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January 31, 2008

Docket EPA-HQ-OPP-2007-1088

Submitted to [[www.regulations.gov]{.underline}](../www.regulations.gov)

CC to Sharlene R. Matten

FR Nov 20, 2007, Volume 72, Number 223, Page 65336-65339

Natural Resources Defense Council

*On behalf of our 1.2 million members and online activists, NRDC
advocates for disclosure of information, regard for scientific inquiry
and facts, justice for disempowered people, honesty by government, and
corporate accountability. We seek to establish sustainability and good
stewardship of the Earth as central ethical imperatives of human society
(www.nrdc.org)*

**Comments to the FIFRA Scientific Advisory Panel on the**

**EPA Notice of Intent to Cancel Carbofuran**

Feb 5-8, 2008

**BACKGROUND**

The N-methyl carbamates are among the most toxic category of pesticides.
For example, the Material Safety Data Sheet (MSDS) provided by the
registrant (FMC Corp) for carbofuran warns that "Effects from
overexposure result from either swallowing, inhaling or coming into
contact with the eyes or skin. Conditions of increased temperature and
humidity may aid skin absorption of this product and, therefore,
increase toxicity. Symptoms of overexposure include headache,
light-headedness, weakness, abdominal cramps, nausea, excessive
salivation, perspiration, blurred vision, tearing, pin-point pupils,
blue skin color, convulsions, tremor and coma."[^1] This is a typical
description of the health effects of all the NMC pesticides.

The approximate acute oral dose that is lethal for half of test animals
(LD50) following oral dosing to male rats is: 0.5 mg/kg body wt for
aldicarb, 2.5 mg/kg for oxamyl, and 5 mg/kg for carbofuran.[^2] These
pesticides are far more acutely toxic than nicotine (LD50=50 mg/kg), DDT
(LD50=100 mg/kg), or ethanol (LD50=5600 mg/kg) by oral dosing. The LD50
for aldicarb (0.5) is only 25-fold less potent than dioxin (0.02 mg/kg;
TCDD), the most toxic substance known.

Because it is acutely toxic, fetotoxic, and neurotoxic, and because of
the availability of reduced-risk chemicals and non-chemical
alternatives, on November 26, 2007, the Natural Resources Defense
Council (NRDC) petitioned the U.S. Environmental Protection Agency (EPA)
to revoke all tolerances of carbofuran. [^3] NRDC and the American Bird
Conservancy (ABC) subsequently submitted an amended petition to provide
more detailed facts to support NRDC's original petition.[^4]

**NRDC RESPONSE TO SELECTED CHARGE QUESTIONS**

**[Point of Departure (PoD) and FQPA Safety Factor Determination for
Dietary Risk Assessment for Infants and Children]{.underline}**

***Please comment on whether the scientific evidence currently before
the Agency supports the Agency's conclusion that brain AChE data provide
a more robust PoD than the RBC AChE data.***

NRDC supports the use of whole brain acetyl-cholinesterase (AChE) data
as preferable to blood AChE data because whole brain data tends to be
more stable (less variation between measurements), and it is a
reflection of the target organ of interest for toxicity.

***Please also comment on whether the scientific evidence currently
before the Agency supports the EPA's conclusion that the Agency's
benchmark dose analysis of the brain AChE data from three studies
provides a scientifically appropriate basis for assessing carbofuran
risk to infants and children.***

NRDC supports the Agency's approach to conducting a benchmark dose
analysis from the three studies it was provided. However, NRDC disagrees
that sole reliance on these AChE data are sufficiently
health-protective; this has not been established scientifically. Use of
these data fails to identify possible regional effects, non-cholinergic
effects, and effects at various time points of development, and is
therefore likely to underestimate the toxicity of carbofuran.

Rigorous independent studies of a related AChE-inhibitor, chlorpyrifos,
have demonstrated both cholinergic and non-cholinergic toxicity.[^5]
Through the non-cholinergic mechanism, chlorpyrifos elicited widespread
neural damage, and disrupted cell development. Through the cholinergic
mechanism, chlorpyrifos induced apoptosis during neurulation, resulting
in reduced cell numbers in brain regions that are enriched in
cholinergic neurons. These regional effects would be undetectable in the
toxicology protocols used by the Agency to evaluate carbofuran toxicity.
Behavioral and cognitive testing, including learning and memory tests,
reflex tests, and others, are key to assessing the true toxic effects of
any neurotoxic and fetotoxic chemicals.

