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Diazinon Diazinon
is an organophosphate insecticide; common trade names include SpectracideTM,
KnoxoutTM,
BasudinTM.
It is the fifth most commonly used pesticide used by homeowners, with two
to four million pounds used annually. In December 2000, the U.S. Environmental Protection Agency announced a four-year phase-out, without any warning to consumers about its neurotoxic properties, of the home and garden insecticide. The voluntary move by the manufacturer of diazinon raises concerns about continued sales to unsuspecting consumers. The agreement allows sales to continue through the phase-out period and allows uses to continue until stocks are depleted. For more information on the phase-out of diazinon products, see Beyond Pesticides' press release from December 5, 2000. Diazinon
originated with Ciba-Geigy in 1952. Various diazinon formulations are
widely used in agriculture and for structural pest control, besides being
used on lawns, and home gardens. Important target pests for diazinon
applications include cockroaches, aphids, scales, mites, ants, crickets,
fleas and ticks, flies, and grubs, and in the Western U.S. yellow jackets.
Diazinon may be found in formulations with a variety of other pesticides.
Depending on form, the EPA has classified diazinon as a toxicity class II
or III pesticide, based on a scale of I to IV, I being the most toxic
class. Health
Effects
A
review of the preliminary risk assessment of diazinon reveals numerous
data gaps, a failure on the part of EPA to fully assess aggregate risks,
as well as extreme health risks from both occupational and
non-occupational exposure to this pesticide. Diazinon
is a moderately acutely toxic broad-spectrum insecticide, with a LD50
of 350 to 400 mg/kg for humans. Like other organophosphate pesticides,
diazinon affects the nervous system through the inhibition of AchE, an
enzyme needed for proper nervous system function. Diazinon is easily
absorbed through the skin, and is synergistic with other chemicals
(meaning that the two together are more toxic than either alone),
including pyrethrins and certain chemicals used in pharmaceuticals. Exposure
to diazinon may cause headache, dizziness, profuse sweating, blurred
vision, nervousness, nausea, vomiting, reduced heart beat, stomach cramps,
diarrhea, loss of coordination, slow and weak breathing, fever, loss of
consciousness, coma, uncontrollable twitching, loss of reflexes, loss of
sphincter control and death. It can cause irritation to the eyes and skin,
and sensitization has been reported in animal tests, though there are some
questions as to whether this is due to the “inert” ingredients in
tested formulations. Repeated
exposure to low doses may cause muscle twitching, anorexia, malaise,
depression, irritability, confusion, anxiety, and dizziness. Damage to the
pancreas has developed in some people and in laboratory animals exposed to
large amounts of diazinon. Diazinon
is a mutagen. Long-term exposure may damage the developing fetus or cause
birth defects, nerve damage and/or liver damage. It has been shown to
cause birth defects in chick embryos (parrot beak, abnormal feathering,
and development of disproportionately small limbs). These effects are
thought to occur because of diazinon’s ability to inhibit the synthesis
of pyridine nucleotides, and possibly also the amino acid tryptophan. A
two generation reproductive study in rats showed that diazinon exposure
affected both mothers and offspring. Diazinon caused increased numbers of
still births and neonatal deaths in beagle dogs and birth defects in pigs.
In
1999, the Health Effects Division, Office of Prevention, Pesticides and
Toxic Substances, EPA, reported that “diazinon is one of the leading
causes of acute reactions to insecticide use reported as poisoning
incidents in the U.S.” The Health Effects Division also stated that
there were 11,808 unintentional residential diazinon exposures reported to
Pest Control Centers from 1993-1996. EPA’s now defunct Pesticide
Incident Monitoring System (PIMS) reported 903 diazinon related human
poisonings between 1966-1980. In the 1980’s, there were 126 reports of
SpectracideTM
pressurized container explosions in 27 states. Ecological
Effects
Diazinon
is highly toxic to bees. It has been known for some time that birds,
especially grazing fowl like ducks and geese, are highly susceptible to
diazinon poisoning, as are predatory or parasitic insects and mites, soil
microbes, fish and aquatic invertebrates. According
to the Prince George’s Journal diazinon caused the deaths of 14
ducks in September of 1997 in Virginia. The ducks were found dead in a
small pond and sent to laboratories were Robert D. Pritchett, chief of
Alexandria’s Environmental Health Department stated to the Journal
that the ducks died from “acute poisoning from the pesticide diazinon.” Diazinon
has been linked to hundreds of reports of bird kills due to diazinon
application on golf courses and sod farms. These reports in the 1980’s
involved over 23 species in at least 18 states. Diazinon poisoning also
caused more than 700 Atlantic brant in New York and over 85 wigeon on a
golf course in Bellingham, WA to die. Due to the large number of die offs
of birds that congregated on golf courses and sod farms, EPA canceled
registration of diazinon in these areas in 1988. Although
diazinon use on golf courses and sod farms has been cancelled, bird
mortalities continue to occur due to exposure to diazinon used on other
outdoor areas. The preliminary risk assessment released in 2000 for
diazinon states that around 300 incidents of wildlife mortality, mostly
birds, have been documented in the EPA, Office of Pesticide Program,
Environmental Fate and Effects Division’s Ecological Incidents Database
(EIID), from diazinon use, which is about 10% of all ecological incidents
in the database. The
preliminary risk assessment also stated that there is “a trend of
steadily increasing numbers of incidents over the years.” The
preliminary risk assessment for diazinon reported that the endangered
species level of concern are exceeded for wildlife, aquatic life and
terrestrial plants in semi-aquatic areas for all currently registered uses
and application rates of diazinon. Environmental
Fate
In
soil, degradation occurs by hydrolysis and microbial degradation, with a
half-life between 14 and 80 days. Diazinon can move through the soil and
contaminate groundwater. It is moderately persistent in water. Diazinon
was detected in surface water in 24 states and the District of Columbia
and in 54 wells in the state of California alone. The U.S. Geological
Survey data show that “diazinon is the most commonly found insecticide
in surface water nationally.” Residues
are taken up by plants and metabolized, while some remain behind on the
surface. These residues should dissipate in a few days to a week.
