Rachel's #977: Chemicals and Diabetes

From: New Scientist (pg. 36) ………………………..[This story printer-friendly]
September 10, 2008

COULD THE DIABETES EPIDEMIC BE DOWN TO POLLUTION?

[Rachel’s introduction: “Ask why diabetes is epidemic in the 21st century and most people will point the finger at bad diet, laziness and obesity. According to a small but growing group of scientists, though, the real culprit is a family of toxic chemicals known as persistent organic pollutants, or POPs… including dioxins, DDT and PCBs….”]

By Phyllida Brown

On July 10, 1976, a reactor at a chemical plant near the small town of Seveso in northern Italy exploded, sending a toxic cloud drifting into the summer sky. Around 18 square kilometres of land was contaminated with TCDD, a member of the notorious class of industrial chemicals known as dioxins.

The immediate after-effects were relatively mild: 15 children landed in hospital with skin inflammation and around 3300 small animals were killed. Today, however, the accident casts a long shadow over the people of Seveso, who are suffering increased numbers of premature deaths from cancer, cardiovascular disease and, perhaps surprisingly, diabetes (American Journal of Epidemiology, vol 167, p 847).

To some diabetes researchers, Seveso serves as a warning to us all. Ask why diabetes is epidemic in the 21st century and most people will point the finger at bad diet, laziness and obesity. According to a small but growing group of scientists, though, the real culprit is a family of toxic chemicals known as persistent organic pollutants, or POPs. If these researchers are right, POPs — which include some of the most reviled chemicals ever created, including dioxins, DDT and PCBs — may be key players in the web of events that lead people to develop the disease.

The claim has yet to attract widespread attention from mainstream diabetes research. Even its champions were initially surprised by it. “I had never even heard of POPs until 2005,” says Duk-Hee Lee, an epidemiologist at Kyungpook National University in Daegu, Korea, who led the work. Lee and her co-workers are now convinced, albeit reluctantly, that they are onto something. “The hypothesis is one that I wish were not true,” says her colleague David Jacobs of the University of Minnesota, Minneapolis.

Diabetes, and particularly its commonest form, type 2 (see “Sidebar: Diabetes basics”), is practically everyone’s business. The World Health Organization estimates that it already affects 180 million people worldwide, with the number predicted to more than double by 2030. Last year the epidemic cost $174 billion in the US alone, according to the American Diabetes Association.

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Sidebar: Diabetes basics

Diabetes has two main forms: type 1 and type 2. About 90 per cent of diabetics have type 2.

Type 1 diabetes is an autoimmune disease in which insulin-producing cells in the pancreas are progressively destroyed.

Type 2 diabetes usually develops in adulthood, although it is now increasingly common in children. In this form, the pancreas either produces too little insulin, or cells in the liver, muscles and fat tissues fail to use it properly. Type 2 is most common in inactive, overweight people who carry their fat on their midriff.

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The standard explanation for type 2 diabetes is that it is a “lifestyle disease” caused by laziness and gluttony. For at least a decade, however, epidemiologists have known that people briefly exposed to high concentrations of POPs face a modest increase in their risk of developing diabetes later in life. Those affected include the people of Seveso and US veterans who were exposed to dioxin- contaminated Agent Orange during the Vietnam war.

Two years ago, Lee, Jacobs and others decided to see whether everyday exposure to POPs is also linked to diabetes. To their surprise and horror, they found that it is.

For most people, POPs are inescapable: meat, fish and dairy products all contain them. They enter the food chain from sources such as pesticides, chemical manufacturing and incinerated waste, and accumulate in animals higher up in the chain. Once in the body they take up residence in fat.

POPs have long been recognised as nasty substances: their effects include birth defects, cancer, immune dysfunction and endocrine disruption. Since the 1970s, various measures have been put in place to phase them out — 12 of the worst POPs, known as the “dirty dozen”, were banned in 2004 — but despite these efforts, POPs remain a significant presence in the environment and food chain, partly because many are still in use in the developing world, and partly because these chemicals can take decades to break down.

