Frequently
Asked Questions on Pesticides and Birds
Why Pesticides and
Birds
What is a Pesticide
When are Birds Exposed
How Can Pesticides Harm Birds
Why
Pesticides and Birds
Birds are a visible and important
part of the world we share. They are not only
worthy of protection in themselves, but are also environmental
sentinels, forewarning us of potential hazards to our
environment and our own health. They are particularly
sensitive to many pesticides. For example birds are
100 times more sensitive than mammals to the commonly
used insecticide diazinon. Populations may already
be in decline due to other factors, such as habitat
loss due to agriculture, urban development and invasive
species. In her landmark book, Silent Spring,
Rachel Carson called attention to the decline in some
bird species, such as Peregrine Falcons, brought about
by DDT and other pesticides, and argued that these declines
suggested serious effects for other species of wildlife
and for humans.
One study, by David Pimentel of
Cornell University, conservatively estimates the number
of birds lost each year to pesticides at 67 million
on farmland alone, with a potential for ten times that
number to be affected in other ways. We see only
a small fraction of the avian impacts of pesticides
because birds die in places not normally frequented
by people, and when they do, we do not usually look
for them. In addition, poisoned birds hide, carcasses
decompose and scavengers do a very efficient job of
cleanup (77% of birds, on average, are scavenged by
predators within 24 hours of dying - see
paper by Nimish B. Vyas). Sick birds are often
misdiagnosed as victims of trauma and the chemical analyses
required to determine pesticide poisoning are costly
and therefore seldom carried out.
Far from declining in use since Rachel
Carson's time, pesticide use, in terms of pounds applied
and number of active ingredients registered, has actually
increased. In the United States today, 1.2 billion
pounds of pesticides - 20% of the world's total - are
applied annually to crops (see EPA's
web pages on pesticide usage), lawns, households,
golf courses and other areas. Documented and investigated
cases indicate that approximately 50 pesticide active
ingredients currently used in the U.S. have caused bird
kills. When we weigh the risks of these chemicals
against their benefits, we must ask how we can responsibly
use and regulate a tool that inherently poses a risk
to wildlife, especially to one of it's most cherished
ambassadors: birds.
What
is a Pesticide
The term pesticide means 'pest killer'.
Pesticides are chemicals designed to kill target organisms
deemed to be pests because they can contribute to human
diseases (such as malaria), crop destruction (before
or after harvest), livestock disease or are household
pests like ants and mice. The Federal Insecticide,
Fungicide and Rodenticide Act (known as FIFRA) defines
pesticides as ". . . any substance or mixture of
substances intended for preventing, destroying, repelling
or mitigating any pest, and any substance or mixture
of substances intended for use as a plant regulator,
defoliant, desiccant."
Pesticides work by disrupting one
or more vital, biological processes of the target organism
eg. photosynthesis in plants or blood clotting in mammals.
They can be divided into groups based on the organisms
they target (eg. insecticides, rodenticides,
herbicides and fungicides), by their mode of action
(eg. cholinesterase inhibitors kill by interfering with
nerve impulse transmission) or by their chemical class.
The two classes encompassing the majority of insecticides
in use today are carbamates and organophosphates.
Others are pyrethroids and biological controls such
as viruses and bacteria. One particular class
of insecticides, widely used after WWII - organochlorines
- was found to have a variety of severe adverse effects
on wildlife soon after their introduction. In
1972, all uses of the organochlorine DDT were cancelled
in the US, closely followed by most other persistent
chlorinated pesticides. There are still some persistent
organochlorines in use in the US today, such as endulfosan
(Thiodan). DDT is still used in six countries
in the Western Hemisphere (Argentina, Belize, Ecuador,
Guyana, Peru, Mexico). While less persistent in
the environment than traditional organochlorines, carbamates
and organophosphates are generally more acutely toxic
to birds.
Most rodenticides are anti-coagulants.
First generation anti-coagulants such as Warfarin cause
hemorrhage. Second generation types bring about
neurological and cardio-pulmonary injury in the target
organism before the onset of hemorrhage.
Herbicides act on biochemical pathways
specific to plants, for example photosynthesis.
They can act on contact or by root absorption and their
effect can be non-systemic (e.g. diquat) or systemic
(e.g. glyphosate). Generally, they are not directly
responsible for bird mortalities but declines in bird
populations can be attributed to habitat loss and depletion
of food resources caused by these chemicals.
New classes of pesticides are constantly
being developed and introduced, some less acutely toxic
to wildlife but nevertheless raising concerns about
accumulation in soils, long-term ecological effects
and synergistic action when different classes of pesticide
used simultaneously. While testing procedures
for human health risks have been greatly improved over
recent years, tests for wildlife toxicity have advanced
little thus restricting our ability to adequately assess
potential wildlife effects prior to registration or
widespread use. To view detailed information on
individual pesticides go to our Pesticide
Profiles page.
