DICHLORVOS
Human Health Effects:
Evidence for Carcinogenicity:
Evaluation: There is inadequate evidence in humans for the carcinogenicity of dichlorvos. There is sufficient evidence in
experimental animals for the carcinogenicity of dichlorvos.
Overall evaluation: Dichlorvos is possibly
carcinogenic to humans (2B).
CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Significant
increases in forestomach tumors in female and male B6C3F1 mice and leukemias and
pancreatic acinar adenomas in Fischer 344 rats. Supporting evidence included observation
of tumors at other sites in the rat and observation of mutagenicity for both dichlorvos and a major metabolite
dichloroacetaldehyde. A structurally related material, dichloropropene , also induces
forestomach tumors in rodents. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY
DATA: Sufficient.
Human Toxicity Excerpts:
HUMANS EXPOSED AT CONCN ... VARYING FROM 0.14 TO 0.33 MG/CU M FOR 30 MIN EACH HR, 10 HR
A DAY FOR 14 DAYS, SHOWED NO CHANGES IN CHOLINESTERASE OR IN NUMBER OF PHYSIOLOGICAL
FUNCTIONS. ... ON THE OTHER HAND, WHEN 28 HUMAN VOLUNTEERS WERE EXPOSED TO DICHLORVOS BY INHALATION AT A CONCN OF 1 MG/CU M,
SINGLE EXPOSURES OF 7.5-8.5 HR RESULTED IN PLASMA CHOLINESTERASE DEPRESSION OF 20-25%.
... PESTICIDE WORKERS HANDLING DICHLORVOS
/WERE SEEN TO HAVE A/ REDUCTION ... IN BLOOD CHOLINESTERASE AS WELL AS LEUKOCYTOSIS,
NEUTROPHILIA, & DECR IN LYMPHOCYTES & MONOCYTES. THESE WERE BACK TO NORMAL @ A 2
WK FOLLOW-UP FOLLOWING EXPOSURE.
After inhalation of dichlorvos, breathing and
eye effects are the first to appear. These include tightness of the chest, wheezing, a
bluish discoloration of the skin, small pupils, aching in and behind the eyes, blurring of
vision, tearing, runny nose, headache, and watering of the mouth. After /ingestion/ of dichlorvos, loss of appetite, nausea, vomiting,
abdominal cramps, and diarrhea may appear within two hours. After skin absorption,
sweating and twitching in the area of absorption may occur ... within 15 minutes to four
hours. With severe intoxication by all routes, in addition to all the symptoms /previously
mentioned/, weakness, generalized twitching, and paralysis may /result/ and breathing may
stop. In addition, dizziness, confusion, staggering, slurred speach, generalized sweating,
irregular or slow heart beat, convulsions, and coma /may result/.
RAPID DEGRADATION ... BOTH IN AIR & IN BODY, IS PROBABLY RESPONSIBLE FOR WIDE
MARGIN BETWEEN THAT CONCN WHICH CAUSES DETECTABLE EFFECT ON MOST SENSITIVE INDICATOR OF
EXPOSURE, PLASMA CHOLINESTERASE, & CONCN WHICH PRODUCES NOTICEABLE SYMPTOMS OF
ILLNESS.
The potency of dichlorvos to inhibit human
complement (C') activities of a panel of normal human sera was investigated in a modified
assay using human complement mediated lysis of sheep red cells (1) incorporating
suboptimal concn of sensitizing antibody, and (2) exhibiting incr sensitivity to serine
esterase inhibitors. Dichlorvos was added to
diluted sera 2 hr prior to incorporation into human complement reaction mixtures.
Potencies to inhibit human complement and serum cholinesterase were compared to potencies
of diisopropylfluorophosphate, a potent serine esterase inhibitor and a standard probe for
human complement esterases. At 0.5 to 3.0 mM, dichlorvos
produced a dose dependent inhibition of lysis. Mean IC50 for inhibition of cholinesterase
(a marker for occupational exposure to organophosphates and carbamates) by dichlorvos was 1.0x10-7 M. Potency of the insecticide
to inhibit cholinesterase did not predict absolute or relative potency to inhibit serum
human complement activity.
In man, dichlorvos inhibits plasma
cholinesterase more readily than red cell cholinesterase.
Mortality surveys and death certificate studies have suggested an association between
leukemia and farming. To investigate whether exposure to carcinogens in an agricultural
setting is related to risk of leukemia, a population based control interview study of 578
white men with leukemia and 1245 controls living in Iowa and Minnesota /was conducted/.
Consistent with recent mortality studies, there were slight, but significant, elevations
in risk for all leukemia (odds ratio 1.2) and chronic lymphocytic leukemia (odds ratio
1.4) for farmers compared to nonfarmers. There were no significant associations with
leukemia for exposure to specific fungicides, herbicides (including 2,4-D and 2,4,5-T), or
crop insecticides. However, significantly elevated risks for leukemia of \ 2.0 were seen
for exposure to specific animal insecticides including the organophosphates crotoxyphos
(odds ratio 11.1), dichlorvos (odds ratio 2.0),
and famphur (odds ratio 2.2) and the natural product pyrethrins (odds ratio 3.7) and the
chlorinated hydrocarbon methoxychlor (odds ratio 2.2). There were also smaller, but
significant, risks associated with exposure to nicotine (odds ratio 1.6) and DDT (odds
ratio 1.3). This finding of elevated risks for insecticides used on animals deserves
further evaluation.
MUTAGENICITY: SISTER CHROMATID EXCHANGE - IN VITRO CHROMOSOMAL EFFECT STUDIES, HUMAN:
NEGATIVE.
Skin, Eye and Respiratory Irritations:
Dichlorvos is not known to be an eye
irritant.
Drug Warnings:
VET: DO NOT USE IN CONJUNCTION WITH OR WITHIN FEW DAYS OF (BEFORE &/OR AFTER) ANY
OTHER CHOLINESTERASE INHIBITORS & AVOID USE WITH PHENOTHIAZINE, PHENOTHIAZONE
TRANQUILIZERS, ARSENICALS, PURGATIVES, OR DRUGS PRODUCING PURGATION AS SIDE EFFECT.
DO NOT ADMINSTER TASK /A FORMULATION/ ... DOG
ANTHELMINTIC IN CONJUNCTION WITH OTHER ANTHELMINTICS, TAENIACIDES, ANTIFILARIAL AGENTS
(DIETHYLCARBAMAZINE EXCEPTED), MUSCLE RELAXANTS OR TRANQUILIZERS. /TASK/
DO NOT ADMIN TO DOGS SHOWING SIGNS OF SEVERE CONSTIPATION, MECHANICAL BLOCKAGE OF
INTESTINAL TRACT, IMPAIRED LIVER FUNCTION, CIRCULATORY FAILURE, OR TO DOGS RECENTLY
EXPOSED TO OR SHOWING SIGNS OF INFECTIOUS DISEASES.
Medical Surveillance:
A complete history and physical examination. ... Examination of the respiratory system,
nervous system, cardiovascular system, and attention to the cholinesterase levels in the
blood should be stressed. The skin should be examined for chronic disorders. ... The
cholinesterase activity in the serum and erythrocytes should be determined by using
acceptable biochemical tests prior to any new period of exposure. ... Medical examinations
should be repeated on annual basis, with the exception of cholinesterase determination
which should be performed quarterly or at any time overexposure is suspected or signs or
symptoms of toxicity occur.
... Workers ... must undergo an annual medical exam at the beginning of each
agricultural season. Contraindications for work with organophosphorus pesticides are
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). 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 ... until
/cholinesterase level/ is completely restored. /Organophosphorus pesticides/
PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in
particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken
concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory.
/Chemical Carcinogens/
SERUM OR PLASMA: The literature search did not reveal reports of monitoring tests for
assessment of organophosphate pesticide absorption. Reference Ranges: Normal - Not
established; Exposed - Not established; Toxic - Not established. /Organophosphate
pesticides/
URINE: The assessment of organophosphate pesticide exposure can be accomplished through
measurement of the following alkyl phosphate metabolites: dimethylphosphate (DMP),
diethylphosphate (DEP), dimethylthiophosphate (DMTP), diethylthiophosphate (DETP),
dimethyldithiophosphate (DMDTP), and diethyldithiophosphate (DEDTP). Detection of
dimethylphosphate and diethylphosphate have been found to be directly attributable to
pesticide exposure. Detection of dimethyldithiophosphate and diethyldithiophosphate is
difficult since they are rapidly degraded and are less directly associated with pesticide
exposure, while dimethylthiophosphate and diethylthiophosphate levels can be produced from
other non-pesticide sources, limiting their usefulness as markers for pesticide
absorption. The one limitation to measurement of urinary alkyl metabolites is that this
test is only useful for assessing recent exposure, due to the short half-life of
organophosphate pesticides. In addition, there are tests for specific urinary phenolic
metabolites of certain organophosphate pesticides such as parathion (metabolite,
p-nitrophenol). However, since each pesticide gives rise to a different phenol metabolite,
it is probably not feasible to identify each urinary metabolite. Reference Ranges: Normal
- Not established; Exposed - Not established; Toxic - Not established. /Organophosphate
pesticides/
BAT for Acetylcholinesterase inhibitors (sampling time is end of exposure or end of
shift, or for long-term exposures sampling time is after several shifts: both measured as
acetylcholinesterase in erythrocytes): Reduction of activity to 70% of reference value.
/Organophosphate pesticides/
BEI (sampling time is discretionary): 70% of individual's baseline. /Organophosphate
pesticides/
Urine Albumin: Albuminuria has been shown to be a specific marker of glomerular
dysfunction. Tubular damage, however, can also result in increased levels of albumin in
the urine. /Organophosphate pesticides/
Urinary Beta-2-Microglobulin and/or Retinal Binding Protein (RBP): Measurements for the
presence of either of these low molecular weight proteins are useful in detection of early
impairment of proximal tubular function. However, beta-2-microglobulin is unstable at
urinary pH less than 6, and may degrade in the bladder prior to collection and subsequent
neutralization of the urine sample. Measurement of RBP appears to be a better marker for
early tubular dysfunction due to its stability in the urine subsequent to collection and
analysis. However, RBP is produced in the liver and not a constitutive protein of the
kidney, so that its presence in the kidney provides only indirect evidence of tubular
damage.
Urinary Alpha and Pi Isoenzymes of Glutathione S-Transferase: Radio-immunological and
Elisa techniques have been developed for quantitation of and isoenzymes of glutathione
S-transferase (GST), which are constitutive proteins in the kidney. The isoenzyme is
located only in the proximal tubule, while the isoenzyme is located in the distal
convoluted tubule, the loop of Henle, and the collecting ducts of the kidney. Damage to
epithelial cell membranes can result in the increased excretion of these isoenzymes in the
urine. This test for assessing renal tubular damage appears to have many advantages over
other available tests, such as: (1) the alpha and pi isoenzymes are constitutive proteins
in the kidney; (2) these isoenzymes are stable in the urine; (3) the test is simple and
reproducible; and (4) due to selective localization of the isoenzymes, differential
diagnosis of specific tubular damage is possible. In addition, increased levels of these
isoenzymes were seen in patients previously exposed to nephrotoxicants where conventional
tests for kidney function were normal, indicating a high degree of sensitivity.
/Organophosphate pesticides/
Urinary Enzyme N-acetylglucosaminidase: This lysosomal enzyme has shown promise in
assessment of subclinical nephrotoxic injury. This enzyme is not normally filtered at the
glomerulus due to its high molecular weight. In the absence of glomerular injury, this
enzyme will be detected in the urine as a result of leakage or exocytosis from damaged,
stimulated, or exfoliated renal cells. The sensitivity of measurement for this enzyme has
not been thoroughly studied, but its usefulness has shown some promise. However, this
enzyme is unstable at urinary pH greater than 8, which could diminish the sensitivity of
measurement due to enzyme degradation. /Organophosphate pesticides/
Routine Urinalysis: Performing a routine urinalysis including parameters such as
specific gravity, glucose, and a microscopic examination may be useful for assessing renal
toxicity. /Organophosphate pesticides/
Evaluation of Peripheral Neuropathy: nerve conduction study, electromyography (EMG),
quantitative sensory testing, thermography. /Organophosphate pesticides/
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 test. The areas that
the neuropsychology test batteries focus on include the domains of memory and attention;
visuoperceptual, visual 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. /Organophosphate pesticides/
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 - standardized odor threshold and identification testing; vision assessment -
standard acuity test, visual field tests, contrast sensitivity, and color vision
measurements (vision assessment); facial and trigeminal nerve assessment - blink reflex
(pontogram); vestibular assessment - pure tone audiometry for bone- and air-conducted
sounds, threshold decay at 4 kHz, speech discrimination and speech reception thresholds,
tympanograms and acoustic thresholds, electronystagmograms; hearing assessment -
audiometry testing. /Organophosphate pesticides/
Populations at Special Risk:
... Persons with a history of reduced pulmonary function, convulsive disorders, or
recent exposure to anticholinesterase agents would be expected to be at increased risk
from exposure.
DICHLORVOS IS RAPIDLY INACTIVATED BY ...
LIVER ENZYMES. ... PATIENTS WITH HEPATIC INSUFFICIENCY MAY BE LESS TOLERANT TO THE TOXIC
EFFECTS OF DICHLORVOS.
Work ... must not be carried out by young persons under 18 yr, expectant or nursing
mothers, or persons for whom work with toxic chemicals is contraindicated on account of
their state of health; the same applies to alcoholics. Contraindications for work with
organophosphorus pesticides are 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).
/Organophosphorus pesticides/
Probable Routes of Human Exposure:
Dichlorvos can affect the body if it is
inhaled, if it comes in contact with the eyes or skin, or is swallowed. ...
NIOSH (NOES Survey 1981-1983) has statistically estimated that 11,182 workers (2,182 of
these are female) are potentially exposed to dichlorvos
in the US(1). The NOES Survey does not include agricultural workers. Occupational exposure
to dichlorvos may occur through inhalation of
ambient air and dermal contact with this compound at workplaces where dichlorvos
is produced or used for household and public health insect control, flea collars and
no-pest strips(2,SRC). Similarly, the general population may be exposed to dichlorvos via inhalation of air and dermal contact
when no-pest strips, sprays or flea collars containing this insecticide are used. Exposure
could also result from ingestion of food which has been prepared in rooms where dichlorvos is used for insect control(SRC). As part of
EPA's Non-Occupational Pesticide Exposure Study (NOPES) conducted in the Summer 1986,
Spring 1987 and Winter 1988 in Jacksonville, FL and Springfield/Chicopee, MA the estimated
mean personal air concn of dichlorvos for
Jacksonville residents was 147.6, 40.2, and 21.4 ng/cu m in summer, spring and winter,
respectively(3). The estimated spring and winter concns for Springfield/Chicopee residents
were 3.7 and 2.1 ng/cu m in spring and winter. In Jacksonville, it was estimated that the
percentage of residents with detectable levels of dichlorvos
in personal air was 35%, 11%, and 16% in summer, spring and winter, respectively. In
Springfield/Chicopee only 2% and 1% of residents were exposed in spring and winter.
Exposure from air inhalation was the primary route of exposure to dichlorvos(3).
Dichlorvos was detected in the workplace
environment in concns of 77 ppb in air during production and processing of a dichlorvos-releasing vaporizer(1). During spraying of
an orchard 130 ppb was detected in air and a rate of skin contamination of 72 ug/100 sq
cm/hr was reported(1). After spraying, 114-765 ug/sq m of dichlorvos
was deposited on worker's clothing(3). A study was performed to determine the level of
exposure to 5 workers after 1.85 kg of dichlorvos
was sprayed on an apple orchard for 5.5 hr with an airblast sprayer(4). The air and
breathing zone dichlorvos concns were 1.0-15.4
ug/cu m, and 113.6-765.3 ug/cu m, respectively. Ambient air in storage rooms of four North
Carolina commercial pest control firms (4 hr period) contained 147-1501 ng/cu m, (617
ng/cu m avg)(2). Ambient air in offices of four North Carolina commercial pest control
firms (4 hr period) contained 19-66 ng/cu m, (41 ng/cu m avg)(2). A 1993 study of
insecticide concns in the air of 10 North Carolina pest control firms (19 samples)
resulted in mean dichlorvos air levels of 1.48
ug/cu m(5). Levels were higher in summer than in winter. In a study to determine the
dissipation of dislodgeable residues of dichlorvos
on turf, the residue level was 0.10 ug/sq cm immediately post application (<2 hr) and
rapidly declined to below the safe level for reentry, 0.06 mg/sq cm after two hours and
was undetectable (<1 ug/sample) after 23 hr(5). There was no significant difference in
post application dissipation of dislodgeable residues between irrigated and non-irrigated
plots. Dichlorvos was detected in air samples
immediately post-spray at 1.9 ppb(5). Three hours after application of dichlorvos
to greenhouse crops using low-volume (<50 l/ha) techniques, the atmospheric concn of dichlorvos had declined to 12% of the initial concn
but was still exceeding the 1000 ug/cu m threshold limit value (TLV)(6).
Body Burden:
Two pest control operators in Japan involved in spraying and mixing a combined
emulsifiable concentrate of fenithrothion and dichlorvos
to exterminated cockroaches in household construction contained mean and maximum alkyl
phosphate levels in urine of 0.099 and 0.22 ug/mg creatinine(1).
Average Daily Intake:
AIR INTAKE: 1.25 ug (Jacksonville, FL; assuming a weighted estimate of average daily
air concns of 62.4 ng/cu m(1)); 0.066 ug (Springfield/Chicopee, MA; assuming a weighted
estimate of average daily air concns of 3.3 ng/cu m(1)).
