Pesticide Poisoning in
Avian Communities
Laura O’Byrne
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Abstract
Pesticide application has become an integral part of agricultural practices as
anthropogenic population increase has accelerated the demand for food crops.
Pesticides increase crop yields by chemically destroying pests such as weeds,
insects and fungi. This increase in pesticide use has increased the concentration and
amount of pesticides or they’re by -products that remains in soils and water bodies.
Residence time of pesticides in environment and extent of the contaminants are
reliant on many dynamic variables, biotic and abiotic. Therefore it is difficult to
predict residence time, or what concentrations of pesticides will remain in the
environment after application.
Birds are omnivores whose diet includes seeds, insects and in some cases small
rodents or other birds. Subsequently, avian communities often accidentally ingest
environmental pesticides or their residues and this causes lethal or sub lethal
effects.
Introduction
Soil, food chain relationships of pesticides have been extensively studied and have
become increasingly important since Rachel Carson’s Silent Spring was published in
the 1962. This book was instrumental in raising awareness of pesticide (DDT)
poisoning in non-target organisms, specifically birds.
A pesticide is intentionally applied to the environment and is designed to kill or
harm living organisms (Cox, 2006). The top ten most common pesticides are shown
in Table 1, with insecticides being the most prevalent in use today.
Pesticide application (Figure 1) is succeeded by absorption by crop, adsorption to
soil particles and the possibility of leaching or surface run off. Microorganisms,
ultraviolet light or vaporization degrades pesticides. Multiple factors determine the
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fate of a pesticide after application. The specific pesticide applied, the dose and
concentration applied will be significant in determining how much of the compound
is taken up by the intended pest and how much remains in the environment.
Factors influencing infiltration and residence time include, soil type and condition of
soil including soil texture, moisture and pH, soil organic matter, hydrologic
conditions and how strongly a particular pesticide is bound by soil components.
Pesticides disable pests by neurotoxicity, genotoxicity or impaired hormone
function. (Cox, 2006). Neurotoxicity would commonly result in the death of an
organism. Secondary poisonings are frequent in the food chain, where one
organism ingests another who has consumed a pesticide. This process where toxins
are magnified in the environment through food webs is called biomagnification.
Toxins which were are lower levels when first taken into an organism become
increasingly concentrated in its tissues which are then ingested by the next animal
on the food chain and so on.
Genotoxicity is a process that is not directly toxic to an organism but impairs it’s
reproductive functioning through damage to the DNA or RNA.
The likelihood that wildlife will be subjected to pesticides in their environment is
great due to the widespread use of pesticides in agriculture. Pesticide compounds
have a potential to remain in their environment for long periods of time and to
travel far distances due aeolian, hydrologic and biological dispersion.
A birds diet is varied and commonly they consume a combination of seeds, fruit and
insects. These crops are very likely contaminated with pesticides. This makes the
avian community vulnerable to unintentional poisoning by pesticides ingestion.
Discussion
Pesticide toxic effects:
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Many insecticides are AChE inhibitors such as Malathion and Parathion (George,
1995). AChE inhibition, acetylcholoinesterase is a key enzyme in the nervous
system down the neurotransmitter acetylcholine to choline and acetic acid at the
synoptic cleft resulting in the next nerve impulse transmitting across the synaptic
gap. Inhibition of this enzyme results in paralysis, convulsions and possible death.
In George’s 1995 study of grasshoppers, he found that dead birds had been
secondarily poisoned by ingesting grasshoppers and the dead birds were found to
have and large amount of AChE in their bodies. In addition, this study found that
AChE levels of 50% or greater resulted in sub-lethal of lethal effects on avian
communities and Blus’ 1997 field studies concurred. According to Mullie and Keith
1993, pesticide application and bird mortality linked but it is unclear whether
interaction is direct or indirect, via ingestion or reduction of food supply. Lee et al
found evidence of airborne pesticide contamination levels of AChE in animals
indicating that point sources of poisoning are not easily traced.
Chemistry of Pesticides
The EPA (Environmental Protection Agency) sets maximum contamination levels
based on individual pesticides, but mixtures are most common in the environment.
Many studies, including Reylea, 2008 and Stromberg, 1977 agree that multiple
pesticide contamination in the environment is standard and that negative
synergistic interactions between pesticides are not well understood. Current
laboratory testing is only done on singular pesticides and lab testing is not
comparable to the biological factors influencing a natural environment.