Any given pesticide product contains
one or more active ingredient and any number of inert
ingredients to enhance the effect of the product.
The active ingredient is the component designed to kill
or otherwise harm the target organism and must, by law,
be listed on the pesticide label, but inerts can be
toxic too, or may enhance the toxicity of the active
ingredient, and yet need not be listed on pesticide
labels. In fact, the mixture of inert and active
ingredients are often closely guarded trade secrets.
Synergists increase the toxicity of the active ingredient,
diluents give the product greater volume for ease of
application, and surfactants reduce surface tension,
thereby aiding the spread of the chemical. Pesticides
can take a variety of forms: liquid, powder, gel bait
granular etc. Pesticides manufactured in granular form
may be subsequently dissolved in spray tanks and applied
as liquid. Others are applied in particle form.
Not long ago these particles were embedded in silica
or processed corn cob, both of which are highly attractive
to birds. More recently clay granules have been
developed which come in many varieties and can break
apart in soil much quicker. While less attractive
to birds due to their lower visibility, these clay granules
may adhere to food items and so may be eaten by birds
inadvertently. The forms a pesticide takes are
generally determined by agronomic and human health concerns
- wildlife effects are rarely considered.
All pesticide use in the US is regulated
via a complex system of registration and review, under
the auspices of the Environmental Protection Agency
(EPA). The governing legal act for product registration
and use is the Federal Insecticide, Fungicide and Rotenticide
Act (FIFRA). The initial version of this act was
passed in 1947, for implementation by the USDA.
It required chemicals to be registered but provided
no means of controlling use. It was not until
1972 that amendments were made to FIFRA to provide mechanisms
for risk-benefit analysis and use restrictions, with
control handed over to the newly formed EPA. Today,
chemical manufacturers bear the burden of proposing
new chemicals, testing their toxicity and presenting
the case for their use. EPA scientists and other
staff are responsible for evaluating the manufacturers
case and making decisions on where and when a chemical
may be used and how it should be applied. The
part the U.S. public can play in this procedure is by
voicing their concern - an increasing role - which can
effect the outcome of an EPA decision.
There are 20,700 pesticide products
on the market today containing 890 registered, active
ingredients. Pesticide users spend about $11.9
billion on 4.5 billion pounds of active ingredient each
year and 3/4 of all households
use them. They are ubiquitous, a fact of modern
life and are found in wood preservatives, soaps, disinfectants,
Christmas trees and home lawn products. They are
used in zoos, parks and swimming pools and we rely on
them to control disease and to guarantee and protect
our food supply. They can be effective tools but
are, in the end, poisons and using them entails risk
to birds and other wildlife.
When
are Birds Exposed
Birds are rarely the target of pesticide
application but are often caught in the crossfire of
a never ending war between humans and pests. Peregrine
Falcons were nearly wiped out due to DDT poisoning throughout
the 50's and 60's. In 1996 it is estimated that
over 20,000 Swainson's hawks, 8% of the species, died
in Argentina from 1995-96, due to poisoning by the insecticide
monocrotophos (Azodrin, Nuvacron) and the EPA estimated
that a single carbamate, carbofuran (Furadan) killed
two million birds or more each year in the early 1990's.
Birds are, by their very nature,
mobile creatures and cannot usually be kept out of areas
where pesticides are applied. Their ability to
cover large distances in a short period of time increases
their susceptibility to pesticide exposure. Birds
can come into contact with pesticides by three Routes
of exposure:
-
Ingestion
-
on/in the food they eat
-
Primary exposure - birds
eat seeds, insects or vegetation sprayed with
a pesticide.
-
Secondary exposure -
birds eat a small mammal or other vertebrate
which has itself been exposed by eating seed,
insects or vegetation sprayed with a pesticide.
-
by drinking
-
Inhalation
-
of chemical spray
-
of treated dust
-
Dermal absorption
-
from bathing in tainted water
-
absorption through the feet
when standing on treated vegetation/soil
-
through preening, which works
the pesticide past the feathers and onto the
skin
-
through the brood patch -
when spray falls on a nest where birds are incubating
The differences in toxicity of any
one chemical varies tremendously between species, sometimes
by a factor of 10 or more. Variations in the application
method, time of year, route of exposure and application
rate can also have a significant outcome on avian toxicity.
Field studies have shown that 77% of bird carcasses
are scavenged by predators within 24 hours and those
that remain are often extremely difficult to locate,
hampering efforts at assessing the number and scale
of pesticide kills. This suggests that kills that
have been identified are only the tip of the iceberg.
