Rachel's Democracy & Health News #909
"Environment, health, jobs and justice--Who gets to decide?"
Thursday, May 31, 2007..................Printer-friendly version
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^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ Featured stories in this issue... A Response To Paul Hawken's 'To Remake the World' Activist and author Kate Davies responds to Paul Hawken about the nature and future of the worldwide social movement that has arisen in response to widespread ecological devastation and global warming. The Faroes Statement In this powerful consensus statement, more than 200 scientists from five continents call for a precautionary approach to toxic chemicals, to protect fetuses and children from chemical exposures that may cause serious disease later in life, and which may also afflict their children and grandchildren. The Faroes Statement defines a "new paradigm of understanding in toxicology." Scientists Warn of Dangers Chemicals Pose To Fetuses, Kids The Los Angeles Times put the blockbuster "Faroes Statement" story on page 1. So far, not a peep from the Boston Globe, the Washington Post or the New York Times. The Developmental Basis of Health and Disease A new hypothesis undergoing scientific testing and scrutiny is called the developmental basis of health and disease: "If true, then it says that the focus on disease prevention and intervention must change from the time of disease onset to perhaps decades prior: during the in utero and neonatal period. Perhaps the reason it has been so difficult to link environmental exposure to disease susceptibility is that scientists have been looking at the wrong time!" Watching TV Before Age 2 Leads To Attention Deficits and Obesity Early exposure to TV can have a negative impact on an infant's rapidly developing brain and put children at a higher risk for attention problems, diminished reading comprehension, and obesity, researchers say. The Link Between Early Childhood Education and Health The health of adults is determined not only by early nutrition and exposure to chemicals, but also by early educational experiences, which shape the architecture of the brain. An Important Conference on Corporate Power -- June 8-10 An important conference to be held June 8-10 in Washington, DC. "Taming the Giant Corporation" will investigate the evolving sources and forms of corporate power, and how it can be subordinated to people's control (including by displacing corporations altogether from certain segments of the economy and society). Learn more about the conference at http://www.tamethecorporation.org/. :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Rachel's Democracy & Health News #909, May 31, 2007 [Printer-friendly version] A RESPONSE TO PAUL HAWKEN'S 'TO REMAKE THE WORLD' By Kate Davies Hooray for Paul Hawken! His article "To Remake the World" in Rachel's News #908 and his new book "Blessed Unrest: How the Largest Movement in the World Came into Being and Why No One Saw it Coming" are extremely timely and thought-provoking. Hawken has put his finger on a global phenomenon that has been growing since the 1999 protests against the World Trade Organization in Seattle. Largely unacknowledged by the spotlight of media attention, a new social movement has been quietly gaining strength in the U.S. and internationally. In bringing it to light, Hawken has revealed a trend that is positive and hopeful at a time when these qualities are sorely needed in the world. Although he has done an outstanding job of describing the new movement, several points call out for further exploration. First, Hawken shies away from giving the new movement the full recognition of a name, calling it instead "this unnamed movement." This is a little strange because it has already been given several names. My favorite is "the new progressive movement," in homage to the U.S. Progressive Movement of the late 19th and early 20th centuries. The new progressive movement embraces many of the same principles as its predecessor, including beliefs in truly democratic institutions and processes, efficient government and the elimination of corruption, social and economic justice, regulation of large corporations and monopolies, and environmental protection. He also asserts that the new movement lacks many basic attributes of previous social movements, specifically an ideology, leaders, and internal organization. Let's look at each of these in more detail. Ideology Hawken says the new movement does not have an ideology and its "big contribution is the absence of one big idea." He is right -- in a sense. The new movement does not impose a rigid article of faith on its members, but it is guided by one big, inspirational idea. Indeed, Hawken acknowledges as much in the article's title. The movement's big, inspirational idea is that ordinary people, acting together, can "remake the world." Collectively, empowered citizens can do more than just succeed on individual issues, like climate change or immigration. They can do more than just win legislative victories, like banning toxic flame retardants or protecting endangered species. The new movement is motivated by the transformative idea that by working together citizens can recreate the whole of society. This is not a new concept. It is the same one that stimulated the birth of this country. But it is an idea that most Americans seem to have forgotten of late. In today's social and political climate, the thought that ordinary people can shape society -- rather than just relying on politicians, corporate leaders and economists -- is truly radical. This may not be "ideology" in the sense that Hawken uses the word, but it is a "big idea" that motivates the entire movement. In addition to this, there are four goals or aspirations that unite much of the movement: ** Creating an open, participatory and fully accountable democracy; ** Social and economic justice; ** Sustainability for people and the planet; and ** Health and wellbeing for all. Most members of the new movement are committed to all these goals, even if they work on only one. Collectively, they provide an inspiring and world-changing ideology, especially when combined with the idea that empowered citizens really can remake society. Leaders Hawken states that the new movement has few recognizable leaders. He says: "Its leaders are farmers, zoologists, shoemakers, and poets." In short, there is no Martin Luther King Jr. or Mahatma Gandhi to look up to and venerate. Going one step further, I would say that the un-acclaimed leaders of the new movement exemplify new types of leadership. Transcending traditional concepts of charismatic and authoritative leadership, they are extremely low key and modest. They are people who emerge in response to specific situations and then relinquish their role when circumstances change. And they are people who serve a group rather than impose their will upon it. The new movement is not alone in embodying new types of leadership. Many organizations are now experimenting with different approaches. Indeed, innovative ways of thinking about leadership have become very fashionable lately. Many authors, including Ronald Heifetz, Peter Senge and Meg Wheatley, have advocated many innovative ideas, such as: ** Seeing leadership as a process of relationship, rather than control; ** Recognizing that there are many different types of leaders; ** Thinking about leadership from a systems perspective; and ** Focusing on the adaptive challenges of long term change, rather than imposing immediate technical fixes. They highlight that the concept of leadership itself is changing. So it should not be surprising that the leaders of the emerging movement are different from those of previous movements. Internal Organization Hawken asserts that the new movement does not have any internal organization, saying: "It forms, gathers and dissipates quickly," an organic process that is "dispersed, inchoate, and fiercely independent." This is true, but the idea that the emerging movement is more of a loose network than a coherent organization is not new. In early 2004, Gideon Rosenblatt, Executive Director of ONE/Northwest, published