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Author: ScienCentral Added: Mon, 22 Sep 2008 22:53:14 -0800 Duration: 109Could a change in the rules governing commercial fishing actually reverse a worldwide trend of declining fish populations? As this ScienCentral video explains, a just-released study of where those rules have changed says, "yes".

Author: ScienCentral Added: Mon, 22 Sep 2008 22:53:14 -0800 Duration: 109Could a change in the rules governing commercial fishing actually reverse a worldwide trend of declining fish populations? As this ScienCentral video explains, a just-released study of where those rules have changed says, "yes".

Could a change in the rules governing commercial fishing actually reverse a worldwide trend of declining fish populations? As this ScienCentral video explains, a just-released study of where those rules have changed says, "yes."

In this video podcast, Dr. Oren Shriki, a science teacher at the Israel Arts and Sciences Academy, speaks about Intel s International Science and Engineering Fair, taking place in Atlanta, May 11-16. (As excitement builds toward the event s opening, you can follow along on a dedicated Intel ISEF blog.) Many of the best young scientists from around the world will attend, selected through regional science fairs for a wide range of skills, from identifying and addressing important scientific challenges or questions to using organized and logical thought to reach conclusions. The participants in Intel ISEF are very likely to be tomorrow s leaders in technology, medicine and health, agriculture, environmental science and engineering. During Intel ISEF, their work will be judged by professional scientists who will look for gifted communicators with excellent foundational understanding in specific research and the scientific process. No matter what the judges decide, however, participants in the annual event will benefit from meeting their peers from around the world, hearing from Nobel laureates and scientists involved in the same kinds of research as theirs, and also creating lasting memories, like those found on the blog of 2004 ISEF alum (and member of a Fourth Award-winning team) Jayson Reggie Obos. Here s more information about the science fair as well as a quick look at recent ISEF events, including the 2007 Intel ISEF in Albuquerque, N.M. Tags: Oren Shriki, Intel, International Science and Engineering Fair, ISEF, science fair, environmental science, Nobel laureate

stre"> Stress Reaction Ozone and Co-pollutants Linked with Oxidation Past studies have hinted that several air pollutants can cause oxidative stress in people, suggesting one mechanism behind diseases such as lung cancer, asthma, and increased cardiopulmonary illnesses and deaths. The evidence has gained more support with the discovery that chronic exposure to ambient ozone, nitrogen dioxide, or particulates is strongly linked with lipid peroxidation, an indicator of oxidative stress [EHP 115:1732-1737; Chen et al.]. Moreover, more damage was seen at higher pollutant concentrations. Researchers evaluated two oxidative stress indicators in the blood of 120 University of California, Berkeley, students aged 18 to 22 years. Each student was a lifelong resident of either the Los Angeles or San Francisco area, where they had experienced variable seasonal exposures to pollutants including ozone. To assess lipid peroxidation, the researchers measured 8-isoprostaglandins-F2 (8-iso-PGF), which has been found in several studies to be a useful indicator. To assess total antioxidant capacity, they measured ferric-reducing ability of plasma (FRAP), which has a more limited history as an indicator. Pollutant concentrations were estimated from data at monitoring stations near where the students lived. The lifelong Los Angeles residents had received much higher average ozone exposure over the course of a lifetime (42.9 ppb versus 26.9 ppb for the San Francisco residents), and 8-iso-PGF was twice as high in these students (195.3 pg/mL versus 97.2 pg/mL). There was also a link between relatively higher ambient ozone concentrations during 2-week and 1-month periods and increased 8-iso-PGF. Neither sex, ethnicity, nor weight affected the results, but there was a wide range in 8-iso-PGF among individuals (17.4-940.7 pg/mL), perhaps due to genetic differences. The researchers also found a significant link between 8-iso-PGF and increased concentration of nitrogen dioxide or particulates, independent of the effects of ozone. The FRAP assay showed no significant difference in antioxidant capacity between the residents of the two cities. However, there was a threefold difference among all study subjects in antioxidant capacity, and males had about 23% more antioxidant capacity than females. Although acknowledging that much more study of other populations and locations needs to be done with more precise measures of personal pollutant exposure, the researchers conclude that each of the three pollutants studied can significantly increase oxidative stress. They also report that 8-iso-PGF is an accurate indicator of oxidative stress, while noting that other indicators, such as cytogenetic damage, may also prove useful. Bob Weinhold

uran"> Uranium in Drinking Water Low Dose Acts as Endocrine Mimic Uranium, the heaviest naturally occurring element, is well known as a radioactive toxicant capable of damaging the kidneys and DNA. A new study has shown for the first time that uranium also acts as an estrogen mimic in mice at concentrations below the U.S. EPA's safety limit of 30 g/L in drinking water [EHP 115:1711-1716; Raymond-Whish et al.]. Other metals, including arsenic, cadmium, lead, and mercury, also are known estrogen mimics. Mine memory. Navajo miners work the Kerr-McGee uranium mine, 7 May 1953. Today, uranium from unremediated abandoned mines contaminates nearby water supplies. image: AP Photo The researchers manipulated the reproductive status of female mice in several ways. They exposed one group of immature female mice to uranium as they matured, a second group of mature female mice to uranium at environmentally relevant concentrations for 30 days prior to breeding and through gestation, and a third group of female mice to uranium immediately after their ovaries were removed. In a fourth group, they removed the ovaries of female mice, then exposed subgroups of this cohort to either uranium or the synthethic estrogen diethylstilbestrol (DES) alone or in combination with the antiestrogen ICI 182,780. All uranium exposures were via the mice's drinking water at concentrations of 0.5 g/L-60.0 mg/L. Uranium had estrogen-like effects at varying dose ranges throughout the suite of experiments. In the first group, exposure resulted in fewer primary and more secondary ovarian follicles among adult females. In the second group, female pups of exposed dams had significantly fewer small primary ovarian follicles. The researchers conjecture that this primary-to-secondary follicle ratio may lead to fewer ovulated eggs and early-onset menopause. In the ovariectomized mice, the researchers found higher uterine weights and accelerated vaginal opening (indicators of earlier puberty onset). In addition, estrogenic activity was blocked in the mice exposed to ICI 182,780 after DES or uranium exposure. The current study is of immediate relevance to the Navajo Nation of Arizona and New Mexico, where many rural Navajo water supplies currently contain uranium at concentrations exceeding the U.S. EPA standard. The uranium boom of the 1950s and 1960s left thousands of abandoned mine sites and derelict milling operations on Navajo lands. Uranium mining has been banned there, but there are active efforts to revive uranium mining in the Navajo town of Crownpoint, New Mexico. The findings may also soon apply to other populations living amid the uranium boom now under way in central Colorado, Canada, Australia, and elsewhere. Valerie J. Brown