Role of fat

Prior to her 2005 introduction to POPs, Lee was working on a humble enzyme called gamma-glutamyltransferase (GGT), which is essential for maintaining antioxidant levels in the liver. She was puzzled to find that obesity combined with an elevated level of GGT is a strong predictor of diabetes, but obesity alone isn’t. “I searched the literature and finally got an idea,” she says.

As it turns out, GGT has an essential role to play in removing some pollutants, including POPs, from inside cells (Diabetologia, vol 51, p 402). Could increased GGT activity simply be a marker of exposure to POPs?

To find out, Lee and her colleagues analysed data from more than 2000 people in the US National Health and Nutrition Examination Survey (NHANES), which measured both diabetes status and bloodstream levels of POPs, among other things. They discovered that people with high levels of six different POPs in their bloodstream were much more likely to have diabetes, regardless of obesity (see diagram). The six POPs were chosen because they were detectable in at least 80 per cent of the participants.

Taking into account factors such as weight, age, waist circumference and ethnic group, Lee calculated that in people with the highest combined levels of all six POPs the rate of diabetes was a massive 38 times greater than in those with the lowest levels (Diabetes Care, vol 29, p 1638). “The people who disagree with us will say it’s all noise,” says Jacobs, “but it’s pretty hard to get odds ratios of 38 with noise.”

To her even greater surprise, Lee found that in people with undetectable levels of POPs the expected link between diabetes and body weight melted away — those who were obese were no more likely to have diabetes than their lean counterparts. “This suggests that POPs may be a more fundamental factor in the risk of diabetes than obesity,” says Lee. “The absolute risk of diabetes was extremely low among subjects with very low concentrations of POPs.”

“The expected link between diabetes and body weight melted away” But fat is not off the hook just yet. While obesity alone appears not to be linked with diabetes, the study suggests that POPs plus obesity is bad news, and the fatter you are the worse it gets. When the researchers examined the link with body mass index, they found that in people with high levels of POPs the odds of being diabetic were much higher for the obese than the lean. This suggests that something about excess fat may be enhancing the toxicity of POPs. “It appears that obesity can increase the harmful effects,” says Lee.

Of course, the findings do not prove that POPs cause diabetes. “This is an association between two things, not direct evidence of a causal link,” warns Oliver Jones, an environmental biochemist at the University of Cambridge. The idea deserves further investigation, though, he says.

Lee and her colleagues acknowledge that their interpretation could be stood on its head. If diabetes causes the body to become less efficient at dealing with POPs, then higher levels of POPs in people with diabetes could be an effect of the disease, rather than its cause. Lee does not rule out this possibility, but thinks it unlikely. She points to a 2003 study by other researchers that found no relationship between diabetes and the rate at which POPs are eliminated from the body (Journal of Toxicology and Environmental Health, vol 66, p 211).

The team also examined the link between POPs and a metabolic disorder called insulin resistance, in which muscle, fat and liver cells fail to use insulin properly and which often progresses to full-blown diabetes. Once again, they found that people whose blood contained the highest levels of POPs were most likely to have insulin resistance (Diabetes Care, vol 30, p 622). The results add weight to the idea that POPs may be playing a vital role in the disease pathway from insulin resistance to diabetes, says Lee. “I am really excited about this.”

Even so, she acknowledges two obvious objections to her work. First, while levels of POPs in the blood of Americans have been falling for a couple of decades, the diabetes epidemic is just taking off. Lee suggests that as obesity seems to make POPs more dangerous, its rising prevalence may have cancelled out any health improvements that should have followed the decline in POPs.

A second question is why, if POPs are central to diabetes, the incidence of the disease is soaring not only in the meat-addicted west but also in countries such as India, where many millions are vegetarian. Lee’s answer is that, while many POPs are banned in the west, some are still used as pesticides in developing countries. “The highest rate of increasing risk of type 2 diabetes is observed in Asia and Africa, not North America with the highest obesity rate,” she says.

