Low levels of BPA exposure may be considered safe, but new research suggests otherwise

In the report, researchers from Yale show that the genome is permanently altered in the uterus of mice that had been exposed to BPA during their fetal development. These changes were found to mainly affect genes that are regulated by estrogen and are implicated in the formation of estrogen-related diseases such as infertility, endometriosis, endometrial cancer, osteoporosis, prostate cancer, neurodegenerative disease, obesity and breast cancer.

“Our study demonstrates that fetal exposure to BPA leads to a detrimental change in the adult uterine response to estrogens,” said Hugh S. Taylor, M.D., a senior researcher involved in the work and Chief of Obstetrics and Gynecology at Yale-New Haven Children’s Hospital at the Yale School of Medicine in New Haven, Connecticut. “Our study confirms that BPA is an active compound and can negatively impact fetal development and confirms that steps should be taken to reduce maternal consumption of BPA during gestation.”

To make this discovery, Taylor and colleagues used two groups of pregnant mice. One group was exposed to human ranges of BPA by intraperitoneal infusion and the other group was not. The researchers then analyzed the genetic and epigenetic profile of the uterus in the female offspring before sexual maturation and examined how the uterine genes responded to estrogen in each of these groups. They found that even though changes to the uterus may not be present at birth or in early post-natal life, changes become apparent after sexual maturity. The study demonstrated a direct change in the estrogen responses of almost 1,000 genes after fetal BPA exposure.

“This study reaches into the antecedent fetal exposure axis and reveals a striking, delayed onset of uterine gene expression effects in the offspring,” said Thoru Pederson, Ph.D., Editor-in-Chief of The FASEB Journal. “To the extent that these findings could be envisioned to translate to the human, we have in this study a very important body of information.”  Science Daily Original web page at Science Daily


Wood toxin could harm zoo animals

When those cute animals gnaw on wood enclosures at a zoo, they may be risking their health by ingesting toxic levels of arsenic, so zoo managers need to pay attention to the potential risk of the wood on zoo animals, a new University of Florida Institute of Food and Agricultural Sciences study shows.

The wood in question is treated with chromated copper arsenate (CCA), which can be toxic.

After visiting a zoo with her family, Julia Gress, a former post-doctoral researcher in the UF/IFAS soil and water sciences department, recognized that animals living in enclosures made from CCA-treated wood might face health risks.

Gress wanted to assess the impact of CCA-treated wood on arsenic exposures in zoo animals. She measured arsenic concentrations in soil from inside enclosures and on wipe samples of CCA-treated wood. Samples were taken from inside 17 wood enclosures, and also included crocodilian eggs, bird feathers, marmoset hair and porcupine quills.

Researchers found arsenic levels in soil that were higher than the U.S. Environmental Protection Agency’s risk-based level for birds and mammals. As well, arsenic levels in some animal tissues were also higher than those in other studies. Those findings should encourage zoo managers to limit animal exposure to arsenic found on the wood surface and in nearby soil, Gress said.

“Zoos care about the animals, which are often worth a lot of money,” said Gress, who conducted her search under the guidance of UF/IFAS soil and water sciences professor Lena Ma. Gress now works at the California Department of Toxic Substances Control in the Safer Consumer Products program.

CCA-treated wood is used in many structures. CCA preserves wood and extends its life by 20 to 40 years, but it contains large amounts of arsenic. CCA was withdrawn from use in most residential applications in 2004 because of health concerns over arsenic. Still, CCA-treated poles, fencing and plywood are still commonly used in areas where animals are housed, including barns, feedlots and zoos, according to the study.

“CCA wood is marketed for us in all types of agricultural applications, and there are instances of animals being poisoned from chewing on CCA wood in their animal enclosures, which is normal animal behavior,” Gress said.

In zoo settings, animals can experience long-term, daily exposure to contaminants, which concerns scientists trying to conserve threatened and endangered species, Gress said. The study is published in the journal Science of the Total Environment.  Science Daily  Original web page at Science Daily


Botulism in waterbirds: Mortality rates and new insights into how it spreads

Outbreaks of botulism killed large percentages of waterbirds inhabiting a wetland in Spain. During one season, more than 80 percent of gadwalls and black-winged stilts died. The botulinum toxin’s spread may have been abetted by an invasive species of water snail which frequently carries the toxin-producing bacterium, Clostridium botulinum, and which is well adapted to wetlands polluted by sewage. Global warming will likely increase outbreaks, said corresponding author Rafael Mateo, PhD. The research was published March 25th in Applied and Environmental Microbiology, a journal of the American Society for Microbiology.

Botulism is a major killer of waterbirds, including some endangered species. In earlier studies, some also published in Applied and Environmental Microbiology, these investigators had found that eutrophication of some of these wetlands, due to effluent from waste water treatment plants, was encouraging growth of C. botulinum and other bacterial pathogens of birds.

In the current study, the investigators surveyed mortality among the resident waterbirds, and investigated how the bacterium is spread. During two outbreaks, the investigators collected 43 dead white-headed ducks, representing seven percent and 17 percent of their maximum population on Navaseca lake during 2011 and 2012, respectively, said Mateo, who is Head of the Group of Wildlife Toxicology, at the Spanish Institute of Game and Wildlife Research, Cuidad Real, Spain. White-headed ducks are highly endangered, with only about ten thousand surviving individuals worldwide.

Additionally, the team found death rates of greater than 80 percent among gadwalls and black-winged stilts in 2011. Mortality estimates for white-headed ducks are probably low, said Mateo, explaining that scavengers frequently devour dead birds, and that it is difficult to find ailing or expired avians in the dense vegetation along the lake shore.

The team also investigated how the disease spreads. The main source of spread, previously known, is the “carcass-maggot cycle,” said Mateo. “Birds feed on maggots growing in a carcass containing C. botulinum and its neurotoxin,” and then die, with the cycle beginning anew as the dead birds become food for more maggots. “The spread of the outbreak is exponential,” said Mateo.

Additionally, the investigators found that 30 percent of an invasive species of freshwater snail, collected during outbreaks, carried C. botulinum. These snails, Physa acuta, are an invasive species that is well adapted to wetlands polluted by sewage. They are likely sources of food for a number of different waterbird species, including mallards, gulls, and coots, said Mateo.

Differences in diets result in different levels of vulnerability among bird species. Flamingos and grebes appeared untouched by outbreaks, likely because they appear to feed mainly on prey species that do not carry C. botulinum, such as certain crustaceans, and/or possibly because they are more resistant genetically than other species to this pathogen.

Mateo warned that outbreaks would likely occur more frequently due to global warming. In earlier research, also published in Applied and Environmental Microbiology, his group showed that higher summer temperatures are associated with higher mortality rates among waterbirds during outbreaks. “We have observed that outbreaks occur when the mean temperature in July exceeds 26˚C [79˚F.],” he said. Additionally, when water is scarce due to drought, wetlands eutrophy more frequently, which favors anaerobic bacteria such as C. botulinum. Finally, birds tend to concentrate in the few wetlands that are maintained with treated sewage, which boosts mortality from botulism and other diseases, he said.

These wetlands, which are located in La Mancha, which was made famous by the novel, Don Quixote, and which are rich in biodiversity, are a UNESCO “biosphere reserve.” Their unique habitat is important for many bird species, including migratory birds that breed there, such as the afore-mentioned white-headed duck. But outbreaks of botulism are common. “We wanted to characterize the ecology of the avian botulism in these wetlands to know to what degree human action–notably poor treatment of sewage–was determining the outbreaks’ occurrence,” said Mateo.  Science Daily  Original web page at Science Daily


Testing detects algal toxins in Alaska marine mammals

Toxins from harmful algae are present in Alaskan marine food webs in high enough concentrations to be detected in marine mammals such as whales, walruses, sea lions, seals, porpoises and sea otters, according to new research from NOAA and its federal, state, local and academic partners.

The findings, reported online today in the journal Harmful Algae, document a major northward expansion of the areas along the Pacific Coast where marine mammals are known to be exposed to algal toxins. Since 1998, algal toxin poisoning has been a common occurrence in California sea lions in Central California. However, this report is the first documentation of algal toxins in northern ranging marine mammals from southeast Alaska to the Arctic Ocean.

“What really surprised us was finding these toxins so widespread in Alaska, far north of where they have been previously documented in marine mammals,” said Kathi Lefebvre, a NOAA Fisheries research scientist who led the study. “However, we do not know whether the toxin concentrations found in marine mammals in Alaska were high enough to cause health impacts to those animals. It’s difficult to confirm the cause of death of stranded animals. But we do know that warming trends are likely to expand blooms, making it more likely that marine mammals could be affected in the future.”

The Wildlife Algal-toxin Research and Response Network for the West Coast (WARRN-West) tested samples from more than 900 marine mammals that were harvested or found stranded in Alaska from 2004 to 2013. Testing found the algal toxins, domoic acid and saxitoxin, present in low levels in some animals from each of the 13 marine mammal species examined, and from all regions in Alaska.

The levels of these algal toxins were well below the seafood safety regulatory limits. Gay Sheffield of the University of Alaska Fairbanks and coauthor of this study, however, warned that clams found in the stomachs of harvested walruses and bearded seals that are often eaten in several coastal communities throughout western and northern Alaska may contain algal toxins. Commonly eaten animal parts like muscle and blubber are not likely to accumulate these toxins in levels of concern for human consumption, and there is no change in the current guidance from the Alaska Department of Health regarding seafood safety.

Lefebvre highlighted the critical role the WARRN-West Network partners played by providing samples for the study. “By consistently submitting samples from stranded and harvested marine mammals, their work was essential to our research,” said Lefebvre. The WARRN-West network, funded by NOAA Fisheries with support from network partners, will continue surveillance for algal toxins in marine mammals.  Science Daily  Original web page at Science Daily


Its complicated: Benefits and toxicity of antiprion antibodies in the brain

Immunotherapy to ameliorate neurodegeneration by targeting brain protein aggregates with antibodies is an area of intense investigation. A study published on January 28th in PLOS Pathogens examines seemingly contradictory earlier results of targeting the prion protein and proposes a cautionary way forward to further test related therapeutic approaches.

