From: Rachel's Democracy & Health News #919, Aug. 09, 2007
TWO RULES FOR DECISIONS: TRUST IN ECONOMIC GROWTH VS. PRECAUTION
By Joseph H. Guth
[Joseph H. Guth, JD, PhD, is Legal Director of the Science and Environmental Health Network. He holds a PhD in biochemistry from University of Wisconsin (Madison), and a law degree from New York University. His work has appeared previously in Rachel's #846, #861, #892, #901 and #905.]
Everyone knows the role of law is to control and guide the economy. From law, not economics, springs freedom from slavery, child labor and unreasonable working conditions. Law, reflecting the values we hold dear, governs our economy's infliction of damage to the environment.
Our law contains what might be called an overarching environmental decision rule that implements our social choices. The structure of this decision rule is an intensely political issue, for the people of our democracy must support its far-reaching consequences. Today we (all of us) are rethinking our current environmental decision rule, which our society adopted in the course of the Industrial Revolution.
The "trust in economic growth" environmental decision rule
Our overarching environmental decision rule (which is also prevalent in much of the rest of the world) constitutes a rarely-stated balance of social values that is hard to discern even though it pervades every aspect of our society.
This decision rule relies extensively on cost-benefit analysis and risk assessment, but the decision rule itself is even broader in scope. The foundation of the rule is the assumption that economic activity usually provides a net benefit to society, even when it causes some damage to human health and the environment. (This conception of "net benefit" refers to the effect on society as a whole, and does not trouble itself too much with the unequal distribution of costs and benefits.)
From this assumption, it follows that we should allow all economic activities, except those for which someone can prove the costs outweigh the benefits. This, then, is the prevailing environmental decision rule of our entire legal system: economic activity is presumed to provide a net social benefit even if it causes some environmental damage, and government may regulate (or a plaintiff may sue) only if it can carry its burden of proof to demonstrate that the costs outweigh the benefits in a particular case. Let's call this the "trust in economic growth" decision rule.
The "precautionary principle" environmental decision rule
The "precautionary principle" is equal in scope to the "trust in economic growth" decision rule, but incorporates a profoundly different judgment about how to balance environment and economic activity when they come into conflict. Under this principle, damage to the environment should be avoided, even if scientific uncertainties remain. This rule implements a judgment that we should presumptively avoid environmental damage, rather than presumptively accept it as we do under the "trust in economic growth" rule.
The role of "cost-benefit" analysis
"Cost-benefit" analysis is a subsidiary tool of both decision rules. However, it is used in very different contexts under the two rules. It can sometimes be employed under the "precautionary" decision rule as a way to compare and decide among alternatives. But under the "trust in economic growth" decision rule, cost-benefit analysis appears as the only major issue and often masquerades as the decision rule itself. This is because most of our laws implicitly incorporate the unstated presumption that economic activities should be allowed even if they cause environmental damage. By and large, our laws silently bypass that unstated presumption and start out at the point of instructing government to develop only regulations that pass a cost-benefit test.
Thus, the foundational presumption of the "trust in economic growth" decision rule is simply accepted as a received truth and is rarely examined or even identified as supplying our law's overarching context for cost-benefit calculations. Almost all economists probably agree with it (except those few who are concerned with the global human footprint and are trying to do full cost accounting for the economy as a whole).
The role of "sound science"
How does science, particularly "sound science," relate to all this? Science supplies a critical factual input used by governments and courts in implementing environmental decision rules. Science is employed differently by the two decision rules, but science does not constitute or supply a decision rule itself. Like cost-benefit analysis, science is a subsidiary tool of the decision rules and so cannot properly be placed in "opposition" to either decision rule. A claim that the precautionary principle, as an overarching environmental decision rule implementing a complex balancing of social values, is in "opposition" to science is a senseless claim.
The phrase "sound science" represents the proposition that a scientific fact should not be accepted by the legal system unless there is a high degree of scientific certainty about it. It is a term used by industry in regulatory and legal contexts and is not commonly used by scientists while doing scientific research. However, it resonates within much of the scientific community because it is a call to be careful and rigorous.
"Sound science" also represents a brake on the legal system's acceptance of emerging science, of science that cuts across disciplines, and of science that diverges from the established traditions and methodologies that characterize many specific disciplines of science. "Sound science" encourages scientists who are concerned about the world to remain in their silos, to avoid looking at the world from a holistic viewpoint, and to avoid professional risks.
But, why does it work for industry? The call for government and law to rely only on "sound science" when they regulate is a call for them to narrow the universe of scientific findings that they will consider to those that have a high degree of certainty.