To try to slot POPs into the complex diabetes jigsaw, it is worth taking a brief step into the mainstream to look at the role of fats, or lipids, in the disease. Type 2 diabetes was once seen mainly as a disorder of glucose metabolism. Now, says diabetes researcher Evan Rosen of Beth Israel Deaconess Medical Center in Boston, the focus has shifted, with many scientists considering that the primary problem lies with the metabolism of fats.

For years, physiologists largely ignored fat cells, or adipocytes, seeing them as little more than passive energy silos. Recently, though, they have been revealed for what they are: highly active in producing both hormones that regulate energy, and inflammatory messenger chemicals that are important to the immune system (New Scientist, 16 September 2000, p 36). If adipocytes malfunction, the consequences can be widespread.

When we eat energy-rich foods, our bodies have to store any excess energy not burned up by physical activity. Most is stored as fat in adipocytes, but when these eventually fill up, excess lipid spills over into other tissues, particularly the liver, muscles and the area around the heart. The presence of this “ectopic fat” has been linked to all sorts of health problems, including insulin resistance and diabetes.

Just how might ectopic fat help to trigger diabetes, though? There is no simple answer and researchers still disagree about the possible mechanism. However, there are some clues.

In animals ectopic fat is known to attract the attention of the immune system, which produces inflammatory messenger chemicals around it as though it were an infection. Interestingly, people with diabetes have chronically raised levels of these inflammatory chemicals, raising the question of whether inflammation caused by ectopic fat could be a factor in the disease.

Ectopic fat also causes problems when muscle cells try to burn it to generate energy. In obese people this is a highly inefficient process, probably because their mitochondria — the cell’s power plants – function at a reduced capacity, says Rosen. Mitochondria in muscle cells are already known to work less efficiently in people with diabetes, and this year a team at Helsinki University Central Hospital in Finland found similar changes in obese people with no symptoms of diabetes (American Journal of Physiology — Endocrinology and Metabolism, vol 295, p E148).”You end up with a half-burned lipid,” says Rosen.

He speculates that this half-burned lipid acts like a magnet for reactive oxygen species (ROS), including free radicals and peroxides, which then inflict damage to the muscle cells themselves. There is now clear evidence that chronic damage from ROS — known as oxidative stress — helps to drive cells into insulin resistance. “If you block ROS, you can block insulin resistance,” says Rosen.

If Lee is right, however, and POPs are at the root of diabetes, these ideas tell only half the story. So how might POPs be involved? Again, there are tantalising hints. Jones points out that POPs are known to bind to a family of receptors on cell nuclei known as PPARs. These are involved in lipid metabolism and are known not to work properly in people with diabetes; the diabetes drug troglitazone works by activating one member of the family, PPAR-gamma. People with an inherited disorder of this receptor are unusually prone to insulin resistance. Another intriguing link is that POPs are known to cause mitochondrial dysfunction, which some researchers think is the root cause of diabetes (Science, vol 307, p 384).

But none of this explains how POPs interact with obesity. It may be that obese people simply have a higher load of POPs in their bodies. Another possibility is that POPs in ectopic fat are particularly dangerous. Perhaps, speculates Lee, adipocytes are a relatively safe storage site for POPs. “Our body has to find some place to store them,” she says, “and in this sense, adipose tissue is a relatively safe organ.” The trouble might start when POP-contaminated ectopic fat starts to build up in the muscles and liver, exposing the organs to a direct toxic assault. “That way, the harmful effects of POPs could become more serious,” Lee suggests.

Clearly more work is needed to establish the precise link between POPs and diabetes. For Jones, it is surprising that Lee’s research has remained relatively neglected, especially given its public health implications. He does note, though, that other teams are starting to investigate the hypothesis. Julian Griffin and others at Cambridge have found that low-level mixtures of POPs can cause metabolic disturbances similar to those seen in type 2 diabetes.

Rosen stresses that the lack of attention given to this research should not be seen as an indictment of the work, but instead reflects how deeply scientists specialise in their own areas. “We generally stay inside our silos,” he says. “It’s incredibly difficult to move outside of them.” Another problem, says Jacobs, is that testing the hypothesis to destruction would require complex and long-term studies of the type that funding bodies are often reluctant to commit money to.

