Cyfluthrin Fact Sheet by Caroline Cox.

FLUORIDE ACTION NETWORK PESTICIDE PROJECT

Cyfluthrin Fact Sheet
By Caroline Cox

Published in JOURNAL OF PESTICIDE REFORM/ SUMMER 1994 • VOL.14, NO. 2

*INTRODUCTION*

Cyfluthrin is a relatively new insecticide that is
classified as a synthetic pyrethroid because its
chemical structure is a synthetic analog of naturally-
occurring pyrethrins. Many pesticide users and
regulators agree with toxicologists who report that
synthetic pyrethroids are economically successful
because they have "a degree of potency not previously
demonstrated in any class of insecticides," and are
"generally recognized as safe to mammalian species."
However, a closer look at cyfluthrin reveals a variety
of hazards associated with its use.

Cyfluthrin is a neurotoxin, with a mode of action
similar to that of the organochlorine insecticide DDT.
Acute exposures cause stinging skin, tremors,
convulsions, decreased blood pressure, and labored
breathing. Chronic exposure of laboratory animals to
cyfluthrin has resulted in weight loss, kidney
inflammation, vomiting, diarrhea, and a decrease in body
temperature. Exposure through inhalation causes symptoms
at very low doses; concentrations of as little as 150
parts per billion are enough to cause lethargy and a
failure to gain weight.

Cyfluthrin also appears to affect reproduction. Rabbits
exposed to cyfluthrin during pregnancy miscarried more
frequently than unexposed rabbits. Synthetic pyrethroids
as a class appear to disrupt androgen (male sex hormone)
function. Consistent with this, cyfluthrin interferes
with receptors that are part of this hormone system.

Cyfluthrin is highly acutely toxic to bees and fish.
(Just one part per billion can kill some fish species.)
Sublethal effects occur at even lower doses; less than
one part per trillion caused adverse effects on juvenile
minnows. Ecosystem-level tests have shown that
cyfluthrin affects many organisms in pond ecosystems,
including algae, zooplankton, nematodes, insects, and
fish.

Cyfluthrin-containing insecticide products also have at
least four ingredients other than cyfluthrin that are
known to cause acute and chronic health hazards.

Cyfluthrin was first registered for use in the United
States in 1987.(2) It is used to kill unwanted insects
in agriculture, in or around buildings, and on
ornamental plants.(2,3)

In California, where pesticide use reporting is more
comprehensive than in other states, the amount used in
agriculture is much smaller than that used for other
purposes.(4) However, agricultural uses are significant:
about 10 percent of the U.S. cotton acreage (over a
million acres) is treated with cyfluthrin, as is about
60 percent of the U.S. pear acreage.(5,6)

A recent survey of household pesticide use conducted for
the U.S. Environmental Protection Agency (EPA) showed
that cyfluthrin use is extensive. While cyfluthrin was
used by less than 2 percent of the households surveyed,
this represented almost 40 million applications annually
in the U.S. The bulk of these treatments (over 33
million annually) were made indoors.(7)

*MODE OF ACTION*

Many synthetic pyrethroids, including cyfluthrin, are
complex molecules and have a variety of three-
dimensional configurations called isomers. All of the
isomers, however have the same mode of action.(8)
Like all synthetic pyrethroids, cyfluthrin is a
neurotoxin. It causes hyperexcitation of the nervous
system, which leads to convulsions and ultimately
death.(9) The peripheral nervous system appears to be
the most vulnerable to synthetic pyrethroids. The
notorious organochlorine insecticide DDT has structural
similarities, has a "broadly similar mode of
action,"(10) and acts on "the same, or a very similar
site"(8) in the nervous system.

