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DIMEFOX
CASRN: 115-26-4
For other data, click on the Table of Contents
Human Health Effects:
Human Toxicity Excerpts:
AMT TOO SMALL FOR CHEM DETECTION CAN CAUSE BLURRED VISION. PREDOMINANT EFFECTS
ARE ON PERIPHERAL TISSUE & NOT ON CNS.
In a study lasting 70 days, whole blood cholinesterase was not inhibited in
a total of four men and women who ingested the compound at a dosage of 0.002
mg/kg/day, but it was reduced about 25% by a dosage of 0.0034 mg/kg/day. In
another study, a dosage of 0.004 mg/kg/day gradually caused a 40% reduction
in whole blood cholinesterase by the 49th day of exposure when inhibition stabilized
until dosing ended on the 95th day. This effect was entirely due to lowering
of red cell cholinesterase since the plasma enzyme remained unchanged. Whole-blood
activity recovered to 90% of normal within 56 days after dosing stopped ...
.
SYMPTOMATOLOGY: 1. NAUSEA...VOMITING, ABDOMINAL CRAMPS, DIARRHEA, EXCESSIVE
SALIVATION... 2. HEADACHE, GIDDINESS, VERTIGO & WEAKNESS. 3. RHINORRHEA
& SENSATION OF TIGHTNESS IN CHEST ARE COMMON IN INHALATION EXPOSURE. 4.
BLURRING OR DIMNESS OF VISION, MIOSIS... TEARING, CILIARY MUSCLE SPASM, LOSS
OF ACCOMMODATION & OCULAR PAIN... MYDRIASIS...SOMETIMES SEEN...PROBABLY
DUE TO SYMPATHO-ADRENAL DISCHARGE. 5. LOSS OF MUSCLE COORDINATION, SLURRING
OF SPEECH, FASCICULATIONS & TWITCHING OF MUSCLES (PARTICULARLY OF TONGUE
& EYELIDS), & GENERALIZED PROFOUND WEAKNESS. 6. MENTAL CONFUSION, DISORIENTATION
& DROWSINESS. /PARATHION/
SYMPTOMATOLOGY: 7. DIFFICULTY IN BREATHING, EXCESSIVE SECRETION OF SALIVA
& OF RESP TRACT MUCUS, ORONASAL FROTHING, CYANOSIS, PULMONARY RALES &
RHONCHI & HYPERTENSION, (PRESUMABLY DUE TO ASPHYXIA). 8. RANDOM JERKY MOVEMENTS,
INCONTINENCE, CONVULSIONS, & COMA. 9. DEATH PRIMARILY DUE TO RESP ARREST
ARISING FROM FAILURE OF RESP CENTER, PARALYSIS OF RESP MUSCLES, INTENSE BRONCHOCONSTRICTION
OR ALL THREE. /PARATHION/
...HAZARDS OF VAPOR TOXICITY ARE HIGH.
Caution: A highly toxic cholinesterase inhibitor.
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/
Organophosphate insecticides ... are potent cholinesterase enzyme inhibitors
that act by interfering with the metabolism of acetylcholine, which results
in accumulation of acetylcholine at neuroreceptor transmission sites. Exposure
produces a broad spectrum of clinical effects indicative of massive overstimulation
of the chlorinergic system, including muscarinic effects (parasympathetic),
nicotinic effects (sympathetic and motor), and CNS effects. These effects present
clinically as feeling of headache, weakness, dizziness, blurred vision, psychosis,
respiratory difficulty, paralysis, convulsions, and coma. Typical findings are
given by the mnemonic "SLUD." which stands for salivation, lacrimation, urination,
and defecation. A small percentage of patients may fail to demonstrate miosis,
a classic diagnostic hallmark. Onset of clinical manifestation of organophosphate
poisoning usually occurs within 12 hr of exposure. /Organophosphate insecticides/
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 possile 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/
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/
Human Toxicity Values:
The no-effect dosage of dimefox based on the most sensitive criterion, red
cell cholinesterase, is 0.002 mg/kg/day in humans.
Drug Warnings:
Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or
Symptom in Infant or Effect on Lactation: Fluorides: None. /from Table 7/
Medical Surveillance:
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/
... There is no change in red blood cell cholinesterase activity in adults
associated with age. ... Activity of this enzyme increases progressively during
the first year of life, it is higher in children under 3 yr of age than in older
children, and it is markedly higher in 5 yr old children than in 3 yr olds.
/Organic phosphorus pesticides/
Cholinesterase activity of plasma is significantly higher in men than in women,
and this is true no matter which of several choline esters are used as substrate
in measuring the enzyme activity. According to some, the difference is confined
to young people. There is no sex difference in the red cell enzyme activity.
Serum cholinesterase activity of blacks tends to be lower than whites of the
same sex. /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:
DIMEFOX IS INCL ON LIST OF COMPD CONSIDERED MOST DANGEROUS TO PESTICIDE APPLIERS.