a paper called "Movement as Network: Connecting People and Organizations in the Environmental Movement." In it, Rosenblatt made the point that the strength of the environmental movement is the countless links between people and organizations, rather than the people or the organizations themselves. Although the "movement as network" idea espoused by Hawken and Rosenblatt has much to commend it, social movements need at least some internal organization. Without any lasting internal structures, it can be difficult to sustain the long-term political momentum needed to successfully confront the entrenched power elites. So what types of structures would be helpful? There are many candidates including policy "think tanks" to facilitate strategic planning, national or regional groups to help local ones mobilize the public, research units to provide information, educational institutions to provide training and support, groups with expertise in communications, and last but not least, organizations with fundraising experience. Beyond "To Remake the World" and "Blessed Unrest" The next step beyond Paul Hawken's article and book is to ask: "How can we build the new movement?" The answer may determine not only the success of the movement itself but also whether it can truly "remake the world." I believe that the emerging movement needs to deepen its understanding of what it takes to achieve systemic social change. This will require a greater understanding of the culture it wants to transform and a more strategic approach to advance progressive change. Understanding Culture Many members of the new movement are natural activists -- me included. By this, I mean we want to identify problems and solve them. We want to fix what's wrong with the world! Our strengths lie in targeting specific issues and promoting solutions. But this emphasis on particular problems means that we pay less attention to the cultural origins that cause the problems we seek to correct. Developing an in-depth understanding of the fundamental economic, political and social forces that shape western culture is essential to identify the leverage points for change. If the new movement does not have a comprehensive knowledge of the culture in which it operates, how can it hope to intervene effectively? This is challenging because issues are usually represented separately from each other by the media and other mainstream social institutions. Unemployment is portrayed as a different issue from racism. Racism is framed independently of environmental quality. Environmental quality is described without any connection to the economy. This fragmentation makes the public perceive individual issues in isolation from one another and prevents them from seeing the common cultural origins that connect different issues. A Strategic Approach to Progressive Change Activists' usual emphasis on immediate solutions also means that the new movement pays less attention to strategies for long term success. As a result, it is relatively unskilled at achieving lasting, resilient change. Although the emerging movement is good at winning battles, it needs a better understanding of the strategies necessary to win the war. Developing a strategic approach to progressive change will require knowledge of how social change actually happens. So how can the new movement acquire such knowledge? 1. One key source of information is previous movements, such as the civil rights, anti-Vietnam War, and women's movements. These and other movements have not yet been adequately studied for what they can teach the new movement about progressive social change. 2. Current thinking about the process of social change provides another source. Ideas about social constructivism will be particularly relevant. 3. A third source is adult learning theory. Much work has already been done on the relationship between learning and change that will be helpful. In summary, the emerging movement could learn a lot about the process of progressive social change that will enable it to be more strategic. Closing Comment Paul Hawken's article and book make an important contribution to progressive social change. They describe what has previously been an unnoticed, but widespread, movement and in doing they so make it much more visible. But Hawken's work is double-edged. At the same time as he describes the new movement, he asserts that it is fundamentally indescribable, saying: "No book can explain it, no person can represent it, no words can encompass it." This remark runs the risk of being more poetic than helpful. Indeed, on the basis of these words, Hawken's readers may question the existence of a movement at all. If it cannot be explained, is it in fact real? If it cannot be represented, does it actually exist? If it cannot be encompassed, is it really a single entity? I fear that Hawken's dualistic representation of the movement could dilute its significance and effectiveness. It also threatens to undermine his central thesis -- that there is a new global movement for progressive social change. Hawken's true gift is to help us all see just how real this movement is -- real enough "to remake the world." ============== Kate Davies is Core Faculty in the Center for Creative Change at Antioch University Seattle. She is currently working on a book called "Making Change: Ideas, Values and Strategies for Building the New Progressive Movement." Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: PPTOX 2007, May 24, 2007 [Printer-friendly version] THE FAROES STATEMENT Human health effects of developmental exposure to environmental toxicants Consensus statement issued by the International Conference on Fetal Programming and Developmental Toxicity [Introduction: This consensus statement was issued March 24, 2007, by the International Conference on Fetal Programming and Developmental Toxicity held May 20-24, 2007, at Torshavn, Faroe Islands, which was attended by more than 200 biologists, toxicologists, epidemiologists, nutrion researchers, and pediatricians. The conference was organized jointly with, and sponsored by, BCPT (the journal, Basic & Clinical Pharmacology and Toxicology); the World Health Organization; the European Environment Agency; the Centers for Disease Control and Prevention; National Institute of Environmental Health Sciences and National Institute of Child Health and Human Development, National Institutes of Health. The conference was co-chaired by Philippe Grandjean (University of Southern Denmark and Harvard School of Public Health) and Pal Weihe (The Faroese Hospital System).] Background Fetal life and early infancy are periods of remarkable susceptibility to environmental hazards. Toxic exposures to chemical pollutants during these windows of increased susceptibility can cause disease and disability in infants, children, and across the entire span of human life. Among the effects of toxic exposures recognised in the past have been congenital malformations and other adverse pregnancy outcomes. These outcomes may be readily apparent and have been linked to toxicant exposures during or prior to pregnancy. Even subtle effects caused by chemical exposures during early development may lead to important functional deficits and increased risks of disease later in life. The notion of developmental plasticity of organ functions and disease risks has gained much support from both experimental and epidemiological studies. The timing of exposure -- with an emphasis on critical windows of susceptibility -- has therefore become a crucial factor to be considered in toxicological assessments. During May 20-24, 2007, researchers in the fields of environmental health, environmental chemistry, developmental biology, toxicology, epidemiology, nutrition, and paediatrics gathered at the International Conference on Fetal Programming and Developmental Toxicity, in Torshavn, Faroe Islands. The conference goal was to highlight new insights into the effects of prenatal and early postnatal exposure to toxicants, and their sustained effects on the individual throughout their lifespan. The Conference brought together, for the first time, key researchers to focus on human data and translation of laboratory results