Featured stories in this issue…
Environmental Agents Associated with Neurodevelopmental Disorders
More than 50 scientists and health professionals this week released an important Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders.
Poverty Mars Formation of Infant Brains
“Many children growing up in very poor families with low social status experience unhealthy levels of stress hormones, which impair their neural development. That effect is on top of any damage caused by inadequate nutrition and exposure to environmental toxins.”
EJ Groups Vow To Fight Carbon Emissions Cap-and-trade Plan
“A cap-and-trade program would allow heavy polluters, often located in poor neighborhoods, to partly buy their way out of lowering their emissions.”
DNA Pollution May Be Spawning Killer Microbes
“A potentially colossal new health threat: DNA pollution.” Ocean Map Charts Path of Human Destruction “Human activity has left a mark on nearly every square kilometer of sea, severely compromising ecosystems in more than 40% of waters.”
Killer Whales Loaded with Fire Retardant
“It’s not very reassuring for humans to find high levels of endocrine-disrupting chemicals in animals at the top of the food chain. We would be unwise to ignore what we are seeing.”
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From: Institute for Children’s Environmental Health, Feb. 20, 2008
ENVIRONMENTAL AGENTS ASSOCIATED WITH NEURODEVELOPMENTAL DISORDERS
A new
Scientific Consensus Statement on Environmental Agents Associated with Neurodevelopmental Disorders, released this week, summarizes the latest science about environmental contaminants associated with neurodevelopmental disorders, such as learning disabilities, autism spectrum disorder, attention deficit hyperactivity disorder (ADHD), intellectual disabilities and developmental delays.
The statement was published by the Collaborative on Health and the Environment’s Learning and Developmental Disabilities Initiative.
The statement, which summarizes over 200 studies, was drafted and reviewed by a prestigious committee of scientists and health professionals based in North America. They concluded:
“The scientific evidence reviewed in this statement indicates environmental contaminants are an important cause of learning and developmental disabilities (LDDs)….
“The consequences of learning and developmental disabilities are most significant for the affected individual but also have profound implications for the family, school system, local community and greater society. Despite some uncertainty, there is sufficient knowledge to take preventive action to reduce fetal and childhood exposures to environmental contaminants. Given the serious consequences of LDDs, a precautionary approach is warranted to protect the most vulnerable of our society.
“Given the established knowledge, protecting children from neurotoxic environmental exposures from the earliest stages of fetal development through adolescence is clearly an essential public health measure if we are to help reduce the growing numbers of those with learning and developmental disorders and create an environment in which children can reach and maintain their full potential.”
“We know enough now to move on with taking steps to protect our children. This document pulls that knowledge together to further this vital effort,” said reviewer Martha Herbert, PhD, MD, an assistant professor of neurology at Harvard Medical School and a pediatric neurologist with subspecialty certification in neurodevelopmental disabilities at the Massachusetts General Hospital in Boston.
Other researchers on the review committee underscored the cost- savings, policy-related and ethical implications of this consensus statement. “We could cut the health costs of childhood disabilities and disease by billions of dollars every year by minimizing contaminants in the environment,” said Phil Landrigan, MD, MSc, of the Children’s Environmental Health Center at the Mount Sinai School of Medicine. “Investing in our children’s health is both cost-effective and the right thing to do.”
“The overwhelming evidence shows that certain environmental exposures can contribute to life-long learning and developmental disorders,” noted Ted Schettler, MD, MPH, with the Science and Environmental Health Network. “We should eliminate children’s exposures to substances that we know can have these impacts by implementing stronger health-based policies requiring safer alternatives. Further, we must urgently examine other environmental contaminants of concern for which safety data are lacking. “
“The proportion of environmentally induced learning and developmental disabilities is a question of profound human, scientific and public policy significance,” said lead author Steven G. Gilbert, PhD, DABT, of the Institute of Neurotoxicology & Neurological Disorders, “and has implications for individuals, families, school systems, communities and the future of our society. The bottom line is, it is our ethical responsibility to ensure all children have a healthy future.”
This document is designed for researchers, health professionals, health-affected groups, environmental health and justice organizations, policymakers and journalists to use as a resource for understanding and addressing concerns about links between environmental factors and neurodevelopmental disorders.
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From: Financial Times, Feb. 16, 2008
POVERTY MARS FORMATION OF INFANT BRAINS
By Clive Cookson in Boston
Poverty in early childhood poisons the brain, the American Association for the Advancement of Science meeting in Boston heard on Friday.