Most importantly, with any developmental neurotoxic chemical such as
carbofuran, effects are the result the dose, the duration of the effect,
and the stage of development at which the exposure takes place.
Exposures during key windows of susceptibility during neural
development, even at very low doses, are most likely to have permanent,
devastating effects on neural function, including behavior and cognition
(reviewed in Colborn, EHP, 2006[^6]). These endpoints are not
incorporated into the benchmark dose analysis. Failure to consider these
cognitive and neurobehavioral endpoints is likely to result in an
underestimation of carbofuran toxicity.

The benchmark dose analysis failed to incorporate the impact of human
genetic variability in response to carbofuran. Genetic polymorphisms
that impair the activity of paraoxonase 1 (PON1) to hydrolyze AChE can
result in abnormally sustained cholinesterase activity. There is a
substantial literature database on the variability of activity of the
human paraoxonase 1 (PON1)-mediated detoxification pathway, and most
recently a 2006 published study reported that children may be up to
164-fold more sensitive than adults to the toxic impacts of chlorpyrifos
and diazinon, based on rigorous assessments of mothers and children of
the Salinas Valley, CA (Furlong et al, Pharmacogenetics and Genomics,
2006). [^7]

***Please comment on whether you agree with the Agency's conclusion
that, based on the available scientific evidence, there is remaining
uncertainty regarding lack of dose response data at the low end of the
dose response curve for RBC AChE inhibition with respect to
extrapolating risk to infants and children. Please provide a basis for
your conclusion.***

NRDC agrees with EPA that there is considerable uncertainty regarding
toxicity at the low end of dose response curve for AChEi, particularly
with respect to risks resulting from exposure during early life stages.
The magnitude of this uncertainty has not been analyzed, and even the
contributors to this uncertainty have not been fully documented. For
example, the sole reliance on whole brain AChEi data from female adult
rodents to calculate a benchmark dose fails to incorporate possible
regional effects, non-cholinergic effects, and long-term or permanent
effects. Behavioral and cognitive testing, including learning and memory
tests, reflex tests, and others, are key to assessing the true toxic
effects of any developmental neurotoxic and fetotoxic chemicals.

Experts have warned that, "the fact that alterations in neurodevelopment
occur with organophosphate exposures below the threshold for
cholinesterase inhibition reinforces the inadequacy of this biomarker
\[cholinesterase inhibition\] for assessing exposure or outcome related
to developmental neurotoxicity."[^8]

Published studies on the toxicity of a related family of pesticides, the
organophosphates, have reported that exposures during fetal and newborn
life-stages affect diverse cellular functions by mechanisms of toxicity
that may be independent of cholinesterase inhibition, or occur at doses
at the low end of observable cholinesterase inhibition. This is
important because while the systemic toxicity that results from
cholinesterase inhibition is reasonably well characterized, it does not
explain why rodents exposed pre- and perinatally seem to recover from
cholinesterase inhibition relatively rapidly, yet display persistent and
more severe damage to the central nervous system.[^9] Evidence points to
non-cholinergic mechanisms that disrupt multiple distinct brain
targets.[^10]

EPA recognizes that the database is not adequate to speculate with
confidence on what the sensitivity may be at doses below the observable
range. Human genetic epidemiology has demonstrated a large range of
variability in the human population for PON1 that can exceed 10X
(Furlong et al., 2005; Costa et al., 2005). Davies et al. (1996) have
reported up to 13-fold variation in PON1 levels in adults. More
recently, Furlong et al. (2006) reported a 26-fold variation in
sensitivity among newborns to diazinon, a 14-fold variation in
sensitivity among mothers, and a 65-fold variation in sensitivity to
diazonon between the most sensitive newborn and the least sensitive
mother. The same study reported that for chlorpyrifos the sensitivity
ranged as high as 164-fold. While carbofuran has not been studied using
these protocols, variations in PON1 activity would be expected to impact
sensitivity to carbofuran poisoning. Failure to consider this likely
scenario is a significant uncertainty biasing the benchmark dose towards
the null, i.e. underestimating risk to sensitive populations.

