Rachel's Democracy & Health News #841
"Environment, health, jobs and justice--Who gets to decide?"
Thursday, February 9, 2006
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^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ Featured stories in this issue... Twiddling Our Thumbs as We Turn Our Boys into Girls Chemicals widely used in toys, cosmetics and pharmaceutical drugs can interfere with the sexual development of male rodents. In recent years, studies have began to accumulate showing similar effects on the sexual development of baby boys. Spokeswomen for the chemical industry, supported by risk assessors within the U.S. Environmental Protection Agency, deny there's evidence of harm. Sick of Poverty: A Broader Vision of Environmental Health Many, many studies suggest that social exclusion, relative poverty, and pyramids of status create stresses that have a strongly harmful influence on health. Thus the "social determinants of health" is a bridging idea, anchored in science, that could allow environmentalists to get beyond their single issues and contribute to a larger social movement for change. The social determinants of health can connect people concerned about justice, fairness, poverty, inequality, urban decay, sprawl, shabby housing, rising personal debt, racism, sexism, mysogyny, homophobia, intolerance, white privilege, street crime, corporate power, public health, hunger, access to a decent diet, obesity, lousy schools, depression, suicide, domestic violence, waste (of all kinds), economic growth, and low-wage jobs that are boring and stressful -- plus many other aspects of our culture that make people insecure, unhappy, stressed out and sick. This is what "environmental health" really means. It's not just about chemicals anymore. The Richest Americans Are Getting Richer Getting rich by owning stock in publicly traded corporations has gotten easier over the last twenty years. As taxes on income from stock sales have declined -- so-called 'capital gains' tax rates are now only 15% -- the few who have wealth to invest in stocks have gained tremendously. More Bad News About Common Household and Lawn-care Pesticides "The Environmental Protection Agency needs to take a closer look at pyrethroids" with an eye toward changing how those 22 compounds are marketed and used, argues Michael J. Lydy, an environmental toxicologist at Southern Illinois University in Carbondale. Ample and growing data, he says, challenge "the suggestion that in the environment, pyrethroids will be innocuous." :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Rachel's Democracy & Health News #841, Feb. 9, 2006 TWIDDLING OUR THUMBS AS WE TURN OUR BOYS INTO GIRLS By Peter Montague [DHN introduction: One of the watershed events of 2005 was a four-part series on chemicals published in the Wall Street Journal (WSJ), written by Peter Waldman, a WSJ reporter. The series basically showed that the U.S. chemical regulation system is utterly broken and is not much more than a public relations scam. In Rachel's News #839 and #840 we discussed the first two parts of Mr. Waldman's WSJ series; here we discuss part 3. In some quotations from WSJ we have added explanatory links.--DHN Editors] In part 3 of his series, Peter Waldman begins by offering his mostly male audience a lesson in reproductive biology: "In the 12th week of a human pregnancy, the momentous event of gender formation begins, as X and Y chromosomes trigger biochemical reactions that shape male or female organs. Estrogens carry the process forward in girls, while in boys, male hormones called androgens do." "Phthalate syndrome" in rodents Mr. Waldman goes on: "Now scientists have indications the process may be influenced from beyond the womb, raising a fresh debate over industrial chemicals and safety. In rodent experiments, common chemicals called phthalates, used in a wide variety of products from toys to cosmetics to pills, can block the action of fetal androgens. The result is what scientists call demasculinized effects in male offspring, ranging from undescended testes at birth to low sperm counts and benign testicular tumors later in life. 'Phthalate syndrome,' researchers call it." In other words, these common chemicals, phthalates -- found in toys, cosmetics, and pharmaceutical drugs -- can interfere with the development of male rodents so reliably that there's a name for the effect: "phthalate syndrome." Now I don't know about you, but it I were a scientist studying a group of chemicals commonly found in toys, cosmetics and drugs, and I discovered that my chemicals could reliably demasculinize male baby rodents, I'd be asking myself, "Wouldn't it be smart to keep these chemicals away from human babies?" That would be called a "precautionary approach" to phthalates -- but this is a noxious idea to U.S. chemical executives and regulators alike. In the U.S., you've got to prove harm to a scientific certainty before you are officially allowed to become concerned about a chemical. And even then the chemical corporations have the right to drag you into court for a decade or two while they continue to sell product (because the corporations are considered legal "persons" and they have arranged for the burden of proof of harm to rest on the public, not on the corporations). So what kind of evidence do we have about harm from phthalates? First WSJ tells us that "...last year, federal scientists found gene alterations in the fetuses of pregnant rats that had been exposed to extremely low levels of phthalates, levels no higher than the trace amounts detected in some humans." OK, so it isn't just high doses that causes problems in rodents. Next we learn that two studies in 2005 found "direct links" to humans: "First, a small study found that baby boys whose mothers had the greatest phthalate exposures while pregnant were much more likely than other baby boys to have certain demasculinized traits." And: "...another small study found that 3-month-old boys exposed to higher levels of phthalates through breast milk produced less testosterone than baby boys exposed to lower levels of the chemicals." Testosterone is male sex hormone and it is what turns boys into boys instead of girls during the 12th week of pregnancy. "Testicular dysgenesis syndrome" in humans WSJ goes on to explain that scientists in Europe "have identified what some see as a human counterpart to rodents' phthalate syndrome, one they call "testicular dysgenesis syndrome," which they think may be due in part to exposure to phthalates and other chemicals that interfere with male sex hormones. These problems begin while the baby is still in the womb. Richard Sharpe of the University of Edinburgh in Scotland, a researcher on male reproduction, told the WSJ, "We know abnormal development of the fetal testes underlies many of the reproductive disorders we're seeing in men. We do not know what's causing this, but we do know high doses of phthalates induce parallel disorders in rats." Now the chemists who make this stuff have known for a long time that it leaks into the environment and then gets into people. How could it not? Phthalates were measured in the Charles and Merrimack Rivers in Massachusetts in 1973. That same year, a study reported finding phthalates in environmental samples. That same year, 1973, researcher reported measuring phthalates in cosmetics. The following year, 1974, we find an article describing phthalates measured in food. So it's definitely no surprise that they're in our mothers' wombs. WSJ acknowledges all this: "It isn't surprising to find traces of phthalates in human blood and urine, because they are used so widely. Nearly five million metric tons [11 billion pounds] of phthalates are consumed by industry every year, 13% in the U.S. They are made from petroleum byproducts and chemically known as esters, or compounds of organic acid and alcohol. The common varieties with large molecules are used to plasticize, or make pliable, otherwise rigid plastics -- such as polyvinyl chloride, known as PVC -- in things like construction materials, clothing, toys and furnishings. Small-molecule phthalates are used as solvents and in adhesives, waxes, inks, cosmetics, insecticides and drugs." Let's see now. In the U.S. we use 1,430,000,000 (1.43 billion) pounds of this stuff each year in products that everyone knows will end up in our homes, then in our bodies, and we know it causes baby boy rats to start to turn into sickly baby girl rats -- and we don't have the sense to call a halt? I suppose the Bible had it right: "The love of money is the root of all evil" -- because the actions of chemists, corporate executives and risk assessors who allow this to continue surely qualify as evil by any normal definition. Marian Stanley of the American