Neuroscientists said many children growing up in very poor families with low social status experience unhealthy levels of stress hormones, which impair their neural development. That effect is on top of any damage caused by inadequate nutrition and exposure to environmental toxins.
Studies by several US universities have revealed the pervasive harm done to the brain, particularly between the ages of six months and three years, from low socio-economic status.
Martha Farah, director of the University of Pennsylvania’s centre for cognitive neuroscience, said: “The biggest effects are on language and memory. The finding about memory impairment — the ability to encounter a pattern and remember it — really surprised us.”
Jack Shonkoff, director of Harvard University’s centre on the developing child, said policymakers had to take note of the research because “the foundation of all social problems later in life takes place in the early years”.
“The earlier you intervene [to counteract the impact of poverty], the better the outcome in the end, because the brain loses its plasticity [adaptability] as the child becomes older,” he said.
Stress hormone levels tend to be higher in young children from poor families than in children growing up in middle-class and wealthy families, said Prof Shonkoff. Excessive levels of these hormones disrupt the formation of synaptic connections between cells in the developing brain — and even affect its blood supply. “They literally disrupt the brain architecture,” he said.
The findings explain why relatively unfocused programmes to prepare poor children for school, such as Head Start in the US, have produced only modest results, the scientists said.
More focused interventions could give more substantial benefits, said Courtney Stevens of the University of Oregon. She gave the preliminary results of an eight-week programme aimed at poor parents of pre-school children in Oregon.
Parents attended weekly coaching sessions to improve their family communications skills and show them how to control their children’s bad behaviour. At the end of the programme, participating parents reported big reductions in family stress compared with a control group that did not take part. Brain scans of the children suggested neural improvements, too.
“Our findings are important because they suggest that kids who are at high risk for school failure can be helped through these interventions,” said Dr Stevens. “Even with these small numbers of children, the parent training appears very promising.”
Well-tailored programmes can help, Prof Shonkoff agreed. But in the end, the only way to remove the “toxic” impact of poverty on young brains is to abolish poverty itself, he said.
Copyright The Financial Times Limited 2008
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From: Los Angeles Times, Feb. 20, 2008
GROUPS VOW TO FIGHT CARBON EMISSIONS CAP-AND-TRADE PLAN
By Margot Roosevelt, Los Angeles Times Staff Writer
Low-income community groups in five California cities launched a statewide campaign Tuesday to “fight at every turn” any global-warming regulation that allows industries to trade carbon emissions, saying it would amount to “gambling on public health.”
The 21-point “Environmental Justice Movement Declaration” challenges the stance of Gov. Arnold Schwarzenegger, a national advocate of a cap-and-trade program that would allow heavy polluters, often located in poor neighborhoods, to partly buy their way out of lowering their emissions.
“Under a trading scheme, 11 power plants to be built around Los Angeles could offset emissions by extracting methane from coal seams in Utah or planting trees in Manitoba,” said Jane Williams of the California Communities Against Toxics, which fights pollution in low- income areas.
The defiant tone of news conferences in Los Angeles, Fresno, Oakland, Sacramento and San Diego indicated that political turbulence might be ahead as the state Air Resources Board hammers out a strategy to drastically reduce greenhouse gas emissions, as required under a 2006 law.
Until now, the debates over how to implement the law have been conducted in polite workshops with industry and environmental groups offering technical testimony to state air board officials. The agency must design a plan, due at the end of this year, to ratchet down emissions to 1990 levels by 2020, an effort that is likely to affect virtually every industry in the state.
“Cap and trade is a charade to continue business as usual,” said Angela Johnson Meszaros, director of the California Environmental Rights Alliance.
Environmental justice groups instead favor carbon fees on polluting industries, a strategy endorsed by many economists as simpler and more transparent, although politically tough to enact.
Williams and Meszaros are co-chairs of the Air Board’s Environmental Justice Advisory Committee, set up under the 2006 global warming law to counsel the state on how to avoid disproportionate effects on low- income communities.
The global warming legislation requires the board to consider cap and trade, and the governor’s strong advocacy of the system makes its adoption likely. The debate is likely to center on how to design such a regulatory regime. One issue is whether to auction off carbon emissions permits or simply give them to polluting industries.
A group of Western states and Canadian provinces is designing a regional trading program. And the climate bill with the most support in Congress, sponsored by Sens. John W. Warner (R-Va) and Joe Lieberman (I-Conn.), includes a cap-and-trade system.