This serves industrial interests under our prevailing "trust in economic growth" decision rule because it restricts the harms to human health and the environment that can be considered by government and law to those that are sufficiently well established to constitute "sound science."
Because the burden of proof is on government, requiring government to rely only on facts established by "sound science" reduces the scope of possible regulatory activity by making it harder for government to carry its burden to show that the benefits of regulation (avoidance of damage to health and environment) outweigh the costs to industry. Exactly the same dynamic is at play when plaintiffs try to carry their burden of proof to establish legal liability for environmental damage.
Shifting the burden of proof would shift the effect of "sound science"
"Sound science" can help industrial interests under a precautionary decision rule, but it also contains a seed of disaster for them.
Precaution is triggered when a threat to the environment is identified, so that the more evidence required to identify a threat as such, the fewer triggers will be pulled. While the precautionary principle is designed to encourage environmental protection even in the face of uncertainty, those opposed to environmental protection urge that the threshold for identification of threats should require as much certainty as possible, and preferably be based only on "sound science."
The seed of disaster for industrial interests is this: the burden of proof can be switched under the precautionary principle (so that when a threat to the environment is identified the proponent of an activity must prove it is safe -- just as a pharmaceutical company must prove that a drug is safe and effective before it can be marketed). When that happens, a call for "sound science" actually would cut against such proponents rather than for them. This is because proponents of an activity would have to provide proof of safety under a "sound science" standard. In other words, the call for "sound science" creates higher burdens on those bearing the burden of proof. In fact, while debates about "sound science" masquerade as debates about the quality of science, the positions that different actors take are actually driven entirely by the underlying legal assignment of the burden of proof.
Why precaution? Because of cumulative impacts.
One of the reasons for adopting the precautionary principle, rather than the "trust in economic growth" decision rule, is "cumulative impacts."
The foundational assumption of the "trust in economic growth" rule (that economic activity is generally to the net benefit of society, even if it causes environmental damage) is further assumed to be true no matter how large our economy becomes. To implement the "trust in economic growth" rule, all we do is eliminate any activity without a net benefit, and in doing this we examine each activity independently. The surviving economic activities, and the accompanying cost-benefit- justified damage to the environment, are both thought to be able to grow forever.
Not only is there no limit to how large our economy can become, there is no limit as to how large justified environmental damage can become either. The "trust in economic growth" decision rule contains no independent constraint on the total damage we do to Earth -- indeed the core structure of this decision rule assumes that we do not need any such constraint. People who think this way see no need for the precautionary principle precisely because they see no need for the preferential avoidance of damage to the environment that it embodies.
But, as we now know, there is in fact a need for a limit to the damage we do to earth. Unfortunately, the human enterprise has now grown so large that we are running up against the limits of the Earth -- if we are not careful, we can destroy our only home. (Examples abound: global warming, thinning of Earth's ozone shield, depletion of ocean fisheries, shortages of fresh water, accelerated loss of species, and so on.)
And it is the cumulative impact of all we are doing that creates this problem. One can liken it to the famous "straw that broke the camel's back." At some point "the last straw" is added to the camel's load, its carrying capacity exceeded. Just as it would miss the larger picture to assume that since one or a few straws do not hurt the camel, straw after straw can be piled on without concern, so the "trust in economic growth" decision rule misses the larger picture by assuming that cost-benefit-justified environmental damage can grow forever.
Thus, it is the total size of our cumulative impacts that is prompting us to revisit our prevailing decision rule. This is why we now need a decision rule that leads us to contain the damage we do. It is why we now must work preferentially to avoid damage to the Earth, even if we forego some activities that would provide a net benefit if we lived in an "open" or "empty" world whose limits were not being exceeded. We can still develop economically, but we must live within the constraints imposed by Earth itself.
Ultimately, the conclusion that we must learn to live within the capacity of a fragile Earth to provide for us, painful as it is, is thrust upon us by the best science that we have -- the science that looks at the whole biosphere, senses the deep interconnections between all its parts, places us as an element of its ecology, recognizes the time scale involved in its creation and our own evolution within it, and reveals, forever incompletely, the manifold and mounting impacts that we are having upon it and ourselves.
STAGE OF A CHILD'S GROWTH DETERMINES HARM FROM TOXIC EXPOSURES
Geneva, Switzerland -- An increased risk of cancer, heart and lung disease in adults can result from exposures to certain environmental chemicals during childhood, the World Health Organization said today. This finding is part of the first report ever issued by the agency focusing on children's special susceptibility to harmful chemical exposures at different stages of their growth.