Emergency Medical Treatment:
Emergency Medical Treatment:
| EMT Copyright Disclaimer: |
| Portions of the POISINDEX(R) database are provided here for general
reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE
CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright
1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication,
replication or redistribution of all or part of the POISINDEX(R) database is a violation
of Micromedex' copyrights and is strictly prohibited. The following Overview, *** DICHLORVOS ***, 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 Dichlorvos is a very toxic poison by ingestion,
inhalation and eye or dermal contact. The most common
route of exposure is spillage on the skin, followed by
rapid absorption through the skin. Inhalation is the
second most common route; oral exposure is usualy only
by accident or suicide. Dichlorvos exposure symptoms
have a remarkably rapid onset and recovery.
o The following are general symptoms due to
anticholinesterase activity of the organophosphate
class of compounds. Not all of these effects may be
documented for dichlorvos, but could potentially occur
in individual cases.
1. MUSCARINIC EFFECTS (PARASYMPATHETIC) - Bradycardia,
hypotension, bronchospasm, bronchorrhea, salivation,
lacrimation, diaphoresis, urinary incontinence,
vomiting, diarrhea, miosis.
2. NICOTINIC EFFECTS (SYMPATHETIC/MOTOR) - Tachycardia,
hypertension, fasciculations, muscle cramps,
mydriasis, weakness, respiratory paralysis.
3. CENTRAL EFFECTS - CNS depression, agitation,
confusion, restlessness, anxiety, headache, psychosis,
delirium, coma, seizures.
o CHILDREN may have different predominant signs/symptoms
than adults: CNS depression, stupor, flaccidity,
dyspnea, and coma are the most common. Classic
muscarinic signs may not develop.
o Inhalation of dichlorvos may result in chest tightness,
wheezing, cyanosis, miosis, aching in and behind the
eyes, blurred vision, tearing, rhinorrhea, headache,
and excessive salivation. Symptoms after ingestion may
include anorexia, nausea, vomiting, abdominal cramps,
and diarrhea. Sweating and twitching in the area of
absorption may occur following dermal exposure.
o Severe intoxication from all routes of exposure may
include, in addition to all previously mentioned signs
and symptoms, weakness, generalized twitching,
paralysis, dizziness, slurred speech, generalized
sweating, irregular or slow heart beat, seizures, and
coma.
o Because dichlorvos is an organic ester of phosphoric
acid, it does not require metabolism to an active form
and may produce rapid onset of symptoms. Because of
its rapid metabolic detoxification, dichlorvos has an
unusually wide margin between inhibition of serum
cholinesterase and onset of clinical effects; recovery
is also rapid relative to other organophosphates.
o Hydrocarbon diluents and/or impurities in formulated
pesticides can enhance or contribute to toxicity.
VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
o Vital sign changes can include bradycardia or
tachycardia, hypotension or hypertension, tachypnea,
respiratory paralysis or fever.
HEENT
0.2.4.1 ACUTE EXPOSURE
o Miosis, lacrimation, blurred vision and salivation are
common; mydriasis may occur in severe poisonings.
CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
o Bradycardia or tachycardia, hypotension, cyanosis and
chest pain may occur. Arrhythmias and conduction
defects may occur in severe cases.
RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
o Dyspnea, rales, bronchorrhea, tachypnea, Cheyne-Stokes
respiration, or apnea may occur, with pulmonary edema
or paralysis of respiratory muscles and death 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, profound weakness,
paralysis, confusion, slurred speech and loss of
reflexes are common symptoms of dichlorvos
overexposure. Altered level of consciousness, seizures
and coma may occur. Seizures may be more common in
children.
o Delayed neuropathy has been reported.
GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
o Vomiting, diarrhea, fecal incontinence, pancreatitis
and abdominal pain may occur after exposure to
dichlorvos.
GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
o Increased urinary frequency or incontinence may occur
after exposure to dichlorvos.
ACID-BASE
0.2.11.1 ACUTE EXPOSURE
o Metabolic acidosis may occur in 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 Sweating is a consistent but not universal sign.
o Rare cases of primary irritant contact dermatitis have
occurred; dichlorvos may induce allergic contact
dermatitis.
MUSCULOSKELETAL
0.2.15.1 ACUTE EXPOSURE Muscle weakness, fatigability and
twitching may occur after dichlorvos exposure.
ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
o Hyperglycemia and glycosuria (with or without ketosis)
may occur in severe poisoning.
METABOLISM
0.2.17.1 ACUTE EXPOSURE
o The hallmark of organophosphate poisoning is inhibition
of plasma pseudocholinesterase or erythrocyte
acetylcholinesterase, or both.
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.
IMMUNOLOGIC
0.2.19.1 ACUTE EXPOSURE
o Pesticide workers exposed to dichlorvos were reported
to have temporary leukocytosis, neutrophilia and a
decrease in lymphocytes and monocytes; this resolved
in 2 weeks (HSDB, 2000).
REPRODUCTIVE HAZARDS
o Studies have produced conflicting results on the
teratogenicity of dichlorvos; there is evidence of
links to specific developmental abnormalities in
experimental animals. Dichlorvose also increased
post-implantation mortality and fetotoxiticity in
rabbits, and produced changes in rat and mouse
spermatogenesis.
o It does not appear in the milk of cattle or rats.
o Sporadic reports of human birth defects related to
organophosphates have not been fully verified.
CARCINOGENICITY
0.2.21.1 IARC CATEGORY
o IARC (Dichlorvos) (IARC, 1997) -
1. Human: Inadequate evidence; Experimental animals:
Sufficient evidence.
2. Group 2B: "possibly carcinogenic to humans"
0.2.21.2 HUMAN OVERVIEW
o Dichlorvos has been categorized as a "probable human
carcinogen", as "possibly carcinogenic to humans", and
as having inadequate data to determine its
carcinogenic classification.
0.2.21.3 ANIMAL OVERVIEW
o Dichlorvos is considered carcinogenic and neoplastic by
RTECS criteria for rats and mice. However, studies
have produced conflicting results about the
tumorigenicity of dichlorvos in experimental animals.
GENOTOXICITY
o Dichlorvos has reportedly induced DNA damage, repair,
and unsceduled synthesis, mutations, chromosome
aberrations and sister chromatid exchanges, sex
chromosome loss and nondisjunction, and morphological
transformations in short-term assays in vitro.
|
| Laboratory: |
o Dichlorvos is not detectable in tissues because of its
rapid degradation.
o Determine plasma and red blood cell cholinesterase
activities. Although there may be poor correlation
between cholinesterase values and clinical effects, a
depression in excess of 50 percent activity is generally
associated with severe symptoms. The correlation between
cholinesterase levels and clinical effects in milder
poisonings may be poor.
o Monitor cardiac rhythm, pulse oximetry and arterial blood
gasses, and follow chest X-rays in patients with
substantial respiratory or nicotinic signs or symptoms.
|
| 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.
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.
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 Decreases in serum and erythrocyte cholinesterase
activities without adverse clinical effects have been
reported from occupational exposures.
o Acute toxicity is variable and depends strongly on 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 compound.
|
Antidote and Emergency Treatment:
Exptl Therapy: Acidosis in dogs /resulting from/ poisoning with DDVP
(30 mg/kg iv) was treated effectively by injections of sodium bicarbonate (10
milliequivalent IV/kg IV, given in 3 injections). Sodium bicarbonate increased the
survival rate of DDVP poisoned dogs to 84.62%.
...
Exptl Therapy: Diethyxime, a non-quaternary cholinesterase reactivator was evaluated
for its antidotal efficacy against organophosphorus intoxication in rats using the
protection index, cholinesterase reactivation and neuromuscular function as the
experimental protocol. Diethyxime along with atropine produced a marked antidote against dichlorvos on all the parameters studied. The action
of diethyxime was mainly peripheral. ...
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 TKO /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
... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organophosphates and
Related compounds/
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. ... IN MODERATELY SEVERE POISONING: ADULT DOSAGE AND CHILDREN
OVER 12 YR: 0.4-2.0 MG REPEATED EVERY 15 MIN UNTIL ATROPINIZATION IS ACHIEVED. MAINTAIN
ATROPINIZATION WITH REPEATED DOSAGE OF 0.02-0.05 MG/KG BODY WEIGHT. /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. ... ADULT DOSAGE AND CHILDREN OVER 12): GIVE 1.0-2.0
G IV @ NO MORE THAN 0.2 G/MIN. CHILD'S DOSE (UNDER 12 YR): GIVE 20-50 MG/KG (DEPENDING ON
SEVERITY) IV, INJECTING NO MORE THAN HALF TOTAL DOSE/MIN. DOSAGE...MAY BE REPEATED IN 1-2
HR, THEN @ 10-12 HR INTERVAL IF NEEDED. IN VERY SEVERE POISONINGS, DOSAGE...MAY BE
DOUBLED. /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 GASTRIC CONTENTS. 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. ADULTS AND CHILDREN OVER 12 YEARS:
50-100 G IN 300-800 ML WATER. CHILDREN UNDER 12: 1.0-1.5 G/KG BODY WEIGHT TO A MAXIMUM OF
50 G PER DOSE. ALTERNATIVE CATHARTICS THAT MAY BE USED INSTEAD ARE SODIUM OR MAGNESIUM
SULFATE OR CITRATE: DOSAGE OF SODIUM OR MAGNESIUM SULFATE: ADULTS AND CHILDREN OVER 12
YEARS: 20-30 G. CHILDREN UNDER 12 YEARS: 250 MG/KG BODY WEIGHT. DOSAGE OF MAGNESIUM
CITRATE SOLUTION: ADULTS AND CHLIDREN: 4 ML/KG BODY WEIGHT OF PROPRIETARY SOLUTION, UP TO
A MAXIMUM OF 300 ML. 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/
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Evaluation: There is inadequate evidence in humans for the carcinogenicity of dichlorvos. There is sufficient evidence in
experimental animals for the carcinogenicity of dichlorvos.
Overall evaluation: Dichlorvos is possibly
carcinogenic to humans (2B).
CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Significant
increases in forestomach tumors in female and male B6C3F1 mice and leukemias and
pancreatic acinar adenomas in Fischer 344 rats. Supporting evidence included observation
of tumors at other sites in the rat and observation of mutagenicity for both dichlorvos and a major metabolite
dichloroacetaldehyde. A structurally related material, dichloropropene , also induces
forestomach tumors in rodents. HUMAN CARCINOGENICITY DATA: None. ANIMAL CARCINOGENICITY
DATA: Sufficient.
Non-Human Toxicity Excerpts:
MUTAGENICITY; MAMMALIAN CYTOGENETICS - IN VIVO BONE MARROW STUDIES, NON-HUMAN:
NEGATIVE; MALE GERM CELL STUDIES, NON-HUMAN: NEGATIVE.
MUTAGENICITY: DNA REPAIR-DEFICIENT BACTERIAL TESTS: POSITIVE.
MUTAGENICITY: ESCHERICHIA COLI WP2,UVRA - REVERSE MUTATION STUDIES: POSITIVE;
ESCHERICHIA COLI WP2 - REVERSE MUTATION STUDIES: POSITIVE.
MUTAGENICITY: ASPERGILLUS DOMINANT LETHAL MUTATION: POSITIVE; ASPERGILLUS ANEUPLOIDY:
POSITIVE; ASPERGILLUS CROSSING OVER: POSITIVE.
/IN MALLARDS & PHEASANTS/, THE SYMPTOMOLOGY /(ACUTE ORAL TOXICITY)/ INCLUDED:
GOOSE-STEPPING ATAXIA, USE OF WINGS TO AID IN BALANCE, TREMORS, CONVULSIONS. VARIOUS
INTERNAL HEMORRHAGES WERE FOUND AT AUTOPSY IN SACRIFICED SURVIVORS OF BOTH SPECIES.
... DICHLORVOS ... /WEAKLY/ TERATOGENIC IN
SHERMAN STRAIN OF RAT, WHEN ADMIN IP ON DAY 11 OF GESTATION @ DOSE LEVEL WHICH CAUSED
SEVERE TOXIC SYMPTOMS IN DAMS. ... DECR FETAL BODY WT WAS MOST SENSITIVE INDICATOR /OF
TOXICITY/. ...
... CHOLINERGIC POISONING ... INCLUDES MUSCULAR FASCICULATIONS, RETCHING, EMESIS,
FREQUENT DEFECATION OF WATERY STOOLS, PUPIL CONTRACTION, SECRETION OF TEARS, & LABORED
BREATHING ASSOCIATED WITH CONSTRICTION OF BRONCHIOLES.
RATS FED NINETY DAYS ON DIET ... 1000 PPM ... NO SIGNS OF INTOXICATION.
SINGLE ORAL TOXIC DOSE (THAT PRODUCES OBSERVABLE DEVIATION IN ANIMAL'S BEHAVIOR) IS
GIVEN ... AS 10 MG/KG ... & 25 MG/KG ... IN CALVES & SHEEP RESPECTIVELY. WHEN
APPLIED AS SPRAY TO CATTLE AT CONCN OF 1% HAD NO OBSERVABLE TOXICITY.
DICHLORVOS A 2 YR INHALATION CARCINOGENESIS
STUDY IN RATS; SPECIES- CARWORTH FARM E; DEPRESSED GROWTH; INCR SURVIVAL IN RATS EXPOSED
TO 5 MG/CU M/2 YR; NO DOSE RELATED INCREASE IN TUMOR RISK.
BIOASSAY FOR CARCINOGENICITY OF TECHNICAL GRADE DICHLORVOS
ADMIN IN DIET TO RATS AND MICE FOR 80 WK AT 150 AND 326 PPM (RATS) OR 318 AND 635 PPM
(MICE); NO STATISTICALLY SIGNIFICANT INCR IN TUMOR INCIDENCE.
DICHLORVOS WAS A MUTAGEN IN THE SCREENING
TEST FOR MUTAGENICITY USING A REC-ASSAY PROCEDURE, WITH H17 REC(+) AND M45 REC(-) STRAINS
OF BACILLUS SUBTILIS AND REVERSION ASSAYS ON AUXOTROPHIC STRAINS OF ESCHERICHIA COLI (WP2)
AND SALMONELLA TYPHIMURIUM (AMES SERIES).
FEMALE MICE WERE TREATED WITH 25 OR 50 MG/KG ORALLY OR 2 OR 8 UG/L BY INHALATION; NO
EFFECT ON % PREGNANT, NUMBER FETAL IMPLANT, OR NUMBER OF EARLY FETAL DEATHS; NO DOMINANT
LETHAL MUTATIONS WERE INDUCED AFTER /ORAL/ DOSING WITH HIGH CONCN OF DICHLORVOS.
MODERATE NEUROPATHIC RESPONSE WAS OBTAINED IN HENS 2 WK AFTER BEING GIVEN SINGLE
MASSIVE SC DOSE OF DICHLORVOS (100 MG/KG OF
ACTIVE INGREDIENT IN COMMERCIAL 50% FORMULATION).
INCUBATION OF QUAIL EMBRYOS IN DDVP ENRICHED
ATMOSPHERE REVEALS BOTH EMBRYOTOXIC & TERATOGENIC EFFECTS OF THIS PESTICIDE. MULTIPLE
MALFORMATIONS ASSOC TO THOSE ASCRIBED TO ANTICHOLINESTERASE ACTION: LORDOSIS, SCOLIOSIS.
Effects of various neuropharmacologic agents on the motility of Dipylidium caninum were
studied ... paralytic effects were caused by ... dichlorvos.
...
Inhalation of dichlorvos at 0.0071 mg/l/hr in
rats caused polyuria, dyspnea, paralysis, restlessness, heavy gasping, salivation, and
loss of muscular coordination, balance, and body weight, but an increase in lung weight
with mild to severe cellular infiltration around the bronchioles causing a mild edema in
the lungs.
/Dichlorvos was/ tested for toxicity and
mutagenicity in the forward mutation test system ade6 of the yeast Schizosaccharomyces
pombe. Dichlorvos showed a linear dose response
relationship for mutagenicity.
The effect of sublethal (1/4th, 1/8th, and 1/16th of 96 hr LC50) of dichlorvos
on blood glucose, lactate, and liver and muscle glycogen levels of Clarias batrachus,
Saccobranchus fossilis, and Mystus vittatus exposed for 30 days. There was an increase in
blood glucose and lactate levels from 10.88 to 36.36% and a decrease in liver and muscle
glycogen from 5.19 to 32.19%.
Effects of O,O-dimethyl O-(2,2-dichlorovinyl) phosphate on the brain cholinergic system
in Japanese quail /were investigated/. Cholinergic signs, such as salivation and
convulsions in legs and wings, were seen 7-15 minutes after administration of DDVP. In the DDVP-treated
quail (10 min after dosage of 3 mg/kg), free acetylcholine and labile-bound acetylcholine
increased significantly while acetylcholinesterase decreased to 28% of the value
determined in untreated quail.
MUSCARINIC SIGNS OF /ORGANOPHOSPHORUS CMPD/ ... 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 ... CMPD, BUT ROUTE OF
ABSORPTION MAY INFLUENCE ONE SYSTEM MORE THAN ANOTHER. /ORGANOPHOSPHORUS CMPD/
The effect of dichlorvos on various lipid
fractions and lipid peroxidation in the discrete areas of the brain and spinal cord were
studied in the fresh water teleost Heteropneustes fossilis exposed to three different
doses (3.0, 6.0, and 9.0 ppm) of dichlorvos
daily for 7 days. Dose related incr in the levels of total lipids, cholesterol and
esterified fatty acids was detected in the fore brain, optic lobes, cerebellum, medulla
oblongata and spinal cord. However, phospholipids were significantly decreased in the
aforementioned regions of the central nervous system. The rate of lipid peroxidation was
significantly increased in all the regions of the central nervous system.