diet"> Dietary Dose Rodent Feed Affects ED Screening Results As the U.S. EPA begins its program to test endocrine-disrupting effects of pesticides, researchers caution that routine screening methods could distort results [EHP 115:1717-1726; Thigpen et al.]. The team discovered that some commercially available rodent diets can cause early sexual maturation similar to that induced by chemical endocrine disruptors. Furthermore, one rat strain commonly used by many researchers is not the most sensitive to the effects of endocrine disruptors and thus may not provide optimal results. image: Matthew Ray/EHP The U.S. EPA Endocrine Disruptor Screening Program was mandated by Congress in 1996 amid mounting evidence that hormone-mimicking chemicals in the environment alter sexual traits in exposed wildlife. Research suggests these chemicals might also contribute to increases in human male reproductive disorders including poor sperm quality, cryptorchidism, and hypospadias. In June 2007 the U.S. EPA published a list of 73 suspect chemicals for initial screening. According to the authors of the current study, some rodent diets could distort screening results because they contain high levels of plant estrogens. The phytoestrogens genistein and daidzein are found in the soybeans used in many rodent diets. U.S. EPA guidelines allow a limited amount of genistein and daidzein in the diets of rodents used for screening. The authors report, however, that even approved levels of these compounds are sufficient to adversely impact sexual end points that researchers use to measure endocrine disruption. Furthermore, genistein and daidzein levels vary significantly among different batches of the same diet. Rats on a diet with the highest genistein and daidzein concentrations reached sexual maturity several days earlier than those fed a different batch of the same diet containing lower levels of the compounds. In addition, rodents on high-calorie diets grew faster and reached sexual maturity earlier than those fed a low-calorie diet. The researchers measured sexual maturity by observing the day each rodent's vagina opened. Vaginal opening provides a noninvasive measurement that does not require the animal to be sacrificed. In contrast, sexual maturity is typically measured by uterine weight, which increases at puberty. The results revealed that dietary estrogens had a lesser effect on the vaginal opening day of Sprague-Dawley rats than on Fischer 344 rats or CD-1 mice. This indicates that the latter two species may be more sensitive to exogenous estrogens and thus are preferable for screening. The authors call on scientists screening suspected endocrine disruptors to choose the most sensitive rodents, to minimize the animals' exposure to dietary estrogens, and to control their caloric intake. Only then, they write, will scientists obtain results that are the most accurate, reproducible, and easiest to compare among laboratories. Cynthia Washam

keep"> Keep the Sprays Away? Home Pesticides Linked to Childhood Cancers Previous studies have suggested a link between pesticide use in the home and childhood hematopoietic tumors, the most common type of childhood cancer. A new epidemiologic study of French children diagnosed with leukemia or lymphoma in 2003 or 2004 suggests that a child has about twice the risk of developing acute leukemia (AL) or non-Hodgkin lymphoma (NHL) if his or her mother used insecticides in the home while pregnant [EHP 115:1787-1793; Rudant et al.]. The researchers interviewed 1,060 children diagnosed within the prior 6 months and 1,681 control children. When analyzing the data on the children, the team controlled for other factors that may alter a child's risk of getting cancer, including family cancer history and whether the child was breastfed. The children with cancer were part of the French National Registry of Childhood Blood Malignancies, begun in 1990, which documents all children in the country under age 15 year who have had hematopoietic tumors. The researchers asked the children's mothers about their use while pregnant of pesticides in their homes, on pets, and in the garden. They also asked about the father's use of pesticides while the mother was pregnant and after the child's birth. Just over 50% of the parents who had a child with AL or NHL had used pesticides at least once during the pregnancy, as did just under 40% of the parents of the control group. Children had 2.1 and 1.8 times the risk of developing AL or NHL, respectively, with maternal use of pesticides during pregnancy. Mothers' use of insecticides during pregnancy was significantly associated with childhood AL, NHL, and mixed-cell Hodgkin lymphomas (HLs). Use of pesticides by fathers was also related to AL and NHL. The association was stronger for common B-cell acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia than for T-cell ALL or mature B-cell ALL. It was also stronger for Burkitt lymphoma than for the other NHLs. Of the HLs, the study linked only the mixed-cell subtype to pesticide use. The strength of the association between pesticide use in the home and cancer did not change as the children grew older. This is the first study to tease out the different types of hematopoietic cancers as they relate to pesticide use in the home. Other studies have found a link between parents' occupational exposure to pesticides and childhood cancers, but few of the parents in the French study were exposed to pesticides at work or through farming. Whether a family was rural or urban didn't alter a child's risk of developing cancer. The two types of lymphoma associated with maternal pesticide use during pregnancy have also both been linked to the Epstein-Barr virus, which may suggest a link between pesticide exposure and susceptibility to a viral lymphoma. According to the authors, the consistency of the findings suggests pregnant women may want to avoid pesticide use. Tina Adler

