECHANICALLY FOR SEVERAL DAYS. 2. ADMIN ATROPINE SULFATE IV, OR IM IF IV
INJECTION IS NOT POSSIBLE. ... /ORGANOPHOSPHATE PESTICIDES/
2. SEVERELY POISONED INDIVIDUALS MAY EXHIBIT REMARKABLE TOLERANCE TO ATROPINE; TWO OR
MORE TIMES THE DOSAGES SUGGESTED ABOVE MAY BE NEEDED. THE DOSE OF ATROPINE MAY BE
INCREASED AND THE DOSING INTERVAL DECREASED AS NEEDED TO CONTROL SYMPTOMS. CONTINUOUS
INTRAVENOUS INFUSION OF ATROPINE MAY BE NECESSARY WHEN ATROPINE REQUIREMENTS ARE MASSIVE.
REVERSAL OF MUSCARINIC SYMPTOMS AND SIGNS, NOT AN ARBITRARY DOSE LIMIT, IS THE DESIRED
END-POINT. PRESERVATIVE-FREE ATROPINE PRODUCTS SHOULD BE USED WHENEVER POSSIBLE. NOTE:
PERSONS NOT POISONED OR ONLY SLIGHTLY POISONED BY ORGANOPHOSPHATES MAY DEVELOP SIGNS OF
ATROPINE TOXICITY FROM SUCH LARGE DOSES. FEVER, MUSCLE FIBRILLATIONS, AND DELIRIUM ARE THE
MAIN SIGNS OF ATROPINE TOXICITY. IF THESE APPEAR WHILE THE PATIENT IS FULLY ATROPINIZED,
ATROPINE ADMINISTRATION SHOULD BE DISCONTINUED, AT LEAST TEMPORARILY, WHILE THE SEVERITY
OF POISONING IS REEVALUATED. /ORGANOPHOSPHATE PESTICIDES/
3. DRAW BLOOD SAMPLE (HEPARINIZED) FOR CHOLINESTERASE ANALYSIS BEFORE ADMINISTRATION OF
PRALIDOXIME, WHICH TENDS TO REVERSE THE CHOLINESTERASE DEPRESSION. 4. ADMIN PRALIDOXIME
(PROTOPAM, 2-PAM) IN CASES OF SEVERE POISONING ... IN WHICH RESP DEPRESSION, MUSCLE
WEAKNESS & TWITCHINGS ARE SEVERE. ... /ORGANOPHOSPHATE PESTICIDES/
4. BE PREPD TO ASSIST PULMONARY VENTILATION MECHANICALLY IF RESP ... DEPRESSED ... . 5.
IN PATIENTS WHO HAVE BEEN POISONED BY ORGANOPHOSPHATE CONTAMINATION OF SKIN, CLOTHING,
HAIR, AND/OR EYES, DECONTAMINATION MUST PROCEED CONCURRENTLY WITH WHATEVER RESUSCITATIVE
AND ANTIDOTAL MEASURES ARE NECESSARY TO PRESERVE LIFE. ... 6. IF ... INGESTED IN QUANTITY
PROBABLY SUFFICIENT TO CAUSE POISONING, THE STOMACH AND INTESTINE MUST BE EMPTIED. A.
EMPTY THE STOMACH BY INTUBATION, ASPIRATION, AND LAVAGE, USING SLURRY OF ACTIVATED
CHARCOAL IN ISOTONIC SALINE. RIGOROUS PRECAUTIONS MUST BE TAKEN TO PROTECT THE AIRWAY FROM
ASPIRATION OF REGURGITATED. IF VICTIM IS UNCONSCIOUS OR OBTUNDED, INSERT A CUFFED
ENDOTRACHEAL TUBE PRIOR TO GASTRIC INTUBATION. KEEP VICTIM'S HEAD BELOW LEVEL OF STOMACH
DURING GASTRIC INTUBATION AND LAVAGE ... KEEP VICTIM'S HEAD TURNED TO THE LEFT.
/ORGANOPHOSPHATE PESTICIDES/
6B. AFTER ASPIRATION OF STOMACH CONTENTS AND LAVAGE, INSTILL ACTIVATED CHARCOAL ...
TOGETHER WITH A CATHARTIC IN THE CHARCOAL SLURRY. ... ALTERNATIVE CATHARTICS THAT MAY BE
USED INSTEAD ARE SODIUM OR MAGNESIUM SULFATE OR CITRATE: DOSAGE OF SODIUM OR MAGNESIUM
SULFATE ... C. IF GASTRIC ASPIRATION AND LAVAGE IS NOT PERFORMED DUE TO DELAY IN
TREATMENT, AND IF PATIENT IS FULLY ALERT, ADMINISTER DOSES OF CHARCOAL AND CATHARTIC
ORALLY. WHEN SORBITOL IS GIVEN ORALLY, IT SHOULD BE DILUTED WITH AN EQUAL VOLUME OF WATER
TO YIELD A 35% SOLUTION. D. SAVE A SAMPLE OF EMESIS OR INITIAL GASTRIC WASHINGS FOR
CHEMICAL ANALYSIS. E. IN SOME CASES OF ORGANOPHOSPHATE INGESTION THERE MAY BE BENEFIT FROM
REPEATED ADMINISTRATION OF ACTIVATED CHARCOAL, EITHER BY INGESTION OR STOMACH TUBE ...
/ORGANOPHOSPHATE PESTICIDES/
7. OBSERVE PATIENT CLOSELY FOR AT LEAST 72 HOURS (LONGER IN CASES OF ORGANOPHOSPHATE
INGESTION) TO INSURE THAT SYMPTOMS (SWEATING, VISUAL DISTURBANCES, VOMITING, DIARRHEA,
CHEST AND ABDOMINAL DISTRESS, AND SOMETIMES PULMONARY EDEMA) DO NOT RECUR AS
ATROPINIZATION IS WITHDRAWN. IN VERY SEVERE POISONINGS BY INGESTED ORGANOPHOSPHATES,
PARTICULARLY THE MORE LIPOPHILIC AND SLOWLY HYDROLYZED COMPOUNDS, METABOLIC DISPOSITION OF
TOXICANT MAY REQUIRE AS MANY AS 5-14 DAYS. /ORGANOPHOSPHATE PESTICIDES/
8. PARTICULARLY IN POISONINGS BY LARGE INGESTED DOSES OF ORGANOPHOSPHATE, MONITOR
PULMONARY VENTILATION CAREFULLY, EVEN AFTER RECOVERY FROM MUSCARINIC SYMPTOMATOLOGY, TO
FORESTALL RESPIRATORY FAILURE. 9. IN SEVERELY POISONED PATIENTS, MONITOR CARDIAC STATUS BY
CONTINUOUS ECG RECORDING. /ORGANOPHOSPHATE PESTICIDES/
10. FUROSEMIDE MAY BE CONSIDERED FOR RELIEF OF PULMONARY EDEMA IF RALES PERSIST IN THE
LUNGS EVEN AFTER FULL ATROPINIZATION. ... 11. THE FOLLOWING DRUGS ARE PROBABLY
CONTRAINDICATED IN NEARLY ALL ORGANOPHOSPHATE POISONING CASES: MORPHINE, THEOPHYLLINE,
PHENOTHIAZINES, AND RESERPINE. ADRENERGIC AMINES SHOULD BE GIVEN ONLY IF THERE IS A
SPECIFIC INDICATION, SUCH AS MARKED HYPOTENSION. /ORGANOPHOSPHATE PESTICIDES/
For immediate first aid: ensure that adequate decontamination has been carried out. If
victim is not breathing, start artificial respiration, preferably with a demand-valve
resuscitator, bag-valve-mask device, or pocket mask as trained. Perform CPR if necessary.
Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If
vomiting occurs, lean patient forward or place on left side (head-down position, if
possible) to maintain an open airway and prevent aspiration. Keep victim quiet and
maintain normal body temperature. Obtain medical attention. /Organophosphates and related
compounds/
Preservative-free atropine should be used to avoid toxicity from preservative agents.
Mydriasis may occur early in the administration of atropine; however the endpoint for
atropine administration is the drying of pulmonary secretions. /Organophosphates and
related compounds/
Never give morphine, theophylline, and theophylline ethylenediamine ... Large amounts
of iv fluids generally are contraindicated because of the threat of pulmonary edema.
/Organic phosphorous pesticides/
Succinylcholine, other cholinergic agents, and aminophylline are contraindicated.
/Organophosphates and related compounds/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
THERE WAS /NO/ EVIDENCE OF TERATOLOGIC OR REPRODUCTIVE EFFECTS IN MALE & FEMALE
RATS FED 1 MG CHLORPYRIFOS/KG/DAY DURING A
THREE-GENERATION REPRODUCTION & FERTILITY STUDY.
... THE ONLY EFFECT IN DOGS & SHEEP ... EXPOSED FOR A 4-HR PERIOD TO A THERMAL FOG
OR LIQUID AEROSOL OF CHLORPYRIFOS @ CONCN OF 4
OR 8 MG/CU FT (140-280 MG/CU M) WAS A MILD DEPRESSION OF PLASMA CHOLINESTERASE IN THE DOGS
EXPOSED @ THE HIGHER CONCN. ... DOGS & RATS FED ... FOR 2 YR SHOWED NO EFFECTS DUE TO
CHOLINESTERASE DEPRESSION OR SIGNS OF ANY SYSTEMIC TOXICITY @ ... 3.0 MG/KG BODY
WEIGHT/DAY.
DURSBAN WAS SCREENED FOR MUTAGENICITY BY THE
REC-ASSAY PROCEDURE USING DIFFERENT STRAINS OF BACILLUS SUBTILIS, AS WELL AS REVERSION
ASSAYS ON PLATES UTILIZING AUXOTROPHIC STRAINS OF ESCHERICHIA COLI (WP2) AND SALMONELLA
TYPHIMURIUM (AMES SERIES). RESULTS WERE NEGATIVE.
DIETARY 11-DAY TOXICANT FEEDING TESTS WERE USED TO DETERMINE EFFECTS OF CHLORPYRIFOS ON MALLARDS. AVOIDANCE OF FOOD WAS NOTED
AT ALL CONCENTRATIONS TESTED (56-1124 PPM) WITH CONSEQUENTIAL DECR IN WT GROWTH.
PREGNANT CF-1 MICE WERE GIVEN 0, 1, 10, OR 25 MG/KG/DAY CHLORPYRIFOS
BY GAVAGE ON DAYS 6-15 OF GESTATION. FETOTOXICITY WAS NOTED AMONG LITTERS OF MICE GIVEN 25
MG/KG AS EVIDENCED BY DECR FETAL BODY MEASUREMENTS & INCR INCIDENCE OF MINOR SKELETAL
VARIANTS. CHLORPYRIFOS WAS NOT TERATOGENIC IN
MICE AT DOSE LEVELS UP TO 25 MG/KG/DAY.
FATHEAD MINNOWS (PIMEPHALES PROMELAS) WERE EXPOSED TO DURSBAN
FOR 200 DAYS INCLUDING A REPRODUCTIVE PERIOD OF THEIR LIFE CYCLE. SURVIVAL OF 1ST
GENERATION WAS ADVERSELY AFFECTED AT 2.6 UG/L WITHIN 60 DAYS. A SIGNIFICANT NUMBER OF
DEFORMITIES OCCURRED AT 2.68 UG/L WITHIN 30 DAYS. GROWTH WAS SIGNIFICANTLY DECREASED AT
2.68 UG/L WITHIN 30 DAYS & AT 1.21 UG/L BY 60 DAYS. MATURATION OF THE FIRST-GENERATION
FISH WAS REDUCED AT ALL EXPOSURE LEVELS & REPRODUCTION WAS SIGNIFICANTLY REDUCED AT
0.63 UG/L & ABOVE. GROWTH & ESTIMATED BIOMASS OF 30-DAY-OLD SECOND GENERATION FISH
WAS GREATLY REDUCED AT 0.12 UG/L. BRAIN ACETYLCHOLINESTERASE (ACHE) ACTIVITY WAS INHIBITED
AT O.27 UG/L & ABOVE. ACHE INHIBITION RANGED FROM NEAR 10% IN FISH EXPOSED TO 0.12
UG/L TO 89% FOR THOSE EXPOSED TO 2.68 UG/L.
EFFECT OF CHLORPYRIFOS ON THE FIELD &
LAB-DEVELOPED ESTUARINE BENTHIC COMMUNITIES WAS STUDIED. LAB COMMUNITIES WERE CONTINUOUSLY
EXPOSED TO TOXICANT FOR 8 WK DURING COLONIZATION BY PLANKTONIC LARVAE IN UNFILTERED SANTA
ROSA SOUND, FL, SEAWATER. FIELD COMMUNITIES WERE DEVELOPED FOR 8 WK IN AQUARIA PLACED IN
SANTA ROSA SOUND, THEN REMOVED TO LAB FOR EXPOSURE TO CHLORPYRIFOS
FOR 1 WK. NUMBER OF ARTHROPODS WAS DECR BY APPROX 0.1 UG/L TECHNICAL GRADE CHLORPYRIFOS IN WATER IN LAB COMMUNITIES & BY 5.9
UG/L IN WATER IN FIELD COMMUNITIES. ONE SPECIES OF ANNELID, CISTENIDES GOULDII, WAS MORE
ABUNDANT IN FIELD AQUARIA RECEIVING 1.0 UG/L OR 5.9 UG/L THAN IN CONTROL & LOWEST
CONCN. MOLLUSCAN LARVAE COLONIZING LAB AQUARIA WERE SENSITIVE TO APPROX 0.1 UG/L; HOWEVER,
LATER DEVELOPMENTAL STAGES CHARACTERIZING FIELD AQUARIA WERE NOT SENSITIVE TO APPROX 5.9
UG/L. ALTHOUGH ONLY 20 OF 78 SPECIES APPEARED IN BOTH LAB & FIELD COMMUNITIES,
SENSITIVITY OF ANIMALS IN THESE TESTS & IN SINGLE SPECIES TESTS COULD BE COMPARED.
ACUTE TOXICITY TESTS PROVIDED THE FOLLOWING DECREASING ORDER OF TOXICITY TO ESTUARINE
CRUSTACEANS & FISHES: AC 222,705, FENVALERATE, PERMETHRIN, CHLORPYRIFOS,
METHYL PARATHION, & BENTHIOCARB. THE ESTUARINE MYSID (MYSIDOPSIS BAHIA) WAS MOST
SENSITIVE SPECIES WITH MEDIAN LETHAL CONCN AS LOW AS 0.008 MG/L. THE SHEEPHEAD MINNOW
(CYPRINODON VARIEGATUS) WAS GENERALLY THE LEAST SENSITIVE (RANGE OF LC50 VALUES 1.1-1.37
MG/L /TIME INTERVAL NOT GIVEN IN SOURCE/).
A COMPARATIVE STUDY OF 5 ORGANOPHOSPHORUS INSECTICIDES, LEPTOPHOS, EPN, CYANOFENPHOS, CHLORPYRIFOS & DIAZINON, WAS CONDUCTED USING
1/10TH THE LD50 VALUES TO STUDY THEIR IN VIVO INTERACTION WITH 6 SERUM ENZYMES FROM ORAL
ADMIN FOR 4 WK IN WHITE RATS. LEPTOPHOS, CHLORPYRIFOS
& DIAZINON EXERTED SIGNIFICANT INHIBITION OF GLUTAMIC OXALOACETIC TRANSAMINASE,
GLUTAMIC PYRUVIC TRANSAMINASE, GLUTAMYLTRANSFERASE & LACTATE DEHYDROGENASE.
GENOTOXICITY & EMBRYOTOXICITY OF CHLORPYRIFOS
(CPF) & 2 METABOLITES WERE EVALUATED USING CHICK EMBRYO, CHINESE HAMSTER OVARY CELL
(CHO), & BY EXAM BLASTOCYSTS FROM SUPEROVULATED COWS CROSSED TO CHLORPYRIFOS-TREATED
BULLS. TEST COMPOUNDS WERE ADMIN TO 3-DAY OLD EMBRYOS BY AIR CELL METHOD. LD50 WAS 1,500
UG/L/EMBRYO WHEN MORTALTIY WAS CHECKED THROUGH & INCL 17 DAYS OF DEVELOPMENT. THE
METABOLITES WERE MORE EMBRYOTOXIC THAN THE CPF. CPF & ITS METABOLITES DID NOT INCR THE
SISTER CHROMATID (SCE) FREQUENCY ABOVE BACKGROUND AT ANY DOSAGE IN 3-DAY OLD CHICK EMBRYO
ASSAY. NONE OF THE COMPOUNDS INCR SISTER CHROMATID FREQUENCIES IN 3-POINT DOSAGE TESTS (1,
10, 100 UG/L) USING CHINESE HAMSTER OVARY CELLS. STUDIES OF BOVINE BLASTOCYSTS DID NOT
REVEAL EVIDENCE OF CHROMOSOME ABERRATIONS OR DEVELOPMENTAL ANOMALIES ASSOCIATED WITH
PESTICIDE APPLICATION.
Toxic to bees
Chicken pullets 203 days of age at start of experiment, were exposed by feeding 25
mg/kg technical grade chlorpyrifos (2.48
mg/kg/day daily dose) for 365 days. /Toxic signs/ observed were reduced blood
cholinesterase activity (78% of normal). Chicken pullets (same as parameter) fed 50 mg/kg
technical grade chlorpyrifos (20.4 mg/kg/day
daily dose) for 365 days, exhibited no effect on feed consumption, body weight, egg
production, feed efficiency, egg weight, interior egg quality, and egg shell thickness.