Air and water contaminants, pesticides in food, lead in soil, as well many other environmental threats which alter the delicate organism of a growing child may cause or worsen disease and induce developmental problems, said the World Health Organization, WHO, releasing the report at its Geneva headquarters.
The peer-reviewed report highlights the fact that in children, the stage in their development when exposure to a threat occurs may be just as important as the magnitude of the exposure.
"Children are not just small adults," said Dr. Terri Damstra, team leader for WHO's Interregional Research Unit. "Children are especially vulnerable and respond differently from adults when exposed to environmental factors -- and this response may differ according to the different periods of development they are going through."
"For example, their lungs are not fully developed at birth, or even at the age of eight, and lung maturation may be altered by air pollutants that induce acute respiratory effects in childhood and may be the origin of chronic respiratory disease later in life," Dr. Damstra said.
Over 30 percent of the global burden of disease in children can be attributed to environmental factors, the WHO study found.
The global health body said this report is the most comprehensive work yet undertaken on the scientific principles to be considered in assessing health risks in children.
The work was undertaken by an advisory group of 24 scientific experts, representing 18 countries. They were convened by WHO to provide insight, expertise, and guidance, and to ensure scientific accuracy and objectivity. Once the text was finalized, it was sent to more than 100 contact points throughout the world for review and comment, and also made available on WHO's International Programme of Chemical Safety website for external review and comment.
The central focus of the study is on the child from embryo through adolescence and on the need to have a good understanding of the interactions between exposure, biological susceptibility, and socioeconomic and nutritional factors at each stage of a child's development.
The scientific principles proposed in the document for evaluating environmental health risks in children will help the health sector, researchers and policy makers to protect children of all ages through improved risk assessments, appropriate interventions and focused research to become healthy adults.
Children have different susceptibilities during different life stages, due to their dynamic growth and developmental processes, the authors said.
Health effects resulting from developmental exposures prenatally and at birth may include miscarriage, still birth, low birth weight and birth defects.
Young children may die or develop asthma, neurobehavioral and immune impairment. Adolescents may experience precocious or delayed puberty.
The vulnerability of children is increased in degraded and poor environments, the report confirms. Neglected and malnourished children suffer the most. These children often live in unhealthy housing, lack clean water and sanitation services, and have limited access to health care and education. For example, lead is known to be more toxic to children whose diets are deficient in calories, iron and calcium.
WHO warns, "One in five children in the poorest parts of the world will not live longer than their fifth birthday -- mainly because of environment-related diseases."
This new volume of the Environmental Health Criteria series, Principles for Evaluating Health Risks in Children Associated with Exposure to Chemicals, is online here.
Copyright Environment News Service (ENS) 2007
From: Voice of America
SCIENTISTS STUDY HEALTH RISKS OF PLASTIC INGREDIENT
By Melinda Smith
Bisphenol A is everywhere. BPA, as it is also called, can be found in the plastic milk bottle used to feed your baby, the cola bottle or food container you pick up for a fast food meal, the kidney dialysis machine patients need to keep them alive, and the dental sealant used to help prevent tooth decay.
A recent study in the journal Reproductive Toxicology raises concerns about adverse effects of BPA in fetal mice, at levels even lower than U.S. government standards permit.
The scientists say widespread exposure through food and liquid containers occurs when the chemical bonds which hold bisphenol A in the plastic degrades. BPA then leaches into the containers.
Frederick vom Saal, a professor of biological sciences at the University of Missouri, says he is concerned about what we absorb and then transmit to our infants. "Very low doses of this -- below the amounts that are present in humans. When particularly exposure occurs in fetuses, in fetuses and newborns, you end up with those babies eventually developing prostate cancer, breast cancer -- they become hyperactive."
Kimberly Lisack is a mother who wants more information about what she feeds her baby. "I get concerned looking at a lot of the packaged baby foods. It's a lot of chemicals and things I don't know what they are."
Bisphenol A has been produced in polycarbonate plastic for decades. A statement released by the American Chemistry Council says the report is at odds with other international studies that say BPA levels pose no health risks to consumers.