If Lee is right, it is not good news for the diabetes epidemic. Even though many POPs are being phased out, they will take decades to clear from the food chain. Meanwhile, newer POPs such as brominated flame retardants continue to be manufactured in large quantities.

There is perhaps one silver lining. If you need an extra incentive to stay lean, eat less meat and keep active, then knowing that toxic chemicals lurking in your body fat could be a sure route to diabetes might just be the motivation you’re looking for.

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Phyllida Brown is a writer based in Exeter, UK

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From: Reuters health ……………………………….[This story printer-friendly]
August 15, 2008

HIGH PCB EXPOSURE TIED TO DIABETES RISK

[Rachel’s introduction: Women who had been exposed to PCB-laced oil were twice as likely as other women to develop type 2 diabetes over 24 years. And women who had been most severely affected by the PCB exposure had a more than five-times higher diabetes risk.]

NEW YORK (Reuters Health) — People who have been exposed to high levels of toxic polychlorinated biphenyls (PCBs) may face an elevated risk of type 2 diabetes, a new study shows.

The findings, reported in the journal Diabetes Care, come from a long-term study of Taiwanese adults who, in the 1970s, had been poisoned by cooking oil contaminated with PCB pollutants.

Once used in products ranging from fluorescent lights and appliances to insulation and insecticide, PCBs were banned in the late 1970s as carcinogens and general health hazards. They linger in the environment, however.

In the new study, Dr. Yueliang Leon Guo, from the National Taiwan University in Taipei, and colleagues examined the incidence of type 2 diabetes among 378 Taiwanese “oil disease” victims and 370 of their neighbors who had not been poisoned.

They found that women who had been exposed to the PCB-laced oil were twice as likely as other women to develop type 2 diabetes over 24 years. And women who had been most severely affected by the PCB exposure had a more than five-times higher diabetes risk.

There were no similar risks seen in men, however.

Other studies have found that people with diabetes tend to have relatively higher levels of organic pollutants, such as PCBs, in their blood. In comments to Reuters Health, Guo said that since “everyone” has detectable PCB levels in his or her body, it’s possible that exposure to such pollutants has helped feed the widespread rise in diabetes in recent decades.

“The public health implication of these findings can be huge,” Guo added, “considering the burden of diabetes and its multiple long-term complications.”

SOURCE: Diabetes Care 2008, August 2008.

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From: The Telegraph (London, U.K.) …………………..[This story printer-friendly]
September 9, 2008

POLLUTION LINKED TO OBESITY, NEW STUDY FINDS

[Rachel’s introduction: Dr. Pete Myers, chief scientist at the US- based Environmental Health Sciences, said: “This is very important. It is the first good study of the effects on the foetus. Its conclusions are not surprising, given what we know from the animal experiments, but it firmly links such chemicals to the biggest challenge facing public health today.”]

By Chris Irvine

Pollution could determine whether a child is fat or not before they have even been born, a new study has found.

Exposure to a range of common chemicals before birth increases the chance of a baby to growing up overweight or obese, the research indicates.

The study by scientists at Barcelona’s Municipal Institute of Medical Research is the first to link obesity with chemical contamination in the womb, where humans are most vulnerable.

A quarter of all British adults and a fifth of children suffer from obesity, with at least 300 million obese worldwide.

Published in the current issue of the journal Acta Paediatrica, the research measured levels of hexachlorobenzene (HCB) in the umbilical cords of 403 children born on the Spanish island of Menorca.

HCB is a pesticide banned internationally but which continues to remain in the environment and can be found in food.

Those with the highest levels of HCB were twice as likely to be obese when they reached the age of six and a half.

The report’s authors are now calling for exposure to similar pesticides to be minimised, including bisphenol A (BPA), used in baby bottles and cans of food, and phthalates, found in cosmetics and shampoos.

Tests have shown BPA is found in 95 per cent of Americans, while 90 per cent have been found to be exposed to phthalates in the womb.