p>Communique de presse 5 juillet 2006 p>Contacts presse : Laetitia Gouffe-Benadiba (InVS) 01 41 79 67 08 Elsa Vidal (InVS) 01 41 79 69 59 Le Programme de Surveillance Air et Sante (PSAS-9)* - coordonne par l Institut de veille sanitaire publie dans la revue scientifique internationale Environmental Health Perspectives un article1 presentant l analyse des effets de la pollution atmospherique photo-chimique pendant la vague de chaleur de l ete 2003 dans neuf villes fran aises (Bordeaux, Le Havre, Lille, Lyon, Marseille, Paris, Rouen, Strasbourg et Toulouse).A la suite de la vague de chaleur de l ete 2003, l objectif du programme** etait d actualiser les relations estimees anterieurement entre la pollution atmospherique photo-chimique, dont l ozone est un indicateur, et le risque de deces a court terme2. En effet, pendant la vague de chaleur de l ete 2003, des niveaux eleves de ce polluant ont ete observes en France, conjointement a de fortes temperatures.Dans cet article, les auteurs presentent des resultats concernant l impact sanitaire de l ozone pour la periode du 3 au 17 aout 2003, periode majeure de la vague de chaleur : pour les neuf villes, 379 deces supplementaires sont ainsi attribuables a la pollution observee, par comparaison a la meme periode des trois annees precedentes. Pour la meme periode, l exces de risque de mortalite lie conjointement a la temperature et a l ozone ainsi que la part relative de chacun des deux facteurs dans cet effet conjoint ont ete estimes.Les resultats different selon les villes. Pour les agglomerations ou la surmortalite a ete importante lors de la vague de chaleur (Paris et Lyon), l ozone a joue un role minoritaire par rapport a celui des temperatures dans l impact sanitaire (respectivement 7,3 et 2,6 %). Dans les autres villes, les resultats sont plus heterogenes : l ozone a un effet minoritaire (moins de 35 %) dans deux villes (Bordeaux et Rouen), majoritaire (plus de 75 %) dans deux autres (Strasbourg et Toulouse) et comparable (entre 40 et 60 %) a celui des temperatures dans les trois autres villes (Lille, Le Havre et Marseille). Ces resultats dependent des niveaux atteints dans chaque ville par les deux facteurs etudies mais egalement des risques estimes localement. Par ailleurs, il semble que l effet des temperatures sur la mortalite persiste entre 2 et 3 jours.Ainsi, parmi les neuf villes considerees, il existe une heterogeneite importante, non seulement pour ce qui concerne l ampleur de la surmortalite attribuable a l effet conjoint de l ozone et des temperatures pendant la vague de chaleur de l ete 2003, mais egalement pour ce qui concerne la part relative de ces deux facteurs. Ces resultats confirment par ailleurs l importance non negligeable des effets de la pollution atmospherique photo-chimique rencontree en milieu urbain en termes de sante publique.* Programme de Surveillance Air et Sante 9 villes (PSAS-9). Vague de chaleur de l ete 2003 : relations entre temperature, pollution atmospherique et mortalite dans neuf villes fran aises (le rapport complet avec son resume est disponible sur le site http://www.invs.sante.fr) (1) http://www.ehponline.org/members/2006/8328/8328.pdf ** Deux rapports (et syntheses) ont ete publies anterieurement par le programme PSAS-9, en 1999 et 2002 respectivement. Ils portaient sur les relations a court terme entre la pollution atmospherique urbaine et des indicateurs de l etat de sante de la population : mortalite, admissions hospitalieres. Des evaluations de l impact sanitaire a court terme de la pollution atmospherique urbaine avaient ete realisees. (2)Le croisement des variations journalieres d indicateurs sante et d indicateurs pollution permet de determiner des relations exposition/risque, exprimees en pourcentage d augmentation du risque de mortalite a court terme et pour une augmentation de 10 microg/m3 par jour des niveaux d indicateur de pollution.

shif"> Shift in the Sexes Are Endocrine Disruptors Changing Birth Ratios? According to demographic data compiled by the United Nations, an average of 105 boys are born for every 100 girls. The male proportion of births, equal to 0.515, varies slightly between years and populations, but these factors do not fully explain consistently shifting ratios in several industrialized countries over recent decades. A new study examines birth and fetal death sex ratios in Japan and the United States and reveals significant male-to-female shifts in both nations [EHP 115:941 946; Davis et al.]. image: Brent Bossom The research team calculated birth and fetal death sex ratios in Japan based on 1949 1999 data from the Japanese Vital Statistics Bureau. The proportion of male births varied yearly before 1970 but declined steadily since then, from 0.5172 to 0.5135. Between 1960 and 1999, the male proportion of fetal deaths increased from 56% to 67.7%. The male fetal death rate is approximately four times higher in Japan than in the United States. For U.S. calculations, the researchers drew 1983 1995 fetal death data and 1970 2002 birth data from the National Center for Health Statistics. The proportion of male births dropped in the United States, from 0.5134 in 1970 to 0.5117 in 2002. There are significant racial differences, however: between 1970 and 2002 the proportion of non-Hispanic white male births fell from 0.5143 to 0.5122, whereas the proportion of black male births rose slightly from 0.5076 to 0.5079. The male proportion of black fetal deaths also increased, rising from 53.5% to 54.5%; among whites, the male proportion of fetal deaths rose by less than 0.5%. Why birth sex ratios differ so much between white and black women is unknown, but hormonal differences due to race and to incidence of obesity may be involved. A possible explanation for the increased ratio among black births may stem from improved prenatal and obstetric care in general, reducing the overall number of fetal deaths. The researchers speculate that parental exposures to endocrine-disrupting chemicals, including metalloestrogens such as methylmercury, might be factors undermining the conception and survival of male children. They suggest particular scrutiny of Japanese body burden of mercury and other metalloestrogens to understand this difference. Additionally, future investigations of declining sex ratios should consider the types and timing of prenatal and parental exposures to endocrine-disrupting chemicals. The researchers hypothesize that paternal exposures prior to conception might affect expression of the SRY gene on the Y chromosome.