Reduced blood cholinesterase activity (24% of normal).
An aerosol preparation containing 2.5% chlorpyrifos
was applied to the tail and umbilicus of new born pigs. Mortality was 7/7 pigs treated 0-3
hr after birth, 3/5 pigs treated at 24-30 hr, and 0/3 pigs treated 30-36 hr after birth.
Clinical signs consistent with organophosphate toxicosis were demonstrated by pigs that
/later/ died or were euthanized in extremis. Blood and brain cholinesterase activities
were depressed in affected pigs compared to controls. Only 1/3 pigs treated 30-36 hr after
birth had a diagnostically significant depression in blood cholinesterase. These results
indicate that piglets one day or less of age are susceptible to organophosphate toxicosis
by cutaneous absorption of chlorpyrifos.
This /study/ was designed to determine the effect of using two different ages of
mallard (Anas platyrhynchos) adults within the first breeding season on reproductive tests
under standard Toxic Substances Control Act avian reproductive guidelines. The adult age
groups were 7 and 11 months at test initiation. The test chemical was an organophosphate
insecticide, chlorpyrifos. Chlorpyrifos
exposure reduced adult body weight, brain acetylcholinesterase activity, egg production,
egg shell thickness, egg weight, and day 0 duckling weight in both age groups.
Statistically, adult age affected only duckling day 14 weight. However, three of the 7
month hens produced phenotypically different ducklings, suggesting the presence of a
different genotype which may have impacted the day 14 weight. Overall age ranging between
7 and 11 months at test initiation did not affect this mallard reproductive test. In
addition, the results of this study demonstrate the importance of using phenotypically and
genotypically similar test birds.
No significant reproductive effects were observed for mallards receiving 8 ppm (mg/kg
of feed) chlorpyrifos in their diet. Birds
receiving 80 ppm chlorpyrifos hatched
significantly (p <0.05) fewer ducklings per successful nest (5.8) than control (10.2).
None of the ducklings on treatment ponds survived to 7 days. Control birds produced 8.4
ducklings per successful nest surviving 7 days or longer. Birds in the 80 ppm treatment
group consumed less feed than did controls (p <0.01). Weight loss from reduced feed
/intake/ did not /result/ to the extent expected, indicating that the birds supplemented
their diets with natural foods found in and around the the ponds. In spite of the
relatively low treated feed consumption, brain acetylcholinesterase was significantly (p
<0.05) depressed (57% of controls) for 80 ppm treated birds. Studies on indoor penned
mallards fed 80 ppm chlorpyrifos in their diet
also resulted in acetylcholinesterase depression to the same extent but at much higher
feed consumption levels.
Methodologic aspects of the determination of the in vivo effect of chlorpyrifos
on acetylcholinesterase in guppies were investigated. There was a linear relationship
between the amount of homogenate (highest volume tested, 100 ul) and the
acetylcholinesterase activity. It was found that the contribution of pseudocholinesterase
to the total cholinesterase activity can be neglected. This was demonstrated by addition
of the acetylcholinesterase inhibitor, 1,5-bis(4-allyldimethylammonium
phenyl)pentane-3-one dibromide. During homogenization of the guppies it was necessary to
protect the acetylcholinesterase from artifactual in vitro enzyme inhibition. For this
purpose, the fish were homogenized in pyrophosphate buffer with 0.00635 M
phenyltrimethylammonium iodide, which bind reversibly to the active site of
acetylcholinesterase. The acetone used to dilute the stock solution of chlorpyrifos
reduced the oxygen content of the water, potentially affecting the uptake rate of the
toxic compound. Very low, sublethal concentrations (1 or 3 ppb) of chlorpyrifos
produced high inhibition levels of acetylcholinesterase (80 to 90%) in guppies within 2
weeks of continuous exposure. Although the enzyme activity recovered after maintenance in
a clean medium for 4 days, the rate of recovery was considerably lower than the rate of
inhibition.
A major spillage of the insecticide Dursban
(500 l) occurred along 19 km of the River Roding, Essex, UK on 2 Apr 1985. Within 30 to 40
hr, Dursban had entered tidal reaches of the
river, 26 km downstream from the spillage point. 90% of the previous biomass of fish (4740
kg) and all aquatic arthropods were killed over a 23 km stretch of the River Roding.
Initial concn in water reached 14 mg/l in Brookhouse Brook (spill site) and 2.5 mg/l in
the Roding, 15.7 km from the spillage point. The entire affected 23 km of the freshwater
Roding was subject to > 0.3 mg/l of the active ingredient chlorpyrifos,
but concn were considerably less (< 30 ug/l) in tidal water. River sediment was
contaminated with up to 818 mg/kg (fresh wt) chlorpyrifos
at Brookhouse Brook and 21 mg/kg 5 km from the spillage point. Concn in water had declined
to below 10 ug/l within 3 wk of the spill, and by 64 wk was not detectable in the Roding.
Five affected macroinvertebrate riffles and an upstream control were kick-sampled at
approx 10 wk intervals for 2 yr following the spill; results are compared with species
composition and relative abundance data collected from the same sites during the previous
6 yr. Initial concn of chlorpyrifos in river
water (up to 2.5 mg/l) exceeded the level lethal to all the aquatic arthropods present by
at least lO fold, and this group of macroinvertebrates was eliminated. Mollusks and
annelids, which are relatively tolerant of chlorpyrifos,
survived. Since these groups already dominated the lowermost urban reaches, the impact of
the spill was greatest further upstream, where reaches with a better quality previously
supported a more diverse and abundant arthropod fauna. Chlorpyrifos
residues in water declined below 1 ug/l within 11 wk, but sediment within 5 km of the
spillage site remained highly contaminated for considerably longer. Of 10 arthropod taxa
previously common to all sites, chironomid larvae were first to recolonize affected
reaches, 13 wk after the spill. The isopod Asellus aquaticus, was also quick to recover.
Although other arthropods had recolonized most sites within 79 wk, the coleopteran
Oulimnius tuberculatus and the ephemeropteran Caenis moesta had failed to return to the
lowermost reaches after 108 wk.
Tests were conducted to determine the dietary concn at which 14-day old bobwhite
(Colinus virginianus) chicks could discriminate between food treated with chlorpyrifos (7 groups at 0 to 4467 ppm) and untreated
food. Results of 5 day subacute dietary LC50 tests using one feeder of treated food per
cage (n > 10 per cage) were compared with those of tests in which birds were presented
with 2 feeders (treated and untreated), 1:1) or 10 feeders (5 treated and 5 untreated,
5:5; or 9 treated and 1 untreated, 9:1). The position of feeders was changed each day
during the 5 days of treatment. Intoxication in the bobwhite was characterized by reduced
food consumption and diarrhea in 48 hr, followed by lethargy, wing droop, muscular
incoordination, tremors and tetany immediately preceding death. Mean body wt of controls
increased more than 50% during the treatment period, while remaining unchanged or decr in
all dietary concn that caused mortality. Dead birds lost 20 to 47% of their body wt during
treatment, with an avg loss of 38 +/- 1%. Total food consumption decr sharply as dietary
concn increased in LC50 tests. The dietary concn above which birds discriminated between
treated and untreated feeders by consuming a greater proportion of untreated food was
defined at the discrimination threshold. The discrimination threshold occurred at
sublethal dietary concn in all chlorpyrifos
tests (discrimination threshold = 45 ppm in 1:1 test, 24 ppm in 5:5 test and 69 ppm in 9:1
test; LC50 = 647 ppm). In all tests, mortality was inversely related to total food
consumption. No relationship was found between mortality and the amount of methyl
parathion ingested per bird-day. Consequently, the ability to locate untreated feeders was
more important than the amount of chemical ingested. Average brain ChE activity was
similar to that of controls in the 1:1 and 5:5 tests regardless of the amount of chemical.
There was a significant correlation between ChE activity and total food consumption for chlorpyrifos (r = 0.78, n = 21, p < 0.001).
Groups of 50 small (50 to 70 mg) and 50 large (300 to 400 mg) freshwater leeches
(Nephelopsis obscura) were exposed to 16, 32, 64, 128, and 144 ppb chlorpyrifos
(Dursban) for as long as 6 wk. There was no
mortality, and no behavioral changes were observed in exptl animals, except for transient
(3 hr) curling and cutaneous mucus secretion at 128 and 144 ppb chlorpyrifos.
RNA synthesis in neurons of the cerebral ganglion, epithelial cells of the intestine, and
the tegument of small immature and large mature Nephelopsis obscura was examined
histochemically. No pathological changes were observed in the intensity of RNA
fluorescence or in the distribution of RNA within the cytoplasm of neurons or epithelial
cells in any specimen.
When chlorpyrifos was administered to monkeys
for 6 mos, both plasma and red cell cholinesterases were inhibited at dosages of 2.0 and
0.4 mg/kg/day, but only the plasma enzyme was inhibited at a dosage of 0.08 mg/kg/day.
The clinical signs associated with organophosphorus cmpd poisoning are due to
accumulation of acetylcholine & hence over-stimulation of the parasympathetic nervous
system. It is usual to divide them under 3 categories, namely, muscarinic, nicotinic &
central effects. Muscarinic signs ... consist of hypersalivation, lacrimation, sweating
& nasal discharge. Miosis, dyspnea, vomiting, diarrhea & frequent urination also
occur. The nicotinic effects consist of fasciculation of the muscles, weakness &
paralysis. The central effects include nervousness, apprehension, ataxia, convulsions
& coma. Death is due to resp failure, or sometimes cardiac arrest. There is little
difference between the signs produced by the different organophosphorus compounds, but the
route of absorption may influence one system more than another. /Organophosphorus
insecticides/
In adult cattle the minimum toxic oral dose of organophosphate pesticides varies from 1
to 125 mg/kg; the minimum toxic dermal concentration varies from 0.5 to 3%, but these
figures are not sacred. The literature is not complete with regard to animal toxicity of
organophosphates; even if it were, toxicity values would not be reliable because of the
number of factors that influence toxicity of these chemicals under different conditions of
use. /Organophosphorus pesticides/
Biologic factors also influence toxicity of organophosphates. Species is very important
here. ... Age of the animal is another biologic factor that alters toxicity of
organophosphate pesticides. Compounds that do not require enzymatic activation are more
toxic in very young animals in which the enzymes of pesticide degradation are deficient.
Compounds that require enzymatic activation are not so toxic for very young animals
because the enzymes of activation are deficient during the early weeks of life. Sex of the
animals can also alter toxicity of organophosphates ... /Organophosphate pesticides/
Some anticholinesterase organic phosphorous compounds interfere with temperature
control and make the body temperature of rats and mice abnormally dependent on the
environmental temperature ... No such effect was observed in guinea pigs or rabbits. The
effect in rats ... and in mice ... was partially prevented by atropine, suggesting that it
is related to cholinesterase inhibition. /Organic phosphorous pesticides/
The cause of death in poisoning by organic phosphorous compounds is usually respiratory
failure and consequent anoxia but may be cardiovascular in origin. Four factors (excessive
secretion of the respiratory tract, bronchoconstriction, weakness of the muscles of
respiration, and failure of the respiratory center) may contribute to respiratory failure.
... In a few instances, death has followed profound brain damage that occurred, usually
early in the course of poisoning, as a result of severe anoxia ... /Organic phosphorous
pesticides/
Some organic phosphorous compounds produce an immediate /CNS depressant/ effect,
ranging from incoordination to deep anesthesia following iv injection. At the same time
respiration may be affected. A large dosage is required for all compounds for which the
effect has been demonstrated and, by necessity, all of them are of low toxicity. /Organic
phosphorous pesticides/
Non-Human Toxicity Values:
LD50 ALBINO RATS MALES ORAL 151 MG/KG, (95% CONFIDENCE LIMIT 179-252 MG/KG) /PURITY
99%/
LD50 ROCK DOVES (DOMESTIC PIGEONS) ORAL 26.9 MG/KG (95% CONFIDENCE LIMIT 19.0-38 MG/KG)
/PURITY 94.5%/
LD50 DOMESTIC GOATS FEMALES ORAL 500-1000 MG/KG /PURITY 94.5%/
LD50 Rat oral 82 mg/kg
LC50 Rat ihl >200 mg/cu m/4 hr
LD50 Rat skin 202 mg/kg
LD50 Mouse oral 60 mg/kg
LD50 Mouse ip 192 mg/kg
LD50 Rabbit oral 1000 mg/kg
LD50 Rabbit skin 2000 mg/kg
LD50 Guinea pig acute oral 504 mg/kg
Ecotoxicity Values:
LC50 Coturnix (Japanese quail) oral 293 ppm (95% confidence limit 112-767 ppm)
/Technical material, 97% active ingredient/
LD50 MALLARDS FEMALE ORAL 75.6 MG/KG (95% CONFIDENCE LIMIT 35.4-161 MG/KG) /PURITY 99%/
LD50 PHEASANT 3-5 MONTH-OLD MALES, ORAL 8.41 MG/KG (95% CONFIDENCE LIMIT 2.77-25.5
MG/KG) /PURITY 99%/
LD50 CHUKAR 3-5 MONTH-OLD MALES, ORAL 60.7 MG/KG (95% CONFIDENCE LIMIT 43.8-84.1 MG/KG)
/PURITY 99%/
LD50 COTURNIX COTURNIX (JAPANESE QUAIL) 2.5 MONTH-OLD MALES, ORAL 15.9 MG/KG (95%
CONFIDENCE LIMIT 10.5-24.0 MG/KG) /PURITY 94.5%/
LD50 HOUSE SPARROWS MALES, ORAL 21.0 MG/KG (95% CONFIDENCE LIMIT 5.59-79.1 MG/KG)
/PURITY 94.5%/
LD50 BRANTA CANADENSIS (CANADIAN GEESE) MALES & FEMALES ORAL MORE THAN 80 MG/KG
/PURITY 99%/
LD50 LESSER SANDHILL CRANE MALES ORAL 25-50 MG/KG /PURITY 94.5% & 99%/
LD50 ANAS PLATYRHYNCHOS (MALLARD DUCKLINGS) 15-19 DAY-OLD MALES & FEMALES ORAL 167
MG/KG (95% CONFIDENCE LIMIT 11.5-1089 MG/KG) /PURITY 99%/
LD50 PHEASANT (PHEASANT SP) 3-5 MONTH OLD FEMALES ORAL 17.7 MG/KG (95% CONFIDENCE LIMIT
12.5-25.0 MG/KG) /PURITY 99%/
LD50 CHUKAR 3-5 MO-OLD FEMALES ORAL 61.6 MG/KG (95% CONFIDENCE LIMIT 47.5-78.6 MG/KG
/PURITY 99%/
LD50 COTURNIX COTURNIX (JAPANESE QUAIL) 2-MO-OLD MALES ORAL 17.8 MG/KG (95% CONFIDENCE
LIMIT 15.0-21.2 MG/KG) /PURITY 94.5%/
LD50 RANA CATESBIANA (BULLFROGS) MALES ORAL MORE THAN 400 MG/KG /PURITY 94.5%/
/CONDITIONS OF BIOASSAY NOT SPECIFIED/
LD50 Quiscalus quiscula (common grackle) oral 13 mg/kg adult
LD50 Corvus brachyrhynchos (crow) oral > 32 mg/kg adult
LC50 Cyprinodon variegatus (sheepshead minnow) juvenile > 1000 ug/l/24 hr at a
salinity of 24 g/kg /99% purity; Conditions of bioassay not specified/
LC50 Leiostomus xanthurus (spot) juvenile 7 ug/l/48 hr at a salinity of 26 g/kg /99%
purity; Conditions of bioassay not specified/
LC50 Fundulus similis (longnose killifish) 3.2 ug/l/48 hr at a salinity of 24 g/kg /99%
purity; Conditions of bioassay not specified/
LC50 Poecilia reticulata (guppy) 220 ug/l/48 hr /Technical; Conditions of bioassay not
specified/
LC50 Anopheles freeborni (mosquito) 4th instar 0.9-7.0 ug/l/24 hr
LC90-95 Hydropsyche pellucidula (trichloptera) > 0.5 ppm/1 hr /Conditions of
bioassay not specified/
LC90-95 Simulium ornatum (diptera) 0.05-0.1 ppm/1 hr /Conditions of bioassay not
specified/
LC50 Palaemon macrodactylus (korean shrimp) 0.01; 0.25 ug/l/96 hr /Conditions of
bioassay not specified/
TL50 Palaemon macrodactylus (korean shrimp) 0.01 (0.002-0.046) ppm/96 hr intermittent
flow lab bioassay
LC90-95 Bactis rhodani (ephimeroptera) 0.01-0.02 ppm/1 hr /Conditions of bioassay not
specified/
LC90-95 Brachycentrus subnubilis (trichoptera) 0.2-0.5 ppm/1 hr /Conditions of bioassay
not specified/
LC50 Gammarus lacustris (crustacean) 0.11 ug/l/96 hr /Conditions of bioassay not
specified/
LC50 Gammarus fasciatus (crustacean) 0.32 ug/l/96 hr /Conditions of bioassay not
specified/
LC50 Cymatogaster aggregata (shiner perch) 3.5; 3.7 ug/l/96 hr /Conditions of bioassay
not specified/
LC50 Salmo gairdneri (rainbow trout) 15 ug/l/96 hr at 7.2 deg C; 51 ug/l/96 hr at 1.6
deg C /Technical material/
LD50 Periplaneta americana (American cockroach) 5.7 ug/g/24 hr nymph; 0.67 ug/insect/24
hr adult /Topical application/
LD50 Blatella germanica (German cockroach) adult male 1.92 ug/g (0.092 ug/insect)/24 hr
/Topical application/
LD50 Leptocoris trivittatus (Boxelder bug) >4.9 ug/g/24 hr, >0.2 ug/insect nymph,
/Topical application/
LD50 Schizaphis graminum (green bug) <41.6 ug/g/24 hr, <0.5 ug/insect adult
/Topical application/
LD50 Sinea diadema (Assassin bug) <0.5 ug/insect/24 hr /Topical application/
LD50 Leptinotarsa decemlineata (Colorado potato beetle) > 2.0 ug/insect/24 hr larva
/Topical application/
LD50 Apis mellifera (honeybee) approx 1.14 ug/bee (as dust) adult worker /Topical
application/
LD50 Musca domestica (housefly) 2.2 ug/g/24 hr, 0.075 ug/fly adult female /Topical
application/
LD50 Stomoxys calcitrans (stable fly) 1.5 ug/g/24 hr, 0.024 ug/fly adult female; 1.13
ug/g/24 hr, 0.093 ug/fly adult male /Topical application/
LC50 Culex pipens (mosquito) 4th instar 1.2 ug/l/24 hr /Technical material/
LC50 Aedes species (mosquito) 4th instar 0.5-3.5 ug/l/24 hr /Technical material/
LC50 Aedes aegypti (mosquito) 2nd instar 0.0011 ug/l/24 hr; 4th instar 0.0014 ug/l/24
hr /Technical material,96%/
LC50 Aedes aegypti (mosquito) 3rd, 4th instar, 10 ug/l/18 hr /Technical material,96%/
LC50 Belostoma sp (giant water bug) adult, 15 ug/l/24 hr /Technical material/
LC50 Hygrotus sp (predaceous diving beetle) adult, 40 ug/l/24 hr /Technical material/
LC50 Laccophilus decipiens (predaceous diving beetle) adult, 4.6 ug/l/24 hr /Technical
material/
LC50 Thermonectus basillaris (predaceous diving beetle) 6 ug/l/24 hr /Technical
material/
LC50 Berosus styliferus (water scavenger beetle) adult 9 ug/l/24 hr /Technical
material/
LC50 Hydrophilus triangularis (water scavenger beetle) larva, 20 ug/l/24 hr; 30 ug/l/24
hr, adult /Technical material/
LC50 Tropisternus lateralis (water scavenger beetle) larva, 52 ug/l/24 hr; Adult, 8
ug/l/24 hr /Technical material/
LC50 Daphnia sp (cladoceran) 0.88 ug/l/4 hr /Encapsulated formulation, conditions of
bioassay not specified/
LC50 Hyalella azteca (amphipod) 1.28 ug/l/24 hr /Encapsulated formulation/
LC50 Ephemerella sp (mayfly) 0.33 ug/l/72 hr /Encapsulated formulation/
LC50 Neoplea striola (pygmy backswimmer) 0.97 ug/l/144 hr /Encapsulated formulation/
TSCA Test Submissions:
Chlorpyrifos (CAS # 2921-88-2) was evaluated
for acute oral toxicity in fasted Fischer 344-derived CDF albino rats (6/sex/group)
receiving doses of 250, 500, 1000, and 2000 mg/kg by oral gavage. Like female groups also
received the low doses of 63 and 130 mg/kg, while 2 additional groups of males received
doses of 630 and 800 mg/kg bodyweight. Mortality associated with treatment occurred from
Day 2 to Day 4 post-gavage and, based on the moving average method of Thompson and Weil,
was consistent with oral LD50's (with 95% confidence limits) of 774 (687-913) and 235
(164-386) mg/kg bodyweight, respectively, for male and female rats. During 14-day
post-gavage observation, all levels of treatment were associated with signs of toxicity
including lethargy, rough hair coat, anorexia, diarrhea, excess salivation, watery eyes,
labored or rapid shallow breathing, body tremors, and convulsions. All surviving rats
gained weight during observation and lacked any treatment-related gross lesions upon
necropsy. Accumulated secretions about periocular, perinasal and perioral hair, and fluid
fecal-soiled perineum characterized the nonspecific lesions among male and female
decedents. Internally, lesions of the gastrointestinal tract were more common among female
lethalities, and included decreased ingesta with gaseous distention, peritonitis, and
gastric hyperemia with erosions, ulcers and hemorrhage. Isolated cases of thymic atrophy
or lobular irregularities of the liver, and thymic hemorrhage were also reported in the
male study victims.