Clinical and pulmonary function changes induced by iv administration of dichlorvos, the toxicosis and reversibility of these
changes after atropine treatment were investigated using six Friesian calves one to three
months old. From one minute after dosage, all animals exhibited severe respiratory
distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decr
in dynamic lung compliance and arterial oxygen tension and incr in total pulmonary
resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly
significant (p< 0.01). Body secretions, heart rate, respiratory rate, tidal volume and
arterial carbon dioxide tension were not significantly affected by dichlorvos
injection. Atropine promptly and completely reversed these changes, except for muscle
fasciculations, central depression and cholinesterase inhibition which disappeared
progressively within 24 hours.
Three organophosphate compounds, dichlorvos,
parathion, and diisopropylfluorophosphate were tested as an unconditioned stimulus in the
conditioned taste aversion test. All three compounds caused a dose dependent CTA in rats
at doses which did not induce any other signs of toxicity. Experiments with dichlorvos indicated that the minimum dose which
caused conditioned taste aversion did not alter the rat's sensitivity to pain or their
behavior in either an open field or an inclined plane. Cholinesterase activity was
inhibited in a dose dependent manner in brain and plasma after administration of the
organophosphates and conditioned taste aversion was correlated with the degree of plasma
cholinesterase inhibition. CTA appears to be a sensitive indicator of neurobehavioral
effects of mild exposure to organophosphates which causes only 30-40% inhibition of plasma
cholinesterase.
Alanine aminotransferase and aspartate transferase activities in the liver, brain, and
muscle were increased following ip administration of dichlorvos
to mice (4 mg/kg/day for 5 days). The incr was the highest in the liver. Dichlorvos
also increased the glutamate dehydrogenase activity. The incr was more in the liver than
in the muscle and brain.
Snails (Thiara torulosa) were exposed in 2 liter tanks to dichlorvos
at concn causing 5 to 95% mortality. Oxygen consumption was measured before and after 24
hr of exposure to the insecticide. At 24, 48, 72, and 96 hr of dichlorvos
exposure, the LD50 (mg/ml) and 95% confidence limits, respectively, were as follows: 12.66
(11.44-14.00), 10.69 (9.73-11.75), 9.40 (8.39-10.47), and 8.70 (7.58-10.02). Oxygen
consumption values after insecticide exposure showed a significant incr at sublethal
concn, but decr at concn > LC50.
Three of 12 dogs given 22 mg/kg of dichlorvos
orally died. The effect of dichlorvos on plasma
and erythrocyte cholinesterase activity in the dog and the rate at which these
subsequently return to normal have been studied ... . No adverse effects, other than a
reversible erythema and loss of hair in one animal, were produced in dogs wearing plastic
collars, containing dichlorvos. ... Dogs wearing
either collars impregnated with 9.3% of dichlorvos
or medallions containing 18.3% of this material were unaffected, whereas those wearing
collars, with 16.5% of dichlorvos plus 1%
chlorpyrifos developed characteristic skin lesions after four weeks.
Horses: Signs of intoxication developed in two of four foals given 50 mg/kg body weight
of dichlorvos orally, whereas all the animals
given twice this level or more were affected.
Administration of dichlorvos does not result
in residues in the tissues or the eggs of poultry. Suspected malicious dichlorvos
poisoning which resulted in the death of 27,000 one month old chickens has been described
... . Dichlorvos can cause decreased
hatchability and laying capacity and an increase in the number of abnormal chicks in
pheasants.
Cats wearing dichlorvos impregnated collars
in a warm, dry atmosphere have developed clinical signs including an ataxia depression
syndrome and cervical contact dermatitis. Many of the severely affected cats were anemic
and some animals died. Cats wearing three impregnated collars developed classical acute
organophosphorus compound poisoning. Although some initial and transient inhibition of
whole blood and tissue cholinesterase activity can occur, the wearing of a single flea
control collar should not produce any untoward effects in cats.
Application of dichlorvos to cattle does not
result in residues in the tissue or milk. The minimum toxic concentration of dichlorvos in spray form to baby calves 0.05-0.1%, and
the lethal concentration 0.25%.
Recovery of plasma and erythrocyte cholinesterase is slow in pigs treated with dichlorvos. The piglets of dichlorvos
treated gilts have a higher liver glycogen level and show a slower increase in body weight
during the first 72 hours of age than the piglets of untreated gilts. Dichlorvos
does not have any teratogenic effect in the pig. No intact dichlorvos
is found in the blood or tissues of treated pigs.
The question has remained open, whether or not the pesticide dichlorvos
(DDVP) should be classified as a carcinogen. The
results of a long term experiment of testing DDVP
in male and female C57B1/6/B1n mice ... did not indicate the development of neoplastic
lesions due to the administration of the compound. /Results of a/ long term administration
of DDVP to male and female BD IX/Bln rats /has
been reported/. In the groups of male rats a increased incidence of proliferations of bile
duct cells and of oval cells of the liver was observed, which was statistically
significant (p< 0.05) in the group of the higher dosed animals when compared with the
group of the vehicle control male rats. Among the DDVP
treated female rats a significantly decreased incidence of tumors of the adrenal glands
and of mammary tumors was observed as compared to the vehicle control group. Similar
results were obtained in earlier experiments, when rats were treated with Trichlorofon,
which easily converts to DDVP. In comparison to
the corresponding control group DDVP treated
male rats showed a higher incidence of focal, hyperplasias of the urinary bladder, of
focal hyperplasias of the pelvis and of transitional cell carcinomas of the renal pelvis. DDVP treated female rats showed the opposite, namely
lower incidences of these types of tumors, when compared with the control group. In our
study on rats there were no neoplastic lesions found which could be attributed to the
treatment of the animals with DDVP.
Up to now the question remained open, whether or not the pesticide dichlorvos,
should be classified as a carcinogen. /Results of a/ long time oral administration /study/
to male and female C57B1/6/B1n mice of dichlorovos to test the compound for carcinogenic
activity /has been reported/. Dichlorvos
significantly increased the incidence of focal hyperplasias (transitional cell
hyperplasias) of the urinary bladder in male and female mice and decreased significantly
the incidence of mixed lymphomas in mice of both sexes as compared with control animals
(treated with solvent or untreated). There were no neoplastic lesions found including
papillomas of the urinary bladder which could be attributed to the treatment of the
animals with dichlorvos.
The induction of chromosomal aberrations by insecticides was studied in hamsters.
Female Syrian golden hamsters were injected ip with a median lethal dose (LD50), 0.5 LD50,
0.25 LD50, or 0.1 LD50 of demeton, dimethoate, dichlorvos,
endosulfan, trichlorofon, a carbaryl and lindane mixture, a methoxychlor and propoxur
mixture, malathion, or 40 mg/kg cyclophosphamide, the positive control. After 22 hours,
animals were injected with 0.8% colchicine. After 24 hours, bone marrow was isolated,
chromosome preparations were made, and the average mitotic index was calculated. At least
50 metaphases obtained from bone marrow of each animal were analyzed. The activity of the
insecticides was compared with those of positive and negative controls. Cyclophosphamide
induced aberrations in 9% of the analyzed cells, significantly higher than 1.3% in the
negative controls. Chromosomal aberrations increased after insecticide administration. The
most commonly observed abnormalities were gaps and breaks, mainly chromatid type, and some
single dicentric and ring chromosomes. Demeton, dichlorvos,
endosulfan, propoxur mixture, malathion, and dimethoate caused statistically significant
increases in aberrant cells. Dimethoate was weakly clastogenic. Demeton was clastogenic in
the three highest doses used. Aberrant cells observed after administration of the highest
doses of dichlorvos and endosulfan did not
differ from those of the positive control. Statistically significant increases in aberrant
cells after some doses of malathion and propoxur mixture indicated that these compounds
were potential carcinogens. Lindane mixture and trichlorfon did not induce chromosomal
aberrations. It was concluded that dichlorvos,
demeton, dimethoate, and malathion induce chromosomal aberrations in the bone marrow of
Syrian hamsters.
The efficacy of a leukemia cell transplant model to measure potential chemotherapeutic
activity was tested with five different chemicals that had previously been evaluated in 2
year studies. Leukemic spleen cells from Fischer rats were injected subcutaneously into
syngeneic recipients and the effects of chemical treatment on tumor progression were
evaluated at 70 days post transplant. The data from the short term assay were in all cases
correlated with the trends reported for mononuclear cell leukemia in 2 year studies, where
two chemicals were reported to decease the incidence and three chemicals were reported to
increase the incidence of leukemia. Short term treatment with the two chemicals which
caused negative trends for leukemia (2-ethoxyethanol or ethylene glycol monoethyl ether;
4-hexylresorcinol) delayed and/or reduced tumor growth in the transplant model in a dose
related fashion, as exhibited by reduction or elimination of splenomegaly and
leukoblastosis, and a reversal in the depression of red blood cell indices or platelet
counts. By contrast, the rate of tumor progression was increased in the short term assay
of the three chemicals which previously caused increased trends for leukemia in 2 year
studies (pyridine; 2,4,6-trichlorophenol, dichlorvos).
The severity of the mononuclear cell leukemia in the transplant recipients, as measured by
histopathological examination of spleen and liver, was correlated with the changes in
tumor growth rates. The in vivo leukemia transplant model is a short term assay that could
be used to screen a variety of potential chemotherapeutic agents, or to study structure
activity relationships within one class of chemicals.
The neurotoxic effect on the central and peripheral nervous system of dichlorvos
(DDVP) was investigated by a computer system in
acute and subchronic experiments in CFY male rats. The administered peroral doses were
given by gavage; the acute group was given a single 88 mg/kg dose and the 2 subchronic
groups were given 1.6 mg/kg or 0.8 mg/kg daily for a period of 6 weeks. Significant
changes of the function of CNS, increase of EEG mean frequency, decrease of EEG amplitude,
that of activity of EEG bands (power density), and peripheral nervous system, decrease of
conduction velocity, increase of relative and absolute refractory periods, were found
after treatment with both the single large and repeated small doses of dichlorvos.
There were no correlations between the functional disturbances of the central and
peripheral nervous systems and the inhibition of the cholinesterase activity in various
organs and the blood.
The organophosphate pesticide, dichlorvos (DDVP), is used commonly to control ectoparasites in
laboratory rodent colonies. This compound is relatively nontoxic to Mus musculus at
dosages several times the therapeutic level. However, usage of a similar therapeutic level
in the white-footed mouse (Peromyscus leucopus) resulted in substantial mortality. To
determine whether Peromyscus leucopus is more susceptible than Mus musculus to the toxic
effects of DDVP, both species were exposed to 0,
3 and 6 g of pelleted DDVP per cage. In a
subsequent experiment, Peromyscus leucopus were exposed to 0 and 1 g of DDVP
per cage. Mortality was not observed in Mus musculus at any dosage level. Peromyscus
leucopus exposed to 1, 3 and 6 g of DDVP
exhibited mortalities of 3%, 20% and 53%, respectively. Mean serum cholinesterase in
Peromyscus leucopus exposed to 3 and 6 g of DDVP
was 0.35 and 0.21 U/ml as compared to 3.13 U/ml in unexposed mice. The analogous values
for Mus musculus were 1.60 and 0.79 U/ml while the level in unexposed mice was 6.79 U/ml.
In the second experiment, mean serum cholinesterase in Peromyscus leucopus exposed to 1 g
of DDVP was 0.32 U/ml as compared to 2.33 U/ml
in unexposed mice. Histopathology revealed no lesions in the brain, liver or kidneys. The
increased susceptibility of Peromyscus leucopus to the toxic effects of DDVP
was related to the lowered serum cholinesterase. This indicates that DDVP
should not be used for control of ectoparasites in Peromyscus leucopus.
Dichlorvos (dichlorovinyl dimethyl phosphoric
acid ester) is a cholinesterase inhibitor used widely as a contact and stomach insecticide
for control of internal and external parasites. Carcinogenesis studies were conducted by
administering dichlorvos in corn oil by gavage 5
times a week for 103 weeks to groups of 50 male and 50 female Fischer rats at 0, 4, or 8
mg/kg body weight, to groups of 50 male B6C3F1 mice at 0, 10, or 20 mg/kg, and to groups
of 50 female B6C3F1 mice at 0, 20, or 40 mg/kg. During the course of the studies, body
weights and survival rates of the male and female rats and mice were not different from
those of their respective controls; females of both species appeared to gain more weight
than controls. Neoplasms induced by dichlorovos included adenomas of the exocrine pancreas
(male rats), mononuclear cell leukemia (male rats), and squamous cell papilloma of the
forestomach (male and female mice; two other female mice had squamous cell carcinomas).
Lesions observed in female rats that may have been due to dichlorvos
administration included adenomas of the exocrine pancreas and fibroadenomas of the mammary
gland. The results demonstrated that dichlorvos
is carcinogenic for Fischer rats and B6C3F1 mice.
To test whether exposure to dichlorvos vapors
for treatment of mouse ectoparasites resulted in temporary cessation of breeding, we
exposed harem breeding groups of mice to varying concentrations of dichlorvos
vapors and examined the effects of exposure on litter frequency and litter size. All
exposure levels resulted in decreased plasma cholinesterase concentrations in treated mice
for up to 10 days following the completion of exposure. Litter freqency and size were
unaffected by dichlorvous exposure, and gestation times were not prolonged. Therefore,
treatment with dichlorvos vapors during breeding
did not affect reproduction in exposed mice.
National Toxicology Program Studies:
Two yr studies of dichlorvos were conducted
by admin 0, 4, or 8 mg/kg dichlorvos 5 days/wk
for 103 wk, to groups of 50 F344/N rats of each sex. Groups of 50 male B6C3F1 mice were
admin 0, 10, or 20 mg/kg dichlorvos on the same
schedule, and groups of 50 B6C3F1 female mice were admin 0, 20, or 40 mg/kg dichlorvos. Body Weight and Survival in the Two Year
Studies: Mean body weights of dosed and vehicle control rats and mice were similar. No
significant differences in survival were observed between any groups of rats or mice of
either sex (Rats male: vehicle control, 31/50; low dose, 25/50; high dose, 24/50; Rats
female: 31/50; 26/50; 26/50; Mice male: 35/50; 27/50; 29/50; Mice female: 26/50; 29/50;
34/50). Neoplastic Effects in the Two Year Studies: Adenomas of the exocrine pancreas
occurred at greater incidence in dosed rats than in vehicle controls (male: vehicle
control, 25/50; low dose, 30/49; high dose 33/50; female: 2/50; 3/47; 6/50). Mononuclear
cell leukemia in both dosed groups of male rats occurred more frequently than in vehicle
controls (11/50; 20/50; 21/50). Mammary gland fibroadenomas and fibroadenomas or adenomas
(combined) in dosed female rats occurred at incr incidence relative to the vehicle
controls (9/50; 19/50; 17/50). Multiple fibroadenomas occurred in dosed female rats but
not in vehicle controls (0/50; 6/50; 3/50); carcinomas occurred in two vehicle control and
two low dose female rats. In mice, incidence of squamous cell papillomas of the
forestomach was incr in the high dose groups compared with those in the vehicle controls
(1/50; 1/50; 5/50; female: 5/49; 6/49; 18/50). Two high dose female mice developed
forestomach carcinomas. Conclusions: Under the conditions of these 2 yr gavage studies,
there was some evidence of the carcinogenic activity of dichlorvos
for male F344/N rats as shown by incr incidence of adenomas in the exocrine pancreas and
mononuclear cell leukemia. There was equivocal evidence of carcinogenic activity of dichlorvos in female F344/N rats as shown by incr
incidence of adenomas of the exocrine pancreas and mammary gland fibroadenomas. There was
some evidence of the carcinogenic activity of dichlorvos
for male B6C3F1 mice as shown by incr incidence of forestomach squamous cell papillomas.
There was clear evidence of carcinogenic activity of dichlorvos
for female B6C3F1 mice as shown by incr incidence of forestomach squamous cell papillomas.
A bioassay for the possible carcinogenicity of technical grade dichlorvos
was conducted using Osborne-Mendel rats and B6C3F1 mice. The test material was admin in
the diet at two concn for 80 wk to groups of 50 animals of each species and sex. The test
animals were held for observation, and surviving rats were /sacrificed/ at 110-111 wk and
surviving mice at 92-94 wk from the initiation of the study. Initial doses in both species
were not well tolerated and they were lowered after a few wk. Time weighted avg doses for
both males and females were 150 and 326 ppm for the rats and 318 and 635 ppm for mice. The
matched controls consisted of 60 rats of each sex, 100 male mice, and 80 female mice. All
surviving rats were /sacrificed/ at 106 to 109 wk; surviving mice at 92-94 wk. After the
doses were reduced, no toxic signs directly attributable to the cmpd were observed.
However, avg weights of high dose animals were slightly depressed. Survival was not dose
related in either species. Microscopic study of the tissues of treated animals and matched
and pooled controls revealed no statistically significant incr in the incidence of tumors
attributable to exposure to dichlorvos in either
animal species. The significance of the three esophageal tumors in male and female mice
and of malignant fibrous histiocytomas in male mice is unclear and there is insufficient
evidence to indicate they were associated with dichlorvos
treatment. Thus under the conditions of this study, dichlorvos
was not demonstrated to be carcinogenic. Levels of Evidence of Carcinogenicity: Male Rats:
Negative; Female Rats: Negative; Male Mice: Negative; Female Mice: Negative.