The 18 groups that signed the declaration included the San Joaquin Valley Latino Environmental Advance Project, Oakland’s West County Toxics Coalition, the L.A. chapter of the Physicians for Social Responsibility and Delano’s Assn. of Irritated Residents.
Notably absent were any of the big mainstream environmental groups, such as the Natural Resources Defense Council or the Sierra Club, both of which declined to comment publicly on the environmental justice declaration.
For the most part, national environmental groups are backing cap-and- trade plans, even though many of them would prefer the politically unpalatable carbon fee or tax. The proceeds of auctioning off credits, some groups argue, could be distributed to low-income communities.
Meszaros said she didn’t trust an auction system. “We’re concerned that proceeds from an auction won’t be applied to transitioning us to a zero-carbon future. State law requires that fees be used for the issue for which the fee is assessed. But with budget shortfalls in California, proceeds from an auction are going to be sucked into filling the holes.”
Mary Nichols, chairwoman of the air board, said the global warming law requires “the most cost-effective solution to reducing emissions,” and that her agency would “run the numbers” on various systems, including cap and trade and fees. “This problem is too big and complicated to rule any technique off the table.”
Further Information:
Copyright 2008 Los Angeles Times
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From: Discover Magazine, Feb. 16, 2008
DNA POLLUTION MAY BE SPAWNING KILLER MICROBES
Rogue genetic snippets spread antibiotic resistance all over the environment.
By Jessica Snyder Sachs
On a bright winter morning high in the Colorado Rockies, a slight young woman in oversize hip boots sidles up to a gap of open water in the icy Cache la Poudre River. Heather Storteboom, a 25-year-old graduate student at nearby Colorado State University, is prospecting for clues to an invisible killer.
Storteboom snaps on a pair of latex gloves and stretches over the frozen ledge to fill a sterile plastic jug with water. Then, setting the container aside, she swings her rubber-clad legs into the stream. “Ahh, no leaks,” she says, standing upright. She pulls out a clean trowel and attempts to collect some bottom sediment; in the rapid current, it takes a half dozen tries to fill the small vial she will take back to the DNA laboratory of her adviser, environmental engineer Amy Pruden. As Storteboom packs to leave, a curious hiker approaches. “What were you collecting?” he asks. “Antibiotic resistance genes,” she answers.
Storteboom and Pruden are at the leading edge of an international forensic investigation into a potentially colossal new health threat: DNA pollution. Specifically, the researchers are seeking out snippets of rogue genetic material that transforms annoying bacteria into unstoppable supergerms, immune to many or all modern antibiotics. Over the past 60 years, genes for antibiotic resistance have gone from rare to commonplace in the microbes that routinely infect our bodies. The newly resistant strains have been implicated in some 90,000 potentially fatal infections a year in the United States, higher than the number of automobile and homicide deaths combined.
Among the most frightening of the emerging pathogens is invasive MRSA, or methicillin-resistant Staphylococcus aureus. Outbreaks of MRSA in public schools recently made headlines, but that is just the tip of the iceberg. Researchers estimate that invasive MRSA kills more than 18,000 Americans a year, more than AIDS, and the problem is growing rapidly. MRSA caused just 2 percent of staph infections in 1974; in the last few years, that figure has reached nearly 65 percent. Most reported staph infections stem from MRSA born and bred in our antibiotic-drenched hospitals and nursing homes. But about 15 percent now involve strains that arose in the general community.
It is not just MRSA that is causing concern; antibiotic resistance in general is spreading alarmingly. A 2003 study of the mouths of healthy kindergartners found that 97 percent harbored bacteria with genes for resistance to four out of six tested antibiotics. In all, resistant microbes made up around 15 percent of the children’s oral bacteria, even though none of the children had taken antibiotics in the previous three months. Such resistance genes are rare to nonexistent in specimens of human tissue and body fluid taken 60 years ago, before the use of antibiotics became widespread.
In part, modern medicine is paying the price for its own success. “Antibiotics may be the most powerful evolutionary force seen on this planet in billions of years,” says Tufts University microbiologist Stuart Levy, author of The Antibiotic Paradox: How the Misuse of Antibiotics Destroys Their Curative Powers. By their nature, anti-biotics support the rise of any bug that can shrug off their effects, by conveniently eliminating the susceptible competition.