Chemistry Council (formerly the Chemical Manufacturer's Association) told the WSJ that phthalates are among the most widely studied chemicals and have proved safe for more than 50 years. So the chemical manufacturers admit they have been pumping this stuff into the public for 50 years while evidence of harm has accumulated. You have to appreciate their candor, and marvel at their gall. Government researcher L. Earl Gray told the WSJ that -- even today -- EPA is "moving cautiously" because, "All this work on the effects of phthalates on the male reproductive system is just five years old." But wait. Mr. Gray himself published his first studies of the ability of certain industrial chemicals to interfere with hormones and alter the development of rodent fetuses at least 25 years ago. If you go to the government's oldest database on chemicals and health, known as Pub Med, and type in "phthalates" your retrieve 467 scientific and medical articles going back to 1965. Back in 1987 -- almost 20 years ago -- U.S. EPA listed one phthalate (bis(2-ethylhexyl)phthalate) as among the 100 most toxic chemicals found at Superfund sites. In 1991, Mr. Gray signed the Wingspread Statement, which was titled, "Chemically Induced Alterations in Sexual Development: The Wildlife/Human Connection." Why were phthalates identified as a major problem in 1987 and then ignored for 15 years? Surely the EPA had knowledgable staff who must have suspected a problem. Were they ignored? Silenced? What? Last summer Mr. Gray told WSJ, "There appears to be clear disruption of the androgen pathway, but how? What are phthalates doing?" Who CARES exactly what phthalates are doing? Pregnant moms don't want the government to sit around while its scientists tease out the precise mechanism by which phthalates cause undescended testicles, hypospadias (a malformation of the penis, often requiring surgery), reduced sperm count, diminished sperm quality, and testicular cancer. They just want phthalates kept out of their babies. Is this too difficult for government scientists and corporate spokeswomen to grasp? But here's a breath of fresh air. At least one corporate scientist, Dr. Rochelle Tyl, a toxicologist, told the WSJ that the broader question is: "If we know something bad is happening, or we think we do, do we wait for the data or do we act now to protect people?" Exactly so. But U.S. EPA and the Chemical Manufacturers Association both give the same answer: "Definitely, let's wait for something bad to happen." Now I can understand why corporations would want to wait for something bad to happen -- most companies in the business of making harmful chemicals also have some fiduciary interest in medical technology, or in "environmental remediation." Many of them have figured out that they can get paid to create problems and then get paid again to fix them. It's that love of money thing again -- it keeps the wheels turning and the economy growing. But why would government not ask the same precautionary question that Dr. Tyl asked and answer it in a way that protects public health? Very mysterious. Perhaps the government is beholden to the corporations at election time and there is no longer any such thing as an independent moral agent making decisions inside the regulatory system. I'm speculating because I don't know. The Japanese have banned phthalates in certain food-handling equipment. The Europeans have banned phthalates from cosmetics and toys. Last summer the European Parliament asked the European Commission (the regulatory body of the European Union) to review products "made from plasticised material which may expose people to risks, especially those used in medical devices." Late last year, Unilever, Revlon Inc., and L'Oreal SA's American subsidiary -- hounded wonderfully by the safe cosmetics campaign -- agreed to go along with whatever the Europeans decide to ban from products. Procter & Gamble Co. said last year it would no longer use phthalates in nail polish. It's a start. Other firms are resisting. Exxon Mobil Corp. and BASF dominate the $7.3 billion phthalates market. According to WSJ, "An Exxon Mobil spokeswoman says risk assessments by government agencies in Europe and the U.S. confirm 'the safety of phthalates in their current applications.'" Risk assessment is definitely the polluter's most useful pseudo-scientific tool. As first EPA administrator William Ruckelshaus said in 1984, "We should remember that risk assessment data can be like the captured spy: If you torture it long enough, it will tell you anything you want to know." Despite these assurances from the polluters' spokeswomen, the WSJ raises serious concerns about the safety of phthalates: "For instance, a 2003 study divided 168 male patients at a fertility clinic into three groups based on levels of phthalate metabolites in their urine. The study found that men in the highest third for one of the phthalates were three to five times as likely as those in the lowest third to have a low sperm count or low sperm activity. Men highest in a different phthalate also had more abnormally shaped sperm, according to the study, which was done by researchers at the Harvard School of Public Health and published in the journal Epidemiology," WSJ reports And "The latest human study, on 96 baby boys in Denmark and Finland, found that those fed breast milk containing higher levels of certain phthalates had less testosterone during their crucial hormonal surge at three months of age than baby boys exposed to lower levels." Of course, as you would expect, not all studies of phthalates show health effects in humans, so industry clings to these "negative" studies and keeps pumping out the pollutants. Studies that create doubt about the science allow polluters to continue polluting for decades -- so there's now a large and growing industrial enterprise devoted simply to ginning up faulty studies that don't find anything because they were designed not to, thus creating doubt. No one could ever accuse the Chemical Manufacturers of missing a trick. But -- to its credit -- the WSJ keeps offering new evidence: "A human study of 85 subjects published in June linked fetal exposure to phthalates to structural differences in the genitalia of baby boys. "Researchers measured phthalate levels in pregnant women and later examined their infant and toddler sons. For pregnant women who had the highest phthalate exposure -- a level equivalent to the top 25% of such exposure in American women -- baby sons had smaller genitalia, on average. And their sons were more likely to have incompletely descended testicles. "Most striking was a difference in the length of the perineum, the space between the genitalia and anus, which scientists call AGD, for anogenital distance. In rodents, a shortened perineum in males is closely correlated with phthalate exposure. A shortened AGD also is one of the most sensitive markers of demasculinization in animal studies," WSJ reported. And: "Males' perineums at birth are usually about twice as long as those of females, in both humans and laboratory rodents. In this study, the baby boys of women with the highest phthalate exposures were 10 times as likely to have a shortened AGD, adjusted for baby weight, as the sons of women who had the lowest phthalate exposures." WSJ continued to explore the meaning of this study: "Some endocrinologists call this the first study to link an industrial chemical measured in pregnant women to altered reproductive systems in offspring. 'It is really noteworthy that shortened AGD was seen,' says Niels Skakkebaek, a reproductive-disorder expert at the University of Copenhagen, who wasn't an author of the study. 