to elucidate the environmental risks to human health. Research state of the art The developing fetus is extraordinarily susceptible to perturbation of the intrauterine environment. Fetal development is adjusted to the intrauterine environment of nutrients and energy supply to fit the anticipated postnatal environmental conditions. If a disparity arises between prenatal and postnatal environments, it can cause abnormalities in energy metabolism, endocrine functions, and organ development. Evolution seems to have favoured a "thrifty" phenotype that optimizes the energy use, but which, in an environment with ample food and limited energy expenditure, can increase the likelihood of developing obesity, metabolic syndrome, and associated diseases. The physiological mechanisms involved in the development of energy and nutrient metabolism are also highly vulnerable to toxic effects of environmental chemicals. Chemical exposures during prenatal and early postnatal life can bring about important effects on gene expression, which determines normal development and also predisposes to disease risks during adolescence and adult life. Many environmental chemicals can alter gene expression by DNA methylation and chromatin remodelling. These epigenetic changes can cause lasting functional changes in specific organs and tissues and increased susceptibility to disease that may even affect successive generations. New research on rodent models shows that developmental exposures to toxic chemicals, such as the hormonally active substances, diethylstilbestrol, tributyl tin, bisphenol A, genistein, can increase the incidence of reproductive abnormalities, metabolic disorders, including obesity and diabetes, and cancer, presumably through epigenetic mechanisms that do not involve changes to DNA sequences but may be heritable. Prenatal exposure to diethylstilbestrol, an estrogenic drug no longer used on pregnant women, causes an increased risk of vaginal, uterine, and breast cancer. Low-level developmental exposure to a plastics ingredient, bisphenol A, can result in increased susceptibility to breast cancer or prostate cancer, and prenatal exposure to vinclozoline, a common fungicide, also promotes later development of cancer. These substances are only weak carcinogens, if at all, in the adult organism but are nonetheless hazardous to the growing fetus. In addition, when exposure to a carcinogenic substance occurs during early development, the expected life-span will exceed the normal latency period for development of the disease. Functioning of the human reproductive system is highly vulnerable to changes in the intrauterine hormonal environment. In men, increasing occurrence of testicular cancer, poor semen quality, and cryptorchidism have all been linked to developmental exposures to maternal smoking and endocrine disrupting chemicals, such as diethylstilbestrol. Additional risk factors include fertility treatment of the mother, phthalate exposure, and occupational exposure to pesticides with suspected estrogenic and antiandrogenic activity. Perinatal exposure to endocrine disrupting chemicals, such as polychlorinated or polybrominated biphenyls, endosulfan, or DDT compounds, may affect puberty development and sexual maturation at adolescence. Expression of some of these effects may be promoted by predisposing genetic traits. The brain is particularly sensitive to toxic exposures during development, which involves a complex series of steps that must be completed in the right sequence and at the right time. Slight decrements in brain function may have serious implications for social functioning and economic activities, even in the absence of mental retardation or obvious disease. Each neurotoxic contaminant may perhaps cause only a negligible effect, but the combination of several toxic chemicals, along with other adverse factors, such as maternal stress or decreased thyroid function, may trigger substantial decrements in brain function and may predispose to the development of serious degenerative disease. The immune system also undergoes important development both before and after birth. New evidence suggests that exposure to some immunotoxic chemicals, such as polychlorinated biphenyls and atrazine, and maternal stress may cause aberrant reactions of the immune system to foreign proteins, including vaccines. Such effects may be related to a shift in immune system balance, with an increased susceptibility to infections and an increased risk of development of allergy in the child. While the research on developmental toxic effects has to date emphasised maternal exposures and the neonatal environment, the possibility exists that paternal exposures may also affect the child's development. Experimental studies suggest that ionizing radiation, smoking, and certain chemicals may be of importance, and some exposures may also affect the sex ratio of the children. Conclusions Three aspects of children's health are important in conjunction with developmental toxicity risks. First, the mother's chemical body burden will be shared with her fetus or neonate, and the child is then likely to be exposed to larger doses relative to the body weight. Second, susceptibility to adverse effects is increased during development, from preconception through adolescence. Third, developmental exposures to toxicants can lead to life-long functional deficits and manifestations of increased disease risks. Research into the environmental influence on developmental programming of health and disease has therefore led to a new paradigm of toxicologic understanding. The old paradigm, developed over four centuries ago by Paracelsus, was that "the dose makes the poison". However, for exposures sustained during early development, the most important issue is that "the timing makes the poison". This extended paradigm deserves wide attention to protect the fetus and child against preventable hazards. Part of the new insight derives from numerous animal studies on fetal programming being responsible for reproductive, immunological, neurobehavioural, cardiovascular, and endocrine dysfunctions and diseases, as well as certain cancers and obesity. These adverse effects have been linked to chemical pollutants at realistic human exposure levels similar to those occurring from environmental sources. Among the mechanisms involved, particular concern is raised about changes in gene expression due to altered epigenetic marking, which may not only lead to increased susceptibility to diseases later in life, but the effects may also be passed on to subsequent generations. Most chronic disease processes are characterised by multi-causality and complexity. Understanding such processes requires a more holistic approach that focuses on systems and tissue biology. Recommendations ** Studies on the etiology of human disease therefore need to incorporate early development and characterise appropriately the factors that determine organ functions and subsequent disease risks. Such associations can best be examined in long-term prospective studies, and existing and planned birth cohorts should be utilized for this purpose. ** Cross-disciplinary approaches and translation of animal data on exposure biomarkers and disease susceptibility need to be promoted for application in studies of the etiology of human disease. Communication and clarification of key concepts and terms needs to be stimulated between the scientific disciplines involved and between these scientists and policymakers. Environmental chemical exposure assessment should emphasise the time period of early development. Exposure data already routinely collected need to be optimised for application in epidemiological studies. Cord blood, cord tissue, human milk and other biological samples can be applied for assessment of exposure biomarkers and for determination of gene expression changes. Since humans are exposed to numerous chemicals during development and throughout life, mixed exposures need to be considered in a life- course approach to disease. Further, the interaction due to other life-style factors, such as intake of essential nutrients and societal environment, needs to be explored. This research