Turning Boys into Girls?

[Guest guest]

^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^Rachel's Democracy & Health News #841"Environment, health, jobs and justice--Who gets to decide?"www.rachel.org^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^ 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." :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: 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-partseries on chemicals published in the Wall Street Journal (WSJ),written by Peter Waldman, a WSJ reporter. The series basically showedthat the U.S. chemical regulation system is utterly broken and is notmuch 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 addedexplanatory links.--DHN Editors] In part 3 of his series, Peter Waldman begins by offering his mostlymale audience a lesson in reproductive biology: "In the 12th week of a human pregnancy, the momentous event of genderformation begins, as X and Y chromosomes trigger biochemical reactionsthat shape male or female organs. Estrogens carry the process forwardin girls, while in boys, male hormones called androgens do.Phthalate syndrome" in rodents Mr. Waldman goes on: "Now scientists have indications the process maybe influenced from beyond the womb, raising a fresh debate overindustrial chemicals and safety. In rodent experiments, commonchemicals called phthalates, used in a wide variety of products fromtoys to cosmetics to pills, can block the action of fetal androgens.The result is what scientists call demasculinized effects in maleoffspring, ranging from undescended testes at birth to low spermcounts and benign testicular tumors later in life. 'Phthalatesyndrome,' researchers call it." In other words, these common chemicals, phthalates -- found in toys,cosmetics, and pharmaceutical drugs -- can interfere with thedevelopment of male rodents so reliably that there's a name for theeffect: "phthalate syndrome." Now I don't know about you, but it I were a scientist studying a groupof chemicals commonly found in toys, cosmetics and drugs, and Idiscovered that my chemicals could reliably demasculinize male babyrodents, I'd be asking myself, "Wouldn't it be smart to keep thesechemicals away from human babies?" That would be called a"precautionary approach" to phthalates -- but this is a noxious ideato U.S. chemical executives and regulators alike. In the U.S., you'vegot to prove harm to a scientific certainty before you are officiallyallowed to become concerned about a chemical. And even then thechemical corporations have the right to drag you into court for adecade or two while they continue to sell product (because thecorporations are considered legal "persons" and they have arranged forthe burden of proof of harm to rest on the public, not on thecorporations). So what kind of evidence do we have about harm from phthalates? First WSJ tells us that "...last year, federal scientists found genealterations in the fetuses of pregnant rats that had been exposed toextremely low levels of phthalates, levels no higher than the traceamounts 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 thegreatest phthalate exposures while pregnant were much more likely thanother baby boys to have certain demasculinized traits." And: "...another small study found that 3-month-old boys exposed tohigher levels of phthalates through breast milk produced lesstestosterone than baby boys exposed to lower levels of the chemicals."Testosterone is male sex hormone and it is what turns boys into boysinstead of girls during the 12th week of pregnancy. "Testicular dysgenesis syndrome" in humans WSJ goes on to explain that scientists in Europe "have identified whatsome see as a human counterpart to rodents' phthalate syndrome, onethey call "testicular dysgenesis syndrome," which they think may bedue in part to exposure to phthalates and other chemicals thatinterfere with male sex hormones. These problems begin while the baby is still in the womb. RichardSharpe of the University of Edinburgh in Scotland, a researcher onmale reproduction, told the WSJ, "We know abnormal development of thefetal testes underlies many of the reproductive disorders we're seeingin men. We do not know what's causing this, but we do know high dosesof phthalates induce parallel disorders in rats." Now the chemists who make this stuff have known for a long time thatit leaks into the environment and then gets into people. How could itnot? Phthalates were measured in the Charles and Merrimack Rivers inMassachusetts in 1973. That same year, a study reported findingphthalates in environmental samples. That same year, 1973,researcher reported measuring phthalates in cosmetics. The followingyear, 1974, we find an article describing phthalates measured infood. 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 andurine, because they are used so widely. Nearly five million metrictons [11 billion pounds] of phthalates are consumed by industry everyyear, 13% in the U.S. They are made from petroleum byproducts andchemically known as esters, or compounds of organic acid and alcohol.The common varieties with large molecules are used to plasticize, ormake pliable, otherwise rigid plastics -- such as polyvinyl chloride,known as PVC -- in things like construction materials, clothing, toysand furnishings. Small-molecule phthalates are used as solvents and inadhesives, waxes, inks, cosmetics, insecticides and drugs." Let's see now. In the U.S. we use 1,430,000,000 (1.43 billion) poundsof this stuff each year in products that everyone knows will end up inour homes, then in our bodies, and we know it causes baby boy rats tostart to turn into sickly baby girl rats -- and we don't have thesense to call a halt? I suppose the Bible had it right: "The love ofmoney is the root of all evil" -- because the actions of chemists,corporate executives and risk assessors who allow this to continuesurely qualify as evil by any normal definition. Marian Stanley of the American Chemistry Council (formerly theChemical Manufacturer's Association) told the WSJ that phthalates areamong the most widely studied chemicals and have proved safe for morethan 50 years. So the chemical manufacturers admit they have beenpumping this stuff into the public for 50 years while evidence of harmhas accumulated. You have to appreciate their candor, and marvel attheir gall. Government researcher L. Earl Gray told the WSJ that -- even today --EPA is "moving cautiously" because, "All this work on the effects ofphthalates on the male reproductive system is just five years old." But wait. Mr. Gray himself published his first studies of the abilityof certain industrial chemicals to interfere with hormones and alterthe 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 467scientific 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 chemicalsfound at Superfund sites. In 1991, Mr. Gray signed the Wingspread Statement, which was titled,"Chemically Induced Alterations in Sexual Development: TheWildlife/Human Connection." Why were phthalates identified as a majorproblem in 1987 and then ignored for 15 years? Surely the EPA hadknowledgable staff who must have suspected a problem. Were theyignored? Silenced? What? Last summer Mr. Gray told WSJ, "There appears to be clear disruptionof the androgen pathway, but how? What are phthalates doing?" Who CARES exactly what phthalates are doing? Pregnant moms don't wantthe government to sit around while its scientists tease out theprecise 