'If it is proven the environment changed the [physical characteristics] of these babies in such an anti-androgenic manner, it is very serious.' Then the WSJ drops a bombshell from the Chemical Manufacturers: "Ms. Stanley of the American Chemistry Council doubts that any study can 'tease out' the cause of a human health condition, given the wide variety of chemical exposures in people's lives." In other words, the Chemical Manufacturers are pumping out 1.43 billion pounds of a chemical that is increasingly linked to sexual dysfunction, including genital cancer in boys, and they don't believe there is any way to definitively learn the truth about that chemical -- or any other chemical -- because the Chemical Manufacturers are pumping out so many other chemicals! Think about that. The U.S. regulatory system requires a very high level of proof of harm before action can be taken to curtail production of a chemical. And the chemical manufacturers don't believe science can EVER "tease out the cause of a human health condition" because we're all exposed to too many industrial poisons simultaneously. So the Chemical Manufacturers must think they're home free -- no amount of scientific study can ever trip them up. And of course the Chemical Manufacturers are right. Science cannot definitively "tease out" the effects of a single chemical when we are all exposed to a toxic soup of industrial poisons from the moment of conception onward. Scientists who insist otherwise are either fooling themselves, or trying to fool us. No matter how many studies are done, some uncertainty will always remain -- some variable that wasn't studied could always confound the results. The only way to pull back from the edge of this cliff is to alter our standards of proof, shift the burden onto the polluter to show that each of his or her products is the least-harmful one available to do the job -- and take precautionary action by insisting on safer substitutes for chemicals that seem harmful based on the weight of the evidence, not waiting for scientific certainty. Insist that every chemical on the market be accompanied by rigorous and thorough data. No data? No market. But of course different people will weigh the evidence differently. WSJ quotes Dr. Tyl, the chemical-industry toxicologist, saying "her own rat studies confirm that AGD is very sensitive to phthalates. She says that in rats that had very high phthalate exposures, a shortened AGD at birth was closely associated with a number of serious reproductive disorders later in life. However, in rats exposed to much lower doses of phthalates, a shortened AGD at birth did not always lead to later troubles. Many of these rats grew up to breed normally, she says, despite their slightly altered anatomy." And, says WSJ, "Dr. Tyl suggests that the same may be true of humans.... Dr. Tyl theorizes, that the boys with shortened AGD will grow up normally. 'At what point do changes like this cross the line' to become dangerous, she asks." And she answers her own question: "We don't know yet." OK, we don't know. We may never know. But we can ask 1000 pregnant moms one question: "Is it OK with you if I pump teensy amounts of a few dozen industrial poisons into your womb and alter the anatomy of your baby?" How many women out of a thousand would say, "Yes?" Maybe a few. Perhaps the wives of chemical company executives would answer, "Of course!. I love having those industrial chemicals in my baby. I'm tickled with the idea of Exxon-Mobil and BASF altering my child's anatomy before birth!" Maybe Marian Stanley (the flak for the Chemical Manufacturers) and the anyonymous spokeswoman for Exxon Mobil would say they are happy to have their babies' anatomy altered so their bosses can continue to consummate their love of money. But somehow I doubt it. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Scientific American, Dec. 15, 2005 SICK OF POVERTY By Robert Sapolsky [DHN introduction: We have added a few explanatory links to the text. --DHN Editors] Rudolph Virchow, the 19th-century German neuroscientist, physician and political activist, came of age with two dramatic events -- a typhoid out-break in 1847 and the failed revolutions of 1848. Out of those experiences came two insights for him: first, that the spread of disease has much to do with appalling living conditions, and second, that those in power have enormous means to subjugate the powerless. As Virchow summarized in his famous epigram, "Physicians are the natural attorneys of the poor." Physicians (and biomedical scientists) are advocates of the underprivileged because poverty and poor health tend to go hand in hand. Poverty means bad or insufficient food, unhealthy living conditions and endless other factors that lead to illness. Yet it is not merely that poor people tend to be unhealthy while everyone else is well. When you examine socio-economic status (SES), a composite measure that includes income, occupation, education and housing conditions, it becomes clear that, starting with the wealthiest stratum of society, every step downward in SES correlates with poorer health. This "SES gradient" has been documented throughout Westernized societies for problems that include respiratory and cardiovascular diseases, ulcers, rheumatoid disorders, psychiatric diseases and a number of cancers. It is not a subtle statistical phenomenon. When you compare the highest versus the lowest rungs of the SES ladder, the risk of some diseases varies 10-fold. Some countries exhibit a five- to 10-year difference in life expectancy across the SES spectrum. Of the Western nations, the U.S. has the steepest gradient; for example, one study showed that the poorest white males in America die about a decade earlier than the richest. So what causes this correlation between SES and health? Lower SES may give rise to poorer health, but conversely, poorer health could also give rise to lower SES. After all, chronic illness can compromise one's education and work productivity, in addition to generating enormous expenses. Nevertheless, the bulk of the facts suggests that the arrow goes from economic status to health -- that SES at some point in life predicts health measures later on. Among the many demonstrations of this point is a remarkable study of elderly American nuns. All had taken their vows as young adults and had spent many years thereafter sharing diet, health care and housing, thereby controlling for those lifestyle factors. Yet in their old age, patterns of disease, incidence of dementia and longevity were still significantly predicted by their SES status from when they became nuns, at least half a century before. Inadequate Explanations So, to use a marvelous phrase common to this field, how does SES get "under the skin" and influence health? The answers that seem most obvious, it turns out, do not hold much water. One such explanation, for instance, posits that for the poor, health care may be less easily accessible and of lower quality. This possibility is plausible when one considers that for many of the poor in America, the family physician does not exist, and medical care consists solely of trips to the emergency room. But that explanation soon falls by the wayside, for reasons made clearest in the famed Whitehall studies by Michael G. Marmot of University College London over the past three decades. Marmot and his colleagues have documented an array of dramatic SES gradients in a conveniently stratified population, namely, the members of the British civil service (ranging from blue-collar workers to high-powered executives). Office messengers and porters, for example, have far higher mortality rates from chronic heart disease than administrators and professionals do. Lack of access to medical attention cannot explain the phenomenon, because the U.K., unlike the U.S., has universal health care. Similar SES gradients also occur in other countries with socialized medicine, including the health care Edens of Scandinavia, and the differences remain significant even after researchers factor in how much the subjects actually use the medical services. Another telling finding is that SES gradients exist for diseases for which health care access is irrelevant. No amount of medical checkups, blood tests and scans will change the likelihood of someone getting type 1 (juvenile-onset) diabetes or rheumatoid arthritis, yet both conditions are more common among the poor. The next "obvious" explanation centers on unhealthy life-styles. As you descend the SES ladder in Westernized societies, people are more likely to smoke, to drink excessively, to be obese, and to live in a violent or polluted or densely populated neighborhood. Poor people are also less likely to have access to clean water, healthy food and health clubs, not to mention adequate heat in the winter and air- conditioning in the summer. Thus, it seems self-evident that lower SES gets under the skin by increasing risks and decreasing protective factors. As mordantly stated by Robert G. Evans of the University of British Columbia, "Drinking sewage is probably unwise, even for Bill Gates." What is surprising, though, is how little of the SES gradient these risk and protective factors explain. In the Whitehall studies, controlling for factors such as smoking and level of exercise accounted for only about a third of the gradient. This same point is made by studies comparing health and wealth among, rather than within, nations. It is reasonable to assume that the wealthier a country, the more financial resources its citizens have to buy protection and avoid risk. If so, health should improve incrementally as one moves up the wealth gradient among nations, as well as among the citizens within individual nations. But it does not. Instead, among the wealthiest quarter of countries on earth, there is no relation between a country's wealth and the