On a biochemical level, cyfluthrin has a complex mode of
action and affects normal nerve function in several
ways. It induces alterations in nerve membranes, causing
abnormal sodium and potassium flows.(11) This results in
the repetitive discharges from the neurons, causing
convulsions and also blockage of further nerve
impulses.(8) Cyfluthrin also affects calcium
concentrations in nervous tissue by inhibiting an enzyme
involved in calcium transport. This in turn increases
the amount of the neurotransmitter acetylcholine
released at the junction between nerves.(12) In
addition, two receptors found in nervous tissue, the
gamma-aminobutyric acid receptors and the peripheral
benzodiazepine receptors, are inhibited by cyfluthrin.
Inhibition of either of these receptors can cause
convulsions.(13,14)

*ACUTE TOXICITY*

The most common symptom of acute exposure to cyfluthrin
(and other synthetic pyrethroids) is paresthesia (a
stinging, burning, itching, and tingling of the skin
particularly common on the face), progressing to
numbness.(15) This is not an allergic or sensitizing
reaction, although one cyfluthrin-containing product
(Baythroid C2 EC; also called Tempo 2 and Baythroid 240)
is a skin sensitizer when tested on guinea pigs.(11)

Acute oral toxicity: Large doses of cyfluthrin cause
excess salivation, irritability, tremors,
incoordination, convulsions, and a fall in blood
pressure.(15) Larger doses, greater than 647-695
milligrams per kilogram (mg/kg) of body weight, cause
death in rats.(11) Mice die from smaller doses (291-609
mg/kg).(2) In some tests, the LD50 (the dose that will
kill half of the population of test animals) is up to
forty times smaller (16 mg/kg).(16) If humans are as
susceptible to cyfluthrin, the amount required to cause
death in an average-sized (60 kg) adult could be from
0.03 (based on the most sensitive test) to 1.5 ounces
(based on the first tests cited).

Like many pyrethroids, the acute toxicity of cyfluthrin
is negatively related to temperature, so that higher
toxicity is found at low temperatures. For example,
cyfluthrin is 10 times more acutely toxic to
cockroaches at 20!C (68!F) than it is at 30!C
(86!F).(17)

Inhalation toxicity: Cyfluthrin is also acutely toxic
when inhaled. Exposure of laboratory animals to 0.7 -
0.9 mg per liter of air caused convulsions, excess
salivation, incoordination, decreased activity, and
death.(11) Other studies of laboratory animals who have
inhaled cyfluthrin noted symptoms of labored breathing,
reduced movement, nasal discharge, and ungroomed
fur.(18)

Eye irritation: Cyfluthrin causes "mild irritation" of
rabbit eyes in laboratory tests. Several cyfluthrin-
containing products are more irritating to eyes.
Baythroid 20% WP (similar to Tempo 20% WP) causes
lesions of the conjunctive membrane, swelling around the
cornea, and a discharge for up to 7 days after
exposure.(19) Baythroid C2 EC (Tempo 2) caused opaque
corneas, lesions in the iris, and swelling around the
cornea for 21 days after exposure.(11) According to the
manufacturer, exposure to Tempo 2 EC may cause "severe
eye irritation."(20)

*CHRONIC TOXICITY*

Long-term exposure of laboratory animals to cyfluthrin
has caused adverse effects that range from diarrhea to
reduced body temperature and weight loss. For example,
in rats fed cyfluthrin for two weeks, weight loss,
slight brain hemorrhages, and death of muscle fibers was
observed. Cyfluthrin-contaminated diets over longer
periods (four weeks) caused weight loss, changes in
several blood chemistry parameters, and changes in liver
weights. In a feeding study that lasted for two years,
weight loss was also noted, as well as kidney
inflammation in females. Dogs fed cyfluthrin for six
months suffered from vomiting and diarrhea; in a year-
long study vomiting, diarrhea, and weight loss were
noted.(16)

Long-term inhalation of cyfluthrin can also cause
adverse effects. In studies with rats, inhalation of
cyfluthrin for three weeks caused a decrease in body
temperature, weight loss, and changes in the weight of
the liver and spleen. Inhalation over a three month
period at the alarmingly low rate of 150 parts per
billion (ppb), also caused a decrease in body
temperature and a failure to gain weight at a normal
rate.(16)

Neurotoxicity: Acute exposure to cyfluthrin can cause
chronic symptoms of damage to the nervous system. For
example, a single acute exposure of hens to cyfluthrin
caused disturbed behavior, prostration, and a limping
gait over two weeks later. Multiple acute exposures over
a one or three week period caused "delayed neurotoxic
signs and moderate fiber alterations in the sciatic
nerve."(11)