Non-Human Toxicity Values:
LD50 Rat acute oral 56 to 80 mg/kg.
LD100 Dog 30 mg/kg in 27 minutes
LD50 Rat oral 17 mg/kg
LC50 Rat ihl 15 mg/cu m/4 hr
LD50 Rat skin 70,400 ug/kg
LD50 Rat ip 23,300 ug/kg
LD50 Rat sc 10,800 ug/kg
LD50 Mouse oral 61 mg/kg
LC50 Mouse ihl 13 mg/cu m/4 hr
LD50 Mouse skin 206 mg/kg
LD50 Mouse ip 22 mg/kg
LD50 Rabbit skin 107 mg/kg
LD50 Rabbit oral 10 mg/kg
LD50 Dog oral 100 mg/kg
LD50 Mouse iv 18 mg/kg
LD50 Mouse sc 24 mg/kg
LD50 Rat male oral 80 mg/kg
LD50 Rat female oral 55 mg/kg
LD50 Rat male dermal 107 mg/kg
LD50 Rat female dermal 75 mg/kg
Ecotoxicity Values:
LC50 FATHEAD MINNOW 11,600 UG/L/96 HR @ 17 DEG C (95% CONFIDENCE LIMIT 7,830-17,200
UG/L) WT 0.7 G IN A STATIC BIOASSAY /TECHNICAL MATERIAL, 93%/
LC50 BLUEGILL 869 UG/L/96 HR @ 18 DEG C (95% CONFIDENCE LIMIT 700-1,080 UG/L), WT 1.5 G
IN A STATIC BIOASSAY /TECHNICAL MATERIAL, 100%/
LC50 MOSQUITOFISH 5,270 UG/L/96 HR @ 17 DEG C (95% CONFIDENCE LIMIT 2,660-10,400 UG/L),
WT 0.2 G IN A STATIC BIOASSAY /TECHNICAL MATERIAL, 100%/
LC50 CUTTHROAT TROUT 170 UG/L/96 HR @ 12 DEG C (95% CONFIDENCE LIMIT 143-203 UG/L), WT
2.5 G IN A STATIC BIOASSAY /TECHNICAL MATERIAL, 100%/
LC50 PTERONARCYS 0.10 UG/L/96 HR @ 15 DEG C (95% CONFIDENCE LIMIT 0.07-0.15 UG/L), 2ND
YR CLASS IN A STATIC BIOASSAY /TECHNICAL MATERIAL 100%/
LC50 GAMMARUS LACUSTRIS 0.50 UG/L/96 HR @ 21 DEG C (95% CONFIDENCE LIMIT 0.37-0.68
UG/L), MATURE IN A STATIC BIOASSAY /TECHNICAL MATERIAL, 100%/
LC50 Gammarus faciatus 0.40 ug/l/96 hr /Conditions of bioassay not specified/
LC50 Crangon septemspinosa (sand shrimp) 4 ppb/96 hr in a static bioassay
LC50 Palaemonetes vulgaris (grass shrimp) 15 ppb/96 hr in a static bioassay
LC50 Pagurus longicarpus (hermit crab) 45 ppb/96 hr in a static bioassay
LC50 Bluegill 1000 ppm/24 hr /Conditions of bioassay not specified/
LC50 Fundulus heteroclitus (mummichog) 2680 ppb/96 hr in a static bioassay
LC50 Fundulus majalis (striped killifish) 2300 ppb/96 hr in a static bioassay
LC50 Menidia menidia (Atlantic silverside) 1250 ppb/96 hr in a static lab bioassay
LC50 Mugil cephalus (striped mullet) 200 ppb/96 hr in a static lab bioassay
LC50 Anguilla rostrata (American eel) 1800 ppb/96 hr static lab bioassay
LC50 Thalassoma bifasciatum (bluehead) 1440 ppb/96 hr in a static lab bioassay
LC50 Sphaeroides maculatus (Northern puffer) 2250 ppb/96 hr in a static lab bioassay
LC50 Coturnix japonica (Japanese quail) oral 265 ppm
LD50 Thiara torulosa 12.66 and 11.44-14.00, 10.69 and 9.73-11.75, 9.40 and 8.39-10.47,
and 8.70 and 7.58-10.02 mg/l at 95% confidence limits of 24, 48, 72, and 96 hr,
respectively.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
VINYL-1-(14)CARBON- & (36)CLORIDE -DICHLORVOS
WAS ADMIN ORALLY TO ... RATS. ... METABOLITE FROM VINYL CARBONS WAS CO2. URINE ANALYSES
... HIPPURIC ACID (8.3%), 2,2-DICHLOROVINYL METHYL PHOSPHATE (10.9%),
2,2-DICHLOROETHYL-BETA-D-GLUCOPYRANOSIDURONIC ACID (27%), & UREA (3.1%).
IN RATS ... DEGRADED BY TWO ENZYMATIC PATHWAYS. ... GLUTATHIONE DEPENDENT, PROCEEDS VIA
DEMETHYLATION TO DESMETHYL DDVP. ... NOT
DEPENDENT UPON GLUTATHIONE ... VIA HYDROLYSIS TO DIMETHYL PHOSPHATE &
DICHLOROACETALDEHYDE. DESMETHYL DDVP METABOLISM
TO MONOMETHYL PHOSPHATE & DICHLOROACETALDEHYDE WAS GLUTATHIONE-INDEPENDENT ALSO.
USING WHOLE HOMOGENATES OF RAT & RABBIT TISSUES ... METABOLISM OF DDVP-(32)PHOSPHORUS
WAS FOLLOWED. IN LIVER, KIDNEY, SPLEEN, & ADRENAL GLANDS, PRINCIPAL METABOLITE WAS
DIMETHYL PHOSPHATE (50-85%). REMAINDER APPEARED AS O-METHYL 2,2-DICHLOROVINYL PHOSPHATE,
MONOMETHYL PHOSPHATE, & INORGANIC PHOSPHATE.
MAJOR PROPORTION OF DICHLOROACETALDEHYDE OBTAINED FROM VINYL LINKAGE CLEAVAGE APPEARS
TO BE REDUCED TO DICHLOROETHANOL WITH VERY SMALL AMT GOING TO DICHLOROACETIC ACID.
... BLUEGILL ... & CHANNEL CATFISH ... /EXPOSED TO DDVP/
CHROMATOGRAPHY REVEALED PRESENCE OF DIMETHYLPHOSPHATE & DICHLOROACETALDEHYDE.
WHEN APPLIED TO STORED WHEAT, DDVP UNDERWENT
RAPID DEGRADATION TO DIMETHYL PHOSPHATE & PHOSPHORYLATED PROTEIN DERIVATIVES.
AFTER ADMIN OF DDVP TO YOUNG PIGS, ANALYSES
SHOWED PRESENCE OF DIMETHYL DDVP,
DICHLOROACETALDEHYDE, DICHLOROETHANOL, & DICHLOROACETIC ACID IN INTESTINAL LUMEN BUT
ONLY DICHLOROETHANOL IN PORTAL OR PERIPHERAL BLOOD.
Dichlorvos (DDVP)
is a methylating agent. DNA from mice given 1.9E-6 mol/kg of DDVP,
degree of alkylation of guanine-n-7 accounting to 8E-13 mol methyl per gram of DNA was
found. Rate of clearance was (estimated) to be 29 hr .
Dichlorvos, one of the active metabolites of
trichlorofon ... is hydrolyzed to give dimethyl phosphate and dichloroacetaldehyde. The
latter is subsequently reduced to beta,beta-dichloroethyl alcohol, characteristically
converted by rats when administered intraperitoneally. After hydrolysis to a two-carbon
fragment, dichloroacetaldhyde is able to enter a pathway of intermediary metabolism, and
carbon dioxide is the major radioactive metabolic.
IN VITRO STUDIES WITH SERUM INDICATED SMALL AMT OF DESMETHYL DDVP
BUT LARGE AMT OF DIMETHYLPHOSPHATE.
Absorption, Distribution & Excretion:
(14)CARBON DICHLORVOS WAS RAPIDLY
BIOTRANSFORMED AFTER ORAL ADMIN TO RATS. 38% OF (14)CARBON WAS EXCRETED IN EXPIRED AIR,
16% IN URINE, & 4% IN FECES IN 4 DAYS. RETAINED (14)CARBON REPRESENTED MATERIAL
INCORPORATED INTO PATHWAYS OF INTERMEDIARY METABOLISM. SIMILAR EXCRETION-RETENTION DATA
WERE OBTAINED AFTER INHALATION ...
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/
The hazard presented by application of insecticides to indoor surfaces where dermal
exposure (and oral exposure in infants) may occur was investigated. Worst case assumptions
for an infant playing in a room were used to calculate exposure for infant inhalation
exposure, dermal exposure through contact with the floor and oral exposures due to
hand/mouth contact. Surface exposure and total absorption were calculated for
chlorpyrifos, dichlorvos, and propoxur. The dose
calculated with each of these insecticides might reach toxic levels, particularly to an
infant. Dose calculations did not consider metabolic breakdown or cumulative effects. Data
necessary for determining that the levels of insecticides in the air and on treated
surfaces will not be injurious to human health would include the bioavailability of
surface residues, rate of transfer from surfaces and dose response data. According to the
authors, risk assessments based on health protective assumptions should be used in the
meantime to decide the safety of various components.
Inhalation studies with laboratory animals have shown that it is difficult to achieve a
lethal concentration in air with this compound because it is so readily absorbed on
surfaces and hydrolyzed by moisture. Thus, it has been possible to kill animals (rats) by
respiratory exposure only when their complete air supply was bubbled through the liquid
insecticide directly into a small exposure chamber.
Mechanism of Action:
The effect of dichlorvos /in depleting
glycogen stores/ seems to be due to simultaneous stimulation of glycogen phosphorylase and
inhibition of glycogen synthesis.
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/
The effect of dichlorvos on the contractile
response of isolated rat tail arteries /revealed that at a concn of/ 1x10(-8) to 1x10(-4)
M of dichlorvos had no effect on baseline
tension, but relaxed 1x10(-7) M norepinephhrine, 1x10(-7) M 5-HT or 100 mM potassium
chloride contractions dose dependently. Dichlorvos
also inhibited calcium chloride dose response curves in potassium(+) depolarized strips,
as well as depressing both phasic and tonic components of norepinephrine induced
contractions. The results suggest a direct relaxant effect of dichlorvos
on arterial smooth muscle by a mechanism probably related to interference with calcium(2+)
supply.
Interactions:
Metaproterenol (20 mg/kg), terbutaline (10 mg/kg), and salbutamol (10 mg/kg) increased
the protection of atropine + trimedoxime bromide (20 mg/kg, each) against /dichlorvos/ poisoning in mice. The increased
protection from the beta-2-adrenoreceptor agonists might have been due to a greater
relaxation of bronchial musculature. ...
Binding isotherms /exhibited/ a high degree (71-73 %) of reversible binding of DDVP with serum proteins. ... In a related study,
prior administration of sulfadimethoxine to rats increased their sensitivity to DDVP and reduced DDVP
serum binding to less than 65-66%.
Treatment of pregnant rabbits with phenobarbital increased the sensitivity of the
progeny to the cerebrotoxic action of dichlorvos.
...
Acetaminophen failed to potentiate the toxicity of dichlorvos
on esterase /in mice/.
... Oral administration of dichlorvos 60
mg/kg (/to castrated pigs/ 3 times the anthelmintic dosage level) 1 hr before levamisole
injection lowered blood cholinesterase activity to approximately 60% that of controls, but
did not change the LD50 of levamisole. ... /LD50 Levamisole-hydrochloride= 39.8 mg/kg/
In order to clarify whether or not dichlorvos
(DDVP), which did not exert carcinogenic effects
in mice in /previously reported studies/ is cocarcinogenic, male and female mice of the
strain C57B1/6/B1n were sc injected with the carcinogen N-nitrosodiethylamine and received
in addition DDVP orally. For comparison
N-nitrosodiethylamine and DDVP alone was
administered to other groups of mice. The combined application N-nitrosodiethylamine + DDVP did not result in increased incidences of tumors
and preneoplastic lesions as compared with the N-nitrosodiethylamine treated groups of
mice. The incidence of focal (transitional cell) hyperplasias of the urinary bladder
epithelium was increased in the groups treated with N-nitrosodiethylamine + DDVP as compared to the groups with single compound
treatment. There were no development of tumors and no differences in the latency periods
of tumors which could be attributed to the combined treatment with N-nitrosodiethylamine +
DDVP. Under these experimental conditions DDVP was not cocarcinogenic in mice.
Pharmacology:
Therapeutic Uses:
MEDICATION (VET): ORALLY ... ANTHELMINTIC: RECOMMENDED AGAINST HOOKWORMS, WHIPWORMS,
& ROUNDWORMS IN DOGS; ADULT & 4TH STAGE WHIPWORMS, NODULAR WORMS, ... STOMACH
WORMS, & ROUNDWORMS IN SWINE; BOTS, STRONGLES, & PINWORMS IN HORSES. EMBEDDED IN
PLASTIC PELLETS, ITS RELEASE RATE IS GRADUAL AFTER INGESTION.
MEDICATION (VET): DICHLORVOS ... IS UNIQUE
AMONG ORGANOPHOSPHORUS ANTHELMINTICS IN THAT IT CAN BE INCORPORATED INTO POLYVINYL
CHLORIDE RESIN PELLETS. ... RELEASED SLOWLY FROM UNDIGESTIBLE PELLETS AS THEY PASS THE
LENGTH OF DIGESTIVE TRACT. ... CONCN AGAINST PARASITES ALL ALONG DIGESTIVE TUBE.
MEDICATION (VET): ... INTRANASALLY AGAINST BOTS ... OF SHEEP. ... HAVE CURED SOME CASES
OF DEMODECTIC MANGE IN DOGS REFRACTORY TO OTHER TREATMENTS BY HANGING ... FLY STRIPS ...
IN DOG KENNELS.
MEDICATION (VET): TOPICALLY, FOR QUICK KNOCKDOWN OF INSECTS ON ANIMALS & PREMISES
AS FOG, MIST, OR SPRAY (1%), IN SUGAR TYPE BAITS NEAR FLY BREEDING AREAS
Drug Warnings:
VET: DO NOT USE IN CONJUNCTION WITH OR WITHIN FEW DAYS OF (BEFORE &/OR AFTER) ANY
OTHER CHOLINESTERASE INHIBITORS & AVOID USE WITH PHENOTHIAZINE, PHENOTHIAZONE
TRANQUILIZERS, ARSENICALS, PURGATIVES, OR DRUGS PRODUCING PURGATION AS SIDE EFFECT.
DO NOT ADMINSTER TASK /A FORMULATION/ ... DOG
ANTHELMINTIC IN CONJUNCTION WITH OTHER ANTHELMINTICS, TAENIACIDES, ANTIFILARIAL AGENTS
(DIETHYLCARBAMAZINE EXCEPTED), MUSCLE RELAXANTS OR TRANQUILIZERS. /TASK/
DO NOT ADMIN TO DOGS SHOWING SIGNS OF SEVERE CONSTIPATION, MECHANICAL BLOCKAGE OF
INTESTINAL TRACT, IMPAIRED LIVER FUNCTION, CIRCULATORY FAILURE, OR TO DOGS RECENTLY
EXPOSED TO OR SHOWING SIGNS OF INFECTIOUS DISEASES.
Interactions:
Metaproterenol (20 mg/kg), terbutaline (10 mg/kg), and salbutamol (10 mg/kg) increased
the protection of atropine + trimedoxime bromide (20 mg/kg, each) against /dichlorvos/ poisoning in mice. The increased
protection from the beta-2-adrenoreceptor agonists might have been due to a greater
relaxation of bronchial musculature. ...
Binding isotherms /exhibited/ a high degree (71-73 %) of reversible binding of DDVP with serum proteins. ... In a related study,
prior administration of sulfadimethoxine to rats increased their sensitivity to DDVP and reduced DDVP
serum binding to less than 65-66%.
Treatment of pregnant rabbits with phenobarbital increased the sensitivity of the
progeny to the cerebrotoxic action of dichlorvos.
...
Acetaminophen failed to potentiate the toxicity of dichlorvos
on esterase /in mice/.
... Oral administration of dichlorvos 60
mg/kg (/to castrated pigs/ 3 times the anthelmintic dosage level) 1 hr before levamisole
injection lowered blood cholinesterase activity to approximately 60% that of controls, but
did not change the LD50 of levamisole. ... /LD50 Levamisole-hydrochloride= 39.8 mg/kg/
In order to clarify whether or not dichlorvos
(DDVP), which did not exert carcinogenic effects
in mice in /previously reported studies/ is cocarcinogenic, male and female mice of the
strain C57B1/6/B1n were sc injected with the carcinogen N-nitrosodiethylamine and received
in addition DDVP orally. For comparison
N-nitrosodiethylamine and DDVP alone was
administered to other groups of mice. The combined application N-nitrosodiethylamine + DDVP did not result in increased incidences of tumors
and preneoplastic lesions as compared with the N-nitrosodiethylamine treated groups of
mice. The incidence of focal (transitional cell) hyperplasias of the urinary bladder
epithelium was increased in the groups treated with N-nitrosodiethylamine + DDVP as compared to the groups with single compound
treatment. There were no development of tumors and no differences in the latency periods
of tumors which could be attributed to the combined treatment with N-nitrosodiethylamine +
DDVP. Under these experimental conditions DDVP was not cocarcinogenic in mice.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Dichlorvos' production and use as an
insecticide in sprays, household and commercial resin strips, and flea collars that are
applied to animals, including livestock and pets, and crops will result in its direct
release to the environment. If released to air, a vapor pressure of 0.0158 mm Hg at 25 deg
C indicates dichlorvos will exist solely as a
vapor in the ambient atmosphere. Vapor-phase dichlorvos
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 13.6 hours. Dichlorvos hydrolyzes in water by a base-catalyzed
process. After 24 hr, 8% and 90% degradation occurred at pH 6.2 and pH 9.3, respectively.