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 toodifficult for government scientists and corporate spokeswomen tograsp? But here's a breath of fresh air. At least one corporate scientist,Dr. Rochelle Tyl, a toxicologist, told the WSJ that the broaderquestion is: "If we know something bad is happening, or we think wedo, do we wait for the data or do we act now to protect people?"Exactly so. But U.S. EPA and the Chemical Manufacturers Associationboth give the same answer: "Definitely, let's wait for something badto happen." Now I can understand why corporations would want to wait for somethingbad to happen -- most companies in the business of making harmfulchemicals also have some fiduciary interest in medical technology, orin "environmental remediation." Many of them have figured out thatthey can get paid to create problems and then get paid again to fixthem. It's that love of money thing again -- it keeps the wheelsturning and the economy growing. But why would government not ask thesame precautionary question that Dr. Tyl asked and answer it in a waythat protects public health? Very mysterious. Perhaps the governmentis beholden to the corporations at election time and there is nolonger any such thing as an independent moral agent making decisionsinside the regulatory system. I'm speculating because I don't know. The Japanese have banned phthalates in certain food-handlingequipment. The Europeans have banned phthalates from cosmetics andtoys. Last summer the European Parliament asked the EuropeanCommission (the regulatory body of the European Union) to reviewproducts "made from plasticised material which may expose people torisks, especially those used in medical devices." Late last year,Unilever, Revlon Inc., and L'Oreal SA's American subsidiary -- houndedwonderfully by the safe cosmetics campaign -- agreed to go alongwith whatever the Europeans decide to ban from products. Procter & Gamble Co. said last year it would no longer use phthalates in nailpolish. 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 Mobilspokeswoman says risk assessments by government agencies in Europe andthe U.S. confirm 'the safety of phthalates in their currentapplications.'" Risk assessment is definitely the polluter's mostuseful pseudo-scientific tool. As first EPA administrator WilliamRuckelshaus said in 1984, "We should remember that risk assessmentdata can be like the captured spy: If you torture it long enough, itwill tell you anything you want to know." Despite these assurances from the polluters' spokeswomen, the WSJraises serious concerns about the safety of phthalates: "For instance,a 2003 study divided 168 male patients at a fertility clinic intothree groups based on levels of phthalate metabolites in their urine.The study found that men in the highest third for one of thephthalates were three to five times as likely as those in the lowestthird to have a low sperm count or low sperm activity. Men highest ina different phthalate also had more abnormally shaped sperm, accordingto the study, which was done by researchers at the Harvard School ofPublic 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 certainphthalates had less testosterone during their crucial hormonal surgeat three months of age than baby boys exposed to lower levels." Of course, as you would expect, not all studies of phthalates showhealth effects in humans, so industry clings to these "negative"studies and keeps pumping out the pollutants. Studies that createdoubt about the science allow polluters to continue polluting fordecades -- so there's now a large and growing industrial enterprisedevoted simply to ginning up faulty studies that don't find anythingbecause they were designed not to, thus creating doubt. No one couldever 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 exposureto phthalates to structural differences in the genitalia of baby boys. "Researchers measured phthalate levels in pregnant women and laterexamined their infant and toddler sons. For pregnant women who had thehighest phthalate exposure -- a level equivalent to the top 25% ofsuch exposure in American women -- baby sons had smaller genitalia, onaverage. And their sons were more likely to have incompletelydescended testicles. "Most striking was a difference in the length of the perineum, thespace between the genitalia and anus, which scientists call AGD, foranogenital distance. In rodents, a shortened perineum in males isclosely correlated with phthalate exposure. A shortened AGD also isone of the most sensitive markers of demasculinization in animalstudies," WSJ reported. And: "Males' perineums at birth are usually about twice as long asthose of females, in both humans and laboratory rodents. In thisstudy, the baby boys of women with the highest phthalate exposureswere 10 times as likely to have a shortened AGD, adjusted for babyweight, as the sons of women who had the lowest phthalate exposures." WSJ continued to explore the meaning of this study: "Someendocrinologists call this the first study to link an industrialchemical measured in pregnant women to altered reproductive systems inoffspring. 'It is really noteworthy that shortened AGD was seen,' saysNiels Skakkebaek, a reproductive-disorder expert at the University ofCopenhagen, who wasn't an author of the study. 'If it is proven theenvironment changed the [physical characteristics] of these babies insuch 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 widevariety of chemical exposures in people's lives." In other words, the Chemical Manufacturers are pumping out 1.43billion pounds of a chemical that is increasingly linked to sexualdysfunction, including genital cancer in boys, and they don't believethere is any way to definitively learn the truth about that chemical-- or any other chemical -- because the Chemical Manufacturers arepumping out so many other chemicals! Think about that. The U.S. regulatory system requires a very highlevel of proof of harm before action can be taken to curtailproduction of a chemical. And the chemical manufacturers don't believescience can EVER "tease out the cause of a human health condition"because we're all exposed to too many industrial poisonssimultaneously. So the Chemical Manufacturers must think they're homefree -- no amount of scientific study can ever trip them up. And of course the Chemical Manufacturers are right. Science cannotdefinitively "tease out" the effects of a single chemical when we areall exposed to a toxic soup of industrial poisons from the moment ofconception onward. Scientists who insist otherwise are either foolingthemselves, or trying to fool us. No matter how many studies aredone, some uncertainty will always remain -- some variable that wasn'tstudied could always confound the results. The only way to pull back from the edge of this cliff is to alter ourstandards of proof, shift the burden onto the polluter to show thateach of his or her products is the least-harmful one available to dothe job -- and take precautionary action by insisting on safersubstitutes for chemicals that seem harmful based on the weight of theevidence, not waiting for scientific certainty. Insist that everychemical 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 "herown rat studies confirm that AGD is very sensitive to phthalates. Shesays that in rats that had very high phthalate exposures, a shortenedAGD at birth was closely associated with a number of seriousreproductive disorders later in life. However, in rats exposed to muchlower doses of phthalates, a shortened AGD at birth did not alwayslead 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 ofhumans.... Dr. Tyl theorizes, that the boys with shortened AGD willgrow up normally. 