But the rapid rise of bacterial genes for drug resistance stems from more than lucky mutation, Levy adds. The vast majority of these genes show a complexity that could have been achieved only over millions of years. Rather than rising anew in each species, the genes spread via the microbial equivalent of sexual promiscuity. Bacteria swap genes, not only among their own kind but also between widely divergent species, Levy explains. Bacteria can even scavenge the naked DNA that spills from their dead compatriots out into the environment.
The result is a microbial arms-smuggling network with a global reach. Over the past 50 years, virtually every known kind of disease-causing bacterium has acquired genes to survive some or all of the drugs that once proved effective against it. Analysis of a strain of vancomycin- resistant enterococcus, a potentially lethal bug that has invaded many hospitals, reveals that more than one-quarter of its genome — including virtually all its antibiotic-thwarting genes — is made up of foreign DNA. One of the newest banes of U.S. medical centers, a supervirulent and multidrug-resistant strain of Acinetobacter baumannii, likewise appears to have picked up most of its resistance in gene swaps with other species.
So where in Hades did this devilishly clever DNA come from? The ultimate source may lie in the dirt beneath our feet.
For the past decade, Gerry Wright has been trying to understand the rise of drug resistance by combing through the world’s richest natural source of resistance-enabling DNA: a clod of dirt. As the head of McMaster University’s antibiotic research center in Hamilton, Ontario, Wright has the most tricked-out laboratory a drug designer could want, complete with a $15 million high-speed screening facility for simultaneously testing potential drugs against hundreds of bacterial targets. Yet he says his technology pales in comparison with the elegant antibiotic-making abilities he finds encoded in soil bacteria. The vast majority of the antibiotics stocking our pharmacy shelves — from old standards like tetracycline to antibiotics of last resort like vancomycin and, most recently, daptomycin — are derived from soil organisms.
Biologists assume that soil organisms make antibiotics to beat back the microbial competition and to establish their territory, Wright says, although the chemicals may also serve other, less-understood functions. Whatever the case, Wright and his students began combing through the DNA of soil microbes like streptomyces to better understand their impressive antibiotic-making powers. In doing so the researchers stumbled upon three resistance genes embedded in the DNA that Streptomyces toyocaensis uses to produce the antibiotic teicoplanin. While Wright was not surprised that the bug would carry such genes as antidotes to its own weaponry, he was startled to see that the antidote genes were nearly identical to the resistance genes in vancomycin-resistant enterococcus (VRE), the scourge of American and European hospitals.
“Yet here they were in a soil organism, in the exact same orientation as you find in the genome of VRE,” Wright says. “That sure gave us a head-slap moment. If only we had done this experiment 15 years ago, when vancomycin came into widespread use, we might have understood exactly what kind of resistance mechanisms would follow the drug into our clinics and hospitals.” If nothing else, that foreknowledge might have prepared doctors for the inevitable resistance they would encounter soon after vancomycin was broadly prescribed.
Wright wondered what else he might find in a shovelful of dirt. So he handed out plastic bags to students departing on break, telling them to bring back soil samples. Over two years his lab amassed a collection that spanned the continent. It even included a thawed slice of tundra mailed by Wright’s brother, a provincial policeman stationed on the northern Ontario-Manitoba border.
By 2005 Wright’s team had combed through the genes of nearly 500 streptomyces strains and species, many never before identified. Every one proved resistant to multiple antibiotics, not just their own signature chemicals. On average, each could neutralize seven or eight drugs, and many could shrug off 14 or 15. In all, the researchers found resistance to every one of the 21 antibiotics they tested, including Ketek and Zyvox, two synthetic new drugs.
“These genes clearly didn’t jump directly from streptomyces into disease-causing bacteria,” Wright says. He had noted subtle variations between the resistance genes he pulled out of soil organisms and their doppelgängers in disease-causing bacteria. As in a game of telephone, each time a gene gets passed from one microbe to another, slight differences develop that reflect the DNA dialect of its new host. The resistance genes bedeviling doctors had evidently passed through many intermediaries on their way from soil to critically ill patients.
Wright suspects that the antibiotic-drenched environment of commercial livestock operations is prime ground for such transfer. “You’ve got the genes encoding for resistance in the soil beneath these operations,” he says, “and we know that the majority of the antibiotics animals consume get excreted intact.” In other words, the antibiotics fuel the rise of resistant bacteria both in the animals’ guts and in the dirt beneath their hooves, with ample opportunity for cross-contamination.