Damaging aggregation of proteins in the brain is a hallmark of several neurodegenerative diseases, including Alzheimer and Parkinson diseases. In prion diseases such as Creutzfeld-Jakob disease, aggregates of abnormally folded versions of the PrP protein cause the death of brain cells. The use of anti-PrP antibodies to target such aggregates and mediate their destruction by the immune system has been proposed as a therapy, with the caveat that such antibodies could themselves be toxic.

Prompted by the publication of seemingly contradictory reports on the potential neurotoxicity of antibodies against the prion protein in mice, Adriano Aguzzi from the University of Zurich, Switzerland, and colleagues set out to rigorously test several antibodies side-by-side. The researchers examined whether toxicity was influenced by where and how the antibodies were delivered into the brain, the antibody dose, which area on the PrP protein the antibodies bind to, and the genetic background of the mice.

For several of the antibodies, they found, toxicity depended strictly on the administered dose, results that could explain some of the seemingly different earlier results. Other factors tested, including which target regions (or epitopes) on the PrP protein the antibodies bound to, also seemed to affect the toxicity of at least some antibodies.

Because the researchers observed toxicity for most of the antibodies that bind to the so-called globular region of PrP, they conclude that such antibodies might not be suitable for immunotherapy. In contrast, since no toxicity was found in tests of antibodies against the flexible tail region of PrP, they suggest that those might be more promising candidates.

“In summary,” they say, “these data illustrate that the efficacy profile (i.e. the curative effectiveness versus the potential toxicity) of anti-prion antibodies is complex and depends both on intrinsic factors such as, crucially, the nature of the engaged epitope, and extrinsic factors such as the route of administration. Detailed analyses and mapping of the involved epitopes and–most importantly–appropriate dose-escalation studies in vivo are prerequisite not only for preparing clinical trials in humans, but also to avoid the reporting of contradictory, confusing, and potentially misleading results.”  Science Daily  Original web page at Science Daily


*First brain scans of sea lions give clues to strandings

Brain scans and behavioral tests of California sea lions that stranded on shore show how an algal toxin disrupts brain networks, leading to deficits in spatial memory, according to a study to be published Dec. 18 in Science. The new findings by scientists at the University of California Santa Cruz, UC Davis and the Marine Mammal Center in Sausalito, Calif. suggest that chronic exposure to the toxin domoic acid, produced by naturally occurring marine algae, affects sea lions’ ability to navigate in their ocean habitat and survive in the wild.

Blooms of the toxic algae typically occur in the spring and fall along the California coast, but have been increasing in frequency and severity. Hundreds of sea lions strand on California beaches every year with symptoms of domoic acid poisoning, including disorientation and seizures.

A team led by Peter Cook, then a graduate student at UC Santa Cruz and now at Emory University, studied 30 California sea lions undergoing veterinary care and rehabilitation at the Marine Mammal Center in Sausalito. Researchers administered behavioral tests to assess spatial memory and performed brain imaging (MRI) to see the extent of brain lesions in the affected animals.

Damage to the hippocampus, a part of the brain involved in memory, is often seen in sea lions with domoic acid poisoning, Cook said. “In this study, we were able to correlate the extent of hippocampal damage to specific behavioral impairments relevant to the animals’ survival in the wild,” he said.

Working with Professor Charan Ranganath’s Dynamic Memory Laboratory at the UC Davis Center for Neuroscience, Cook adapted behavioral tests usually used to assess memory in rats to sea lions. For example, in a ‘T-maze,’ an animal has to remember that if it got a treat by turning right, the next time it takes the test it gets a treat by turning left. Cook also consulted with the UC Davis Alzheimer’s Disease Center on how to use MRI scans to quantify damage to brain structures such as the hippocampus.

With MRI, the researchers could see structural damage in the brains of affected sea lions, especially in the hippocampus. This looped structure in the center of the brain is known to be important for memory processes in humans and rodents. Animals with damage to the hippocampus showed impaired performance on short-and long-term spatial memory tasks, the researchers found.

“We could see structural differences, so we decided to get some functional data while the animals were in the scanner,” Ranganath said. While an anesthetized animal is in the scanner, brain regions continue to share information back and forth.

With a grant from Siemens, the team was able to use equipment never previously used for marine mammals to look at how different brain regions talk to each other. They found that in addition to visible damage to the hippocampus, there were effects on interactions between the hippocampus and other brain structures, notably the thalamus.

“This is the first evidence of changes to brain networks in exposed sea lions, and suggests that these animals may be suffering a broad disruption of memory, not just spatial memory deficits,” Cook said.

The study provides the missing link, Ranganath said, between the environmental degradation that leads to toxic algal blooms and sea lion strandings.

“We didn’t know exactly why the algae lead to strandings. But sea lions are dynamically foraging — and for an animal like that, if you don’t know where you are, you have a big problem,” he said.

These memory deficits may also help explain anecdotal reports of sea lions showing up in unusual places far outside their normal range, either too far out at sea or inland far from the coast, according to coauthor Colleen Reichmuth, director of the Pinniped Cognition and Sensory Systems Laboratory at UC Santa Cruz where the behavioral tests were conducted.

Brain lesions may develop over time with repeated exposure to the toxin. Sea lions with symptoms of brain damage strand on beaches all year round, even when there is no active bloom of the toxic algae.

“What isn’t well understood yet is the dose response,” Cook said. “We don’t know how heavy the exposure needs to be, or how often repeated, to cause this kind of brain damage, and we don’t know the effects of repeated low-dose exposure.”  Science Daily  Original web page at Science Daily


Data scientists create world’s first therapeutic venom database

What doesn’t kill you could cure you. A growing interest in the therapeutic value of animal venom has led a pair of Columbia University data scientists to create the first catalog of known animal toxins and their physiological effects on humans.

VenomKB, short for Venom Knowledge Base, summarizes the results of 5,117 studies in the medical literature describing the use of venom toxins as painkillers and as treatments for diseases like cancer, diabetes, obesity, and heart failure. Drawn from an automated analysis of the literature, VenomKB documents nearly 42,723 effects on the body. Though modern medicine makes use of only a small fraction of the toxins documented thus far, the researchers hope that the catalog will spur the discovery of new compounds and medical treatments.

“With this list we can take stock of what we know about venoms and their therapeutic effects” said Nicholas Tatonetti, an assistant professor of biomedical informatics at Columbia University Medical Center and a member of the Data Science Institute. “The questions now is: How can we use this information with other databases to discover new compounds and therapies?”

Tatonetti and Joseph Romano, a graduate student, searched on the term “venoms/therapeutic use” in a database of 22 million medical research papers. This produced a list of 5,117 venom-related studies whose results they summarized using a pair of computer algorithms. After cross-referencing toxins and drugs listed under multiple names and correcting other irregularities in the data, they found 42,723 unique mentions of venoms having a specific effect on the body. Their results are published in a companion study to Venom KB in the journal Scientific Data.

Venom’s capacity to heal is paradoxically linked to its fast-acting, lethal effects in the wild. Found in more than 173,000 species, venoms evolved over millions of years to target molecules that are often involved in disease. The toxic proteins and amino acids known as peptides that make up venom act on cell receptors and ion channels, controlling how cells behave.

By mimicking or altering how these toxins act on specific human cells, researchers can develop drugs that inhibit pain or treat diseases, often with fewer side effects than those of drugs already on the market.

About a dozen major drugs have emerged from this strategy so far, National Geographic magazine reported in 2013. One of the first, an anticoagulant called Arvin, gained favor in the late 1960s after a doctor discovered that ancrod, a protein found in the venom of the Malayan pit viper, could treat blood clots in the legs.

The widely used type 2 diabetes drug Byetta, is made from the toxin exenatide, found in the saliva of the venomous Gila monster, a lizard native to the United States and Mexico.

Another drug, bombesin, uses a toxin found in the skin of the venomous European fire-bellied toad to treat gastrointestinal disorders. Bombesin’s ability to bind to neuronal tumors has led to interest in developing a florescent version that could guide surgeons around the edges of a tumor.

Five compounds produced by the venomous cone snail have made it to clinical trials, including ziconotide, the generic term for an analgesic similar to morphine.

The Malayan pit viper, Gila monster, European fire-bellied toad, and cone snail account for about 18 percent of the 5,117 venom-related studies now catalogued in Venom KB. Yet there are 10 million or more venomous species that have yet to be studied. Zoltan Takacs, a toxinologist who earned his PhD in evolutionary studies at Columbia, estimates there are 20 million venom toxins waiting to be screened.

Venom KB got its start after Romano approached Tatonetti, his thesis adviser, about studying medicinal uses of venom. Tatonetti suggested that Romano start looking through the venom database. To their surprise there was neither a database nor a list. Still modest in size, VenomKB is expected to grow more useful as researchers contribute more data. “With a large enough library we can screen for more effective, safer compounds,” said Romano.

Databases of compounds and their biological effects have been used in recent years to discover and develop new drugs as well as uncover problems with drugs already in use. Tatonetti and his colleagues mined a federal database of documented drug side effects, the FDA Adverse Event Reporting System (FAERS), and discovered that the interaction of the anti-depressant paroxetine, sold under the brand name Paxil, and the statin pravastatin, sold as Pravachol, could raise blood glucose levels in diabetic patients.

With VenomKB up and running, Tatonetti and Romano plan to contribute data of their own. Starting with samples of dried venom from the black mamba, they will perform experiments and explore new treatments for chronic pain, diabetes and heart disease.   Science Daily  Original web page at Science Daily


Births down and deaths up in Gulf dolphins

A NOAA-led team of scientists is reporting a high rate of reproductive failure in dolphins exposed to oil from the Deepwater Horizon spill. The team has monitored these bottlenose dolphins in heavily-oiled Barataria Bay for five years following the spill. Their findings, published in Proceedings of the Royal Society today, suggest that the effects of the Deepwater Horizon oil spill will be long-lasting.

The study assessed reproductive success and survival rate for Barataria Bay dolphins. These dolphins had been sampled for health assessments in 2011, and were found to have a high prevalence of lung disease and adrenal dysfunction. Now the team is reporting that only 20% of the sampled dolphins that were pregnant produced viable calves. This is compared to a previously-reported pregnancy success rate of 83% from a similar study in a dolphin population in Sarasota Bay, which was not affected by the spill.