Although “laboratory results showed no toxic effects of DDD (a metabolite of DDT),
1000 pairs of breeding Grebes were completely decimated in one year” following
DDT application (Blus, 1997).
Further complicating the pesticide toxic effects are the solvents or ‘inert’ ingredients
that are added to the commercial pesticide formulations. These ingredients, which
include solvents like ethanol or petroleum, are not required to be disclosed because
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of their function in the product. Pesticide testing is restricted to active ingredients
and for acute toxicity only. This testing does not include inert ingredients or sublethal effects. There is a 30% greater dermal exposure rate with inert ingredients
then with active pesticide ingredients alone (Cox, 2006). In the Cox 2006 studies, he
found that these inert ingredients could be both biologically and chemically active
when added to the pesticide compound. It was determined by Reylea and Cox that
these inert ingredients may have toxic effect independent of the pesticide itself and
that some solvents increase environmental mobility and persistence of the
compound. Metabolites of the pesticide compound themselves are toxic (Schwartz,
1967) and pesticides have a ‘life’ and interact with their surrounding environment.
Physiochemical Factors
Once a pesticide compound is released into the environment, many biotic and
abiotic factors determine its fate. Some of these factors include climate, moisture,
soil type, texture and pH and microclimate. Several studies have shown that an
increase in moisture will increase both pesticide resilience and toxicity. Mullie and
Keith found that shallow depressions also increase concentration and toxicity of
pesticide compounds due to leaching and sediment run off from precipitation.
Reylea found that multiple pesticides usually result in an increase in the soil pH
while Douthwaite and his team determined that although heat increases dissipation
of pesticide residues, it can take up to “12 years “ for pesticide residue breakdown in
temperate soils.
Chemistry and topography dictate pesticide persistence and these vary spatially and
temporally. Blumhurst studied pesticide degradation and found that biological
activity of microorganisms, which encourages pesticide degradation, is greater near
the soil surface. If pesticide leaches, the biological activity decreases which
increases its persistence. In studies by Braverman et al, found that dry soil beds
“inactivate soil applied herbicides”. The same study found that although high
temperatures of +25 degrees Celsius favor herbicide degradation, they also decrease
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herbicide efficacy. This demonstrates how complicated pesticide application,
degradation and persistence are to predict in a natural environment.
Biological Components
Pesticides are hydrologically pervasive and Reylea found that 60-95% of surface
waters contain multiple pesticides.
The trend of multiple pesticides increasing the negative effects to biotic
communities is well documented in scientific studies. These studies agree that
laboratory experiments are one-dimensional and cannot substitute for a natural
habitat. Laboratory experiments test one organism and not a whole biotic
community. Multiple studies agree that “persistence residence time is not
predictable” (Stone, 1984) in a natural environment which is multifactor and not
static like the laboratory (Table 2). A 1995 study by Douthwaite showed that DDT
was still present in fat tissues of animals although DDT was banned over forty years
earlier. In Stones’ study of crickets, they found DDT and it’s metabolites present in
22/25 sampled crickets. This study indicates that pesticide residence time is not
predictable and that ecological pathways should be considered in pesticide
application.
Avian Consequences
Birds are opportunistic feeders whose diet varies according to availability, and their
life cycle requirements. Adult birds who are granivores often change their diet to an
entirely insectivorous diet when mating season begins and continue this diet
through their breeding season and well into their chicks’ development (Sibley,
2001).
The process of biomagnification is well understood in the scientific community and
this process has a crucial effect on avian communities. An avian diet often includes
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insects that accumulate toxins directly from their soil environment. Korschgen
found that pesticide residues or degradation products in soils “directly poison
macro invertebrates”, these include, earthworms, beetles, toads snakes and mice.
These organisms are common prey for many bird species and by ingesting this food
source; the birds accumulate toxins at a much higher rate then in the original
organism. Korschgens’ studies included some examples of biomagnification;
Earthworms and toads in their study had toxin levels of 5.65ppm and 8.30ppm
respectively. The snakes that ingested these organisms further accumulated the
toxins in their tissues at a much higher rate of up to 10.3-14.4ppm.
The fundamental factor influencing effects of pesticides on avian communities is the
timing of the application. Insecticides applied during breeding season have a
“negative effect of reproduction, diet and chick mortality (George, 1995). Avian
parents insectivorous diet is essential in order for chicks to achieve maximum
growth and health (Alsop, 2001). Therefore, a decrease in avian prey during
breeding season can result in many dire consequences for parents and chicks (Table
3). Reproductive failure is a well-documented phenomenon in pesticide treated
avian communities. This can range from eggshell thinning, which makes the shells
more vulnerable to breaking and therefore decreases the viable eggs hatched.