Nobody knows how long free-floating DNA might persist in the water. A 2001 study by University of Illinois microbiologist Roderick Mackie documented this flow. When he looked for tetracycline resistance genes in groundwater downstream from pig farms, he also found the genes in local soil organisms like Microbacterium and Pseudomonas, which normally do not contain them. Since then, Mackie has found that soil bacteria around conventional pig farms, which use antibiotics, carry 100 to 1,000 times more resistance genes than do the same bacteria around organic farms.
“These animal operations are real hot spots,” he says. “They’re glowing red in the concentrations and intensity of these genes.” More worrisome, perhaps, is that Mackie pulled more resistance genes from his deepest test wells, suggesting that the genes percolated down toward the drinking water supplies used by surrounding communities.
An even more direct conduit into the environment may be the common practice of irrigating fields with wastewater from livestock lagoons. About three years ago, David Graham, a University of Kansas environmental engineer, was puzzled in the fall by a dramatic spike in resistance genes in a pond on a Kansas feedlot he was studying. “We didn’t know what was going on until I talked with a large-animal researcher,” he recalls. At the end of the summer, feedlots receive newly weaned calves from outlying ranches. To prevent the young animals from importing infections, the feedlot operators were giving them five-day “shock doses” of antibiotics. “Their attitude had been, cows are big animals, they’re pretty tough, so you give them 10 times what they need,” Graham says.
The operators cut back on the drugs when Graham showed them that they were coating the next season’s alfalfa crop with highly drug-resistant bacteria. “Essentially, they were feeding resistance genes back to their animals,” Graham says. “Once they realized that, they started being much more conscious. They still used antibiotics, but more discriminately.”
While livestock operations are an obvious source of antibiotic resistance, humans also take a lot of antibiotics — and their waste is another contamination stream. Bacteria make up about one-third of the solid matter in human stool, and Scott Weber, of the State University of New York at Buffalo, studies what happens to the antibiotic resistance genes our nation flushes down its toilets.
Conventional sewage treatment skims off solids for landfill disposal, then feeds the liquid waste to sewage-degrading bacteria. The end result is around 5 billion pounds of bacteria-rich slurry, or waste sludge, each year. Around 35 percent of this is incinerated or put in a landfill. Close to 65 percent is recycled as fertilizer, much of it ending up on croplands.
Weber is now investigating how fertilizer derived from human sewage may contribute to the spread of antibiotic-resistant genes. “We’ve done a good job designing our treatment plants to reduce conventional contaminants,” he says. “Unfortunately, no one has been thinking of DNA as a contaminant.” In fact, sewage treatment methods used at the country’s 18,000-odd wastewater plants could actually affect the resistance genes that enter their systems.
Every tested strain in a dirt sample proved resistant to multiple antibiotics. Most treatment plants, Weber explains, gorge a relatively small number of sludge bacteria with all the liquid waste they can eat. The result, he found, is a spike in antibiotic-resistant organisms. “We don’t know exactly why,” he says, “but our findings have raised an even more important question.” Is the jump in resistance genes coming from a population explosion in the resistant enteric, or intestinal, bacteria coming into the sewage plant? Or is it coming from sewage-digesting sludge bacteria that are taking up the genes from incoming bacteria? The answer is important because sludge bacteria are much more likely to thrive and spread their resistance genes once the sludge is discharged into rivers (in treated wastewater) and onto crop fields (as slurried fertilizer).
Weber predicts that follow-up studies will show the resistance genes have indeed made the jump to sludge bacteria. On a hopeful note, he has shown that an alternative method of sewage processing seems to decrease the prevalence of bacterial drug resistance. In this process, the sludge remains inside the treatment plant longer, allowing dramatically higher concentrations of bacteria to develop. For reasons that are not yet clear, this method slows the increase of drug- resistant bacteria. It also produces less sludge for disposal. Unfortunately, the process is expensive.
Drying sewage sludge into pellets — which kills the sludge bacteria — is another way to contain resistance genes, though it may still leave DNA intact. But few municipal sewage plants want the extra expense of drying the sludge, and so it is instead exported “live” in tanker trucks that spray the wet slurry onto crop fields, along roadsides, and into forests.
Trolling the waters and sediments of the Cache la Poudre, Storteboom and Pruden are collecting solid evidence to support suspicions that both livestock operations and human sewage are major players in the dramatic rise of resistance genes in our environment and our bodies. Specifically, they have found unnaturally high levels of antibiotic resistance genes in sediments where the river comes into contact with treated municipal wastewater effluent and farm irrigation runoff as it flows 126 miles from Rocky Mountain National Park through Fort Collins and across Colorado’s eastern plain, home to some of the country’s most densely packed livestock operations.