/FROM TABLE/
Occupational exposure to dimefox may occur through inhalation and dermal contact
with this pesticide during and after its application or at workplaces where
dimefox is produced. (SRC)
Minimum Fatal Dose Level:
5. 5= EXTREMELY TOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) 5-50 MG/KG, BETWEEN
7 DROPS & 1 TEASPOONFUL FOR 70 KG PERSON (150 LB).
Emergency Medical Treatment:
Emergency Medical Treatment:
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is strictly prohibited.
The following Overview, *** DIMEFOX ***, 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 Dimefox is an organophosphate compound. The following
are symptoms from organophosphates in general, which
are due to the anticholinesterase activity of this
class of compounds. All of these effects may not be
documented for dimefox, but could potentially occur in
individual cases.
o MUSCARINIC (PARASYMPATHETIC) EFFECTS may include
bradycardia, bronchospasm, bronchorrhea, salivation,
lacrimation, diaphoresis, vomiting, diarrhea, and
miosis. NICOTINIC (SYMPATHETIC AND MOTOR) EFFECTS may
include tachycardia, hypertension, fasciculations,
muscle cramps, weakness, and RESPIRATORY PARALYSIS.
CENTRAL EFFECTS may include CNS depression, agitation,
confusion, delirium, coma, and seizures.
o Children may exhibit different predominant signs and
symptoms than adults: CNS depression, stupor,
flaccidity, dyspnea, and coma are the most common signs
in children.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Fever, bradycardia and hypotension, or tachycardia and
hypertension may occur.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Miosis, lacrimation, and blurred vision are common;
mydriasis may occur in severe poisonings. Opsoclonus
has been reported in one case. Salivation commonly
occurs.
0.2.4.2 CHRONIC EXPOSURE
o Decreased visual acuity and persistent photophobia may
be seen.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Bradycardia, hypotension, and chest pain may occur.
Tachycardia and hypertension may also be noted.
Arrhythmias and conduction defects may occur in severe
poisonings. Myocarditis may develop.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Dyspnea, rales, bronchorrhea, bronchospasm, or
tachypnea may be noted. Noncardiogenic pulmonary edema
may occur in severe cases. Chemical pneumonitis may be
seen.
o Bronchospasm may occur in previously sensitized
asthmatics or as a pharmacological muscarinic effect.
o Acute respiratory insufficiency is the main cause of
death in acute poisonings.
o Most organophosphate compounds can release toxic and
irritating fumes on thermal decomposition. Exposure to
such fumes could cause chemical pneumonitis,
bronchospasm, or noncardiogenic pulmonary edema.
NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
o Headache, dizziness, muscle spasms and profound
weakness are common. Alterations of level of
consciousness, anxiety, paralysis, seizures and coma
may occur. Seizures may be more common in children.
o Peripheral neuropathy of the mixed sensory-motor type
may be delayed by 6 to 21 days following exposure to
some organophosphates. Recovery may be slow or
incomplete.
o Dyskinesias may develop. Abnormal neuropsychiatric
tests and EEGs may persist for months after acute
exposure.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Vomiting, hypersalivation, diarrhea, fecal incontinence
and abdominal pain may occur.
o Intussusception has been reported in a single pediatric
organophosphate poisoning case.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Increased urinary frequency or, in severe cases,
urinary incontinence has occurred.
o Immune-complex nephropathy with proteinuria and/or
amorphous crystalluria may be possible.
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. Clinically significant bleeding or
hypercoagulability are rare.
o The hallmark of organophosphate poisoning is the
inhibition of plasma pseudocholinesterase or
erythrocyte acetylcholinesterase, or both.
DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
o Sweating is a consistent but not universal sign.
0.2.14.2 CHRONIC EXPOSURE
o Dermal sensitization may occur.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE
o Muscle weakness, fatigability and fasciculations are
common findings and may be delayed by several days.
Paralysis may supervene.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Hyperglycemia and glycosuria without ketosis may be
present.
PSYCHIATRIC
0.2.18.1 ACUTE EXPOSURE
o Decreased vigilance, 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 or
pre-existing psychological conditions.
o Psychosis may be noted following acute poisoning.
o Abnormal neuropsychiatric tests and EEGs may persist
for months after acute exposure.
IMMUNOLOGIC
0.2.19.2 CHRONIC EXPOSURE
o Chronic skin exposure to some organophosphates may lead
to dermal sensitization.
REPRODUCTIVE HAZARDS
o Most of the organophosphates have not been teratogenic
in animals but some have caused lower fetal or birth
weights and/or higher neonatal mortality.
o Sporadic reports of human birth defects related to
organophosphates have not been fully verified.
o No information about possible male reproductive effects
was found in available references at the time of this
review.
CARCINOGENICITY
0.2.21.2 HUMAN OVERVIEW
o In in vitro experiments, dimefox interacted with
nitrite to form potentially carcinogenic
dimethylnitrosamine.
o The widely used organophosphates are thought not to be
carcinogenic; however, some controversy exists in this
area.