Chronic exposures at lower levels can also cause chronic
symptoms of nervous system damage. Rats exposed to
cyfluthrin through inhalation showed chronic symptoms of
neurotoxicity at low doses. Inhaled concentrations of
150 ppb over a three month period caused the rats to
exhibit unkempt fur, lethargy, and agitation. Rats fed
larger amounts of cyfluthrin for two weeks showed
disturbed behavior, uncoordinated walking, excess
salivation, and degeneration of several nerves. Dogs fed
cyfluthrin for six months developed a stiff gait,
incoordination, and arched backs.(16)

*REPRODUCTIVE EFFECTS*

In pregnant rabbits, feeding of cyfluthrin causes both
miscarriages and resorption of fetuses. In a three-
generation study of rats, feeding of cyfluthrin caused
pups to have "decreased viability" and decreased
weight.(16)

Cyfluthrin may also have more subtle effects on the
ability of humans and other animals to reproduce. Recent
(1990) research documented the ability of six synthetic
pyrethroids, as well as the naturally occurring
pyrethrins, to bind with androgen (a male sex hormone)
receptors, and disrupt normal androgen function.(21)
These kinds of effects, broadly called endocrine
disruption, have been linked to a variety of health
problems, including breast cancer, testicular cancer,
and decreased sperm counts. The researchers "advise
protection from any form of contact or ingestion of the
pyrethroids in order to prevent any undesirable effects
on the human reproductive system."(21) While cyfluthrin
was not one of the compounds included in this study, the
results are consistent with research showing that
cyfluthrin binds with peripheral benzodiazepine (PBZ)
receptors. PBZ receptors are found in high concentration
in the testes and appear important in "hormonal
responsiveness."(14)

*CARCINOGENICITY AND MUTAGENICITY*

The tests submitted in support of cyfluthrin's
registration "indicate that cyfluthrin is not an
oncogen" (does not cause cancer) and is "not considered
to be mutagenic" (having the ability to damage genetic
material).(2) It is not known whether cyfluthrin-
containing products are carcinogenic or mutagenic
because tests of the products as they are used
(including all ingredients) are not required by EPA.
Laboratory tests of some of the ingredients in these
products other than cyfluthrin show that they are
associated with increases in the incidence of some kinds
of cancer. For example, crystalline silica causes
increases in lung cancer in laboratory animals and in
exposed workers and also induces lymphoma when injected
into test animals.(22) Xylenes have caused increased
rates of leukemia in workers who inhaled this solvent.
Xylenes also seem to be a cocarcinogen and increase the
number of skin cancers caused by other carcinogens in
laboratory animals.(23) Female rats exposed to
ethylbenzene developed an increased number of malignant
tumors.(24) (For more information, see "Secret 'Inert'
Ingredients," below).

*HUMAN EXPOSURE*

People are exposed to cyfluthrin by eating contaminated
food, from residues persisting after indoor or outdoor
applications, and through making applications of
cyfluthrin-containing products.

Food residues: Australian researchers monitored residues
of cyfluthrin applied to stored wheat over a year-long
period at a variety of temperature and humidity
conditions. They found that much of the cyfluthrin
persisted for the entire length of the study (52 weeks).
The estimated half-life of the cyfluthrin varied from 23
to 114 weeks depending on temperature, humidity, and
which isomer of cyfluthrin was studied.(25 ) A second
study of cyfluthrin used on stored grains found that
residues did not "decrease significantly" with time. In
addition, losses during milling and baking were
small.(26)

A study of cyfluthrin residues on strawberries found
that residues persisted for the entire length of the
study (21 days after spraying).(27)

Contamination of food with residues of cyfluthrin has
made headlines recently because of some fraudulent tests
conducted by Craven Laboratories of Austin, Texas.
Craven contracted with a number of pesticide
manufacturers to provide data on the persistence of food
residues of almost 30 pesticide products, including
cyfluthrin.(28) The data is required by EPA in order to
set tolerances (allowable food contamination levels). In
March 1994, Craven, its owner, and fourteen employees
were sentenced to jail terms (5 years for Craven's
owner), fines (15.5 million dollars), and restitution
(3.7 million dollars) after pleading guilty to charges
that the company had falsified residue tests.(29,30)