Biodegradation may also be a factor in situations where acclimated colonies of
microorganisms exist or under acidic conditions when hydrolysis is slower. The estimated
volatilization half-life of dichlorvos in a
model river is 119 days. Experimental studies indicate that dichlorvos
does not bioconcentrate in fish. The whole and body BCF in carp is <0.5 and the
insecticide's excretion half-life is 0.6 hr. Based upon a Koc of 47, dichlorvos
would be expected to exhibit high mobility in soil and not adsorb to suspended solids and
sediment in water. Volatilization from water surfaces and moist soil surfaces is not
expected to be an important fate process based upon an estimated Henry's Law constant of
4.6X10-7 atm-cu m/mole. When applied to soil, dislodgeable residue levels on foliage and
turf rapidly decline to safe reentry levels in several hours. Dichlorvos
degrades in soil by hydrolysis and biodegradation. Half-lives determined in a variety of
soils range from 1.5 to 17 days. The general population will be primarily exposed to dichlorvos by inhalation of indoor air where dichlorvos is used as an insecticide. Occupational
exposure will primarily be by inhalation and dermal contact in situations where the
insecticide is used or stored. (SRC)
Probable Routes of Human Exposure:
Dichlorvos can affect the body if it is
inhaled, if it comes in contact with the eyes or skin, or is swallowed. ...
NIOSH (NOES Survey 1981-1983) has statistically estimated that 11,182 workers (2,182 of
these are female) are potentially exposed to dichlorvos
in the US(1). The NOES Survey does not include agricultural workers. Occupational exposure
to dichlorvos may occur through inhalation of
ambient air and dermal contact with this compound at workplaces where dichlorvos
is produced or used for household and public health insect control, flea collars and
no-pest strips(2,SRC). Similarly, the general population may be exposed to dichlorvos via inhalation of air and dermal contact
when no-pest strips, sprays or flea collars containing this insecticide are used. Exposure
could also result from ingestion of food which has been prepared in rooms where dichlorvos is used for insect control(SRC). As part of
EPA's Non-Occupational Pesticide Exposure Study (NOPES) conducted in the Summer 1986,
Spring 1987 and Winter 1988 in Jacksonville, FL and Springfield/Chicopee, MA the estimated
mean personal air concn of dichlorvos for
Jacksonville residents was 147.6, 40.2, and 21.4 ng/cu m in summer, spring and winter,
respectively(3). The estimated spring and winter concns for Springfield/Chicopee residents
were 3.7 and 2.1 ng/cu m in spring and winter. In Jacksonville, it was estimated that the
percentage of residents with detectable levels of dichlorvos
in personal air was 35%, 11%, and 16% in summer, spring and winter, respectively. In
Springfield/Chicopee only 2% and 1% of residents were exposed in spring and winter.
Exposure from air inhalation was the primary route of exposure to dichlorvos(3).
Dichlorvos was detected in the workplace
environment in concns of 77 ppb in air during production and processing of a dichlorvos-releasing vaporizer(1). During spraying of
an orchard 130 ppb was detected in air and a rate of skin contamination of 72 ug/100 sq
cm/hr was reported(1). After spraying, 114-765 ug/sq m of dichlorvos
was deposited on worker's clothing(3). A study was performed to determine the level of
exposure to 5 workers after 1.85 kg of dichlorvos
was sprayed on an apple orchard for 5.5 hr with an airblast sprayer(4). The air and
breathing zone dichlorvos concns were 1.0-15.4
ug/cu m, and 113.6-765.3 ug/cu m, respectively. Ambient air in storage rooms of four North
Carolina commercial pest control firms (4 hr period) contained 147-1501 ng/cu m, (617
ng/cu m avg)(2). Ambient air in offices of four North Carolina commercial pest control
firms (4 hr period) contained 19-66 ng/cu m, (41 ng/cu m avg)(2). A 1993 study of
insecticide concns in the air of 10 North Carolina pest control firms (19 samples)
resulted in mean dichlorvos air levels of 1.48
ug/cu m(5). Levels were higher in summer than in winter. In a study to determine the
dissipation of dislodgeable residues of dichlorvos
on turf, the residue level was 0.10 ug/sq cm immediately post application (<2 hr) and
rapidly declined to below the safe level for reentry, 0.06 mg/sq cm after two hours and
was undetectable (<1 ug/sample) after 23 hr(5). There was no significant difference in
post application dissipation of dislodgeable residues between irrigated and non-irrigated
plots. Dichlorvos was detected in air samples
immediately post-spray at 1.9 ppb(5). Three hours after application of dichlorvos
to greenhouse crops using low-volume (<50 l/ha) techniques, the atmospheric concn of dichlorvos had declined to 12% of the initial concn
but was still exceeding the 1000 ug/cu m threshold limit value (TLV)(6).
Body Burden:
Two pest control operators in Japan involved in spraying and mixing a combined
emulsifiable concentrate of fenithrothion and dichlorvos
to exterminated cockroaches in household construction contained mean and maximum alkyl
phosphate levels in urine of 0.099 and 0.22 ug/mg creatinine(1).
Average Daily Intake:
AIR INTAKE: 1.25 ug (Jacksonville, FL; assuming a weighted estimate of average daily
air concns of 62.4 ng/cu m(1)); 0.066 ug (Springfield/Chicopee, MA; assuming a weighted
estimate of average daily air concns of 3.3 ng/cu m(1)).
Natural Pollution Sources:
Dichlorvos is not known to occur as a natural
product(1).
Artificial Pollution Sources:
Dichlorvos' production and use as an
insecticide used in sprays, resin strips, and flea collars that are applied to animals,
including livestock and pets, and crops(1) will result in its direct release to the
environment (SRC). Its extensive use against sea-lice parasites in cage-cultures of salmon
farming in Ireland(2) indicates that it is released into seawater. Dichlorvos
is also a breakdown product of the insecticide trichlorphon(1) and may be released to the
environment when trichlorphon is used.
Environmental Fate:
Octanol water partition coefficients and air water partition coefficients were obtained
for 10 organochlorine pesticides (including dichlorvos)
as basic data for predicting their fate in the environment. The octanol water partition
coefficient is ... 1.45X10+1 for dichlorvos.
These values approximately correlated with the solubilities of these pesticides in water.
The air water partition coefficient is ... 5.0X10-3 for dichlorvos.
TERRESTRIAL FATE: When spilled on soil, dichlorvos
leached into the ground with 18-20% penetrating to 30 cm within 5 days. Dichlorvos
degrades in soil by both hydrolysis and biodegradation(7). In a soil perfusion experiment
using Houston Black Clay (pH 7.7), 71% degradation occurred after 10 days in a non-sterile
system while 50% occurred in a sterile system(1). Half-lives of 7 days were obtained in
clay, sandy-clay, and loose sandy soil(1). A half-life of 1.5 days was obtained in field
plots with chestnut soil(2) and 17 days in an unidentified soil(3). It disappeared from
soil as well as foliage when sprayed on a vineyard in the USSR(4). Dissipation rates of
dislodgeable dichlorvos residues were measured
on lawns with and without postspray irrigation(5). Residue levels for all application
scenarios rapidly declined to below 0.06 ug/sq cm, the safe reentry level, within six
hours post spray(5). The half-life of dichlorvos
was determined in 16 sediment samples (pH ranging from 8.2 to 9.2) from the Bay of
Bengal(6). The half-lives were determined with all exchangeable ions present as well with
the exchangeable ions removed. The half-lives ranged from 36 days (lower pH) to 12 days
(higher pH). With the exchangeable ions removed, the respective half-lives ranged from 40
days to 25 days. The shorter half-lives in the presence of exchangeable ions are believed
to reflect a catalytic effect exerted on the exchangeable ions(6). Half-lives in sediment
were shorter. Based on a classification scheme(11), the experimental Koc value of 47(9),
indicates that dichlorvos will have high
mobility in soil(SRC). Volatilization of dichlorvos
from moist soil surfaces is not expected to be an important fate process (10,SRC) based
upon an estimated Henry's Law constant of 4.6X10-7 atm-cu m/mole(SRC), derived from its
vapor pressure and water solubility and its low adsorption to soil(8).
AQUATIC FATE: When released into the environment, dichlorvos
will partition predominantly to water, reflecting its high water solubility(7). It will
degrade primarily by hydrolysis although biodegradation may be important where acclimated
microorganisms may exist such as some polluted waters or where the water is more acidic
and hydrolysis slower(SRC). Hydrolysis is base catalyzed. In one experiment, a 64%
disappearance was observed in 24 hr at pH 8.7 and only 8% at pH 6.2(1). Below pH 3.3, no
degradation occurred after 96 hr(1). After its addition to seawater at concn of 0.419
mg/l, the concn decreased only slightly to 0.359 mg/l in 9 days(4). Conflicting hydrolysis
data were obtained in water samples prepared with phosphate buffers and NaCl to be the
aqueous counterpart of sediment samples obtained from the Bay of Bengal(5). The half-life
of dichlorvos in fresh water ranged from 40 to
60 days in samples where the pH ranged from 9.2 to 8.2(5). In brackish water of similar pH
values, the half-life ranged from 50 to 70 days(5). The decreasing rate of hydrolysis with
increasing salinity is thought to be due to decreased mobility of the hydroxyl ions(5). In
studies performed on a mixture of pesticides studied over a 6-month period in different
water types at 22 deg C, dichlorvos disappeared
after 81 days, 55 days and 34 days in ultrapure water (pH 6.1), river water (pH 7.3), and
filtered river water (pH 7.3), respectively; it was present after 6 months in seawater (pH
8.1)(6). Based on a classification scheme(8), the experimental Koc value of 47(2),
indicates that dichlorvos will not adsorb to
suspended solids and sediment in water(SRC). Dichlorvos
is not expected to volatilize from water surfaces(3,SRC) based upon an estimated Henry's
Law constant of 4.6X10-7 atm-cu m/mole(SRC), derived from its vapor pressure and water
solubility(9). Its estimated volatilization half-life for a model river is 119
days(3,SRC). Experimental BCF values of <0.5 and 0.8 in carp(10) and willow shiner(11),
respectively and a excretion half-life of 0.6 hr in carp(10) indicate that dichlorvos will not bioconcentrate in fish(SRC).
ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile
organic compounds in the atmosphere(1), dichlorvos,
which has a vapor pressure of 0.0158 mm Hg at 25 deg C(2), is expected to exist solely as
a vapor in the ambient atmosphere. Vapor-phase dichlorvos
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 13.6 hr(SRC) from
its estimated rate constant of 9.4E-12 cu cm/molecule-sec(3). Droplets containing dichlorvos as a result of spraying will be removed
from the air by gravitational settling(SRC). The fact that dichlorvos
has been detected in air a week after spraying has been ascribed to its volatility after
being adsorbed on plants and soil(4).
Environmental Biodegradation:
AEROBIC: Dichlorvos is listed as being
amenable to biological treatment after acclimation(1). It was resistant to degradation
(8-14% of theoretical BOD) in an 8 day laboratory test using a sewage inoculum(2). The
biodegradation rate constant and half-life for dichlorvos
was determined to be 0.20 1/d and 3.5 days, respectively in an aerobic biodegradability
test using an activated sludge inoculum at 20 deg C and GC analysis(8). Dichlorvos
was not completely removed when incubated with sewage for 7 days at 29 deg C;
biodegradation products are dichloroethanol, dichloroacetic acid and ethyl
dichloroacetate(5). There is some evidence that it degrades somewhat faster in polluted
than unpolluted waters(3,4). Dichlorvos is
degraded by soil microorganisms although much of the degradation in soil is chemical in
nature. In a soil perfusion experiment, 71% degradation occurred in 10 days but only 30%
was due to biodegradation(6). The presence of active microorganisms reduced the half-life
of dichlorvos in clay and calcareous soil from
0.9 to 0.75 days and 0.85 to 0.70 days, respectively(7). The average first-order rate
constant and half-life of dichlorvos in an
acidic silty clay soil and a neutral sandy clay soil was 0.0423 and 0.04443,
respectively(8). The half-life in both cases was 16 days. The rate was about 1.4 times
faster with a 10 ppm loading than a 100 ppm loading. Dichlorvos
was completely degraded on passage through a sand column, whereas no degradation occurred
when the sand was sterilized(10).
ANAEROBIC: Low concn of dichlorvos (3 mg-C/l)
degraded within 7 days in an anaerobic biodegradability test at 37 deg C(1). The
biodegradation rate constant and half-life for dichlorvos
was determined to be 0.20 1/d and 3.5 days, respectively in an anaerobic biodegradability
test using 30 mg/l anaerobic microorganisms cultured by an artificial sewage at 20 deg C
under nitrogen and GC analysis(8). The investigators obtained the same rate for aerobic
biodegradation.
Environmental Abiotic Degradation:
Dichlorvos absorbs light in the UV with a
maximum absorbance and extinction coefficient between 295 and 305 nm of 0.0246 and 54
l/mol-cm, respectively(1). Despite this relatively low extinction coefficient, the
degradation of dichlorvos in a thin film (0.67
ug/sq cm) was rapid; the photodegradation rate constant and half-life are 265.2X10-7 1/sec
and 7.25 hr, respectively(1). Dichlorvos
hydrolyzes in water; the rate of hydrolysis increases with pH(2-4), temperature(2,3), and
concentration(2). Dichlorvos is stable at pH
<3.3(4). The neutral and basic hydrolysis rate constants at 20 deg C are reported as
36.7X10-4 1/hr and 20790 1/M-hr, respectively(9). Eight, 18, 64, and 90% degradation was
observed in 24 hr at pH 6.2, 8.2, 8.7 and 9.3, respectively(4). Another study found that
the hydrolysis half-life decreased from 77 hr to 5 hr when the pH increased from 5.4 to 8
at 37.5 deg C(3). At pH 5, the half-life was 10.0, 2.6, and 0.7 days at 10, 20, and 30 deg
C, respectively(3). The half-life was >72 hr in water from 3 Yugoslav rivers(5) and
approximately 100 hr in a German lake whose pH was <6 and temperature below 5 deg C(6).
Hydrolysis is an important degradation mechanism in soils(7). While 71% of dichlorvos added to Houston black clay degraded in 10
days, 70% of the degradation was attributed to hydrolysis(4). The half-lives of dichlorvos in autoclaved clay soil and calcareous soil
were 0.9 and 0.85 days, respectively(8,SRC).
The rate constant for the vapor-phase reaction of dichlorvos
with photochemically-produced hydroxyl radicals has been estimated as 9.41 cu
cm/molecule-sec at 25 deg C(SRC) using a structure estimation method(1). This corresponds
to an atmospheric half-life of 13.6 hours at an atmospheric concentration of 5X10+5
hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of dichlorvos with ozone has been estimated to be
3.58X10-11 cu cm/molecule-sec at 25 deg C(1) which corresponds to an atmospheric half-life
of about 320 days at an atmospheric concentration of 7X10+11 molecules per cu cm(1). The
concentrations of hydroxyl radicals and ozone used to estimate the half-lives are
representative of outdoor air and may not be appropriate for indoor air where dichlorvos is mostly used(SRC).
Environmental Bioconcentration:
The log BCF for dichlorvos estimated from its
log octanol/water partition coefficient, 1.47, is 1.26(1). This value was selected from
results predicted using seven different equations and indicates that dichlorvos
will not bioconcentrate in fish. The whole-body bioconcentration factor measured in carp
was <0.5 after 168 hr(2). The excretion rate and half-life were 0.56 1/hr and 0.6 hr,
respectively indicating that dichlorvos is
readily eliminated from carp(2). The average whole-body BCF of dichlorvos
in willow shiner after 24 and 168 hr was 0.8(3). The concentration of dichlorvos
in the fish was low and rapidly decreased; the excretion rate constant could not be
determined.
Soil Adsorption/Mobility:
The Koc for dichlorvos calculated from its
water solubility and octanol/water partition coefficient are 28(1) and 47(5),
respectively. The Freundlich adsorption constants were determined in 3 Japanese black
soils with organic carbon contents ranging from 2.3% to 6.8% and a sodium-bentonite clay
by shaking in serum bottles for 24 hr at 25 deg C until the system was equilibrated(4).
The Freundlich adsorption constant Kf was 3.6, 2.4 and 1.0 for the 3 black soils and the
Freundlich exponent, 1/n, was 1/0.78; Kf for the clay mineral was <0.2. The Koc derived
from Kf was 47. According to a classification scheme(6), these estimated and measured Koc
values suggest that dichlorvos will have high
mobility in soil(SRC). In a field experiment, 18-20% of the dichlorvos
which was sprayed on the ground had penetrated the soil to a depth of 30 cm within 5
days(2). In a soil TLC study, mobility was measured and the effects of various soil
properties were determined; Rf values ranged from 0.36 to 0.74(3). The mobility of dichlorvos in soil is decreased by the addition of
soil amendments such as calcium carbonate(7). Mobility in soil decreases with increasing
soil pH(8).