GENOTOXICITY
o Cytogenetic studies of organophosphate-exposed workers
have suggested possible increases in frequencies of
chromosome aberrations, but the evidence is not
compelling.
o Two generations of an Israeli family who had been
chronically exposed to organophosphates had 100-fold
amplification of the "silent" allele of the CHE gene on
chromosome 3; the absence of amplification of other
genes on chromosome 3 suggests that the amplification of
the CHE gene was a specific response to exposure to the
organophosphate.
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.
o If respiratory tract irritation, excessive bronchial
secretions, or bronchospasm occur following exposure,
monitor arterial blood gases and chest x-ray.
|
| Treatment Overview: |
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/CATHARTIC: Administer charcoal
slurry, aqueous or mixed with saline cathartic or
sorbitol. The FDA suggests 240 mL of diluent/30 g of
charcoal. Usual charcoal dose is 25 to 100 grams in
adults and adolescents, 25 to 50 grams in children (1 to
12 years old), and 1 gram/kilogram in infants less than
1 year old.
1. Routine use of cathartics is NOT recommended. If used,
administer only ONE dose of cathartic. Administer one
dose of a cathartic, mixed with charcoal or given
separately. See "Treatment: Prevention of Absorption"
in the main document.
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.
o See treatment of oral exposure in the main body of this
document for complete information.
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.
o See treatment of inhalation exposure in the main body of
this document for complete information.
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.
o See treatment of eye exposure in the main body of this
document for complete information.
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.
o See treatment of dermal exposure in the main body of
this document for complete informtion.
|
| Range of Toxicity: |
o Acute toxicity is variable and depends strongly upon the
kinetics of absorption and whether or not metabolic
activation is required. Sudden absorption of a less toxic
compound may have a more severe effect than gradual
absorption of a more toxic agent.
o No cholinesterase inhibition occurred in volunteers who
ingested 0.002 mg/kg of dimefox daily for 70 days. A 25%
reduction in cholinesterase activity was observed in
volunteers who ingested 0.0034 mg/kg of dimefox daily for
70 days.
1. With daily ingestion of 0.004 mg/kg of dimefox,
volunteers gradually developed a 40% decrease in
cholinesterase activity over the first 49 days of the
study. Continuing this dose through the 95th day did not
result in any further cholinesterase inhibition.
o Rats fed 0.024, 0.095, and 0.475 mg/kg of dimefox daily
for 28 days developed a dose-related decrease in
cholinesterase activity. Rats fed 0.01 and 0.25 mg/kg of
dimefox daily for 6 days developed ataxia and decreased
maximum motor nerve conduction velocity in the tail nerve.
|
Antidote and Emergency Treatment:
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/
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/
For 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 ... water for dilution if the patient
can swallow, has a strong gag reflex, and does not drool. Administer activated
charcoal ... /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:
MARKED DIFFERENCE IN SUSCEPTIBILITY OF SEXES IS...SEEN IN CASE OF MANY ORGANO-PHOSPHORUS
INSECTICIDES. ...DIMEFOX.../IS/ SLIGHTLY MORE TOXIC TO MALES.
Repeated intraperitoneal administration of dimefox to rats at a rate of 0.5
mg/kg/day killed half of them within 10 doses; 0.1 mg/kg/day produced marked
inhibition of cholinesterase, but no deaths following 30 injections. The no-effect
dosages of dimefox based on the most sensitive criterion, red cell cholinesterase,
are 0.003 /and/ 0.006...mg/kg/day in rat /&/ pig...
FOR 28 DAYS FEMALE RATS WERE FED 0.024 MG/KG/DAY, 0.095 MG/KG/DAY & 0.475
MG/KG/DAY, RESPECTIVELY RESULTING IN ABOUT 50% INHIBITION OF RBC CHOLINESTERASE
CHE & NO EFFECT ON PLASMA CHE, 75% REDN OF RBC CHE & 25% REDN OF PLASMA
CHE; ALM COMPLETE INHIBITION OF RBC CHE & 75% REDN OF PLASMA CHE RESPECTIVELY.
/FROM TABLE/
Toxic to bees.
Vapor toxicity hazard is high.
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 demonstrate and, by necessity, all of them are
of low toxicity. /Organic phosphorous pesticides/
Although some anticholinergic compounds are teratogenic, most are not. /Organic
phosphorous pesticides/
Non-Human Toxicity Values:
LD50 Rat oral 7.5 mg/kg
LD50 Rat ip 5.0 mg/kg
LD50 Rat oral 1-2 mg/kg
LD50 Rat dermal 5 mg/kg
LD50 Mouse ip 1.4 mg/kg
LD50 Guinea pig ip 2.5 mg/kg
LD50 Dog ip 5-10 mg/kg
The no-effect dosages of dimefox based on the most sensitive criterion, red
cell cholinesterase, are 0.003 and 0.006 mg/kg/day in the rat and pig, respectively.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
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/
Absorption, Distribution & Excretion:
Following oral administration to rats, elimination is via the urine.
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 pesticides/
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/
Mechanism of Action:
Unmetabolized dimefox is a moderately strong inhibitor of cholinesterase in
vitro; the molar concentration required to cause 50% inhibition is 4x10-5. ...
Its action is mainly peripheral, that on the brain
being slower in onset.