Chlorpyrifos (CAS # 2921-88-2) was evaluated
for eye irritation in 9 New Zealand white rabbits administered 0.1 mL instillations in
right eye (6/9) or left eye (3/9) conjunctival sacs, the untreated eyes serving as
controls. Following a 30-minute exposure, the 3 treated left eyes were rinsed and the
rabbits' right eyes treated as before, but left unwashed for the duration of study. All
rabbits blinked excessively upon instillation of the test material indicating minimal
discomfort, however no further signs of irritation were noted at any of 5 interval
examinations for conjunctival, corneal, or iridic changes throughout 8-day post-treatment
observation.
Chlorpyrifos (CAS # 2921-88-2) was evaluated
for primary dermal irritation in 6 New Zealand white rabbits administered 0.5 mL
percutaneous applications upon both abraded and intact sites under semi-occluded wrap for
24 hours. The irritative response to treatment was characterized by moderate erythema,
slight to moderate edema, superficial chemical burn (4/6), and irreversible burn (2/6)
which, by test criteria, established chlorpyrifos
as dermally corrosive in rabbits.
Chlorpyrifos (CAS # 2921-88-2) was evaluated
for acute dermal toxicity in New Zealand white rabbits (2/sex/dose level) administered
undiluted percutaneous applications of 250, 500, 1000, 2000, and 4000 mg/kg upon clipped
trunks under occluded wrap. After 24 hours, all application sites were undressed and
thoroughly washed of any test material for immediate evaluation of any irritative
reactions. Rabbits were also observed frequently throughout the exposure and weekly
thereafter for any signs of systemic toxicity. Mortality from Day 3 to Day 6 was
consistent with an acute dermal LD50 of 1303 (736-3057, 95% confidence limits) mg/kg
bodyweight, based on a moving average method of Thompson and Weil. Irritative signs
included slight to marked erythema, slight to moderate edema, and slight necrosis. All
treated rabbits exhibited lethargy, and 1/4 of the 250 mg/kg exposure also demonstrated
hypersensitivity 4.5 hours post-treatment. Other overt signs of toxicity included
hyperemia or congestion at the application site, perioral matting of fur due to excessive
salivation, and perineal soiling. Upon necropsy, all rabbits exhibited treatment-related
gastrointestinal lesions including gastric hemorrhage and erosions, decreased ingesta,
mucous or gas, fluidity of lower bowel contents, and/or cecal petechial hemorrhage. Among
2000 and 4000 mg/kg rabbits, livers with small pale foci or an exaggerated lobular pattern
were also observed. Local reactions persisted in 2 rabbits surviving 3 weeks
post-treatment and were characterized by slightly roughened skin and flaky debris at the
application sites.
Subchronic dermal toxicity was evaluated in a group of 5 Mongrel and Beagle dogs (sex
not reported) treated with an aerosol spray of Dursban
(directed toward the hair roots; sprayed for 30 seconds) one time/day, 5 days/week fora
total of 10 applications. There were no treatment-related mortalities, clinical findings,
body weight changes, changes in food consumption rates, hematological findings, or
clinical chemistry findings. No additional parameters were evaluated.
The effect of DURSBAN (CAS No. 2921-88-2)
dust and aerosols on erythrocyte and plasma cholinesterase levels was evaluated in 3
humans during inhalation exposure periods of approximately 30 seconds in duration in a
given day. The number of exposure periods over 14 consecutive days ranged between 3 and 10
for the 3 individuals. Air concentrations were not reported, and the 3 exposed individuals
wore different types of protective clothing and masks. Pre-exposure cholinesterase levels
were obtained to serve as controls for the respective subjects. An apparent but not
statistically significant decrease in plasma cholinesterase levels was observed in all 3
subjects 14 days after the initial exposure. This decrease disappeared by 56 days
following the initial exposure in all 3 subjects. Erythrocyte cholinesterase levels were
reported to be normal after exposure. No clinical signs were reported either during or
after the exposures.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
A metabolite was recovered from the liver of a /61 yr old man/ who had ingested chlorpyrifos. It was similar to the parent compound,
except for substitution of a methylthio- (SCH3) group for a chlorine on the pyridinol
ring.
BIOTRANSFORMATION OF DURSBAN AFFORDS UP TO
80% OF DOSE AS 3,5,6-TRICHLORO-2-PYRIDYL PHOSPHATE & UP TO 20% AS
3,5,6-TRICHLORO-2-PYRIDINOL.
CRANBERRY BEANS WERE GROWN IN NUTRIENT SOLN CONTAINING 50 PPM (36)CL-DURSBAN.
... CHROMATOGRAPHY OF PLANT EXTRACTS INDICATED PRESENCE OF 7 METABOLITES. OF THESE, 4 WERE
IDENTIFIED AS: 3,5,6-TRICHLORO-2-PYRIDYL PHOSPHATE; 3,5,6-TRICHLORO-2-PYRIDINOL; ETHYL
3,5,6-TRICHLORO-2-PYRIDYL PHOSPHATE; O-ETHYL-O-3,5,6-TRICHLORO-2-PYRIDYL PHOSPHOROTHIOATE.
RATS METABOLIZED CHLORPYRIFOS ... VERY
RAPIDLY YIELDING MAINLY (90%) URINARY METABOLITES. ... /3,5,6-TRICHLORO-2-PYRIDINOL/
(9.6%) & ITS GLUCURONIDE (72%) WERE MAJOR METABOLITES BUT THEY WERE ACCOMPANIED BY
SMALL AMT (3.6%) OF GLUCOSE CONJUGATE OF ... /PARENT HETEROCYCLE/.
Oxidative desulfurization of chlorpyrifos
gives its oxone, and via oxidation and hydrolysis, trichloropyridole is produced. Although
dechlorination of chlorpyrifos has not been
reported in plants and rat and fish metabolisms, reductive dechlorinated
3-dechlorochlorpyrifos has been identified in insects.
(14)C- & (36)CL-LABELED DURSBAN WAS
APPLIED TO CRANBERRY BEAN & CORN LEAVES. WITHIN 3 DAYS ABOUT 80% OF RADIOACTIVITY WAS
LOST PRESUMBABLY BY VOLATILIZATION. THE REMAINDER WAS SLOWLY METABOLIZED. (36)CL-CHLORIDE
WAS FOUND IN PLANTS, INDICATING DEHALOGENATION OF PYRIDINOL ... ANALYSES ALSO SHOWED
PRESENCE OF 3,5,6-TRICHLORO-2-PYRIDINOL.
CHLORPYRIFOS WAS METABOLIZED TO CHLORPYRIFOS OXON & TO 3,5,6-TRICHLORO-2-PYRIDINOL
BY MOUSE HEPATIC MICROSOMES. FORMATION OF BOTH METABOLITES REQUIRED NADPH, AND WAS
INHIBITED BY CO (CARBON MONOXIDE).
The metabolism of (14)C-chlorpyrifos in
goldfish /exposed/ to the chemical in a static-flow model system ... was investigated. ...
Chlorpyrifos was rapidly absorbed from the water
and degraded by goldfish. Five metabolites were identified: Chlorpyrifos,
ethyl O-3,5,6-trichloro-2-pyridyl phosphorothioate, ethyl O-3,5,6-trichloro-2-pyridyl
phosphate, and 3,5,6-trichloro-2-pyridinol.
... (14)C-chlorpyrifos /metabolism was
investigated using/ Reticulitermes flavipes (subterranean termites). Ten metabolites were
detected, three ... were identified as: chlorpyrifos,
its oxon, and 3,5,6-trichloro-2-pyridinol. ...
Plasma and tissue enzymes are responsible for hydrolysis /of organophosphorus
compounds/ to the corresponding phosphoric and phosphonic acids. However, oxidative
enzymes are also involved in the metabolism of some organophosphorus compounds.
/Anticholinesterase agents/
The organophosphorus anticholinesterase agents are hydrolyzed in the body by a group of
enzymes known as A-esterases or paraoxonases. These enzymes are found in the plasma and
liver and hydrolyze a large number of organophosphorus compounds ... by cleaving the
phosphoester, anhydride, P-F, or P-CN bonds. /Anticholinesterase agents/
Unmetabolized chlorpyrifos at concentrations
of 0.21, 0.47, and 0.08 ppm was found in the blood, brain, and liver, respectively, of a
61 yr old man who survived about 1 day after ingesting the compound accidentally. The
parent compound was not detected in urine, but diethylphosphate, diethylthiophosphate, and
/other hydroxalated/ derivative were found at concentrations of 24.5, 23.6 and 13.8 ppm,
respectively; traces of the first two were found in some tissues.
Absorption, Distribution & Excretion:
MAJOR ELIMINATIVE ROUTE IS VIA KIDNEYS. BIOTRANSFORMATION OF DURSBAN
AFFORDS UP TO 80% OF DOSE AS 3,5,6-TRICHLORO-2-PYRIDYL PHOSPHATE & UP TO 20% AS
3,5,6-TRICHLORO-2-PYRIDINOL. TRACES OF UNCHANGED /DURSBAN/
ARE EXCRETED IN FECES. UNCHANGED DURSBAN
ACCUMULATES IN ADIPOSE TISSUES FROM WHICH IT IS SLOWLY EXCRETED.
WHEN FED TO COWS, SOME UNCHANGED DURSBAN WAS
FOUND IN FECES BUT NOT IN URINE OR MILK. DIETHYLTHIOPHOSPHATE & DIETHYLPHOSPHATE WERE
EXCRETED IN URINE. OXON OCCURRED IN SPRAYED CATTLE.
AFTER SINGLE DOSES OF (36)CL-DURSBAN WERE FED
TO RATS, 90% OF RADIOACTIVITY ... APPEARED IN URINE & 10% IN FECES. ... DURSBAN ... /AND NOT ITS METABOLITES/ SEEMED TO
ACCUMULATE IN TISSUES AND THIS WAS ESSENTIALLY IN FAT.
METABOLISM OF DURSBAN IN FISH WAS STUDIED IN
A TANK ... AFTER EXPOSURE TO DURSBAN, THE FISH
WERE SACRIFICED & THE FISH & SOME WATER EXAMINED BY PAPER CHROMATOGRAPHY. IN
ADDITION TO OXYGEN ANALOG (II) OF DURSBAN, THE
MONOETHYL ANALOG (III) OF DURSBAN & ITS
OXYGEN ANALOG (IV), 3,5,6-TRICHLORO-2-PYRIDYL PHOSPHATE (V), &
3,5,6-TRICHLORO-2-PYRIDINOL (VI) WERE ALSO FOUND. IN THE FISH TISSUES THEMSELVES,
COMPOUNDS II, IV, V, VI WERE FOUND.
HEIFERS FED CHLORPYRIFOS DAILY FOR 30 DAYS @
LOW CONCN (3, 10, 30 & 100 PPM OF FEED) ACCUMULATED NO CHLORPYRIFOS
IN LIVER OR KIDNEYS, BUT SMALL AMT (1-2 PPM) OF THE PARENT HETEROCYCLE WERE PRESENT. OXON
WAS SOUGHT BUT NOT DETECTED BOTH IN THESE ORGANS & IN ADIPOSE TISSUES (WHEREIN SMALL
AMOUNTS OF CHLORPYRIFOS WERE EVIDENT- ABOUT 3
PPM IN CATTLE FED 100 PPM).
NECROPSIES OF CANADIAN GEESE THAT HAD BEEN EXPOSED TO CHLORPYRIFOS
ON A GOLF COURSE SHOWED ACCUMULATION IN GIZZARD AND LIVER.
CHLORPYRIFOS APPEARS TO ACCUMULATE
PREDOMINATELY IN BODY FAT ... IN SWINE, RESIDUES OF CHLORPYRIFOS
ARE FOUND PRIMARILY IN FAT TISSUE FOLLOWING INGESTION OF THE CHEMICAL IN DIET FOR 30 DAYS.
CONCENTRATIONS LESS THAN 0.05 PPM ARE FOUND IN FAT FOLLOWING FEEDING OF 10 PPM CHLORPYRIFOS IN THE RATIONS. WITHIN 7 DAY PERIOD AFTER
WITHDRAWAL OF THE CHEMICAL, RESIDUES DROP TO UNDETECTABLE OR VERY LOW LEVELS. SIMILAR
FINDINGS HAVE BEEN REPORTED IN CHICKENS FED THE DRUG.
Chlorpyrifos ... is rapidly and efficiently
absorbed via the oral, ... dermal, and inhalation routes. /Based on laboratory and
domestic animal studies/
Chlorpyrifos ... readily penetrates the
cuticle of houseflies, thus rapid cuticular uptake rates, in combination with relatively
poor detoxification mechanisms, may explain properties of chlorpyrifos.
Most organophosphate compounds are ... absorbed from skin, conjunctiva,
gastrointestinal tract, & lung. /Organophosphate compounds/
The rate of dermal absorption /of organophosphorus pesticides/ may be ... influenced by
the solvent used. /Organophosphorus insecticides/
Many of /the organophosphorus insecticides/ are excreted in the milk ...