After nearly four years of monitoring, scientists were also able to estimate the survival rate of the dolphins sampled in 2011. They found that only 86.8% of the dolphins survived each year, as compared to other populations where roughly 95% of the dolphins survived. The reduced reproductive potential, along with decreased survival, will have long-term consequences for the Barataria Bay dolphin population.

In August of 2011, a team of independent and NOAA scientists evaluating the health of bottlenose dolphins in Louisiana’s Barataria Bay gave dolphin Y35 a good health outlook. Based on the ultrasound, she was in the early stages of pregnancy, but unlike many of the other dolphins examined that summer day, Y35 was in pretty good shape. She wasn’t extremely underweight or suffering from moderate-to-severe lung disease, conditions connected to exposure to Deepwater Horizon oil in the heavily impacted Barataria Bay.

Veterinarians did note, however, that she had alarmingly low levels of important stress hormones responsible for behaviors such as the fight-or-flight response. Normal levels of these hormones help animals cope with stressful situations. This rare condition–known as hypoadrenocorticism–had never been reported before in dolphins, which is why it was not used for Y35 and the other dolphins’ health prognoses.

Less than six months later, researchers spotted Y35 for the last time. It was only 16 days before her expected due date. She and her calf are now both presumed dead, a disturbingly common trend among the bottlenose dolphins that call Barataria Bay their year-round home.

This trend of reproductive failure and death in Gulf dolphins over five years of monitoring after the 2010 Deepwater Horizon oil spill is outlined in a November 2015 study led by NOAA and published in the peer-reviewed journal Proceedings of the Royal Society.

Of the 10 Barataria Bay dolphins confirmed to be pregnant during the 2011 health assessment, only two successfully gave birth to calves that have survived. This unusually low rate of reproductive success–only 20%–stands in contrast to the 83% success rate in the generally healthier dolphins being studied in Florida’s Sarasota Bay, an area not affected by Deepwater Horizon oil.

While hypoadrenocorticism had not been documented previously in dolphins, it has been found in humans. In human mothers with this condition, pregnancy and birth–stressful and risky enough conditions on their own–can be life-threatening for both mother and child when left untreated. Wild dolphins with this condition would be in a similar situation.

Mink exposed to oil in an experiment ended up exhibiting very low levels of stress hormones, while sea otters exposed to the Exxon Valdez oil spill experienced high rates of failed pregnancies and pup death. These cases are akin to what scientists have observed in the dolphins of Barataria Bay after the Deepwater Horizon oil spill.

Among the pregnant dolphins being monitored in this study, at least two lost their calves before giving birth. Veterinarians confirmed with ultrasound that one of these dolphins, Y31, was carrying a dead calf in utero during her 2011 exam. Another pregnant dolphin, Y01, did not successfully give birth in 2012, and was then seen pushing a dead newborn calf in 2013. Given that dolphins have a gestation of over 12 months, this means Y01 had two failed pregnancies in a row.

The other five dolphins to lose their calves after the Deepwater Horizon oil spill, excluding Y35, survived pregnancy themselves but were seen again and again in the months after their due dates without any young. Dolphin calves stick close to their mothers’ sides in the first two or three months after birth, indicating that these pregnant dolphins also had calves that did not survive.

At least half of the dolphins with failed pregnancies also suffered from moderate-to-severe lung disease, a symptom associated with exposure to petroleum products. The only two dolphins to give birth to healthy calves had relatively minor lung conditions.

Dolphin Y35 wasn’t the only one of the 32 dolphins being monitored in Barataria Bay to disappear in the months following her 2011 examination. Three others were never sighted again in the 15 straight surveys tracking these dolphins. Or rather, they were never seen again alive. One of them, Y12, was a 16-year-old adult male whose emaciated carcass washed up in Louisiana only a few weeks before the pregnant Y35 was last seen. In fact, the number of dolphins washing up dead in Barataria Bay from August 2010 through 2011 was the highest ever recorded for that area.

Survival rate in this group of dolphins was estimated at only 86%, down from the 95-96% survival seen in dolphin populations not in contact with Deepwater Horizon oil. The marshy maze of Barataria Bay falls squarely inside the footprint of the Deepwater Horizon oil spill, and its dolphins and others along the northern Gulf Coast have repeatedly been found to be sick and dying in historically high numbers. Considering how deadly this oil spill has been for Gulf bottlenose dolphins and their young, researchers expect recovery for these marine mammals to be a long time coming.   Science Daily  Original web page at Science Daily


Chernobyl: At site of world’s worst nuclear disaster, the animals have returned

In 1986, after a fire and explosion at the Chernobyl Nuclear Power Plant released radioactive particles into the air, thousands of people left the area, never to return. Now, researchers reporting in the Cell Press journal Current Biology on October 5 have found that the Chernobyl site looks less like a disaster zone and more like a nature preserve, teeming with elk, roe deer, red deer, wild boar, and wolves.

The findings are a reminder of the resilience of wildlife. They may also hold important lessons for understanding the potential long-term impact of the more recent Fukushima disaster in Japan.

“It’s very likely that wildlife numbers at Chernobyl are much higher than they were before the accident,” says Jim Smith of the University of Portsmouth in the UK. “This doesn’t mean radiation is good for wildlife, just that the effects of human habitation, including hunting, farming, and forestry, are a lot worse.”

Earlier studies in the 4,200 km2 Chernobyl Exclusion Zone showed major radiation effects and pronounced reductions in wildlife populations. The new evidence, based on long-term census data, now shows that mammal populations have bounced back.

The relative abundance of elk, roe deer, red deer, and wild boar within the exclusion zone are now similar to those in four uncontaminated nature reserves in the region, the researchers report. The number of wolves living in and around the Chernobyl site is more than seven times greater than can be found in those nature reserves.

Helicopter survey data also reveal rising trends in the abundance of elk, roe deer, and wild boar from 1 to 10 years after the accident. A dip in the wild boar population at one point was traced to a disease outbreak unrelated to radiation exposure.

“These results demonstrate for the first time that, regardless of potential radiation effects on individual animals, the Chernobyl Exclusion Zone supports an abundant mammal community after nearly three decades of chronic radiation exposure,” the researchers conclude. They note that these increases came at a time when elk and wild boar populations were declining in other parts of the former Soviet Union.

“I’ve been working, studying, and taking photos of the wonderful wildlife in the Chernobyl area for over 20 years and am very pleased our work is reaching an international scientific audience,” says Tatiana Deryabina from the Polessye State Radioecological Reserve in Belarus, a few miles from the site of the Chernobyl accident.

“These unique data showing a wide range of animals thriving within miles of a major nuclear accident illustrate the resilience of wildlife populations when freed from the pressures of human habitation,” says Jim Beasley, a study co-author at the University of Georgia.  Science Daily  Original web page at Science Daily


* Mice exposed to environmental chemicals may show decreased physical activity in offspring

Endocrine disruptors are contaminants that interfere with endocrine or hormone systems and can cause tumors, birth defects and developmental disorders in mammals. Often, these contaminants are used in a variety of consumer products, such as water bottles, dental composites and resins used to line metal food and beverage containers. Now, a University of Missouri study suggests that female mice exposed to these environmental chemicals may cause decreases in their daughter’s metabolism and the amount of exercise and voluntary physical activity they engage in later in life. These disruptors when introduced in developmental stages, are essentially creating “couch potatoes” among female mice and could predict future metabolic complications, researchers say.

“We found that if we exposed mice to one of two common endocrine disruptors- bisphenol A (BPA) or ethinyl estradiol (EE), which is the estrogen present in birth control pills, during development, it caused later disruptions in voluntary physical activity once the mice became adults,” said Cheryl Rosenfeld, associate professor of biomedical sciences in the College of Veterinary Medicine and a researcher in the Bond Life Sciences Center at MU. “Mice exposed to endocrine disruptors move around less, are more likely to sleep and engage in less voluntary physical activity.”

To test the chemicals’ impact on metabolism and activity, Rosenfeld’s lab exposed mice to BPA and EE in the womb and during weaning through the mother’s diet. A third group of mice whose mothers were placed on a control diet and were thus not exposed to either chemical. At weaning, the scientists then placed all the mice on the same control diet and measured their energy expenditure, body composition and level of voluntary physical activity as adults.

To further test the effects of voluntary exercise, the lab rigged bicycle computers to “hamster wheels” to track how far, fast and for how long the mice ran. Researchers monitored the mice’s energy expenditure by measuring oxygen consumption and carbon dioxide production, and tracked the rodents’ movements during the day and at night.

“Female mice exposed to BPA and EE were less active than the control mice,” Rosenfeld said. “They moved around less at night–when these mice are typically most active–and moved more slowly, drank less water, and spent more time sleeping. In addition, BPA-exposed females burned more carbohydrates relative to fats, as compared to control mice. This is similar to the difference between obese and slender humans, and many researchers believe that burning more carbohydrates relative to fats can lead to fats gradually accumulating in the body.”

The researchers currently are conducting follow-up studies to determine if the changes caused by exposure to BPA and EE predispose mice to obesity and other metabolic disorders. “Our findings are significant because decreased voluntary physical activity, or lack of exercise, can predispose animals or humans to cardiovascular diseases, metabolic disorders and even cancer,” Rosenfeld said.  Science Daily  Original web page at Science Daily


* Plastic in 99 percent of seabirds by 2050

Researchers from CSIRO and Imperial College London have assessed how widespread the threat of plastic is for the world’s seabirds, including albatrosses, shearwaters and penguins, and found the majority of seabird species have plastic in their gut.

The study, led by Dr Chris Wilcox with co-authors Dr Denise Hardesty and Dr Erik van Sebille and published today in the journal PNAS, found that nearly 60 per cent of all seabird species have plastic in their gut. Based on analysis of published studies since the early 1960s, the researchers found that plastic is increasingly common in seabird’s stomachs. In 1960, plastic was found in the stomach of less than 5 per cent of individual seabirds, rising to 80 per cent by 2010.