The signs of poisoning due to organophosphorus cmpd are those due to accumulation
of acetylcholine & hence overstimulation of parasympathetic nervous system.
It is usual to divide them under 3 headings: muscarinic, nicotinic & central.
Muscarinic signs ... consist of hypersalivation, lacrimation, sweating &
nasal discharge. Miosis, dyspnea, vomiting, diarrhea & frequency of urination
... Nicotinic effects consist of fasciculation of muscles, weakness & paralysis.
Central nervous system effects include nervousness, apprehension, ataxia, convulsions
& coma. Death is due to resp failure, or sometimes cardiac arrest. There
is little difference between signs produced by different organophosphorus compounds,
but route of absorption may influence one system more than another. /Organophosphorus
cmpd/
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/
Organophosphorus derivatives act by combining with and inactivating the enzyme
acetylcholinesterase. ... 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 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/
Interactions:
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:
Drug Warnings:
Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or
Symptom in Infant or Effect on Lactation: Fluorides: None. /from Table 7/
Interactions:
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/
Minimum Fatal Dose Level:
5. 5= EXTREMELY TOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) 5-50 MG/KG, BETWEEN
7 DROPS & 1 TEASPOONFUL FOR 70 KG PERSON (150 LB).
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Dimefox's use as an insecticide and acaricide will result in its release to
the environment. If released to the atmosphere, dimefox is expected to exist
solely in the vapor phase in the ambient atmosphere based on its measured vapor
pressure of 0.11 mm Hg at 20 deg C. Vapor-phase dimefox will be readily degraded
in the atmosphere by reaction with photochemically-produced hydroxyl radicals
(estimated half-life 6.4 hours). If released to soil, an estimated Koc of 9.8
suggests dimefox will have very high mobility in soil. Dimefox is not expected
to volatilize from dry or wet soil surfaces based on the measured vapor pressure
and an estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole, respectively.
If released into water, dimefox is not expected to adsorb to suspended solids
and sediment in water based on an estimated Koc of 9.8. Volatilization, hydrolysis,
and bioconcentration are not expected to be environmentally important processes
in aquatic systems. Occupational exposure to dimefox may occur through inhalation
or dermal contact with this pesticide during or after its application or at
workplaces where it is produced. (SRC)
Probable Routes of Human Exposure:
DIMEFOX IS INCL ON LIST OF COMPD CONSIDERED MOST DANGEROUS TO PESTICIDE APPLIERS.
/FROM TABLE/
Occupational exposure to dimefox may occur through inhalation and dermal contact
with this pesticide during and after its application or at workplaces where
dimefox is produced. (SRC)
Natural Pollution Sources:
Dimefox is of anthropogenic origin, and is not known to be produced by natural
sources. (SRC)
Artificial Pollution Sources:
Dimefox's use as an insecticide and acaricide(1) will result in its release
to the environment(SRC).
Environmental Fate:
TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 9.8(SRC), determined from a structure estimation method(2), indicates
that dimefox is expected to have very high mobility in soil(SRC). Volatilization
of dimefox from moist soil surfaces is not expected(SRC) given an estimated
Henry's Law constant of 2.2X10-8 atm-cu m/mole(SRC), determined from experimental
values for water solubility(3) and vapor pressure(4). Dimefox is not expected
to volatilize from dry soil surfaces based on a measured vapor pressure of 0.11
mm Hg(4).
AQUATIC FATE: Based on a recommended classification scheme(1), an estimated
Koc value of 9.8(SRC), determined from a structure estimation method(2), indicates
that dimefox is not expected to adsorb to suspended solids and sediment in water(SRC).
Dimefox is not expected to volatilize from water surfaces(3,SRC) based on an
estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole(4,5,SRC). According
to a classification scheme(6), an estimated BCF value of 0.28(3,SRC), from an
estimated log Kow(7,SRC), suggests that bioconcentration in aquatic organisms
is low(SRC). Hydrolysis is not expected to be an environmentally important removal
process(8,9,SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), dimefox, which has a measured vapor
pressure of 0.11 mm Hg at 20 deg C(2), is expected to exist solely as a vapor
in the ambient atmosphere. Vapor-phase dimefox 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 about 6.4 hours(3,SRC).
Environmental Biodegradation:
Little oxidation of dimefox occurred when exposed to the green alga, Chlorella
pyrenoidosa, at a concentration of 1000 ppm(1).
Environmental Abiotic Degradation:
The rate constant for the vapor-phase reaction of dimefox with photochemically-produced
hydroxyl radicals has been estimated as 6.0X10-11 cu cm/molecule-sec at 25 deg
C(SRC) using a structure estimation method(1,SRC). This corresponds to an atmospheric
half-life of about 6.4 hours at an atmospheric concentration of 5X10+5 hydroxyl
radicals per cu cm(1,SRC). Dimefox is resistant to hydrolysis with a half-life
of greater than ten years at pH 7(2). The hydrolysis half-life of dimefox at
70 deg C in ethanol, pH 6 buffer solution, was 8.8 days(3). Dimefox is not expected
to undergo direct photolysis in the environment due to its lack of ability to
absorb light in the environmental spectrum(SRC).