/Organophosphorus insecticides/
Following their absorption, most organophosphorus cmpd are excreted almost entirely as
hydrolysis products in the urine. /Anticholinesterase agents/
TOXICANTS CAN BE ABSORBED BY INHALATION, INGESTION, AND SKIN PENETRATION. ... ALL
UNDERGO HYDROLYTIC DEGRADATION IN LIVER AND OTHER TISSUES, USUALLY WITHIN HR OF
ABSORPTION. DEGRADATION PRODUCTS ARE OF LOW TOXICITY, AND ARE EXCRETED IN URINE AND FECES.
/ORGANOPHOSPHATE CHOLINESTERASE-INHIBITING PESTICIDES/
/THEY/ ... ARE RAPIDLY ABSORBED THROUGH MUCOUS MEMBRANE OF DIGESTIVE SYSTEM,
RESPIRATORY SYSTEM & THE SKIN, & CONVEYED BY THE BLOOD TO VARIOUS BODY TISSUES.
... THE MAIN ROUTE OF ELIMINATION ... /IS/ THE KIDNEYS. /ORGANOPHOSPHORUS PESTICIDES/
Organic phosphorous insecticides are absorbed by the skin, as well as by the
respiratory and GI tracts. Absorption by the skin tends to be slow, but, because the
insecticides are difficult to remove, such absorption is frequently prolonged. Skin
absorption is somewhat greater at higher temperatures and may be much greater in the
presence of dermatitis. /Organic phosphorous pesticides/
Biological Half-Life:
The half-life in aqueous methanolic solution at pH 6 in 1930 days; at pH 9.96 it is 7.2
days.
Mechanism of Action:
The toxicity of chlorpyrifos is probably the
result of metabolic conversion to its oxygen analog, chlorpyrifos-oxon,
and its subsequent inhibition of various enzymes (eg, cholinesterases, carboxylases,
acetylcholinesterases, and mitochondrial oxidative phosphorylases).
Organophosphorus derivatives act by combining with and inactivating the enzyme
acetylcholinesterase (AChE). ... The inactivation of cholinesterase by cholinesterase
inhibitor pesticides allows the accumulation of large amounts of acetylcholine, with
resultant widespread effects that may be ... separated into 4 categories: (1) Potentiation
of postganglionic parasympathetic activity. ... (2) Persistent depolarization of skeletal
muscle ... (3) Initial stimulation following depression of cells of central nervous system
... (4) Variable ganglionic stimulation or blockade ... /Cholinesterase inhibitor
pesticides/
The characteristic pharmacological effects of the anti-ChE agents are due primarily to
the prevention of hydrolysis of ACh by AChE at sites of cholinergic transmission.
Transmitter thus accumulates, and the response to ACh that is liberated by cholinergic
impulses or that is spontaneously released from the nerve ending is enhanced. With most of
the organophosphorus agents ... virtually all the acute effects of moderate doses are
attributable to this action. /Anticholinesterase agents/
The cardiovascular actions of anticholinesterase agents are complex, since they reflect
both ganglionic and postganglionic effects of accumulated ACh on the heart and blood
vessels. The predominant effect on the heart from the peripheral action of accumulated ACh
is bradycardia, resulting in a fall in cardiac output. Higher doses usually cause a fall
in blood pressure, often as a consequence of effects of anticholinesterase agents on the
medullary vasomotor centers of the CNS. /Anticholinesterase agents/
The main feature of the toxic mechanism of organophosphorus pesticides is inhibition of
the esterase enzyme activity, in particular of cholinesterase, which plays an important
physiological part. Organophosphorus pesticides can also indirectly interact with the
biochemical receptors of acetylcholine. /Organophosphorus pesticides/
Phosphorylated enzymes, like acetylated acetylcholinesterase, are esters and may be
hydrolyzed by nucleophilic agents, including water. The rate at which phosphorylated
enzymes are reactivated by water is extremely low, compared to the rate for
acetylcholinesterase combined with acetate. When inhibition is by isopropyl phosphate, the
rate is essentially zero. /Organic phosphorous pesticides/
Organophosphates poison insects and humans primarily by phosphorylation of the
acetylcholinesterase enzyme at nerve endings. /Organophosphate cholinesterase-inhibiting
pesticides/
Organophosphate insecticides ... are potent cholinesterase enzyme inhibitors that act
by interfering with the metabolism of acetylcholine, resulting in the accumulation of
acetylcholine at neuroreceptor transmission sites. Exposure produces a broad spectrum of
clinical effects that are indicative of massive overstimulation of the cholinergic system,
including muscarinic effects (parasympathetic), nicotinic effects (sympathetic and motor),
and CNS effects. These effects present clinically as feelings of headache, weakness,
dizziness, blurred vision, psychosis, respiratory difficulty, paralysis, convulsions, and
coma. Typical findings are given by the mnemonic SLUD (salivation, lacrimation, urination,
and defecation). A small percentage of patients may fail to demonstrate miosis, a classic
diagnostic hallmark. The onset of the clinical manifestation of organophosphate poisoning
usually occurs within 12 hr of exposure. /Organophosphate insecticides/
LIVER RNA & DNA ISOLATED FROM MALE MICE IP INJECTED WITH 2 DOSES (5 & 15 MG/KG
BODY WT) OF LABELED CHLORPYRIFOS WERE
HYDROLYZED. RADIOACTIVITY RESULTING FROM INCORPORATION & ALKYLATION OF RNA & DNA
WAS MEASURED. LABELED 7-ETHYLGUANINE WAS FOUND IN RNA HYDROLYSATE. IN DNA HYDROLYSATE
(14)C7-ETHYLGUANINE WAS MISSING & MAJOR RADIOACTIVITY WAS FOUND IN 2 UNKNOWN PEAKS,
ONE OF WHICH CORRESPONDS TO 3X10-2% OF THE APPLIED DOSE. THE RESULTS INDICATE THAT THE
EXTENT OF ALKYLATION OBTAINED WITH CHLORPYRIFOS
IS HIGH AS COMPARED WITH OTHER ORGANOPHOSPHATES WITH METHYL ESTERS.
Interactions:
ADDITION OF ASCORBIC ACID TO THE DIET (0.5%) ENHANCED THE ACUTE TOXICITY OF LEPTOPHOS, CHLORPYRIFOS & DIAZINON & PROTECTED A NUMBER
OF THE MONITORED SERUM ENZYMES FROM BEING DECREASED EXCEPT FOR LEPTOPHOS.
/The solvent which/ chlorpyrifos /is
dissolved in/ ... may also have significant toxic effects in addition to those associated
with chlorpyrifos.
Some phenothiazines may antagonize & some may potentiate the toxic
anticholinesterase effects of ... /organophosphorus insecticides/. /Organophosphate
cholinesterase inhibitors/
In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of
anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the miotic
(antiglaucoma) & other muscarinic effects of anticholinesterases on the autonomic
& central nervous systems. Tricyclic antidepressants (anticholinergic effects)
antagonize the antiglaucoma (miotic) effects of anticholinesterases in glaucoma. ...
Antihistamines with anticholinergic effects antagonize the miotic (antiglaucoma) & CNS
effects of anticholinesterases. Anticholinesterases potentiate tranquilizing &
behavioral changes induced by antihistamines. The actions of anticholinesterase agents on
autonomic effector cells, & to some extent those on CNS, are antagonized by atropine,
an antidote of choice. Barbiturates are potentiated by anticholinesterases. ...
Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate insecticides
potentiate the effects of other anticholinesterases. /Anticholinesterases/
BARBITURATES ARE POTENTIATED BY ANTICHOLINESTERASES. ALTHOUGH BARBITURATES MAY BE USED
CAUTIOUSLY IN TREATING CONVULSIONS, EXTREME CARE IS ESSENTIAL IN HANDLING POISONINGS DUE
TO ANTICHOLINESTERASES, PARTICULARLY ORGANOPHOSPHORUS PESTICIDES. ECHOTHIOPHATE, A
CHOLINESTERASE INHIBITOR USED AS MIOTIC, POTENTIATES OTHER SUCH INHIBITORS ... USED FOR
OTHER PURPOSES (ADDITIVE EFFECTS) OR POSSIBLY SYNERGISTIC. THOSE EXPOSED TO
ORGANOPHOSPHATE INSECTICIDES MUST TAKE STRICT PRECAUTIONS. ... ORGANOPHOSPHORUS
INSECTICIDES: ADDITIVE ANTICHOLINESTERASE EFFECTS. HAZARDOUS. PATIENTS ON
ANTICHOLINESTERASES (EVEN TOPICAL, SUCH AS EYE DROPS) SHOULD AVOID AREAS WHERE
ORGANOPHOSPHORUS INSECTICIDES ... RECENTLY ... USED. /ANTICHOLINESTERASE/
ANTICHOLINESTERASE (ORGANOPHOSPHORUS) INSECTICIDES ANTAGONIZE POLARIZING MUSCLE
RELAXANTS. PHENOTHIAZINES /AND THIOXANTHENES/: ... MAY ENHANCE TOXIC EFFECTS OF
ORGANOPHOSPHORUS INSECTICIDES. /INSECTICIDES, ORGANOPHOSPHORUS/
Pharmacology:
Interactions:
ADDITION OF ASCORBIC ACID TO THE DIET (0.5%) ENHANCED THE ACUTE TOXICITY OF LEPTOPHOS, CHLORPYRIFOS & DIAZINON & PROTECTED A NUMBER
OF THE MONITORED SERUM ENZYMES FROM BEING DECREASED EXCEPT FOR LEPTOPHOS.
/The solvent which/ chlorpyrifos /is
dissolved in/ ... may also have significant toxic effects in addition to those associated
with chlorpyrifos.
Some phenothiazines may antagonize & some may potentiate the toxic
anticholinesterase effects of ... /organophosphorus insecticides/. /Organophosphate
cholinesterase inhibitors/
In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of
anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the miotic
(antiglaucoma) & other muscarinic effects of anticholinesterases on the autonomic
& central nervous systems. Tricyclic antidepressants (anticholinergic effects)
antagonize the antiglaucoma (miotic) effects of anticholinesterases in glaucoma. ...
Antihistamines with anticholinergic effects antagonize the miotic (antiglaucoma) & CNS
effects of anticholinesterases. Anticholinesterases potentiate tranquilizing &
behavioral changes induced by antihistamines. The actions of anticholinesterase agents on
autonomic effector cells, & to some extent those on CNS, are antagonized by atropine,
an antidote of choice. Barbiturates are potentiated by anticholinesterases. ...
Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate insecticides
potentiate the effects of other anticholinesterases. /Anticholinesterases/
BARBITURATES ARE POTENTIATED BY ANTICHOLINESTERASES. ALTHOUGH BARBITURATES MAY BE USED
CAUTIOUSLY IN TREATING CONVULSIONS, EXTREME CARE IS ESSENTIAL IN HANDLING POISONINGS DUE
TO ANTICHOLINESTERASES, PARTICULARLY ORGANOPHOSPHORUS PESTICIDES. ECHOTHIOPHATE, A
CHOLINESTERASE INHIBITOR USED AS MIOTIC, POTENTIATES OTHER SUCH INHIBITORS ... USED FOR
OTHER PURPOSES (ADDITIVE EFFECTS) OR POSSIBLY SYNERGISTIC. THOSE EXPOSED TO
ORGANOPHOSPHATE INSECTICIDES MUST TAKE STRICT PRECAUTIONS. ... ORGANOPHOSPHORUS
INSECTICIDES: ADDITIVE ANTICHOLINESTERASE EFFECTS. HAZARDOUS. PATIENTS ON
ANTICHOLINESTERASES (EVEN TOPICAL, SUCH AS EYE DROPS) SHOULD AVOID AREAS WHERE
ORGANOPHOSPHORUS INSECTICIDES ... RECENTLY ... USED. /ANTICHOLINESTERASE/
ANTICHOLINESTERASE (ORGANOPHOSPHORUS) INSECTICIDES ANTAGONIZE POLARIZING MUSCLE
RELAXANTS. PHENOTHIAZINES /AND THIOXANTHENES/: ... MAY ENHANCE TOXIC EFFECTS OF
ORGANOPHOSPHORUS INSECTICIDES. /INSECTICIDES, ORGANOPHOSPHORUS/
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Chlorpyrifos' production and use as an
insecticide is expected to result in its direct release to the environment. If released to
air, a vapor pressure of 2X10-5 mm Hg at 25 deg C indicates chlorpyrifos
will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase
chlorpyrifos will be degraded in the atmosphere
by reaction with photochemically-produced hydroxyl radicals; the half-life for this
reaction in air is estimated to be 4 hours. Particulate-phase chlorpyrifos
will be removed from the atmosphere by wet and dry deposition. The photolysis half-life of
a thin film of chlorpyrifos on a glass plate
exposed to environmentally significant wavelengths from a UV light was reported to be
52.45 hours. If released to soil, chlorpyrifos
is expected to have low to no mobility based upon Koc values of 995-31,000 reported in a
variety of soils. Volatilization from moist soil surfaces is expected to be an important
fate process based upon a Henry's Law constant of 2.9X10-6 atm-cu m/mole. The
volatilization half-life of chlorpyrifos from 3
moist soils was in the range of 45-163 hours. Chlorpyrifos
is not expected to volatilize from dry soil surfaces based on its vapor pressure.
Biodegradation may be an important environmental fate process based on half-lives of about
2 to 81 days measured in a variety of soils. If released into water, chlorpyrifos
is expected to adsorb to suspended solids and sediment in the water column based upon the
Koc data. Volatilization from water surfaces is expected to be an important fate process
based upon this compound's Henry's Law constant. Estimated volatilization half-lives for a
model river and model lake are 16 and 179 days, respectively, but volatilization may be
attenuated by adsorption. The hydrolysis half-life of chlorpyrifos
in distilled water at 25 deg C was reported as 62 days (pH 4.7), 35 days (pH 6.9) and 22
days pH 8.1. Photolysis may be important in sunlit surface waters based on a half-life of
22 days experimentally determined under midday summer sunlight in California. Measured BCF
values of 100-4,667 in fish suggests bioconcentration in aquatic organisms is high.
Occupational exposure to chlorpyrifos may occur
through inhalation and dermal contact with this compound at workplaces where chlorpyrifos is produced or used. The general
population may be exposed to chlorpyrifos via
inhalation of ambient air and ingestion of food. (SRC)
Probable Routes of Human Exposure:
Those involved in the manufacture, formulation, and application of this pesticide /are
at risk of exposure/.
An occupational study of pest control operators in Texas using chlorpyrifos
determined a mean air concentration of 7540 ng/cu m during an eight hour work shift with a
maximum concn of 27600 ng/cu m measured(1). Airborne levels of chlorpyrifos
in a test room (simulating a typical American home) containing pest control strips
(gradual release) ranged from 100 to 230 ng/cu m over a 30 day period after
application(2). Airborne average concentration of chlorpyrifos
in dormitory rooms receiving spray applications to cracks and crevices were 100, 1100,
1100, 800 and 300 ng/cu m before treatment, immediately after treatment, one day after,
two days after and three days after treatment, respectively(3). Airborne concentration in
rooms receiving either spray or aerosol application of chlorpyrifos
to cracks and crevices ranged from 2700 ng/cu m immediately after application to 50 ng/cu
m three days later(4). Mean levels of 220, 126 and 96 ng/cu m were detected in storage
rooms, offices and vehicles, respectively, of commercial pest control operators(5).
Airborne levels found after spraying cracks and crevices in food-preparation serving areas
were 20-1488 ng/cu m immediately after spraying and 4-361 ng/cu m 24 hours later(5). Five
occupants of an office demonstrated organophosphate intoxication after chloropyrifos
application(6).
NIOSH (NOES Survey 1981-1983) has statistically estimated that 10,493 workers (588 of
these are female) are potentially exposed to chlorpyrifos
in the US(1). The NOES Survey does not include farm workers who may be exposed to chlorpyrifos through its application as an
insecticide. Occupational exposure to chlorpyrifos
may occur through inhalation and dermal contact with this compound at workplaces where chlorpyrifos is produced or used(SRC). The general
population may be exposed to chlorpyrifos via
inhalation of ambient air and ingestion of food products that contain this compound(SRC).
Body Burden:
A urinary metabolite (3,5,6-trichloro-2-pyridinol) of chlorpyrifos
was detected in the urine of 5.8% of 6990 samples collected from the general population
(persons 12-74 years old) during 1976-1980(1). The mean concentration of urinary chlorpyrifos metabolites found in the urine of pest
control operators in Texas was 5.6-8.3 ug/8 hours(2).
Average Daily Intake:
AIR INTAKE: Insufficient data. WATER INTAKE: Insufficient data. FOOD INTAKE: Based on
the FDA's Total Diet Study of food composites collected between Oct 1979 and Sept 1980,
the FDA has estimated the average daily food intake of chlorpyrifos
to be 0.04 ug(1).