Dr Pete Myers, chief scientist at the US-based Environmental Health Sciences, said: “This is very important. It is the first good study of the effects on the foetus. Its conclusions are not surprising, given what we know from the animal experiments, but it firmly links such chemicals to the biggest challenge facing public health today.”

The research comes after Conservative leader David Cameron said that obesity is purely a matter of “personal responsibility”.

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From: Reuters ………………………………………[This story printer-friendly]
September 16, 2008

COMMON PLASTICS CHEMICAL LINKED TO HUMAN DISEASES

[Rachel’s introduction: Is your baby drinking from a bottle made out of the common plastic BPA? The U.S. Food and Drug Administration says it’s completely safe, though other government agencies disagree. Now, for the first time, we have direct evidence of human disease from exposure to BPA.]

London, Sept 16 — A study has for the first time linked a common chemical used in everyday products such as plastic drink containers and baby bottles to health problems, specifically heart disease and diabetes.

Until now, environmental and consumer activists who have questioned the safety of bisphenol A, or BPA, have relied on studies showing harm from exposure in laboratory animals.

But British researchers, who published their findings on Tuesday in the Journal of the American Medical Association, analyzed urine and blood samples from 1,455 U.S. adults aged 18 to 74 who were representative of the general population.

Using government health data, they found that the 25 percent of people with the highest levels of bisphenol A in their bodies were more than twice as likely to have heart disease and, or diabetes compared to the 25 percent of with the lowest levels.

“Most of these findings are in keeping with what has been found in animal models,” Iain Lang, a researcher at the University of Exeter in Britain who worked on the study, told a news conference.

“This is the first ever study (of this kind) that has been in the general population,” Lang said.

Steven Hentges of the American Chemistry Council, a chemical industry group, said the design of the study did not allow for anyone to conclude BPA causes heart disease and diabetes.

“At least from this study, we cannot draw any conclusion that bisphenol A causes any health effect. As noted by the authors, further research will be needed to understand whether these statistical associations have any relevance at all for human health,” Hentges said in a telephone interview.

A U.S. Food and Drug Administration panel of outside experts on Tuesday will hear testimony on health effects from BPA as it reviews a draft report it issued last month calling BPA safe.

“The study, while preliminary with regard to these diseases in humans, should spur U.S. regulatory agencies to follow recent action taken by Canadian regulatory agencies, which have declared BPA a ‘toxic chemical’ requiring aggressive action to limit human and environmental exposures,” Frederick vom Saal of the University of Missouri and John Peterson Myers of the nonprofit U.S.-based Environmental Health Sciences, wrote in a commentary accompanying the study.

BOTTLES TO UTENSILS

BPA is used to make polycarbonate plastic, a clear shatter-resistant material in products ranging from baby and water bottles to plastic eating utensils to sports safety equipment and medical devices.

It also is used to make durable epoxy resins used as the coating in most food and beverage cans and in dental fillings.

People can consume BPA when it leaches out of plastic into liquid such as baby formula, water or food inside a container.

In the study, the team said the chemical is present in more than 90 percent of people, suggesting there is not much that can be done to avoid the chemical of which over 2.2 million tonnes is produced each year.

The researchers, who will also present their findings at the U.S. FDA session on Tuesday, added it was too early to identify a mechanism through which the chemical may be doing harm.

Animal studies have suggested the chemical may disrupt hormones, especially estrogen.

The researchers also cautioned that these findings are just the first step and more work is needed to determine if the chemical actually is a direct cause of disease.

“Bisphenol A is one of the world’s most widely produced and used chemicals, and one of the problems until now is we don’t know what has been happening in the general population,” said Tamara Galloway, a University of Exeter researcher who worked on the study.

Canada’s government in April decided BPA was harmful to infants and toddlers and announced plans to ban some products.

The European Union’s top food safety body said in July the amount of BPA found in baby bottles cannot harm human health.

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From: New Scientist (pg. 7) …………………………[This story printer-friendly]
July 14, 2008

CONTAMINATED U.S. SITE FACES ‘CATASTROPHIC’ NUCLEAR LEAK

[Rachel’s introduction: “More than 210 million litres of radioactive and chemical waste are stored in 177 underground tanks at Hanford in Washington State. Most are over 50 years old. Already 67 of the tanks have failed, leaking almost 4 million litres of waste into the ground.”]