LOOKING DEEP, DEEP INTO YOUR GENES
By Laura Wright
Martha Herbert, a pediatric neurologist at Boston's Massachusetts General Hospital, studies brain images of children with autism. She was seeing patients one day a few years ago when a 3-year-old girl walked in with more than the usual cognitive and behavioral problems. She was lactose intolerant, and foods containing gluten always seemed to upset her stomach. Autistic children suffer profoundly, and not just in their difficulty forming emotional bonds with family members, making friends, or tolerating minor deviations from their daily routines. Herbert has seen many young children who've had a dozen or more ear infections by the time they made their way through her door, and many others -- "gut kids" -- with chronic diarrhea and other gastrointestinal problems, including severe food allergies. Such symptoms don't fit with the traditional explanation of autism as a genetic disorder rooted in the brain, and that was precisely what was on Herbert's mind that day. She's seen too many kids whose entire systems have gone haywire.
During the course of the little girl's appointment, Herbert learned that the child's father was a computer scientist -- a bioinformatist no less, someone trained to crunch biological data and pick out patterns of interest. She shared with him her belief that autism research was overly focused on examining genes that play a role in brain development and function, to the exclusion of other factors -- namely, children's susceptibility to environmental insults, such as exposure to chemicals and toxic substances. Inspired by their conversation, Herbert left the office that day with a plan: She and the girl's father, John Russo, head of computer science at the Wentworth Institute of Technology, would cobble together a team of geneticists and bioinformatists to root through the scientific literature looking for genes that might be involved in autism without necessarily being related to brain development or the nervous system.
The group scanned databases of genes already known to respond to chemicals in the environment, selecting those that lie within sequences of DNA with suspected ties to autism. They came up with more than a hundred matches, reinforcing Herbert's belief that such chemicals interact with specific genes to make certain children susceptible to autism.
Although some diseases are inherited through a single genetic mutation -- cystic fibrosis and sickle cell anemia are examples -- the classic "one gene, one disease" model doesn't adequately explain the complex interplay between an individual's unique genetic code and his or her personal history of environmental exposures. That fragile web of interactions, when pulled out of alignment, is probably what causes many chronic diseases: cancer, obesity, asthma, heart disease, autism, and Alzheimer's, to name just a few. To unravel the underlying biological mechanisms of these seemingly intractable ailments requires that scientists understand the precise molecular dialogue that occurs between our genes and the environment -- where we live and work, what we eat, drink, breathe, and put on our skin. Herbert's literature scan was a nod in this direction, but actually teasing out the answers in a laboratory has been well beyond her or anyone else's reach -- until now.
Consider for a moment that humans have some 30,000 genes, which interact in any number of ways with one or more of the 85,000 synthetic, commercially produced chemicals, as well as heavy metals, foods, drugs, myriad pollutants in the air and water, and anything else our bodies absorb from the environment. The completion of the Human Genome Project in 2003 armed scientists with a basic road map of every gene in the human body, allowing them to probe more deeply into the ways our DNA controls who we are and why we get sick, in part by broadening our understanding of how genes respond to external factors. In the years leading up to the project's completion, scientists began developing powerful new tools for studying our genes. One is something called a gene chip, or DNA microarray, which came about through the marriage of molecular biology and computer science. The earliest prototype was devised about a decade ago; since then these tiny devices, as well as other molecular investigative tools, have grown exponentially in their sophistication, pushing medical science toward a new frontier.
Gene chips are small, often no larger than your typical domino or glass laboratory slide, yet they can hold many thousands of genes at a time. Human genes are synthesized and bound to the surface of the chip such that a single copy of each gene -- up to every gene in an organism's entire genome -- is affixed in a grid pattern. The DNA microarray allows scientists to take a molecular snapshot of the activity of every gene in a cell at a given moment in time.
The process works this way: Every cell in your body contains the same DNA, but DNA activity -- or expression -- is different in a liver cell, say, than it is in a lung, brain, or immune cell. Suppose a scientist wishes to analyze the effect of a particular pesticide on gene activity in liver cells. (This makes sense, since it is the liver that processes and purges many toxins from the body.) A researcher would first expose a liver cell culture in a test tube to a precise dose of the chemical. A gene's activity is observed through the action of its RNA, molecules that convey the chemical messages issued by DNA. RNA is extracted from the test tube, suspended in a solution, then poured over the gene chip. Any given RNA molecule will latch on only to the specific gene that generated it. The genes on the chip with the most RNA stuck to them are the ones that were most active in the liver cells, or most "highly expressed." The genes that don't have any RNA stuck to them are said to be "turned off" in those cells. Scientists use the microarray to compare the exposed cells to non-exposed, control cells (see sidebar). Those genes that show activity in the exposed cells but not in the control cells, or vice versa, are the ones that may have been most affected by the pesticide exposure.
