Public Information and Records Integrity Branch (PIRIB) (7502C)

Office of Pesticide Programs

Environmental Protection Agency

1200 Pennsylvania Avenue, NW

Washington, DC 20461-0001

Attn: Docket ID Number OPP-2003-0237

2 August 2004

Dear Office of Pesticide Programs:

We are writing to you in response to the public comment period for the
methyl parathion IRED (OPP-2003-0237). Our initial comment is that we
believe that this comment period (60 days) was insufficient to
thoroughly and completely respond to a document that is complex and
exceeds 100 pages (including attachments), so we are requesting some
additional time in which to complete our response. We are intent on
providing you a set of comments that reflect a thorough review of this
document, as we feel that this particular issue is extremely important
and requires nothing short of a thorough review by the public. We
greatly appreciate your consideration of our request.

As for our preliminary response to the methyl parathion IRED, we are in
**STRONG OPPOSITION** to this proposed risk assessment, and detail some
of our concerns regarding this risk assessment as follows:

\(1\) Methyl parathion has been in use in the United States for 51 years
now. In 1970, the EPA was formed, and a few years later in 1978, the new
agency determined that methyl parathion was so hazardous to humans and
birds that they designated it as "restricted use" only. Methyl parathion
has been restricted use now for 26 years. This is totally unacceptable.
There has been plenty of time to find acceptable alternatives and over
this large amount of time "wean" our country away from the use of this
overly hazardous chemical. However, that has not happened. Instead, what
has happened is that the EPA has continued to find new ways to keep it
on the market. In late 1998, the EPA conducted a "preliminary" risk
assessment of methyl parathion and concluded that is posed an
"unacceptable risk" as currently used. So, in 1999, the EPA and the
registrants came up with some mitigation measures, including the
cancellation of uses of certain fruits and vegetables consumed
frequently by children, and modification of product labels in an attempt
to increase worker protection. Overall, these cancellations made up only
a miniscule fraction of the total acreage in which methyl parathion is
used in the United States. Now, five years later, methyl parathion is
still one of the most widely used insecticides in the US, with an
estimated annual use of 2-4 million lbs of active ingredient annually
(Donaldson et al. 2002). This document states that it will continue to
have at least 27 registered uses, including on such major crops as corn,
cotton, wheat, soybeans, and rice. So, in effect, what the EPA has done
is to allow methyl parathion to be continued to be used on a vast
majority of the acreage that it was being used on prior to the 1999
action with the addition of a few weak mitigation measures. Exactly how
is that protecting humans and the environment from this significantly
hazardous pesticide? The action by the EPA in 1999 stopped well short of
what should have been done at the time, which is to cancel all uses of
methyl parathion in the United States. By comparison, ethyl parathion,
registered in the US since 1948, was used for 55 years before its use
was finally cancelled by the EPA in October 2000 (used until October
2003). This insecticide is chemically and toxicologically very similar
to methyl parathion, and it is our assertion that the EPA should have
taken the outstanding opportunity that they had in 1999 to cancel
further uses of methyl parathion as well.

The risk assessments (human, occupational, ecological) presented in this
IRED have completely failed to accurately quantify or even realistically
consider the real health implications to humans and the environment from
the continued registration of methyl parathion. Further, the mitigation
measures proposed by this document generally are weak and will prove to
be ineffective towards decreasing the overall hazard presented by methyl
parathion in the environment. For example, the ecological risk
assessment found that methyl parathion exceeds the Agency's LOC for all
aquatic and terrestrial species considered. This indicates a
significantly hazardous pesticide, yet on p. 9, the document proposes
that, to address ecological risks, the EPA will lower the maximum number
of applications for several crops. This is such a minimal, token measure
that it will do virtually nothing to address ecological risks posed by
methyl parathion. There are many other examples (too numerous to list)
of this contained in the document. Therefore, we call on the EPA to
completely rework this reregistration IRED so that it cancels all
remaining used of methyl parathion by the end of this year.