should also involve the impact of genetic variation and genetic predisposition to disease. ** Toxicological tests and risk assessment of environmental chemicals need to take into account the susceptibility of early development and the long-term implications of adverse programming effects. Although test protocols exist to assess reproductive toxicity or developmental neurotoxicity, such tests are not routinely used, and the potential for such effects is therefore not necessarily considered in decisions on safety levels of environmental exposures. The accumulated research evidence suggests that prevention efforts against toxic exposures to environmental chemicals should focus on protecting the fetus and small child as highly vulnerable populations. Given the ubiquitous exposure to many environmental toxicants, there needs to be renewed efforts to prevent harm. Such prevention should not await detailed evidence on individual hazards to be produced, because the delays in decision-making would then lead to propagation of toxic exposures and their long-term consequences. Current procedures therefore need to be revised to address the need to protect the most vulnerable life stages through greater use of precautionary approaches to exposure reduction. Note: This statement has been developed by the International Scientific Committee of the conference, taking into account comments and suggestions from the conference participants. The statement (pending minor editorial revision) will be included in the conference proceedings. Members of the International Scientific Committee David Barker (UK) David Bellinger (USA) Ake Bergman (Sweden) Roberto Bertollini (WHO) Sylvaine Cordier (France) Terri Damstra (WHO) George Davey-Smith (UK) Erik Dybing (BCPT) Brenda Eskenazi (USA) David Gee (EEA) Kimberly Gray (NIEHS) Mark Hanson (UK) Peter van den Hazel (The Netherlands) Jerry Heindel (NIEHS) Birger Heinzow (Germany) Irva Hertz-Picciotto (USA) Howard Hu (USA) Terry Huang (NICHD) Tina Kold Jensen (Denmark) Philip J Landrigan (USA) Caroline McMillen (Australia) Katsuyuki Murata (Japan) Larry L Needham (USA) Sjśršur Olsen (Denmark) Beate Ritz (IARC) Greet Schoeters (Belgium) Niels E Skakkebęk (Denmark) Staffan Skerfving (Sweden) Copyright 2006 by Thomas Steen Christensen Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Los Angeles Times, May 24, 2007 [Printer-friendly version] SCIENTISTS WARN OF DANGERS CHEMICALS POSE TO FETUSES, KIDS By Marla Cone In a strongly worded declaration, many of the world's leading environmental scientists warned Thursday that exposure to common chemicals makes babies more likely to develop an array of health problems later in life, including diabetes, attention deficit disorders, prostate cancer, fertility problems, thyroid disorders and even obesity. The declaration by about 200 scientists from five continents amounts to a vote of confidence in a growing body of evidence that humans are vulnerable to long-term harm from toxic exposures in the womb and during the first years after birth. Convening in the Faroe Islands in the North Atlantic, toxicologists, pediatricians, epidemiologists and other experts warned that when fetuses and newborns encounter various toxic substances, growth of critical organs and functions can be skewed. In a process called "fetal programming," the children then are susceptible to diseases later in life -- and perhaps could even pass on those altered traits to their children and grandchildren. The scientists' statement also contained a rare international call to action. The effort was led by Dr. Philippe Grandjean of Harvard University and University of Southern Denmark, and Dr. Pal Weihe of the Faroese Hospital System, who both have studied children exposed to mercury for more than 20 years. Many governmental agencies and industry groups, particularly in the United States, have said there is no or little human evidence to support concerns about most toxic residue in air, water, food and consumer products. About 80,000 chemicals are registered in the United States. Yet, the scientists urged government leaders not to wait for more scientific certainty and recommended that governments revise regulations and procedures to take into account subtle effects on fetal and infant development. "Given the ubiquitous exposure to many environmental toxicants, there needs to be renewed efforts to prevent harm. Such prevention should not await detailed evidence on individual hazards," the scientists wrote in the four-page statement. The scientists are particularly concerned that the newest animal research suggests that chemicals can alter gene expression -- turning on or off genes that predispose people to disease. Although the DNA itself would not be altered, such genetic misfires in the womb may be permanent, and all of the subsequent generations could be at greater risk of diseases, too. "Toxic exposures to chemical pollutants during these windows of increased susceptibility can cause disease and disability in childhood and across the entire span of human life," the scientists concluded. "Recent research now shows that even subtle effects caused by chemical exposures during early development may lead to important functional deficits and increased risks of disease." The Barker Hypothesis, conceived by a British scientist in 1992, says human fetuses are "programmed" for diseases by their early environment. The scientists concluded that this is now well-documented for toxic exposures by a large collection of animal experiments and some human data. "A sad aspect with many of these prenatal exposures is that they leave the mother unscathed while causing injury to her fetus," said Dr. Philip Landrigan, a pediatrician who chairs the Mount Sinai School of Medicine's Department of Community and Preventive Medicine. He was one of the statement's authors. In a more optimistic vein, the researchers said that if contaminants do play a big role in human health problems, some diseases could be prevented. "Reducing exposure would lead to tremendous benefits," said Dr. Bruce Lanphear, director of the Environmental Health Center at Cincinnati Children's Hospital Medical Center. "We shouldn't wait for an epidemic to fully mature before we develop policies to protect children." For centuries, the basic rule of toxicology has been "the dose makes the poison." Now, the scientists say "the timing makes the poison" -- in other words, when a toxic exposure occurs is as important as how much people are exposed to. The fetus "is extraordinarily susceptible to perturbation of the intrauterine environment," they wrote. The growing brain is the most sensitive. Mothers' exposure to mercury and polychlorinated biphenyls (PCBs) in fish and other seafood can cause slight declines in IQ and motor skills. In addition, early exposure to pesticides might trigger Parkinson's and Alzheimer's diseases. Also, children exposed to lead, organophosphate pesticides or cigarette smoke have greater risk of attention deficit hyperactivity disorder. One of every three cases of the neurological disorder, affecting an estimated 560,000 children in the United States, can be attributed to either lead exposure or prenatal tobacco smoke exposure, Lanphear reported in a study published last December. The immune, reproductive and cardiovascular systems also are vulnerable to early damage. Children exposed prenatally to PCBs have a high rate of infections and weak response to vaccinations. Many chemicals also can mimic hormones, and in animal tests, they feminize newborns, lowering sperm counts and promoting prostate, testicular, uterine and breast cancers. In the newest area of research, metabolic systems -- which control how nutrients are converted into energy -- have been altered by chemicals administered in animal experiments, changes that may contribute to obesity and diabetes. "These adverse effects have been linked to chemical pollutants at realistic human exposure levels similar to those occurring from environmental sources," the scientists wrote. Among the risky chemicals they named are bisphenol A, found in polycarbonate plastic food and water containers, the pesticides atrazine, vinclozolin and