Decrease in avian parents diet may result in a lower birth weight of chicks and
higher chick mortality due to starvation or malnutrition (George, 1995). Stromberg
also found a direct relationship between pheasant egg laying, which declined with
an increase in seed treated by pesticides. Mullie and Keith documented a decrease
in “fledgling weight, decreased singing and mating rituals that result in a decrease in
breeding and future populations of birds". Adult weights of birds also decreased in
pesticide treated areas and parents have been known to abandon chicks as a result
of sub-lethal toxicity or decrease in food supply. Lethal and sub-lethal effects of
pesticide poisoning are at times more subtle and difficult to ascertain.
Although rarely documented, farmers have been known to intentionally use
insecticides to kill birds in an attempt to preemptively save their crops (Schwartz,
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1967). This has been confirmed through necropsies of masses of corpses in
agricultural areas and subsequent confessions of farmers. The number of
intentionally poisoned birds may be vastly underestimated due to the mobility of
birds and sub-lethal effects.
In human studies dermal and inhalation exposure is the most common form of
pesticide absorption. Adverse health effects have been documented in agricultural
workers and persons living in close proximity to agricultural fields. Human
exposure yields similar health effects to animals exposed that include reproductive
disruption, increase in blood pressure and heart rate (Ward, 2000). Wennergren
and Stark found evidence of second-generation effects and increased infant
mortality in birds from pesticides in environment.
Indirect effects of pesticide poisoning include a decrease or alteration in native
vegetation due to herbicide application. The result of this is a decrease in potential
or preferred habitat of birds that alters the biological community in unpredictable
ways. Herbicides have the potential to decrease food supply, reduce possible prey
that can culminate in extirpation or even extinction of species in an area (Blus,
1997).
Studies by Blus showed that DDT and its metabolites, DDD and DDE have been
shown to biomagnify in the food chain. DDT metabolites, which do not have
directly toxic effects, can accumulate in body tissues as AChE inhibitors. Geluso
determined that pesticides could accumulate in fatty tissues in most organisms.
These fat stores of toxin are released during times of stress. Avian lives often
include two migrations per year. Migrations, breeding, molt, illness and cold
temperatures would all be classified as stress to birds. During these times, the
toxins stored in the fatty tissues become released and accumulate in the brain that
causes a delayed lethal effect.
In studies done by Cox, it was found that birds, specifically gulls and terns that have
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come into contact with pesticides have initiated homosexual pairings, which results
in a zero reproductive success rate.
Birds’ exposure to pesticides is considerable given their life cycle and feeding
strategies. Exposure can be lethal to sub-lethal but both may be difficult to identify
due to the mobility of birds, predation of bird corpses and the secretive nature of
certain avian species (Mullie and Keith).
Toxicity through biomagnifications, AChe inhibition, reproductive success or
intentional poisoning are constant risks for avian communities.
Conclusion
Bait application has proven to be a less toxic option to pesticide control by reducing
non-target organism poisonings due to reduction in dermal or inhalation exposure
and reduction in amount chemicals applied (George, 1995).
The ripple effect of decreased prey or ingestion of contaminated prey results in wide
ranging effects on the food web. A particular species may be eradicated or
extirpated which will affect its predators and it’s biotic habitat.
Western Meadowlarks declined in Luke’s study due to a decrease in food supply
(grasshoppers), an increase in toxicity of surrounding environment, and decreased
productivity or reproduction due to sub-lethal effects (George, 1995).
IPM goals should be considered, before pesticide applications. In the case of
grasshoppers, birds reduce grasshopper populations and maintain them at endemic
levels. Adverse effect of pesticides on grasshopper predators may be
counterproductive to long-term pest management goals. If the predator is
extirpated, the prey may develop a pesticide resilience that would increase the
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pressure to use more pesticides that would potentially exacerbate the initial
problem.
Life histories are important factors to consider when determining sensitivity to
birds and treated areas. Different organisms have varying sensitivity to various
pesticides. Factors such as habitat preference, diet, feeding strategies and
systematic relationships vary between species.
Although lethal and sub-lethal effects are at times difficult to ascertain, there is
enough evidence through laboratory and field studies to show that pesticide toxicity
will continue to increase with an increase in pesticide use. Using a ‘cocktail ‘ of
pesticides will result in more detrimental effects on all organisms.