DNA microarrays open the door to an entirely new way of safety-testing synthetic chemicals: Each chemical alters the pattern of gene activity in specific ways, and thus possesses a unique genetic fingerprint. If a chemical's genetic fingerprint closely matches that of another substance already known to be toxic, there is good reason to suspect that that chemical can also do us harm. Ultimately, government agencies charged with regulating chemicals and protecting our health could use this method, one aspect of a field called toxicogenomics, to wade through the thousands of untested or inadequately studied chemicals that circulate in our environment. In other words, these agencies could make our world safer by identifying -- and, one hopes, banning -- hazardous substances.
For such a young field, toxicogenomics has already begun to challenge some fundamental assumptions about the origins of disease and the mechanisms through which chemicals and various environmental exposures affect our bodies. Consider the case of mercury, which was identified as poisonous many centuries ago. Its potential to wreak havoc on the human nervous system was most tragically demonstrated in the mass poisoning of the Japanese fishing village of Minamata in the 1950s. More recently, scientists have begun to amass evidence suggesting that mercury also harms the immune system. In 2001, Jennifer Sass, a neurotoxicologist and senior scientist at the Natural Resources Defense Council (NRDC), who was then a postdoctoral researcher at the University of Maryland, designed an experiment that included the use of microarrays and other molecular tools to figure out how, exactly, mercury was interfering with both our nervous and immune systems. She grew cells in test tubes -- one set for mouse brain cells, another for mouse liver cells -- and exposed them to various doses of mercury so that she could see which genes were being switched on and off in the presence of the toxic metal. In the brain and the liver cells, she noticed unusual activity in the gene interleukin-6, which both responds to infection and directs the development of neurons.
"We thought we had mercury figured out," says Ellen Silbergeld, a professor of environmental health sciences at Johns Hopkins University, who collaborated with Sass on the study. Genomic tools may identify effects of other chemicals by allowing scientists to "go fishing," as Silbergeld puts it, for things they didn't know to look for.
The findings of Sass, Silbergeld, and others indicate that mercury might play a role in the development of diseases involving immune system dysfunction. These diseases perhaps include autism -- think of Herbert's patients with their inexplicable collection of infections and allergies -- but also the spate of autoimmune disorders that we can't fully explain, from Graves' disease and rheumatoid arthritis to multiple sclerosis and lupus.
"Do we need to reevaluate our fish advisories?" Silbergeld asks. "Are our regulations actually protecting the most sensitive people?" We target pregnant women and children because we've presumed that mercury's neurotoxic effects are most damaging to those whose brains are still developing. Sass and Silbergeld's findings don't contradict that assumption, but they do suggest that there might be other adults who are far more vulnerable than we'd realized -- who simply can't tolerate the more subtle effect the metal has on their immune system because of a peculiarity in their genetic makeup. Designing fish advisories for those people, whose sensitivities are coded in their DNA, is a challenge we've never tackled before.
Translating new findings about how chemicals affect gene activity into something of broader public health value will require that we understand precisely the tiny genetic differences among us that make one person or group of people more vulnerable than others to certain environmental exposures. One way to do that is by slightly modifying the gene chip to allow researchers to scan up to a million common genetic variants -- alternate spellings of genes, so to speak, that differ by just a single letter -- to look for small differences that might make some people more likely to get sick from a toxic exposure.
Our attempts to identify those who are most genetically susceptible to developing a particular disease as a result of environmental exposures have already yielded important insights. Patricia Buffler, dean emerita of the School of Public Health at the University of California, Berkeley, has found that children with a certain genetic variant may be susceptible to developing leukemia in high-traffic areas, where they're likely to be exposed to benzene compounds in auto exhaust. Other studies have found that a particular genetic variation in some women who drink chlorinated municipal water leads to an increased likelihood that they'll give birth to underweight babies. Still others have found that a specific version of an immune gene, HLA-DP, renders people vulnerable to the toxic effects of the metal beryllium, which causes a chronic lung condition in the genetically sensitive population. This particular vulnerability raises some sticky workplace issues. Toxic exposure to beryllium occurs almost exclusively in industrial settings where welders and other machinists come in contact with the metal while making defense industry equipment, computers, and other electronics. Should employers test their workers for genetic variants that may put them at risk for developing a disease? Could that information be used to bar someone from a job? Such ethical considerations, and their legal and public policy ramifications, will only multiply as we learn more.