DDT, lead, mercury, phthalates used in some cosmetics and soft plastics, brominated flame retardants, arsenic, which contaminates some water supplies, and PCBs, banned but ubiquitous, particularly in fish. Some of the chemicals already have been regulated in the United States, but many have not. Moreover, the scientists said, tests for developmental effects are not routinely required, so "the potential for such effects is therefore not necessarily considered in decisions on safety levels of environmental exposures." "We have absolutely solid evidence for certain chemicals -- lead, methyl mercury, PCBs, arsenic and the organophosphate pesticides," Landrigan said. "We know with great certainty that prenatal exposure to any of these materials can damage the developing brain with resulting lifelong loss of intelligence and disruption of behavior." Yet there is "an incredible gap," he said, because 80 percent of major chemicals in commerce have never been tested to see if they damage early development. Although the statement did not include any reference to it, some of the U.S. scientists said Congress should adopt a new law, similar to one enacted by the European Union last year, that requires more chemical testing and could ban many hazardous substances. The conference was funded by the World Health Organization, National Institutes of Health, European Environment Agency and the Centers for Disease Control and Prevention. Denmark's Faroe Islands, just south of the Arctic Circle, was the venue because it is home to the longest-running human experiment analyzing prenatal toxic exposure. Since 1986, Grandjean and Weihe have tracked Faroese children from the womb to adolescence to monitor neurological effects of mercury in seafood. Their findings prompted U.S. advisories that women of childbearing age and children avoid swordfish and other highly contaminated fish. Ten U.S. scientists served on the 28-member committee that wrote the consensus: Landrigan; Brenda Eskenazi of the University of California, Berkeley; Irva Hertz-Picciotto of UC Davis; Beate Ritz of UCLA; Jerry Heindel and Kimberly Gray of the National Institute of Environmental Health Sciences; Larry Needham of the CDC; Terry Huang of the National Institute of Child Health and Human Development; David Bellinger of Harvard University; and Howard Hu of University of Michigan. Copyright 2007, Los Angeles Times Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Reproductive Toxicology, May 1, 2007 [Printer-friendly version] THE DEVELOPMENTAL BASIS OF HEALTH AND DISEASE Role of exposure to environmental chemicals in the developmental basis of disease and dysfunction By Jerrold J. Heindel** There is a major paradigm shift taking place in science that while simple is profound. It states that the root of many diseases, including reproductive diseases and dysfunctions, will not be found by examination of disease onset or etiology hours, days, weeks, or even years prior to disease onset. The new paradigm suggests that susceptibility to disease is set in utero or neonatally as a result of the influences of nutrition and exposures to environmental stressors/toxicants. In utero nutrition and/or in utero or neonatal exposures to environmental toxicants alters susceptibility to disease later in life as a result of their ability to affect the programming of tissue function that occurs during development. This concept, that is still a hypothesis undergoing scientific testing and scrutiny, is called the developmental basis of health and disease. If true, then it says that the focus on disease prevention and intervention must change from the time of disease onset to perhaps decades prior: during the in utero and neonatal period. Perhaps the reason it has been so difficult to link environmental exposure to disease susceptibility is that scientists have been looking at the wrong time! Certainly not all exposures that result in increased disease or dysfunction occur during development. This paradigm shift just suggests that this is a sensitive window of exposure that should be examined more thoroughly. This concept has its origins in two disciplines, epidemiology studies of humans and developmental toxicology studies in animals. The underlying scientific hypothesis behind the developmental basis of adult diseases has been developed by epidemiology studies and emphasized by Dr. David Barker in the United Kingdom. He has shown that during development fetuses respond to adverse conditions, mainly severe undernutrition, by favoring the metabolic demands of the growing brain/CNS and heart at the expense of other tissues. The growing brain/CNS and heart tissue may not, however, escape entirely unscathed. The long-term consequences of this response are that the fetus is protected from death, is live-born, but has a low birth weight and is more prone to diseases later in life. These epidemiology studies show that low birth weight (LBW), small for gestation age (SGA), frank intra-uterine growth retardation (IUGR) or clinically abnormal thinness at birth strongly predicts the subsequent occurrence of hypertension, hyperlipidemia, insulin resistance, type 2 diabetes, ischemic heart disease, breast or prostate cancer in adult life. Fetuses that are clinically malnourished during the first trimester of development are also three times more likely to be obese as adults (reviewed in ). The concept of fetal programming of structural-functional formations during development has been proposed to explain these findings. Programming is the term used to describe lifelong changes in function that follow a particular event in an earlier period of the life span. While epidemiology studies have identified the phenomenon of metabolic programming, little is known about the mechanism(s) by which fetal insults lead to altered programming and to disease later in life. In addition, emphasis thus far has been on alterations in nutrition during development with virtually no focus on the role that exposures to environmental agents, such as air or water pollution, either alone or in combination with qualitative alterations in macro- or micro- nutrition (i.e. soy protein, phytoestrogens, isoflavones or other chemicals in herbal supplements or dietary sources), might have on this phenomenon. With regard to developmental toxicology, it is known that between 2 and 5% of all live-born infants have major developmental defects. Up to 40% of these defects have been estimated to result from maternal exposure(s) to harmful environmental agents that directly or indirectly create an unfavorable intrauterine environment. A spectrum of adverse effects can occur, including death, structural malformation, and/or functional alteration of the fetus/embryo. The traditional focus of the science of developmental toxicology has been on the role of agents (environmental or drugs) that cause either premature death of the fetus or birth defects. In recent years, attention has turned to examining the effects of in utero or neonatal exposure to environmental agents on functional changes in tissues, e.g. permanent changes in tissue function that are not the result of overtly or grossly teratogenic effects but that result in increased susceptibility to disease/dysfunction later in life. This new focus on functional changes has been made possible by the development and use of "omics" technology that has allowed the examination of gene expression changes in tissues during development. It should be noted that this hypotheses was actually formulated over 20 years ago by Dr. Howard Bern when he described the "fragile fetus syndrome" . It has been revived and is now receiving significant attention due to advancement in genomics and proteomics technology that has allowed scientist to detect changes in gene expression and protein levels in tissues, presenting a possible mechanism for the phenomenon described. The epidemiology data that support the Barker hypothesis on the fetal basis of adult disease, together with the preliminary data showing alterations in gene expression and tissue imprinting due to in utero or neonatal exposures to some environmental agents, provide an attractive framework for understanding delayed functional