Biotic and abiotic conditions in the environment are not static and the
precautionary principle should be considered before bombarding the environment
with more pesticides. Biological controls could be a consideration in order to
increase crop yields while decreasing a growing reliance on pesticides.
Ecological toxicity is complicated and both short term and long term studies should
be employed to gain a stronger understanding of this complex process of pesticide
poisoning in avian communities and non target organisms.
Ecological toxicity is complicated and need long-term studies to begin to understand
pieces of this complex process.
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Table 1
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Table 2
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Table 3
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Figure 1
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Bibliography
Alsop, Fred, Smithsonian Birds of North America, 2001.
Blumburst, Michael, Experimental Parameters Used to Study Pesticide Degradation
in Soil, 1996. Weed Technology, Vol. 10, No.1, p 169-173.
Blus, L., and Henry, C., Field Studies on Pesticides and Birds: Unexpected and
Unique Relations, 1997. Ecological Applications, Vol. 7, No.4, p-1125-1132.
Braverman, M., Dusky, J., Locascio, S., Hornsby, A., Sorption and Degradation of
Thiobencarb in Three Florida Soils, 1990. Weed Science, Vol. 38, No. 6, p 583-588.
Carson, Rachel, Silent Spring, 1962
Cox, C. and Surgan, M., Unidentified Inert Ingredients in Pesticides: Implications for
Human and Environmental Health, 2006. Environmental Health Perspectives, Vol.
114, No. 12, p 1803-1806.
Douthwaite, R.J., Occurrence and Consequences of DDT Residues in Woodland Birds
Following Tsetse Fly Spraying Operations in NW Zimbabwe, 1995. Journal of
Applied Ecology, Vo. 32, No. 4, p 727-738.
Geluso, K., Altenbach, J., and Wilson, D., Bat Mortality: Pesticide Poisoning and
Migratory Stress, 1976. Science, New Series, Vol. 194, No. 4261, p 184-186.
George, L., McEwen, L., Petersen, B., Effects of Grasshopper Control Programs on
Rangeland Breeding Bird Populations, 1995. Journal of Range Management, Vol. 48,
No. 4, p 336-342.
16
Korschgen, Leroy, Soil-Food-Chain-Pesticide Wildlife Relationships in AldrinTreated Fields, 1970. The Journal of Wildlife Management, Vol. 34, No. 1, p 186-199.
Lee, S., McLaughlin, R., Harnly, M., Gunier, R., and Kreutzer, R., Community
Exposures to Airborne Agricultural Pesticides in California: Ranking of Inhalation
Risks, 2002. Environmental Health Perspectives, Vol. 110, No. 12, p 1175-1184.
Mullie, W., and Keith, J., The Effects of Aerially Applied Fenithrothion and
Chlorpyrifos on Birds in the Savannah of Northern Senegal, 1993. Journal of Applied
Ecology, Vol. 30, No. 3, p 536-550.
Relyea, Rick, A Cocktail of Contaminants: How Mixtures of Pesticides at Low
Concentrations Affect Aquatic Communities, 2008. Oecologia, Vol 159, p 363-376.
Schwartz, Henry, Microbial Degradation of Pesticides in Aqueous Solutions, 1967.
Water Pollution Control Federation, Vol. 39, No. 10, Part 1, p 1701-1714.
Sibley, D.A., The Sibley Guide to Bird Life and Bevohavior, 2001.
Stone, W., Overmann, S., and Okeniewski, J., Intentional Poisoning of Birds with
Parathion, 1984. The Condor, Vol. 86, No. 3, p 333-336.
Stromberg, K., Seed Treatment Pesticide Effects on Pheasant Reproduction at Sub
lethal Doses, 1977. The Journal of Wildlife Management, Vol. 41, No.4, p 632-642.
Ward, M., Nuckols, J., Weigel, S., Maxwell, S., Cantor, K., and Miller, R., Identifying
Populations Potentially Exposed to Agricultural Pesticides Using Remote Sensing
and a Geographic Information System, 2000. Environmental Health Perspectives,
Vol, 108, No. 1, p 5-12.
17
Wennergren, U., and Stark, J., Modelling Long-Term Effects of Pesticides on
Populations: Beyond Just Counting Dead Animals, 2000. Ecological Applications,
Vol. 10, No. 1, p 295-302.