health of its people. Thus, health care access, health care utilization, and exposure to risk and protective factors explain the SES/health gradient far less well than one might have guessed. One must therefore consider whether most of the gradient arises from a different set of considerations: the psychosocial consequences of SES. ====================================================== Sidebar: Overview: Status and Health Researchers have long known that people with low socioeconomic status (SES) have dramatically higher disease risks and shorter life spans than do people in the wealthier strata of society. The conventional explanations that the poor have less access to health care and a greater incidence of harmful lifestyles such as smoking and obesity cannot account for the huge discrepancy in health outcomes. ** New studies indicate that the psychosocial stresses associated with poverty may increase the risks of many illnesses. The chronic stress induced by living in a poor, violent neighborhood, for example, could increase one's susceptibility to cardiovascular disease, depression and diabetes. ** Other studies have shown a correlation between income inequality and poor health in the U.S. Some researchers believe that the poor feel poorer, and hence suffer greater stress, in communities with wide gaps between the highest and lowest incomes. ====================================================== Psychosocial Stress Ideally, the body is in homeostatic balance, a state in which the vital measures of human function heart rate, blood pressure, blood sugar levels and so on are in their optimal ranges. A stressor is anything that threatens to disrupt homeostasis. For most organisms, a stressor is an acute physical challenge for example, the need for an injured gazelle to sprint for its life or for a hungry predator to chase down a meal. The body is superbly adapted to dealing with short- term physical challenges to homeostasis. Stores of energy, including the sugar glucose, are released, and cardiovascular tone increases to facilitate the delivery of fuel to exercising muscle throughout the body. Digestion, growth, tissue repair, reproduction and other physiological processes not needed to survive the crisis are suppressed. The immune system steps up to thwart opportunistic pathogens. Memory and the senses transiently sharpen. But cognitively and socially sophisticated species, such as we primates, routinely inhabit a different realm of stress. For us, most stressors concern interactions with our own species, and few physically disrupt homeostasis. Instead these psycho- social stressors involve the anticipation (accurate or otherwise) of an impending challenge. And the striking characteristic of such psychological and social stress is its chronicity. For most mammals, a stressor lasts only a few minutes. In contrast, we humans can worry chronically over a 30-year mortgage. Unfortunately, our body's response, though adaptive for an acute physical stressor, is pathogenic for prolonged psychosocial stress. Chronic increase in cardiovascular tone brings stress-induced hypertension. The constant mobilization of energy increases the risk or severity of diseases such as type 2 (adult-onset) diabetes. The prolonged inhibition of digestion, growth, tissue repair and reproduction increases the risks of various gastrointestinal disorders, impaired growth in children, failure to ovulate in females and erectile dysfunction in males. A too-extended immune stress response ultimately suppresses immunity and impairs disease defenses. And chronic activation of the stress response impairs cognition, as well as the health, functioning and even survival of some types of neurons. An extensive biomedical literature has established that individuals are more likely to activate a stress response and are more at risk for a stress-sensitive disease if they (a) feel as if they have minimal control over stressors, (b) feel as if they have no predictive information about the duration and intensity of the stressor, (c) have few outlets for the frustration caused by the stressor, (d) interpret the stressor as evidence of circumstances worsening, and (e) lack social support for the duress caused by the stressors. ===================================================== Sidebar: Chronic Stress CHRONIC STRESS may explain how poverty "gets under the skin" and exerts a harmful influence on health. The risk of stress-sensitive diseases increases if individuals lack social support, have no outlets for their frustration and feel that their circumstances are worsening exactly the conditions in many poor communities in the U.S. ====================================================== Psychosocial stressors are not evenly distributed across society. Just as the poor have a disproportionate share of physical stressors (hunger, manual labor, chronic sleep deprivation with a second job, the bad mattress that can't be replaced), they have a disproportionate share of psychosocial ones. Numbing assembly-line work and an occupational lifetime spent taking orders erode workers' sense of control. Unreliable cars that may not start in the morning and paychecks that may not last the month inflict unpredictability. Poverty rarely allows stress-relieving options such as health club memberships, costly but relaxing hobbies, or sabbaticals for rethinking one's priorities. And despite the heartwarming stereotype of the "poor but loving community," the working poor typically have less social support than the middle and upper classes, thanks to the extra jobs, the long commutes on public transit, and other burdens. Marmot has shown that regardless of SES, the less autonomy one has at work, the worse one's cardiovascular health. Furthermore, low control in the workplace accounts for about half the SES gradient in cardiovascular disease in his Whitehall population. Feeling Poor Three lines of research provide more support for the influence of psychological stress on SES-related health gradients. Over the past decade Nancy E. Adler of the University of California, San Francisco, has explored the difference between objective and subjective SES and the relation of each to health. Test subjects were shown a simple diagram of a ladder with 10 rungs and then asked, "In society, where on this ladder would you rank yourself in terms of how well you're doing?" The very openness of the question allowed the person to define the comparison group that felt most emotionally salient. As Adler has shown, a person's subjective assessment of his or her SES takes into account the usual objective measures (education, income, occupation and residence) as well as measures of life satisfaction and of anxiety about the future. Adler's provocative finding is that subjective SES is at least as good as objective SES at predicting patterns of cardiovascular function, measures of metabolism, incidences of obesity and levels of stress hormones -- suggesting that the subjective feelings may help explain the objective results. ===================================================================== Sidebar: The Good and Bad Effects of Stress The human body is superb at responding to the acute stress of a physical challenge, such as chasing down prey or escaping a predator. The circulatory, nervous and immune systems are mobilized while the digestive and reproductive processes are suppressed. If the stress becomes chronic, though, the continual repetition of these responses can cause major damage. ** Acute stress: Brain Increased alertness and less perception of pain ** Chronic stress: Brain Impaired memory and increased risk of depression === ** Acute stress: Thymus Gland and Other Immune Tissues Immune system readied for possible injury ** Chronic stress: Thymus Gland and Other Immune Tissues Deteriorated immune === ** Acute stress: Circulatory System Heart beats faster, and blood vessels constrict to bring more oxygen to muscles ** Chronic stress: Circulatory System Elevated blood pressure and higher risk of cardiovascular disease === ** Acute stress: Adrenal Glands Secrete hormones that mobilize energy supplies ** Chronic stress: Adrenal Glands High hormone levels slow recovery from acute stress === ** Acute stress: Reproductive Organs Reproductive functions are temporarily suppressed ** Chronic stress: Reproductive Organs Higher risks of infertility and miscarriage ===================================================== This same point emerges from comparisons of the SES/health gradient among nations. A relatively poor person in the U.S. may objectively have more financial resources to purchase health care and protective factors than a relatively wealthy person in a less developed country yet, on average, will still have a shorter life expectancy. For