***Based on the currently available data, does the panel agree that
basing its safety factor on the ratio of BMD~50~ estimates in brain AChE
and RBC AChE in juvenile animals is a reasonable approach? Please
provide a basis for your conclusion.***

The Agency's use of nothing more than a comparative ratio of brain:
blood AChE measurements for determination of the FQPA factor is wholly
inadequate and unscientific. NRDC recommends that the EPA increase the
FQPA factor to reflect uncertainties associated with its failure to test
for non-cholinergic toxicity, regional variations in toxicity, impacts
from exposure during multiple ages and developmental stages, and
possible long-term or permanent cognitive and behavioral impacts.
Behavioral and cognitive testing, including learning and memory tests,
reflex tests, and others, are key to assessing the true toxic effects of
any neurotoxic and fetotoxic chemicals.

When reviewing the EPA assessment of a related family of
cholinesterase-inhibiting pesticides, the organophosphates, the SAP
(2002) raised the concern that, "reliance on a single biochemical assay
to measure brain damage may become problematic."[^11] This is supported
by evidence from rigorous studies of chlorpyrifos that have demonstrated
both cholinergic and non-cholinergic toxicity (Slotkin, EHP, 1999;
Slotkin et al, Brain Res, 2001; Song et al, Toxicol Appl Pharmacol,
1997). Through the non-cholinergic mechanism, chlorpyrifos elicited
widespread neural damage, and disrupted cell development. Through the
cholinergic mechanism, chlorpyrifos induced apoptosis during
neurulation, resulting in reduced cell numbers in brain regions that are
enriched in cholinergic neurons. These regional effects would be
undetectable in the toxicology protocols used by the Agency to assess
carbofuran. With any developmental neurotoxic chemical such as
carbofuran, effects are the result the dose, the duration of the effect,
and the stage of development at which the exposure takes place.
Exposures during key windows of susceptibility during neural
development, even at very low doses, may have permanent, devastating
effects on neural function, including behavior and cognition (reviewed
in Colborn, EHP, 2006[^12]). This was never examined in the current
carbofuran assessment, and is a very serious gap in the understanding of
the toxic effects of carbofuran.

**[Point of Departure (PoD) Determination for Dermal Risk Assessment for
Workers]{.underline}**

In the 2006 and 2007 human health risk assessment for carbofuran, the
Agency has relied on oral studies in adult rats for deriving the PoD for
dermal risk assessment for workers. The Agency applied a dermal
absorption factor of 6% to extrapolate from the oral route to the dermal
route. The Agency acknowledges the uncertainties associated with route
to route extrapolation.

In 2007, FMC submitted a 21-day dermal rat toxicity study (MRID
47143702) that also included a 7-day range-finding study (MRID
47143701). In these studies, carbofuran at various doses was applied to
shaved skin for 6 hours/day, 5 days/week with the skin occluded after
application. These studies failed to provide measurements to address
time of onset, time of peak, or time to recovery information necessary
for the dermal risk assessment. Furthermore, the RBC AChE measurements
from both studies were unreliable. The Agency has therefore relied on
oral studies for assessing dermal risk of carbofuran to workers.

***Do you agree with the Agency's conclusion that the dermal toxicity
studies in rats (MRID 47143701-2) are not acceptable for use in
extrapolating dermal risk to workers? Please provide a basis for your
conclusions.***

NRDC disagrees that EPA must use either inadequate data from
poorly-conducted studies on rodents, or inappropriate data from an
unrelated route of exposure. EPA could and should have required the
needed data during the early stages of the reregistration and tolerance
reassessment processes. In the absence of reliable data from
pre-validated test methods, NRDC recommends that EPA assume 100% dermal
absorption.

Since repeatability is one of the most fundamental tenets of the
scientific method, the reliance on single studies for route/dose
assessment is inadequate as it precludes confirmation of the results.
Further, orally ingested residues are subject to digestion and
subsequent metabolisms in the liver, while dermally absorbed and inhaled
residues do not pass through the digestive tract but instead have direct
access to the blood stream and lymphatic circulation. EPA's failure to
require robust dermal testing from pre-validated study protocols during
the reregistration and tolerance reassessment processes adds an
unnecessary uncertainty to the final risk assessment and risk management
decisions.