“Over the course of the river, we saw the concentration of resistance genes increase by several orders of magnitude,” Pruden says, “far more than could ever be accounted for by chance alone.” Pruden’s team likewise found dangerous genes in the water headed from local treatment plants toward household taps.
Presumably, most of these genes reside inside live bacteria, but a microbe doesn’t have to be alive to share its dangerous DNA. As micro-biologists have pointed out, bacteria are known to scavenge genes from the spilled DNA of their dead.
“There’s a lot of interest in whether there’s naked DNA in there,” Pruden says of the Poudre’s waters. “Current treatment of drinking water is aimed at killing bacteria, not eliminating their DNA.” Nobody even knows exactly how long such free-floating DNA might persist.
All this makes resistance genes a uniquely troubling sort of pollution. “At least when you pollute a site with something like atrazine,” a pesticide, “you can be assured that it will eventually decay,” says Graham, the Kansas environmental engineer, who began his research career tracking chemical pollutants like toxic herbicides. “When you contaminate a site with resistance genes, those genes can be transferred into environmental organisms and actually increase the concentration of contamination.”
Taken together, these findings drive home the urgency of efforts to reduce flagrant antibiotic overuse that fuels the spread of resistance, whether on the farm, in the home, or in the hospital.
For years the livestock pharmaceutical industry has played down its role in the rise of antibiotic resistance. “We approached this problem many years ago and have seen all kinds of studies, and there isn’t anything definitive to say that antibiotics in livestock cause harm to people,” says Richard Carnevale, vice president of regulatory and scientific affairs at the Animal Health Institute, which represents the manufacturers of animal drugs, including those for livestock. “Antimicrobial resistance has all kinds of sources, people to animals as well as animals to people.”
The institute’s own data testify to the magnitude of antibiotic use in livestock operations, however. Its members sell an estimated 20 million to 25 million pounds of antibiotics for use in animals each year, much of it to promote growth. (For little-understood reasons, antibiotics speed the growth of young animals, making it cheaper to bring them to slaughter.) The Union of Concerned Scientists and other groups have long urged the United States to follow the European Union, which in 2006 completed its ban on the use of antibiotics for promoting livestock growth. Such a ban remains far more contentious in North America, where the profitability of factory-farm operations depends on getting animals to market in the shortest possible time.
On the other hand, the success of the E.U.’s ban is less than clear- cut. “The studies show that the E.U.’s curtailing of these compounds in feed has resulted in more sick animals needing higher therapeutic doses,” Carnevale says.
“There are cases of that,” admits Scott McEwen, a University of Guelph veterinary epidemiologist who advises the Canadian government on the public-health implications of livestock antibiotics. At certain stressful times in a young animal’s life, as when it is weaned from its mother, it becomes particularly susceptible to disease. “The lesson,” he says, “may be that we would do well by being more selective than a complete ban.”
McEwen and many of his colleagues see no harm in using growth- promoting livestock antibiotics known as ionophores. “They have no known use in people, and we see no evidence that they select for resistance to important medical antibiotics,” he says. “So why not use them? But if anyone tries to say that we should use such critically important drugs as cephalosporins or fluoroquinolones as growth promoters, that’s a no-brainer. Resistance develops quickly, and we’ve seen the deleterious effects in human health.”
A thornier issue is the use of antibiotics to treat sick livestock and prevent the spread of infections through crowded herds and flocks. “Few people would say we should deny antibiotics to sick animals,” McEwen says, “and often the only practical way to administer an antibiotic is to give it to the whole group.” Some critics have called for restricting certain classes of critically important antibiotics from livestock use, even for treating sick animals. For instance, the FDA is considering approval of cefquinome for respiratory infections in cattle. Cefquinome belongs to a powerful class of antibiotic known as fourth-generation cephalosporins, introduced in the 1990s to combat hospital infections that had grown resistant to older drugs. In the fall of 2006, the FDA’s veterinary advisory committee voted against approving cefquinome, citing concerns that resistance to this vital class of drug could spread from bacteria in beef to hospital superbugs that respond to little else. But the agency’s recently adopted guidelines make it difficult to deny approval to a new veterinary drug unless it clearly threatens the treatment of a specific foodborne infection in humans. As of press time, the FDA had yet to reach a decision.