'At what point do changes like this cross the line'to become dangerous, she asks." And she answers her own question: "Wedon't know yet." OK, we don't know. We may never know. But we can ask 1000 pregnantmoms one question: "Is it OK with you if I pump teensy amounts of afew dozen industrial poisons into your womb and alter the anatomy ofyour baby?" How many women out of a thousand would say, "Yes?" Maybe a few. Perhaps the wives of chemical company executives wouldanswer, "Of course!. I love having those industrial chemicals in mybaby. I'm tickled with the idea of Exxon-Mobil and BASF altering mychild's anatomy before birth!" Maybe Marian Stanley (the flak for theChemical Manufacturers) and the anyonymous spokeswoman for Exxon Mobilwould say they are happy to have their babies' anatomy altered sotheir bosses can continue to consummate their love of money. But somehow I doubt it. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: 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, physicianand political activist, came of age with two dramatic events -- atyphoid out-break in 1847 and the failed revolutions of 1848. Out ofthose experiences came two insights for him: first, that the spread ofdisease has much to do with appalling living conditions, and second,that those in power have enormous means to subjugate the powerless. AsVirchow summarized in his famous epigram, "Physicians are the naturalattorneys of the poor." Physicians (and biomedical scientists) are advocates of theunderprivileged because poverty and poor health tend to go hand inhand. Poverty means bad or insufficient food, unhealthy livingconditions and endless other factors that lead to illness. Yet it isnot merely that poor people tend to be unhealthy while everyone elseis well. When you examine socio-economic status (SES), a compositemeasure that includes income, occupation, education and housingconditions, it becomes clear that, starting with the wealthieststratum of society, every step downward in SES correlates with poorerhealth. This "SES gradient" has been documented throughout Westernizedsocieties for problems that include respiratory and cardiovasculardiseases, ulcers, rheumatoid disorders, psychiatric diseases and anumber of cancers. It is not a subtle statistical phenomenon. When youcompare the highest versus the lowest rungs of the SES ladder, therisk of some diseases varies 10-fold. Some countries exhibit a five-to 10-year difference in life expectancy across the SES spectrum. Ofthe Western nations, the U.S. has the steepest gradient; for example,one study showed that the poorest white males in America die about adecade earlier than the richest. So what causes this correlation between SES and health? Lower SES maygive rise to poorer health, but conversely, poorer health could alsogive rise to lower SES. After all, chronic illness can compromiseone's education and work productivity, in addition to generatingenormous expenses. Nevertheless, the bulk of the facts suggests that the arrow goes fromeconomic status to health -- that SES at some point in life predictshealth measures later on. Among the many demonstrations of this pointis a remarkable study of elderly American nuns. All had taken theirvows as young adults and had spent many years thereafter sharing diet,health care and housing, thereby controlling for those lifestylefactors. Yet in their old age, patterns of disease, incidence ofdementia and longevity were still significantly predicted by their SESstatus 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 mostobvious, it turns out, do not hold much water. One such explanation,for instance, posits that for the poor, health care may be less easilyaccessible and of lower quality. This possibility is plausible whenone considers that for many of the poor in America, the familyphysician does not exist, and medical care consists solely of trips tothe emergency room. But that explanation soon falls by the wayside, for reasons madeclearest in the famed Whitehall studies by Michael G. Marmot ofUniversity College London over the past three decades. Marmot and hiscolleagues have documented an array of dramatic SES gradients in aconveniently stratified population, namely, the members of the Britishcivil service (ranging from blue-collar workers to high-poweredexecutives). Office messengers and porters, for example, have farhigher mortality rates from chronic heart disease than administratorsand professionals do. Lack of access to medical attention cannotexplain the phenomenon, because the U.K., unlike the U.S., hasuniversal health care. Similar SES gradients also occur in othercountries with socialized medicine, including the health care Edens ofScandinavia, and the differences remain significant even afterresearchers factor in how much the subjects actually use the medicalservices. Another telling finding is that SES gradients exist for diseases forwhich health care access is irrelevant. No amount of medical checkups,blood tests and scans will change the likelihood of someone gettingtype 1 (juvenile-onset) diabetes or rheumatoid arthritis, yet bothconditions are more common among the poor. The next "obvious" explanation centers on unhealthy life-styles. Asyou descend the SES ladder in Westernized societies, people are morelikely to smoke, to drink excessively, to be obese, and to live in aviolent or polluted or densely populated neighborhood. Poor people arealso less likely to have access to clean water, healthy food andhealth clubs, not to mention adequate heat in the winter and air-conditioning in the summer. Thus, it seems self-evident that lower SESgets under the skin by increasing risks and decreasing protectivefactors. As mordantly stated by Robert G. Evans of the University ofBritish Columbia, "Drinking sewage is probably unwise, even for BillGates." What is surprising, though, is how little of the SES gradient theserisk and protective factors explain. In the Whitehall studies,controlling for factors such as smoking and level of exerciseaccounted for only about a third of the gradient. This same point ismade by studies comparing health and wealth among, rather than within,nations. It is reasonable to assume that the wealthier a country, themore financial resources its citizens have to buy protection and avoidrisk. If so, health should improve incrementally as one moves up thewealth gradient among nations, as well as among the citizens withinindividual nations. But it does not. Instead, among the wealthiestquarter of countries on earth, there is no relation between acountry's wealth and the health of its people. Thus, health care access, health care utilization, and exposure torisk and protective factors explain the SES/health gradient far lesswell than one might have guessed. One must therefore consider whethermost 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 spansthan do people in the wealthier strata of society. The conventionalexplanations that the poor have less access to health care and agreater incidence of harmful lifestyles such as smoking and obesitycannot account for the huge discrepancy in health outcomes. ** New studies indicate that the psychosocial stresses associatedwith poverty may increase the risks of many illnesses. The chronicstress 