The researchers predict that plastic ingestion will affect 99 per cent of the world’s seabird species by 2050, based on current trends. The scientists estimate that 90 per cent of all seabirds alive today have eaten plastic of some kind. This includes bags, bottle caps, and plastic fibres from synthetic clothes, which have washed out into the ocean from urban rivers, sewers and waste deposits.

Birds mistake the brightly coloured items for food, or swallow them by accident, and this causes gut impaction, weight loss and sometimes even death. “For the first time, we have a global prediction of how wide-reaching plastic impacts may be on marine species — and the results are striking,” senior research scientist at CSIRO Oceans and Atmosphere Dr Wilcox said.

“We predict, using historical observations, that 90 per cent of individual seabirds have eaten plastic. This is a huge amount and really points to the ubiquity of plastic pollution.” Dr Denise Hardesty from CSIRO Oceans and Atmosphere said seabirds were excellent indicators of ecosystem health.

“Finding such widespread estimates of plastic in seabirds is borne out by some of the fieldwork we’ve carried out where I’ve found nearly 200 pieces of plastic in a single seabird,” Dr Hardesty said.

The researchers found plastics will have the greatest impact on wildlife where they gather in the Southern Ocean, in a band around the southern edges of Australia, South Africa and South America. Dr van Sebille, from the Grantham Institute at Imperial College London, said the plastics had the most devastating impact in the areas where there was the greatest diversity of species. “We are very concerned about species such as penguins and giant albatrosses, which live in these areas,” Erik van Sebille said. “While the infamous garbage patches in the middle of the oceans have strikingly high densities of plastic, very few animals live here.

Dr Hardesty said there was still the opportunity to change the impact plastic had on seabirds.

“Improving waste management can reduce the threat plastic is posing to marine wildlife,” she said. “Even simple measures can make a difference. Efforts to reduce plastics losses into the environment in Europe resulted in measureable changes in plastic in seabird stomachs with less than a decade, which suggests that improvements in basic waste management can reduce plastic in the environment in a really short time.

The work was carried out as part of a national marine debris project supported by CSIRO and Shell’s Social investment program as well as the marine debris working group at the National Center for Ecological Analysis and Synthesis, University of California, Santa Barbara, with support from Ocean Conservancy. Science Daily  Original web page at

Science Daily


* Novel fatigue syndrome in feedlot cattle discovered

Researchers at Kansas State University’s College of Veterinary Medicine, in collaboration with colleagues at Iowa State University and Texas Tech University, have discovered a novel fatigue syndrome affecting feedlot cattle. The syndrome is similar to one affecting the swine industry.

The researchers’ landmark paper, “Description of a novel fatigue syndrome of finished feedlot cattle following transportation,” appeared as a special report in the July 15 issue of the Journal of the American Veterinary Medical Association.

“This syndrome has been identified in the swine industry and had not been identified in cattle until our work that started in 2013,” Thomson said. “Our landmark paper places an emphasis on cattle stress at the end of the feeding period with items such as heat load, animal size, cattle handling at shipping, time of day of shipping, animal transportation and other issues that could be causing stress of large cattle during the summer time.”

The study was spurred by observations made during summer 2013. Abattoirs throughout the United States reported concerns about slow and difficult-to-move cattle and other mobility problems that developed soon after arrival at the facilities. Affected cattle had various clinical signs, including rapid breathing with an abdominal component to respiration, lameness and reluctance to move. Many of the cattle affected with mobility problems had clinical signs similar to those of pigs with fatigued pig syndrome, a multifactorial condition in which affected pigs become nonambulatory without obvious injury, trauma or disease, and refuse to walk.

“I think this paper is the first publication of the interaction between beta-agonists and lameness issues in cattle,” Ensley said. “The beta-agonists are widely used in cattle and pig feeding and there is very little information about adverse effects. More work needs to be done, but this is a great start.”

Beta-agonists are supplements fed to cattle. Part of the pathophysiology points to a metabolic overload of sorts that result in or from respiratory insufficiency and muscle damage, Loneragan said. “While we don’t know the cause, it appears to be multifactorial in nature, but warrants further investigation,” Loneragan said. “It is important to be able to share case reports like the ones described. While it is not always as thorough as a case report of hospitalized animals, these field-based observations are nevertheless of value and under Dr. Thomson’s leadership, we were able to dig relatively deeply into these events and provide a report to share with our profession.”

Also described in the manuscript is a problematic condition — possibly an extreme endpoint of the fatigued cattle syndrome — where animals sloughed one or more hooves. “Based on microscopic examination, this appears to be a distinct condition and is likely not laminitis resulting from dietary disturbances,” Loneragan said. “It is clear this results in intense pain for the animals. The abattoir companies have decided that events like these are unacceptable, and I applaud their dedication and commitment to protecting the welfare of the animals they depend on for their business and we depend on for food.”

The study concludes it would be imperative for the beef industry and affiliated veterinarians to learn quickly as much as possible about fatigue cattle syndrome so measures can be implemented to prevent the condition, or at least minimize its impact on cattle welfare.  Science Daily  Original web page at   Science Daily


Racehorses at risk from misuse of cobalt, new study finds

In a new study published in The Veterinary Journal, scientists from the University of Surrey warn about the numerous risks posed to racehorses from the misuse of cobalt chloride, a banned performance-enhancing agent that has been used illegally by trainers in Australia and USA. The team of researchers have uncovered that when excessive levels of the alleged performance-enhancing substance are administered to a horse, it can cause serious cardiovascular issues, potential nerve problems, thickening of the blood and thyroid toxicity. The researchers also pointed to the lack of evidence for enhanced performance in horses and human athletes.

Cobalt, required by all horses in order to survive, is normally present at very low levels through various feedstuffs. However, excessive amounts of impure formulations of the substance, which can be administered easily as a powder, feed supplement or injection, can lead to severe side effects, such as long-term damage to vital organs such as the heart. Indeed in humans, cobalt salts have been used in the past to treat rare forms of anemia. However, it has been associated with a variety of adverse effects, including gastrointestinal neurologic, cardiovascular, and thyroid problems, and as a result, its use has been discontinued.

Not a prescription medication, various cobalt salts are available from a variety of commercial sources. The salts are impure and are inexpensive, easily accessible and not subject to medicines regulation. “We have grave concerns over a potentially lethal practice in the race horsing industry, and are most concerned that some trainers continue to use Google as their source of information,” said lead author Professor Ali Mobasheri from the University of Surrey.

“It is the duty of veterinary surgeons working in the industry to ensure that horse trainers are aware of the dangers of its ‘amateur’ use. “Currently there is no evidence to suggest that cobalt chloride can enhance human or equine athletic performance. It is our hope that this study will increase greater awareness and prompt a broader discussion about the misuse of this substance.”  Science Daily  Original web page at Science Daily


Neurotoxin found in commercial seafood

Popular commercial seafood purchased from Swedish supermarkets at the Stockholm region contains Beta-Methylamino-L-Alanine (BMAA). BMAA is a naturally-occurring amino acid with a possible link to neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease and Amyotrophic lateral sclerosis. It is the first screening study to measure BMAA in commercial seafood from metropolitan markets.

Popular commercial seafood purchased from Swedish supermarkets at the Stockholm region contains Beta-Methylamino-L-Alanine (BMAA), shows a doctoral thesis from Stockholm University. BMAA is a naturally-occurring amino acid with a possible link to neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease and Amyotrophic lateral sclerosis. It is the first screening study to measure BMAA in commercial seafood from metropolitan markets. “We detected BMAA in blue mussel, oyster, shrimp, plaice, char and herring but not in salmon, cod, perch and crayfish,” says Liying Jiang, PhD student at the Department of Environmental Science and Analytical Chemistry (ACES), Stockholm University.

Amino acids are the building blocks of proteins. There are 20 amino acids commonly used in making proteins but BMAA is not one of them. It is not clear how BMAA should be able to lead to the onset of neurodegenerative diseases. It has been discussed that BMAA may be mistakenly incorporated into proteins during synthesis and, in turn, goes on to change their normal shape and function leading to the onset or the speeding up the progress of neurodegenerative diseases.

The amino acid BMAA was first isolated and identified in extracts from the seeds of cycad trees in the West Pacific island of Guam in 1967. BMAA was potentially linked to the neurodegenerative diseases that were prevalent in Guam during the 1950’s, as an important environmental risk factor. “The BMAA producers in nature were reported to be phytoplankton, found at the bottom of the food chain. In this scenario, the entry of BMAA into the food web is inevitable.” says Liying Jiang, PhD student at the Department of Environmental Science and Analytical Chemistry (ACES), Stockholm University.

According to the Food and Agricultural Organisation of the United Nations, the average consumption of seafood per capita in Sweden during 2005-2007 was estimated at 28.7 kg/year, i.e. 0.6 kg/week. Liying Jiang points out that consumers can rest assured knowing that the levels of BMAA she and her colleagues measured in commercial seafood are too low to have any direct toxic effects on animals and let alone in humans. However, Liying Jiang emphasises that we should exercise caution due to the limited data available on the distribution and function of BMAA.

“It has been suggested that BMAA may be a slow toxin, possibly with a biomagnification potential, meaning that its levels could rise the higher up in the food chain it is found. Consequently it is important to monitor its distribution in our environment and understand the means by which it gets stored and released by organisms. These are necessary aspects that need to be addressed,” says Liying Jiang, PhD student at the Department of Environmental Science and Analytical Chemistry (ACES), Stockholm University.  Science Daily  Original web page at Science Daily


* ‘Flameproof’ falcons and hawks: Most polluted bird on record found in Vancouver

A Cooper’s hawk, found in Greater Vancouver, is the most polluted wild bird that has been found anywhere in the world. A team of Canadian researchers made this startling discovery while analyzing liver samples from birds of prey that were discovered either injured or dead in the Vancouver area.

The levels of polybrominated diphenyl ethers (PBDEs) in the contaminated Cooper’s hawk were 196 parts per million, significantly higher than those recorded in birds found either in cities in California or in an electronic waste site in China. PBDEs are a group of chemicals that act as flame retardants and were once used widely in computers, stereos, televisions, vehicles, carpets and furniture. Although many of the PBDEs have been banned since the 2000s in Canada, they continue to accumulate in landfill sites where people dispose of PBDE-rich items. In British Columbia’s Fraser River delta, for example, the quantity of PBDEs has doubled every four years over the past four decades. This can have a significant effect on the bird populations that live nearby.