\(2\) Methyl parathion is one of only 27 hazardous chemicals included in
the Rotterdam Convention on Prior Informed Consent Treaty -- this is a
very significant fact; methyl parathion is so highly toxic and hazardous
to humans, wildlife and the environment that it was included in the
initial list of hazardous pesticides listed in the Rotterdam Convention,
which requires exporters of these hazardous chemicals to notify
importing countries that they are on this list of hazardous chemicals.
The Director General of the UN Food and Agriculture Organization,
Jacques Diouf, referred to pesticides on this list as "inappropriate
pesticides" because they pose such great hazard to developing countries
that supposedly don't know any better. Well, we supposedly do know
better, so why is it that the federal agency that we trust to protect
our environment continues to register this inappropriate pesticide in
this country? Of the 22 pesticides on the initial list, methyl
parathion, lindane and methamidophos are all still registered in the
United States.

Further, many countries around the world (at least 27 that we are aware
of) have banned the use of methyl parathion outright (or never allowed
its use in the first place), including developing countries such as
Indonesia, Sri Lanka, and Tanzania, as well as developed nations such as
Canada, the United Kingdom, and Denmark. Many countries, such as Iraq,
United Arab Emirates, Ecuador, Peru, Jamaica, Trinidad and Tobago, and
many of the countries in the European Union, Asia, and Africa, as well
as Canada are countries listed as "no consent to import", meaning that
they refuse to import (use) methyl parathion (PANNA 2004). Now, what do
they all know that we don't?

We find it incredibly ironic that Denmark, the country that is home to
Cheminova, the largest manufacturer of methyl parathion sold in the
United States, has banned (because it was too hazardous) the use of this
chemical in their own country!!!

\(3\) Contradiction between the reason for its continued use and the
facts -- as far as we can ascertain, the main non-economic reason that
methyl parathion is still on the market is that it supposedly has a
short environmental persistence. This is stated in the methyl parathion
IRED document. In fact, we find that the half-life for methyl parathion
in aquatic media is 175 days and the half-life for methyl parathion in
soil is anywhere from 10 days to two months (PAN-UK 1998). These
half-lives for both aquatic and terrestrial media are not all that short
and still result in what we believe to be significant opportunities for
exposure in humans, fish and wildlife and the environment. After all,
you have to keep in mind that the acute toxicity of methyl parathion is
so high, and uptake is so efficient (oral, dermal, and inhalation or any
combination thereof) that in many instances it only takes one exposure
to kill an organism. Further, one fact that is not considered in this
"short persistence" reasoning is that, as methyl parathion breaks down
in the environment, the initial degradation (and metabolic) product is
methyl paraoxon, a compound that is considered at least three orders of
magnitude **MORE TOXIC** than the parent compound methyl parathion due
to its incredible cholinesterase-inhibiting abilities. So, the argument
that methyl parathion is not persistent in the environment used by EPA
to rationalize continued use of methyl parathion is incorrect because it
fails to consider the continued toxicity of any of its
degradation/metabolic products, including methyl paraoxon, its most
toxic degradation/metabolic product. Methyl parathion is widely used
throughout the United States, applied to at least 5 million acres each
year. Because it is aerially applied to many of these acres, drift can
be significant, so substantially more than 5 million acres each year are
impacted by methyl parathion. Not surprisingly, methyl parathion and its
degradation products are found in groundwater, surface waters,
precipitation, fog, and air in the United States.

\(4\) High toxicity concerns - methyl parathion has high acute, chronic,
and sublethal toxicity by all routes of exposure (oral, dermal,
inhalation), is readily taken up through all routes of exposure (oral,
dermal, inhalation), and although not known as a carcinogen, is a
probable mutagen and teratogen, and is embryotoxic (Tanimura et al.
1967). Human fatalities have been caused through all three routes of
exposure. The World Health Organization (WHO) classifies methyl
parathion as an "extremely hazardous" pesticide. Currently, there are 15
products registered by the EPA with methyl parathion as the active
ingredient (PANNA 2004). Of note is that fact that 14 of the 15 products
are listed as Toxicity Class 1, which is classified in the "Danger"
category. Clearly, this organophosphorus insecticide is so highly toxic
in so many ways (acute, chronic, sublethal) that its continued use poses
a significant hazard to any human or any other animal with a nervous
system unfortunate enough to be exposed to it.