**NRDC RECOMMENDS CANCELLING IMPORT TOLERANCES**

In July 2006, EPA issued its proposed decision to cancel all domestic
uses of the toxic pesticide carbofuran. However, EPA did, inexplicably,
choose to retain four import tolerances for coffee, bananas, sugarcane,
and rice. While we applauded the decision to cancel carbofuran domestic
uses, we petitioned EPA to also revoke all import tolerances.[^13] By
continuing to allow the import tolerances, EPA is allowing food and
products that are contaminated with carbofuran to enter the U.S. without
triggering any type of action. Since FDA, and not EPA, checks imports
for such violations, only by updating the list of tolerances to reflect
risk management decisions correctly can EPA ensure that appropriate
action be taken to keep America's food supply safe.

[Revoking import tolerances protects both the U.S. population and the
international community through PIC reporting requirements]{.underline}

Generally, pesticide manufacturers prefer to voluntarily cancel high
risk products, or voluntarily withdraw high risks uses, rather than have
EPA issue a ban on those products. This practice highlights a separate,
but equally important, reason to revoke tolerances for pesticides that
are voluntarily withdrawn or cancelled. When a ban is issued, Prior
Informed Consent (PIC) listing is triggered, according to the Rotterdam
Convention which entered into force in early 2004.[^14] The Convention
creates legally binding obligations for the implementation of the Prior
Informed Consent (PIC) procedure for pesticides that have been banned or
severely restricted for health or environmental reasons. PIC
requirements include labelling and obligations to inform other parties
of a national ban or restrictions. At this time, there are 24 pesticides
subject to PIC procedures.[^15]

To avoid PIC listing, that is, to avoid alerting the international
community of an unacceptably high risk pesticide, manufacturers will
instead issue a quiet voluntary withdrawal, thereby leaving open
international markets and trade options. We find this practice morally
reprehensible as it results in the transfer of high risk chemicals to
the developing countries, where environmental, occupational, and public
health protections are generally far weaker than the protections in the
U.S. Such countries often rely on the U.S. risk evaluations and risk
management decisions as guides and goals in managing their own chemical
risks. The U.S. can best serve the international community, and best
protect U.S. imports, by making public its risk assessments and risk
management determinations, including tolerance revocations.

[Failing to revoke import tolerances leads to unacceptable ecological
risks]{.underline}

EPA has consistently identified that carbofuran use raises many
environmental concerns and acted on that information. In 1992, EPA
cancelled the granular formulation with a prolonged phase-out period and
in 2002 it also cancelled all liquid formulations because of
unacceptably high risks. The 2006 carbofuran Interim Reregistration
Eligibility Determination (IRED) concluded that, "based on the
assessment of ecological and human health risks associated with
carbofuran uses, the Agency has determined that all uses of carbofuran
are ineligible for reregistration."[^16] The same IRED also concluded
that, "carbofuran is very highly toxic to birds on an acute basis, and
highly toxic on a sub-acute basis. A chronic effect level could not be
established due to the fact that all concentrations tested caused
mortality in the test subjects." [^17] And, "carbofuran is very highly
toxic to freshwater and estuarine/marine fish on an acute basis." [^18]

The continuing foreign use of pesticides cancelled in the U.S. presents
an unacceptable risk to North American migratory birds wintering in
Central and South American countries. Billions of U.S. migratory birds
over-winter in countries that currently have registrations for
carbofuran, including the major countries listed for importation of
coffee, bananas, sugarcane and rice. In fact, carbofuran use on rice was
the first major crop use documented to kill birds in significant
numbers, and the major reason for cancellation of the granular
formulation in 1992. Maintaining a U.S. import tolerance for carbofuran
allows Central and South American countries to continue using any
formulation of this pesticide on crops for which the U.S. has already
determined there are unacceptable risks for protected U.S. migratory
birds. EPA must protect U.S. migratory birds on their wintering grounds
as well as in the U.S. by cancelling tolerances for these crops. Doing
so will encourage the use of legal, safer pesticides and non-chemical
practices by foreign growers, at least for those crops that are imported
into the U.S.

The ABC "Birds in Agricultural Areas" database contains data from 60
peer reviewed publications documenting the use of U.S. rice fields by
183 species of birds.[^19] Thirty-seven of these species are on the
ABC-Audubon "Watch List" of vulnerable species, and many are species
that migrate to Latin America during the winter season.[^20]
Agricultural use of carbofuran in Latin America occurs during the rice
growing season, which coincides with the seasonal migration pattern of
U.S. birds in these countries.