“Many animals, including coyotes, eagles and hawks benefit from the excess food in our cities. A downside is the high levels of pollution. The levels of flame retardants in starlings, a favourite prey of hawks, which nested near the landfill site were fifteen times higher than levels in starlings found elsewhere in Vancouver,” says Prof. Kyle Elliott, of McGill’s Department of Natural Resource Sciences, one of the authors of the study which was recently published in the journal Science of the Total Environment. “We were surprised to see such high levels of contaminants in what I think of as ‘green’ city. We can only hope that because many forms of PBDEs have now been banned and the levels of these contaminants are rapidly disappearing from herons and cormorants in Vancouver, the same will be true for other bird species.”  Science Daily

Original web page at Science Daily


Mercury levels in Hawaiian yellowfin tuna increasing

Mercury concentrations in Hawaiian yellowfin tuna are increasing at a rate of 3.8 percent or more per year, according to a new University of Michigan-led study that suggests rising atmospheric levels of the toxin are to blame. Mercury is a potent toxin that can accumulate to high concentrations in fish, posing a health risk to people who eat large, predatory marine fish such as swordfish and tuna. In the open ocean, the principal source of mercury is atmospheric deposition from human activities, especially emissions from coal-fired power plants and artisanal gold mining.

For decades, scientists have expected to see mercury levels in open-ocean fish increase in response to rising atmospheric concentrations, but evidence for that hypothesis has been hard to find. In fact, some studies have suggested that there has been no change in mercury concentration in ocean fish. By compiling and re-analyzing three previously published reports on yellowfin tuna caught near Hawaii, U-M’s Paul Drevnick and two colleagues found that the concentration of mercury in that species increased at least 3.8 percent per year from 1998 to 2008. A paper about the study is scheduled for online publication in the journal Environmental Toxicology and Chemistry on Feb. 2. The other authors are Carl Lamborg of the Woods Hole Oceanographic Institution, now at the University of California at Santa Cruz, and Martin Horgan.

“The take-home message is that mercury in tuna appears to be increasing in lockstep with data and model predictions for mercury concentrations in water in the North Pacific,” said Drevnick, an assistant research scientist at the U-M School of Natural Resources and Environment and at the U-M Biological Station. “This study confirms that mercury levels in open ocean fish are responsive to mercury emissions.” Drevnick and his colleagues reanalyzed data from three studies that sampled the same yellowfin tuna population near Hawaii in 1971, 1998 and 2008. In each of the three studies, muscle tissues were tested for total mercury, nearly all of which was the toxic organic form, methylmercury. In their re-analysis, Drevnick and his colleagues included yellowfins between 48 and 167 pounds and used a computer model that controls for the effect of fish body size. Data from 229 fish were analyzed: 111 from 1971, 104 from 1998 and 14 from 2008. The researchers found that mercury concentrations in the yellowfins did not change between the 1971 and 1998 datasets. However, concentrations were higher in 2008 than in either 1971 or 1998. Between 1998 and 2008, the mercury concentration in yellowfins increased at a rate greater than or equal to 3.8 percent a year, according to the new study. “Mercury levels are increasing globally in ocean water, and our study is the first to show a consequent increase in mercury in an open-water fish,” Drevick said. “More stringent policies are needed to reduce releases of mercury into the atmosphere. If current deposition rates are maintained, North Pacific waters will double in mercury by 2050.” Yellowfin tuna, often marketed as ahi, is widely used in raw fish dishes — especially sashimi — or for grilling. The Natural Resources Defense Council’s guide to mercury in sushi lists yellowfin tuna as a “high mercury” species. Science Daily Original web page at Science Daily


Are all rattlesnakes created equal? No, maybe not

But new research by a team of biologists at Florida State University has revealed that creating antivenom is a bit tricky. That’s because the type of venom a snake produces can change according to where it lives. Mark Marges, a Florida State doctoral student in Professor Darin Rokyta’s laboratory, led a research study that examined the venom of 65 eastern diamondback rattlesnakes and 49 eastern coral snakes from all over the state of Florida to determine whether snake venoms varied by geography. The venom from an eastern diamondback rattlesnake in the Florida panhandle is very different than the venom from a rattlesnake 500 miles south in the Everglades, and this has huge implications for snakebite treatment. “So if you use just southern venoms when making the antivenom, it would be ineffective against some of the more common toxins found in northern diamondback rattlesnakes,” said Florida State University doctoral student Mark Margres. In the rattlesnakes, they found significant variation linked to geography. But, in the coral snakes, they found the venom to be identical no matter where the snakes were found. “This can tell us a bit of the history and evolutionary patterns of the snakes,” said Kenny Wray, a post-doctoral research associate in Rokyta’s lab. “This suggests that the coral snakes may be recent invaders to the region and haven’t had time to evolve different venoms in different areas.” This information also will help with the development of coral snake antivenom, because scientists now know there is uniformity in coral snake venom. According to a 2012 estimate by the Center for Disease Control, 7,000 to 8,000 people in the United States are bitten by venomous snakes every year. Not only are there medical implications, this information is also important for conservation purposes. The eastern diamondback rattlesnake is being considered for federal protection under the Endangered Species Act. But, if the snakes are removed from one geographic area, they will be irrevocably deleted sfrom the ecosystem altogether. “If we lose some of these populations, we lose a whole venom type,” Rokyta said. “That really changes conservation.”  Science Daily  Original web page at Science Daily


Poisoning Tibet’s rabbit relatives may be a bad move

The plateau pika doesn’t have many friends. This small burrowing relative of the rabbit, weighing only around 140 grams, is the most abundant mammal on the vast grasslands of the Tibetan plateau, but it is widely condemned as a cause of soil erosion and an  ecosystem wrecker. There is a government-funded campaign to exterminate them by poisoning their burrows all across the flatlands, also known as the “roof of the world”. But the tide could be turning. Recent studies have found that the pika is not a pest after all, but a “keystone species”. It is being recast as protector of the 2.5 million square kilometres of grasslands across Tibet. It could be essential for supporting birds of prey and the Tibetan fox, as well as being a vital ecological engineer, affecting the flow of water to some of the planet’s largest rivers. Pika poisoning is government policy in China. Each winter, teams of workers soak grain in Clostridium botulinum, a bacterium that produces the neurotoxin botulinum, and stuff it down pika burrows. In many areas, this assault is now eliminating the animal, says Andrew Smith of Arizona State University in Tempe. “You can drive for hundreds of kilometres across the plateau and fail to see a single pika,” he says. his pogrom is damaging the many species that prey on the plateau pika. According to Richard Harris of the University of Montana animals such as buzzards are suffering, as well as the Tibetan fox, which has an almost identical territory to the pika and is found nowhere else. His detailed study of fox scat revealed for the first time that the fox is almost entirely dependent on the pika for food. It turns out that no pika will mean no foxes, too. And there is more to these rabbit relatives than just being food to larger species. The Tibetan plateau has been called Asia’s water tower, and it is where giant rivers such as the Yangtze, Mekong, Indus and Yellow River originate. Smith found  that soils in areas where pika are still at large hold more water. This is down to their burrowing behaviour, which mixes the wetter top layer with dryer soil deeper down. By holding more water, the soil reduces surface run-off that can cause floods. Exterminating the pika means the poisoners are making the rivers downstream more flood-prone in the wet season, and more likely to dry up at other times, Smith argues. Chinese researchers, led by Lü Zhi, director of the Center for Nature and Society at Peking University, lobbied state officials in December to end the extermination campaign, arguing that the pika is not a pest but a vital element of a fragile ecosystem. Smith is hopeful that the new evidence and campaign to save the pika will deliver. “Maybe change is in the air,” says Smith.  NewScientist Original web page at New Scientist


Seabird losses from deepwater horizon oil spill estimated at hundreds of thousands

The 2010 Deepwater Horizon oil spill is often cited as the worst environmental disaster in U.S. history—yet its impacts on the marine life of the Gulf of Mexico have gone largely undetermined. Now, new findings published this month in Marine Ecology Progress Series estimate that the number of seabirds lost as a result of the spill may number well into the hundreds of thousands. Birds are especially vulnerable to oil, which can coat their feathers and cause death by dehydration, starvation, or drowning. Seabird mortalities can easily be underestimated following a spill as bodies are lost at sea or go undiscovered. So researchers turned to two different estimation methods—one whereby total mortalities were estimated from the actual number of dead birds recovered, and another in which information on the geographic extent of the oil slick and seabird densities were used to estimate potential mortalities. The scientists found that although the two approaches were based on different data sets, they returned roughly similar estimates of 600,000 and 800,000 oil-related seabird deaths, respectively. Although the number of seabird mortalities from the spill likely centers around 700,000, sources of uncertainty in the estimates indicate the number of deaths could actually lie anywhere between 300,000 and 2 million. In comparison, an estimated 250,000 seabirds were lost during the Exxon Valdez oil spill, and longline fisheries are estimated to contribute to 160,000 to 320,000 seabird deaths globally each year. For some seabirds, such as the laughing gull (Leucophaeus atricilla), the Deepwater Horizon impact translates into an estimated loss of more than 30% of its Gulf of Mexico population. Energy company BP faces civil penalties based in part on the number of birds and other wildlife lost in the spill, therefore the mortality estimates could influence the amount the company will be required to pay.  Science Magazine  Original web page at Science Magazine


* Poisoned vulture could herald European bird crisis

India’s vultures have suffered catastrophic declines since the 1990s, with populations of certain species such as Gyps indicus falling by more than 95%, and considered critically endangered. Scientists have blamed the drug diclofenac, which vets give to farm animals to treat conditions ranging from pneumonia to arthritis — but which can be deadly to vultures that feed on their carcasses as they are unusually sensitive to the compound. Last week, a paper in Conservation Biology reported that a Eurasian griffon vulture (Gyps fulvus) found dead in Spain in 2012 had suffered from severe visceral gout — which in Indian vultures is a classic sign of diclofenac poisoning. Laboratory tests showed that liver and kidney samples contained high levels of flunixin, another drug in the same class as diclofenac, known as non-steroidal anti-inflammatory drugs, or NSAIDs. This is the first case of a wild vulture being felled by an NSAID outside Asia, according to Mark Taggart, lead author of the paper and a pollutants researcher at the University of the Highlands and Islands in Thurso, UK. It is also the first instance of a bird death from an NSAID other than diclofenac, he adds. The researchers also say that this corpse may be the tip of the iceberg in terms of vulture deaths, and stress it was only found due to the transparency of the local government in Andalusia and ongoing monitoring efforts on the health of the local vulture population. “What is needed now is further research to safety test all NSAIDs on scavenging raptors,” says Taggart. According to the Vulture Conservation Foundation (VCF) in Zurich, Switzerland, Spain hosts around 70,000 griffon vultures, 5,000 cinereous vultures (Aegypius monachus), 3,000 Egyptian vultures (Neophron percnopterus) and 300 bearded vultures (Gypaetus barbatus).