In addition, sublethal effects documented for methyl parathion exposure
are numerous. In addition to the many different impacts on the nervous
(target) system, methyl parathion is listed by the Illinois EPA as a
probable endocrine disruptor, and by Benbrook (1996) as an endocrine
disruptor. Further, it is a known immunotoxicant in mammals (Street and
Sharma 1975). Of particular concern to us is the risk that methyl
parathion poses to vertebrate species. In amphibians, Johnson and Prine
(1976) found that exposure to only 25 μg/l methyl parathion over 24 hrs
caused juvenile western toads (*Bufo boreas*) to lose their tolerance to
temperature, a sublethal effect that likely becomes lethal rather
rapidly. Methyl parathion (Folidol M50 formulation) contained in
simulated rice paddy overflow water was found to cause mortality in
giant toads (*Bufo marinus*) at levels as low as 280 μg/l (Calumpang et
al. 1997). In another study, frogs exposed to 1.0 mg/l methyl parathion
suffered changes in the composition of their connective tissue matrices,
which resulted in malformations of the spinal column (scoliosis) and/or
limbs (short and think long bones with the epiphyses grossly twisted;
Alvarez et al. 1995). Further, a study by Fleming et al. (1982) showed
that parathion actually bioaccumulated in cricket frogs (*Acris
crepitans*), thereby posing a serious secondary poisoning hazard to
American kestrels (*Falco sparverius*). Studies by Hall and Kolbe (1980)
and Hall (1990) further document bioaccumulation of parathion and other
organophosphorus insecticides in amphibians, which is cause for great
concern, particularly for amphibian predators that are likely to die
from secondary poisoning.

In birds, a number of mass mortality events involving numerous avian
species have been documented in the scientific literature. But even more
troubling is the fact that **methyl parathion kills birds even at
recommended label application rates!** This is very troubling to us and
we would really like to see the EPA act to put an end to allowing
pesticides to be used whose recommended label application rates
routinely cause mortality and morbidity in fish and wildlife species as
well as in humans. In addition to lethal effects, there are a wide range
of debilitating sublethal effects seen following exposure to methyl
parathion. Both methyl parathion and its closely related chemical analog
ethyl parathion have been found to cause reproductive, physiological,
biochemical, and behavioral effects that ultimately lead to premature
mortality in exposed organisms. Reproductive effects such as decreased
productivity (% eggs hatching/% nests successful) have been documented
in songbirds exposed to parathion. Physiological effects such as reduced
daily food consumption (anorexia) and decreased body temperature
(hypothermia) have been documented in songbirds and upland game birds
exposed to parathion. Behavioral effects may be the most insidious and
damaging of the sublethal effects. Decreased ability to avoid predators,
decreased nest attentiveness during incubation and maternal care
following hatching, and increased brood abandonment by females have been
documented in upland gamebirds, gulls, and waterfowl (King et al. 1984,
White et al. 1979, 1983). Research from studies conducted with other OP
insecticides suggests that many other debilitating sublethal effects may
occur following exposure to methyl or ethyl parathion. As sublethal
effects are generally difficult to document in the field, there is great
concern for continued use of a pesticide such as methyl parathion that
has so many documented cases of lethal and sublethal poisonings, both
experimentally and in the field.