Volatilization from Water/Soil:
The Henry's Law constant for dichlorvos is
estimated as 4.6X10-7 atm-cu m/mole(SRC) from its vapor pressure, 0.0158 mm Hg(1), and
water solubility, 10,000 mg/l(2). This Henry's Law constant indicates that dichlorvos should slowly volatilize from water
surfaces(3). 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)(3) is estimated as 119
days(SRC). The volatilization half-life from a model pond, which considers the effect of
adsorption(5), has been estimated to be over 400 days(SRC). The average decrease of dichlorvos after seven days of aeration in water was
16%/day(4). Without aeration, the average decrease was 6%/day(4). Dichlorvos'
estimated Henry's Law constant(1,2) indicates that slow volatilization from moist soil
surfaces may also occur(SRC). Based upon its vapor pressure, dichlorvos
is not expected to volatilize from dry soil surfaces(SRC).
Environmental Water Concentrations:
SURFACE WATER: Dichlorvos has been detected
in a water reservoir and water supply-irrigation system in the USSR and in 4 polluted
rivers(1). On September 9 to 11, 1988, dichlorvos
was detected in marine waters of Beirtreach Bay, Ireland at concentrations up to 0.13
ug/l(2). Dichlorvos was found in the Yamaska
River and its tributaries in Quebec, Canada in 1986-7(3). Its concn at a site near the
mouth of the river was 8.2 and 1.7 ng/l on two occasions; it was not detected on two other
occasions. Dichlorvos was detected in the
Neya-gawa River in Osaka City and Osaka Bay, Japan during monitoring studies conducted in
1989-1990; concn levels were not reported(4). Dichlorvos
was not found in monthly samples of surface water taken at six sites between August 1989
and January 1990 in an area of the Netherlands used for bulb culture(5).
DRINKING WATER: No dichlorvos was detected in
California well water performed between 7/1/94 and 6/30/95 as part of the state's well
water inventory in which 46 wells in 7 counties were sampled(1).
Effluent Concentrations:
Dichlorvos was detected in wastewater from a dichlorvos production plant in Bulgaria 16 g/l(1). As
a result of a fire at Sandoz Ltd near Basel, Switzerland in November 1986, it was
estimated that 1-3 kg was discharged into the Rhine River; the estimated water concn at
Village-Neuf was 0.15-0.65 ug/l(2).
Atmospheric Concentrations:
URBAN/SUBURBAN: As part of EPA's Non-Occupational Pesticide Exposure Study (NOPES)
conducted in the Summer 1986, Spring 1987 and Winter 1988 in Jacksonville, FL and
Springfield/Chicopee, MA the estimated mean outdoor air concn of dichlorvos
in Jacksonville was 0, 0, and 3.2 ng/cu m in summer, spring and winter, respectively(2). Dichlorvos was not detected in outdoor air in
Springfield/Chicopee in spring and winter. It was not detected in the air of Kitakyushu
City, Japan(1).
INDOOR AIR: As part of EPA's Non-Occupational Pesticide Exposure Study (NOPES)
conducted in the Summer 1986, Spring 1987 and Winter 1988 in Jacksonville, FL and
Springfield/Chicopee, MA the estimated mean indoor air concn of dichlorvos
for Jacksonville residents was 134.5, 86.2, and 24.5 ng/cu m in summer, spring and winter,
respectively(3). The estimated spring and winter concns for Springfield/Chicopee residents
were 4.3 and 1.5 ng/cu m in spring and winter. In Jacksonville, it was estimated that the
percentage of residents with detectable levels of dichlorvos
in indoor air was 33%, 14%, and 10% in summer, spring and winter, respectively. In
Springfield/Chicopee only 2% and 1% of residents were exposed in spring and winter. A
study comparing the concn of indoor pesticides in air and household dust that determined dichlorvos levels in 7 representative New Jersey
homes, found only one house with detectable air concn of dichlorvos;
the average level in this house was 254.7 ng/cu m(4). No dichlorvos
was found in household dust in this house. Concn levels in households and food shops in
which commercial pesticide strips were used were 0-26 ppb and <1-3 ppb,
respectively(1). Trials were conducted in the U.K., Australia and France between 1967 and
1970 to determine the concn of dichlorvos in the
air of homes using "Vapona" strips(2).
Results from more than 3000 samples of air indicated that the great majority of values
were 0.1 ug dichlorvos/liter of air or less;
values ranged from <0.01 to 0.24 ug/l with the higher values being associated with
closed up homes or the use of multiple strips. In each trial the concn of dichlorvos rose rapidly and then fell exponentially.
In temperate area trials, the concn was highest 1-2 weeks after placing the strips; the
geometric mean of all values at this time was 0.04 ug/l and 3 months after placement the
mean concn was 0.01 ug/l(2).
Food Survey Values:
In FDA's Total Diet Study (1986-1991) in which foods prepared for consumption from
different regions of the country are analyzed and mean daily intakes for diet for a
variety of age-sex groups determined, the mean daily intake per unit body weight of dichlorvos was <0.0001 ug/kg body weight-day(1).
Less than 2% of the 4914 items of food analyzed contained dichlorvos.
A further FDA study in which 234 ready-to-eat foods were tested 37 times each over a 10
year period found only one item containing dichlorvos
at 0.0100 ug/g(2). The FDA found no dichlorvos
residues in a targeted 1992-1993 study of 1219 domestic and 144 imported samples of
tomatoes(3). In a 1993-1994 FDA study of domestic and imported apples (1831 samples) and
rice (1210 samples), dichlorvos was only found
on 1 sample of domestic rice at 0.08 ppm(4). A pesticide residue screen program
(1989-1991) involving 6970 produce samples found only 1 sample of radishes containing dichlorvos above the detection limit of 0.25 ppm(5).
The percent occurrence of dichlorvos in FDA's
Residue Monitoring studies in 1978-1982 and 1982-1986 was <1% and <2%,
respectively(6,7). The concn of dichlorvos on
postharvest-treated potatoes declined with half-lives of 45 days at a storage temperature
of -5 deg C (single phase) and 1.6 days, 11 days (two-phase) at a storage temperature of
19.7 deg C(12). After the sixth week when some potatoes were processed into starch, 3% of
the residue remained on the potatoes after washing and no residue was found in the
starch(12). Detected in 5.3% of fruits and vegetables produced in Gifu Prefecture,
Japan(8). Dichlorvos was detected in 1 of 47
samples from France at a concn of 0.2 mg/kg(10). A 1964 to 1968 survey of Swedish fruits
and vegetables showed apples, lettuce and potatoes contained dichlorvos(11).
Dichlorvos concns reported in various food items
(item, concn): Stored wheat, 2.4-6.0 ppm decreasing to 0.5 ppm or less over 6 weeks;
Cereal products, 0 ppm; flour, 0-5.8 ppm; Crude soy bean oil and meal, <1 ppm; Malt and
worts, 0-2 ppm; Raspberries, 0.2-7.0 ppm; Vegetable food products, 0.24 ppm(9). Dichlorvos was also detected in mushrooms(9). Prepared
food which was experimentally exposed to air containing 3 to 60 ppb dichlorvos
contained concns of 5 to 1653 ppm(9). Foods prepared in households and food shops in which
commercial pest strip were used contained dichlorvos
at concns ranging from <10 to 120 ppb and <50 ppb, respectively, when the dichlorvos in the ambient air ranged from 0 to 26 ppb
and <1-3 ppb, respectively(9).
Plant Concentrations:
Dichlorvos was detected in the leaves of
cabbage and onion plants during the first 7 days after spraying(1). The half-life of
dislodgeable foliar residues of dichlorvos
applied by low-volume spraying of and emulsifiable concentrate (550 g/l) at 50 g ai/1000
sq m on chrysanthemum seedlings was estimated as 0.2 days in each of two experiments(2).
This indicates that dichlorvos residues on
plants would rapidly decline(SRC).
Fish/Seafood Concentrations:
None of the 92 samples of farmed salmon analyzed as part of a farmed fish surveillance
in the U.K. between 10/87 and 2/89 contained residues of dichlorvos(1).
Animal Concentrations:
Dichlorvos was found in sheep organs and in
the tissue of cattle, 7 days and 15-22 days after application of trichlorphon,
respectively.
Milk Concentrations:
Dichlorvos was detected in milk and dairy
products(1,2).
Environmental Standards & Regulations:
FIFRA Requirements:
Tolerances for residues of the insecticide 2,2-dichlorovinyl dimethyl phosphate are
established for the following agricultural products: Cattle, (fat, cattle, meat, and
meat-by-products); cucumbers; eggs; goats, (fat, meat, and meat-by-products); horses,
(fat, meat, and meat-by-products); lettuce: milk; mushrooms; poultry, (fat, meat; and
meat-by-products); radishes; raw agricultural commodities non-perishable; sheep, (fat,
meat, and meat-by-products);and tomatoes.
Pesticide chemicals that cause related pharmacological effects will be regarded as
having an additive deleterious action. Where residues from two or more chemicals in the
same class are present in or on a raw agricultural commodity the tolerance for the total
of such residues shall be the same as that for the chemical having the lowest numerical
tolerance in the class, unless a higher tolerance level is specifically provided for the
combined residues by a regulation ... 2,2-Dichlorovinyl dimethyl phosphate is a member of
the class of cholinesterase-inhibiting pesticides.
The food additive 2,2-dichlorovinyl dimethyl phosphate may be present as a residue from
application as an insecticide on packaged or bagged nonperishable processed food in an
amount in such food not in excess of 0.5 ppm.
A Registration Standard was issued Sept 1987 for dichlorvos
used as an insecticide.
EPA is staying the effective date of an order which was published in 58 FR 59663
(11/10/93) regarding the revocation of the food additive regulation for dichlorvos.
EPA received a petition to stay the March 10, 1994 effective date for the revocation of
the food additive regulation 40 CFR 185.1900. EPA is staying the effective date in order
to review the petition and determine whether to grant a stay, and if so, for what period.
As the federal pesticide law FIFRA directs, 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. Dichlorvos 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, as amended in
1988. Case No: 0310; Pesticide type: insecticide; Case Status: 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
Reregistration Eligibility Decision (RED) document.; Active ingredient (AI): Dichlorvos; Data Call-in (DCI) Date(s): 09/20/91,
02/24/94, 11/01/94, 03/03/95, 10/13/95; AI Status: The producers of the pesticide has 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 10 lb or 4.54 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).
This regulation establishes the list of extremely hazardous substances, threshold
planning quantities, and facility notification responsibilities necessary for the
development and implementation of State and local emergency response plans. 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. Dichlorovos is an extremely hazardous substance subject to reporting requirements
when stored in amounts in excess of its threshold planning quantity of 1000 lbs.
Atmospheric Standards:
Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious
health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards
requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is
required to establish and phase in specific performance based standards for all air
emission sources that emit one or more of the listed pollutants. Dichlorvos
is included on this list.
Clean Water Act Requirements:
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.
State Drinking Water Guidelines:
(FL) FLORIDA 0.1 ug/l
FDA Requirements:
Oral dosage form new animal drugs not subject to certification: Conditions of use of
2,2-dichlorvinyl dimethyl phosphate are given for (1) swine; (2) dogs; (3) horses when
administered in grain; horses when administered orally by syringe; (4) cats and puppies.
Dichlorvos: Conditions of use: It is used in
feed for swine as follows: Indications for use. For the removal and control of mature,
immature, and/or fourth-stage larvae of the whipworm (Trichuris suis), nodular worm
(Oesophagostomum spp), large roundworm (Ascaris suum) and the thick stomach worm (Ascarops
strongylina) of the gastrointestinal tract. ... An aid in improving litter production
efficiency by increasing pigs born alive, birth weights, survival to market, and rate of
weight gain.
A tolerance of 0.1 ppm is established for negligible residues of dichlorvos
in the edible tissues of swine.
Allowable Tolerances:
Tolerances for residues of the insecticide 2,2-dichlorovinyl dimethyl phosphate are
established as follows (expressed in ppm; N = negligible residues): Cattle, fat: 0.02 (N);
cattle, meat: 0.02 (N); cattle meat-by-products: 0.02 (N); cucumbers: (residues expressed
as naled): 0.5; eggs: 0.05 (N); goats, fat: 0.02 (N); goats, meat: 0.02 (N); goats,
meat-by-products: 0.02 (N); horses, fat: 0.02 (N); horses, meat 0.02: (N); horses,
meat-by-products: 0.02 (N); lettuce (residues expressed as naled): 1.0; milk: 0.02 (N);
mushrooms (residues expressed as naled): 0.5; poultry, fat: 0.05 (N); poultry, meat: 0.05
(N); poultry, meat-by-products: 0.05 (N); radishes: 0.5; raw agricultural commodities
non-perishable, bulk stored regardless of fat content (post-harvest): 0.5; raw
agricultural commodities, non-perishable, packaged or bagged, containing 6% fat or less
(post-harvest): 0.5; raw agricultural commodities, non-perishable packaged or bagged,
containing more than 6% fat (post-harvest): 2.0; sheep, fat: 0.02 (N); sheep, meat: 0.02
(N); sheep meat-by-products: 0.02 (N); tomatoes (pre- and post-harvest) (residues
expressed as naled): 0.05.
The food additive 2,2-dichlorovinyl dimethyl phosphate may be present as a residue from
application as an insecticide on packaged or bagged nonperishable food in an amt in such
food not in excess of 0.5 ppm.
A tolerance of 0.1 ppm is established for negligible residues of dichlorvos
in the edible tissues of swine.
Chemical/Physical Properties:
Molecular Formula:
C4-H7-Cl2-O4-P
Molecular Weight:
220.98
Color/Form:
Colorless to amber liquid /technical grade/
Odor:
Aromatic odor
Mild, chemical odor.
Boiling Point:
140 deg C @ 20 mm Hg
Corrosivity:
CORROSIVE TO IRON & MILD STEEL
Density/Specific Gravity:
1.415 @ 25 deg C/4 deg C
Octanol/Water Partition Coefficient:
log Kow= 1.43
Solubilities:
Solubility in water: about 0.5 g/100 ml; in glycerol: about 0.5 g/100 ml
SOL IN CHLOROFORM, ACETONE
SOLUBILITY IN KEROSENE 2 TO 3 G/KG
MISCIBLE WITH MOST ... AEROSOL PROPELLANTS
Water solubility: 10,000 mg/l @ 20 deg C
Completely miscible with aromatic hydrocarbons, chlorinated hydrocarbons, and alcohols;
moderately soluble in diesel oil, kerosene, isoparaffinic hydrocarbons, and minerals oils
Miscible in dichloromethane, 2-propanol, toluene
Spectral Properties:
INDEX OF REFRACTION: 1.451 @ 25 DEG C/D
Intense mass spectral peaks: 109 m/z (100%), 185 m/z (31%), 79 m/z (21%), 202 m/z (12%)
Intense mass spectral peaks: 145 m/z, 220 m/z
Vapor Pressure:
0.0158 mm Hg @ 25 deg C
Other Chemical/Physical Properties:
The air water partition coefficient is 5.0X10-3 for dichlorvos.
The octanol water partition coefficient is 1.45X10+1 for dichlorvos.
Slowly hydrolyzed in water and in acid media; rapidly hydrolyzed by alkalis to dimethyl
hydrogen phosphate and dichloroacetaldehyde.
Chemical Safety & Handling:
Hazards Summary:
The major hazards encountered in the use and handling of dichlorvos
stem from its toxicologic properties as an organophosphate pesticide. Direct contact with dichlorvos may cause burns to the skin and eyes.
Systemic effects from skin absorption, ingestion, or inhalation range from depression of
blood cholinesterase, dizziness, and confusion, to convulsions, coma, and death. The
airborne level of dichlorvos reported by NIOSH
to be immediately dangerous to life and health (IDLH) is 200 mg/cu m. The OSHA PEL and
ACGIH TLV are both set at 1 mg/cu m, with an indication that skin contact be avoided. To
avoid skin exposure, wear overalls made of tight fabric or polyvinyl chloride, gloves,
rubber boots (some forms of rubber are attacked by dichlorvos),
and a face shield or splash-proof goggles. To avoid inhalation wear a full facepiece
supplied-air respirator or self-contained breathing apparatus. Clothing that becomes
contaminated with dichlorvos should be promptly
removed and any contaminated skin immediately washed with soap and water. Protect from
exposure persons under 18 yr of age, expectant or nursing mothers, alcoholics, or those
having diseases of the CNS, respiratory system, liver, kidney, or eyes. Dichlorvos
will not ignite easily (flashpoint > 175 deg C open cup), but will burn with the
possible release of toxic gases and vapors such as hydrogen chloride, phosphoric acid
mist, and carbon monoxide. For small fires involving dichlorvos,
extinguish with dry chemical, CO2, water spray, foam, and for large fires, use water
spray, fog, or foam. Runoff from fire control water may give off poisonous gases or cause
water polution and should, therefore, be diked for later disposal. Dichlorvos
should be stored in a cool (< 80 deg F) and dry place (to avoid hydrolysis); away from
strong acids and alkalis. In choosing an appropriate storage container, the fact that dichlorvos is corrosive to iron and mild steel should
be considered. Containers of dichlorvos may be
shipped by air, rail, road, water, and for both domestic and international compliance,
should should be affixed with labels stating, "Keep Away From Food", and
"Poison". For small spills of dichlorvos,
absorb in vermiculite, dry sand or earth and collect for reclamation. Large land spills
should be deposited in excavated pits, ponds, or other holding areas and the bulk material
absorbed with fly ash or cement powder. Surface flow should be diked with sand bags or
soil. Spills of dichlorvos in bodies of water,
first may need to be treated with activated carbon, then the immobilized masses removed
with mechanical dredges or lifts. Before permanent land disposal of dichlorvos,
consult with environmental regulatory agencies.