Environmental Bioconcentration:
An estimated BCF value of 0.28 was calculated for dimefox(SRC), using an estimated
log Kow of -0.43(1,SRC) and a recommended regression-derived equation(2). According
to a classification scheme(3), this BCF value suggests that bioconcentration
in aquatic organisms is low(SRC).
Soil Adsorption/Mobility:
Using a structure estimation method based on molecular connectivity indices(1),
the Koc for dimefox can be estimated to be about 9.8(SRC). According to a recommended
classification scheme(2), this estimated Koc value suggests that dimefox is
expected to have very high mobility in soil(SRC).
Volatilization from Water/Soil:
The Henry's Law constant for dimefox is estimated as 2.2X10-8 atm-cu m/mole(SRC)
from its experimental values for vapor pressure, 0.11 mm Hg(1), and water solubility,
1X10+6 mg/l(2). This value indicates that dimefox will be essentially nonvolatile
from water surfaces(3,SRC). Dimefox's Henry's Law constant(1,2,SRC) indicates
that volatilization from moist soil surfaces is not expected (SRC). Dimefox
is not expected to volatilize from dry soil surfaces based on a measured vapor
pressure of 0.11 mm Hg(1).
Environmental Standards & Regulations:
CERCLA Reportable Quantities:
Releases of CERCLA hazardous substances are subject to the release reporting
requirement of CERCLA section 103, codified at 40 CFR part 302, in addition
to the requirements of 40 CFR part 355. Dimefox is an extremely hazardous substance
(EHS) subject to reporting requirements when stored in amounts in excess of
its threshold planning quantity (TPQ) of 500 lbs.
Chemical/Physical Properties:
Molecular Formula:
C4-H12-F-N2-O-P
Molecular Weight:
154.13
Color/Form:
Colorless liquid
Odor:
FISHY ODOR
Boiling Point:
86 DEG C @ 15 MM HG; 67 DEG C @ 4.0 MM HG
Corrosivity:
Corrosive to metals
Density/Specific Gravity:
1.1151 @ 20 DEG C/4 DEG C
Solubilities:
FREELY SOL IN ETHER, BENZENE
MISCIBLE WITH MOST ORG SOLVENTS
Miscible with water at 20 deg C.
Spectral Properties:
Index of Refraction: 1.4267 at 20 deg C/D
Vapor Pressure:
0.11 mm Hg at 20 deg C
Other Chemical/Physical Properties:
IT HAS CHLOROFORM/WATER PARTITION COEFFICIENT 15:1 IN FAVOR OF CHLOROFORM
Vapor pressure: 0.36 mm Hg at 25 deg C
Decomposes more rapidly in acidic media than in alkaline media.
Resistant to hydrolysis with half-life over ten years at pH 7.
Slowly oxidized by vigorous oxidizing agents and rapidly decomposed by chlorine.
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. /Organophosphorus
pesticide, liquid, poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus
pesticide, solid, poisonous; Organophosphorus pesticide, solid, toxic/
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. /Organophosphorus pesticide, liquid, poisonous;
Organophosphorus pesticide, liquid, toxic; Organophosphorus pesticide, solid,
poisonous; Organophosphorus pesticide, solid, toxic/
Public safety: CALL Emergency Response Telephone Number. ... 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.
/Organophosphorus pesticide, liquid, poisonous; Organophosphorus pesticide,
liquid, toxic; Organophosphorus pesticide, solid, poisonous; Organophosphorus
pesticide, solid, toxic/
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. /Organophosphorus
pesticide, liquid, poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus
pesticide, solid, poisonous; Organophosphorus pesticide, solid, toxic/
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. /Organophosphorus pesticide,
liquid, poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus
pesticide, solid, poisonous; Organophosphorus pesticide, solid, toxic/
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. /Organophosphorus
pesticide, liquid, poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus
pesticide, solid, poisonous; Organophosphorus pesticide, solid, toxic/
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. /Organophosphorus pesticide, liquid, poisonous; Organophosphorus
pesticide, liquid, toxic; Organophosphorus pesticide, solid, poisonous; Organophosphorus
pesticide, solid, toxic/
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. /Organophosphorus pesticide, liquid,
poisonous; Organophosphorus pesticide, liquid, toxic; Organophosphorus pesticide,
solid, poisonous; Organophosphorus pesticide, solid, toxic/
Health: Toxic; may be fatal if inhaled, ingested or absorbed through skin.
Inhalation or contact with some of these materials will irritate or burn skin
and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors
may cause dizziness or suffocation. Runoff from fire control or dilution water
may cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous;
Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide,
liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/
Fire or explosion: Highly flammable: Will be easily ignited by heat, sparks
or flames. Vapors may form explosive mixtures with air. Vapors may travel to
source of ignition and flash back. Most vapors are heavier than air. They will
spread along ground and collect in low or confined areas (sewers, basements,
tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Some
may polymerize (P) explosively when heated or involved in a fire. Runoff to
sewer may create fire or explosion hazard. Containers may explode when heated.