In mammals, exposure to the OP insecticide methyl parathion has been
found to result in loss of motor coordination in bats (Clark 1986),
reduced predator escape response (Galindo et al. 1985), altered hearing
ability in squirrel monkeys (Reischl et al. 1975), a decreased ability
to learn (Reiter et al. 1973), and suppression of the immune system
(Street and Sharma 1975). In rats, Zhu et al. (2001) found that repeated
dermal exposures of as little as 1 mg/kg/day methyl parathion resulted
in sustained inhibition of cholinesterase activity and impairment of
both motor function and memory. These subtle yet insidious sublethal
effects are never monitored in wildlife species, so they almost always
go undetected unless morbid animals are found by accident. It seems that
we often miss these types of sublethal effects in humans even when we
are looking hard for them, so it is clear that we are barely seeing the
tip of the iceberg when it comes to negative impacts of methyl parathion
on ourselves and our environment.

\(5\) Endangered Species issues -- on p. 49 of the document, it states
that "the endangered species LOCs are exceeded for acute and chronic
risks to birds, mammals, and freshwater and estuarine/marine
invertebrates, fish, amphibians, reptiles and terrestrial invertebrates
(including insects)." So, the LOCs are exceeded for both short- and
long-term for just about every animal species on Earth, and you're not
concerned enough to act? It is clear that methyl parathion has the real
potential for killing any listed species that is unlucky enough to be
exposed. Further, we are greatly concerned about the discussion on p. 49
regarding the Section 7 consultations under the ESA that you say you are
engaged in at present. You use these consultations as justification for
your overall environmental effects mitigation strategy. It is our
understanding that the ESA counterpart regulations are now in place, so
we do not believe that you will be completing your consultations as you
state in this document. Failure to complete these consultations negates
your overall environmental effects mitigation strategy and you will then
not have any interim protection measures to reduce the likelihood that
endangered and threatened species may be exposed to methyl parathion at
levels of concern.

\(6\) Mass mortalities of fish and wildlife -- on p. 49 in the document,
it is noted that there are relatively few bird and fish kill incidents
which are strongly linked to methyl parathion use. The discussion
continues with speculation on why there might be so few incident
reports. Just because there are relatively few incident reports for
methyl parathion in EPA's EIIS database does not then mean that methyl
parathion is not hazardous to everything in the environment that is
exposed to it.

Well, there may be relatively few incident reports in the EPA's EIIS
database; however, there are many other databases for incident reports,
at the state, regional, national and international levels, and we
question whether or not any of these were ever consulted by the EPA.

It should be noted that methyl parathion has been implicated in mass
mortality events on at least four of the six continents in which it is
used, including North America, South America, Africa, and Europe. In
1992, a massive avian mortality event occurred in Costa Rica following
the aerial application of methyl parathion to a cotton field (PAN-UK
1998). Methyl parathion is also implicated in deaths of waterfowl in
Spain, and the deaths of fish, birds, cattle, and wildlife in Sudan
(PAN-UK 1998). Finally, parathion (methyl and/or ethyl) is commonly used
in other countries (e.g., Venezuela) as an avicide to intentionally kill
songbirds. The work of Basili and Temple (1999) has documented huge mass
mortality events involving dickcissels (*Spiza americana*) that flock in
agricultural areas. These international mortality incidents cannot be
ignored and must be included in any ecological risk assessment of methyl
parathion.

Finally, it should be further noted that methyl parathion is at least as
effective on the many beneficial invertebrate species as it is on target
pests, so every time methyl parathion is applied to a field, it causes a
mass mortality event for beneficial invertebrate species in and around
the sprayed area. This likely includes honey bees (*Apis mellifera*) and
other pollinators, which continue to decline in the US with our
continued heavy reliance on organophosphorus insecticides.

Extensive field incident data for almost 30 years indicate that methyl
parathion poses a very high risk to bees and that bee mass mortalities
continue to occur following application of both EC and microencapsulated
(ME) formulations. The LD~50~s for each formulation (0.111 μg/bee and
0.214 μg/bee, respectively) indicate very high toxicity to bees. The
ecosystem service that bees and other pollinators provide to humans is
invaluable and many of our most important food crops require pollination
by bees and other organisms that continue to decline in the face of our
continued heavy reliance on pesticides.