Consumers may contribute to the problem of DNA pollution whenever they use antibacterial soaps and cleaning products. These products contain the antibiotic-like chemicals triclosan and triclocarban and send some 2 million to 20 million pounds of the compounds into the sewage stream each year. Triclosan and triclocarban have been shown in the lab to promote resistance to medically important antibiotics. Worse, the compounds do not break down as readily as do traditional antibiotics. Rolf Halden, cofounder of the Center for Water and Health at Johns Hopkins University, has shown that triclosan and triclocarban show up in many waterways that receive treated wastewater — more than half of the nation’s rivers and streams. He has found even greater levels of these two chemicals in sewage sludge destined for reuse as crop fertilizer. According to his figures, a typical sewage treatment plant sends more than a ton of triclocarban and a slightly lesser amount of triclosan back into the environment each year.
For consumer antibacterial soaps the solution is simple, Halden says: “Eliminate them. There’s no reason to have these chemicals in consumer products.” Studies show that household products containing such anti– bacterials don’t prevent the spread of sickness any better than ordinary soap and water. “If there’s no benefit, then all we’re left with is the risk,” Halden says. He notes that many European retailers have already pulled these products from their shelves. “I think it’s only a matter of time before they are removed from U.S. shelves as well.”
Finally, there is the complicated matter of the vast quantity of anti-biotics that U.S. doctors prescribe each year: some 3 million pounds, according to the Union of Concerned Scientists. No doctor wants to ignore an opportunity to save a patient from infectious disease, yet much of what is prescribed is probably unnecessary — and all of it feeds the spread of resistance genes in hospitals and apparently throughout the environment.
“Patients come in asking for a particular antibiotic because it made them feel better in the past or they saw it promoted on TV,” says Jim King, president of the American Academy of Family Physicians. The right thing to do is to educate the patient, he says, “but that takes time, and sometimes it’s easier, though not appropriate, to write the prescription the patient wants.”
Curtis Donskey, chief of infection control at Louis Stokes Cleveland VA Medical Center, adds that “a lot of antibiotic overuse comes from the mistaken idea that more is better. Infections are often treated longer than necessary, and multiple antibiotics are given when one would work as well.” In truth, his studies show, the longer hospital patients remain on anti-biotics, the more likely they are to pick up a multidrug-resistant super-bug. The problem appears to lie in the drugs’ disruption of a person’s protective microflora — the resident bacteria that normally help keep invader microbes at bay. “I think the message is slowly getting through,” Donskey says. “I’m seeing the change in attitude.”
Meanwhile, Pruden’s students at Colorado State keep amassing evidence that will make it difficult for any player — medical, consumer, or agricultural — to shirk accountability for DNA pollution.
Late in the afternoon, Storteboom drives past dairy farms and feedlots, meatpacking plants, and fallow fields, 50 miles downstream from her first DNA sampling site of the day. Leaving her Jeep at the side of the road, she strides past cow patties and fast-food wrappers and scrambles down an eroded embankment of the Cache la Poudre River. She cringes at the sight of two small animal carcasses on the opposite bank, then wades in, steering clear of an eddy of gray scum. “Just gross,” she mutters, grateful for her watertight hip boots.
Of course, the invisible genetic pollution is of greater concern. It lends an ironic twist to the river’s name. According to local legend, the appellation comes from the hidden stashes (cache) of gunpowder (poudre) that French fur trappers once buried along the banks. Nearly two centuries later, the river’s hidden DNA may pose the real threat.
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From: ScienceNOW Daily News, Feb. 14, 2008
OCEAN MAP CHARTS PATH OF HUMAN DESTRUCTION
By Eli Kintisch
BOSTON–Four years in the making, a groundbreaking new map of the state of the world’s oceans was released today, and its message is stark: Human activity has left a mark on nearly every square kilometer of sea, severely compromising ecosystems in more than 40% of waters.
The map, presented here at the annual meeting of the American Association for the Advancement of Science (publisher of ScienceNOW) — and published tomorrow in Science — combines 17 anthropogenic stressors, including coastal runoff and pollution, warming water temperature due to human-induced climate change, oil rigs that damage the sea floor, and five different kinds of fishing. Hundreds of experts worked to weigh and compare the stressors, overlaying them on top of maps that the scientists built of various ecosystems, with data obtained from shipping maps, satellite imagery, and scientific buoys. Then marine scientists modeled how different ecosystems would be affected by the stressors, mapping so-called impact scores onto square-kilometer-sized parcels worldwide. The scores correspond to colored pixels on the new map.