Many liquids are lighter than water. /Organophosphorus pesticide, liquid, flammable,
poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus
pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid,
toxic, flammable/
Public safety: Call Emergency Response Telephone Number. ... Isolate spill
or leak area immediately for at least 100 to 200 meters (330 to 660 feet) in
all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low
areas. Ventilate closed spaces before entering. /Organophosphorus pesticide,
liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable,
toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus
pesticide, liquid, toxic, flammable/
Protective clothing: Wear positive pressure self-contained breathing apparatus
(SCBA). Wear chemical protective clothing which is specifically recommended
by the manufacturer. It may provide little or no thermal protection. Structural
firefighters' protective clothing is recommended for fire situations only; it
is not effective in spill situations. /Organophosphorus pesticide, liquid, flammable,
poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus
pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid,
toxic, flammable/
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. /Organophosphorus pesticide,
liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable,
toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus
pesticide, liquid, toxic, flammable/
Fire: CAUTION: All these products have a very low flash point. Use of water
spray when fighting fire may be inefficient. Small fires: Dry chemical, CO2,
water spray or alcohol-resistant foam. Large fires: Water spray, fog or alcohol-resistant
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. 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. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus
pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous,
flammable; Organophosphorus pesticide, liquid, toxic, flammable/
Spill or leak: Fully encapsulating, vapor protective clothing should be worn
for spills and leaks with no fire. ELIMINATE all ignition sources (no smoking,
flares, sparks or flames in immediate area). All equipment used when handling
the product must be grounded. Do not touch or walk through spilled material.
Stop leak if you can do it without risk. Prevent entry into waterways, sewers,
basements or confined areas. A vapor suppressing foam may be used to reduce
vapors. Small spills: Absorb with earth, sand or other non-combustible material
and transfer to containers for later disposal. Use clean non-sparking tools
to collect absorbed material. Large spills: Dike far ahead of liquid spill for
later disposal. Water spray may reduce vapor; but may not prevent ignition in
closed spaces. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus
pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous,
flammable; Organophosphorus pesticide, liquid, toxic, flammable/
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. Wash skin with
soap and water. 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. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus
pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous,
flammable; Organophosphorus pesticide, liquid, toxic, flammable/
Fire Fighting Procedures:
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/
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:
IT HAS HIGH VAPOR PRESSURE & SHOULD BE HANDLED IN ENCLOSED PLACES WITH
RESPIRATOR.
Respiratory protection (supplied-air respirator with full facepiece or self-contained
breathing apparatus) should be available where these compounds are manufactured
or used and should be worn in case of emergency and overexposure. /Phosphorus
compounds/
WORKERS HANDLING AND APPLYING ORGANOPHOSPHATE PESTICIDES (OPP) MUST ... BE
GIVEN PERSONAL PROTECTIVE EQUIPMENT COMPRISING OVERALLS MADE OF A TIGHT FABRIC
OR POLYVINYL CHLORIDE, GLOVES, AND RUBBER BOOTS. THEY MUST WEAR A RESPIRATOR
WITH AN ACTIVATED-CARBON GAS FILTER CARTRIDGE AFFORDING PROTECTION FOR A DETERMINED
NUMBER OF WORKING HOURS. THE EYES SHOULD BE PROTECTED BY GOGGLES. THE SIGNALMEN
FOR AERIAL DUSTING OPERATIONS SHOULD BE EQUIPPED WITH A HAT AND CAPE MADE OF
POLYVINYL CHLORIDE OR A FABRIC IMPREGNATED WITH A WATER REPELLENT. /PESTICIDES,
ORGANOPHOSPHORUS/
Preventive Measures:
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/
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/
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/
Stability/Shelf Life:
AQ SOLN ARE STABLE
DIMEFOX IS RESISTANT TO HYDROLYSIS BY ALKALI. IT IS HYDROLYZED BY ACIDS, SLOWLY
OXIDIZED BY VIGOROUS OXIDIZING AGENTS, AND RAPIDLY OXIDIZED BY CHLORINE.
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 Air Transport Association (IATA) Dangerous Goods Regulations
are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions
618 and 619 and constitute a manual of industry carrier regulations to be followed
by all IATA Member airlines when transporting hazardous materials.
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:
...MUST BE STORED IN ITS SEALED ORIGINAL CONTAINERS, IN WELL-AIRED, FRESH
& DRY STOREHOUSES OR IN SHADED & POSSIBLY WELL-AIRED PLACES. IT IS RECOMMENDED
THAT THE PRODUCT'S TEMP...NOT EXCEED 25-30 DEG C, & KEEP...AWAY FROM SOURCES
OF HEAT, FREE FLAMES OR SPARK-GENERATING EQUIPMENT. CONTAINERS MUST BE STACKED
IN SUCH A WAY AS TO PERMIT FREE CIRCULATION OF AIR...AT BOTTOM & INSIDE
OF PILES. STORAGE AREAS MUST BE LOCATED AT SUITABLE DISTANCE FROM INHABITED
BUILDINGS, ANIMAL SHELTERS, & FOOD STORES; MOREOVER, THEY MUST BE INACCESSIBLE
TO UNAUTHORIZED PERSONS, CHILDREN, & DOMESTIC ANIMALS. /PROTHOATE/
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/
Pesticides 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/
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.