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 inequalityand poor health in the U.S. Some researchers believe that the poorfeel poorer, and hence suffer greater stress, in communities with widegaps between the highest and lowest incomes. ====================================================== Psychosocial Stress Ideally, the body is in homeostatic balance, a state in which thevital measures of human function heart rate, blood pressure, bloodsugar levels and so on are in their optimal ranges. A stressor isanything that threatens to disrupt homeostasis. For most organisms, astressor is an acute physical challenge for example, the need for aninjured gazelle to sprint for its life or for a hungry predator tochase down a meal. The body is superbly adapted to dealing with short-term physical challenges to homeostasis. Stores of energy, includingthe sugar glucose, are released, and cardiovascular tone increases tofacilitate the delivery of fuel to exercising muscle throughout thebody. Digestion, growth, tissue repair, reproduction and otherphysiological processes not needed to survive the crisis aresuppressed. The immune system steps up to thwart opportunisticpathogens. Memory and the senses transiently sharpen. But cognitively and socially sophisticated species, such as weprimates, routinely inhabit a different realm of stress. For us, moststressors concern interactions with our own species, and fewphysically disrupt homeostasis. Instead these psycho- social stressorsinvolve the anticipation (accurate or otherwise) of an impendingchallenge. And the striking characteristic of such psychological andsocial stress is its chronicity. For most mammals, a stressor lastsonly a few minutes. In contrast, we humans can worry chronically overa 30-year mortgage. Unfortunately, our body's response, though adaptive for an acutephysical stressor, is pathogenic for prolonged psychosocial stress.Chronic increase in cardiovascular tone brings stress-inducedhypertension. The constant mobilization of energy increases the riskor severity of diseases such as type 2 (adult-onset) diabetes. Theprolonged inhibition of digestion, growth, tissue repair andreproduction increases the risks of various gastrointestinaldisorders, impaired growth in children, failure to ovulate in femalesand erectile dysfunction in males. A too-extended immune stressresponse ultimately suppresses immunity and impairs disease defenses.And chronic activation of the stress response impairs cognition, aswell as the health, functioning and even survival of some types ofneurons. An extensive biomedical literature has established that individualsare more likely to activate a stress response and are more at risk fora stress-sensitive disease if they (a) feel as if they have minimalcontrol over stressors, (b) feel as if they have no predictiveinformation about the duration and intensity of the stressor, © havefew outlets for the frustration caused by the stressor, (d) interpretthe stressor as evidence of circumstances worsening, and (e) lacksocial support for the duress caused by the stressors. ===================================================== Sidebar: Chronic Stress CHRONIC STRESS may explain how poverty "gets under the skin" andexerts a harmful influence on health. The risk of stress-sensitivediseases increases if individuals lack social support, have no outletsfor their frustration and feel that their circumstances are worseningexactly the conditions in many poor communities in the U.S. ====================================================== Psychosocial stressors are not evenly distributed across society. Justas 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 disproportionateshare of psychosocial ones. Numbing assembly-line work and anoccupational lifetime spent taking orders erode workers' sense ofcontrol. Unreliable cars that may not start in the morning andpaychecks that may not last the month inflict unpredictability.Poverty rarely allows stress-relieving options such as health clubmemberships, costly but relaxing hobbies, or sabbaticals forrethinking one's priorities. And despite the heartwarming stereotypeof the "poor but loving community," the working poor typically haveless social support than the middle and upper classes, thanks to theextra jobs, the long commutes on public transit, and other burdens. Marmot has shown that regardless of SES, the less autonomy one has atwork, the worse one's cardiovascular health. Furthermore, low controlin the workplace accounts for about half the SES gradient incardiovascular disease in his Whitehall population. Feeling Poor Three lines of research provide more support for the influence ofpsychological stress on SES-related health gradients. Over the pastdecade Nancy E. Adler of the University of California, San Francisco,has explored the difference between objective and subjective SES andthe relation of each to health. Test subjects were shown a simplediagram of a ladder with 10 rungs and then asked, "In society, whereon this ladder would you rank yourself in terms of how well you'redoing?" The very openness of the question allowed the person to definethe comparison group that felt most emotionally salient. As Adler has shown, a person's subjective assessment of his or her SEStakes into account the usual objective measures (education, income,occupation and residence) as well as measures of life satisfaction andof anxiety about the future. Adler's provocative finding is thatsubjective SES is at least as good as objective SES at predictingpatterns of cardiovascular function, measures of metabolism,incidences of obesity and levels of stress hormones -- suggesting thatthe 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 aphysical challenge, such as chasing down prey or escaping a predator.The circulatory, nervous and immune systems are mobilized while thedigestive and reproductive processes are suppressed. If the stressbecomes chronic, though, the continual repetition of these responsescan 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 oxygento 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 gradientamong nations. A relatively poor person in the U.S. may objectivelyhave more financial resources to purchase health care and protectivefactors than a relatively wealthy person in a less developed countryyet, on average, will still have a shorter life expectancy. Forexample, as Stephen Bezruchka of the University of Washingtonemphasizes, people in Greece on average earn half the income ofAmericans yet have a longer life expectancy. Once the minimalresources are available to sustain a basic level of health throughadequate food and housing, absolute levels of income are of remarkablylittle importance to health. Although Adler's work suggests that theobjective state of being poor adversely affects health, at the core ofthat result is the subjective state of feeling poor. Being Made to Feel Poor Another body of research arguing that psychosocial factors mediatemost of the SES/health gradient comes from Richard Wilkinson of theUniversity of Nottingham in England. Over the past 15 years he and hiscolleagues have reported that the extent of income inequality in acommunity is even more predictive than SES for an array of healthmeasures. In other words, absolute levels of income aside, greaterdisparities in income between the poorest and the wealthiest in acommunity predict worse average health. (David H. Abbott of theWisconsin National Primate Research Center and I, along with ourcolleagues, found