One of “the most contaminated places on Earth” will only get dirtier if the US government doesn’t get its act together — clean-up plans are already 19 years behind schedule and not due for completion until 2050.

More than 210 million litres of radioactive and chemical waste are stored in 177 underground tanks at Hanford in Washington State. Most are over 50 years old. Already 67 of the tanks have failed, leaking almost 4 million litres of waste into the ground.

There are now “serious questions about the tanks’ long-term viability,” says a Government Accountability Office report [2.1 Mbytes PDF], which strongly criticises the US Department of Energy for delaying an $8 billion programme to empty the tanks and treat the waste. The DoE says the clean-up is “technically challenging” and argues that it is making progress in such a way as to protect human health and the environment.

The DoE’s plan, however, is “faith-based”, says Robert Alvarez, an authority on Hanford at the Institute for Policy Studies in Washington DC. “The risk of catastrophic tank failure will sharply increase as each year goes by,” he says, “and one of the nation’s largest rivers, the Columbia, will be in jeopardy.”

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From: New Scientist ………………………………..[This story printer-friendly]
July 10, 2008

CORALS JOIN FROGS AND TOADS AS WORLD’S MOST ENDANGERED

[Rachel’s introduction: Of the 704 species of corals that have been studied, scientists say 32.8% are at risk of extinction. The fate of the other 141 coral species remains unknown.]

By Catherine Brahic

Within one generation, diving on coral reefs could be a very rare holiday opportunity. The first comprehensive review of tropical coral species reveals that over one-quarter reef-building coral species already face extinction.

This means corals join frogs and toads as the most threatened group of animal species on the planet.

There are 845 known species of corals that build reefs and live in symbiosis with algae. Not enough is known about 141 of these to determine how threatened they are. But of the 704 remaining species, scientists say 32.8% are at risk of extinction.

The team, which was led by Kent Carpenter of the International Union for the Conservation of Nature (IUCN) and gathered experts from around the world, used the IUCN Red List criteria to assess the 845 species.

Sewage and climate

Two hundred and thirty one species (27%) were found to be threatened with extinction. A further 176 (21%) were deemed “near-threatened”.

“It was a huge surprise because there is only one other group of animals that has been assessed that exceed that level of threat,” says Alex Rogers of the Zoological Society of London, who participated in the survey, “and that’s the amphibians.”

Humans directly threaten corals by dumping fertilisers and sewage into the oceans and by overfishing with destructive methods.

All this encourages the growth of larger algae, which smother corals. “Outside of the US and Europe, 80% of human sewage is released into the oceans without treatment,” says Rogers.

Global warming increases sea temperatures which causes “bleaching” events, where the reefs expel the tiny algae upon which they depend. Warming has also been associated with an increased incidence of coral diseases.

Large-scale disaster

In 1998, a world-wide coral bleaching triggered by unusually warm seas irreversibly destroyed 16% of the coral reef area worldwide.

Coral reefs are home to 25% of all fish species, and as many as 2 million species of animals and plants.

In this sense, they are the tropical rainforests of the oceans and the 1998 bleaching event can be compared to irreversibly wiping out 240 million hectares of forest — equivalent to half of the Amazon.

“If this happened in terrestrial ecosystems we would all be shouting from the treetops,” says Rogers. “And yet, it has now completely passed out of public memory.”

Valuable resource

“I have two children that are under one-and-a-half years old. I expect that by the time they are 40, coral reefs will have massively declined and in some regions, such as the Caribbean, they will be pretty much gone. By the end of the century there could be virtually nothing left.”

Conserving corals will require doing more than addressing the causes of climate change, but the benefits will be considerable. Reef fish feed more than 1 billion people in the developing world and the overall value of coral reefs is estimated at more than $30 billion a year.

There is a little good news, though. The 1998 bleaching event revealed that some species of corals appear to be resistant to coral bleaching, suggesting that these species may become hardy survivors.