Simply because a bird does not feed
on vegetation or insects which have been the target
of pesticide application (primary exposure), does not
mean that it cannot come into contact with that chemical.
Predatory or scavenging species may be exposed when
they feed on target or non-target vertebrate species
(e.g. rats) that have themselves been exposed.
This is called secondary exposure. Runoff or wind
can carry pesticides to nearby ponds and fields where
birds feed, bathe, drink or gather tainted brush or
mud for their nests.
Finally, when we think of pesticides,
we generally think of agricultural use, but homeowners
share some of the responsibility. In one study
in Illinois, homeowners used four times as much pesticide
per acre as farmers, on their lawns and gardens.
How
can Pesticides Harm Birds
When we think of birds being affected
by pesticides, the image conjured up in many minds is
of media headlines citing mass mortalities, accompanied
by graphic pictures of fields of dead birds. In
reality, while these do occur from time to time, actual
effects may be much more subtle and hard to isolate.
Some incidents may eventually cause death in a slower
more insidious way, making carcasses harder to find.
Others may cause species numbers to decline indirectly
by weakening the animal or reducing food supply, and
others still may reduce species numbers without killing
individuals, by reducing breeding success.
To simplify matters, we can think
of pesticide hazard to birds in two ways; exposure and
effect:
Exposure can be either acute or chronic;
-
Acute: These are sudden, short
exposures to high levels of pesticides. Responses
of birds to acute exposure can vary significantly.
Acute exposure to organophospates often leads to
death of the bird within 30 minutes after symptoms
of feather fluffing, labored breathing, muscle tremors
and convulsions.
-
Chronic: these are defined as
long-term exposures. The problem with these
exposures is that because the poisoning takes place
over a prolonged period birds are more likely to
become scattered over a wider geographical area
and may never be seen. If they are recovered
it is much harder to correlate the death with specific
pesticide applications.
Effects from acute exposures can
be immediate or delayed. Chronic exposure, by
definition produces delayed effects. Both types of exposure
lead to a range of potential DIRECT EFFECTS, which might
be lethal or sub-lethal:
-
Lethal: in addition to the highly
visible mass mortalities, birds can die in a variety
of other ways due to pesticides, from both acute
and chronic exposures. Again, the slower the
reaction, the harder it can be to detect.
-
Sub-lethal:
-
Weakening: If a bird is hit
by a car, we might simply put that down to bad
luck for the bird or careless driving by the
driver. But if the bird's vision or reactions
are impaired by chronic exposure to pesticide
it is neither. These victims of
road accidents are often left unanalyzed by
the side of the highway and we are none the
wiser of the underlying cause. Birds that
are suffering from pesticide poisoning are more
likely to be killed by predators - this may
be especially true of females on the nest, as
was the case in a study on the one-time treatment
of fields with methyl parathion and nearby nesting
ducks. In an unusual reversal,
a Great Horned Owl died in 1999 after being
wounded by its intended prey, a muskrat.
These wounds are a common occurrence but in
this case the owl was suffering from the effects
of brodifacoum poisoning, an anti-coagulant
rodenticide, causing it to bleed to death.
Tolerance to extreme temperatures and disease
may also be reduced after pesticide exposure.
-
Reproductive: these effects
include egg shell thinning (as was the case
with DDT, which caused Peregrine Falcon eggs
to break while being incubated), deformed embryos,
reduced fertility and decreased hatchability
of fertile eggs. Most of these effects
are never seen unless specifically studied because
eggs that fail to hatch may do so for a number
of reasons not necessarily attributable to pesticides
(parental inexperience, genetic defects, nest
disturbance). Fertility reduction is only
noticeable when looked at over successive generations.
-
Behavioral: these changes
are perhaps the most subtle of all potential
pesticide effects. Changes in territoriality,
vocalization, courtship and breeding behaviors,
reduced attention to young and a reduced response
to human presence may all result after pesticide
exposure, with latent effects on individuals
or populations.
INDIRECT EFFECTS: Birds that use
roadside margins or hedgerows for nesting, roosting,
cover or food can decline when these areas are 'cleaned
up' by civic authorities' 'beautification' programs.
Birds will likewise be effected if their primary food
source is also regarded as a pest or is a non-target
species that is affected nonetheless by insecticide
or herbicide application. While the pesticide
does not necessarily poison the bird, it is nevertheless
the indirect effects of the chemicals that are ultimately
responsible for reduction in populations. In addition
to the effects on birds to direct exposure to pesticides,
birds can be affected by the pesticide without ever
coming into contact with it. These are called Indirect
Effects.
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