The AVDI of chlorpyrifos estimated for
farmworkers was reported as 2.9X10-6 to 2.1X10-4 mg/kg/day(1). The AVDI for children
residing in farmworkers homes was 1.95X10-5 to 4.7X10-5 mg/kg/day(1). The AVDI of chlorpyrifos from 1986-1991 was estimated as 0.0147
ug/kg/day (6-11 months old), 0.0138 ug/kg/day (2 years old), 0.0038 ug/kg/day (14-16 years
old female), 0.006 ug/kg/day (14-16 years old male), 0.0038 ug/kg/day (25-30 years old
female), 0.0038 ug/kg/day (25-30 years old male), 0.0041 ug/kg/day (60-65 years old
female) and 0.0040 (60-65 years old male)(2). The AVDI of chlorpyrifos
from 1984-1986 was estimated as 0.0125 ug/kg/day (6-11 months old), 0.0172 ug/kg/day (2
years old), 0.0044 ug/kg/day (14-16 years old female), 0.006 ug/kg/day (14-16 years old
male), 0.0045 ug/kg/day (25-30 years old female), 0.0039 ug/kg/day (25-30 years old male),
0.0047 ug/kg/day (60-65 years old female) and 0.0046 (60-65 years old male)(3). Based on
data from 78,882 adult females and 38,075 adult males in 1990, the mean AVDI of chlorpyrifos in the US was reported as 0.8 ug/day(4).
Artificial Pollution Sources:
Chlorpyrifos' production and use as an
insecticide(1) is expected to result in its direct release to the environment(SRC).
Environmental Fate:
MODERATELY RESIDUAL ON PLANT SURFACES, QUITE RESIDUAL ON INERT SURFACES /SUCH AS WOOD/.
VOLATILE ENOUGH TO FORM RESIDUES ON NEARBY SURFACES ...
TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 995-31,000
reported in a variety of soils(2), indicates that chlorpyrifos
is expected to have very low to no mobility in soil(SRC). Volatilization of chlorpyrifos from moist soil surfaces is expected to
be an important fate process(SRC) given a Henry's Law constant of 2.9X10-6 atm-cu
m/mole(3). The volatilization half-life of chlorpyrifos
from 3 moist soils was in the range of 45-163 hours using an airstream of 1 km/hr passed
over the soil(2). Chlorpyrifos is not expected
to volatilize from dry soil surfaces(SRC) based on a vapor pressure of 2X10-5 mm Hg at 25
deg C(4). The half-life of chlorpyrifos in
Hessaraghatta soil (pH 7.09, clay content 20.2%) was 2.8-11.5 days, the half-life in
Chettalli soil (pH 6.24, clay content 22.5%) was 10-25.1 days and the half-life in Bellary
soil (pH 9, clay content 33.2%) was 1.6-8.7 days(5). The half-life of chlorpyrifos
in a field measurement using a sandy soil was 81 days(6).
AQUATIC FATE: Based on a classification scheme(1), Koc values of 995-31,000 reported in
a variety of soils(2), indicates that chlorpyrifos
is expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from
water surfaces is expected(3) based upon a Henry's Law constant of 2.9X10-6 atm-cu
m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization
half-lives for a model river and model lake are 16 and 179 days, respectively(SRC), but
adsorption may attenuate this process. In a laboratory study, 50 ppb of chlorpyrifos
added to 10 liters of water was volatilized 85% in 24 hours(2). The hydrolysis half-life
of chlorpyrifos in distilled water at 25 deg C
was reported as 62 days (pH 4.7), 35 days (pH 6.9) and 22 days pH 8.1(5). According to a
classification scheme(6), BCF values of 100-4,667 measured in fish(2) suggests that
bioconcentration in aquatic organisms is high. In a shake-flask screening test similar to
a river die-away test, chlorpyrifos degraded
about 40% faster in active (natural) water as compared to the same water which had been
sterilized with formalin(7). The reported half-life in active water was 24.5 days and with
sterilzed water was 35 days(7).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), chlorpyrifos,
which has a vapor pressure of 2X10-5 mm Hg at 25 deg C(2), is expected to exist in both
the vapor and particulate phases in the ambient atmosphere. Vapor-phase chlorpyrifos
is degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals(SRC); the half-life for this reaction in air is estimated to be 4 hours(SRC),
from its rate constant of 9.2X10-11 cu cm/molecule-sec at 25 deg C(3) determined using a
structure estimation method(3). Particulate-phase chlorpyrifos
will be removed from the atmosphere by wet and dry deposition(SRC). The photodegradation
half-life of a thin film of chlorpyrifos on a
glass plate exposed to environmentally significant wavelengths from a UV light was
reported to be 52.45 hours(4).
Environmental Biodegradation:
HALF-LIFE OF CHLORPYRIFOS IN SEDIMENT-WATER
STUDIES RANGED FROM 1.2 TO 34 DAYS & WERE IN THE FOLLOWING ORDER OF INCREASING
PERSISTENCE: METHYL PARATHION, PERMETHRIN, BENTHIOCARB, AC 222,705, CHLORPYRIFOS,
& FENVALERATE. AFTER TERMINATION OF THE EXPOSURE, EACH INSECTICIDE WAS DEPURATED BY
OYSTERS TO NONDETECTABLE CONCENTRATIONS WITHIN 1 WK.
Measured half-life of 4 weeks (clay loam) and 12 weeks (silt loam) in non-sterile soils
versus 24 weeks in both soils sterilized by autoclaving was indicative of significant
biodegradation(1). Half-lives of one week (sandy loam) and 2.5 weeks (organic) in
non-sterile soils versus half-life of 17 and 40 weeks, respectively, in the sterilized
soils(2). After 4 weeks of incubation, 33-38% of applied chlorpyrifos
was degraded in a clay loam sterilized by autoclaving or gamma irradiation while 62% was
degraded in the non-sterile soil(3). No significant difference in the degradation rate was
observed in a natural water versus the natural water which had been sterilized(4). The
degradation rate in non-sterile sandy loam and muck soils was found to be significantly
faster than in the sterilized soils with the degradation rate in non-sterile soil
decreasing with a decrease in temperature (3 to 28 deg C) and variable with moisture
content(5,6). The half-life of chlorpyrifos in a
sea water-sediment system was 24 days but was well in excess of the 28 day experimental
period when the system was sterilized with formalin(7). In a shake-flask screening test
similar to a river die-away test, chlorpyrifos
degraded about 40% faster in active (natural) water as compared to the same water which
had been sterilized with formalin(8). The reported half-life in active water was 24.5 days
and in sterilized water was 35 days(8).
After applying 300 ppm chlorpyrifos to
autoclaved soil, approximately 80% remained after 30 days, but only 50% remained in a
non-sterile soil(1). The half-life of chlorpyrifos
in Hessaraghatta soil (pH 7.09, clay content 20.2%) was 2.8-11.5 days, the half-life in
Chettalli soil (pH 6.24, clay content 22.5%) was 10-25.1 days and the half-life in Bellary
soil (pH 9, clay content 33.2%) was 1.6-8.7 days(2). The half-life of chlorpyrifos
in a field measurement using a sandy soil was 81 days(3).
Environmental Abiotic Degradation:
The hydrolysis half-life of chlorpyrifos at
20 deg C buffered solution was measured to be 53.0 days at pH 7.4 and 120 days at pH
6.1(1,2). At 25 deg C, the hydrolysis rate was found to be relatively independent of pH
from pH 1 to pH 7 with a half-life of about 78 days(3). In buffered distilled water,
half-lives of 62.7, 35.3, and 22.8 days were measured at pH 4.7, 6.9, and 8.1,
respectively at 25 deg C; half-lives of 210, 99,and 54 days were measured at pH 4.7, 6.9,
and 8.1, respectively at 15 deg C(4). The products of the aqueous hydrolysis of chlorpyrifos include 3,5,6-trichloro-2-pyridinol and
various trichloropyridyl phosphorothioates(4). The aqueous hydrolysis of chlorpyrifos
is catalyzed significantly by the presence of Cu(+2) ions(4,5,6,7); the addition of Cu(+2)
ions to both a distilled water and natural water solution of chlorpyrifos
at pH 8.2-8.3 lowered the half-lives from several weeks to less than one day(7). Chlorpyrifos hydrolyzed 16 times faster in natural
canal water containing metal ions than in distilled water at the same pH and
temperature(4); however, the level of catalyzing metal ions present in most natural waters
is about an order of magnitude lower than necessary to enhance the hydrolysis rate(8). The
hydrolysis half-life in three different natural waters at 25 deg C was measured to be
about 48 days with metal catalysis unimportant(8). The neutral and acid rate of hydrolysis
of chlorpyrifos was not significantly altered
when absorbed to sediments in laboratory studies as compared to hydrolysis in natural
water only; however, the hydrolysis rate was retarded somewhat under alkaline conditions
in the sorbed-state(8).
The rate constant for the vapor-phase reaction of chlorpyrifos
with photochemically-produced hydroxyl radicals has been estimated as 9.2X10-11 cu
cm/molecule-sec at 25 deg C(SRC) using a structure estimation method(1). This corresponds
to an atmospheric half-life of about 4 hours at an atmospheric concentration of 5X10+5
hydroxyl radicals per cu cm(1). The hydrolysis half-life of chlorpyrifos
in distilled water at 25 deg C was reported as 62 days (pH 4.7), 35 days (pH 6.9) and 22
days pH 8.1 (2). A 16-fold rate enhancement was demonstrated in canal and pond water at 25
deg C with the following hydrolysis products identified: 3,5,6-trichloro-2-pyridinol;
O-ethyl,O-hydrogen-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate;
O,O-dihydrogen-O-(3,5,6-trichloro-2-pyridyl)phosphorothioate(2). Reported hydrolysis
half-lives of 120 and 53 days were reported at pH 6.1 and 7.4, respectively(3). It was
also noted that the aqueous hydrolysis of chlorpyrifos
may be enhanced significantly by the presence of dissolved copper cations(3). It was
reported that chlorpyrifos (2.8 ppm) was
completely hydrolyzed within 24 hours in an aqueous methanol (50%) solution containing
1X10-4 mols/l copper(II)(3). Limited hydrolysis occurred in the presence of magnesium
chloride and negligible hydrolysis was observed for a variety of other metal salts
tested(3). The environmental significance of these results are limited since natural
concns of metal cations are low. Chlorpyrifos
absorbs light greater than 295 nm and photolysis has been observed in air and aqueous
environments(3). Based on laboratory experimental data, the following photolysis
half-lives in water at 40 deg N latitude have been estimated: mid-summer surface
conditions - 31 days, mid-winter surface conditions - 345 days, mid-summer 1 m depth pure
water - 43 days, mid-summer 1 m depth river water with average light attenuation - 2.7
years(4). Photolysis half-life of 22 days in pure water (at surface conditions)
experimentally determined under midday summer sunlight in California(5). The photochemical
conversion half-life in air has been reported to be 2.27 hours(6). The photodegradation
half-life of a thin film of chlorpyrifos on a
glass plate exposed to environmentally significant wavelengths from a UV light was
reported to be 52.45 hours(7). 3,5,6-Trichloro-2-pyridinol was identified as a
photodegradation product of chlorpyrifos in both
air and aqueous environments(3). The following compounds were identified as
photodegradation products of chlorpyrifos in
either hexane or methanol solution: O,O-diethyl
O-(3,5-dichloro-2-pyridyl)phosphorothioate, O,O-diethyl
O-(3,6-dichloro-2-pyridyl)phosphorothioate, O,O-diethyl
O-(5,6-dichloro-2-pyridyl)phosphorothioate and O,O-diethyl
O-(monochloro-2-pyridyl)phosphorothioate(3).
Environmental Bioconcentration:
A measured log BCF value for chlorpyrifos of
2.67 was determined from a 35-day flowing-water study using mosquito fish (1). An
experimental log BCF value of 2.50 was determined from a static ecosystem study using
mosquito fish(2). In a review of the environmental fate of chlorpyrifos,
BCF values of 100-4,667 were reported in a variety of fish under field conditions(3). BCF
values of 58-5,100 were reported in a variety of fish using flow-through aquariums(3).
According to a classification scheme(4), this BCF data suggests that bioconcentration in
aquatic organisms is moderate to very high(SRC).
Soil Adsorption/Mobility:
Soil sorption constants based on the organic carbon content of 15 pesticides were
measured using 2 soils (clay loam and high clay) at 0.01, 0.1 and 1.0 ppm pesticide. The
soil sorption coefficients ((ug pesticide/g soil)/(ug pesticide/g water)) for chlorpyrifos were 116.2 + or - 66.2 in clay loam and
13.4 + or - 1.5 in high clay soil. The soil sorption constants were 2740 and 995
respectively, with a mean of 1868. Significant correlations were found between organic
carbon content and water solubility, octanol/water partition coefficient, retention time
in reversed phase high pressure liquid chromatography and molecular wt.
Koc values of 4,381 to 6,129 were measured in four different soils with organic carbon
content varying from 0.88 to 6.55%; virtually complete adsorption was noted in soil of
organic content of 31.65%(1). Average Koc values of 6,070 were determined in soil column
studies using 3 agricultural soils(2). An experimental Koc value of 13,600 was reported
for a single soil type(3). Greater than 99% of chlorpyrifos
applied to a loam soil remained in the upper 2.5 cm soil layer after periodic irrigation
with overhead sprinklers indicating relative immobility(4). In laboratory studies using a
sandy loam soil, chlorpyrifos was determined to
be relatively immobile(5). In a simulated ecosystem study, the chlorpyrifos
concentration in the sediment was as much as 4 times greater than in the water-phase(6). Chlorpyrifos applied to a natural pond was observed to
rapidly absorb to bottom sediments(7). In a review of the environmental fate of chlorpyrifos, Koc values of 995-31,000 were reported
in a variety of soils(8). According to a classification scheme(9), this Koc data suggests
that chlorpyrifos is expected to have low to no
mobility in soils(SRC).
Volatilization from Water/Soil:
(14)C- & (36)CL-LABELED DURSBAN WAS
APPLIED TO CRANBERRY BEAN & CORN LEAVES. WITHIN 3 DAYS ABOUT 80% OF RADIOACTIVITY WAS
LOST PRESUMBABLY BY VOLATILIZATION.
The Henry's Law constant for chlorpyrifos is
2.9X10-6 atm-cu m/mole(1). This Henry's Law constant indicates that chlorpyrifos
is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the
volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3
m/sec)(2) is estimated as 16 days if adsorption is ignored(SRC). The volatilization
half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2)
is estimated as 179 days if adsorption is ignored(SRC). The volatilization half-life from
a model pond is 17 years if adsorption is considered(3). In a laboratory study, 50 ppb of chlorpyrifos added to 10 l of water was volatilized
85% in 24 hours(3). Chlorpyrifos' Henry's Law
constant(1) indicates that volatilization from moist soil surfaces may occur(SRC). The
volatilization half-life of chlorpyrifos from 3
moist soils was in the range of 45-163 hours using an airstream of 1 km/hr passed over the
soil(4). The volatility of chlorpyrifos was
studied under field conditions(5,6). Following application of 1.5 kg/ha, the highest flux
rates were observed in the first few hours after application, with particularly large
values when heavy dew was present on the surface(5,6). Flux rates usually declined to
non-detectable levels by about noon each day(5,6). Chlorpyrifos
is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of
2X10-5 mm Hg(7).
Environmental Water Concentrations:
Waters from 21 wells and 2 springs located in a typically farmed, mostly agricultural
PA watershed (the Mahantango Creek Watershed) were analyzed for 11 pesticides, including chlorpyrifos. Pesticides were selected according to a
farm use survey, and samplings were made during Dec 1985, Aug 1986, and Mar/Apr 1987. Chlorpyrifos was applied in 1985 but not in 1986. No chlorpyrifos was found in any sampling (< 4 ng/l).
GROUNDWATER: Chlorpyrifos was detected at a
concn of 0.04 ug/l in groundwater of a golf course in Cape Cod, MA(1).
SURFACE WATER: Chlorpyrifos was detected in 3
of 949 water samples taken from 11 agricultural watersheds in southern Ontario during
1975-1977 at concentrations ranging from less than 0.01 ppb to 1.6 ppb(1,2). Chlorpyrifos was qualitatively identified in waters
from Lake Erie and Lake St. Clair(3). Chlorpyrifos
was detected in 5 out of 6 samples from the Segre River, Spain at 0.01 ug/l(4). Chlorpyrifos was detected at concns of less than 1
ng/l in the San Joaquin River and its tributaries(5). Chlorpyrifos
was detected at concns of 0.045 to 1.67 ng/l in the Susquhanna River, VA(6). Chlorpyrifos was detected at 0-0.6 ppb in surface
water in golf courses in North Carolina(7). Chlorpyrifos
was detected in the South Platte River, CO at a max concn of 0.22 ug/l in agricultural
areas and a max concn of 0.30 ug/l in urban areas(8).
RAIN/FOG: Chlorpyrifos was detected in fog
deposition from San Joaquin Valley, CA at concns of 17.8-171.9 ng/cu m and an avg concn of
64.9 ng/cu m(1). Chlorpyrifos was detected in
atmospheric deposition at trace concns in Regina, Saskatchewan(2).
Effluent Concentrations:
Chlorpyrifos was identified, not quantified,
in water runoff from golf courses in Singapore where it was applied as an insecticide(1). Chlorpyrifos was measured at concns of less than 0.025
to 0.26 ug/l in stormwater runoff in California(2).
Sediment/Soil Concentrations:
Chlorpyrifos was detected in suspended
particulates of the San Joaquin River and its tributaries at less than 0.5 to 153 ng/l and
sediment at concns of less than 0.5 to 7.2 ng/g(1). Chlorpyrifos
was detected in sediment of the Chesapeake Bay at a concn of 0.0016 ug/kg(2). Chlorpyrifos was detected at a concn of 1.106 ppb in
soil near a factory in Kafr El-Zayat, Egypt(3). Chlorpyrifos
was detected in soil from households of farmers and farm workers at a mean concn of 17
ng/g and in soil from non agriculturally employed households at a mean concn of 11
ng/g(4). Chlorpyrifos was detected at mean
concns of 0-40 ng/g in sediment of Sarasota Bay, FL(5).