Persistence (outdoor): Residents whose yards or house
foundations are treated with cyfluthrin are often
concerned about how long they can expect residues to
remain. This is a difficult question to answer in a
simple way because persistence depends on a variety of
conditions. However, under laboratory conditions,
cyfluthrin residues in soil persisted up to 120 days,
with an estimated half-life up to 75 days.(31) EPA
reports a half-life of between 56 and 63 days.(2)

Persistence (indoor): Like persistence in soil,
persistence indoors also varies considerably depending
on conditions. A study that measured cyfluthrin residues
following an aerosol (spray-can) application inside an
apartment found that cyfluthrin persisted during the
entire length of the study (60 hours). Cyfluthrin
residues were constant throughout the study, so that no
estimate could be made of its persistence.(32) Another
study found cyfluthrin-treated dormitory rooms had floor
residues for three days following treatment.(33)

Occupational exposure: Inhalation of cyfluthrin over a
several month period caused adverse effects at lower
doses than any of the other tests required for
registration of cyfluthrin. As a result, EPA has been
concerned about the potential exposure of pest control
applicators who routinely apply cyfluthrin. In 1987,
just prior to registering cyfluthrin, EPA estimated
risks to pest control operators and concluded that there
was not an adequate margin of safety for applicators who
used cyfluthrin over a three month period. EPA's
Exposure Assessment Branch suggested that exposures
could be reduced by requiring applicators to wear
respirators when using cyfluthrin.(34) However, this
protective clothing was never required. Instead, EPA
revised its estimates of how much cyfluthrin an
applicator might use (both the number of apartments
treated and the amount of cyfluthrin used per apartment)
in order to achieve an adequate margin of safety.(35)

The cyfluthrin product for which this risk assessment
was done, Tempo 2, was also registered for use in
hospitals, nursing homes, schools, restaurants, and food
handling establishments that, according to EPA's
Toxicology Branch, "may pose special exposure
scenarios." The toxicologists did not believe that the
pest control operator use in apartments would
"necessarily represent a 'worst case' exposure scenario
for the many uses listed on the label."(34) However, EPA
appears to have taken no further action to remedy these
problems.(35)

Another concern about occupational exposure comes from
studies of how well laundering removes cyfluthrin
residues from fabric. Depending on detergent type,
fabric finish, and the type of cyfluthrin product used,
between 5 and 100 percent of cyfluthrin residues were
not removed by machine washing. The researchers state,
"across all specimens as much as 90 percent I of
pesticide remained after washing. Although laundering
made a difference in pyrethroid residue, it was not
particularly successful."(36) This means pest control
applicators who apply cyfluthrin may have a difficult
time removing contamination from their work clothing. A
second study found laundering to be somewhat more
successful at removing cyfluthrin from fabric, but still
found that between 20 and 30 percent of the cyfluthrin
contamination was not removed.(37)

*EFFECTS ON NONTARGET ORGANISMS*

Cyfluthrin affects a variety of living things in
addition to the unwanted insects it is designed to kill.
Such effects have been demonstrated for honey bees,
spiders, fish, birds, and aquatic invertebrates. In
addition, studies of model aquatic ecosystems have shown
that cyfluthrin has the potential to disrupt normal
ecosystem processes.

Bees: Cyfluthrin is highly toxic to bees. The median
lethal dose (LD50) is less than 0.04 micrograms (a
millionth of a gram) per bee.(38) In several field
tests, cyfluthrin was more acutely toxic to bees the day
after it had been applied than it was at the time of
application.(39) Cyfluthrin also appears to have
sublethal effects on bees; treated bees learn at a
slower rate (using an odor training test) and never
achieve as high a level of positive responses as do
untreated bees. Cyfluthrin appears to have stronger
effects on learning than do several other common
synthetic pyrethroids.(40)

Other Beneficial Arthropods: Kentucky entomologists have
studied the impact of cyfluthrin on predators whose prey
includes two turf pest species, the Japanese beetle and
the fall armyworm. A single application of cyfluthrin
reduced the abundance of predatory spiders, and effects
persisted for five weeks following treatment.(41)