Researchers have been warning of the risks posed to Spanish vultures by diclofenac. And Antoni Margalida, a conservation biologist at the University of Bern in Switzerland who researches scavenging birds, agrees that the latest paper shows that wild animals are indeed eating carrion from medicated animals  a key point of controversy, because the drugs are not supposed to be used in animals that may enter wildlife food chains. Margalida points out that other threatened species also feed on carrion, such as eagles and kites. What was once a risk is now “a demonstrated concern that requires an urgent response by administrations to ban as soon as possible the use of diclofenac”, says Margalida. The European Medicines Agency is currently considering the threat posed by diclofenac to Europe’s vultures, and is due to produce a decision by the end of November. It could ban use of the drug in livestock, or recommend restrictions on its use or on how carcasses are disposed of. Products containing diclofenac were approved for veterinary use in livestock in Spain only last year, and it is not clear how widely they are being used. Estimates from the VCF suggest that if diclofenac use grows, the number of contaminated carcasses could quickly reach the levels that caused the near disappearance of Indian vultures. José Tavares, the director of the VCF, says that the drug needs to be banned because of the practical and cost issues involved with controlling wildlife access to potentially toxic carcasses. Some of the animals are in remote areas, where they can lie unnoticed. And in parts of Spain, carcasses are left in the open for wild animals to eat, at sites called muladares.

“We are now asking the European Union to ban diclofenac as a first step,” Tavares says. Europe should then consider banning other potentially harmful drugs, including the flunixin that killed the Spanish bird. Failure to act could have “a significant impact on European vultures”, he warns. Some researchers suggest switching to an alternative drug — meloxicam — which treats the same problems as diclofenac, but is less toxic to vultures. They also express concern that allowing diclofenac use to continue in Europe could undermine efforts to limit access to it in other parts of the world. “Other countries would not have any reason to ban the drug,” says Tavares. And those that already have “may reopen the question and say, ‘Why do we have to ban the drug here if in Europe they have approved it?’.”

Nature doi:10.1038/nature.2014.16161  Nature  Original web page at Nature


New poison dart frog species discovered in Donoso, Panama

A bright orange poison dart frog with a unique call was discovered in Donoso, Panama, and described by researchers from the Smithsonian Tropical Research Institute and the Universidad Autónoma de Chiriquí in Panama, and the Universidad de los Andes in Colombia. In the species description published this week in Zootaxa, it was named Andinobates geminisae for Geminis Vargas, “the beloved wife of [coauthor] Marcos Ponce, for her unconditional support of his studies of Panamanian herpetology.” Every new species name is based on a representative specimen. The specimen for this species was collected Feb. 21, 2011, in the headwaters of the Rio Caño, in the district of Donoso, Colón Province, Panama, by Samuel Valdés, who was then the MWH Global Inc. environment office director, and his field assistant, Carlos de la Cruz. Additional specimens were collected between the Rio Coclé del Norte and the Rio Belen by biologists Marcos Ponce and Abel Batista, then a student at the Universidad Autónoma de Chiriquí. The specimens were deposited in the Museo de Vertebrados at the University of Panama, the Museo Herpetólogico de Chiriquí at the Universidad Autónoma de Chiriquí and in the Círculo Herpetólogico de Panamá. “Abel Batista and Marcos Ponce were the first to note the presence of this species,” said Cesar Jaramillo, Smithsonian herpetologist. “They’ve known it was there for several years. However, they were not sure if it was only a variety of another poison dart frog species, Oophaga pumilio, which exhibits tremendous color variation. Based on morphological characteristics of the adult and the tadpole, I thought it might be a new species of Andinobates.” Andrew Crawford, professor at Universidad de Los Andes and former STRI postdoctoral fellow, sequenced the DNA, confirming that this was a new species of Andinobates. Genetic information about this species is available in the Barcode of Life Data System and in GenBank. A recording of the call is available at Because this new frog species appears to be found in only a very small area, habitat loss and collecting for the pet trade are major threats to its existence. The authors recommend the formulation of special conservation plans to guarantee its survival. A. geminisae is included in the captive breeding program of the Panama Amphibian Rescue and Conservation project, a consortium of six zoos and research institutions dedicated to saving amphibians from the chytrid fungal disease, which is decimating amphibians worldwide, and habitat loss. Original web page Science Daily


Exposure to toxins makes great granddaughters more susceptible to stress

Scientists have known that toxic effects of substances known as endocrine disrupting chemicals (EDCs), found in both natural and human-made materials, can pass from one generation to the next, but new research shows that females with ancestral exposure to EDC may show especially adverse reactions to stress. According to a new study by researchers from The University of Texas at Austin and Washington State University, male and female rats are affected differently by ancestral exposure to a common fungicide, vinclozolin. Female rats whose great grandparents were exposed to vinclozolin become much more vulnerable to stress, becoming more anxious and preferring the company of novel females to familiar females. Males who have the same combination of ancestral exposure and stress do not have the same adverse effects. These results should concern us all because we have been exposed to endocrine disrupting chemicals for decades and we all go through natural challenges in life,” said David Crews, the Ashbel Smith Professor of Zoology and Psychology at The University of Texas at Austin and lead author of the study. “Those challenges are now being perceived differently because of this ancestral exposure to environmental contamination.”

The study was published July 22 online in the journal Endocrinology. Vinclozolin is a fungicide commonly used by farmers to treat fruits and vegetables. To test the effects of stress on rats, the researchers confined some of them to soft, warm cylinders for six hours a day for three weeks. This was done during adolescence, a developmentally sensitive time of life for rats, just as for humans. Months later, the researchers tested the brain chemistry, brain function, gene expression and behavior of the rats as adults.

They discovered that for female rats, ancestral exposure to vinclozolin alone or stress during the animal’s adolescence alone had negligible effects on the rats’ hormonal balance and behavior. However, the combination of ancestral exposure and stress caused the female rats to have dramatically higher levels of corticosterone (a stress hormone similar to cortisol in humans), higher expression of genes associated with anxiety and more anxious behaviors. Other research has shown that stress hormones cause degeneration of a region of the brain associated with memory and learning. Crews said that following exposure to EDCs, what is being passed down from generation to generation is not a change in the genetic code of the animals, but rather a change in the way specific genes are expressed. Gene expression is the process by which a cell uses the genetic code to make useful products such as proteins. If a section of a person’s genetic code were a cookie recipe, gene expression would refer to how many cookies, if any, a cook makes with the recipe. The observation that changes in gene expression can be passed on to future generations has led to a new field of research known as epigenetics. Crews and others have shown that EDCs can increase the risk in future generations for human illnesses such as autism, obesity and cardiovascular disease. Crews noted that environmental levels of EDCs are continuing to rise, as well as the rates of these diseases, particularly mental disorders.  Science Daily  Original web page at Science Daily


Toxic toads threaten ‘ecological disaster’ for Madagascar

The unique wildlife of Madagascar is facing an invasion of toxic toads that could devastate the island’s native species. Snakes feeding on the toads are especially at risk of poisoning, as are a host of other animals unique to the island — such as lemurs and endemic birds — and the species could cause harm to humans as well. In a letter to Nature,  11 researchers warn that Asian common toads (Duttaphrynus melanostictus) were observed near Toamasina, the African country’s largest seaport, in March. It is suspected that the amphibians arrived from Asia in shipping containers, and are now taking advantage of what the writers describe as “ideal resources and climate” to establish themselves. “Time is short, so we are issuing an urgent call to the conservation community and governments to prevent an ecological disaster,” say Jonathan Kolby, a wildlife-health researcher at James Cook University in Townsville, Australia, and his colleagues. The discovery of the invasive amphibians recalls the Australian plague of cane toads (Rhinella marina). These animals, relatives of the Asian common toad, were deliberately introduced to Australia in 1935; they proceeded to devastate native animal populations and have spread across much of the country, defying attempts to eradicate them. Kolby and his colleagues warn that something similar could now happen in Madagascar. The toads are already reported to have been deadly to snakes, including the ground boa (Acrantophis spp.), which is found nowhere else, Kolby tells Nature. Drawing parallels with the cane-toad situation, he warns that more than 50 species of endemic snake could be threatened, because they are likely to eat the toxic toads. Iconic Madagascan species such as the cat-like fossa (Cryptoprocta ferox), lemurs and endemic birds are also in jeopardy. And the toads could spread diseases to other amphibians and even contaminate drinking water and transmit parasites to humans.

The species is not yet widespread in Madagascar, but it has been found a mere 25 kilometres away from the important Betampona nature reserve, and a short distance further from other internationally important biodiversity hotspots. It is unclear how fast it can travel, but cane toads have been clocked expanding their range at 50 kilometres per year. The potential tragedy is not restricted to Madagascar. “There is now a high dispersal risk of these toads spreading from Madagascar to other Indian Ocean islands such as the Mascarene Islands, Comoros and Seychelles,” says Kolby. Toads are already being collected and removed, he says, and the Madagasikara Voakajy, a non-governmental organization in Antananarivo devoted to biodiversity, is tracking the spread of the amphibians. The toads should be hunted, their spawn should be destroyed and ponds should be drained to stop their breeding, says Kolby. “We are still within the early stages of population growth,” he says. An eradication programme should be developed swiftly, “while populations are still relatively small and manageable”. Mark Hoddle, director of the Center for Invasive Species Research at the University of California, Riverside, notes that to be considered invasive, a non-native species must have established a reproductive population that spreads and causes environmental and economic damage. On this basis it may be too early to declare the Asian toad in Madagascar a problem species, he says, but there are “very good reasons to be concerned”.