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: ... 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: Spill: 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:
Dichlorvos is not known to be an eye
irritant.
Fire Fighting Procedures:
If material is on fire or involved in a fire: Do not extinguish fire unless flow can be
stopped; 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 foam, carbon dioxide, or dry chemical. Keep
run-off water out of sewers and water sources.
Fire fighting: Self-contained breathing apparatus with a full facepiece operated in
pressure demand or other positive pressure mode.
Toxic Combustion Products:
Toxic gases and vapors (such as hydrogen chloride gas, phosphoric acid mist, and carbon
monoxide) may be released in a fire involving dichlorvos.
Hazardous Reactivities & Incompatibilities:
HYDROLYZES IN WATER
Special precautions: Dichlorvos will attack
some forms of plastics, rubber, and coatings.
Strong acids, strong alkalis [Note: Corrosive to iron & mild steel].
Hazardous Decomposition:
READILY DECOMP IN STRONG ACID OR ALKALI
Decomposition products may include toxic gases and vapors of hydrogen chloride gas,
phosphoric acid mist, and carbon monoxide.
Prior History of Accidents:
After a fire at the Sandoz Ltd. storehouse at Schweizerhalle, Switzerland, which stored
pesticides, dichlorvos was released to Rhine
River water.
Immediately Dangerous to Life or Health:
100 mg/cu m
Protective Equipment & Clothing:
EMPLOYEES SHOULD BE PROVIDED WITH & REQUIRED TO USE IMPERVIOUS CLOTHING, GLOVES,
FACE SHIELD (8-INCH MINIMUM), & OTHER APPROPRIATE PROTECTIVE CLOTHING NECESSARY TO
PREVENT REPEATED OR PROLONGED SKIN CONTACT WITH DICHLORVOS.
... REQUIRED TO USE SPLASH-PROOF SAFETY GOGGLES WHERE LIQ ... MAY CONTACT EYES.
Respiratory protection from dichlorvos is as
follows: 10 mg/cu m or less: Any supplied-air respirator or any self-contained breathing
apparatus; 50 mg/cu m or less: Any supplied-air respirator with a full facepiece, helmet
or hood or any self-contained breathing apparatus with a full facepiece; 200 mg/cu m or
less; A Type-C supplied-air respirator operated in pressure-demand or other positive
pressure or continuous-flow mode; Greater than 200 mg/cu m or entry or escape from unknown
concentrations; A combination respirator which includes a Type-C supplied-air respirator
with a full facepiece operated in pressure-demand or other positive pressure or
continuous-flow mode and an auxiliary self-contained breathing apparatus operated in
pressure-demand or other positive pressure mode; Escape: Any gas mask providing protection
against organic vapors and particulates including pesticide respirations which meet the
requirements of this class or any self-contained breathing apparatus. Use of supplied-air
suits may be necessary to prevent skin contact while providing respiratory protection from
airborne concentrations of dichlorvos. ... Where
supplied-air suits are used above a concentration of 200 mg/cu m, an auxiliary
self-contained breathing apparatus operated in positive pressure mode should also be worn.
WORKERS HANDLING AND APPLYING ORGANOPHOSPHORUS PESTICIDES ... 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. ... /ORGANOPHOSPHORUS PESTICIDES/
Wear appropriate personal protective clothing to prevent skin contact.
Wear appropriate eye protection to prevent eye contact.
Recommendations for respirator selection. Max concn for use: 10 mg/cu m. Respirator
Class(es): Any supplied-air respirator.
Recommendations for respirator selection. Max concn for use: 25 mg/cu m. Respirator
Class(es): Any supplied-air respirator operated in a continuous flow mode.
Recommendations for respirator selection. Max concn for use: 50 mg/cu m. Respirator
Class(es): Any supplied-air respirator that has a tight-fitting facepiece and is operated
in a continuous-flow mode. Any self-contained breathing apparatus with a full facepiece.
Any supplied-air respirator with a full facepiece.
Recommendations for respirator selection. Max concn for use: 100 mg/cu m. Respirator
Class(es): Any supplied-air respirator operated in a pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection. Condition: Emergency or planned entry into
unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing
apparatus that has a full facepiece and is operated in a pressure-demand or other
positive-pressure mode. Any supplied-air respirator that has a full facepiece and is
operated in a pressure-demand or other positive-pressure mode in combination with an
auxiliary self-contained breathing apparatus operated in pressure-demand or other
positive-pressure mode.
Recommendations for respirator selection. Condition: Escape from suddenly occurring
respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator
(gas mask) with a chin-style, front- or back-mounted organic vapor canister having a
high-efficiency particulate filter. Any appropriate escape-type, self-contained breathing
apparatus.
PRECAUTIONS FOR "CARCINOGENS": ... Dispensers of liq detergent /should be
available./ ... Safety pipettes should be used for all pipetting. ... In animal
laboratory, personnel should ... wear protective suits (preferably disposable, one-piece
& close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... In
chemical laboratory, gloves & gowns should always be worn ... however, gloves should
not be assumed to provide full protection. Carefully fitted masks or respirators may be
necessary when working with particulates or gases, & disposable plastic aprons might
provide addnl protection. ... Gowns ... /should be/ of distinctive color, this is a
reminder that they are not to be worn outside the laboratory. /Chemical Carcinogens/
Preventive Measures:
Do not consume alcohol before, or during spraying.
In case of spill notify local health and wildlife officials. Notify operators of nearby
water intakes.
If material is not on fire and not involved in a 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; Attempt to stop leak if without hazard; Use water spray to
knock-down vapors.
Avoid breathing vapors. Keep upwind. Do not handle broken packages without protective
equipment. Wash away any material which may have contacted the body with copious amounts
of water, or soap and water.
Good industrial hygiene practices recommend that engineering controls be used to reduce
environmental concentrations to the permissible level, however, there are some exceptions
where respirators may be used to control exposure. Respirators may be used when
engineering and work practice controls are not technically feasible, when such controls
are in the process of being installed, or when they fail and need to be supplemented.
Respirators may also be used for operations which require entry into tanks or closed
vessels, and in emergency situations. If the use of respirators is necessary, the only
respirators permitted are those that have been approved by the Mine Safety and Health
Administration (formerly Mining Enforcement and Safety Administration) or by the National
Institute for Occupational Safety and Health. In addition to respirator selection, a
complete respiratory protection program should be instituted which includes regular
training, maintenance, inspection, cleaning, and evaluation.
Clothing contaminated with dichlorvos should
be placed in closed containers for storage until it can be discarded or until provision is
made for the removal of dichlorvos from the
clothing. If the clothing is to be laundered or otherwise cleaned to remove the dichlorvos, the person performing the operation should
be informed of dichlorvos's hazardous
properties.
Non-impervious clothing which becomes contaminated with dichlorvos
should be removed immediately and not reworn until the dichlorvos
is removed from the clothing.
Skin that becomes contaminated with dichlorvos
should be immediately washed or showered with soap or mild detergent and water to remove
any dichlorvos. Employees who handle dichlorvos should wash their hands thoroughly with
soap and mild detergent and water before eating, smoking, or using toilet facilities.
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/
THE STRICT OBSERVANCE OF HYGIENE RULES- NO SMOKING AND NO FOOD INTAKE DURING WORK,
THOROUGH WASHING WITH SOAP AFTER WORK, CHANGING PROTECTIVE CLOTHING BEFORE GOING HOME- IS
OF THE UTMOST IMPORTANCE. /ORGANOPHOSPHORUS PESTICIDES/
THE PROTECTIVE CLOTHING SHOULD BE KEPT IN SEPARATE PLACES WHERE IT CANNOT BE
CONTAMINATED WITH TOXIC CHEMICALS. IT SHOULD BE FORBIDDEN TO KEEP THIS CLOTHING IN LIVING
QUARTERS. PROTECTIVE CLOTHING MUST BE WASHED AT LEAST ONCE A WEEK AND EACH TIME IT IS
CONTAMINATED WITH PESTICIDES. BEFORE WASHING THE CLOTHING SHOULD BE SOAKED FOR SEVERAL
HOURS IN A CALCIUM CARBONATE SOLUTION. /PESTICIDES/
Smoking, eating, and drinking before washing should be absolutely prohibited when any
pesticide ... is being handled or used. /Pesticides/
Contact lenses should not be worn when working with this chemical.
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.
The worker should immediately wash the skin when it becomes contaminated.
Work clothing that becomes wet or significantly contaminated should be removed and
replaced.
PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or
of food & beverage containers or utensils, & the application of cosmetics should
be prohibited in any laboratory. All personnel should remove gloves, if worn, after
completion of procedures in which carcinogens have been used. They should ... wash ...
hands, preferably using dispensers of liq detergent, & rinse ... thoroughly.
Consideration should be given to appropriate methods for cleaning the skin, depending on
nature of the contaminant. No standard procedure can be recommended, but the use of
organic solvents should be avoided. Safety pipettes should be used for all pipetting.
/Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove
their outdoor clothes & wear protective suits (preferably disposable, one-piece &
close-fitting at ankles & wrists), gloves, hair covering & overshoes. ... Clothing
should be changed daily but ... discarded immediately if obvious contamination occurs ...
/also,/ workers should shower immediately. In chemical laboratory, gloves & gowns
should always be worn ... however, gloves should not be assumed to provide full
protection. Carefully fitted masks or respirators may be necessary when working with
particulates or gases, & disposable plastic aprons might provide addnl protection. If
gowns are of distinctive color, this is a reminder that they should not be worn outside of
lab. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ... Operations connected with synth &
purification ... should be carried out under well-ventilated hood. Analytical procedures
... should be carried out with care & vapors evolved during ... procedures should be
removed. ... Expert advice should be obtained before existing fume cupboards are used ...
& when new fume cupboards are installed. It is desirable that there be means for
decreasing the rate of air extraction, so that carcinogenic powders can be handled without
... powder being blown around the hood. Glove boxes should be kept under negative air
pressure. Air changes should be adequate, so that concn of vapors of volatile carcinogens
will not occur. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Vertical laminar-flow biological safety
cabinets may be used for containment of in vitro procedures ... provided that the exhaust
air flow is sufficient to provide an inward air flow at the face opening of the cabinet,
& contaminated air plenums that are under positive pressure are leak-tight. Horizontal
laminar-flow hoods or safety cabinets, where filtered air is blown across the working area
towards the operator, should never be used ... Each cabinet or fume cupboard to be used
... should be tested before work is begun (eg, with fume bomb) & label fixed to it,
giving date of test & avg air-flow measured. This test should be repeated periodically
& after any structural changes. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Principles that apply to chem or biochem lab
also apply to microbiological & cell-culture labs ... Special consideration should be
given to route of admin. ... Safest method of administering volatile carcinogen is by
injection of a soln. Admin by topical application, gavage, or intratracheal instillation
should be performed under hood. If chem will be exhaled, animals should be kept under hood
during this period. Inhalation exposure requires special equipment. ... Unless
specifically required, routes of admin other than in the diet should be used. Mixing of
carcinogen in diet should be carried out in sealed mixers under fume hood, from which the
exhaust is fitted with an efficient particulate filter. Techniques for cleaning mixer
& hood should be devised before expt begun. When mixing diets, special protective
clothing &, possibly, respirators may be required. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When ... admin in diet or applied to skin,
animals should be kept in cages with solid bottoms & sides & fitted with a filter
top. When volatile carcinogens are given, filter tops should not be used. Cages which have
been used to house animals that received carcinogens should be decontaminated.
Cage-cleaning facilities should be installed in area in which carcinogens are being used,
to avoid moving of ... contaminated /cages/. It is difficult to ensure that cages are
decontaminated, & monitoring methods are necessary. Situations may exist in which the
use of disposable cages should be recommended, depending on type & amt of carcinogen
& efficiency with which it can be removed. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": To eliminate risk that ... contamination in
lab could build up during conduct of expt, periodic checks should be carried out on lab
atmospheres, surfaces, such as walls, floors & benches, & ... interior of fume
hoods & airducts. As well as regular monitoring, check must be carried out after
cleaning-up of spillage. Sensitive methods are required when testing lab atmospheres. ...
Methods ... should ... where possible, be simple & sensitive. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Rooms in which obvious contamination has
occurred, such as spillage, should be decontaminated by lab personnel engaged in expt.
Design of expt should ... avoid contamination of permanent equipment. ... Procedures
should ensure that maintenance workers are not exposed to carcinogens. ... Particular care
should be taken to avoid contamination of drains or ventilation ducts. In cleaning labs,
procedures should be used which do not produce aerosols or dispersal of dust, ie, wet mop
or vacuum cleaner equipped with high-efficiency particulate filter on exhaust, which are
avail commercially, should be used. Sweeping, brushing & use of dry dusters or mops
should be prohibited. Grossly contaminated cleaning materials should not be re-used ... If
gowns or towels are contaminated, they should not be sent to laundry, but ...
decontaminated or burnt, to avoid any hazard to laundry personnel. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Doors leading into areas where carcinogens are
used ... should be marked distinctively with appropriate labels. Access ... limited to
persons involved in expt. ... A prominently displayed notice should give the name of the
Scientific Investigator or other person who can advise in an emergency & who can
inform others (such as firemen) on the handling of carcinogenic substances. /Chemical
Carcinogens/
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:
STABLE TO HEAT
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.
PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should
be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass
bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top
container that will not open when dropped & will resist attack from the carcinogen.
Both bottle & the outside container should be appropriately labelled. ... National
post offices, railway companies, road haulage companies & airlines have regulations
governing transport of hazardous materials. These authorities should be consulted before
... material is shipped. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following
procedure must be adopted. The carcinogen should be enclosed in a securely sealed,
watertight container (primary container), which should be enclosed in a second,
unbreakable, leakproof container that will withstand chem attack from the carcinogen
(secondary container). The space between primary & secondary container should be
filled with absorbent material, which would withstand chem attack from the carcinogen
& is sufficient to absorb the entire contents of the primary container in the event of
breakage or leakage. Each secondary container should then be enclosed in a strong outer
box. The space between the secondary container & the outer box should be filled with
an appropriate quantity of shock-absorbent material. Sender should use fastest & most
secure form of transport & notify recipient of its departure. If parcel is not
received when expected, carrier should be informed so that immediate effort can be made to
find it. Traffic schedules should be consulted to avoid ... arrival on weekend or holiday
... /Chemical Carcinogens/
Storage Conditions:
IT MUST BE STORED @ TEMP BELOW 80 DEG F TO ASSURE PROPER SHELF LIFE.
Store in origional container, preferably in a locked area, away from children, food,
feed.
PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical
to lab in which carcinogens are to be used, so that only small quantities required for ...
expt need to be carried. Carcinogens should be kept in only one section of cupboard, an
explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that
bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen
& date it was acquired ... Facilities for dispensing ... should be contiguous to
storage area. /Chemical Carcinogens/
Cleanup Methods:
Land spill: Dig a pit, pond, lagoon, 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 surface flow using soil, sand bags,
foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, or cement
powder.
Water spill: If dissolved, apply activated carbon at ten times the spilled amount in
region of 10 ppm or greater concn. Use mechanical dredges, or lifts to remove immobilized
masses of pollutants and precipitates.
Air spill: Apply water spray or mist to knock down vapors.
Ventilate area of spill or leak. Collect for reclamation or absorb in vermiculite, dry
sand, earth, or similar material.
PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA)
or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated
safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is
designed so that used filters can be transferred into plastic bag without contaminating
maintenance staff is avail commercially. Filters should be placed in plastic bags
immediately after removal ... The plastic bag should be sealed immediately ... The sealed
bag should be labelled properly ... Waste liquids ... should be placed or collected in
proper containers for disposal. The lid should be secured & the bottles properly
labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ...
is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken
glassware ... should be decontaminated by solvent extraction, by chemical destruction, or
in specially designed incinerators. /Chemical Carcinogens/
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.
Treat dichlorvos by alkali, (64%
disappearance in Zahn at pH 8.7) mix the product with a portion of soil rich in organic
matter before burying. Recommendable methods: Incineration, hydrolysis, & landfill.