a roughly equivalent phenomenon in animals: amongmany nonhuman primate species, less egalitarian social structurescorrelate with higher resting levels of a key stress hormone an indexfor 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 haveswhen you are a have-not. ===================================================== Wilkinson's subtle and critical finding has generated considerablecontroversy. One dispute concerns its generality. His original worksuggested that income inequality was relevant to health in manyEuropean and North American countries and communities. It has becomeclear, however, that this relation holds only in the developed countrywith the greatest of income inequalities, namely, the U.S. Whether considered at the level of cities or states, income inequalitypredicts mortality rates across nearly all ages in the U.S.. Why,though, is this relation not observed in, say, Canada or Denmark? Onepossibility is that these countries have too little income variabilityto tease out the correlation. Some critics have questioned whether the linkage between incomeinequality and worse health is merely a mathematical quirk. Therelation between SES and health follows an asymptotic curve: droppingfrom the uppermost rung of society's ladder to the next-to-top stepreduces life expectancy and other measures much less drastically thanplunging from the next-to-bottom rung to the lowest level. Because acommunity with high levels of income inequality will have a relativelyhigh number of individuals at the very bottom, where health prospectsare so dismal, the community's average life expectancy will inevitablybe lower than that of an egalitarian community, for reasons that havenothing to do with psychosocial factors. Wilkinson has shown, however,that decreased income inequality predicts better health for both thepoor and the wealthy. This result strongly indicates that theassociation between illness and inequality is more than just amathematical artifact. Wilkinson and others in the field have long argued that the moreunequal income in a community is, the more psychosocial stress therewill be for the poor. Higher income inequality intensifies acommunity's hierarchy and makes social support less available: trulysymmetrical, reciprocal, affiliative support exists only among equals.Moreover, having your nose rubbed in your poverty is likely to lessenyour sense of control in life, to aggravate the frustrations ofpoverty and to intensify the sense of life worsening. If Adler's work demonstrates the adverse health effects of feelingpoor, Wilkinson's income inequality work suggests that the surest wayto feel poor is to be made to feel poor to be endlessly made aware ofthe haves when you are a have-not. And in our global village, we areconstantly made aware of the moguls and celebrities whose resourcesdwarf ours. John W. Lynch and George A. Kaplan of the University of Michigan atAnn Arbor have recently proposed another way that people are made tofeel poor. Their "neomaterialist" interpretation of the incomeinequality 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 toimprove the quality of life for the average person. But by definition,the bigger the income inequality in a society, the greater thefinancial distance between the average and the wealthy. The biggerthis distance, the less the wealthy have to gain from expenditures onthe public good. Instead they would benefit more from keeping theirtax money to spend on their private good a better chauffeur, a gatedcommunity, bottled water, private schools, private health insurance.So the more unequal the income is in a community, the more incentivethe wealthy will have to oppose public expenditures benefiting thehealth of the community. And within the U.S., the more incomeinequality there is, the more power will be disproportionately in thehands of the wealthy to oppose such public expenditures. According tohealth economist Evans, this scenario ultimately leads to "privateaffluence and public squalor." This "secession of the wealthy" can worsen the SES/health gradient intwo ways: by aggravating the conditions in low- income communities(which account for at least part of the increased health risks for thepoor) and by adding to the psychosocial stressors. If social andpsychological stressors are entwined with feeling poor, and even moreso with feeling poor while being confronted with the wealthy, theywill be even more stressful when the wealthy are striving to decreasethe goods and services available to the poor. Social Capital A third branch of support for psychosocial explanations for therelation between income inequality and health comes from the work ofIchiro Kawachi of Harvard University, based on the concept of "socialcapital." Although it is still being refined as a measure, socialcapital refers to the broad levels of trust and efficacy in acommunity. Do people generally trust one another and help one anotherout? Do people feel an incentive to take care of commonly heldresources (for example, to clean up graffiti in public parks)? And dopeople feel that their organizations such as unions or tenantassociations actually have an impact? Most studies of social capitalemploy two simple measures, namely, how many organizations peoplebelong to and how people answer a question such as, "Do you think mostpeople 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 badhealth, bad self-reported health and high mortality rates. Using acomplex statistical technique called path analysis, Kawachi hasdemonstrated that (once one controls for the effects of absoluteincome) the strongest route from income inequality to poor health isthrough the social capital measures to wit, high degrees of incomeinequality come with low levels of trust and support, which increasesstress and harms health. None of this is surprising. As a culture, America has neglected itssocial safety nets while making it easier for the most successful tosit atop the pyramids of inequality. More- over, we have chosen toforgo the social capital that comes from small, stable communities inexchange for unprecedented opportunities for mobility and anonymity.As a result, all measures of social epidemiology are worsening in theU.S. Of Westernized nations, America has the greatest incomeinequality (40 percent of the wealth is controlled by 1 percent of thepopulation) and the greatest discrepancy between expenditures onhealth care (number one in the world) and life expectancy (as of 2003,number 29). The importance of psychosocial factors in explaining the SES/healthgradient generates a critical conclusion: when it comes to health,there is far more to poverty than simply not having enough money. (AsEvans once stated, "Most graduate students have had the experience ofhaving very little money, but not of poverty. They are very differentthings.") The psychosocial school has occasionally been accused ofpromulgating an antiprogressive message: don't bother with universalhealth care, affordable medicines and other salutary measures becausethere will still be a robust SES/health gradient after all thereforms. But the lesson of this research is not to abandon suchsocietal change. It is that so much more is needed. Additional Reading: Wilkinson, Richard. Mind the Gap: Hierarchies, Health and HumanEvolution. London, UK: Weidenfeld and Nicolson, 2000. Kawachi, Ichiro and Bruce P. Kennedy, The Health of Nations: WhyInequality Is Harmful to Your Health. New York: New Press, 2002. Marmot, Michael. The Status Syndrome. New York: Henry Holt andCompany, 2004. Sapolsky, Robert. Why Zebras Don't Get Ulcers: A Guide to Stress,Stress-Related Diseases and Coping. Third edition. New York: HenryHolt and Company, 2004. ============== Robert Sapolsky is professor of biological sciences, neurology andneurological sciences at Stanford University and a research associateat the National Museums of Kenya. In his laboratory work, he focuseson how stress can damage the brain and on gene therapy for the nervoussystem. In addition, he studies populations of wild baboons in EastAfrica, trying to determine the relation between the social rank of ababoon and its health. His latest book is Monkeyluv and Other Essayson Our Lives as Animals (Scribner, 2005). Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: 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 corporatewealth among the highest-income Americans grew significantly in 2003,as a trend that began in 1991 accelerated in the first year thatPresident Bush and Congress cut taxes on capital. In 2003 the top 1 percent of households owned 57.5 percent ofcorporate wealth, up from 53.4 percent the year before, according to aCongressional Budget Office analysis of the latest income tax data.The top group's share of corporate wealth has grown by half since1991, 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 wealthhave declined since 1991. These declines ranged from 12.7 percent forthose on the 96th to 99th rungs on the income ladder to 57 percent forthe poorest fifth of Americans, who made less than $16,300 andtogether owned 0.6 percent of corporate wealth in 2003, down from 1.4percent in 1991. The analysis did not measure wealth directly. It looked at taxes oncapital gains, dividends, interest and rents. Income from securitiesowned by retirement plans and endowments was excluded, as were gainsfrom noncorporate assets such as personal residences. This technique for measuring wealth has long been used in standardeconomic studies, though critics have challenged that tradition. Among them is Stephen J. Entin, president of the Institute forResearch on the Economics of Taxation in Washington, which favorseliminating most taxes on capital and teaches that an unintendedconsequence of the corporate income tax is depressed wage rates. Mr.Entin said the report's approach was so flawed that the data wereuseless. He said reduced tax rates on long-term capital gains may have promptedwealthy investors to sell profitable investments. That would show upin tax data as increased wealth that year, even though the increasemay have built up over decades. Long-term capital gains were taxed at 28 percent until 1997, and at 20percent until 2003, when rates were cut to 15 percent. The top rate ondividends was cut to 15 percent from 35 percent that year. The White House said it did not believe that the 2003 tax cuts hadmuch influence on wealth shares. It also said that since wealth istransitory for many people, a more important issue is how incomes andwealth are influenced by the quality of education. ''We want to lift all incomes and wealth,'' said Trent Duffy, a WhiteHouse spokesman. ''We are starting to see that the income gap islargely an education gap.'' ''The president thinks we need to close the income gap, and he hastalked about ways in which we can do that,'' especially througheducation, Mr. Duffy said. The data showing increased concentration of corporate wealth wereposted last month on the Congressional Budget Office Web site. IsaacShapiro, associate director of the Center on Budget and PolicyPriorities in Washington, spotted the information last week and wrotea report analyzing it. Mr. Shapiro said the figures added to the center's ''concerns over theincreasingly regressive effects'' of the reduced tax rates on capital.Continuing those rates will ''exacerbate the long-term trend towardgrowing income inequality,'' he wrote. The center, which studies how government affects the poor and supportspolicies that it believes help alleviate poverty, opposes Mr. Bush'stax policies. The center plans to release its own report on Monday that questionsthe wisdom of continuing the reduced tax rates on dividends andcapital gains, saying the Congressional Budget Office analysisindicates that the benefits flow directly to a relatively fewAmericans. Return to Table of Contents :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: 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. InSilent Spring, she documented how long-lived organochlorinepesticides, most notoriously DDT, were not only ridding croplands ofinsects, streets of mosquitoes, and homes of spiders but also exactinga high toll on songbirds and other nontargeted species. The chemicals'broad-spectrum potency and resistance to breakdown, advantages intheir use against pests, emerged as hazards. Shortly after the publication of Carson's book, industrializedcountries began phasing out such persistent organic pollutants, orPOPs. There's now a United Nations treaty aiming at their globalelimination (SN: 11/8/03, p. 301: Available to rs athttp://www.sciencenews.org/articles/20031108/note14.asp). In the wake of organochlorine pesticides came organophosphate agents.Although these agents are highly effective, their toxicity tonontarget animals -- including people -- echoed the perils of DDT.Regulators responded, and by the middle 1990s, once-popular members ofthis 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 toproducts based on pyrethrins, chemicals made by certain members of thechrysanthemum family. Farmers in various parts of the world have formillennia used preparations from these flowers to protect crops frominsects. Since the 1960s, manufacturers have produced syntheticanalogs -- called pyrethroids -- of the herbal products' activeingredients. Although pyrethroids have greater toxicity to insects and somewhatmore resistance to breakdown than their natural counterparts do,studies have demonstrated that these synthetic chemicals pose littlerisk to most vertebrates, from songbirds to people. Pyrethroids stand poised to overtake organophosphate insecticides forfarm use and are already the leading insecticides sold to homeowners.However, emerging data show that even pyrethroids can pose seriousenvironmental hazards. At concentrations found in streams, thechemicals can kill beneficial insects and crustaceans and may even beacting -- below the radar screen -- to poison fish and lizards. Most of these findings came to light in some dozen presentations inBaltimore last November at the Society of Environmental Toxicology andChemistry (SETAC) annual meeting. The research described theresuggests that, at least where the mum-based pesticides might enterstreams, these compounds should be used sparingly. "The Environmental Protection Agency needs to take a closer look atpyrethroids" with an eye toward changing how the 22 such compoundsthat it has registered are marketed and used, argues Michael J. Lydy,an environmental toxicologist at Southern Illinois University inCarbondale. Ample and growing data, he says, challenge "the suggestionthat in the environment, pyrethroids will be innocuous." Hunting thrins "Walk down the pesticide aisle of your local hardware store and readthe 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 -- lackthat 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 launchedseveral surveys to check whether pyrethroids were causing harm instreams. Because these