Researchers don’t know what the impact scores, which mostly ranged from 0 to 20, mean in terms of specific damage for different ecosystems. And without hard data sets, marine ecologists must rely on fuzzy terms such as “degraded” or “severe.” But previous studies of devastated coral reefs provide some context. A 2003 paper (Science, 15 August 2003, p. 955) showed that certain coral reef ecosystems in the Caribbean Sea and off the coast of Australia had lost as much as half of their species since preindustrial times. This level of damage corresponds to an impact score of 13 or 14 in the current map, values found in wide swaths of orange on the map of the world’s oceans.
Those figures are sobering, says marine ecologist Benjamin Halpern of the National Center for Ecological Analysis and Synthesis in Santa Barbara, California, who led the effort. The data suggest, for example, that ecosystems found in rocky reefs and on continental shelves “are being impacted even more” than coastal coral reefs, which get much more attention. But coral reefs are in bad shape themselves: The map indicates that nearly half of global reefs are experiencing serious, multiple impacts, including damage from fishing and ocean acidification.
“The takeaway message of the paper is that one needs to take into account the cumulative effects of different threats to the ocean,” says Duke University marine ecologist Larry Crowder, who wasn’t part of the effort. Still, although the map is a “bold attempt,” Crowder notes that it is far from comprehensive. Some very severely threatened ecosystems, such as certain rare reefs, are too small to show up on the map, he notes, and other data, such as the cumulative impact of fishing historically, are simply not available. Scientists in the broader community will be able to update the various data sets that form the map, which could fill some of these gaps.
Copyright 2008 American Association for the Advancement of Science
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From: Victoria (B.C.) Times-Colonist, Feb. 10, 2008
KILLER WHALES LOADED WITH FIRE RETARDANT
PBDEs can disrupt reproductive and immune systems, researcher says
By Judith Lavoie, Times Colonist
They wow tourists and remind people of the mysteries and majesty of the ocean, but killer whales swimming around the waters of Vancouver Island are the most contaminated animals on Earth.
Information, which is slowly and painstakingly being gathered about the whales that live along the coast of North America, reveals alarming trends and offers a graphic illustration of looming environmental problems.
Blubber studies on the two salmon-eating populations of resident killer whales — the endangered southern residents with 88 members and the threatened northern residents with 230 members — have found a significant buildup of toxins in their systems.
Furthermore, the studies also discovered the chemicals remain in their systems long after the chemicals themselves, such as PCBs, have been removed from the environment.
A growing concern is the rapid buildup of PBDEs, the chemicals found in fire retardants, says Peter Ross, toxicology research scientist at the Institute of Ocean Sciences in Sidney.
“This is a major concern, a major emerging issue,” he said.
PBDEs (polybrominated diphenyl ethers) can disrupt the endocrine system, affecting both the reproductive and immune systems.
Ross, who published a scientific paper entitled “Fireproof killer whales” believes there is overwhelming evidence to justify the ban of those chemicals in Canada.
Two varieties of the chemical have been withdrawn from North American and European markets, but a third variety, deca-PBDE, is still in use.
If nothing is done to curb it, PBDEs are poised to surpass PCBs as the predominant chemical in killer whales by 2025, according to research.
And the legacy of PCBs is still haunting the oceans.
PCBs were banned in 1977, but Ross and his fellow sci-entists predict they will not be expunged from the bodies of the southern resident whales until 2089.
Whale contamination illustrates how ignorant people are about effect of the thousands of chemicals being dumped in the ocean, Ross said.
“It’s not very reassuring for humans to find high levels of endocrine- disrupting chemicals in animals at the top of the food chain. We would be unwise to ignore what we are seeing,” he said.
Killer whales illustrate the shortcomings of traditional science and research, which is geared to small animals, living short lives within a limited area, Ross said.
Whale researcher Paul Spong, of OrcaLab on Hanson Island, has his toxic nightmares about oil.
Last year a barge spilled its load, including a fuel truck, into Robson Bight, smack in the middle of prime whale territory, but that is nothing compared to what could happen if the provincial and federal governments allow offshore oil and gas exploration, Spong said.
“It potentially poses huge problems for cetaceans and other marine life,” he said.
Copyright Times Colonist (Victoria) 2008
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