Peer-review: Adsorb residues on sawdust and incinerate @ high temp in a unit with effluent
gas scrubbing. (Peer-review conclusions of an IRPTC expert consultation (May 1985))
PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that
has been proved satisfactory for all carcinogenic compounds & specific methods of chem
destruction ... published have not been tested on all kinds of carcinogen-containing
waste. ... summary of avail methods & recommendations ... /given/ must be treated as
guide only. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ... Incineration may be only feasible method
for disposal of contaminated laboratory waste from biological expt. However, not all
incinerators are suitable for this purpose. The most efficient type ... is probably the
gas-fired type, in which a first-stage combustion with a less than stoichiometric air:fuel
ratio is followed by a second stage with excess air. Some ... are designed to accept ...
aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb soln onto
suitable combustible material, such as sawdust. Alternatively, chem destruction may be
used, esp when small quantities ... are to be destroyed in laboratory. /Chemical
Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": HEPA (high-efficiency particulate arrestor)
filters ... can be disposed of by incineration. For spent charcoal filters, the adsorbed
material can be stripped off at high temp & carcinogenic wastes generated by this
treatment conducted to & burned in an incinerator. ... LIQUID WASTE: ... Disposal
should be carried out by incineration at temp that ... ensure complete combustion. SOLID
WASTE: Carcasses of lab animals, cage litter & misc solid wastes ... should be
disposed of by incineration at temp high enough to ensure destruction of chem carcinogens
or their metabolites. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ... Small quantities of ... some carcinogens
can be destroyed using chem reactions ... but no general rules can be given. ... As a
general technique ... treatment with sodium dichromate in strong sulfuric acid can be
used. The time necessary for destruction ... is seldom known ... but 1-2 days is generally
considered sufficient when freshly prepd reagent is used. ... Carcinogens that are easily
oxidizable can be destroyed with milder oxidative agents, such as saturated soln of
potassium permanganate in acetone, which appears to be a suitable agent for destruction of
hydrazines or of compounds containing isolated carbon-carbon double bonds. Concn or 50%
aqueous sodium hypochlorite can also be used as an oxidizing agent. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Carcinogens that are alkylating, arylating or
acylating agents per se can be destroyed by reaction with appropriate nucleophiles, such
as water, hydroxyl ions, ammonia, thiols & thiosulfate. The reactivity of various
alkylating agents varies greatly ... & is also influenced by sol of agent in the
reaction medium. To facilitate the complete reaction, it is suggested that the agents be
dissolved in ethanol or similar solvents. ... No method should be applied ... until it has
been thoroughly tested for its effectiveness & safety on material to be inactivated.
For example, in case of destruction of alkylating agents, it is possible to detect
residual compounds by reaction with 4(4-nitrobenzyl)-pyridine. /Chemical Carcinogens/
Occupational Exposure Standards:
Threshold Limit Values:
8 hr Time Weighted Avg (TWA) 0.9 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.
BEI (Biological Exposure Index): Cholinesterase activity in red cells (timing is
discretionary) is 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/
A4. A4= Not classifiable as a human carcinogen.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m, skin.
Immediately Dangerous to Life or Health:
100 mg/cu m
Other Occupational Permissible Levels:
Australia: 0.1 ppm, skin (1990); Federal Republic of Germany: 0.1 ppm, short-term level
1 ppm, 30 min, once per shift, skin, Pregnancy group C, no reason to fear a risk of damage
to the developing embryo or fetus when MAK and BAT values are adhered to (1990); United
Kingdom: 0.1 ppm, 10-min STEl 0.3 ppm, skin (1991)
Manufacturing/Use Information:
Major Uses:
CHLORINATED ORGANIC PHOSPHATE INSECTICIDE WITH APPRECIABLE VAPOR PRESSURE. INCORPORATED
INTO PLASTIC STRIPS IT SLOWLY RELEASES ... VAPOR. ... HAS BEEN APPROVED FOR USE IN
DISINFECTION OF ... AIRCRAFT.
... CONTACT & STOMACH INSECTICIDE WITH FUMIGANT & PENETRANT ACTION. ... USED AS
HOUSEHOLD & PUBLIC HEALTH FUMIGANT ...
MEDICATION (VET)
Controls household, public health, stored product insects. Controls mushroom flies,
aphids, spider mites, caterpillers, thrips, white flies in glasshouse crops, outdoor
fruit, vegetables.
Manufacturers:
Amvac Chemical Corporation, Hq: 4695 MacArthur Court Suite 1250 Newport Beach, CA 92660
(714)260-1212; Production site: 4100 E. Washington Blvd, Los Angeles, CA 90023
(213)264-3910
Methods of Manufacturing:
REACTION OF TRIMETHYL PHOSPHITE & CHLORAL
Dehydrochlorination of trichlorphon
Trimethyl phosphite + chloral (Perkow reaction); trichlorfon
(dehydrochlorination/rearrangement)
General Manufacturing Information:
Above pH 6, trichlorfon rearranges to form dichlorvos.
A slow release insecticide preparation for use in rooms, warehouses, etc, is
manufactured using inert aluminum silicate enhancer. Thus, an aluminum silicate plate (60
g) is soaked in a solution containing 20 g dichlorvos
and 0.5 g xanthine derivative. The preparation lasted 3-4 months, and the effective space
for its activity was 20-30 cu m.
Sustained release PVC incorporated insecticidal formulations are given, which also
contain insect stimulating materials (dyes, flavors, etc). Thus, a formulation contains
PVC 100, di-(2-ethylhexyl)phthalate 47, metal soap 2, stearic acid 0.2, dichlorvos
10-30, gelatin 2, and aluminum hydroxide 10 parts.
Finely dispersed carriers are impregnated with a compound containing a urethane
prepolymer isocyanates, polyols and pesticides. The compound is polymerized, molded, and
made into a pest control collar for pets. The pesticide containing particles in the
urethane polymer gradually flake off from the collar by friction and control pests for a
prolonged period. The compound contains an organic isocyanate-polyester polyol (molecular
weight 3000) 15, isocyanate-polyether polyol (molecular weight 1000) 8, Ti-coupled
aluminum hydroxide particles (80 u m/40 u m= 1/4) 75.5, and insecticide (eg, dichlorvos, allethrin) 1.5%.
... non-phytotoxic (except to some Chrysanthemum cultivars) ... & Non-persistent.
Formulations/Preparations:
Aerosols; soluble concentrates; multi-layered laminated strip
Impurities:
Dichlorvos is available in the USA as a
technical grade containing not less than 93 wt% of the pure chemical and not more than 7
wt% of insecticidally active related cmpd. Technical grade dichlorvos
can contain trichlorphon.
Consumption Patterns:
ESSENTIALLY 100% AS A PESTICIDE
Laboratory Methods:
Clinical Laboratory Methods:
ESTIMATION OF CHOLINESTERASE ACTIVITY OF ORGANOPHOSPHORUS INSECTICIDES IN HUMAN RED
BLOOD CELLS AND PLASMA BY INCUBATION WITH KNOWN EXCESS OF CHOLINESTERASE & ADDN OF
KNOWN EXCESS OF ACETYLCHOLINE. ACETIC ACID PRODUCED DETERMINED FROM CHANGE IN PH (PH
METER). /ORGANOPHOSPHORUS INSECTICIDES/
Analytic Laboratory Methods:
PRODUCT ANALYSIS: ... BY IR SPECTROSCOPY ... RESIDUES MAY BE DETERMINED BY GLC ...
NIOSH Method 295. Analyte: Dichlorvos.
Matrix: Air. Procedure: Gas chromatography/flame photometric detector. Method was
validated over the range of 0.382 to 1.707 mg/cu m using a 120 liter sample. Method
detection limit 0.2 ug/sample. Precision (CVt): 0.054. Interference: A compound with the
same retention time as the analyte is an interference.
Product analysis is by reaction with excess of iodine which is estimated by titration
or by glc.
A colorimetric method for the determination of the organic phosphate metabolites of dichlorvos in urine requires extraction with ether and
uses ascorbic acid as the chromogenic reagent. The resultant colored solution is analyzed
with a visible spectrophotometer at a wavelength of 820 nm. Calculation is based on a
response factor derived from a standard curve. This method has a sensitivity of 0.2 mg/l.
Determination of organophosphorus pesticide residues in food with two-dimensional gas
chromatography using capillary columns and flame photometric detection is described.
/Organophosphorus pesticide/
ASTM Method D3695: Volatile Alcohols in Water by GC: Standard Test Method for Volatile
Alcohols in Water by Direct Aqueous-Injection Gas Chromatography; GC with flame ionization
detection, wastewater, detection limit of 1.0 mg/l.
Sampling Procedures:
Trap in acetone using spectrophotometry of resorcinol complex at 490 nm; detection
limit of 0.14 mg/cu m. /From table/
NIOSH Method 295. Analyte: Dichlorvos.
Matrix: Air. Procedure: Adsorption on XAD-2 and desorption with toluene. Flow Rate: 0.5
and 1 l/min. Sample Size: 120-liters.
Special References:
Special Reports:
Dichlorvos is found in an EPA document
entitled Chemical Emergency Preparedness Program: Interim Guidance (Nov, 1985). This
voluntary program provides two goals: to increase community awareness of chemical hazards
and to develop state and local emergency response plans for dealing with chemical
accidents.
Santodonato J; Monograph on Human Exposure to Chemicals in the Workplace: Dichlorvos 31 pp. NTIS PPB86-148343 (1985)
Sternberg SS; Int Encycl Pharmacol Ther 113: 561-80 (1984). The carcinogenesis,
mutagenesis of insecticides is presented. Reviews both animal and human data.
World Health Organization; Monograph on Dichlorvos
(1989). Topics covered in this literature review are: physical and chemical properties and
analytical methods; sources of human and environmental exposure; kinetics and metablism;
effects on organisms; effects on experimental animals; effects on man; evaluation of human
health risks and effects on the environment.
Synonyms and Identifiers:
Related HSDB Records:
881 [TRICHLORFON] (METABOLIC PRECURSOR)
Synonyms:
Apavap
**PEER REVIEWED**
Astrobot
**PEER REVIEWED**
Atgard
**PEER REVIEWED**
Atgard C
**PEER REVIEWED**
BAY-19149
**PEER REVIEWED**
Benfos
**PEER REVIEWED**
BIBESOL
**PEER REVIEWED**
Brevinyl
**PEER REVIEWED**
BREVINYL E50
**PEER REVIEWED**
CANOGARD
**PEER REVIEWED**
Cekusan
**PEER REVIEWED**
CHLORVINPHOS
**PEER REVIEWED**
Cypona
**PEER REVIEWED**
DDVP
**PEER REVIEWED**
Dedevap
**PEER REVIEWED**
DERIBAN
**PEER REVIEWED**
DERRIBANTE
**PEER REVIEWED**
Des
**PEER REVIEWED**
Devikol
**PEER REVIEWED**
(2,2-DICHLOOR-VINYL)-DIMETHYL-FOSFAAT (DUTCH)
**PEER REVIEWED**
(2,2-Dichloor-vinyl)-dimethyl-phosphat (German)
**PEER REVIEWED**
DICHLOORVO (DUTCH)
**PEER REVIEWED**
Dichlorfos (Polish)
**PEER REVIEWED**
Dichlorman
**PEER REVIEWED**
2,2-Dichloroethenyl dimethyl phosphate
**PEER REVIEWED**
2,2-DICHLOROETHENYL PHOSPHORIC ACID DIMETHYL ESTER
**PEER REVIEWED**
DICHLOROVAS
**PEER REVIEWED**
(2,2-DICHLORO-VINIL)DIMETIL-FOSFATO (ITALIAN)
**PEER REVIEWED**
2,2-DICHLOROVINYL DIMETHYL PHOSPHATE
**PEER REVIEWED**
Dichlorovos
**PEER REVIEWED**
DICHLORPHOS
**PEER REVIEWED**
O-(2,2-DICHLORVINYL)-O,O-DIMETHYLPHOSPHAT (GERMAN)
**PEER REVIEWED**
DIMETHYL 2,2-DICHLOROETHENYL PHOSPHATE
**PEER REVIEWED**
O,O-DIMETHYL DICHLOROVINYL PHOSPHATE
**PEER REVIEWED**
O,O-DIMETHYL O-2,2-DICHLOROVINYL PHOSPHATE
**PEER REVIEWED**
DIMETHYL 2,2-DICHLOROVINYL PHOSPHATE
**PEER REVIEWED**
Divipan
**PEER REVIEWED**
Duo-kill
**PEER REVIEWED**
Duravos
**PEER REVIEWED**
ENT 20738
**PEER REVIEWED**
EQUIGEL
**PEER REVIEWED**
ESTROSEL
**PEER REVIEWED**
Estrosol
**PEER REVIEWED**
ETHENOL, 2,2-DICHLORO-, DIMETHYL PHOSPHATE
**PEER REVIEWED**
FECAMA
**PEER REVIEWED**
HERKAL
**PEER REVIEWED**
HERKOL
**PEER REVIEWED**
KRECALVIN
**PEER REVIEWED**
MAFU
**PEER REVIEWED**
Mafu strip
**PEER REVIEWED**
MARVEX
**PEER REVIEWED**
NCI-C00113
**PEER REVIEWED**
Nefrafos
**PEER REVIEWED**
NERKOL
**PEER REVIEWED**
NOGOS
**PEER REVIEWED**
No-pest
**PEER REVIEWED**
NO-PEST STRIP
**PEER REVIEWED**
NUVA
**PEER REVIEWED**
NUVAN
**PEER REVIEWED**
OMS 14
**PEER REVIEWED**
PHOSPHATE DE DIMETHYLE ET DE 2,2-DICHLOROVINYLE (FRENCH)
**PEER REVIEWED**
PHOSPHORIC ACID, 2,2-DICHLOROETHENYL DIMETHYL ESTER
**PEER REVIEWED**
PHOSPHORIC ACID, 2,2-DICHLOROVINYL DIMETHYL ESTER
**PEER REVIEWED**
PHOSVIT
**PEER REVIEWED**
SD 1750
**PEER REVIEWED**
SZKLARNIAK
**PEER REVIEWED**
TASK
**PEER REVIEWED**
Tetravos
**PEER REVIEWED**
Unifos
**PEER REVIEWED**
VAPONA
**PEER REVIEWED**
VAPONITE
**PEER REVIEWED**
Vinylofos
**PEER REVIEWED**
Winylophos
**PEER REVIEWED**
Formulations/Preparations:
Aerosols; soluble concentrates; multi-layered laminated strip
Shipping Name/ Number DOT/UN/NA/IMO:
NA 2783; Dichlorvos
UN 2783; Organophosphorus pesticides, solid, toxic, NOS
UN 3018; Organophosphorus pesticides, liquid, toxic, NOS
UN 2784; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint 23 deg C
or more
UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, NOS, flashpoint less than
23 deg C
IMO 6.1; Organophosphorus pesticides, solid, toxic, NOS; Organophosphorus pesticides,
liquid, toxic, flammable, NOS, flashpoint 23 deg C or more; Organophosphorus pesticides,
liquid, toxic, flammable, NOS, flashpoint less than 23 deg C; Organophosphorus pesticides,
liquid, toxic, NOS
Standard Transportation Number:
49 215 34; Dichlorvos (agricultural
insecticides, not elsewhere classified, liquid)
49 215 35; Dichlorvos (agricultural
insecticides, not elsewhere classified, other than liquid)
49 215 36; Dichlorvos (insecticides, other than
agricultural, not elsewhere classified)
49 215 37; Dichlorvos mixture, dry (agricultural
insecticides, other than liquid)
RTECS Number:
NIOSH/TC0350000
Administrative Information:
Hazardous Substances Databank Number: 319
Last Revision Date: 20010809
Last Review Date: Reviewed by SRP on 1/31/1999
Update History:
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/15/2001, 1 field added/edited/deleted.
Complete Update on 05/25/2000, 3 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 09/21/1999, 1 field added/edited/deleted.
Field Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 08/06/1999, 66 fields added/edited/deleted.
Field Update on 03/17/1999, 1 field added/edited/deleted.
Field Update on 11/17/1998, 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 05/08/1997, 1 field added/edited/deleted.
Complete Update on 04/01/1997, 3 fields added/edited/deleted.
Complete Update on 03/17/1997, 2 fields added/edited/deleted.
Complete Update on 03/07/1997, 4 fields added/edited/deleted.
Field Update on 03/06/1997, 1 field added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 09/10/1996, 1 field added/edited/deleted.
Complete Update on 07/11/1996, 1 field added/edited/deleted.
Complete Update on 06/06/1996, 1 field added/edited/deleted.
Complete Update on 05/09/1996, 1 field added/edited/deleted.
Complete Update on 04/16/1996, 7 fields added/edited/deleted.
Complete Update on 01/18/1996, 1 field added/edited/deleted.
Complete Update on 01/18/1995, 1 field added/edited/deleted.
Complete Update on 12/19/1994, 1 field added/edited/deleted.
Complete Update on 10/11/1994, 1 field added/edited/deleted.
Complete Update on 09/26/1994, 1 field added/edited/deleted.
Complete Update on 09/08/1994, 8 fields added/edited/deleted.
Field Update on 07/22/1994, 1 field added/edited/deleted.
Field Update on 05/05/1994, 1 field added/edited/deleted.
Field Update on 03/21/1994, 1 field added/edited/deleted.
Field Update on 01/25/1994, 1 field added/edited/deleted.
Field Update on 09/02/1993, 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 09/14/1992, 69 fields added/edited/deleted.
Complete Update on 08/17/1992, 69 fields added/edited/deleted.
Field Update on 04/16/1992, 1 field added/edited/deleted.
Field Update on 01/13/1992, 1 field added/edited/deleted.
Field Update on 09/13/1991, 1 field added/edited/deleted.
Field Update on 09/12/1991, 1 field added/edited/deleted.
Field Update on 09/11/1991, 1 field added/edited/deleted.
Field Update on 09/10/1991, 1 field added/edited/deleted.
Complete Update on 05/08/1991, 1 field added/edited/deleted.
Complete Update on 10/22/1990, 15 fields added/edited/deleted.
Field Update on 05/14/1990, 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, 12 fields added/edited/deleted.
Field Update on 05/05/1989, 1 field added/edited/deleted.
Field Update on 03/01/1989, 1 field added/edited/deleted.
Field Update on 05/12/1988, 1 fields added/edited/deleted.
Complete Update on 03/04/1988, 91 fields added/edited/deleted.
Complete Update on 05/02/1985
Record Length: 239020