Bacterial enzymes can speed the breakdown of diazinon in soil and have
been used in treating emergency situations such as spills. It
has been reported that some forms of the compound can be degraded to more
toxic forms. This transformation may occur in air, particularly in the
presence of moisture, and by ultraviolet radiation. Diazinon
was one of five pesticides found to be able to concentrate in fog droplets
in California agriculture areas. In April 1995, the U.S. Geological Survey
began a study to determine the occurrence and temporal distribution of 49
pesticides and pesticide metabolites in air and rain samples from an urban
and an agricultural sampling site in Mississippi. The study found that
every rain and air sample collected from the urban and agricultural sites
had detectable levels of multiple pesticides. Diazinon was found to have
the highest concentration in the urban air site. It has also been found in
at least 18 of the 1,430 National Priorities List (Superfund) sites
identified by the EPA. Metabolism
and excretion rates for diazinon are relatively rapid. The half-life of
diazinon in animals is about 12 hours. The product is passed out of the
body through urine and in the feces. Cattle exposed to diazinon may store
the compound in their fats for two weeks. Application of diazinon to the
skin of cows resulted in trace amounts in milk 24 hours after the
application. References: Aspelin,
A. (1999). Pesticides Industry Sales and Usage: 1996 and 1997 Market
Estimates. Document No. 733-E-99-001. U.S. EPA, Office of Prevention,
Pesticides and Toxic Substances. Washington, DC. Coupe,
R., et al. (2000). “Occurrence of pesticides in rain and air in urban
and agricultural areas of Mississippi, April – September 1995.” Science
Total Environment 248(2-3):227-240. Cox,
Caroline. (1992). “Diazinon.” Journal of Pesticide Reform
12(3):30-35. “Diazinon
ban is suspended in first such U.S. court order,” Chemical Marketing
Reporter, July 10, 1989. Doherty,
M., et al. (1982). A survey of the scientific literature on selected
pesticides used in the City of Berkeley, CA: Diazinon. School of Public
Health, University of California-Berkeley. Extension
Toxicology Network. (1996). “Diazinon.” Pesticide Information
Profiles. http://ace.orst.edu/cgi-bin/mfs/01/pips/diazinon.htm. Glotfelty,
D., et al. (1987). “Pesticides in fog.” Nature 325:602-605. Kriner,
R. (1985). “Final report on the results of a national survey of
pesticide usage on golf courses in the U.S. conducted in July-September,
1982.” American Association of Retired Persons – U.S. EPA. Washington,
DC. Kushaba-Rugaaju,
S., et al. (1985). “Effects of diazinon on nucleotide and amino acid
contents of chick embryos.” Biochemical Pharmacology
34(11):1937-1943. “Low-dose
diazinon golf-course test results in kill of 85 wigeons.” Pesticide
& Toxic Chemical News, November 26, 1985. Meister,
R. (2000). Farm Chemicals Handbook. Meister Publishing Company,
Willoughby, OH. “New
York emergency rule bans diazinon on golf courses, sod farms.” Pesticide
& Toxic Chemical News, July 16, 1986. Plott,
W. (1988). “News release: Emergency pesticide warning notice (exploding
cans of diazinon).” Pesticide Complaint Monitoring Service.
Jacksonville, FL. Pohanish,
R. (1997). Hazardous Substances Resource Guide. Gale Publishing,
Detroit, MI. Rostker,
M. (1988). Personal communication re: bird mortality connected to diazinon
use. Office of Pesticide Programs. Washington, DC. Stone,
W., et al. (1985). “Wildlife mortality related to use of the pesticide
diazinon.” NE Environmental Science 4(1):30-38. Thomson,
W. (1992). Agricultural Chemicals: Insecticides. Thompson
Publications, Fresno, CA. U.S.
Department of Health and Human Services. (1996). Toxicological Profile for
Diazinon. Agency for Toxic Substances and Disease Registry, Public Health
Service. Atlanta, GA. U.S.
EPA. (2000). Diazinon Revised HED Preliminary Human Health Risk Assessment
for the Reregistration Eligibility Decision. Office of Pesticide Programs.
Washington, DC. U.S.
EPA. (1989). Guidance for the reregistration of pesticide products
containing diazinon as the active ingredient. Office of Pesticide
Programs. Washington, DC. U.S.
EPA. (1986). Notice of intent to cancel registrations and denial of
applications for registration of pesticide products containing diazinon:
Conclusion of Special Review. Office of Pesticide Programs. [51 FR 35034]
Washington, DC. U.S.
EPA. (1986). “Diazinon.” EPA Pesticide Fact Sheet, No. 96. Office of
Pesticide Programs. Washington, DC. U.S.
EPA. (1985). Diazinon Support Document. Office of Pesticide Programs.
Washington, DC. U.S.
EPA. (1980). “Summary of Reported Pesticide Incidents Involving Diazinon.”
Pesticide Incident Monitoring System Report No. 361. Office of Pesticide
Programs. Washington, DC. Whitmore,
R., et al. (1992). National home and garden pesticide use survey final
report. Volume I. Research Triangle Park, NC: Research Triangle Institute. Wright, C., et al. (1981). “Insecticides in the ambient air of rooms following their application for control of pests.” Bulletin of Environmental Contamination Toxicology 26:548-553.
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