example, as Stephen Bezruchka of the University of Washington emphasizes, people in Greece on average earn half the income of Americans yet have a longer life expectancy. Once the minimal resources are available to sustain a basic level of health through adequate food and housing, absolute levels of income are of remarkably little importance to health. Although Adler's work suggests that the objective state of being poor adversely affects health, at the core of that result is the subjective state of feeling poor. Being Made to Feel Poor Another body of research arguing that psychosocial factors mediate most of the SES/health gradient comes from Richard Wilkinson of the University of Nottingham in England. Over the past 15 years he and his colleagues have reported that the extent of income inequality in a community is even more predictive than SES for an array of health measures. In other words, absolute levels of income aside, greater disparities in income between the poorest and the wealthiest in a community predict worse average health. (David H. Abbott of the Wisconsin National Primate Research Center and I, along with our colleagues, found a roughly equivalent phenomenon in animals: among many nonhuman primate species, less egalitarian social structures correlate with higher resting levels of a key stress hormone an index for worse health among socially subordinate animals.) ===================================================== Sidebar: The surest way to feel poor The surest way to feel poor is to be endlessly made aware of the haves when you are a have-not. ===================================================== Wilkinson's subtle and critical finding has generated considerable controversy. One dispute concerns its generality. His original work suggested that income inequality was relevant to health in many European and North American countries and communities. It has become clear, however, that this relation holds only in the developed country with the greatest of income inequalities, namely, the U.S. Whether considered at the level of cities or states, income inequality predicts mortality rates across nearly all ages in the U.S.. Why, though, is this relation not observed in, say, Canada or Denmark? One possibility is that these countries have too little income variability to tease out the correlation. Some critics have questioned whether the linkage between income inequality and worse health is merely a mathematical quirk. The relation between SES and health follows an asymptotic curve: dropping from the uppermost rung of society's ladder to the next-to-top step reduces life expectancy and other measures much less drastically than plunging from the next-to-bottom rung to the lowest level. Because a community with high levels of income inequality will have a relatively high number of individuals at the very bottom, where health prospects are so dismal, the community's average life expectancy will inevitably be lower than that of an egalitarian community, for reasons that have nothing to do with psychosocial factors. Wilkinson has shown, however, that decreased income inequality predicts better health for both the poor and the wealthy. This result strongly indicates that the association between illness and inequality is more than just a mathematical artifact. Wilkinson and others in the field have long argued that the more unequal income in a community is, the more psychosocial stress there will be for the poor. Higher income inequality intensifies a community's hierarchy and makes social support less available: truly symmetrical, reciprocal, affiliative support exists only among equals. Moreover, having your nose rubbed in your poverty is likely to lessen your sense of control in life, to aggravate the frustrations of poverty and to intensify the sense of life worsening. If Adler's work demonstrates the adverse health effects of feeling poor, Wilkinson's income inequality work suggests that the surest way to feel poor is to be made to feel poor to be endlessly made aware of the haves when you are a have-not. And in our global village, we are constantly made aware of the moguls and celebrities whose resources dwarf ours. John W. Lynch and George A. Kaplan of the University of Michigan at Ann Arbor have recently proposed another way that people are made to feel poor. Their "neomaterialist" interpretation of the income inequality phenomenon which is subtle, reasonable and, ultimately, deeply depressing runs as follows: Spending money on public goods (better public transit, universal health care and so on) is a way to improve the quality of life for the average person. But by definition, the bigger the income inequality in a society, the greater the financial distance between the average and the wealthy. The bigger this distance, the less the wealthy have to gain from expenditures on the public good. Instead they would benefit more from keeping their tax money to spend on their private good a better chauffeur, a gated community, bottled water, private schools, private health insurance. So the more unequal the income is in a community, the more incentive the wealthy will have to oppose public expenditures benefiting the health of the community. And within the U.S., the more income inequality there is, the more power will be disproportionately in the hands of the wealthy to oppose such public expenditures. According to health economist Evans, this scenario ultimately leads to "private affluence and public squalor." This "secession of the wealthy" can worsen the SES/health gradient in two ways: by aggravating the conditions in low- income communities (which account for at least part of the increased health risks for the poor) and by adding to the psychosocial stressors. If social and psychological stressors are entwined with feeling poor, and even more so with feeling poor while being confronted with the wealthy, they will be even more stressful when the wealthy are striving to decrease the goods and services available to the poor. Social Capital A third branch of support for psychosocial explanations for the relation between income inequality and health comes from the work of Ichiro Kawachi of Harvard University, based on the concept of "social capital." Although it is still being refined as a measure, social capital refers to the broad levels of trust and efficacy in a community. Do people generally trust one another and help one another out? Do people feel an incentive to take care of commonly held resources (for example, to clean up graffiti in public parks)? And do people feel that their organizations such as unions or tenant associations actually have an impact? Most studies of social capital employ two simple measures, namely, how many organizations people belong to and how people answer a question such as, "Do you think most people would try to take advantage of you if they got a chance?" What Kawachi and others have shown is that at the levels of states, provinces, cities and neighborhoods, low social capital predicts bad health, bad self-reported health and high mortality rates. Using a complex statistical technique called path analysis, Kawachi has demonstrated that (once one controls for the effects of absolute income) the strongest route from income inequality to poor health is through the social capital measures to wit, high degrees of income inequality come with low levels of trust and support, which increases stress and harms health. None of this is surprising. As a culture, America has neglected its social safety nets while making it easier for the most successful to sit atop the pyramids of inequality. More- over, we have chosen to forgo the social capital that comes from small, stable communities in exchange for unprecedented opportunities for mobility and anonymity. As a result, all measures of social epidemiology are worsening in the U.S. Of Westernized nations, America has the greatest income inequality (40 percent of the wealth is controlled by 1 percent of the population) and the greatest discrepancy between expenditures on health care (number one in the world) and life expectancy (as of 2003, number 29). The importance of psychosocial factors in explaining the SES/health gradient generates a critical conclusion: when it comes to health, there is far more to poverty than simply not having enough money. (As Evans once stated, "Most graduate students have had the experience of having very little money, but not of poverty. They are very different things.") The psychosocial school has occasionally been accused of promulgating an antiprogressive message: don't bother with universal health care, affordable medicines and other salutary measures because there will still be a robust SES/health gradient after all the reforms. But the lesson of this research is not to abandon such societal change. It is that so much more is needed. Additional Reading: Wilkinson, Richard. Mind the Gap: Hierarchies, Health and Human Evolution. London, UK: Weidenfeld and Nicolson, 2000. Kawachi, Ichiro and Bruce P. Kennedy, The Health of Nations: Why Inequality Is Harmful to Your Health. New York: New Press, 2002. Marmot, Michael. The Status Syndrome. New York: Henry Holt and Company, 2004. Sapolsky, Robert. Why Zebras Don't Get Ulcers: A Guide to Stress, Stress-Related Diseases and Coping. Third edition. New York: Henry Holt and Company, 2004. ============== Robert Sapolsky is professor of biological sciences, neurology and neurological sciences at Stanford University and a research associate at the National Museums of Kenya. In his laboratory work, he focuses on how stress can damage the brain and on gene therapy for the nervous system. In addition, he studies populations of wild baboons in East Africa, trying to determine the relation between the social rank of a baboon and its health. His latest book is Monkeyluv and Other Essays on Our Lives as Animals (Scribner, 2005). Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Mercury News (San Jose, Calif.), Jan. 29, 2006 CORPORATE WEALTH SHARE RISES FOR TOP-INCOME AMERICANS By David Cay Johnston New government data indicate that the concentration of corporate wealth among the highest-income Americans grew significantly in 2003, as a trend that began in 1991 accelerated in the first year that President Bush and Congress cut taxes on capital. In 2003 the top 1 percent of households owned 57.5 percent of corporate wealth, up from 53.4 percent the year before, according to a Congressional Budget Office analysis of the latest income tax data. The top group's share of corporate wealth has grown by half since 1991, when it was 38.7 percent. In 2003, incomes in the top 1 percent of households ranged from $237,000 to several billion dollars. For every group below the top 1 percent, shares of corporate wealth have declined since 1991. These declines ranged from 12.7 percent for those on the 96th to 99th rungs on the income ladder to 57 percent for the poorest fifth of Americans, who made less than $16,300 and together owned 0.6 percent of corporate wealth in 2003, down from 1.4 percent in 1991. The analysis did not measure wealth directly. It looked at taxes on capital gains, dividends, interest and rents. Income from securities owned by retirement plans and endowments was excluded, as were gains from noncorporate assets such as personal residences. This technique for measuring wealth has long been used in standard economic studies, though critics have challenged that tradition. Among them is Stephen J. Entin, president of the Institute for Research on the Economics of Taxation in Washington, which favors eliminating most taxes on capital and teaches that an unintended consequence of the corporate income tax is depressed wage rates. Mr. Entin said the report's approach was so flawed that the data were useless. He said reduced tax rates on long-term capital gains may have prompted wealthy investors to sell profitable investments. That would show up in tax data as increased wealth that year, even though the increase may have built up over decades. Long-term capital gains were taxed at 28 percent until 1997, and at 20 percent until 2003, when rates were cut to 15 percent. The top rate on dividends was cut to 15 percent from 35 percent that year. The White House said it did not believe that the 2003 tax cuts had much influence on wealth shares. It also said that since wealth is transitory for many people, a more important issue is how incomes and wealth are influenced by the quality of education. ''We want to lift all incomes and wealth,'' said Trent Duffy, a White House spokesman. ''We are starting to see that the income gap is largely an education gap.'' ''The president thinks we need to close the income gap, and he has talked about ways in which we can do that,'' especially through education, Mr. Duffy said. The data showing increased concentration of corporate wealth were posted last month on the Congressional Budget Office Web site. Isaac Shapiro, associate director of the Center on Budget and Policy Priorities in Washington, spotted the information last week and wrote a report analyzing it. Mr. Shapiro said the figures added to the center's ''concerns over the increasingly regressive effects'' of the reduced tax rates on capital. Continuing those rates will ''exacerbate the long-term trend toward growing income inequality,'' he wrote. The center, which studies how government affects the poor and supports policies that it believes help alleviate poverty, opposes Mr. Bush's tax policies. The center plans to release its own report on Monday that questions the wisdom of continuing the reduced tax rates on dividends and capital gains, saying the Congressional Budget Office analysis indicates that the benefits flow directly to a relatively few Americans. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: From: Science News (Vol. 169, No. 5, pg. 74), Feb. 5, 2006 A LITTLE LESS GREEN? HN Are Pyrethroid Insecticides Dangerous? Studies challenge the benign image of pyrethroid insecticides By Janet Raloff Rachel Carson turned the pest-control world upside down in 1962. In Silent Spring, she documented how long-lived organochlorine pesticides, most notoriously DDT, were not only ridding croplands of insects, streets of mosquitoes, and homes of spiders but also exacting a high toll on songbirds and other nontargeted species. The chemicals' broad-spectrum potency and resistance to breakdown, advantages in their use against pests, emerged as hazards. Shortly after the publication of Carson's book, industrialized countries began phasing out such persistent organic pollutants, or POPs. There's now a United Nations treaty aiming at their global elimination (SN: 11/8/03, p. 301: Available to subscribers at http://www.sciencenews.org/articles/20031108/note14.asp). In the wake of organochlorine pesticides came organophosphate agents. Although these agents are highly effective, their toxicity to nontarget animals -- including people -- echoed the perils of DDT. Regulators responded, and by the middle 1990s, once-popular members of this class of agents -- such as dursban, malathion, and chlorpyrifos -- were being phased out or severely restricted in their uses. In recent years, farmers and others have increasingly turned to products based on pyrethrins, chemicals made by certain members of the chrysanthemum family. Farmers in various parts of the world have for millennia used preparations from these flowers to protect crops from insects. Since the 1960s, manufacturers have produced synthetic analogs -- called pyrethroids -- of the herbal products' active ingredients. Although pyrethroids have greater toxicity to insects and somewhat more resistance to breakdown than their natural counterparts do, studies have demonstrated that these synthetic chemicals pose little risk to most vertebrates, from songbirds to people. Pyrethroids stand poised to overtake organophosphate insecticides for farm use and are already the leading insecticides sold to homeowners. However, emerging data show that even pyrethroids can pose serious environmental hazards. At concentrations found in streams, the chemicals can kill beneficial insects and crustaceans and may even be acting -- below the radar screen -- to poison fish and lizards. Most of these findings came to light in some dozen presentations in Baltimore last November at the Society of Environmental Toxicology and Chemistry (SETAC) annual meeting. The research described there suggests that, at least where the mum-based pesticides might enter streams, these compounds should be used sparingly. "The Environmental Protection Agency needs to take a closer look at pyrethroids" with an eye toward changing how the 22 such compounds that it has registered are marketed and used, argues Michael J. Lydy, an environmental toxicologist at Southern Illinois University in Carbondale. Ample and growing data, he says, challenge "the suggestion that in the environment, pyrethroids will be innocuous." Hunting thrins "Walk down the pesticide aisle of your local hardware store and read the active ingredients in insecticides. Nearly every one ends in 'thrin,'" a dead giveaway that it is a pyrethroid, observes Donald P. Weston, an environmental toxicologist at the University of California, Berkeley. Only a few pyrethroids -- most notably esfenvalerate -- lack that suffix. Although many of these compounds have been used for decades, especially on farms, "no one had looked for them in the environment," Weston notes. In the past few years, he and his colleagues