Nature doi:10.1038/nature.2014.15309  Nature

June 24, 2014  Original web page at Nature



* Mouse model would have predicted toxicity of drug that killed 5 in 1993 clinical trial

Over 20 years after the fatal fialuridine trial, a study published this week in PLOS Medicine demonstrates that mice with humanized livers recapitulate the drug’s toxicity. The work suggests that this mouse model should be added to the repertoire of tools used in preclinical screening of drugs for liver toxicity before they are given to human participants in clinical trials. A retrospective analysis by the US National Academy of Sciences of all preclinical fialuridine toxicity tests, which included studies in mice, rats, dogs, and monkeys, concluded that the available animal data provided no indication that the drug would cause liver failure in humans. Working on a mouse model in which approximately 90% of the animal’s liver cells are replaced by human liver cells, Jeffrey Glenn and Gary Peltz, from Stanford University, USA, and colleagues now show that it is possible to detect the toxicity of fialuridine, and possibly other drugs that poison human liver cells. When the researchers treated mice with humanized livers with fialuridine, they found that the drug caused liver failure. The clinical symptoms (jaundice and lethargy), laboratory abnormalities (elevated transaminase and lactate levels), and anatomical changes to the liver in the drug-treated mice mirrored those observed in human participants in the fialuridine trial. To test whether the mouse model could specifically identify the toxicity of fialuridine but would not raise “false alarm” on other drugs, the researchers treated the humanized liver mice with a second drug called sofosbuvir. Sofosbuvir belongs to the same class of drugs as fialuridine, but it has been tested in humans and was found not to have liver toxicity at doses within a few orders of magnitude of the effective dose. Sofosbuvir-treated mice did not show symptoms of liver failure.

Because the humanized mice used in these studies have an impaired immune system, they cannot be used to warn of toxicity that is mediated by the immune system. Nevertheless, since the liver is the “detox” organ, toxicity caused by drugs that act directly on the liver is a common problem in drug development. And because of important differences between human and animal livers, the researchers say “toxicology studies using mice with humanized livers could have a large impact on drug development and could improve the safety of drugs that will subsequently be tested in humans.” They express hope that, as suggested by their findings, “the use of 21st century methodologies could improve the safety of 21st century drug development.”  Science Daily

May 13, 2014  Original web page at Science Daily


* This chip can tell if you’ve been poisoned

When you are dealing with a deadly poison that can be found in food and is a potential terrorist weapon, you want the best detection tools you can get. Now, researchers in France have demonstrated an improved method to detect the most deadly variant of the botulinum neurotoxin, which causes botulism. Their test provides results faster than the standard method and accurately detects even low concentrations of the toxin. Botulinum neurotoxin—one of the deadliest poisons known to humans—is produced by the bacterium Clostridium botulinum. This toxin can be found in improperly canned foods and is considered a potential terrorist weapon due to its ability to kill at very low concentrations if added to food, water, or the air supply. Individuals who become sick from the toxin develop progressive paralysis that is fatal 60% of the time if left untreated. But if a patient receives treatment in time, the likelihood of death falls to less than 5%. Unfortunately, the current standard blood test for detecting the botulinum toxin in adults is slow—and gruesome. Blood from the patient is injected into mice; if the rodents develop symptoms of botulism and die, the test is positive. But it can take as long as four days to get results from the mouse test, which limits its usefulness in situations where treatment decisions need to be made quickly. What’s more, the patients who have the least amount of time to spare often don’t test positive at all. The botulinum toxin moves out of the blood and into muscle as the disease progresses. As the concentration of the toxin in the blood falls, the mice become less likely to react to it in time—even as the patient becomes sicker and sicker. Molecular neurobiologist Christian Lévêque of the French biomedical research agency INSERM in Marseille and Aix-Marseille University in Provence thought it was high time for a change. So he and his team set out to design a new test that took advantage of the molecular processes behind the botulinum neurotoxin’s paralyzing effect. They focused on botulinum neurotoxin A, which causes most of the botulism cases in the United States. (Botulinum neurotoxins B, E, and F can also cause disease.)

Botulinum neurotoxin A causes paralysis by breaking apart a protein called SNAP-25, which helps nerves and muscles communicate. Lévêque and his team affixed SNAP-25 to a tiny chip and exposed it to blood containing the A toxin. Then, the researchers introduced an engineered antibody that reacts with SNAP-25 only after it has been dismantled in the manner particular to the A neurotoxin. If the antibody reacted with the chip, they knew the blood sample contained A toxin. Using this method, Lévêque and his team could detect the toxin in a matter of hours, instead of days, and at much lower concentrations than the mouse test, they report in an upcoming issue of Biosensors and Bioelectronics. Attaching SNAP-25 to the chip proved to be a key advantage of the new method, Lévêque says. This trick allows the test to react directly to a patient’s blood, which means very little precious time is wasted preparing the sample for analysis. “Sample preparation often represents a bottleneck” in clinical tests, Lévêque explains. His team’s test, on the other hand, “is very simple, as samples just need to be diluted and introduced into the apparatus.” The new test “is very fast and sensitive,” says Luis Polo-Parada, a medical nanotechnologist at University of Missouri, Columbia, who was not involved with the research. However, he cautions that additional labs will need to confirm the test’s effectiveness before it will be ready for use in patients. Both Polo-Parada and disease detection researcher Markus Kalkum of the Beckman Research Institute of City of Hope in Duarte, California, who was not involved with the research, hope the test will be expanded to cover the B, E, and F neurotoxins, too. Lévêque says his group is already working on that.  ScienceNow

May 13, 2014  Original web page at ScienceNow


Surprise finding, blood clots absorb bacterial toxin

Blood clots play an unexpected role in protecting the body from the deadly effects of bacteria by absorbing bacterial toxins, researchers at the University of California, Davis, have found. The research was published Dec. 2 in the journal PLoS ONE. It’s a significant addition to the short list of defenses that animals use to protect themselves against toxin-induced sepsis,” said Peter Armstrong, professor of molecular and cellular biology at UC Davis and senior author on the paper. Even with modern antibiotics, septic shock from bacterial infections afflicts about 300,000 people a year in the U.S., with a mortality rate of 30 to 50 percent. Septic shock is caused by Gram-negative bacteria, which release a toxin called lipopolysaccharide or endotoxin. In small amounts, lipopolysaccharide triggers inflammation. When infections with these bacteria get out of hand, lipopolysaccharide courses through the bloodstream, causing catastrophic damage to organs and tissues. These toxins cause disease in a variety of animal species — lipopolysaccharide is also toxic to both horseshoe crabs and lobsters, separated from humans by hundreds of millions of years of evolution. In humans and other mammals, blood clots quickly form from a mix of specialized blood cells and protein fibers. Arthropods like horseshoe crabs and lobsters can also form clots in response to injury, with a different mix of cells and proteins.

Clots protect and help to seal wounds, prevent blood or body fluids from leaking out and form a physical barrier that entangles and blocks bacteria from entering the body. The new study shows that they also actively soak up lipopolysaccharide, reducing its release from the wound site into the body, where it could cause disease or even death. Armstrong’s laboratory had previously developed fluorescent labels to show that a lipopolysaccharide-like molecule is present in chloroplasts, structures inside cells of green plants that carry out photosynthesis and are thought to be descended from bacteria. As he also studies the role of blood clots in resisting infections, Armstrong decided to test the same techniques on blood clots that had been exposed to bacteria or to bacterial lipopolysaccharide. The fluorescent probes lit up the clots, showing that the clot fibers bound lipopolysaccharide to their surfaces. “I was ecstatic,” Armstrong said. “It was one of those moments that makes the rest of the slogging worthwhile.”

Armstrong and colleagues Margaret Armstrong at UC Davis and Frederick Rickles at George Washington University looked at clots of blood, or its equivalent, from humans, mice, lobsters and horseshoe crabs. In all four species, they found that fluorescently tagged lipopolysaccharide was bound to the fibers of the blood clot. The toxin was too tightly attached to be readily removed by chemical treatments that remove weakly bound macromolecules from proteins. During a sabbatical leave in the laboratory of Dr. Bruce Furie at Beth Deaconess Medical Center and Harvard University, Armstrong was also able to film clots in blood vessels of live mice and showed that these in vivo clots took up lipopolysaccharide in real time. These in vivo experiments, he said, confirm the bench-top observations and offer new insights into the pathology of sepsis. One of the deadly consequences of septic shock is disseminated intravascular coagulation, when blood clots form rapidly throughout the body. But the new results suggest that on a small and local scale, this might be part of a protective mechanism against sepsis — these intravascular clots can soak up quantities of lipopolysaccharide from the blood. They also show that rather than being a simple physical barrier, blood clots play an active and dynamic role in protecting the body from infections.

Science Daily
January 7, 2014

Original web page at Science Daily


Early-life exposure of frogs to herbicide increases mortality from fungal disease

The combination of the herbicide atrazine and a fungal disease is particularly deadly to frogs, shows new research from a University of South Florida laboratory, which has been investigating the global demise of amphibian populations. USF Biologist Jason Rohr said the new findings show that early-life exposure to atrazine increases frog mortality but only when the frogs were challenged with a chytrid fungus, a pathogen implicated in worldwide amphibian declines. The research is published in the new edition of Proceedings of the Royal Society B. “Understanding how stressors cause enduring health effects is important because these stressors might then be avoided or mitigated during formative developmental stages to prevent lasting increases in disease susceptibility,” Rohr said. The study was conducted by Rohr and Lynn Martin, Associate Professors of USF’s Department of Integrative Biology; USF researchers Taegan McMahon and Neal Halstead; and colleagues at the University of Florida, Oakland University, and Archbold Biological Station. Their experiments showed that a six-day exposure to environmentally relevant concentrations of atrazine, one of the most common herbicides in the world, increased frog mortality 46 days after the atrazine exposure, but only when frogs were challenged with the chytrid fungus. This increase in mortality was driven by a reduction in the frogs’ tolerance of the infection.