\(7\) Serious resistance issues -- methyl parathion was first registered
in the US in 1954, thereby having been used in this country for 51 years
now. Further, it has been used fairly consistently on many of the same
crops and same locations for 51 years! As a result, many pest species
that methyl parathion is used to protect against have evolved a genetic
resistance to methyl parathion. For example, this has been clearly
documented by Parimi et al. (2003) for the western corn rootworm
(*Diabrotica virgifera virgifera*) in the corn belt of the midwestern
US. The timespan of 51 years is more than enough time for **all** pest
species targeted by methyl parathion to have evolved genetic resistance
to it. Further, there is evidence suggesting that, as seen with
organochlorine insecticides, there is cross-resistance with the
organophosphorus insecticides as well, so this only compounds the
resistance problem.

\(8\) Methyl parathion has resulted in excessive costs to society --
since 1994, in excess of 6,000 homes and businesses have been
contaminated with methyl parathion in MS, LA, TN, AR, IL, OH, MI, and
TX. Through their Superfund program, the EPA has been decontaminating
homes and businesses to habitable condition at a response cost in excess
of \$65,000,000!!! As a result of misuse alone, the Agency has had to
work extensively with the registrants, come up with a new, more
aggressive enforcement strategy, and develop a national strategy for
outreach to deal with the problems that methyl parathion has caused. The
costs for all of this extra work over a period of years are likely
staggering as well. Then there are all of the costs occurred by the
people that inhabited the over 6,000 homes/businesses affected that
either died or were sickened by methyl parathion exposure and the
funeral bills, hospital bills, lost work hours, residual health effects,
court/legal fees, etc. that occurred. The taxpayers are footing the
entire cleanup and response costs, which is simply unacceptable to us.
The costs to the people affected by methyl parathion are real and they
are completely unnecessary. There is absolutely no reason that society
should have to shoulder costs such as these for keeping this badly
outdated product on the market.

\(9\) Benefits? -- on p. 4 of the document, there is a statement that
says "Based on the use cancellation on tree fruits and vegetables, and
considering the implementation of mitigation measures discussed above,
the Agency has determined that pesticides containing methyl parathion
generally will still present risk to humans and the environment. But
there are significant benefits associated with the remaining uses which
balance this risk." Well, what exactly are these benefits? And how is it
that we could not be the recipient of these exact same benefits if we
used a much less hazardous alternative to methyl parathion, of which
many exist today. Then we would be the recipient of even more benefits
by not having to worry about any further exposure to (and effects from)
methyl parathion!

To summarize, the comments submitted herein are but a brief synopsis of
what would have been a full set of comments we would have provided had
we had sufficient time to do so. However, there was not enough time
allotted in this comment period to thoroughly and completely assess the
methyl parathion IRED. We can say without hesitation, though, that the
current methyl parathion IRED, as well as the mitigation measures
proposed within, are grossly insufficient. The risk assessments (human,
occupational, ecological) presented in this IRED have completely failed
to accurately quantify or even realistically consider the real health
implications to humans, fish and wildlife species, and the environment
from the continued registration of methyl parathion. It is our assertion
that the EPA should have taken the opportunity that they had in 1999 to
cancel further uses of methyl parathion. We therefore request that the
EPA act to cancel all current uses of methyl parathion before the end of
this year. Thank you for the opportunity to provide comments on this
document, and we hope to be able to provide you with more substantial
comments if and when the comment period is extended.

Respectfully submitted,

Steven R. Sheffield, Ph.D.

Affiliate Professor

Department of Environmental Science and Policy

George Mason University

Fairfax, VA

Caroline Kennedy, Director

Conservation Initiatives

Defenders of Wildlife

Washington, DC

Patti Bright, MS, DVM

VP for Pesticide Programs

American Bird Conservancy

The Plains, VA and Washington, DC

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