Birds: High exposures are required to kill the bird
species on which cyfluthrin has been tested and EPA has
classified cyfluthrin as "practically nontoxic"(38) to
both upland game birds and waterfowl. However, several
reproductive effects seem worthy of concern. In mallard
ducks, "statistically significant reduction in
production of normal hatchlings"(38) was observed at all
levels tested. "Statistically significant impairment of
reproduction"(38) was observed in bobwhite quail. In
addition, "eggshell thinning was statistically
significant at all levels tested."(38) Although the
eggshell thinning study seems serious, particularly
because of the significant consequences of eggshell
thinning caused by exposure to DDT (whose mode of action
is similar to that of cyfluthrin), it appears that
little has been done to follow up on these studies. A
second eggshell thinning study was submitted which found
no thinning at any dose level, but NCAP is aware of no
explanation from EPA for the inconsistent results.(38)

Fish: Cyfluthrin is also very highly toxic to fish.
Median lethal concentrations (LC50s; the concentration
required to kill half of a population of test animals)
are close to one part per billion for the fish species
that have been tested. As might be expected, sublethal
effects occur at much lower doses; in the sheepshead
minnow exposures of less than one tenth as much as the
lethal dose, 84 parts per trillion (ppt), reduced
survival of juveniles and effects were measured on
juvenile rainbow trout with even lower exposures,18
ppt.(38) In one study, effects on juvenile fathead
minnows were measured at the startlingly low
concentration of 0.14 ppt.(42) Cyfluthrin is estimated
to bioconcentrate (concentrate in animals whose diets
are higher up the food chain) by a factor of over 800
times,(38) thus increasing its potential effects on
fish.

Other aquatic invertebrates: Cyfluthrin is very highly
toxic to a variety of aquatic organisms. The median
lethal dose for water fleas (Daphnia magna and
Ceriodaphnia dubia) was less than 1 ppt;(43) for mysid
shrimp was less than 3 ppt;(2) and for Eastern oyster
was about 3 parts per billion.(2) Sublethal effects
occurred at lower concentrations. For example,
reproductive success of mysid shrimp was affected at
1.25 ppt,(38) and uncoordinated swimming was observed in
water fleas at concentrations below the LC50 of 1
ppt.(43)

Ecosystem-level effects: EPA has recently (1992)
reviewed a study designed to measure any effects of
cyfluthrin on aquatic ecosystems. The study involves the
use of mesocosms, small artificial ponds into which are
introduced a variety of plankton, aquatic insects, and
fish. While EPA found many deficiencies in the study,
including the contamination of ponds that were supposed
to serve as control (untreated) mesocosms, the study
does point out how cyfluthrin can impact an entire
ecosystem. Cyfluthrin affected "the majority of the
lower tiers of the ecosystem": During most of the study,
treated ponds had a lower weight of phytoplankton
(algae) than did untreated ponds, and by the end of the
study abundances were also lower. Zooplankton
(microscopic animals) were also affected: some species
were less abundant in treated ponds, while their
competitors (other species of zooplankton eating the
same kinds of food) increased in abundance. Nematodes
increased in treated ponds, while diversity of surface-
dwelling insects decreased. These effects were evident
at concentrations in the water in the parts per trillion
range. The study also provides evidence that these
effects "cascaded throughout the pond ecosystem" and are
important to the larger organisms. Fish biomass in
untreated ponds was greater than treated ponds "at all
test doses" and fish weight gain was "markedly greater"
in untreated ponds.(42)

*RESISTANCE*

Insect resistance, the ability of unwanted insects to
tolerate exposure to an insecticide in amounts that
would be lethal to a typical individual, is an
increasing problem. Over 500 insect species, including
"most of the economically important species" have
developed resistance to at least one insecticide and
twelve economically important insect pests have
developed resistance to nearly all available
insecticides. Synthetic pyrethroids as a class have
played a prominent role in recent discussions of
resistance because resistance to pyrethroids has
developed quickly and many insects that are resistant to
other classes of insecticides easily evolve pyrethroid
resistance.(44)