effects of toxicant exposures. Thus it has been proposed that exposure to certain environmental chemicals alone or in combination with altered nutrition, leads to aberrant developmental programming that permanently alters gland, organ or system potential. These states of altered potential or compromised function are hypothesized to result from epigenetic changes, e.g. altered gene expression due to toxicant- induced effects on imprinting, and the underlying methylation-related protein-DNA relationships associated with chromatin remodeling. The end result is an animal that is sensitized so that it will be more susceptible to diseases later in life. The following key points serve to elaborate this general hypothesis: ** There is a unique sensitivity to the developing fetus which may be due to multiple factors including undeveloped DNA repair, or immature immune system, lack of detoxifying enzymes, primitive liver metabolism, lack of blood/brain barrier, increased metabolic rate and increased sensitivity to epigenetic changes. ** This unique sensitivity is during tissue development, which in many cases extends well into neonatal life. ** The initiating in utero environmental insult may act alone or in concert with in utero nutrition and/or with later exposures. That is, there could be an in utero exposure that would lead by itself to pathophysiology later in life or there could be in utero exposure combined with a neonatal exposure (same or different compound(s)) or adult exposure that would trigger or exacerbate the pathophysiology. ** The pathophysiology may manifest as: the occurrence of a disease that otherwise would not have happened; an increase in risk for a disease that would normally be of lower prevalence or an earlier onset of a disease that would normally have occurred; or an exacerbation of the disease. ** The pathophysiology may have a variable latent period from onset in the neonatal period, early childhood, puberty, early adulthood, or late adulthood; depending on the toxicant, time of exposure and tissue/organ affected. ** The effects may be transmitted to future generations through the germ line. ** The effects of in utero exposure to toxic environmental chemicals may occur in the absence of reduced birth weight. This makes it more difficult to assess, than effects due to severe nutritional deficits during development. In addition, extrapolation of risk may be difficult since effects may not follow a monotonic dose-response relationship, the toxicant may have an entirely different effect on the embryo, fetus, or perinatal organism, compared to the adult and exposure of one individual to an environmental toxicant may have little effect, whereas another individual will develop overt disease or dysfunctions. The short-term approach to addressing this paradigm is to produce in utero or neonatal exposure to an environmental agent at environmentally relevant doses. Then to correlate exposure measurements with measurements of gene expression in target tissues at or near birth or the termination of dosing. Some animals are then allowed to mature and onset of disease/dysfunction is quantitated. Gene expression studies are carried out on the diseased tissues. Finally gene expression changes noted after dosing are correlated with gene expression changes in the diseased tissue to show that in utero exposure has resulted in altered programming of gene expression and this effect correlates with disease. In the long term it is necessary to show cause and effect relationship between in utero or neonatal exposures, altered gene expression in target tissues and disease. Finally, the mechanism responsible for the altered gene expression that is responsible for the increased incidence or severity of disease must be determined. Once completed, the intervention and prevention strategies can be developed to reduce the incidence of disease. There are several recent reviews on this paradigm , ,  and . This special edition of reproductive toxicology is intended to highlight recent data that show proof-of-principle for the hypothesis that in utero or neonatal exposures to environmental agents alone or in combination with altered nutrition can provide the developmental basis for a number of later-occurring diseases. Some articles are research manuscripts, some are reviews and some are combinations, all are focused on the developmental basis of adult disease paradigm. The main focus is on animal studies as the developmental basis of disease paradigm is particularly difficult to assess in humans at this point in time; as in utero exposures must be linked to gene expression or other tissue potential changes at birth and then linked to an adult disease. Nonetheless, humans are exposed to a variety of environmental chemicals in utero, many are the same chemicals that have been shown to cause increased incidences of disease/dysfunction later in life in animal studies and at similar concentrations to those used in the animal studies ,  and . Indeed a recent publication by The Environmental Working Group  showed that a variety of industrial chemicals, pollutants, and pesticides could be measured in human umbilical cord blood. They tested newborns for 413 environmental chemicals and found that 287 of them were found at some levels including various PCBs, mercury, DDT and dioxins. In addition, the Centers for Disease Control and Prevention (CDC), has recently released its Third National Report on Human Exposures to Environmental Chemicals . It reports on blood and urine levels for 148 chemicals, 38 for the first time, by age, sex, race or ethnicity, in a random sample from participants from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2002. These data indicate low exposure to multiple chemicals including mercury, phthalates, bisphenol A, phytoestrogens, organochlorine pesticides, herbicides and dioxin-like chemicals. Thus the potential exists for extrapolation of the animal data on the developmental basis of health and disease to human health. Indeed the first article in this edition focuses on human exposures during development. This is followed by an examination of epigenetics as the mechanism for the developmental basis of adult disease. The following 21 articles describe the state of the science in this exciting and emerging area highlighting the developmental basis of obesity, reproductive diseases, cardiovascular disease, respiratory disease, and neurological disease. It will take years to discern the actual importance of this new paradigm to disease processes. It is hoped that this special edition will stimulate research in this direction. **Division of Extramural Research and Training, National Institute of Environmental Health Sciences, Department of Health and Human Service, 79 T.W. Alexander Drive, Building 4401 3rd Floor, Mail Drop: EC-23, Room 3413, Research Triangle Park, NC 27709, United States References  P.D. Gluckman and M.A. Hanson, Developmental origins of disease paradigm: a mechanistic and evolutionary perspective, Pediatr Res 56 (2004), pp. 311-317.  H. Bern, The fragile fetus. In: T. Colborn and C. Clement, Editors, Chemically-induced alternations in sexual and functional development: the wildlife/human connection (1992).  K.P. Miller, C. Gorgeest, C. Greenfeld, D. Tomic and J.A. Flaws, In utero effects of chemicals on reproductive tissues in females, Toxicol Appl Pharmacol 198 (2004), pp. 111-131.  A.C. Vidaeff and L.E. Sever, In utero exposure to environmental estrogens and male reproductive health: a systematic review of biological and epidemiologic evidence, Reprod Toxicol 12 (2005), pp. 5-20.  C. Lau and J.M. Rogers, Embryonic and fetal programming of physiological disorders in adulthood, Birth Defects Res (Part C) 72 (2005), pp. 300-302.  A.J. Drake and B.R. Walker, The intergenerational effects of fetal programming: non-genomic mechanisms for the inheritance of low birth weight and cardiovascular risk, J Endocrinol 180 (2005), pp. 1-16.  L.L. Needam and K. Sexton, Assessing children's exposure to hazardous environmental chemicals: an overview of selected research challenges and complexities, J Expos Anal Environ Epidemiol 10 (2000), pp. 611-629.  