Rice is a very important crop for many shorebirds, waders, waterfowl and
some grassland birds; bananas and coffee (especially shade coffee) are
also very important winter habitats for many neotropical migrant
songbirds. The use of carbofuran in these crops will continue to pose
unreasonable risks for U.S. and many additional bird species.

Pursuant to Executive Order 13186 §3(e)(9), EPA must

> identify where unintentional take reasonably attributable to agency
> actions is having, or is likely to have, a measurable negative effect
> on migratory bird populations, focusing first on species of concern,
> priority habitats, and key risk factors. With respect to those actions
> so identified, the agency shall develop and use principles, standards,
> and practices that will lessen the amount of unintentional take,
> developing any such conservation efforts in cooperation with the \[US
> Fish and Wildlife\] Service.

Setting an import tolerance for carbofuran constitutes an agency action
that is likely to have a measurable negative effect on species of
concern as well as other protected species under the Migratory Bird
Treaty Act. 16 U.S.C. §§ 703-711. Additionally, since the EPA has
already determined in the carbofuran IRED that carbofuran poses an
unreasonable risk to protected bird species, the Agency must cancel the
import tolerances for rice, bananas, coffee and sugarcane.

Thank you for the opportunity to present comments for your
consideration.

Jennifer Sass, Ph.D.

Senior scientist, Health and Environment\
Natural Resources Defense Council\
tel: 202-289-6868 (main); email: <jsass@nrdc.org>

[^1]: http://msds.fmc.com/msds/100000010246-msds_us-e.pdf

[^2]: All LD50 values from Sigma Chem Co.

[^3]: NRDC Petition to Cancel Carbaryl and Propoxur for Pet Collar Uses;
    Petition to Revoke All Tolerances of Carbofuran; and Comments on
    EPA\'s revised cumulative risk assessment for the N-methyl carbamate
    pesticides Nov. 26, 2007, EPA-HQ-OPP-2007-0935-0027 and -0027.1

[^4]: NRDC and Am Bird Conservancy Amend Petition to Revoke Import
    Tolerances of Carbofuran. December 29, 2007. EPA-HQ-OPP-2007-0935

[^5]: Slotkin TA, Seidler FJ. Prenatal chlorpyrifos exposure elicits
    presynaptic serotonergic and dopaminergic hyperactivity at
    adolescence: critical periods for regional and sex-selective
    effects. Reprod Toxicol. 2007 Apr-May;23(3):421-7.

    Slotkin TA, Tate CA, Ryde IT, Levin ED, Seidler FJ. Organophosphate
    insecticides target the serotonergic system in developing rat brain
    regions: disparate effects of diazinon and parathion at doses
    spanning the threshold for cholinesterase inhibition. Environ Health
    Perspect. 2006 Oct;114(10):1542-6.

    Slotkin TA, Levin ED, Seidler FJ. Comparative developmental
    neurotoxicity of organophosphate insecticides: effects on brain
    development are separable from systemic toxicity. Environ Health
    Perspect. 2006 May;114(5):746-51.

    Slotkin TA, Brown KK, Seidler FJ. Developmental exposure of rats to
    chlorpyrifos elicits sex-selective hyperlipidemia and
    hyperinsulinemia in adulthood. Environ Health Perspect. 2005
    Oct;113(10):1291-4.

    Aldridge JE, Meyer A, Seidler FJ, Slotkin TA. Alterations in central
    nervous system serotonergic and dopaminergic synaptic activity in
    adulthood after prenatal or neonatal chlorpyrifos exposure. Environ
    Health Perspect. 2005 Aug;113(8):1027-31.

    Slotkin TA, Seidler FJ. The alterations in CNS serotonergic
    mechanisms caused by neonatal chlorpyrifos exposure are permanent.
    Brain Res Dev Brain Res. 2005 Aug 8;158(1-2):115-9.

    Slotkin TA, Oliver CA, Seidler FJ. Critical periods for the role of
    oxidative stress in the developmental neurotoxicity of chlorpyrifos
    and terbutaline, alone or in combination. Brain Res Dev Brain Res.
    2005 Jun 30;157(2):172-80.

[^6]: Colborn T. A case for revisiting the safety of pesticides: a
    closer look at neurodevelopment. Environ Health Perspect. 2006
    Jan;114(1):10-7. Review.