Moreover, the researchers found no evidence of recovery from the atrazine exposure and the atrazine-induced increase in disease susceptibility was independent of when the atrazine exposure occurred during tadpole development. “These findings are important because they suggest that amphibians might need to be exposed only to atrazine briefly as larvae for atrazine to cause persistent increases in their risk of chytri-induced mortality,” Rohr said. “Our findings suggest that reducing early-life exposure of amphibians to atrazine could reduce lasting increases in the risk of mortality from a disease associated with worldwide amphibian declines.” Until this study, scientists knew little about how early-life exposure to stressors affected the risk of infectious diseases for amphibians later in life. “Identifying which, when, and how stressors cause enduring effects on disease risk could facilitate disease prevention in wildlife and humans, an approach that is often more cost-effective and efficient than reactive medicine,” Rohr said. The findings are also the latest chapter in research Rohr and his lab has conducted on the impact of atrazine on amphibians. These findings are consistent with earlier studies that concluded that, while the chemical typically does not directly kill amphibians and fish, there is consistent scientific evidence that it negatively impacts their biology by affecting their growth and immune and endocrine systems.

Science Daily
November 12, 2013

Original web page at Science Daily


Eating poisonous plants saves life of gemsbok in Namibian desert

In drought periods browsing springbok (Antidorcas marsupialis) feed on all plant material they can find, while grazing gemsbok (Oryx gazella gazella), in contrast, switch their diet to a high proportion of poisonous plants — and they survive. These findings were just published in the scientific online journal PLOS ONE. “We wanted to understand how these quite well-studied ungulates with contrasting feeding strategies can survive and even flourish in an adverse habitat like the Kunene region in Namibia, where the environment is characterised by strong and unpredictable variation in resource availability,” says David Lehmann, doctoral candidate at the German Leibniz Institute for Zoo and Wildlife Research (IZW) and first author of the study. Researchers from the IZW, the University of Namibia and other Namibian partners found that gemsbok (also called oryx) adjusted its diet according to season. During drought periods, they fed on a restricted mixture of plants, including more than 30 % of shrubs and trees. Surprisingly, gemsbok diet also consisted of up to 25 % of Damara milk-bush (Euphorbia damarana), an endemic, large succulent plant which is available all year round but highly toxic. When food was plentiful, gemsbok specialised exclusively on grasses and more ephemeral succulent species.

In contrast, springboks fed on a higher proportion of shrubs and trees than grasses and succulent plants irrespective of environmental conditions. As the researchers expected, springbok opportunistically adjusted their diet in response to variation in food sources availabilities, preferring e.g. grass sprouts during the wet season and browsing predominantly on leaves of bushes when grass quality decreased during drought. Springbok therefore adopted a different dietary strategy than gemsbok when facing a shortage of food sources. The potential effects of the Damara milk-bush on gemsbok health are still unknown. However, by extensively using this poisonous plant, gemsbok succeed in surviving environmental challenges. Gemsbok seem to be well adapted to the toxic effects of special plants growing in dry regions, and they benefit from their high water and nutritious content. Because global climate change increases drought periods and enhances desertification in Southern Africa, it is crucial to understand how wildlife species respond to the impoverishment of their natural environments and the decline of their food sources. Furthermore, gemsbok and springbok are two of the main protein sources for local communities, who would be negatively affected by declining wildlife population sizes. Knowledge about feeding behaviours of local species like gemsbok and springbok is therefore fundamental to establish sustainable wildlife management plans.

Science Daily
September 3, 2013

Original web page at Science Daily


Environmental toxins enter the brain tissue of polar bears

Scientists from Denmark and Canada are worried by their new findings showing that several bioaccumulative perfluoroalkyl substances (PFASs) are crossing the blood brain barrier of polar bears from Scoresby Sound, East Greenland. PerFluoroAlkyl Substances (PFASs) and precursor compounds have been used in a wide variety of commercial and industrial products over the past six decades. Applications include water and oil repellent coatings, e.g. for textiles, paper products, carpets and food packaging, pharmaceuticals and surfactants in cleaning products and fire-fighting foams. PFASs are highly resistant to chemical, thermal and biological degradation. PFASs and their precursor compounds have shown a dramatic increase and dispersal around the world over the past four decades. An increasing amount of information is becoming available on the toxicity of these compounds. Hence, studies have documented the toxicity of PFASs on wildlife and human health, including carcinogenesis, genotoxicity and epigenetic effects as well as reproductive and developmental toxicities, neurotoxicity, effects on the endocrine system and immunotoxicity. Bioaccumulative PFASs enter all parts of the brain.

Despite the fact that the liver is considered the major repository in the body for most PFASs, some shorter chain compounds from this grouping have previously been reported in the brain of chicken embryos, suggesting that they are able to cross the blood-brain barrier. Previous studies have shown a dramatic biomagnification of several PFASs, and particularly one known as perfluorooctane sulfonate (PFOS) as well as several compounds of the perfluorinated carboxylate (PFCAs) grouping, in polar bears. PFOS have been shown to be at concentrations in the liver that are 100 fold higher than the ringed seals on which they are predating. In a new study Arctic researchers from Carleton University in Canada and Aarhus University in Denmark have used the polar bear as a sentinel species for humans and other predators in the top of the food chain. The researchers demonstrated accumulation of PFOS and several PFCAs in eight brain regions of polar bears collected from Scoresby Sound, East Greenland. Dr. Robert Letcher, Carleton University, explains: “We know that fat soluble contaminants are able to cross the brain-blood barrier, but is it quite worrying that the PFOS and PFCAs, which are more associated with proteins in the body, were present in all the brain regions we analyzed.” Professor Rune Dietz, Aarhus University, is also worried about the results: “If PFOS and PFCAs can cross the blood-brain barrier in polar bears, it will also be the case in humans. The brain is one of the most essential parts of the body, where anthropogenic chemicals can have a severe impact. However, we are beginning to see the effect of the efforts to minimize the dispersal of this group of contaminants.”

The eight carbon chain PFOS and perfluorooctane carboxylate (PFOA) are PFASs have been phased out and are no longer produced in the western world. However, production in China, today the only known production source of PFOS and PFOA, has increased by roughly a factor of 10, since it was phased out in the USA. Unfortunately, no emission inventory is so far available from this region. Furthermore, replacements for PFOS and PFOA are now marketed and produced in e.g. the U.S.A. and China, which generally have perfluorinated carbon chains that are shorter or branched. Another recent study from Aarhus University documents that PFOS concentrations in Greenlandic polar bears and ringed seals started to decline after 2006. Other wildlife populations closer to the sources in Europe and North America have shown a decline prior to the Greenlandic animals. Rune Dietz comments: “It is promising to see that the PFAS are on the decline. This development should be encouraged by the authorities globally. In the meantime my best advice to the consumers is to go for environmentally labeled products. But avoiding products is difficult, because PFASs are so widespread in many kind of products and they are rarely declared.” Perfluoroalkyl substances (PFASs) constitute a group of compounds where one end of the molecule consists of a carbon chain in which all the hydrogen atoms are replaced by fluorine atoms. This so-called perfluoroalkyl “tail” can be short or long, but the strong C-F bonds make the tail more or less impossible to degrade, compared to the more well known CFC-bonds. The best known PFAS is PFOS with an eight-chained perfluoroalkyl tail.

Science Daily
August 6, 2013

Original web page at Science Daily


Mercury pollution threatens arctic foxes

New scientific results show that arctic foxes accumulate dangerous levels of mercury if they live in coastal habitats and feed on prey which lives in the ocean. Researchers from the Leibniz Institute for Zoo and Wildlife Research, Moscow State University and the University of Iceland just published their discovery in the science online journal PLOS ONE. Mercury is usually transferred across the food chain, so the researchers checked which items were the main source of food and measured mercury levels in the main prey of Arctic foxes. The scientists compared three fox populations in different environments. Foxes on the small Russian Commander Island of Mednyi fed almost exclusively on sea birds, with some foxes eating seal carcasses. In Iceland, foxes living on the coast ate sea birds whereas those living inland ate non-marine birds and rodents. In all three environments different levels of mercury were present in their hair. Foxes living in coastal habitats such as Iceland and Mednyi Island exhibited high levels of mercury. What does this mean for the foxes? Using museum skin samples from the Commander Islands, the researchers could show that the foxes suffered exposure to mercury for a long time. The researchers confirmed that the source of contamination was their food, as they measured high mercury levels in the prey of foxes such as seals and sea birds.

However, the inland Arctic fox populations of Iceland had low mercury levels. Thus, living inland and eating non-marine birds and rodents instead of eating prey that feeds from the sea protected the inland foxes from mercury exposure. This may have health and conservation implications. The Mednyi Island foxes are almost an opposite example to the inland Icelandic fox population. They live on a small island with no rodents or alternative food source to seals or sea birds. They suffered a tremendous population crash and while the population is currently stable, it is very small and juvenile foxes in particular show high mortality rates. Foxes of all ages exhibit low body weight and have poor coat condition. “When going into this project we thought that an introduced pathogen would explain the poor condition of the foxes and their high mortality but after extensive screening, we did not find anything,” says Alex Greenwood, principal investigator of the study. Instead, the researchers began to suspect that something else was at play. “If pathogens were not the cause, we thought perhaps pollutants could be involved. We thought of mercury because it has been reported in high concentration in other Arctic vertebrates also in remote areas and mercury intoxication is known to increase mortality in mammals. As mercury can have negative effects on overall health, particularly in young individuals, and as we knew that Mednyi foxes were exclusively feeding on potentially contaminated sources, we wanted to see whether contamination with mercury depended on feeding ecology and hence might have been the crucial factor for the population decline on Mednyi Island,” comments Gabriele Treu, one of the lead authors of the study. As it turned out, the observed high mercury demonstrated a tight association with feeding ecology and geographical distribution of the foxes. In terms of conservation and long term population health for the entire arctic food chain of carnivores, mercury pollution must be stopped.

Science Daily
May 28, 2013

Original web page at Science Daily