Restored reefs

At the 11th International Coral Reef Symposium held in Florida this week, a team of scientists presented evidence that some strains of the endangered staghorn coral Acropora cervicornis can resist white band disease.

This disease has caused mass die-offs of staghorn corals in the Caribbean, resulting in them being listed in the US Endangered Species Act. The researchers say the findings suggest it might be possible to propagate resistant strains to restore the endangered reefs.

Recent studies have highlighted the plight of coral reefs in different areas around the world. In 2007, researchers announced that reefs in the Pacific are disappearing twice as fast as tropical rainforests. And in 2003, another team showed that Caribbean corals were dangerously close to extinction.

Journal reference: Science (DOI: 10.1126/science.1159196)

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From: Environmental Health News ……………………..[This story printer-friendly]
September 15, 2008

FEMINIZED TOADS LINKED TO FARMS.

[Rachel’s introduction: “The reality is we are stressing wildlife populations, killing them through habitat loss and disease, and then also modifying them so they cannot reproduce optimally.”]

By Marla Cone, Editor in Chief

Along the shore of Florida’s Lake Okeechobee, male toads seem more like females. Most have ovaries as well as testes, the mottled skin of a female and depleted testosterone.

Nearby, in a Palm Beach suburb, the toads are normal. The difference? The feminized ones live in areas with heavy agriculture while the normal males inhabit suburban areas.

Scientists at University of Florida have documented that proximity to farms increases the chances that amphibians are half-male, half female. The more intense the agriculture, the more feminized the male toads, and the more likely they can’t reproduce.

The new findings intensify the already highly contentious debate over whether pesticides — particularly atrazine, one of the most widely used herbicides in the United States — are messing up the reproductive organs of wildlife.

Some scientists say that pesticide exposure is likely to be a big piece of a puzzle that they have tried to solve for decades: What is wiping out frogs and amphibians around the world?

Louis Guillette The threat from agriculture “is part of a complex response that endangers frog and other wildlife populations,” said Louis Guillette, senior author of the study and a University of Florida Distinguished Professor of Zoology.

You have stacked the deck against healthy populations,” he said. “The reality is we are stressing wildlife populations, killing them through habitat loss and disease, and then also modifying them so they cannot reproduce optimally.”

The new research “adds to the support that agriculture causes these problems,” said Tyrone Hayes, a professor of integrative biology at University of California at Berkeley.

Hayes in 2003 published data that showed frogs exposed in the laboratory to the herbicide atrazine became hermaphroditic.

However, other studies, many of them industry-funded, have found no such effects. The U.S. Environmental Protection Agency concluded last year after a review of existing data that there was insufficient data to suggest that atrazine feminizes amphibians. Its science advisory committee agreed.

Dr. Tim Pastoor, principal scientist at Syngenta, the manufacturer of atrazine, said “a growing body of research conducted by independent labs across the world is showing that atrazine does not affect the sexual development of amphibians.”

Florida’s gender-bending chemicals

University of Florida’s research in the early 1990s, led by Guillette, was considered pivotal science that led to worldwide concern about chemicals that mimic or block hormones. The scientists linked the pesticide dicofol, which contains DDT, to feminized alligators in Florida’s Lake Apopka. The phenomenon, called endocrine disruption, has now been replicated in research on various species and chemicals throughout the world.

In the new study, scientists collected toads from five sites in South Florida. At the two places, Belle Glade and Canal Point, where most land is farmed, about 60% of males had feminized sex organs, including 35% to 40% that were considered intersex, with both ovaries and testes. But at Lake Worth, which has no agriculture, there were no intersex toads and feminized traits were found in less than 10%.

Also, the male toads in the agricultural areas had fewer pads on their thumbs which grow on mating males. Their testosterone levels were low in the farmed areas, similar to those of female toads.

Andrew Blaustein, a zoology professor at Oregon State University who studies environmental threats to frogs, said the more-subtle, feminine changes found in the males — particularly the lack of thumb pads allowing them to hold on to a mate–could have dramatic effects on their ability to breed.