Resistance to cyfluthrin specifically has been
documented in the spotted tentiform leafminer (a pest of
apples),(45) the Egyptian cotton leafworm (a pest of
cotton),(46) flour beetles (a stored products pest),(47)
the German cockroach (a household pest),(48,49) the
cotton aphid (a cotton pest),(50) the tobacco budworm (a
pest on a variety of crops),(51,52) and the cat flea (a
mammal pest).(53) In some cases, the degree of
resistance is astonishing. For example, cockroaches from
an apartment in Gainesville, Florida were found to be
almost 90 times as resistant to cyfluthrin as a
susceptible laboratory strain. (The apartment had been
treated repeatedly with cypermethrin, another synthetic
pyrethroid.) The researchers warned that this "entire
class of compounds may be rendered useless in a short
time."(48)

*SECRET 'INERT' INGREDIENTS*

All cyfluthrin-containing insecticide products contain
ingredients other than cyfluthrin that are called trade
secrets by their manufacturers and classified as "inert"
ingredients by EPA. However, these ingredients are
neither biologically, toxicologically, or chemically
inert. "Inerts" make up 75 percent of Baythroid 254 and
Tempo 2 EC,(20) and 80 percent of Tempo 20% Wettable
Powder(55) is "inert." The following "inert" ingredients
have been identified on the material safety data sheets
produced for at least one cyfluthrin-containing product:

Crystalline silica is a mineral dust . The International
Agency for Research on Cancer has classified evidence
about its ability to cause cancer as sufficient in
animals and limited in humans. In laboratory animals,
inhalation of crystalline silica induced significant
increases in the incidence of lung cancer. Injections
induced lymphomas in the thorax and abdomen. In humans,
a number of studies have shown that lung cancer occurs
more frequently in workers who are exposed to
silica.(22)

Xylenes are solvents. They cause nose and throat
irritation, eye irritation, labored breathing, lung
inflammation, nausea, vomiting, mild liver toxicity,
impaired short-term memory, and hearing loss in exposed
humans and/or laboratory animals. In laboratory tests,
xylene exposure has also caused reduced fertility,
increased number of fetal resorptions, increased
incidence of cleft palate, decreased fetal weight.
Xylene inhalation has been associated with an increased
frequency of leukemia in solvent-exposed workers. In
addition, it may be a cocarcinogen; exposure to xylenes
enhanced the number of skin cancers caused by other
carcinogens.(23)

Ethylbenzene is another solvent. It causes throat irritation, eye irritation, damage to liver and kidneys,
dizziness, and incoordination in humans and/or laboratory animals. In laboratory tests, exposure to
ethylbenzene has caused fetal resorption, retardation of fetal skeletal development, and extra ribs in fetuses.
It has also blocked or delayed the estrus cycle in female rats and damaged testes in a small study of
monkeys. Exposure to ethylbenzene increased the number of malignant tumors in female rats.(24)

Trimethylbenzenes are highly volatile solvents that can cause skin and eye irritation, nervousness, tension,
bronchitis, disruptions of the ability of blood to clot, headaches, fatigue, dizziness, and loss of
consciousness.(56)

*REFERENCES*

1. Bradbury, S.P. and J.R. Coats. 1989. Comparative toxicology of the pyrethroid insecticides. Rev. Environ.
Cont. Toxicol. 108:134-177.

2. U.S. EPA. Office of Pesticides and Toxic Substances. Office of Pesticide Programs. 1987.
Pesticide fact sheet: Cyfluthrin. No. 164. Washington, D.C. (December 30.)

3. Farm Chemicals '92. 1992. Willoughby, OH: Meister Publishing Company.

4. California Dept. of Pesticide Regulation. Information Services Branch. 1993. Summary of pesticide
use report data: Annual 1991. Indexed by chemical. Sacramento, CA (January 25.)

5. U.S. Dept. of Agriculture. National Agricultural Statistics Service. Agricultural Statistics Board. 1994.
Agricultural chemical usage: 1993 field crops summary. Washington, D.C.: (March).

6. U.S. Dept. of Agriculture. National Agricultural Statistics Service. Agricultural Statistics Board. 1992.
Agricultural chemical usage: 1991 fruit and nuts summary. Washington, D.C.: (June).