Atmospheric Concentrations:
INDOOR AIR: Chlorpyrifos was detected at
concns of 0.3-70.3 ug/cu m in dorm rooms 1-7 days following its application for flea
control(1). Chlorpyrifos was detected in 12
homes located in Bloomington, IN at concns of 0.2-150 ng/cu m(2). Chlorpyrifos
was detected in 4 homes in Bloomington, IN at concns of 0-89 ng/cu m(3). Chlorpyrifos
was detected in indoor air at mean concns of 366.6 ng/cu m (summer), 205.4 ng/cu m
(spring) and 120.3 ng/cu m (winter) in Jacksonville, FL(4). Chlorpyrifos
was detected in indoor air at mean concns of 9.8 ng/cu m (spring) and 5.1 ng/cu m (winter)
in Springfield/Chicopee, MA(4).
URBAN/SUBURBAN: Chlorpyrifos was positively
identified in 14 of 123 ambient air samples collected at ten US locations in 1980 with a
mean concn of 2.1 ng/cu m and a max concn of 100 ng/cu m(1). Chlorpyrifos
was detected in the atmosphere of the Chesapeake Bay at concns of 2 to 95 pg/cu m(2). Chlorpyrifos was detected in the air above the
Mississippi River from New Orleans, LA to St Paul, MN at concns of 0.17 to 1.6 ng/cu m(3).
Typical outdoor concns of chlorpyrifos were
reported as 200 ng/cu m and typical indoor air concns were reported as 1 ng/cu m(4). Chlorpyrifos was detected at mean concns of 16.7 ng/cu
m (summer), 3.5 ng/cu m (spring) and 2.5 ng/cu m (winter) in Jacksonville, FL(5). Chlorpyrifos was detected at mean concns of 13.9 ng/cu
m (spring) and less than 0.05 ng/cu m (winter) in Springfield/Chicopee, MA(5). Chlorpyrifos was detected in personal air of residents
of Jacksonville, Fl at concns of 118.2-280.4 ng/cu m and in personal air of residents of
Springfield/Chicopee, MA at 5.9-7.5 ng/cu m(5).
Food Survey Values:
Chlorpyrifos was detected in 2 of 360 food
composites collected between Aug 1972 and July 1973 during the FDA's Total Diet Study at a
concentration of 0.005 ppm in one fruit composite and 0.003 ppm in one grain-cereal
composite(1). It was detected in 4 of 240 food composites collected between Oct 1977 and
Sept 1978 during FDA's Total Diet Study at concentrations of 0.006-0.009 ppm in 3
grain-cereal composites and 0.012 ppm in one fruit composite(2). It was detected in 9 of
240 adult food composites collected between Oct 1978 and Sept 1979 during the FDA's Total
Diet Study at concns of trace to 0.008 ppm(3); it was detected in one of 110 infant and
toddler food composites collected between Oct 1978 and Sept 1979 a concentration of 0.004
ppm in one grain-cereal composite(4). It was detected in 2 of 240 food composites
collected between Oct 1979 and Sept 1980 during the FDA's Total Diet Study at a
concentration of 0.002 ppm in one grain-cereal composite and at a trace level (below
0.0001 ppm) in one garden fruit composite (5). In a summary of monitoring results from
three Federal programs (FDA Total Diet Study, FDA Monitoring Program, USDA National
Residue Program), chlorpyrifos was reported as
infrequently detected in various food products such as fruit, vegetables, grains, and
processed foods(6). Chlorpyrifos was identified,
not quantified, in 3% of adult foods during an FDA survey from 1978-1982(7) and in 8% of
adult foods from 1982-1986(8). During an FDA survey of domestic foods from 1985-1991 chlorpyrifos was detected in 283 of 2,464 apples at a
max concn of 0.9 ppm, 3 of 2,739 milk samples at trace concns, 297 of 862 oranges at a max
concn of 0.76 ppm and 3 of 571 pears at a max concn of 0.01 ppm(9). In an FDA survey of
imported foods from 1985-1991, chlorpyrifos was
detected in 87 of 735 apples at a max concn of 0.11 ppm, 121 of 1,097 bananas at a max
concn of 0.25 ppm, 1 of 64 orange juice samples at trace concns, 17 of 474 oranges at a
max concn of 0.28 ppm and 25 of 816 pears at a max concn of 0.06 ppm(9). In an FDA survey
of children foods, chlorpyrifos was detected in
cereals (max concns 0.001-0.003 ppm), meat dinners (max concn 0.0008-0.004 ppm), poultry
dinners (max concns 0.004-0.005 ppm), deserts (max concns 0.002-0.003 ppm), fruits and
juices (max concn 0.001-0.006 ppm) and vegetables (max concns 0.001-0.004 ppm)(9). Chlorpyrifos was detected in citrus fruit from Spain
in 1994-1995 at concns of 0.1-0.6 mg/kg(10). In an FDA survey of foods in 1993-1994, chlorpyrifos was detected in 132 of 769 domestic
apples at a max concn of 0.21 ppm and in 98 of 1,062 imported apples at a max concn of
0.05 ppm(11).
Fish/Seafood Concentrations:
Chlorpyrifos was identified, not quantified,
from fish in the San Francisco Bay(1). Chlorpyrifos
was identified, not quantified, in mussels from the Mediterranean coast(2). Chlorpyrifos was detected in zebra mussels at concns
of less than 5 ug/kg and eels at concns of less than 20 ug/kg from the Rhine and Meuse
Rivers, Netherlands(3).
Milk Concentrations:
IN STUDY OF CHLORPYRIFOS RESIDUES IN COW
MILK, PARENT COMPOUND & 3,5,6-TRICHLOROPYRIDINOL WERE PRESENT IN VERY SMALL AMT (ABOUT
0.01 UG/G) FOLLOWING DOSE OF 30 PPM DAILY FOR 2 WK.
Other Environmental Concentrations:
Chlorpyrifos was detected in household dust
at a mean concn of 429 ng/g (12-17,100 ng/g) in homes of farmers and farm workers, it was
detected at a mean concn of 168 ng/g (17-483 ng/g) in household dust of non-agriculturally
employed families(1). Chlorpyrifos was detected
in 67% of household dust samples from 9 states in the US at a mean concn of 0.46 ug/g(2).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances are established for combined residues of the pesticide chlorpyrifos
[(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioate] and its metabolite
3,5,6-trichloro-2-pyridinol in or on the following raw agricultural commodities: almonds;
almonds, hulls; apples; beans, lima; beans, lima forage; beans, snap; beans, snap forage;
beets, sugar, roots; beets, sugar, tops; blueberries; citrus fruits; corn fresh (includes
sweet kernel plus cob with husk removed); cranberries; kiwifruit; mushrooms; onions (dry
bulb); peppers; seed and pod vegetables; sorghum, fodder; sorghum, forage; sorghum, grain;
sunflower, seeds; tomatoes; tree nuts; vegetables, leafy, Brassica (cole); walnuts.
Tolerances with regional registration, as defined in 180.1(n), are established for the
combined residues of chlorpyrifos and its
metabolite 3,5,6-trichloro-2-pyridinol in or on the following raw agricultural
commodities: asparagus; dates; grapes; leeks.
Tolerances with regional registration, as defined in 180.1(n), are established for
residues of the pesticide chlorpyrifos
(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioate in or on the following raw
agricultural commodity (expressed as ppm): alfalfa, forage; alfalfa, hay; bananas, whole;
bananas, pulp with peel removed; bean, forage; broccoli; brussels sprouts; cabbage;
caneberries; cattle, fat; cattle, meat and meat byproducts; cauliflower; cherries; chinese
cabbage; corn, field, grain; corn, forage and fodder; cottonseed; cucumbers; eggs; figs;
goats, fat; goats, meat and meat byproducts; hogs, fat; hogs, meat and meat byproducts;
horses, meat, fat, and meat byproducts; legume vegetables, succulent or dried (except
soybeans); milk, fat; milk, whole; mint, hay; pea forage; peanuts; poultry, meat, fat, and
meat byproducts (including turkeys); pumpkins; radishes; rutabagas; sheep, fat; sheep,
meat and meat byproducts; soybean grain; soybean forage; strawberries; sugarcane; sweet
potatoes; turnip greens; turnips; wheat, grain; wheat, straw; wheat, forage.
Tolerances with regional registration, as defined in 180.1(n), are established for
residues of the pesticide chlorpyrifos
(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl)phosphorothioate) in or on the following
commodities: cherimoya; feijoa (pineapple guava); sapote.
Tolerances are established as follows for residues of the insecticide chlorpyrifos
[O,O-diethyl O-3,5,6-trichloro-2-pyridyl) phosphorothioate] in or on the following raw
agricultural commodities: nectarines; peaches; pears; plums.
A tolerance is established for residues of the pesticide chlorpyrifos
[O,O-diethyl O(3,5,6-trichloro-2-pyridyl)phosphorothioate] in or on the raw agricultural
commodities oats and barley when blended together as a mixture containing not more than
97% oats and not less than 3% barley. Such tolerance applies only to oats that were
treated post-harvest with chlorpyrifos on or
before June 15, 1994. Such tolerance applies only to oats to be used as animal feed or as
a constituent of animal feed. Notwithstanding any other provision of law or regulation,
this tolerance does not authorize the presence of residues of chlorpyrifos
in any human food item made from such treated oats, other than residues resulting from the
use of the oats for animal feed purposes. Such tolerance expires on December 31, 1996.
Tolerances are established for the combined residues of the insecticide chlorpyrifos [O,O-diethyl
O-(3,5,6-trichloro-2-pyridyl) phosphorothioate] and its metabolite
3,5,6-trichloro-2-pyridinol resulting from application of the insecticide to growing crops
as follows: citrus oil and corn oil.
The additive chlorpyrifos may be safely used
in accordance with the following prescribed conditions: (1) applications shall be limited
solely to spot and/or crack and crevice treatment in food handling establishments where
food and food products are held, processed, prepared or served. Contamination of food or
food contact surfaces shall be avoided. Food must be removed or covered during treatment;
(2) spray concentration for spot treatment shall be limited to a maximum of 0.5% of the
active ingredient by weight. A course, low-pressure spray shall be used to avoid
atomization or splashing of the spray; (3) paint-on application for spot treatment shall
be limited to a maximum of 2% of the active ingredient by weight; (4) crack and crevice
treatment shall be limited to a maximum of 2% of the active ingredient by weight.
Equipment capable of delivering a pin stream of insecticide shall be used; (5) application
via adhesive strips shall contain a maximum of 10% by weight of the controlled-release
product in food-handling establishments where food and food products are held, processed,
prepared, or served. A maximum of 36 strips (or 5.15 g of chlorpyrifos)
is to be used per 100 sq ft of floor space. The strips are not to be placed in exposed
areas where direct contact with food, utensils, and food-contact surfaces would be likely
to occur; (6) to assure safe use of the insecticide, its label and labeling shall conform
to that registered by the US EPA, and it shall be used in accordance with such label and
labeling.
A tolerance is established for residues of chlorpyrifos,
per se, in or on all food items (other than those already covered by a higher tolerance as
a result of use on growing crops) in food service establishments where food and food
products are prepared and served, as a result of the application of chlorpyrifos
in microencapsulated form. Application of a microencapsulated product shall be limited
solely to spot and/or crack and crevice treatment in foodhandling establishments where
food and food products are prepared and served. All treatments shall be applied in such a
manner as to avoid contamination of food or food contact surfaces. Spray concentrations
shall be limited to a maximum of 0.5% of the active ingredient by weight. For crack and
crevice treatment, equipment capable of delivering a pin stream of spray directly into
cracks and crevices or capable of applying small amounts of insecticide into cracks and
crevices shall be used. For spot treatment, an individual spot shall not exceed 2 sq ft.
To assure safe use of the insecticide, its label and labeling shall conform to that
registered by the US EPA, and it shall be used in accordance with such label and labeling.
Tolerances are established for residues of the inseciticide chlorpyrifos
resulting from application of the insecticide to growing crops as follows: milling
fractions (except flour) of wheat; mint oil; peanut oil.
As the federal pesticide law FIFRA direct, EPA is conducting a comprehensive review of
older pesticides to consider their health and environmental effects and make decisions
about their future use. Under this pesticide reregistration program, EPA examines health
and safety data for pesticide active ingredients initially registered before November 1,
1984, and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act of 1996. Chlorpyrifos is found on List A, which contains most
food use pesticides and consists of the 194 chemical cases (or 350 individual active
ingredients) for which EPA issued registration standards prior to FIFRA 88. Case No: 0100;
Pesticide type: Insecticide; Registration Standard Date: 09/30/84; Case Status: PreRED -
OPP is reviewing data from the pesticide's producers regarding its human health and/or
environmental effects, or OPP is determining the pesticide's eligibility for
reregistration and developing the RED document. Active ingredient (AI): Chlorpyrifos;
Data Call-in (DCI) Date(s): 1984, 08/28/91, 08/12/93, 03/03/95, 10/13/95; AI Status:
Supported - The producers of the pesticide have made commitments to conduct the studies
and pay the fees required for reregistration, and are meeting those commitments in a
timely manner.
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are required to notify the National Response
Center (NRC) immediately, when there is a release of this designated hazardous substance,
in an amount equal to or greater than its reportable quantity of 1 lb or 0.454 kg. The
toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area
(202) 426-2675. The rule for determining when notification is required is stated in 40 CFR
302.4 (section IV. D.3.b).
Clean Water Act Requirements:
Chlorpyrifos is designated as a hazardous
substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and
further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations
apply to discharges of this substance. This designation includes any isomers and hydrates,
as well as any solutions and mixtures containing this substance.
Federal Drinking Water Guidelines:
EPA 20 ug/l
State Drinking Water Guidelines:
(FL) FLORIDA 21 ug/l
(FL) FLORIDA 70 ug/l /Chlorpyrifos-methyl/
Allowable Tolerances:
Tolerances are established for combined residues of the pesticide chlorpyrifos
[(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioate] and its metabolite
3,5,6-trichloro-2-pyridinol in or on the following raw agricultural commodities:
(expressed in ppm): almonds 0.2; almonds, hulls 12.0; apples 1.5; beans, lima 0.05; beans,
lima forage 1.0; beans, snap 0.05; beans, snap forage 1.0; beets, sugar, roots 1.0; beets,
sugar, tops 8.0; blueberries 2 (of which no more than 1 ppm is chlorpyrifos);
citrus fruits 1.0; corn fresh (includes sweet kernel plus cob with husk removed) 0.1;
cranberries 1.0; kiwifruit 2.0; mushrooms 0.1; onions (dry bulb) 0.5; peppers 1.0; seed
and pod vegetables 0.1; sorghum, fodder 6.0; sorghum, forage 1.5; sorghum, grain 0.75;
sunflower, seeds 0.25; tomatoes 0.5; tree nuts 0.2; vegetables, leafy, Brassica (cole) 2.0
(of which no more than 1.0 ppm is chlorpyrifos);
walnuts 0.2.
Tolerances with regional registration, as defined in 180.1(n), are established for the
combined residues of chlorpyrifos and its
metabolite 3,5,6-trichloro-2-pyridinol in or on the following raw agricultural
commodities: asparagus 0.5 ppm; dates 0.5 ppm (of which no more than 0.3 ppm is chlorpyrifos); grapes 0.5 ppm; leeks 0.5 ppm (of which
no more than 0.2 ppm is chlorpyrifos).
Tolerances with regional registration, as defined in 180.1(n), are established for
residues of the pesticide chlorpyrifos
(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl) phosphorothioate in or on the following raw
agricultural commodity (expressed as ppm): alfalfa, forage 3.0; alfalfa, hay 13.0;
bananas, whole 0.1; bananas, pulp with peel removed 0.01; bean, forage 0.7; broccoli 1;
brussels sprouts 1; cabbage 1; caneberries 1.0; cattle, fat 0.3; cattle, meat and meat
byproducts 0.05; cauliflower 1; cherries 1; chinese cabbage 1; corn, field, grain 0.05;
corn, forage and fodder 8; cottonseed 0.2; cucumbers 0.05; eggs 0.01; figs 0.01; goats,
fat 0.2; goats, meat and meat byproducts 0.05; hogs, fat 0.2; hogs, meat and meat
byproducts 0.25; horses, meat, fat, and meat byproducts 0.25; legume vegetables, succulent
or dried (except soybeans) 0.05; milk, fat 0.25; milk, whole 0.01; mint, hay 0.8; pea
forage 0.7; peanuts 0.2; poultry, meat, fat, and meat byproducts (including turkeys) 0.1;
pumpkins 0.05; radishes 2; rutabagas 0.5; sheep, fat 0.2; sheep, meat and meat byproducts
0.05; soybean grain 0.3; soybean forage 0.7; strawberries 0.2; sugarcane 0.01; sweet
potatoes 0.05; turnip greens 0.3; turnips 1; wheat, grain 0.5; wheat, straw 6; wheat,
forage 3.
Tolerances with regional registration, as defined in 180.1(n), are established for
residues of the pesticide chlorpyrifos
(O,O-diethyl O-(3,5,6-trichloro-2-pyridyl)phosphorothioate) in or on the following
commodities: cherimoya 0.05 ppm; feijoa (pineapple guava) 0.05 ppm; sapote 0.05 ppm.