phth"> Phthalates and Metabolism Exposure Correlates with Obesity and Diabetes in Men The prevalence of obesity, insulin resistance, and diabetes has increased considerably in the past few decades. Many plausible contributing factors have been identified for this increase, among them low testosterone levels in men. Research has found that exposure to certain synthetic chemicals adversely affects testicular function in animals and possibly in humans. A new analysis looked for and found that exposure to one class of these chemicals, phthalates, correlated with two metabolic abnormalities in men: abdominal obesity and insulin resistance [EHP 115:876 882; Stahlhut et al.]. image: Paul Cowan/ShutterStock Phthalates are commonly used in products such as cosmetics, soaps, pesticides, lubricants, plastics, and paints. They are widespread; indeed, more than 75% of the U.S. population carries detectable levels of several phthalate metabolites. Studies have also found associations between some phthalate metabolites and antiandrogenic effects in humans, including both infant and adult males. The authors used 1999 2002 data from the CDC National Health and Nutrition Examination Survey (NHANES) to look for a connection between phthalate exposure and metabolic disease in adult men. They compared urine concentrations of six phthalate metabolites to the participants' waist circumference and measures of insulin resistance. The analysis controlled for a variety of potential confounders, including age, ethnicity, fat and calorie consumption, physical activity, and smoking status. Four phthalate metabolites were significantly associated with greater waist circumference and three with increased insulin resistance. When the authors further controlled their models for measures of participants' kidney and liver function, the associations decreased somewhat but remained significant for all but one metabolite. The authors caution that this first look at phthalates, obesity, and insulin resistance is limited by the study's cross-sectional design and the single measurement of urine phthalate metabolites (an imperfect measure of long-term exposure). In addition, although the study was based on the hypothesis that phthalates cause metabolic abnormalities by decreasing androgen levels or function, the authors couldn't examine this mechanism, because the NHANES data do not contain measures of sex hormones in men. They note that other mechanisms could also be involved in a relationship between phthalates and metabolic disease. If phthalates are eventually shown conclusively to contribute to obesity or diabetes in men, it's still not clear how these chemicals would affect the opposite sex, since low testosterone has been associated with a lower (not higher) prevalence of metabolic disease in women. If further longitudinal studies confirm that phthalate exposure contributes to obesity, diabetes, and related disorders, actions to reduce phthalate exposure could effectively lessen the chemicals' contribution to metabolic disorders, because phthalates are quickly metabolized and excreted by the body.

chil"> Childhood Leukemia in Germany Cluster Identified near Nuclear Power Plant Childhood leukemia clusters have been observed at a number of sites near European nuclear facilities. With the identification of the largest cluster to date, a new German study underscores the need to clarify the association [EHP 115:947 952; Hoffmann et al.]. image: vario images GmbH Co. KG/Alamy Between February 1990 and May 1991, five cases of leukemia were diagnosed in children living within 5 kilometers of the Krummel nuclear power plant in Geesthacht and a neighboring nuclear research operation along the Elbe River in northern Germany. By 2005, another nine cases of leukemia had been discovered in the area. Most of the cases were acute lymphatic leukemia in males under five years of age. Several expert commissions investigated, and found moderate levels of cesium in rainwater and air samples, along with plutonium and americium in household dust near the plant. There was also some evidence of chromosomal damage to lymphocytes among the local population. One panel deemed these observations consistent with fallout from a possible accident at the research facility that would have to have occurred around September 1986, but so far no such accident has been proved. Another panel suggested instead that chance or population mixing the commingling of local people with newcomers from various places might have caused the cluster. In the current study, researchers compared the number of observed leukemia cases in the sparsely populated Geesthacht area to the number of predicted cases based on nearby county and national incidence rates from 1990 to 2005. The five cases found in 1990 and 1991 significantly exceeded the expected incidence for that period of 0.45 cases. After studying medical records from all treatment facilities in the vicinity and in Hamburg, the team concluded that the Geesthacht cluster is the "largest series of childhood leukemia cases reported to date" among European leukemia clusters near nuclear facilities, including those at Dounreay, Scotland; LeHague, France; and Sellafield, England. The authors state that population mixing is unlikely to account for the leukemia incidence because the population remained stable over the years studied. Nor would an alleged one-time release of radiation in 1986 readily explain the cluster, given that the excess incidence persisted over at least 15 years. Thus, they conclude, the elevated incidence of childhood leukemia around Geesthacht remains "another piece in a growing puzzle" of childhood leukemia's association with nuclear installations and its severity and persistence emphasize the need to keep investigating.