[^7]: Furlong CE. Genetic variability in the cytochrome P450-paraoxonase
    1 (PON1) pathway for detoxication of organophosphorus compounds. J
    Biochem Mol Toxicol. 2007;21(4):197-205. Review. Erratum in: J
    Biochem Mol Toxicol. 2007;21(5):323.

    Furlong CE. Genetic variability in the cytochrome P450-paraoxonase 1
    (PON1) pathway for detoxication of organophosphorus compounds. J
    Biochem Mol Toxicol. 2007;21(5):323.

    Furlong CE, Holland N, Richter RJ, Bradman A, Ho A, Eskenazi B. PON1
    status of farmworker mothers and children as a predictor of
    organophosphate sensitivity. Pharmacogenet Genomics. 2006:
    16(3):183-90.

    Furlong CE, Cole TB, Jarvik GP, Pettan-Brewer C, Geiss GK, Richter
    RJ, Shih DM, Tward AD, Lusis AJ, Costa LG. Role of paraoxonase
    (PON1) status in pesticide sensitivity: genetic and temporal
    determinants. Neurotoxicology. 2005 Aug;26(4):651-9. Review.

    Furlong CE, Cole TB, Walter BJ, Shih DM, Tward A, Lusis AJ, Timchalk
    C, Richter RJ, Costa LG. Paraoxonase 1 (PON1) status and risk of
    insecticide exposure. J Biochem Mol Toxicol. 2005;19(3):182-3.

    Costa LG, Cole TB, Vitalone A, Furlong CE. Measurement of
    paraoxonase (PON1) status as a potential biomarker of susceptibility
    to organophosphate toxicity. Clin Chim Acta. 2005
    Feb;352(1-2):37-47. Review.

[^8]: Slotkin TA, Tate CA, Ryde IT, Levin ED, Seidler FJ.
    Organophosphate insecticides target the serotonergic system in
    developing rat brain regions: disparate effects of diazinon and
    parathion at doses spanning the threshold for cholinesterase
    inhibition. Environ Health Perspect. 2006 Oct;114(10):1542-6.

[^9]: Slotkin TA, Cousins MM, Tate CA, Seidler FJ. Persistent
    cholinergic presynaptic deficits after neonatal chlorpyrifos
    exposure. Brain Res. 2001 Jun 1;902(2):229-43.

[^10]: Pope CN. Organophosphorus pesticides: do they all have the same
    mechanism of toxicity? J Toxicol Environ Health B Crit Rev. 1999 Apr
    Jun;2(2):161-81. Review.

[^11]: Transmittal of Meeting Minutes of the FIFRA Scientific Advisory
    Panel Meeting Held June 26-27, 2002. Released on July 19, 2002, 26.

[^12]: Colborn T. A case for revisiting the safety of pesticides: a
    closer look at neurodevelopment. Environ Health Perspect. 2006
    Jan;114(1):10-7. Review.

[^13]: Petition to Cancel Carbaryl and Propoxur for Pet Collar Uses;
    Petition to Revoke All Tolerances of Carbofuran; and Comments on
    EPA\'s revised cumulative risk assessment for the N-methyl carbamate
    pesticides Nov. 26, 2007, EPA-HQ-OPP-2007-0935

[^14]: Rotterdam Convention
    http://www.pic.int/home.php?type=t&id=5&sid=16

[^15]: See Annex III of the Rotterdam Convention for a list of chemicals
    currently subject to the PIC procedure
    http://www.pic.int/home.php?type=t&id=29

[^16]: Carbofuran IRED (2006).
    <http://www.epa.gov/pesticides/reregistration/REDs/carbofuran_ired.pdf>

    Carbofuran IRED facts.
    http://www.epa.gov/oppsrrd1/REDs/factsheets/carbofuran_ired_fs.htm

[^17]: Carbofuran IRED facts.
    http://www.epa.gov/oppsrrd1/REDs/factsheets/carbofuran_ired_fs.htm

[^18]: Carbofuran IRED facts.
    http://www.epa.gov/oppsrrd1/REDs/factsheets/carbofuran_ired_fs.htm

[^19]: http://www.abcbirds.org/abcprograms/policy/pesticides/biaa/biaa_form2.cfm

[^20]: http://web1.audubon.org/science/species/watchlist/browsewatchlist.php