pesticides don't readily dissolve, but insteadglom on to particles and quickly settle out of water, his team focusedits analyses on sediments. Their findings proved eye-opening, Weston told Science News. In one study of creeks adjacent to farmlands across a 10-county areain California's Central Valley, researchers looked for fivepyrethroids and found one or more in at least three-quarters of the 70sediments sampled. The researchers then tested two stream dwellers: the amphipod Hyalellaazteca, which is a small, shrimplike crustacean, and a larval midge ofthe species Chironomus tentans. Ecologists use these tiny "lab rats ofthe sediment-testing world" for toxicity assessments, Weston explains. At 42 percent of the sampled sites, the sediment proved deadly to atleast one of two species, his group reported 2 years ago. In a follow-up study, the scientists spiked sediment samples fromclean sites with six common pyrethroids to compare their toxic effectson H. azteca. They measured each compound's LC50 -- the concentrationlethal to 50 percent of animals exposed in a test. In the April 2005 Environmental Toxicology and Chemistry (ET & C), theteam 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, indicatinggreater toxicity. The most toxic: lambda-cyhalothrin and bifenthrin,which have an LC50 of 2 to 6 ppb. The crustaceans' growth was significantly retarded at concentrationsjust one-third of a pyrethroid's LC50. Lawn pollution Farm runoff isn't the only -- or perhaps even the mostimportant -- way in which these agents get into streams. Weston andhis Berkeley colleague Erin L. Amweg reported data at the SETACmeeting showing that pyrethroids are washed into waterways fromsuburban 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 washedinto storm drains, which are a direct conduit to neighborhood streams.Amweg In one recent study, Weston, Lydy, and others surveyed streams inRoseville, a suburb of Sacramento, Calif. Only a decade earlier, landalong these creeks had been arid grassland. Since then, much of it hasbeen converted to subdivisions sporting four homes per acre, most withmanicured lawns. Roughly 90 percent of the stream sediments sampled containedbifenthrin, and the majority of them had bifenthrin concentrationstoxic to Hyalella, the scientists report in the Dec. 15, 2005,Environmental Science & Technology. Often, one to five morepyrethroids were present. In contrast, the pesticides didn't show up in waters drainingRoseville sites free of residential development. In toxicity, bifenthrin dominated the suburban sediments. Indeed, Lydytold Science News, "80 percent of our samples had enough toxicity dueto bifenthrin alone to cause at least half of our [amphipods] to die."The team recorded pesticide concentrations as high as 437 ppb—that'sabout 100 times as great as its LC50 for H. azteca and 15 times thehighest bifenthrin concentration seen in sediments of creeks runningthrough Central Valley croplands. This indicates, Weston says, that the highest concentrations ofpyrethroids in creek sediments trace to "classic suburbia -- we'retalking Mom, Dad, two kids, and a dog." Although pesticides applied by professional exterminators around theperimeters of homes are a possible source of the creek contamination,the research group strongly suspects that much of the bifenthrin comesfrom lawn-care products. Some fertilizers even include bifenthrin, sothat homeowners can feed their grass and kill bugs in one pass. In the Roseville study, the pesticides didn't appear to travel faronce they reached a creek, with the high concentrations appearing onlywithin 100 yards or so of storm-drain outfalls. What's not clear, Weston and others observe, is whether the Californiadata reflect what's occurring nationally or might instead represent aworst-case scenario. For instance, Amweg presented data at the SETACmeeting indicating that creeks near Sacramento and San Franciscoshowed substantial sediment contamination but streams in Nashvilledidn't. The California sites, unlike Nashville, get little summer rainfall todilute stream pollutants. Moreover, many of California's urban areasrely on concrete storm drains to channel lawn runoff directly intostreams, whereas the Nashville sites were separated from waterways bya corridor of greenery. Too excited Joel R. Coats of Iowa State University in Ames and hiscolleagues 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 plantdebris. Ordinarily, a nymph cuts and stacks materials, log-cabinstyle, into an orderly, well-aerated covering (top inset). Pyrethroid-exposed nymphs, however, make chaotically structured dwellings fromuncut 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, Coatsexplains, "there's an electrical ripple that's triggered by sodiumgates in [each cell] opening in sequence." Pyrethroids perturb thenerve cells' sodium gates, however, so that once open, they neverfully close, Coats says. The resulting sodium leaks maintain nervecells in a state of overexcitation that kills the insects. Because the nervous systems of crustaceans and many other soft-bodiedaquatic animals resemble those of insects, these nontargeted animalsare also vulnerable to pyrethroids. Coats observes that mammals and birds gain some protection frompyrethroid poisoning by two mechanisms: production of esterase enzymesthat inactivate the poisons by splitting them in half, and anothermetabolic process that employs oxidation. He reported at the SETACmeeting that although rainbow trout, bluegill, and fathead minnows canall oxidize pyrethroids, their esterase enzyme activity doesn't breakapart the pesticides. Although these pesticides may induce ill effects that fall short oflethality, toxicologists have generally been forced to focus on theirdeadliness, Weston says, because fatal concentrations tend to be at ornear the minimum value at which current technology can detect thepesticides. If the pesticides cause sickness, therefore, it's likelyto happen at concentrations too low to measure, he says. To get aroundthis difficulty, some scientists have added minute amounts of thecompounds to tanks of water containing aquatic animals. At Oregon State University (OSU) in Corvallis, Katherine R. Johnsonand her colleagues administered esfenvalerate to aquatic nymphs of thecaddis fly (Brachycentrus americanus) -- an insect eaten by many fish. For protection from predators, these nymphs enshroud themselves inhard cases. As the OSU researchers increased pyrethroid concentrationsabove 0.05 ppb, formerly resting animals began fleeing their cases inincreasing numbers, notes coauthor Jeffrey J. Jenkins. Among nymphsthat fled, three-quarters of those exposed to as little as 0.2 ppbesfenvalerate didn't rebuild their cases. Rebuilt cases weredisordered and much weaker than the originals, the scientists reportedat the SETAC meeting. Conditional toxicity Environmental stressors can sabotage pesticide-detoxification systems, even in animals that would otherwise withstandthe chemicals, notes Larry G. Talent. At Oklahoma State University inStillwater, he studied adult green anole lizards (Anoliscarolinensis), 6 to 8 inches long, exposed to a pyrethroid productused to treat birds for mites and lice. When he doused the lizards with a solution of the pesticide and thenmaintained the reptiles at a comfortable 95°F, none died. However, 70percent of treated lizards died within 2 days when they were insteadhoused at a cool 68°F. Without pesticide exposure, the lizards showedno mortality at the