atwi"> A Twist in the Ritalin Riddle Drug-Related Genomic Damage Not Confirmed in Children The frequently prescribed central nervous system stimulant methylphenidate (MPH), better known by brand names that include Ritalin, does not cause genomic damage in children, contrary to earlier reports, according to new work published this month [EHP 115:936 940; Walitza et al.]. In use for more than 50 years and now prescribed more than 5 million times a year in the United States, MPH is the drug of choice for attention deficit/hyperactivity disorder (ADHD). ADHD is the most frequently diagnosed psychiatric disorder in children and adolescents, with an estimated 6 12% of minors worldwide thus diagnosed. image: Calvero, GFDL A 2005 report published in Cancer Letters had showed that gross genomic damage reflected by chromosome aberrations including sister chromatid exchanges and formation of micronuclei (smaller-than-normal cell nuclei containing partial genomes) was found in nucleated lymphocytes taken from peripheral circulation of children who had been taking the drug for only three months. Because large chromosomal breaks are associated with cancer, the study raised concerns about the potential for cancer risk in the millions of people who have taken the stimulant. That 2005 study found an increased frequency of chromosomal abnormalities in all of the 12 children whose lymphocytes were examined, lending urgency to future studies. The current study looked at micronuclei as an indicator of genomic damage in the lymphocytes of 38 children newly prescribed the drug, following some but not all of them out to six months. The children, 29 boys and 9 girls, took a variety of doses and formulations of the drug. Some subjects were lost to follow-up during the study; others switched to other medications or dropped out because they did not respond to the drug. Eight children stayed in the study through the whole six months. Overall, there was no significant increase in the formation of micronuclei at any time point, though some individual children had elevated numbers of micronucleated lymphocytes at one time point or another. Further, the lymphocytes of 9 children who had been taking the drug for more than six months at the start of the study did not show increased levels of micronucleation compared to the pretreatment levels seen in drug-naive children. The marked difference in results between the 2005 study and the current one raises the possibility of unexplained genetic differences between the study populations. Whereas the first study population included six white, four black, and two Hispanic children, the latter study focused on a more uniform group of ethnically German children. The authors say further work, especially on the long-terms effects of MPH, is called for.

Neurodevelopmental disorders such as learning disabilities, mental retardation, and autism spectrum disorders affect an estimated 5 10% of the 4 million babies born in the United States annually. In a report released in 2000, the National Research Council concluded that 3% of these disorders are the direct result of environmental exposures to neurotoxicants, with another 25% arising from the interaction between such exposures and genetic susceptibility. Investigators have shown that many of these long-term adverse outcomes can be attributed to genetic damage to immature neurons in the developing brain related to exposure to genotoxicants, chemicals that disrupt the complex, delicate cellular process that regulates development of a fully functional brain. Although the precise mechanisms involved are still poorly understood, scientists are now starting to unravel the molecular ravages caused by genotoxicants [EHP 114:1703 1712; Kisby et al.]. Young and vulnerable. Immature neurons called granule cells are more sensitive to genotoxicants. image: Kisby et al. As reported in this month's issue, a research group exposed cultures of immature neurons known as granule cells and the more developed and more abundant astrocytes to sublethal doses of two well-characterized alkylating genotoxicants: methylazoxymethanol (MAM), a highly toxic compound synthesized from the poison found in plants called cycads, and nitrogen mustard (HN2), a chemotherapeutic agent. The team then analyzed the cultures for cell viability, DNA damage, markers of apoptosis, and corresponding gene expression patterns. The intent of the research is ultimately to identify the key molecular networks that are targeted by genotoxicants, in order to understand how such agents influence brain development. Results showed that granule cells were much more sensitive to the genotoxicants than astrocytes. The exposures caused dose-dependent DNA lesions that persisted and accumulated, apparently because, unlike astrocytes, granule cells lack the ability to repair DNA damage. In other words, once the exposure has wreaked havoc on the developing neurons, the damage is done, and its impact is felt throughout the process of neuronal development, leading to long-term impairment. The authors speculate that these events "could explain why the developing cerebellum is a prime target in several human neurodevelopmental disorders." The team also discovered that the two genotoxicants affected distinctly different sets and functional types of genes. MAM targeted differentiation, stress and immune response, cell signaling, and transcriptional regulation genes, whereas HN2 targeted apoptosis and protein synthesis gene expression. This preferential targeting suggests that different genotoxicants probably cause completely different effects in the developing brain. With a significant proportion of neurodevelopmental disabilities thought to stem directly from early exposures to DNA-damaging agents or gene environment interactions related to such exposures, further investigation of the molecular networks involved in these effects is clearly needed.

Many countries have set guidelines for levels of environmental lead exposure that are considered safe for children. However, relatively few studies have focused exclusively on the role of prenatal lead exposure on infant neurodevelopment. Indeed, studies conducted in the past 20 years have shown inconsistent results, perhaps because of variability in when prenatal lead was measured (first, second, or third trimester) and in what type of sample (maternal plasma, maternal whole blood, or umbilical cord blood). A comprehensive study published this month is the first to compare such variables [EHP 114:1730 1735; Hu et al.]. Early threat. A study of pregnant women in Mexico City showed that fetal lead exposure during the first trimester had a greater impact on later neurodevelopment than exposure in other trimesters. image: Audrey Wade From 1997 to 1999, the investigators measured lead levels of 146 pregnant women living in Mexico City. Leaded gasoline was sold in Mexico City until 1997, and bone lead levels in women there are about three times higher than in the United States. The leaching of lead stored in a mother's bones provides a major source of fetal lead exposure. The investigators obtained samples of plasma and whole blood during each trimester and umbilical cord blood at delivery. They also tested the neurodevelopment of the children at age 24 months using the Mental Development Index (MDI), which evaluates memory, language, and sensory abilities. The authors found that lead exposure during the first trimester of pregnancy was more strongly linked to later decreases in the MDI scores than exposure during the latter two trimesters. Moreover, maternal plasma lead was the best predictor of a child's later neurobehavioral performance because most of the lead in whole blood is attached to red cells and cannot cross the placenta. Each increase of 1 standard deviation unit in plasma lead lowered the MDI score by 3.5 points. Neither maternal levels in the second or third trimester nor cord blood levels impacted MDI scores in as strong a fashion. The results raise two questions: should lead be routinely measured in the first trimester of pregnancy, and are there ways to reduce fetal exposure? Plasma lead is expensive and difficult to measure, according to the authors, making routine clinical testing impractical. Studies suggest that calcium supplements slow the release of lead from bone. An ongoing clinical trial of pregnant women is assessing the efficacy of this intervention.