But first, a more fundamental question: Do we even understand what today's chronic diseases are? It is beginning to appear that what we call autism may in fact be many illnesses that we've lumped together because those who are afflicted seem to behave similarly. Doctors base their diagnosis on behavioral symptoms, not on what caused those symptoms. Some scientists now refer to the condition as "autisms," acknowledging that we've yet to find a single, unifying biological mechanism, despite the identification, in some studies, of a handful of genes that may confer increased vulnerability. But then, genes or environmental exposures that appear to be important causal factors in one study may not show up at all in another. This leaves scientists to wonder whether the problem isn't that the disease is so diverse in its biological origins that only a truly massive study -- involving many thousands of patients -- would have the statistical power to tease apart the various factors involved.
The same difficulty probably holds true for many chronic diseases, explains Linda Greer, a toxicologist and director of the health program at NRDC. "What we think of as asthma, for example, is probably not one condition at all. It's probably many different diseases that today we simply call asthma." Seemingly contradictory explanations for the epidemic could all turn out to be true. Until we are able to sift out what makes one asthmatic child different from the next -- how and why their respective molecular makeups differ -- treatments or preventive measures that work for one child will continue to fail for another.
At the Centers for Disease Control and Prevention, Muin Khoury, the director of the National Office of Public Health Genomics, has created theoretical models to try to figure out just how many different factors may be involved in most chronic diseases. His findings suggest that some combination of 10 to 20 genes plus a similar number of environmental influences could explain most of the complex chronic diseases that plague the population. But to analyze how even a dozen genes interact with a dozen environmental exposures across large populations requires vast studies: immense numbers of people and huge volumes of data -- everything from precise measurements of gene activity inside cells to exact recordkeeping of subject" exposure to environmental hazards. Microarrays and other molecular tools now make such studies possible.
In 2003, Columbia University and the Norwegian government together launched the Autism Birth Cohort, one of the largest autism investigations in history. The study will track 100,000 Norwegian mothers and children -- from before birth through age 18 -- collecting clinical data, blood, urine, and other biological materials. It will also collect RNA in order to analyze gene activity. Though initial results are due in 2011, it will take decades to complete this study, and RNA samples will have to be painstakingly archived while the investigators await additional funding. Although the current study is not focused on environmental health per se, researchers plan to measure a variety of biological exposures -- including infection, environmental toxins, and dietary deficiencies -- in each mother and child. As the children grow up, and as some among them develop disease, scientists will have complete records to analyze for key commonalities and differences. Which genes do the sick children have in common? Which chemical exposures were most meaningful? The answers may provide clues not only to the origins of autism, but to many other disorders, from cerebral palsy to asthma to diabetes. Other archiving projects are even more ambitious, such as the U.K. Biobank project, which has begun to enroll 500,000 people to create the world's largest resource for studying the role of the environment and genetics in health and disease.
As vital to our understanding of human disease as such studies may prove to be, a 50-year-old taking part in the U.K. Biobank project isn't likely to reap the rewards. "It will take a long time to make sense of the data," says Paul Nurse, a 2001 Nobel laureate in medicine and the president of Rockefeller University. According to Nurse, it may well be that most of the researchers starting these studies today won't see the final results -- the data will be analyzed by their children. In his estimation, that's all the more reason "to get on with it."
In response to concern that environmental exposures were affecting children's health, the Clinton administration in 2000 launched the National Children's Study, the largest such undertaking in the United States, under the auspices of the National Institutes of Health. The goal was to enroll 100,000 children; a genetic biobanking component has since been added. Investigators have not yet recruited participants, in part because of financial uncertainties. The Bush administration's 2007 budget proposal completely eliminated money for the study, though Congress reinstated funding in February.
The irony is that cutting funding for such projects may be the most expensive option of all. Even if we successfully address campaign- dominating political issues like skyrocketing medical costs and the growing ranks of the uninsured, our failure to consider the fundamental mechanisms of disease -- the interplay between our genes and the environment -- could still bankrupt us, socially if not financially. Until we're able to interrupt the slide toward disease much earlier, based on our developing knowledge of how genes and the environment interact, medicine will remain the practice of "putting people back together after they've been hit by the train," says Wayne Matson, a colleague of Martha Herbert's who studies Huntington's and other neurodegenerative diseases at the Edith Nourse Rogers Memorial Veterans Hospital in Bedford, Massachusetts. "It would be a lot better if we knew how to pull that person off the tracks in the first place."
Copyright 2007 by the Natural Resources Defense Council
GLOBAL WARMING WILL STEP UP AFTER 2009: SCIENTISTS
Washington (Reuters) -- Global warming is forecast to set in with a vengeance after 2009, with at least half of the five following years expected to be hotter than 1998, the warmest year on record, scientists reported on Thursday.