lower temperature, Talent reports in the December2005 ET & C. Low temperatures, which might mimic night or winter environments, posea double whammy for pyrethroid effects: Not only is the lizard'snervous system more vulnerable to poisoning but its metabolicbreakdown of pollutants also slows. Mark A. Clifford last year reported a similar synergy between twoenvironmental stressors—pyrethroid exposure and a viral infection --in young salmon. The University of California, Davis fish pathologistexposed 2-month-old chinook salmon for 4 days to either esfenvalerateor chlorpyrifos, an organophosphate pesticide. He then seeded some ofthe aquariums holding the fish with infectious hematopoietic necrosisvirus, which can kill juveniles. Fish exposed to low doses of the virus survived, as did those exposedto either pesticide alone, Clifford's team reported in the July 2005ET & C. Deaths occurred only in fish exposed to high concentrations ofthe virus or to both the pyrethroid and virus. Within 3 days of beingexposed 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. Twofollow-up trials confirmed that the initial observation was not afluke. Winds of change? EPA considers new data when it periodically reviewsits approvals of pesticides registered before 1984. Reevaluations forpermethrin, resmethrin, and cypermethrin are slated for completionthis year, and three other pyrethroids are to be reviewed by 2008. Because bifenthrin was registered in late 1985, it's not scheduled forsuch a reevaluation. In a statement to Science News, however, EPA'sOffice of Pesticide Programs (OPP) notes that this pesticide'smanifestation of "certain toxic properties at the level of detection[makes it] challenging for the agency to determine whether risks fromthe use of this pesticide are acceptable." In fact, the statement says, to better understand pyrethroids'toxicity and bioavailability to nontarget organisms, OPP is "reviewingthe sediment toxicity studies on bifenthrin, cypermethrin, cyfluthrin,and esfenvalerate that were recently submitted [by Weston's group andothers]." These pesticides were chosen as "surrogates," the statementsays, 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, pendingfuture evaluation of their sediment toxicity and of the value ofbuffer zones in keeping treated areas from tainting streams. OPP says that it anticipates completing a "comparative assessment forpyrethroids" by December. Pyrethroid manufacturers are already bracing for change. Jim Fitzwater, a spokesman for bifenthrin-maker FMC Corp. ofPhiladelphia, says that homeowners need to be educated about how andwhen to apply lawn-care products containing pyrethroids. He notes thathis company sells to consumer-products companies rather than consumersand says, "We're looking at working with [these] end-use manufacturersto do a better stewardship job." References: 2005. Pyrethroid pesticides found at toxic levels in California urbanstreams. University of California, Berkeley press release. Oct. 25.Available here. 2004. Sediments in many Central Valley streams contain toxic levels ofpyrethroid pesticides. University of California, Berkeley pressrelease. May 6. Available here. Amweg., E.L., D.P. Weston, J. You, and M.J. Lydy. In press. Pyrethroidinsecticides and sediment toxicity in urban creeks from California andTennessee. Environmental Science & Technology.Abstract available here. Amweg, E.L., and J. You. 2005. Pyrethroid pesticide distribution andtoxicity 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 ofpyrethroid pesticides in the Central Valley, California, USA.Environmental Toxicology and Chemistry 24(April):966-972. Abstractavailable here. Clifford, M.A., et al. 2005. Synergistic effects of esfenvalerate andinfectious hematopoietic necrosis virus on juvenile chinook salmonmortality. Environmental Toxicology and Chemistry 24(July):1766-1772.Abstract available here. Coats, J.R. 2005. Toxicology of synthetic pyrethroids to fish. SETACNorth America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. DeLorenzo, M.E., et al. 2005. Toxicity of the pyrethroid insecticidepermethrin 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 toesfenvalerate induces case-leaving in the caddisfly Brachycentrusamericanus. SETAC North America 26th Annual Meeting. Nov. 13-17.Baltimore. Abstract. Lydy, M., D. Weston, and J. You. 2005. Relative contributions ofagricultural or urban pyrethroid usage to toxicity in Californiastreams. SETAC North America 26th Annual Meeting. Nov. 13-17.Baltimore. Abstract. Talent, L.G. 2005. Effect of temperature on toxicity of a naturalpyrethrin 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 toresidential 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 urbanenvironments. SETAC North America 26th Annual Meeting. Nov. 13-17.Baltimore. Abstract. Weston, D.P., J. You, and M.J. Lydy. 2004. Distribution and toxicityof sediment-associated pesticides in agriculture-dominated waterbodies 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 andesfenvalerate to fathead minnows and midge larvae. EnvironmentalToxicology and Chemistry 25(February):623-629. Abstract availablehere. 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. SETACNorth America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Lydy, M.J., and K.R. Austin. 2004. Toxicity assessment of pesticidemixtures typical of the Sacramento- San Joaquin delta using Chironomustentans. Archives of Environmental Contamination and Toxicology48(December):49-55. Abstract available here. Raloff, J. 2003. POPs treaty enacted. Science News 164(Nov. 8):301.Available to rs here. ______. 2000. The case for DDT. Science News 158(July 1):12-13.Available here. ______. 1999. Thyroid linked to some frog defects. Science News156(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. SETACNorth America 26th Annual Meeting. Nov. 13-17. Baltimore. Abstract. Sources: Erin L. Amweg University of California, Berkeley Building 102-RFSBerkeley, CA 94720-3140 Mark Clifford Fish Health Laboratory Medicine and EpidemiologyUniversity of California, Davis Davis, CA 95616 Joel R. Coats Iowa State University Department of Entomology Ames, IA50011 Jim Fitzwater FMC Corporation 1735 Market Street Philadelphia, PA19103 Jeffrey J. Jenkins Department of Molecular Toxicology Oregon StateUniversity 1007 Ag and Life Science Building Corvallis, OR 97331-7301 Katherine R. Johnson Department of Environmental and MolecularToxicology 1007 ALS Building Corvallis, OR 97331-7301 Michael J. Lydy Department of Zoology Southern Illinois UniversityCarbondale, IL 62901-6501 Mah Shamin Environmental Risk Branch 5 Environmental Fate & EffectsDivision 1200 Pennsylvania Avenue, N.W. Washington, DC 20460 Society of Environmental Toxicology and Chemistry 1010 North 12thAvenue Pensacola, FL 32501-3368 Donald P. Weston University of California, Berkeley Building 102-RFSBerkeley, 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 dhn. Rachel's Democracy & Health News is published as often as necessary to provide readers with up-to-date coverage of the subject. Editors: Peter Montague - peter Tim Montague - tim :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: To start your own free Email subscription to Rachel's Democracy & Health News send a blank Email to: join-rachel. In response, you will receive an Email asking you to confirm that you want to . :::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: Environmental Research FoundationP.O. Box 160, New Brunswick, N.J. 08903dhn