The Pesticide Epidemic

The fact is that we have threeglobal epidemics among wildlife and all three vector easily toward a naturalsensitivity to pesticides in particular and to cumulative exposure.  Were it one, we would be looking forconfirmation in the other two and a lack thereof would be a good reason toquestion any linkage.

I have been posting on the beeissue in particular.  That is now wellunderstood except by those who wish to deny it. Bats also accumulate insects and naturally accumulate persistentpesticides.  How much is too much weconveniently do not know.  And then wehave frogs who accumulate toxins through their skins.

In short these are the three atrisk species.

What is not been well measured isthe losses of other wild bees and other pollinators.

We need not just superiorpesticides perhaps, but smart delivery protocols that minimize distributioninto the environment and the farmer’s lungs.

Behind Mass Die-Offs, Pesticides Lurk as Culprit

In the past dozen years, three new diseases have decimated populationsof amphibians, honeybees, and — most recently — bats. Increasingly, scientistssuspect that low-level exposure to pesticides could be contributing to thisrash of epidemics.

by sonia shah

07 JAN 2010: REPORT

http://e360.yale.edu/content/feature.msp?id=2228

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 beentracking the dramatic toll on wildlife of a planet awash in pesticides. Today,drips and puffs of pesticides surround us everywhere, contaminating 90 percentof the nation’s major rivers and streams, more than 80 percent of sampled fish,and one-third of the nation’s aquifers. According to the U.S. Fish and Wildlife Service,fish and birds that unsuspectingly expose themselves to this chemical soup dieby the millions every year.

But as regulators grapple with the lethal dangers of pesticides, scientists arediscovering that even seemingly benign, low-level exposures to pesticides canaffect wild creatures in subtle, unexpected ways — and could even becontributing to a rash of new epidemics pushing species to the brink ofextinction.

In the past dozen years, no fewer than three never-before-seen diseases havedecimated populations of amphibians, bees, and — most recently — bats. Agrowing body of evidence indicates that pesticide exposure may be playing animportant role in the decline of the first two species, and scientists areinvestigating whether such exposures may be involved in the deaths of more than1 million bats in the northeastern United States over the past several years.

White-nose Syndrome, named for the tell-tale white fuzz it leaves onbats’ ears and noses, has killed more than a million bats in the northeastern United States.

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

The recent spate of widespread die-offs began in amphibians. Scientistsdiscovered the culprit — an aquatic fungus called Batrachochytriumdendrobatidis, of a class of fungi called “chytrids” — in 1998. Itsdevastation, says amphibian expert Kevin Zippel, is “unlike anything we’ve seensince the extinction of the dinosaurs.” Over 1,800 species of amphibianscurrently face extinction.

It may be, as many experts believe, that the chytrid fungus is a novelpathogen, decimating species that have no armor against it, much as Europe’s smallpox and measles decimated Native Americansin the sixteenth and seventeenth centuries. But “there is a really goodplausible story of chemicals affecting the immune system and making animalsmore susceptible,” as well, says San Francisco State University conservation biologist CarlosDavidson.

In California, for example, insecticidescoated on the crops of the San JoaquinValley are known to waft upwind to theSierra Nevada mountains, where theysettle 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 1971to 1991, he found a strong correlation between upwind pesticide use — inparticular 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 offungus-fighting compounds called antimicrobial peptides, which may be crucialto amphibians’ ability to fend off chytrid fungus. Further testing has shownthat amphibian species that produce the most effective mixes of antimicrobialpeptides resist experimental chytrid infection, and tend to be those thatsurvive most successfully in the wild.

Six years after scientists discovered the fungal assault on amphibians, amysterious plague began decimating honeybees. Foraging honeybees first startedvanishing from their hives, abandoning their broods and queens to certain deathby starvation, in 2004. Alarmed beekeepers dubbed the devastating malady“colony collapse disorder.” Between 2006 and 2009, colony collapse disorder andother ills destroyed 35 percent of the U.S. honeybee population.