Climate experts have long predicted a general warming trend over the 21st century spurred by the greenhouse effect, but this new study gets more specific about what is likely to happen in the decade that started in 2005.
To make this kind of prediction, researchers at Britain's Met Office -- which deals with meteorology -- made a computer model that takes into account such natural phenomena as the El Nino pattern in the Pacific Ocean and other fluctuations in ocean circulation and heat content.
A forecast of the next decade is particularly useful, because climate could be dominated over this period by these natural changes, rather than human-caused global warming, study author Douglas Smith said by telephone.
In research published in the journal Science, Smith and his colleagues predicted that the next three or four years would show little warming despite an overall forecast that saw warming over the decade.
"There is... particular interest in the coming decade, which represents a key planning horizon for infrastructure upgrades, insurance, energy policy and business development," Smith and his co- authors noted.
The real heat will start after 2009, they said.
Until then, the natural forces will offset the expected warming caused by human activities, such as the burning of fossil fuels, which releases the greenhouse gas carbon dioxide.
"HINDCASTS" FOR THE FUTURE
"There is... particular interest in the coming decade, which represents a key planning horizon for infrastructure upgrades, insurance, energy policy and business development," Smith and his co- authors noted.
To check their models, the scientists used a series of "hindcasts" -- forecasts that look back in time -- going back to 1982, and compared what their models predicted with what actually occurred.
Factoring in the natural variability of ocean currents and temperature fluctuations yielded an accurate picture, the researchers found. This differed from other models which mainly considered human-caused climate change.
"Over the 100-year timescale, the main change is going to come from greenhouse gases that will dominate natural variability, but in the coming 10 years the natural internal variability is comparable," Smith said.
In another climate change article in the online journal Science Express, U.S. researchers reported that soot from industry and forest fires had a dramatic impact on the Arctic climate, starting around the time of the Industrial Revolution.
Industrial pollution brought a seven-fold increase in soot -- also known as black carbon -- in Arctic snow during the late 19th and early 20th centuries, scientists at the Desert Research Institute found.
Soot, mostly from burning coal, reduces the reflectivity of snow and ice, letting Earth's surface absorb more solar energy and possibly resulting in earlier snow melts and exposure of much darker underlying soil, rock and sea ice. This in turn led to warming across much of the Arctic region.
At its height from 1906 to 1910, estimated warming from soot on Arctic snow was eight times that of the pre-industrial era, the researchers said.
Copyright 2007 Reuters Ltd
From: News & Observer (Charlotte, N.C.)
TREES OF LIMITED VALUE VS. WARMING
By Margaret Lillard, The Associated Press
RALEIGH -- A decade-long experiment led by Duke University scientists indicates that trees provide little help in offsetting increased levels of the greenhouse gas carbon dioxide.
That's because the trees grew more, but only those that got the most water and nutrients could store significant levels of carbon.
"The responses are very variable according to how available other resources are -- nutrients and water -- that are necessary for tree growth," said Heather McCarthy, a former graduate student at the private university in Durham who spent 6 1/2 years on the project. "It's really not anywhere near the magnitude that we would really need to offset emissions."
McCarthy, now a postdoctoral fellow at the University of California at Irvine, presented the findings this week at a national meeting of the Ecological Society of America in San Jose, Calif. Researchers from the U.S. Forest Service, Boston University and the University of Charleston also contributed to the report.
All helped in the Free Air Carbon Enrichment experiment, in which pine trees in Duke Forest were exposed to higher-than-normal levels of carbon dioxide.
The scientists also gathered data on whether the forest could grow fast enough to help control predicted increases in the level of carbon dioxide.
The loblolly pines grew more tissue, but only those that got the most water and nutrients were able to store enough carbon to have any impact on global warming, the scientists discovered.
"These trees are storing carbon," McCarthy said Wednesday. "It's just not such a dramatic quantity more."
That means proposals to use trees to bank increasing amounts of carbon dioxide emitted by humans may depend too heavily on the weather and large-scale fertilization to be feasible.
"It would be an attractive solution, for sure," McCarthy said. "I don't know how realistic people thought it was, but I think there were certainly high hopes."
Scientists blame the worldwide buildup of carbon dioxide -- due largely to the burning of fossil fuel -- for global warming. The United States is second only to China in the level of greenhouse gas it emits as a nation.
The experiment site, funded by the U.S. Department of Energy, holds four forest plots dominated by loblolly pines in Duke Forest, in north-central North Carolina.