Tolerances are established as follows for residues of the insecticide chlorpyrifos
[O,O-diethyl O-3,5,6-trichloro-2-pyridyl) phosphorothioate] in or on the following raw
agricultural commodities: nectarines 0.05 ppm; peaches 0.05 ppm; pears 0.05 ppm; plums
0.05 ppm.
A tolerance of 15 ppm is established for residues of the pesticide chlorpyrifos
[O,O-diethyl O(3,5,6-trichloro-2-pyridyl)phosphorothioate] in or on the raw agricultural
commodities oats and barley when blended together as a mixture containing not more than
97% oats and not less than 3% barley. Such tolerance applies only to oats that were
treated post-harvest with chlorpyrifos on or
before June 15, 1994. Such tolerance applies only to oats to be used as animal feed or as
a constituent of animal feed. Notwithstanding any other provision of law or regulation,
this tolerance does not authorize the presence of residues of chlorpyrifos
in any human food item made from such treated oats, other than residues resulting from the
use of the oats for animal feed purposes. Such tolerance expires on December 31, 1996.
Tolerances are established for the combined residues of the insecticide chlorpyrifos [O,O-diethyl
O-(3,5,6-trichloro-2-pyridyl) phosphorothioate] and its metabolite
3,5,6-trichloro-2-pyridinol resulting from application of the insecticide to growing crops
as follows: citrus oil 25.0 ppm and corn oil 3.0 ppm.
A tolerance of 0.1 ppm is established for residues of chlorpyrifos,
per se, in or on all food items (other than those already covered by a higher tolerance as
a result of use on growing crops) in food service establishments where food and food
products are prepared and served, as a result of the application of chlorpyrifos
in microencapsulated form. Application of a microencapsulated product shall be limited
solely to spot and/or crack and crevice treatment in foodhandling establishments where
food and food products are prepared and served. All treatments shall be applied in such a
manner as to avoid contamination of food or food contact surfaces. Spray concentrations
shall be limited to a maximum of 0.5% of the active ingredient by weight. For crack and
crevice treatment, equipment capable of delivering a pin stream of spray directly into
cracks and crevices or capable of applying small amounts of insecticide into cracks and
crevices shall be used. For spot treatment, an individual spot shall not exceed 2 sq ft.
To assure safe use of the insecticide, its label and labeling shall conform to that
registered by the US EPA, and it shall be used in accordance with such label and labeling.
Tolerances are established for residues of the inseciticide chlorpyrifos
resulting from application of the insecticide to growing crops as follows: milling
fractions (except flour) of wheat 1.5 ppm; mint oil 8 ppm; peanut oil 0.4 ppm.
Chemical/Physical Properties:
Molecular Formula:
C9-H11-Cl3-N-O3-P-S
Molecular Weight:
350.59
Color/Form:
White granular crystals
Colorless crystals
Colorless to white crystalline solid [Note: Commercial formulations may be combined
with combustible liquids.]
Odor:
Mild mercaptan odor
Boiling Point:
320 deg F (decomp)
Melting Point:
41-42 deg C
Corrosivity:
Corrosive to copper and brass
Density/Specific Gravity:
1.398 at 43.5 deg C (liquid)
Octanol/Water Partition Coefficient:
log Kow = 5.27
Solubilities:
water solubility = 0.4 mg/l @ 23 deg C
Solubility @ 25 deg C: 1.4 mg/l of water
Solubility @ 25 deg C: 6.5 kg/l acetone
Solubility @ 25 deg C: 7.9 kg/kg benzene
Solubility @ 25 deg C: 6.3 kg/kg chloroform
Solubility @ 25 deg C: 450 g/kg methanol
Solubility @ 25 deg C: 5.9 kg/l in carbon disulfide
Solubility @ 25 deg C: 5.1 kg/l in diethyl ether
Solubility @ 25 deg C: 5.0 kg/l in xylene
Solubility @ 25 deg C: 790 g/l in iso-octanol
Solubility @ 25 deg c: in isooctane 79% wt/wt
Sol in most organic solvents
Spectral Properties:
Intense mass spectral peaks: 97 m/z (100%), 197 m/z (97%), 199 m/z (94%), 314 m/z (64%)
Intense mass spectral peaks: 286 m/z, 349 m/z
UV max: 208, 230, and 290 nm
Vapor Pressure:
2.02X10-5 mm Hg @ 25 deg C
Other Chemical/Physical Properties:
Heat of sublimation 26,800 cal/mol /From table/
Amber solid cake with amber oil /Technical grade/
Henry's Law constant = 2.9X10-6 atm cu-m/mol @ 20 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin
contact. Effects of contact or inhalation may be delayed. Fire may produce irritating,
corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive
and/or toxic and cause pollution.
Fire or explosion: Combustible material: may burn but does not ignite readily.
Containers may explode when heated. Runoff may pollute waterways. Substance may be
transported in a molten form.
Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If
Shipping Paper not available or no answer, refer to appropriate telephone number listed on
the inside back cover. Isolate spill or leak area immediately for at least 25 to 50 meters
(80 to 160 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep
out of low areas.
Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing which is specifically recommended by the manufacturer.
Structural firefighters' protective clothing is recommended for fire situations ONLY; it
is not effective in spill situations.
Evacuation: Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for
800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters
(1/2 mile) in all directions.
Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: Water spray, fog or
regular foam. Move containers from fire area if you can do it without risk. Dike fire
control water for later disposal; do not scatter the material. Do not use straight
streams. Fire involving tanks or car/trailer loads: Fight fire from maximum distance or
use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool
containers with flooding quantities of water until well after fire is out. Withdraw
immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from the ends of tanks. For massive fire, use unmanned hose holders or
monitor nozzles; if this is impossible, withdraw from area and let fire burn.
Spill or leak: Do not touch damaged containers or spilled material unless wearing
appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry
into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent
spreading . Absorb or cover with dry earth, sand or other non-combustible material and
transfer to containers. DO NOT GET WATER INSIDE CONTAINERS.
First aid: Move victim to fresh air. Call emergency medical care. Apply artificial
respiration if victim is not breathing. Do not use mouth-to-mouth method if victim
ingested or inhaled the substance; induce artificial respiration with the aid of a pocket
mask equipped with a one-way valve or other proper respiratory medical device. Administer
oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In
case of contact with substance, immediately flush skin or eyes with running water for at
least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to
substance may be delayed. Ensure that medical personnel are aware of the material(s)
involved, and take precautions to protect themselves.
Skin, Eye and Respiratory Irritations:
May be irritating to skin and eyes.
Flash Point:
82 DEG F (CLOSED CUP) /DURSBAN 4E/
87 DEG F (CLOSED CUP) /LORSBAN 4E/
Fire Fighting Procedures:
If material is on fire or involved in a fire: Extinguish fire using agent suitable for
type of surrounding fire. (Material itself does not burn, or burns with difficulty.) Keep
runoff water out of sewers and water sources.
If material on fire or involved in fire: Do not extinguish fire unless flow can be
stopped or safely confined. Use water in flooding quantities as fog. Solid streams of
water may be ineffective. Cool all affected containers with flooding quantities of water.
Apply water from as far a distance as possible. Use "alcohol" foam, carbon
dioxide or dry chemical. /Organophosphorus pesticides, liquid, NOS/
If material on fire or involved in fire: Extinguish fire using agent suitable for type
of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water
in flooding quantities as fog. Use "alcohol" foam, carbon dioxide or dry
chemical. /Organophosphorus pesticides, solid, NOS/
Hazardous Reactivities & Incompatibilities:
Strong acids, caustics, amines [Note: Corrosive to copper & brass].
Hazardous Decomposition:
Decomposition temperature: approx 160 deg C
When heated to decomposition it emits very toxic fumes of Cl-, nitroxides,
phosphoxides, and sulfoxides.
Other Hazardous Reaction:
A portion of even the most flammable materials is likely to be lost by vaporization.
... The smoke from an open fire used to destroy pesticides will contain some of the
poison. Burning should be attempted only in an isolated place. Inhalation of smoke must be
avoided. /Pesticides/
Protective Equipment & Clothing:
Wear appropriate chemical protective gloves, boots and goggles.
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Preventive Measures:
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend not only
upon the substance, but also on factors including the form of the substance,
characteristics and duration of the exposure, the uses of other eye protection equipment,
and the hygiene of the lenses. However, there may be individual substances whose
irritating or corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn. In any
event, the usual eye protection equipment should be worn even when contact lenses are in
place.
Avoid contact with skin, eyes, and clothing. Wash contaminated clothing before re-use.
Avoid breathing dust, spray, or mist. Do not contaminate food or feed. /Data from table/
Wash away any material which may have contacted the body with copious amounts of water,
or soap and water.
If material is not on fire and not involved in fire: Keep material out of water sources
and sewers.
Keep upwind. Avoid breathing vapors or dusts. Wash away any material which may have
contacted the body with copious amounts of water or soap and water. /Chlorpyrifos,
Agricultural insecticides, not elsewhere classified, liquid; other than liquid; and
insecticides, other than agricultural, not otherwise classified/
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet or significantly contaminated should be removed and
replaced.
Workers whose clothing may have become contaminated should change into uncontaminated
clothing before leaving the work premises.
Contact lenses should not be worn when working with this chemical.
In some situations where personnel may become accidently contaminated ... it is
necessary to provide shower bath in addition to the usual washing facilities. Special
arrangements for cleaning clothing & overalls may be necessary ... /Pesticides/
Special aircraft should preferably be used for spraying or dusting toxic
organophosphorus pesticides. ... Aerial spraying or dusting gives rise to clouds which
spread over larger surfaces than clouds produced by ground application. Aerial spraying
should therefore be carried out on windless days only. Residential areas, water supply
sources, etc must be avoided. ... When aircraft approaches, signalmen /guiding the
aircraft/ should leave the windward side. ... The local population should be informed
about the site & time of aerial pesticide treatment. Access of unauthorized persons
& especially children to the area to be treated must be ... forbidden. Warning signs
should be placed at the limits of the area. Ground spraying must be carried out with
compressed-air spraying equipment towed by tractors with closed cabs. /Organophosphorus
pesticides/
Small packages of pesticides are preferable for individual application in order to
limit the quantities to be weighed & metered. A special vessel with long stirring rod
for dilution & suspension of the poison must be available in order to reduce manual
handling to a minimum. The strict observance of hygiene rules--no smoking & no food
intake during work. Thorough washing with soap after work, changing protective clothing
before going home--is of utmost importance. /Organophosphorus pesticides/
Containers ... should be cleaned with a suspension of bleaching powder in water or with
other alkaline soln after soaking for 24 hr and then be rinsed with hot water.
/Organophosphorus pesticides/
If material not on fire and not involved in fire: Keep sparks, flames, and other
sources of ignition away. Keep material out of water sources and sewers. Build dikes to
contain flow as necessary. Use water spray to knock-down vapors. /Organophosphorus
pesticides, liquid, NOS/
Personnel protection: Keep upwind. Wear appropriate chemical protective gloves, boots
and goggles. Do not handle broken packages unless wearing appropriate personal protective
equipment. Wear positive pressure self-contained breathing apparatus when fighting fires
involving this material. /Organophosphorus pesticides, liquid, NOS/
If material not on fire and not involved in fire: Keep sparks, flames, and other
sources of ignition away. Keep material out of water sources and sewers. /Organophosphorus
pesticides, solid, NOS/
Personnel protection: Avoid breathing dusts, and fumes from burning material. Keep
upwind. Avoid bodily contact with the material. Wear appropriate chemical protective
gloves, boots and goggles. Do not handle broken packages unless wearing appropriate
personal protective equipment. Wash away any material which may have contacted the body
with copious amounts of water or soap and water. Wear positive pressure self-contained
breathing apparatus when fighting fires involving this material. If contact with the
material anticipated, wear appropriate protective clothing. /Organophosphorus pesticides,
solid, NOS/
Parathion and possibly other organophosphate insecticide residues may persist in
clothing, despite repeated laundering. /Organophosphates and related compounds/
Do not drink alcoholic beverages before or during spraying since alcohol promotes
absorption of organic phosphates. /Organic phosphates/
SRP: Contaminated protective clothing should be segregated in such a manner so that
there is no direct personal contact by personnel who handle, dispose, or clean the
clothing. Quality assurance to ascertain the completeness of the cleaning procedures
should be implemented before the decontaminated protective clothing is returned for reuse
by the workers. Contaminated clothing should not be taken home at end of shift, but should
remain at employee's place of work for cleaning.
Stability/Shelf Life:
VERY STABLE UNDER NEUTRAL OR SLIGHTLY ACID CONDITIONS AT ROOM TEMP
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for transportation in
commerce unless that person is registered in conformance ... and the hazardous material is
properly classed, described, packaged, marked, labeled, and in condition for shipment as
required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Maritime Dangerous Goods Code lays down basic principles for
transporting hazardous chemicals. Detailed recommendations for individual substances and a
number of recommendations for good practice are included in the classes dealing with such
substances. A general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be used when
shipping any substance or article.
Storage Conditions:
Keep locked up. Keep away from food, drink and animal feeding stuffs.
Rooms used for storage only should be soundly constructed & fitted with secure
locks. Floors should be kept clear & pesticides clearly identified. If repacking is
carried out in storage rooms, adequate light should be available; floors should be
impervious & sound ... /Pesticides/
Pesticide containers must be provided with labels indicating the degree of toxicity of
the product they contain. The labels must not only give a short description of how to use
the prepn, but also state basic precautions to be taken when applying it.
/Organophosphorus pesticides/
Pesticides of any degree of toxicity should be transported in containers which are
clearly labelled, leak-proof, and not easily damaged. They should never be transported /or
stored/ beside, or above any type of food, and all spillages should be immediately
reported. /Pesticides/
Cleanup Methods:
Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to
contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes,
or holding areas should be sealed with an impermeable flexible membrane liner./ Dike
material surface flow using soil, sand bags, foamed polyurethane, or foamed concrete;
absorb bulk liquid with fly ash or cement powder. /Chlorpyrifos
(Agricultural insecticides, not elsewhere classified), liquid)/
Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to
contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes,
or holding areas should be sealed with an impermeable flexible membrane liner./ Cover
solids with a plastic sheet to prevent dissolving in rain or fire fighting water. /Chlorpyrifos, (agricultural insecticides, not
elsewhere classified), other than liquid; Chlorpyrifos
(insecticides, other than agricultural, not elsewhere classified)/
Environmental considerations: Water spill: Use natural deep water pockets, excavated
lagoons, or sand bag barriers to trap material at bottom. If dissolved, in regions of 10
ppm or greater concentration, apply activated carbon at ten times the spilled amount.
Remove trapped material with suction hoses. Use mechanical dredges or lifts to remove
immobilized masses of pollutants and precipitates. /Chlorpyrifos
(insecticides, other than agricultural, not elsewhere classified; Chlorpyrifos
(agricultural insecticides, not elsewhere classified, other than liquid)/
Disposal Methods:
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill)
disposal practices are subject to significant revision. Prior to implementing land
disposal of waste residue (including waste sludge), consult with environmental regulatory
agencies for guidance on acceptable disposal practices.
This compound should be susceptible to removal from wastewater by air stripping.
Small amt - Adsorption on materials such as sand and bury in locations away from
domestic water supplies. For decontamination of containers triple rinse is recommended.
The use of a caustic soda-methanol or caustic soda-detergent rinse soln will also be
effective in decontaminating the container, but the rinse soln must be disposed of either
by incineration or burial in an area away from water supplies. Recommendable methods:
Incineration, adsorption.
All organic pesticides, whether of botanical or synthetic origin, can be destroyed by
incineration. /Organic pesticides/
Manufacturers or formulators of very large amounts of pesticides may find it
advantageous to build incinerators adequate to destroy all organic pesticides and equipped
with scrubbers to remove acid wastes. /Organic pesticides/
Occupational Exposure Standards:
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 0.2 mg/cu m, skin
Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three
times the TLV-TWA for no more than a total of 30 min during a work day, and under no
circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not
exceeded.
A4. A4= Not classifiable as a human carcinogen.
Biological Exposure Index (BEI) adoption (1989 edition): Determinant: cholinesterase
activity in red cells; Sampling Time: discretionary; BEI: 70% of individual's baseline.
The determinant is usually present in a significant amt in biological specimens collected
from subjects who have not been occupationally exposed. Such background levels are incl in
the BEI value. The determinant is nonspecific, since it is observed after exposure to some
other chemicals. These nonspecific tests are preferred because they are easy to use and
usually offer a better correlation with exposure than specific tests. In such instances, a
BEI for a specific, less quantitative biological determinant is recommended as a
confirmatory test. The biological determinant is an indicator of exposure to the chemical,
but the quantitative interpretation of the measurement is ambiguous (semiquantitative).
These biological determinants should be used as a screening test if a quantitative test is
not practical or as a confirmatory test if the quantitative test is not specific and the
origin of the determinant is in question. /Organophosphorus cholinesterase inhibitors/
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 0.2 mg/cu m.
Recommended Exposure Limit: 15 Min Short-Term Exposure Limit: 0.6 mg/cu m. Skin.
Other Occupational Permissible Levels:
Australia: 0.2 mg/cu m, 0.6 mg/cu m STEL (deletion proposed), skin (1990); United
Kingdom: 0.2 mg/cu m, 10-min STEL 0.6 mg/cu m (1991).