launched several surveys to check whether pyrethroids were causing harm in streams. Because these pesticides don't readily dissolve, but instead glom on to particles and quickly settle out of water, his team focused its analyses on sediments. Their findings proved eye-opening, Weston told Science News. In one study of creeks adjacent to farmlands across a 10-county area in California's Central Valley, researchers looked for five pyrethroids and found one or more in at least three-quarters of the 70 sediments sampled. The researchers then tested two stream dwellers: the amphipod Hyalella azteca, which is a small, shrimplike crustacean, and a larval midge of the species Chironomus tentans. Ecologists use these tiny "lab rats of the sediment-testing world" for toxicity assessments, Weston explains. At 42 percent of the sampled sites, the sediment proved deadly to at least one of two species, his group reported 2 years ago. In a follow-up study, the scientists spiked sediment samples from clean sites with six common pyrethroids to compare their toxic effects on H. azteca. They measured each compound's LC50 -- the concentration lethal to 50 percent of animals exposed in a test. In the April 2005 Environmental Toxicology and Chemistry (ET&C), the team reported that permethrin's LC50 was 60 to 110 parts per billion (ppb), depending on how much organic carbon the sediment contained. The LC50 for the remaining pyrethroids was far lower, indicating greater toxicity. The most toxic: lambda-cyhalothrin and bifenthrin, which have an LC50 of 2 to 6 ppb. The crustaceans' growth was significantly retarded at concentrations just one-third of a pyrethroid's LC50. Lawn pollution Farm runoff isn't the only -- or perhaps even the most important -- way in which these agents get into streams. Weston and his Berkeley colleague Erin L. Amweg reported data at the SETAC meeting showing that pyrethroids are washed into waterways from suburban yards by rain and lawn watering. RUNAWAY RUNOFF. Lawn-watering runoff at this home in Roseville, Calif., illustrates how pyrethroids used on the yard would be washed into storm drains, which are a direct conduit to neighborhood streams. Amweg In one recent study, Weston, Lydy, and others surveyed streams in Roseville, a suburb of Sacramento, Calif. Only a decade earlier, land along these creeks had been arid grassland. Since then, much of it has been converted to subdivisions sporting four homes per acre, most with manicured lawns. Roughly 90 percent of the stream sediments sampled contained bifenthrin, and the majority of them had bifenthrin concentrations toxic to Hyalella, the scientists report in the Dec. 15, 2005, Environmental Science & Technology. Often, one to five more pyrethroids were present. In contrast, the pesticides didn't show up in waters draining Roseville sites free of residential development. In toxicity, bifenthrin dominated the suburban sediments. Indeed, Lydy told Science News, "80 percent of our samples had enough toxicity due to bifenthrin alone to cause at least half of our [amphipods] to die." The team recorded pesticide concentrations as high as 437 ppb—that's about 100 times as great as its LC50 for H. azteca and 15 times the highest bifenthrin concentration seen in sediments of creeks running through Central Valley croplands. This indicates, Weston says, that the highest concentrations of pyrethroids in creek sediments trace to "classic suburbia -- we're talking Mom, Dad, two kids, and a dog." Although pesticides applied by professional exterminators around the perimeters of homes are a possible source of the creek contamination, the research group strongly suspects that much of the bifenthrin comes from lawn-care products. Some fertilizers even include bifenthrin, so that homeowners can feed their grass and kill bugs in one pass. In the Roseville study, the pesticides didn't appear to travel far once they reached a creek, with the high concentrations appearing only within 100 yards or so of storm-drain outfalls. What's not clear, Weston and others observe, is whether the California data reflect what's occurring nationally or might instead represent a worst-case scenario. For instance, Amweg presented data at the SETAC meeting indicating that creeks near Sacramento and San Francisco showed substantial sediment contamination but streams in Nashville didn't. The California sites, unlike Nashville, get little summer rainfall to dilute stream pollutants. Moreover, many of California's urban areas rely on concrete storm drains to channel lawn runoff directly into streams, whereas the Nashville sites were separated from waterways by a corridor of greenery. Too excited Joel R. Coats of Iowa State University in Ames and his colleagues have been probing why pyrethroids "are as nasty as DDT [is] to a lot of aquatic life -- including fish." HOW NEAT? Aquatic caddis fly nymphs build protective cases from plant debris. Ordinarily, a nymph cuts and stacks materials, log-cabin style, into an orderly, well-aerated covering (top inset). Pyrethroid- exposed nymphs, however, make chaotically structured dwellings from uncut parts (bottom inset) or forgo such protection altogether. Johnson/OSU Pyrethroids poison pests by wreaking havoc on their nervous systems, as most insecticides do. When nerves transmit an impulse, Coats explains, "there's an electrical ripple that's triggered by sodium gates in [each cell] opening in sequence." Pyrethroids perturb the nerve cells' sodium gates, however, so that once open, they never fully close, Coats says. The resulting sodium leaks maintain nerve cells in a state of overexcitation that kills the insects. Because the nervous systems of crustaceans and many other soft-bodied aquatic animals resemble those of insects, these nontargeted animals are also vulnerable to pyrethroids. Coats observes that mammals and birds gain some protection from pyrethroid poisoning by two mechanisms: production of esterase enzymes that inactivate the poisons by splitting them in half, and another metabolic process that employs oxidation. He reported at the SETAC meeting that although rainbow trout, bluegill, and fathead minnows can all oxidize pyrethroids, their esterase enzyme activity doesn't break apart the pesticides. Although these pesticides may induce ill effects that fall short of lethality, toxicologists have generally been forced to focus on their deadliness, Weston says, because fatal concentrations tend to be at or near the minimum value at which current technology can detect the pesticides. If the pesticides cause sickness, therefore, it's likely to happen at concentrations too low to measure, he says. To get around this difficulty, some scientists have added minute amounts of the compounds to tanks of water containing aquatic animals. At Oregon State University (OSU) in Corvallis, Katherine R. Johnson and her colleagues administered esfenvalerate to aquatic nymphs of the caddis fly (Brachycentrus americanus) -- an insect eaten by many fish. For protection from predators, these nymphs enshroud themselves in hard cases. As the OSU researchers increased pyrethroid concentrations above 0.05 ppb, formerly resting animals began fleeing their cases in increasing numbers, notes coauthor Jeffrey J. Jenkins. Among nymphs that fled, three-quarters of those exposed to as little as 0.2 ppb esfenvalerate didn't rebuild their cases. Rebuilt cases were disordered and much weaker than the originals, the scientists reported at the SETAC meeting. Conditional toxicity Environmental stressors can sabotage pesticide- detoxification systems, even in animals that would otherwise withstand the chemicals, notes Larry G. Talent. At Oklahoma State University in Stillwater, he studied adult green anole lizards (Anolis carolinensis), 6 to 8 inches long, exposed to a pyrethroid product used to treat birds for mites and lice. When he doused the lizards with a solution of the pesticide and then maintained the reptiles at a comfortable 95°F, none died. However, 70 percent of treated lizards died within 2 days when they were instead housed at a cool 68°F. Without pesticide exposure, the lizards showed no mortality at the lower temperature, Talent reports in the December 2005 ET&C. Low temperatures, which might mimic night or winter environments, pose a double whammy for pyrethroid effects: Not only is the lizard's nervous system more vulnerable to poisoning but its metabolic breakdown of pollutants also slows. Mark A. Clifford last year reported a similar synergy between two environmental stressors—pyrethroid exposure and a viral infection -- in young salmon. The University of California, Davis fish pathologist exposed 2-month-old chinook salmon for 4 days to either esfenvalerate or chlorpyrifos, an organophosphate pesticide. He then