Human studies have shown widespread exposure to phthalates, compounds used in the manufacture of household, consumer, and medical products. The metabolites mono-2-ethylhexyl phthalate (MEHP) and mono-n-butyl phthalate (MBP) have shown testicular toxicity in rats, specifically damage to the cells that produce testosterone and sperm. But animal studies involve higher phthalate exposures than humans typically experience, and there is inconclusive evidence that low exposures affect testicular cells in men. Occupational phthalate exposure tends to be greater and more consistent than the highly variable low levels seen in the general population, however, and research at a Chinese manufacturing plant now reveals that such exposure can be significantly related to decreased blood testosterone concentration [EHP 114:1643 1648; Pan et al.]. Lowered productivity. Men exposed to phthalates in a PVC flooring plant showed decreases in testosterone levels. image: Digital Vision The study participants included 74 men who manufactured polyvinyl chloride (PVC) flooring at a plant in Liaoning Province and 63 men employed at a construction company. All the men completed a questionnaire about lifestyle factors and provided blood and urine samples. Blood samples were analyzed for circulating amounts of free testosterone, luteinizing hormone, follicle-stimulating hormone, and estradiol. Urine analysis provided data on concentrations of MBP and MEHP, which served as biomarkers of exposure. Due to the materials involved in flooring manufacture, the men at the flooring plant were assumed to have dermal and inhalational exposure to dibutyl phthalate (DBP) and di-2-ethylhexyl phthalate (DEHP), the parent compounds of MBP and MEHP. Indeed, all the participants except one construction worker had detectable levels of urinary MBP and MEHP, demonstrating that phthalate exposure was pervasive. However, PVC plant workers had up to 100-fold higher levels of MBP and MEHP and significantly lower blood testosterone concentrations, compared with construction workers. Regression analysis revealed a modest but significant decrease in testosterone as total phthalate esters increased. Based on MEHP concentrations, the investigators estimated that 40.5% of the PVC plant workers had DEHP exposure exceeding the European Union's tolerable daily intake standard of 37.0 microg/kg body weight. The team concluded that high levels of DEHP and DBP exposure seemed to suppress testosterone production in the PVC plant workers, but it is not clear from this study what effect, if any, that might have on their fertility.

Untitled Document FOR IMMEDIATE RELEASE 1 February 2007 CONTACT: Kimberly Thigpen Tart, News Editor, EHP (919) 541-5377 Chelation therapy reduces lead-exposure problems but could create lasting effects for children treated for autism, CU researchers find By Krishna Ramanujan Lead chelation therapy -- a chemical treatment to remove lead from the body -- can significantly reduce learning and behavioral problems that result from lead exposure, a Cornell study of young rats finds. However, in a further finding that has implications for the treatment of autistic children, the researchers say that when rats with no lead in their systems were treated with the lead-removing chemical, they showed declines in their learning and behavior that were similar to the rats that were exposed to lead. Chelating drugs, which bind to lead and other metals in the blood, are increasingly being used for the treatment of autism in children. "Although these drugs are widely used to treat lead-exposed children, there is remarkably little research on whether or not they improve cognitive outcomes, the major area of concern in relation to childhood lead poisoning," said Barbara Strupp, Cornell associate professor of nutritional sciences and of psychology and the senior author of the study, which was published in a recent issue of Environmental Health Perspectives. Studies on the safety or effectiveness of the drugs for treating autism are similarly lacking, Strupp said. Strupp added that to her knowledge this is the first report that shows that chelation therapy can reduce behavioral and learning problems due to lead exposure as well as the first to show that this type of treatment can have lasting adverse effects when administered in the absence of elevated levels of heavy metals. The study used succimer (brand name, Chemet), the most widely prescribed drug for the treatment of lead poisoning. Doctors prefer succimer to other such drugs because it can be given orally on an outpatient basis, and it leaches less zinc, iron and other essential minerals out of the body. Although the Centers for Disease Control recommends chelation therapy only for children whose blood lead levels exceed 45 micrograms per deciliter, such drugs as succimer are commonly administered at much lower levels of exposure, due to concerns about lasting complications with even slightly elevated blood lead levels. It is important to remove lead from the body as quickly as possible to prevent or lessen lasting damage to the developing brain. High-lead exposure from peeling lead-based paint can lead to coma, convulsions and even death. At lower levels, lead exposure causes attention deficits, delinquency and difficulty regulating emotions and can lower IQ scores at a rate of about one IQ point per microgram/deciliter of exposure. The study used rats -- whose mental and behavioral responses to lead exposure are similar to humans' -- and exposed them to moderate- and high-lead levels (administered via mothers' milk). A third group -- the control -- was not exposed. Exposures were followed by a treatment with succimer or placebo. Immediately thereafter, the researchers conducted automated tests over six months on the rats' attention, memory and abilities to learn and regulate emotions. The rats with moderate-lead exposure benefited greatly from the succimer: Their test results were indistinguishable from the control test results. Rats exposed to higher lead levels showed benefits in the emotional domain: After succimer treatment, they behaved similarly to the control group. However, the treatment only slightly improved their learning deficit. In the group that had no lead exposure but were given succimer, "we found lasting cognition and emotion-regulation [deficits] that were as pervasive and large as rats with high lead exposure," said Strupp. She added that one possibility is that succimer, in the absence of lead, may disrupt the balance of such essential minerals as zinc and iron. "These findings raise concerns about the use of chelating agents in treating autistic children," she said. The study was funded by the National Institutes of Health. Among other colleagues, Diane Stangle, a psychology graduate student, and Stephane Beaudin, a research associate in nutritional sciences, contributed to this work.