Some experts believe colony collapse disorder is the result of a“perfect storm” of honeybee-debilitating factors: poor nutrition, immunedysfunction from decades of industrial beekeeping practices, and the opportunismof multiple pathogens, acting in malevolent concert. But many beekeepersbelieve 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 pesticidesthat evaporate or disperse shortly after application, neonicotinoids aresystemic poisons. Applied to the soil or doused on seeds, neonicotinoidinsecticides incorporate themselves into the plant’s tissues, turning the plantitself 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 resultedin a series of bans on the chemicals. In the United States, regulators haveapproved their use, despite the fact that the Environmental Protection Agency’sstandard method of protecting bees from insecticides — by requiring farmers torefrain from applying them during blooming times when bees are most exposed —does little to protect bees from systemic pesticides.

“The companies believe this stuff is safe,” says U.S. Department of Agriculture(USDA) entomologist Jeff Pettis. “It is used at lower levels, and is a boon forfarmers,” since neonicotinoids don’t require repeated application, nor widebroadcasting into the environment, he explains. Plus, years of research have shownthat only very low levels of the chemicals are exuded from the pollen andnectar of treated plants.

But University of Padua entomologistVincenzo Girolami believes he may have discovered an unexpected mechanism bywhich neonicotinoids — despite their novel mode of application — do in factkill bees. In the spring, neonicotinoid-coated seeds are planted usingseeding machines, which kick up clouds of insecticide into the air. “The cloudis 20 meters wide, sometimes 50 meters, and the machines go up and down and upand down,” he says. “Bees that cross the fields, making a trip every tenminutes, have a high probability of encountering this cloud. If they make atrip every five minutes, it is certain that they will encounter this cloud.”

And the result could be immediately devastating. In as-yet-unpublishedresearch, Girolami has found concentrations of insecticide in clouds aboveseeding machines 1,000 times the dose lethal to bees. In the spring, when theseed machines are working, says Girolami, “I think that 90 percent or more ofdeaths of bees is due to direct pesticide poisoning.”

Girolami has also found lethal levels of neonicotinoids in other, unexpected —and usually untested — places, such as the drops of liquid that treated cropssecrete along their leaf margins, which bees and other insects drink. (Thescientific community has yet to weigh in on Girolami’s new,still-to-be-published research, but Pettis, who has heard of the work, calls it“a good and plausible explanation.”)

The Spread of New Diseases: The Climate Connection

As humans encroach on forested lands and as temperatures rise, the transmissionof disease from animals and insects to people is growing. Now a new field,known as “conservation medicine,” is exploring how ecosystem disturbance andchanging interactions between wildlife and humans can lead to the spread of newpathogens.

What’s Killing the Tasmanian Devil?

Scientists have been trying to identify the cause of a cancer epidemic that iswiping out Australia’sTasmanian devils. Now new research points to an alarming conclusion: Because ofthe species’ low genetic diversity, the cancer is contagious and is spreading

from one devil to another.

Two years after the honeybees started disappearing, so, too, did bats.The corpses of hibernating bats were first found blanketing caves in thenortheastern United Statesin 2006. The disease that killed them, caused by a cold-loving funguscalled Geomyces destructans — and dubbed White-nose Syndrome for thetell-tale white fuzz it leaves on bats’ ears and noses — has since destroyed atleast one million bats. University of Florida wildlife ecologist John Hayes calls it “themost precipitous wildlife decline in the past century in North America.”

Like the mysterious Batrachochytrium dendrobatidis fungus infestingamphibians, Geomyces could be a novel pathogen, newly preying upondefenseless bat species. But scientists have also started to investigatewhether pesticide exposure might be playing a role.

Bats are especially vulnerable to chemical pollution. They’re small — thelittle brown bat weighs just 8 grams — and can live for up to three decades.“That’s lots of time to accumulate pesticides and contaminants,” points out Boston Universitybat researcher and Ph.D. candidate Marianne Moore, who is studying whetherenvironmental contaminants suppress bats’ immune function. “We know they areexposed to and accumulate organochlorines, mercury, arsenic, lead, dioxins,”she says, “but we don’t understand the effects.”

Which, in the end, is the central dilemma facing pesticide-reliant societies.Proving, with statistical certainty, that low-level pesticide exposure makesliving things more vulnerable to disease is notoriously difficult. There aretoo many different pesticides, lurking in too many complex, poorly understoodhabitats to build definitively damning indictments. The evidence is subtle,suggestive. But with the rapid decimation of amphibians, bees, and bats, it isaccumulating, fast.