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Behind mass die-offs, pesticides lurk as culprit

By Sonia Shah - posted Monday, 11 January 2010


Ever since Olga Owen Huckins shared the spectacle of a yard full of dead, DDT-poisoned birds with her friend Rachel Carson in 1958, scientists have been tracking the dramatic toll on wildlife of a planet awash in pesticides. Today, drips and puffs of pesticides surround us everywhere, contaminating 90 per cent of the nation’s major rivers and streams, more than 80 per cent of sampled fish, and one-third of the nation’s aquifers. According to the US Fish and Wildlife Service, fish and birds that unsuspectingly expose themselves to this chemical soup die by the millions every year.

But as regulators grapple with the lethal dangers of pesticides, scientists are discovering that even seemingly benign, low-level exposures to pesticides can affect wild creatures in subtle, unexpected ways - and could even be contributing to a rash of new epidemics pushing species to the brink of extinction.

In the past dozen years, no fewer than three never-before-seen diseases have decimated populations of amphibians, bees, and - most recently - bats. A growing body of evidence indicates that pesticide exposure may be playing an important role in the decline of the first two species, and scientists are investigating whether such exposures may be involved in the deaths of more than 1 million bats in the northeastern United States over the past several years.

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For decades, toxicologists have accrued a range of evidence showing that low-level pesticide exposure impairs immune function in wildlife, and have correlated this immune damage to outbreaks of disease. Consumption of pesticide-contaminated herring has been found to impair the immune function of captive seals, for example, and may have contributed to an outbreak of distemper that killed over 18,000 harbour seals along the northern European coast in 1988. Exposure to PCBs has been correlated with higher levels of roundworm infection in Arctic seagulls. The popular herbicide atrazine has been shown to make tadpoles more susceptible to parasitic worms.

The recent spate of widespread die-offs began in amphibians. Scientists discovered the culprit - an aquatic fungus called Batrachochytrium dendrobatidis, of a class of fungi called “chytrids” - in 1998. Its devastation, says amphibian expert Kevin Zippel, is “unlike anything we’ve seen since the extinction of the dinosaurs”. Over 1,800 species of amphibians currently face extinction.

It may be, as many experts believe, that the chytrid fungus is a novel pathogen, decimating species that have no armour against it, much as Europe’s smallpox and measles decimated Native Americans in the 16th and 17th centuries. But “there is a really good plausible story of chemicals affecting the immune system and making animals more susceptible,” as well, says San Francisco State University conservation biologist Carlos Davidson.

In California, for example, insecticides coated on the crops of the San Joaquin Valley are known to waft upwind to the Sierra Nevada mountains, where they settle in the air, snow, and surface waters, and inside the tissues of amphibians. And when Davidson compared historical reports of pesticide use, habitat loss, wind patterns, and amphibian population counts in California for the years 1971 to 1991, he found a strong correlation between upwind pesticide use - in particular cholinesterase-inhibiting chemicals such as the insecticide carbaryl - and declining amphibian populations.

Experimental evidence bolsters Davidson’s findings. In lab experiments, exposure to carbaryl dramatically reduced yellow-legged frogs’ production of fungus-fighting compounds called antimicrobial peptides, which may be crucial to amphibians’ ability to fend off chytrid fungus. Further testing has shown that amphibian species that produce the most effective mixes of antimicrobial peptides resist experimental chytrid infection, and tend to be those that survive most successfully in the wild.

Six years after scientists discovered the fungal assault on amphibians, a mysterious plague began decimating honeybees. Foraging honeybees first started vanishing from their hives, abandoning their broods and queens to certain death by starvation, in 2004. Alarmed beekeepers dubbed the devastating malady “colony collapse disorder.” Between 2006 and 2009, colony collapse disorder and other ills destroyed 35 per cent of the US honeybee population.

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Some experts believe colony collapse disorder is the result of a “perfect storm” of honeybee-debilitating factors: poor nutrition, immune dysfunction from decades of industrial beekeeping practices, and the opportunism of multiple pathogens, acting in malevolent concert. But many beekeepers believe that a new class of chemicals based on nicotine, called neonicotinoids, may be to blame.

Neonicotinoids came into wide use in the early 2000s. Unlike older pesticides that evaporate or disperse shortly after application, neonicotinoids are systemic poisons. Applied to the soil or doused on seeds, neonicotinoid insecticides incorporate themselves into the plant’s tissues, turning the plant itself into a tiny poison factory emitting toxin from its roots, leaves, stems, pollen, and nectar.

In Germany, France, Italy, and Slovenia, beekeepers’ concerns about neonicotinoids’ effect on bee colonies have resulted in a series of bans on the chemicals. In the United States, regulators have approved their use, despite the fact that the Environmental Protection Agency’s standard method of protecting bees from insecticides - by requiring farmers to refrain from applying them during blooming times when bees are most exposed - does little to protect bees from systemic pesticides.

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First published in Yale Environment 360 on January 7, 2010.



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About the Author

Sonia Shah is an author and science journalist whose writing has appeared in The Nation, New Scientist, The Washington Post and elsewhere. Her third book, The Fever: How Malaria Ruled Humankind for 500,000 Years, will be published in 2010.

Creative Commons LicenseThis work is licensed under a Creative Commons License.

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