seeded some of the aquariums holding the fish with infectious hematopoietic necrosis virus, which can kill juveniles. Fish exposed to low doses of the virus survived, as did those exposed to either pesticide alone, Clifford's team reported in the July 2005 ET&C. Deaths occurred only in fish exposed to high concentrations of the virus or to both the pyrethroid and virus. Within 3 days of being exposed to either dose of virus, roughly 70 percent of the pesticide- exposed salmon fry were dead. The pyrethroid's impact "was totally unexpected," Clifford says. Two follow-up trials confirmed that the initial observation was not a fluke. Winds of change? EPA considers new data when it periodically reviews its approvals of pesticides registered before 1984. Reevaluations for permethrin, resmethrin, and cypermethrin are slated for completion this year, and three other pyrethroids are to be reviewed by 2008. Because bifenthrin was registered in late 1985, it's not scheduled for such a reevaluation. In a statement to Science News, however, EPA's Office of Pesticide Programs (OPP) notes that this pesticide's manifestation of "certain toxic properties at the level of detection [makes it] challenging for the agency to determine whether risks from the use of this pesticide are acceptable." In fact, the statement says, to better understand pyrethroids' toxicity and bioavailability to nontarget organisms, OPP is "reviewing the sediment toxicity studies on bifenthrin, cypermethrin, cyfluthrin, and esfenvalerate that were recently submitted [by Weston's group and others]." These pesticides were chosen as "surrogates," the statement says, for assessing the exposures and toxicity of other pyrethroids. Indeed, OPP notes, despite their use on some 50 agricultural crops, some pyrethroids have only "conditional" approval from EPA, pending future evaluation of their sediment toxicity and of the value of buffer zones in keeping treated areas from tainting streams. OPP says that it anticipates completing a "comparative assessment for pyrethroids" by December. Pyrethroid manufacturers are already bracing for change. Jim Fitzwater, a spokesman for bifenthrin-maker FMC Corp. of Philadelphia, says that homeowners need to be educated about how and when to apply lawn-care products containing pyrethroids. He notes that his company sells to consumer-products companies rather than consumers and says, "We're looking at working with [these] end-use manufacturers to do a better stewardship job." References: 2005. Pyrethroid pesticides found at toxic levels in California urban streams. University of California, Berkeley press release. Oct. 25. Available here. 2004. Sediments in many Central Valley streams contain toxic levels of pyrethroid pesticides. University of California, Berkeley press release. May 6. Available here. Amweg., E.L., D.P. Weston, J. You, and M.J. Lydy. In press. Pyrethroid insecticides and sediment toxicity in urban creeks from California and Tennessee. Environmental Science & Technology. Abstract available here. Amweg, E.L., and J. You. 2005. Pyrethroid pesticide distribution and toxicity in urban creeks. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Amweg, E.L., D.P. Weston, and N.M. Ureda. 2005. Use and toxicity of pyrethroid pesticides in the Central Valley, California, USA. Environmental Toxicology and Chemistry 24(April):966-972. Abstract available here. Clifford, M.A., et al. 2005. Synergistic effects of esfenvalerate and infectious hematopoietic necrosis virus on juvenile chinook salmon mortality. Environmental Toxicology and Chemistry 24(July):1766-1772. Abstract available here. Coats, J.R. 2005. Toxicology of synthetic pyrethroids to fish. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. DeLorenzo, M.E., et al. 2005. Toxicity of the pyrethroid insecticide permethrin to adult and larval grass shrimp (Palaemonetes pugio). SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Johnson, K.R., J.J. Jenkins, and P.C. Jepson. 2005. Exposure to esfenvalerate induces case-leaving in the caddisfly Brachycentrus americanus. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Lydy, M., D. Weston, and J. You. 2005. Relative contributions of agricultural or urban pyrethroid usage to toxicity in California streams. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Talent, L.G. 2005. Effect of temperature on toxicity of a natural pyrethrin pesticide to green anole lizards (Anolis carolinensis). Environmental Toxicology and Chemistry 24(December):3113-3116. Abstract available here. Weston, D.P.... and M.J. Lydy. 2005. Aquatic toxicity due to residential use of pyrethroid insecticides. Environmental Science & Technology 39(Dec. 15):9778-9784. Abstract available here. Weston, D.P., R.W. Holmes, and T. English. 2005. A tale of two creeks: an intensive study of pyrethroids and related toxicity in urban environments. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Weston, D.P., J. You, and M.J. Lydy. 2004. Distribution and toxicity of sediment-associated pesticides in agriculture-dominated water bodies of California's Central Valley. Environmental Science & Technology 38(May 15):2752-2759. Abstract available here. Further Readings: Belden, J.B., and M.J. Lydy. 2006. Joint toxicity of chlorpyrifos and esfenvalerate to fathead minnows and midge larvae. Environmental Toxicology and Chemistry 25(February):623-629. Abstract available here. Cheplick, J.M., et al. 2005. National exposure analysis of pyrethroids (Part 2): Erosion assessment using PRZM 3.12 at the watershed level. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Holmes, C.M., et al. 2005. National exposure analysis of pyrethroids (Part 1): Spatial proximity of agriculture to surface water. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Lydy, M.J., and K.R. Austin. 2004. Toxicity assessment of pesticide mixtures typical of the Sacramento- San Joaquin delta using Chironomus tentans. Archives of Environmental Contamination and Toxicology 48(December):49-55. Abstract available here. Raloff, J. 2003. POPs treaty enacted. Science News 164(Nov. 8):301. Available to subscribers here. ______. 2000. The case for DDT. Science News 158(July 1):12-13. Available here. ______. 1999. Thyroid linked to some frog defects. Science News 156(Oct. 2):212. Available here. Ritter, A.M., et al. 2005. National exposure analysis of pyrethroids (Part 3): Sensitivity analysis of exposure to drift and erosion. SETAC North America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Sources: Erin L. Amweg University of California, Berkeley Building 102-RFS Berkeley, CA 94720-3140 Mark Clifford Fish Health Laboratory Medicine and Epidemiology University of California, Davis Davis, CA 95616 Joel R. Coats Iowa State University Department of Entomology Ames, IA 50011 Jim Fitzwater FMC Corporation 1735 Market Street Philadelphia, PA 19103 Jeffrey J. Jenkins Department of Molecular Toxicology Oregon State University 1007 Ag and Life Science Building Corvallis, OR 97331-7301 Katherine R. Johnson Department of Environmental and Molecular Toxicology 1007 ALS Building Corvallis, OR 97331-7301 Michael J. Lydy Department of Zoology Southern Illinois University Carbondale, IL 62901-6501 Mah Shamin Environmental Risk Branch 5 Environmental Fate & Effects Division 1200 Pennsylvania Avenue, N.W. Washington, DC 20460 Society of Environmental Toxicology and Chemistry 1010 North 12th Avenue Pensacola, FL 32501-3368 Donald P. Weston University of California, Berkeley Building 102-RFS Berkeley, CA 94720-3140 From Science News, Vol. 169, No. 5, Feb. 4, 2006, p. 74. Copyright 2006 Science Service. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: Rachel's Democracy & Health News (formerly Rachel's Environment & Health News) highlights the connections between issues that are often considered separately or not at all. The natural world is deteriorating and human health is declining because those who make the important decisions aren't the ones who bear the brunt. Our purpose is to connect the dots between human health, the destruction of nature, the decline of community, the rise of economic insecurity and inequalities, growing stress among workers and families, and the crippling legacies of patriarchy, intolerance, and racial injustice that allow us to be divided and therefore ruled by the few. In a democracy, there are no more fundamental questions than, "Who gets to decide?" And, "How do the few control the many, and what might be done about it?" As you come across stories that might help people connect the dots, please Email them to us at firstname.lastname@example.org. Rachel's Democracy & Health News is published as often as necessary to provide readers with up-to-date coverage of the subject. 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