The trees are exposed to extra levels of carbon dioxide from computer- controlled valves that are mounted on rings of towers above the treetops. The valves can be adjusted to account for wind speed and direction, and sensors throughout the plot monitor carbon dioxide levels, McCarthy said. Four more plots received no extra gas.
Trees exposed to the gas produced about 20 percent more biomass -- wood and vegetation -- than untreated trees. But the researchers said the amounts of available water and nitrogen nutrients varied substantially between plots.
Ram Oren, the project director and a professor of ecology at Duke's Nicholas School of the Environment and Earth Sciences, said in a written statement that replicating the tree growth in the real world would be virtually impossible.
"In order to actually have an effect on the atmospheric concentration of CO2, the results suggest a future need to fertilize vast areas," Oren said. "And the impact on water quality of fertilizing large areas will be intolerable to society."
Copyright Copyright 2007, The News & Observer Publishing Company
From: International Herald Tribune
EXTREME WEATHER: A GLOBAL PROBLEM
By Reuters and The Associated Press
GENEVA: Much of the world has experienced record-breaking weather events this year, from flooding in Asia to heat waves in Europe and snowfall in South Africa, the United Nations weather agency said Tuesday.
The World Meteorological Organization said global land surface temperatures in January and April were the warmest since such data began to be recorded in 1880, at more than one degree Celsius higher than average for those months.
There have also been severe monsoon floods across South Asia; abnormally heavy rains in northern Europe, China, Sudan, Mozambique and Uruguay; extreme heat waves in southeastern Europe and Russia; and unusual snowfall in South Africa and South America this year, the meteorological agency said.
"The start of the year 2007 was a very active period in terms of extreme weather events," Omar Baddour of the agency's World Climate Program said in Geneva.
While most scientists believe extreme weather events will be more frequent as heat-trapping carbon dioxide emissions cause global temperatures to rise, Baddour said it was impossible to say with certainty what the second half of 2007 would bring. "It is very difficult to make projections for the rest of the year," he said.
The Intergovernmental Panel on Climate Change, a UN group of hundreds of experts, has noted an increasing trend in extreme weather events over the past 50 years and said irregular patterns will probably intensify.
South Asia's worst monsoon flooding in recent memory has affected 30 million people in India, Bangladesh and Nepal, destroying croplands, livestock and property and raising fears of new health crises in the densely populated region.
Heavy rains also hit southern China in June, with nearly 14 million people affected by floods and landslides that killed 120 people, the World Meteorological Organization said.
England and Wales this year had their wettest May and June since records began in 1766, resulting in extensive flooding and more than $6 billion in damage, as well as at least nine deaths. Germany swung from its driest April since country-wide observations started in 1901 to its wettest May on record. And torrential rains have followed weeks of severe drought in northern Bulgaria -- officials said Tuesday that at least seven people have been killed in floods.
Mozambique suffered its worst floods in six years in February, followed by a tropical cyclone the same month. Flooding of the Nile River in June caused damage in Sudan.
In May, Uruguay had its worst flooding since 1959.
In June, the Arabian Sea had its first documented cyclone, which touched Oman and Iran.
Temperatures also strayed from the expected this year. Records were broken in southeastern Europe in June and July, and in western and central Russia in May. In many European countries, April was the warmest ever recorded.
Argentina and Chile saw unusually cold winter temperatures in July while South Africa had its first significant snowfall since 1981 in June.
The World Meteorological Organization and its 188 member states are working to set up an early warning system for extreme weather events. The agency also wants to improve monitoring of the impacts of climate change, particularly in poorer countries that are expected to bear the brunt of floods.
As exceptionally heavy rains continued to cut a wide swath of ruin across northern India, a top UN official warned Tuesday that climate change could destroy vast swaths of farmland in the country, ultimately affecting food production and adding to the problems of already desperate peasants, The New York Times reported from New Delhi.
Even a small increase in temperatures, said Jacques Diouf, head of the Food and Agricultural Organization, could push down crop yields in the world's southern regions, even as agricultural productivity goes up in the north. A greater frequency of droughts and floods, one of the hallmarks of climate change, the agency added, could be particularly bad for agriculture.
"Rain-fed agriculture in marginal areas in semi-arid and sub-humid regions is mostly at risk," Diouf said. "India could lose 125 million tons of its rain-fed cereal production -- equivalent to 18 percent of its total production." That is a sign of the steep human and economic impact of extreme weather in India.
Copyright International Herald Tribune
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