C. Mori, M. Komiyama, T. Adachi, T. Sakurai, D. Nishimura and K. Takashima et al., Application of toxicogenomic analysis to risk assessment of delayed long-term effects of multiple chemicals including endocrine disruptors in human fetuses, Environ Health Perspect 111 (2002), pp. 803-809.  E.V. Younglai, W.G. Foster, E.G. Hughes, K. Trim and J.F. Farrell, Levels of environmental contaminants in human follicular fluid serum and seminal plasma of couples undergoing in vitro fertilization, Arch Environ Contamin Toxicol 43 (2002), pp. 121-126.  Environmental Working Group. 2005; http://www.ewg.org/reports/bodyburden2.  CDC. National report on human exposures to environmental chemicals. 2005; http://www.cdc.gov/exposurereport. Reproductive Toxicology Volume 23, Issue 3, April-May 2007, Pages 257-259 Copyright 2007 Elsevier Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Boston Globe, May 27, 2007 [Printer-friendly version] HEAVY TV VIEWING UNDER 2 IS FOUND Ignoring risks, parents cite 'educational' value By Barbara F. Meltz, Globe Staff About 40 percent of 3-month-olds watch television or videos for an average of 45 minutes a day, or more than five hours a week, according to the first-ever study of the viewing habits of children under the age of 2. The study, by pediatric researchers at the University of Washington, also found that by age 2, 90 percent of children are watching television for an average of more than 90 minutes a day. Such early exposure to screens can have a negative impact on an infant's rapidly developing brain and put children at a higher risk for attention problems, diminished reading comprehension, and obesity, researchers said. Researchers said they were surprised not only by the number of hours young children are spending in front of the television but also by the primary reason: Most parents are using television as an educational tool, not for the more conventional explanation of babysitting. Despite nearly a decade of warnings by pediatricians to the contrary, parents believe that the content of programs aimed at babies is good for brain development. "I wouldn't be so upset about this if I thought parents were doing it because they needed a break to take a shower or make dinner," said Dimitri Christakas, the University of Washington pediatrician who co- authored the study. "What I'm troubled by is the notion that parents think it's good for their kids. That's more likely to lead to excessive viewing rather than occasional viewing." The new study, based on 1,009 random telephone interviews with families in Minnesota and Washington, was published in this month's Archives of Pediatrics and Adolescent Medicine. (According to the study, the families interviewed were more likely to be highly educated and higher-income than the general US population.) The top two reasons parents gave for allowing babies to watch television is that the programs "teach something" or are "good for his/her brain" (29 percent), and because it's "something he/she really enjoys doing" (23 percent). Needing to keep a baby occupied scored in third place (20 percent). "That's stunning when you consider that the best evidence shows that early viewing puts children on a trajectory that places them at a high risk for attention deficit, diminished reading ability, and obesity," says Andrew Meltzoff, a developmental psychologist who co-authored the new book, "The Elephant in the Living Room, Make Television Work For Your Kids," with Christakas. "These parents want to do the right thing, but there's a huge discrepancy between what the professional community recommends -- no viewing under 2 -- and what is happening in real life." Kristy Merhib of Milford reflects the dichotomy. She says her 4-month- old, Jake, has been watching practically from birth even though she knows about pediatricians' recommendations to the contrary. "That's why I'm careful to use it in moderation, and only what's educational," she said. "I think even at this age, something is definitely getting through. Colors, numbers -- he really seems to pay attention." The baby video market is a billion-dollar-a-year industry, with Baby Einstein videos, programs aimed at stimulating development and activity in infants and toddlers, generating sales of more than $500 million alone last year. Cathy Davies of Wayland, who has a 2 1/2-year-old and 1-month-old, says the guideline is the reason she waited until her oldest was 18 months before she introduced baby videos. With her second, she won't wait that long. "I bet he'll be watching at a year," she said. "I know it's controversial, but it's geared to babies." Another mother, Renata Wilson of Newton, put Isabella in front of "Baby Einstein" at 2 months. "We're a bilingual family. I only speak Portuguese to her, so I thought it would be a good way for her to get more English," she said, noting that even at a young age her daughter seemed to pay attention. That parents put so much stock in videos such as the wildly popular "Baby Einstein" series has researchers and educators wondering what they can do to support parents' good intentions but wean them away from the baby video market. "We have succeeded in convincing people that the first years are critical to brain development," said Meltzoff, who is co-director of the Institute for Learning and Brain Sciences at the University of Washington. "The unfortunate consequence is that it has spun off to build a brainier baby enterprise, where people think they have to use technology to take advantage of this critical window." What parents identify as attention and learning scientists say is a primitive reflex known as the orienting response. "Yes, the baby is staring at the screen, but it's wrong to think the child likes it," said Christakas, the study's co-author and himself the father of two young children. "He or she has no choice in the matter. He's hard-wired to pay attention to anything that is fast- moving, brightly colored, or loud. It's a survival response." Christakas said he embarked on the study after being perplexed by the results of a 2003 Kaiser Foundation study that found that children under age 6 were spending up to two hours a day in front of a screen, despite the American Academy of Pediatrics recommendation that children under 2 watch no television at all. A baby is born with 100 billion brain cells, but only 17 percent of them are immediately operational. "The rest of the wiring follows in the days, weeks, months, and years to come," said child psychologist David Walsh, president of the National Institute on Media and the Family. What's not hard-wired by genetics gets soft-wired by experience and exposure. "For instance, we don't need to teach babies to make noise; that's hard-wired," Walsh said. "But which language do they end up speaking? That's the soft-wiring." Early screen-viewing has a negative effect on soft-wiring even when the content is baby-safe, he said. "The question to ask isn't, 'What is she watching,' but, 'What else isn't she doing?'?" he said. "When there's screen time at an early age, the brain is wired to respond to screens even before they crawl or say their first words. At a time when they need to be interacting with the environment and with real human beings, they are being conditioned to respond to a screen." What's more, he said, babies who are in front of a screen as early as 3 months are at higher risk for childhood obesity. "Wiring is based on repetition, on patterning. It's a reasonable hypothesis that if a baby is in front of a screen at 3 months, it will be harder to get him away from the screen at 3, 8, 10, or 13," he says. "We're conditioning them to be couch potatoes." Contact Barbara Meltz at email@example.com. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Economic Opportunity Institute, Mar. 24, 2004 [Printer-friendly version] THE LINK BETWEEN EARLY CHILDHOOD EDUCATION AND HEALTH Early Experiences are Important Determinants of Adult Health Status By Jen Brown A child's early experiences are lifelong determinants of health and well-being. Studies in neurobiology, neurodevelopment, and early intervention show that the years birth to school age are critically important for brain development. During this critical time, children develop the essential language and cognitive skills required to learn, develop their ability to manage emotions and stress, and learn to cooperate with others. Properly shaping the architecture of the brain in these earliest years of life has profound benefits in adult life. Many of the risks for the diseases of adult life (e.g. heart disease) are, in part shaped by learning, coping, and decision-making skills that are set in the earliest years of life. These skills determine performance in the school system and set children onto life pathways that in turn, affect their health and well-being over time. Early Childhood Trajectory The Role of Early Childhood Education Early childhood education plays a crucial role in children's development. A key requisite for optimal healthy child development is secure attachment to a trusted caregiver, giving consistent caring, support and affection early in life. Coping skills are strongly influenced by how well children are "nurtured" during the early years of childhood. Spending one's early years in an unstimulating, emotionally and physically unsupportive environment affects brain development in adverse ways, and leads to cognitive, social and behavioral delays. Evaluation of quality early learning and care provision before the age of 5 years has found that it is associated with improvement in a range of educational and social measures, some of which have been documented many years after the care. In one of the studies, the Perry Preschool Project followed participants up to 27 years of age and showed that the people from the preschool group were more likely to have advantageous social outcomes such as high school graduation, employment, fewer arrests, higher earnings, and owning their own home than those who did not participate in the program. These findings have been confirmed by multiple other studies. The Perry Preschool program also measured a significant effect on teen pregnancy, showing that youth who did not receive the program were nearly twice as likely to have a teen pregnancy than those who did receive the program. Similarly, the research demonstrated the benefits of creating opportunities for children to participate in decision making from an early age. The study discovered that children from impoverished inner- city environments who planned and made decisions about their school activities in their preschool years were, in adulthood, significantly less (as much as 50 percent) involved in using drugs. Lack of school readiness puts children at risk of academic, social and behavioral difficulties in school. Those children are more likely to leave school before high school graduation, get involved in criminal behavior, become pregnant as a teenager, and become addicted to tobacco, alcohol, and other drugs. And the combination of behavioral problems and failure in school are also associated with low levels of physical and mental health in adulthood. The reverse is also true. Children from high quality early learning and care programs are more likely to graduate high school, go on to college or higher learning, and earn more. These outcomes are all associated with better physical and mental health as adults. Access to Health Services Early care and learning programs are often a vehicle for health education and promotion to children. Research has shown that early childhood programs can affect children's physical health by requiring that children be properly immunized; by linking them to health services; by conducting vision, hearing, and developmental screenings, and in some cases, by providing them with nutritious meals. Children who attend quality early child programs have greater access to health care and improved physical health, receive better dental care, and demonstrate improved nutritional status and better nutritional practices. Early learning and care programs are also essential in getting children enrolled into low-income children's health insurance programs for which they are eligible, such as Medicaid and the Children's Health Insurance Program (CHIP). Prevention Results in Cost Savings Cost implications are very clear. Loading our energies at the beginning of the children's services continuum makes sense since early childhood development and prevention services are immensely more cost- effective than waiting to pay for health care services later in the life. Endnotes  Shonkoff, J.P., Phillips, D.A. (2000) From Neurons to Neighborhoods: The Science of Early Childhood Development. National Research Council and Institute of Medicine. Washington, D.C.: National Academy Press. pg. 314.  Hertzman, C., Mustard, F. (1997) A Healthy Early Childhood = A Healthy Adult Life. Founders Network Report, The Canadian Institute for Advanced Research: 1(1)  Shonkoff, J.P., Phillips, D.A. (2000).  Barnett, W. S. (1996). Lives in the balance: Age-27 benefit-cost analysis of the High/Scope Perry Preschool Program (Monographs of the High/Scope Educational Research Foundation, 11). Ypsilanti, MI: High/Scope Press. A summary of the Perry study findings up to age 40 is available here.  Reynolds, A.J. et al. (2001) Long-term Effects of an Early Childhood Intervention on Educational Achievement and Juvenile Arrest: a 15-Year Follow-Up of Low-income Children in Public Schools. JAMA (and be sure to get the published correction to this article). "Smart Start: A Six County Study of the Effects of Smart Start Child Care on Kindergarten Entry Skills," Frank Porter Graham Child Development Center Smart Start Evaluation Team, North Carolina. (1999).  The rate for youth not receiving the program is higher than 100 because some youth may have had more than one teen pregnancy during the course of the study.  Hertzman, C., Keating, D. (eds.) Developmental Health and the Wealth of Nations: Social, Biological, and Educational Dynamics. New York: The Guilford Press, 1999.  Acheson, D. (1998) Independent Inquiry into Inequalities in Health. London: The Stationary Office.  Zigler, E., Piotrkowski, C.S., Collins, R. (1994) Health Services in Head Start. Annual Review of Public Health: 15:511-34.  Howes, C. 1990. "Can the age of entry into child care and the quality of child care predict adjustment in kindergarten?" Developmental Psychology, 26(2), 292-303. McKey, R.H., Condelli, L., Ganson, H., Barrett, B.J., McConkey, C., & Plantz, M.C. 1985. The impact of Head Start on children, families, and communities. Final report of the Head Start Evaluation, Synthesis, and Utilization Project. (Washington, DC: CSR Incorporated for the Head Start Bureau, Administration for Children, Youth and Families, U.S. Dept. of Health and Human Services). (A more recent evaluation of the effectiveness of the Head Start program can be found here.)  Centers for Medicare and Medicaid Services. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Essential Action, May 31, 2007 [Printer-friendly version] CORPORATE POWER SINCE 1980 By Robert Weissman The United States Since 1980 (Cambridge University Press, 2007) is a superb short work from Dean Baker of the Center for Economic and Policy Research. In a couple hundred pages, Baker covers enormous territory, reviewing the rightward shift in U.S. politics, the sharpening of inequality (and underlying causes), U.S. unilateralism in global affairs, and much more. He concludes by identifying the U.S. political system's failure to address three overriding problems: provision of healthcare to all at an affordable cost, the spiking trade deficit, and global warming. The distressing effects of corporate power and influence is interwoven into the narrative of The United States Since 1980, but corporate power is not analyzed in its own right. There will be an opportunity to conduct that kind of analysis at an important conference to be held June 8-10 in Washington, DC. "Taming the Giant Corporation" will investigate the evolving sources and forms of corporate power, and how it can be subordinated to people's control (including by displacing corporations altogether from certain segments of the economy and society). You can get information on the conference, and register, at:
Environmental Research Foundation
P.O. Box 160, New Brunswick, N.J. 08903