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:
Manufacturing/Use Information:
Major Uses:
SYSTEMIC ACARICIDE
SYSTEMIC INSECTICIDE (NOT USED IN US)
Manufacturers:
NOT PRODUCED COMMERCIALLY IN US
Methods of Manufacturing:
REACTION OF DIMETHYLAMINE AND POTASSIUM FLUORIDE
WITH PHOSPHORUS OXYCHLORIDE
PREPD BY FLUORINATION OF BIS(DIMETHYLAMIDO)PHOSPHORYL CHLORIDE.
By interaction of dimethylamine, phosphoryl chloride, and potassium fluoride
in chloroform (Brit patent 688,760).
General Manufacturing Information:
IT IS COMPATIBLE WITH OTHER PESTICIDES BUT TECHNICAL PRODUCT SLOWLY ATTACKS
METALS.
THIS COMPD...HAS BEEN USED TO CONTROL MEALYBUG VECTOR OF SWOLLEN SHOOT DISEASE
OF CACAO BY IMPLANTING SOL CAPSULES ABOUT ROOTS. BECAUSE OF ITS VOLATILITY,
DIMEFOX HAS VERY SHORT RESIDUAL ACTIVITY & IS NOT SUITED FOR FOLIAGE APPLICATION.
/ITS/...MAIN USE IS FOR SOIL TREATMENT OF HOPS AGAINST APHIDS & RED SPIDER
MITES, BEING EFFECTIVE, @ NON-PHYTOTOXIC CONCN, FOR 6-8 WK.
A systemic pesticide, primarily for ornamental and non-food plants.
Formulations/Preparations:
TERRA SYTAM BUTANOL SOLN CONTAINING 50% WT/VOL DIMEFOX TOGETHER WITH 17% TOTAL
OF SCHRADAN & HEXAMETHYL PYROPHOSPHORAMIDE, WHICH ACTS AS SYNERGIST. S-14
IS 20% AQ DILUTION OF TERRA SYSTAM.
SOLN.../CONTAINS/ 50 WT/VOL; 10% FOR S 14/10*.
U. S. Production:
(1972) NOT PRODUCED COMMERCIALLY IN US
(1975) NONE
Laboratory Methods:
Analytic Laboratory Methods:
PRODUCT ANALYSIS FOR DIMEFOX...IS PREFERABLY BY GLC (DETAILS OF METHOD ARE
AVAILABLE FROM WACKER-CHEMIE GMBH) OR BY SELECTIVE ACID HYDROLYSIS AT VARIOUS
TEMPERATURES AND THE DETERMINATION OF AMINE IN THE SEPARATED FRACTIONS (CIPAC
HANDBOOK, 1970, 1, 329). RESIDUE ANALYSIS FOR DIMEFOX IS BY GLC WITH FLAME IONIZATION
DETECTION (WACKER-CHEMIE GMBH).
GENERAL SAMPLE, SPECTROPHOTOMETRY, WAVELENGTH 560 NM. DUPEE, LP ET AL, J AGR
FOOD CHEM 4, 233 (1956).
RESIDUES /ARE DETERMINED/...BY GLC USING THERMIONIC DETECTION. ANALYSIS BY
FLAME SPECTROPHOTOMETRY, HAOB, H ET AL, DEUT LEBENSM-RUNDSCH, 66, 317-322, 1970
(GERMAN), DEJONCKHEERE, W ET AL, PESTIC SCI, 4, 549, 1974.
RESIDUE ANALYSIS IS BY EXTRACTION, CHROMATOGRAPHIC SEPARATION & ULTIMATE
PHOSPHORUS DETERMINATION VIA MOLYBDENUM BLUE COMPLEX: FIELD, K & LAWS, EQ,
ANALYST, LOND, 1957, 82, 667.
Analysis of products: alkaline decomposition with heating and titration of
the dimethylamine distilled off (CIPC handbook 1970, 1, 329); elemental analysis:
calculated 18.18% N; 12.33% F; 20.10% P.