Untitled Document FOR IMMEDIATE RELEASE 1 February 2007 CONTACT: Jim Tobin 919-653-2582 Report in Environmental Health Perspectives links prenatal alcohol exposure with increased risk of genital malformation in boys [Research Triangle Park, NC] Pregnant women who consume even moderate amounts of alcohol may be placing their sons' reproductive development at risk, according to a study published today in Environmental Health Perspectives (EHP). Researchers at the University of Copenhagen in Denmark have released findings suggesting that consumption of alcohol during pregnancy may increase the risk of cryptorchidism in sons. Cryptorchidism, or undescended testicles, is one of the most common genital malformations in males. Although its cause is still largely unknown, previous research has indicated several risk factors, including low birth weight, prematurity, and twinning. Recent studies have reported an increase in the prevalence of cryptorchidism in the last few generations, suggesting that environment and lifestyle factors such as smoking, caffeine intake, and alcohol consumption may play a part in its occurrence. The investigators in the current study analyzed lifestyle and medical data for 4,957 pregnant women collected in a joint prospective birth cohort in Denmark (1997-2001) and Finland (1997-1999). By the beginning of the third trimester, each woman had completed a questionnaire reporting how many alcoholic and caffeinated drinks they consumed per week as well as smoking habits. A total of 2,496 sons born to these women were examined at birth and at 3 months of age. At birth 128 boys (94 Danish, 34 Finnish) displayed varying degrees of cryptorchidism, and 33 boys remained cryptorchid at 3 months of age. Data analysis revealed that mothers who regularly consumed alcoholic beverages were more likely to give birth to sons with cryptorchidism, even after controlling for other confounding variables such as premature delivery, birth weight, and maternal smoking and caffeine intake. Results showed no statistically significant adverse effects in boys whose mothers consumed fewer than five drinks per week. However, the researchers caution that there is "no well-established safety level of drinking during pregnancy," and they say this new finding should be considered in counseling of pregnant women regarding alcohol consumption. The lead author of the study was Ida N. Damgaard of the University of Denmark Department of Growth and Reproduction. Other authors included Tina K. Jensen, the Nordic Cryptorchidism Study Group, Jorgen H. Petersen, Niels E. Skakkebaek, Jorma Toppari, and Katharina M. Main. The article is available free of charge at http://www.ehponline.org/members/2006/9608/9608.html. EHP is published by the National Institute of Environmental Health Sciences (NIEHS), part of the U.S. Department of Health and Human Services. EHP is an Open Access journal. More information is available online at http://www.ehponline.org/. Brogan Partners Convergence Marketing handles marketing and public relations for EHP, and is responsible for the creation and distribution of this press release. Editor s note: Working media can register to receive press releases via e-mail by visiting http://www.ehponline.org/press/, calling 919-653-2582, or e-mailing ehpmedia@brogan.com.

FOR IMMEDIATE RELEASE 3 January 2007 CONTACT: Jim Tobin 919-653-2582 Report in Environmental Health Perspectives says proposed heavy use of Tamiflu to combat pandemic avian flu could lead to resistant strains of the virus Research Triangle Park, NC Widespread use of the antiviral Tamiflu to fight pandemic avian flu in humans could actually lead to the development of what public health officials hope to avoid drug-resistant strains of the virus in wild birds. British researchers at the Centre for Ecology and Hydrology in Oxford have released findings in the January 2007 issue of Environmental Health Perspectives (EHP) that demonstrate how Tamiflu's persistence in wastewater and river water could affect the waterfowl that drink from those water sources. Since the World Health Organization's first warning of an avian flu pandemic two years ago, nations worldwide have been stockpiling Tamiflu for treatment and outbreak prevention. The drug, which minimizes flu symptoms and duration, inhibits the movement of the influenza virus from the cells it infects, and also helps uninfected people avoid contracting the flu. However, Tamiflu's active agent, the metabolite oseltamivir carboxylate (OC) would be excreted into sewers for several weeks during a pandemic and is expected to withstand biodegradation. According to the researchers in the current study, once birds drink OC-laced water from catchments receiving treated wastewater, they could produce Tamiflu-resistant strains and pass them on to other birds who share the same waters. The investigators analyzed 11 waterway catchments in the United States and 5 in England using a metabolic pathway prediction system to determine the potential biodegradability of OC. They also measured wastewater discharges into the catchments. They estimated the number of clinically infected people in each catchment area treated with a full 5-day course of Tamiflu with 100% compliance, assuming that 80% of the ingested Tamiflu was released into sewer systems as OC and that all of the OC entering each catchment was flushed out in one day. Their estimates showed a maximum concentration well above that required for development of resistance in vitro for 62 consecutive days in the arid Lower Colorado River catchment area. Overall, the researchers say that because of the lower population density for many of the U.S. catchments, peak concentrations of OC in a pandemic would be approximately 10 times less than the concentrations in British rivers. All but one of the American catchments studied are larger than those in Britain and, with the exception of the Lower Colorado River flow area, have more available dilution per person in each given population. There were no specific ecotoxicological risks from Tamiflu identified at the time the drug was submitted for approval to the European Medicines Agency. The authors, however, suggest that the ecotoxicological risk associated with Tamiflu use needs to be reassessed in light of the hundreds of millions of courses that would be consumed globally during a pandemic. The authors warn that, with the release of the uniquely structured, biochemically resistant OC antiviral into river water, "the range of OC concentrations predicted . . . will have uncharacterized ecotoxicological consequences." They call for more detailed water contamination modeling, especially in high-risk areas of the world such as Southeast Asian countries, where there is more frequent human-to-waterfowl contact and where future use of Tamiflu would be significant. They also recommend development of methods to minimize the release of OC into wastewater systems, such as biological and chemical pretreatment in the toilet. The lead author of the study was Andrew C. Singer. Other authors included Miles A. Nunn, Ernest A. Gould, and Andrew C. Johnson. The article is available free of charge at http://www.ehponline.org/docs/2006/9574/abstract.html. EHP is published by the National Institute of Environmental Health Sciences (NIEHS), part of the U.S. Department of Health and Human Services. EHP is an Open Access journal. More information is available online at http://www.ehponline.org/. Brogan Partners Convergence Marketing handles marketing and public relations for EHP, and is responsible for the distribution of this press release. -30- Editor's note: Working media can register to receive press releases via RSS feed or e-mail by visiting http://www.ehponline.org/press/, calling 919-653-2582, or e-mailing ehpmedia@brogan.com.