7. Whitmore, R.W., J.E. Kelly, and P.L. Reading. 1992. National home and garden pesticide use survey: Final
report, Volume 1. Executive summary, results, and recommendations. Research Triangle Park, NC: Research
Triangle Institute.

8. Cremlyn, R.J. 1991. Agrochemicals: Preparation and mode of action. Chichester, U.K.: John Wiley & Sons.
Pp.68-69.

9. Corbett, J.R., K.W. Wright, and A.C. Baillie. 1984. The biochemical mode of action of pesticides. Second
edition. London, U.K.: Academic Press. p. 151.

10. Corbett, J.R., K.W. Wright, and A.C. Baillie. 1984. The biochemical mode of action of pesticides. Second
edition. London, U.K.: Academic Press. p. 157.

11. U.S. EPA. Office of Pesticides and Toxic Substances. 1986. The review of toxicology data in
support of the registration of Baythroid 240 ornamental pyrethroid insecticide Tempo 2. Memo from J.E. Whalan,
Hazard Evaluation Division, to George LaRocca, Registration Division. Washington, D.C. (August 18.)

12. Al-Rajhi, D.H. 1990. Properties of Ca+2 + Mg2 -ATPase from rat brain and its inhibition by
pyrethroids. Pest. Biochem. Physiol. 37:116-120.

13. Ramadan, A.A. et al. 1988. Action of pyrethroids on GABA receptor function. Pest. Biochem. Physiol. 32:97-
105.

14. Ramadan, A.A. et al. 1988. Actions of pyrethroids on the peripheral benzodiazepine receptor. Pest.
Biochem. Physiol. 32:106-113.

15. Morgan, D.P. 1989. Recognition and management of pesticide poisonings. Washington, D.C.: U.S. EPA. Office
of Pesticide Programs. Health Effects Division.

16. U.S. EPA. Office of Pesticide Programs. 1989. "Tox one-liners": Cyfluthrin. Washington, D.C. (June 28.)

17. Wadleigh, R.W. et al. 1991. Effect of temperature on the toxicities of ten pyrethroids to German
cockroach. (Dictyoptera: Blattellidae). J. Econ. Entomol. 84(5):1433-1436.

18. Pauluhn, J., et al. 1988. Methodological aspects of the determination of the acute inhalation toxicity of
spray-can ingredients. J. Appl. Toxicol. 8(6):431-437.

19. U.S. EPA. Office of Pesticides and Toxic Substances. 1987. Review of acute toxicology data in
support of the registration of Tempo 20% Wettable Powder for use in food handling establishments. Memo from J.E.
Whalan, Hazard Evaluation Division, to George LaRocca, Registration Division. Washington, D.C. (February 24.)

20. Miles Inc. Agriculture Division. 1991. Material Safety Data Sheet: Tempo 2EC. Kansas City, MO. (January
30.)

21. Eil, C. and B.C. Nisula. 1990. The binding properties of pyrethroids to human skin fibroblast
androgen receptors and to sex hormone binding globulin. J. Steroid Biochem. 35(3/4):409-414.

22. U.S. Dept. of Health and Human Services. Public Health Service. 1991. Sixth annual report on
carcinogens. Summary. Research Triangle Park: National Institute of Environmental Health Sciences.

23. U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease
Registry. 1993. Toxicological profile for xylenes. (October.)

24. U.S. Dept. of Health and Human Services. Public Health Service. Agency for Toxic Substances and Disease
Registry. 1990. Toxicological profile for ethylbenzene. (November.)

25. Noble, R.M. and D.J. Hamilton. 1985. Stability of cypermethrin and cyfluthrin on wheat and storage.
Pestic. Sci. 16:179-185.

26. Dicke, W., H.-D. Ocker, and H.-P. Thier. 1988. Rckstandsanalyze von pyrethroid-insecticiden in
getreide, mahlerzeugnissen und brot. Z. Lebensm. Unters Forsch 186:125-129.

27. McEwen, F.L. 1986. Residues of synthetic pyrethroid insecticides on horticultural crops. Pestic. Sci.
17:150-154.

28. CRC Press. 1991. EPA lists 14 more pesticides linked to possibly faulty data. Pesticide & Toxic
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