Manufacturing/Use Information:
Major Uses:
For Chlorpyrifos (USEPA/OPP Pesticide Code:
059101) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but
approved pesticide uses may change periodically and so federal, state and local
authorities must be consulted for currently approved uses./
Acaricide
Used for control of Coleoptera, Diptera, Homoptera, and Lepidoptera in soil or on
foliage in a wide range of crops ... Also used for control of household pests, ...
mosquitoes (larvae and adults) and in animal houses. Also for stored products.
Manufacturers:
Dow AgroSciences LLC, 9330 Zionsville Rd, Indianapolis, IN 46268, (317) 337-3000;
Production Sites: Lafayette, IN 47902; Midland, MI 48667
Drexel Chemical Co., 1700 Channel Ave., Memphis, TN 38106-1412, (901) 774-1412;
Production site: Cordele, GA 31015
Sure Co., Inc., 310 Martin Luther King Dr., P.O. Box 938, Fort Valley, GA 31030, (912)
825-3351; Production site: Fort Valley, GA 31030
Methods of Manufacturing:
By the reaction of 3,5,6-trichloro-2-pyridinol with diethyl phosphorochloridothioate in
the presence of sodium carbonate
Prepn: Rigterink, French patent 1,360,901 corresponding to US patent 3,244,586 (1964,
1966, both to Dow); Rigterink, Kenaga, J Agr Food Chem 14 394 (1966)
General Manufacturing Information:
Types and methods of application: Ground and aerial, spray and dust applications.
Application rates: Range from 0.5 lb active ingredient (ai)/acre to 3 lb active
ingredient (ai)/acre, and crack and crevice treatment to broadcast treatment for indoor
uses.
A composition containing chlorpyriphos is
microencapsulated in a water-soluble N-containing compound (eg, casein or casein
derivative) in the presence of a hardening product (eg, formaldehyde, glutaraldehyde, or
glyoxal). The product is suspended in a solution containing a non-ionic surfactant such as
polyoxyethylene sorbitan fatty acid esters and spray dried to yield a controlled-release
insecticide that is readily suspended in water and free from aggregation. Thus, 120 g of
71.3% chlorpyriphos in xylene was added to 370
ml of 10% gelatin. The mixture was homogenized to a particle size of 5-10 mu m. The
emulsion was diluted with 1 l of warm water at 50 deg C to form a coacervate, and mixed
with 2 g of Reodale TW-L120 (non-ionic surfactant) and 40 g of 25% glutaraldehyde. The
mixture was adjusted to pH> 9, heated to 50 deg C and stirred at that temperature for
30 minutes to yield microcapsules. The mixture was cooled to room temperature to obtain a
microencapsulated slurry. The microcapsules were suspended in a solution containing 1%
Abicel RC-591NF 500 and 4% gum arabic 500 ml. The suspension was spray dried to yield chlorpyriphos capsules. The microcapsules (50 ppm)
were effective in 100% control of cockroaches for 74 weeks.
Dursban /is/ a trademark for insecticides
containing O,O-diethyl-O-3,5,6-trichloro-2-pyridyl phosphorothioate.
... Concentrations of chlorpyrifos ... /were
found still to be toxic/ to mosquito larvae one year after an application of a
slow-release polymer formulation to a natural pond. /Initial concn of application not
specified/
Incompatible with alkaline preparations.
... Chlorpyrifos may be incompatible with
pesticides containing carboxylic acid amide groups or other strongly basic functional
groups such as alpha, alpha'-dithiobis(dimethylthio)formamide (Thiram) and
N-(trichloromethylthio)cyclohex-4-ene-1,2-dicarboximide (Captan).
Formulations/Preparations:
USEPA/OPP Pesticide Code 059101; Trade Names: Lorsban;
Dowco 179; Super Insect Coating A.P.T.; ENT 27311; Dursban
F; Dursban 4E; Dursban
HF; Killmaster; OMS 971; Brodan; Eradex; Detmol
U.A.; Pyrinex.
Emulsifiable concentrate; dust; flowable pellet; spray, granular wettable powder,
microcapsule, and granular bait
/Chlorpyrifos is formulated using carriers
such as/ synthetic clays, talc, and various solvents.
Baits, ... flowables, impregnated plastics, and pressurized liquids.
Chlorpyrifos is available for pesticide
applications as ... wettable powders, ... and controlled-release polymers.
... The commerical formulations are often combined with petroleum products (which may
include No 2 diesel oil and kerosene) to incr the rate of dispersal.
Formulation types: GR; EC; WP; DP; UL; Microcapsule
Chlorpyrifos is available as 25% wettable
powders, 1-10% granules, and emulsifiable concentrates of 2 and 4 lb/U.S. gal.
Mixtures (chlopyrifos +): diflubenzuron; cypermethrin; dimethoate; disulfoton; lindane;
pirimicarb; thiram
87 DEG F (CLOSED CUP) /LORSBAN 4E/
Impurities:
/SRP/: DIETHYL SULFIDE & DIETHYL DISULFIDE ARE VOLATILE CONTAMINANTS WHICH ARE
PARTLY RESPONSIBLE FOR THE OFFENSIVE ODOR OF THE TECHNICAL GRADE.
Impurities /found in the technical product (94.0% active ingredient)/ ... included:
some residual solvent, methylene chloride; unreacted O,O-diethyl-phosphorochloridothioate,
3,5,6-trichloro-2-pyridinol; the S-ethyl isomer of chlorpyrifos,
and other isomeric and related chloropyridyl phosphorothioates and phosphates; compounds
related to 3,5,6-trichloro-2-pyridinol; and trace amounts of sulfotep.
O-Ethyl O,O-bis(3,5,6-trichloro-2-pyridyl) phosphorothioate does not occur as a
significant impurity in /technical product (94.0% of active ingredient)/.
Consumption Patterns:
INSECTICIDE USED ON CORN, 39%; ALFALFA, 6%; COTTON, 3%; SORGHUM, 1%; OTHER FIELD
CROPS-EG, CITRUS & DECIDUOUS FRUITS/NUTS, 21%; NON-AGRICULTURAL USES, 31% (1982)
(1978) 4.00X10+9 G (CONSUMPTION)
(1982) 3.27X10+9 G (CONSUMPTION)
Laboratory Methods:
Clinical Laboratory Methods:
HIGH-PERFORMANCE LIQ CHROMATOGRAPHY WITH 3 DIFFERENT MOBILE PHASES WAS USED TO
DETERMINE CHLORPYRIFOS & ITS OXYGEN ANALOG
IN BIOLOGICAL TISSUES (PLASMA, BRAIN HOMOGENATES, & LIVER MICROSOMES).
Analytic Laboratory Methods:
UV SPECTROPHOTOMETER & GAS CHROMATOGRAPHY.
A METHOD INTENDED FOR REGULATORY PURPOSES IS DESCRIBED FOR DETERMINING RESIDUES OF CHLORPYRIFOS IN FRUITS & VEGETABLES. EXTRACTS WERE
ANALYZED BY GLC USING THERMIONIC DETECTORS.
GAS CHROMATOGRAPHIC PATTERNS FOR COMMERCIAL PESTICIDES ARE DESCRIBED.
METHYLENE CHLORIDE LIQ/LIQ EXTRACTION AND SEP-PAK C18 CARTRIDGE ADSORPTION TECHNIQUES
OF REVERSE-PHASE HIGH PERFORMANCE LIQUID CHROMATOGRAPHY WERE USED TO QUANTIFY DURSBAN IN CONTAMINATED WATER SAMPLES.
AOAC Method 981.03. Chlorpyrifos in Pesticide
Formulations. Liquid Chromatographic Method.
AOAC Method 985.22. Organochlorine and Organophosphorus Pesticide Residues. Gas
Chromatographic Method.
SOME PROCEDURES FOR THE ENZYMATIC DETECTION OF ORGANOPHOSPHORUS PESTICIDES, WHICH HAVE
GIVEN REPRODUCIBLE RESULTS ON A ROUTINE SCALE, ARE DESCRIBED. THE METHODS HAVE
SUCCESSFULLY BEEN APPLIED TO THE DETECTION OF CHLORPYRIFOS
IN FRUIT OR VEGETABLE EXTRACTS. THE METHODS INVOLVE INITIAL THIN-LAYER CHROMATOGRAPHY OF
THE SAMPLE EXTRACTS, THEN OXIDATION WITH BROMINE TO CONVERT THE THIOPHOSPHATES TO ACTIVE
ENZYME INHIBITORS. THE PLATES ARE THEN SPRAYED WITH ESTERASES FROM A SUITABLE SOURCE &
FURTHER SPRAYED WITH A SUITABLE SUBSTRATE WHICH WILL CAUSE THE BACKGROUND TO BECOME
COLORED FOLLOWING HYDROLYSIS. ALTERNATIVELY, THE ENZYME & AN ACID-BASE INDICATOR ARE
INCORPORATED INTO AN AGAR GEL & THE DEVELOPED TLC PLATE PRESSED AGAINST THIS FOR 1 HR
AFTER ACTIVATION WITH BROMINE, THEN THE AGAR IS SPRAYED WITH ACETYLCHOLINE, WHICH RELEASES
ACETIC ACID ON HYDROLYSIS. THE LIMIT OF DETECTION ACHIEVED FOR MOST SUBSTANCES IS 1 TO 10
NG. THE METHOD CAN BE USED AS A SCREENING PROCEDURE FOR ROUTINE ANALYSES.
EPA Method 8140: Organophosphorus Pesticides. Method 8140 is a gas chromatographic
method used to determine the concentration of various organophosphorous pesticides. Prior
to analysis, appropriate sample extraction techniques must be used. ... Organic liquids
may be analyzed by direct injection. A 2 to 5 ul aliquot of the extract is injected into a
gas chromatograph, and compounds in the gas chromatographic effluent are detected with a
flame photometer or thermionic detector. Chlorpyrifos
has a method detection limit of 0.3 ug/l with a retention time of 6.16 min. Single
operator accuracy and precision of 18 analyses results in an average recovery of 98.3%,
and a standard deviation of 5.5%.
EPA Method 8141 is a gas chromatographic method used to determine chlorpyrifos
in ground water, soil, and non-water miscible waste. A gas chromatograph with a flame
photometric or nitrogen-phosphorus detector is used for this multiresidue procedure.
Method detection limits for this compound using a flame photometric detector are 0.07 ug/l
for water, and 5.0 ug/kg for soil.
NIOSH Method 5600. Determination of Organophosphorus Pesticides by Gas Chromatography
with Flame Photometric Detection.
AREAL Method IP-8. Determination of Organochlorine Pesticides in Indoor Air.
AREAL Method TO-10. Determination of Organochlorine Pesticides In Ambient Air Using Low
Volume Polyurethane Foam (PUF) Sampling With Gas Chromatography/Electron Capture Detector
(GC/ECD).
EMSLC Method 508. Determination of Chlorinated Pesticides in Water by Gas
Chromatography with an Electron Capture Detector. Revision 3.0.
EMSLC Method 525.2. Determination of Organic Compounds in Drinking Water by
Liquid-Solid Extraction and Capillary Column Gas Chromatography and Mass Spectrometry.
Revision 1.0.
EMSLC Method 622. The Determination of Organophosphorus Pesticides in Municipal and
Industrial Wastewater by Gas Chromatography with Thermionic Bead or Flame Photometric
Detection in the Phosphorus Mode.
Special References:
Special Reports:
USEPA; Ambient Water Quality Criteria Doc: Chlorpyrifos
(1986) EPA 440/5-86-005
Nat'l Research Council Canada; Ecotoxicology of Chlorpyrifos
(1978) NRCC No. 16079
Matsumura F, Madhukar BV; Pharmacol Ther 9 (1): 27-49 (1980). Review article concerned
with exposure to insecticides which includes chlorpyrifos.
Synonyms and Identifiers:
Synonyms:
CHLOROPYRIFOS
**PEER REVIEWED**
CHLOROPYRIPHOS
**PEER REVIEWED**
CHLORPYRIFOS-ETHYL
**PEER REVIEWED**
CHLORPYRIPHOS
**PEER REVIEWED**
EPA Pesticide Code 059101
**PEER REVIEWED**
O,O-DIAETHYL-O-3,5,6-TRICHLOR-2-PYRIDYLMONOTHIOPHOSPHAT (GERMAN)
**PEER REVIEWED**
O,O-Diethyl O-(3,5,6-trichloro-2-pyridinyl)phosphorothioate
**PEER REVIEWED**
O,O-DIETHYL O-3,5,6-TRICHLORO-2-PYRIDYL PHOSPHOROTHIOATE
**PEER REVIEWED**
Dursban
**PEER REVIEWED**
OMS-0971
**PEER REVIEWED**
PHOSPHOROTHIOIC ACID, O,O-DIETHYL O-(3,5,6-TRICHLORO-2-PYRIDINYL) ESTER
**PEER REVIEWED**
PHOSPHOROTHIOIC ACID, O,O-DIETHYL O-(3,5,6-TRICHLORO-2-PYRIDYL) ESTER
**PEER REVIEWED**
2-PYRIDINOL, 3,5,6-TRICHLORO-, O-ESTER WITH O,O-DIETHYL PHOSPHOROTHIOATE
**PEER REVIEWED**
Formulations/Preparations:
USEPA/OPP Pesticide Code 059101; Trade Names: Lorsban;
Dowco 179; Super Insect Coating A.P.T.; ENT 27311; Dursban
F; Dursban 4E; Dursban
HF; Killmaster; OMS 971; Brodan; Eradex; Detmol
U.A.; Pyrinex.
Emulsifiable concentrate; dust; flowable pellet; spray, granular wettable powder,
microcapsule, and granular bait
/Chlorpyrifos is formulated using carriers
such as/ synthetic clays, talc, and various solvents.
Baits, ... flowables, impregnated plastics, and pressurized liquids.
Chlorpyrifos is available for pesticide
applications as ... wettable powders, ... and controlled-release polymers.
... The commerical formulations are often combined with petroleum products (which may
include No 2 diesel oil and kerosene) to incr the rate of dispersal.
Formulation types: GR; EC; WP; DP; UL; Microcapsule
Chlorpyrifos is available as 25% wettable
powders, 1-10% granules, and emulsifiable concentrates of 2 and 4 lb/U.S. gal.
Mixtures (chlopyrifos +): diflubenzuron; cypermethrin; dimethoate; disulfoton; lindane;
pirimicarb; thiram
87 DEG F (CLOSED CUP) /LORSBAN 4E/
Shipping Name/ Number DOT/UN/NA/IMO:
NA 2783; Chloropyrifos
Standard Transportation Number:
49 411 23; Chlorpyrifos (agricultural
insecticides, not elsewhere classified, liquid)
49 411 24; Chlorpyrifos (agricultural
insecticides, not elsewhere classified, other than liquid)
49 411 25; Chlorpyrifos (insecticides, other
than agricultural not elsewhere classified)
RTECS Number:
NIOSH/TF6300000
Administrative Information:
Hazardous Substances Databank Number: 389
Last Revision Date: 20010809
Last Review Date: Reviewed by SRP on 9/23/1999
Update History:
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 01/04/2001, 3 fields added/edited/deleted.
Complete Update on 03/02/2000, 73 fields added/edited/deleted.
Field Update on 02/08/2000, 1 field added/edited/deleted.
Field Update on 02/02/2000, 1 field added/edited/deleted.
Field Update on 11/18/1999, 1 field added/edited/deleted.
Field Update on 09/28/1999, 1 field added/edited/deleted.
Field Update on 09/21/1999, 1 field added/edited/deleted.
Field Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 03/17/1999, 2 fields added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 10/14/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 02/25/1998, 1 field added/edited/deleted.
Complete Update on 10/17/1997, 1 field added/edited/deleted.
Complete Update on 09/08/1997, 1 field added/edited/deleted.
Complete Update on 08/11/1997, 1 field added/edited/deleted.
Complete Update on 05/08/1997, 1 field added/edited/deleted.
Complete Update on 04/01/1997, 2 fields added/edited/deleted.
Complete Update on 02/27/1997, 5 fields added/edited/deleted.
Complete Update on 01/24/1997, 1 field added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 09/04/1996, 6 fields added/edited/deleted.
Complete Update on 05/10/1996, 1 field added/edited/deleted.
Complete Update on 05/07/1996, 1 field added/edited/deleted.
Complete Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 11/10/1995, 1 field added/edited/deleted.
Complete Update on 01/18/1995, 1 field added/edited/deleted.
Complete Update on 12/21/1994, 1 field added/edited/deleted.
Complete Update on 07/20/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 04/05/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Complete Update on 08/04/1993, 1 field added/edited/deleted.
Field update on 12/12/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Field update on 1/28/1991, 1 field added/edited/deleted.
Field update on 05/18/1990, 1 field added/edited/deleted.
Field Update on 03/07/1990, 1 field added/edited/deleted.
Field Update on 03/07/1990, 1 field added/edited/deleted.
Field Update on 03/07/1990, 1 field added/edited/deleted.
Field Update on 03/07/1990, 1 field added/edited/deleted.
Field Update on 03/06/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 62 fields added/edited/deleted.
Field Update on 05/05/1989, 1 field added/edited/deleted.
Field Update on 05/12/1988, 1 fields added/edited/deleted.
Complete Update on 04/22/1988, 2 fields added/edited/deleted.
Complete Update on 03/05/1988, 80 fields added/edited/deleted.
Complete Update on 10/25/1985
Record Length: 245524