Analysis of residues: gas chromatographic determination with flame-ionization
detection (Wacker-Chemie GmbH, Munich)
Special References:
Synonyms and Identifiers:
Synonyms:
S-14
**PEER REVIEWED**
T-2002
**PEER REVIEWED**
BFP
**PEER REVIEWED**
BFPO
**PEER REVIEWED**
BIS(DIMETHYLAMIDO)FLUOROPHOSPHATE
**PEER REVIEWED**
BIS(DIMETHYLAMIDO)PHOSPHORYL FLUORIDE
**PEER REVIEWED**
BIS(DIMETHYLAMINO)FLUOROPHOSPHATE
**PEER REVIEWED**
BISDIMETHYLAMINOFLUOROPHOSPHINE OXIDE
**PEER REVIEWED**
CR 409
**PEER REVIEWED**
DIFO
**PEER REVIEWED**
DMF
**PEER REVIEWED**
ENT 19,109
**PEER REVIEWED**
FLUOPHOSPHORIC ACID DI(DIMETHYLAMIDE)
**PEER REVIEWED**
FLUORURE DE N,N,N',N'-TETRAMETHYLE PHOSPHORODIAMIDE [FRENCH]
**PEER REVIEWED**
HANANE
**PEER REVIEWED**
PESTOX 14
**PEER REVIEWED**
PESTOX IV
**PEER REVIEWED**
PESTOX XIV
**PEER REVIEWED**
PHOSPHINE OXIDE, BIS(DIMETHYLAMINO)FLUORO-
**PEER REVIEWED**
PHOSPHORODIAMIDIC FLUORIDE, TETRAMETHYL-
**PEER REVIEWED**
TERRA-SYSTAM
**PEER REVIEWED**
TERRA-SYTAM
**PEER REVIEWED**
TERRASYTUM
**PEER REVIEWED**
N,N,N',N'-TETRAMETHYL-DIAMIDOFOSFORZUUR-FLUORIDE
[DUTCH]
**PEER REVIEWED**
TETRAMETHYLDIAMIDOPHOSPHORIC FLUORIDE
**PEER REVIEWED**
N,N,N',N'-TETRAMETHYL-DIAMIDO-PHOSPHORSAEURE-FLUORID [GERMAN]
**PEER REVIEWED**
TETRAMETHYLPHOSPHORODIAMIDIC FLUORIDE
**PEER REVIEWED**
N,N,N',N'-TETRAMETHYLPHOSPHORODIAMIDIC FLUORIDE
**PEER REVIEWED**
N,N,N',N'-TETRAMETIL-FOSFORODIAMMIDO-FLUORURO [ITALIAN]
**PEER REVIEWED**
TETRA SYTAM
**PEER REVIEWED**
TL 792
**PEER REVIEWED**
WACKER S 14/10
**PEER REVIEWED**
Formulations/Preparations:
TERRA SYTAM BUTANOL SOLN CONTAINING 50% WT/VOL DIMEFOX TOGETHER WITH 17% TOTAL
OF SCHRADAN & HEXAMETHYL PYROPHOSPHORAMIDE, WHICH ACTS AS SYNERGIST. S-14
IS 20% AQ DILUTION OF TERRA SYSTAM.
SOLN.../CONTAINS/ 50 WT/VOL; 10% FOR S 14/10*.
Shipping Name/ Number DOT/UN/NA/IMO:
IMO 6.1; Organophosphorus pesticides, liquid, toxic, not otherwise specified;
Organophosphorus pesticides, liquid, toxic, flammable, not otherwise specified,
flashpoint between 23 deg C and 61 deg C; Organophosphorus pesticides, solid,
toxic, not otherwise specified
UN 3018; Organophosphorus pesticides, liquid, toxic, not otherwise specified
UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, not otherwise
specified, flashpoint between 23 deg C and 61 deg C
UN 2784; Organophosphorus pesticides, liquid, flammable, toxic, not otherwise
specified, flashpoint less than 23 deg C
IMO 3.2; Organophosphorus pesticides, liquid, flammable, toxic, not otherwise specified, flashpoint less than 23 deg C
Standard Transportation Number:
49 216 74; Organophosphorus pesticide, liquid, not otherwise specified (compounds
and preparations) (insecticides, other than agricultural, NEC)
49 216 75; Organophosphorus pesticide, liquid, not otherwise specified (compounds
and preparations) (agricultural insecticides, NEC, liquid)
49 105 44; Organophosphorus pesticide, liquid, not otherwise specified (compounds
and preparations) (insecticides, other than agricultural, NEC)
49 105 45; Organophosphorus pesticide, liquid, not otherwise specified (compounds and preparations) (agricultural insecticides, NEC, liquid)
RTECS Number:
NIOSH/TD4025000
Administrative Information:
Hazardous Substances Databank Number: 1775
Last Revision Date: 20010809
Last Review Date: Reviewed by SRP on 9/18/1997
Update History:
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 11/18/1999, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 10/20/1998, 1 field added/edited/deleted.
Complete Update on 09/11/1998, 1 field added/edited/deleted.
Complete Update on 06/03/1998, 50 fields added/edited/deleted.
Field Update on 06/02/1998, 1 field added/edited/deleted.
Field Update on 10/23/1997, 1 field added/edited/deleted.
Field Update on 05/08/1997, 1 field added/edited/deleted.
Field Update on 05/01/1997, 2 fields added/edited/deleted.
Complete Update on 10/15/1996, 1 field added/edited/deleted.
Complete Update on 01/21/1996, 1 field added/edited/deleted.
Complete Update on 11/10/1995, 1 field added/edited/deleted.
Complete Update on 12/28/1994, 1 field added/edited/deleted.
Complete Update on 10/27/1994, 2 fields added/edited/deleted.
Complete Update on 09/16/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Field update on 12/22/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 05/21/1990, 2 fields added/edited/deleted.
Field update on 05/18/1990, 1 field added/edited/deleted.
Complete Update on 10/03/1986