“The secondary sexual traits are really striking,” he said.

Although the new study only looked at cane toads, which are not native to Florida, “we have also studied green tree frogs and southern toads, and both show similar gonadal abnormalities at the agricultural sites,” said Krista McCoy, lead author of the Florida study, which was published in an online edition of Environmental Health Perspectives in July.

“In general amphibian reproductive system development is very sensitive to hormones, natural and man-made,” McCoy said. As a result, she said “what we find in cane toads is likely occurring in other species and might be contributing to their rarity.”

Effects on specific populations, however, have not been documented. Scientists do not know whether any hormone-mimicking pesticides have caused population declines in amphibians

“We know that many pollutants are distributed globally, and we know that amphibian populations are declining globally, faster than birds or mammals actually. But we do not have an understanding of the role that pollutants are playing in amphibian population declines,” McCoy said.

Across all species, hormone systems are strikingly similar, regulating how the reproductive tract develops. Scientists suspect that the same chemicals that feminize toads might be feminizing human boys, too.

“In fact, there is general concern among scientists who study endocrine disrupting chemicals that some of the very chemicals used at the agricultural sites we studied are negatively affecting humans,” McCoy said.

‘The big suspect is atrazine’

About 888 million pounds of active pesticide ingredients were used in 2001, 76% for agriculture, according to EPA data. Of that, 550 million pounds were herbicides. Corn is the major crop using herbicides, accounting for more than one-third of the total. Illinois and Iowa lead the nation in herbicide use.

The Florida team did not implicate any particular chemical. But the primary pesticide used in that area is atrazine, applied to sugarcane fields.

“The big suspect is atrazine,” Hayes said. “What makes atrazine particularly bad is that it is everywhere. It is the one pesticide that’s always there, that’s persistent. There is no other evidence at this point for other pesticides.”

Hayes theorizes that atrazine feminizes animals by activating an enzyme that causes an imbalance between testosterone and estrogen.

“We have effects in fish, and similar effects in alligators and other species, and we have studies on human cell lines,” Hayes said. “To me it’s a no-brainer. That can’t be a coincidence.”

However, the EPA mounted a review of 19 laboratory and field studies exploring the effects on amphibians, and concluded last year that atrazine does not feminize them.

Syngenta’s Pastoor said the new study “contains major uncertainties that render the data interpretation unreliable.” For example, the age of the toads was not reported, and that is important because sexual characteristics vary with age, he said.

While atrazine is used in South Florida, concentrations in water near the places where the toads were collected “are extremely low,” Pastoor said.

Some scientists, however, say there is ample evidence that pesticides are harming frogs and related animals. Hayes has criticized the EPA for relying too heavily on studies conducted by atrazine’s manufacturer.

Said Blaustein, the Oregon State zoology professor: “Not only can these pesticides have direct effects, they can have indirect effects. They can kill you, they can screw up your physiology and anatomy and they can put you under stress and hamper your immune systems, so they are nasty.”

Throughout much of the world, urban development, introduced predators and diseases all play a role in the disappearance of native frogs, toads and other amphibians.

Diseases and parasites have killed many amphibians, but immune- suppressing chemicals might contribute to those deaths.

“In some ways it is the AIDS story,” Guillette said. “If you have reduced immune function you increase the chance of having a full blown infection that then sets you up for every other pathogen you come in contact with.”

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Rachel’s Democracy & Health News highlights the connections between issues that are often considered separately or not at all.

The natural world is deteriorating and human health is declining because those who make the important decisions aren’t the ones who bear the brunt. Our purpose is to connect the dots between human health, the destruction of nature, the decline of community, the rise of economic insecurity and inequalities, growing stress among workers and families, and the crippling legacies of patriarchy, intolerance, and racial injustice that allow us to be divided and therefore ruled by the few.

In a democracy, there are no more fundamental questions than, “Who gets to decide?” And, “How DO the few control the many, and what might be done about it?”

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Peter Montague – peter@rachel.org
Tim Montague – tim@rachel.org

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