As the WHO has begun warning of the potential for an avian flu pandemic, governments worldwide have been stockpiling Tamiflu (oseltamivir phosphate). Tamiflu minimizes flu symptoms and duration by preventing the virus from escaping the cells it infects. It also reduces the likelihood of spreading the virus. Now British researchers are predicting that heavy use of Tamiflu, as during a pandemic, will expose wild waterfowl to enough of the antiviral agent to foster a resistant strain [EHP 115:102 106; Singer et al.]. Release and catch. Release of excreted Tamiflu into the environment could create drug-resistant strains of avian flu in wild waterfowl. image credit: Chris Reuther/EHP The risk that Tamiflu will promote a resistant virus comes from the drug's excreted metabolite, oseltamivir carboxylate (OC), which is in fact the active antiviral. Up to 80% of ingested Tamiflu is excreted as OC in urine and feces. OC withstands degradation through sewage treatment and for several weeks afterward. Birds drinking water from catchments contaminated with OC would ingest the antiviral, which would inhibit nonresistant viruses in the birds' digestive systems while enabling resistant viruses to proliferate. Birds excreting the resistant virus would spread the strain among other waterfowl at the same body of water. To estimate birds' exposure to OC, Singer and his colleagues examined data on OC's biodegradability along with measurements of wastewater discharges into 16 major catchment areas in the United States and the United Kingdom. They estimated the number of flu cases in an outbreak within each catchment. Among other suppositions, the researchers assumed that all cases were treated with a standard five-day regimen of Tamiflu. The team calculated that the most vulnerable catchment in the United States is the Lower Colorado, where they predicted OC concentrations high enough to promote Tamiflu resistance in the virus for up to eight weeks. The most vulnerable British catchment would be the Lee catchment in northeast London. Resistant strains could proliferate within a week after pandemic starts in a region, assuming all patients start taking Tamiflu as soon as they develop symptoms. The authors also note that the range of predicted concentrations could have yet-uncharacterized ecotoxicologic effects. Singer and colleagues call for more detailed modeling of OC water contamination, particularly in Asia, where the virus is most prevalent and human-to-wildfowl contact is more common. They also recommend studies of ways to minimize the release of OC into waterways, which could include biological and chemical pretreatment in the toilet bowl.

Growing evidence links heart attacks with short-term exposures to vehicle exhaust from nearby streets. Now some of the first evidence that long-term exposures also are a culprit has been published by a team of Massachusetts researchers [EHP 115:53 57; Tonne et al.]. Cardiovascular disease, of which heart attacks are one major type, is the leading killer in the United States and much of the world. Hazard near home. New data link small increases in heart attack risk to living within 100 m of local traffic and major roads. image credit: image100/Alamy The team evaluated more than 5,000 cases of acute myocardial infarction that occurred in residents of the mid-sized city of Worcester, Massachusetts, from 1995 to 2003, to determine if there was any connection between the heart attacks and exposure to traffic. They used two measures of exposure: cumulative local traffic within 100 m of the home, and the distance of the individual's house to major roadways. They also factored in variables such as age, sex, income, education, amount of open space in the town, and nearby point sources of fine particulates. They found that local traffic within 100 m of an individual's house was associated with a 4% increase in heart attack risk for each interquartile increase in cumulative traffic volume. The linkage wasn't as strong at 200 m and 300 m, which fits with other findings that local traffic-related pollutants tend to diminish around 100 150 m from the roadside. For major roadways (such as highways), heart attack risk increased by 5% for each kilometer closer to the road. For unknown reasons, there was a link to individuals' age, with those under 65 being most vulnerable. Those aged 65 to 74 were less vulnerable, and there was no link for those aged 75 and older. There also were significant links between increasing heart attack risk and both decreasing open space and increasing poverty. The high number of cases studied is one of the many strengths of the study. However, the authors acknowledge that a number of factors need to be better studied to more fully understand what is going on. For instance, they were unable to study individual income and education. Instead, they relied on census block group data, which reflects some homogeneity of socioeconomic conditions, but doesn't capture individual variations. Other weaknesses included a reliance on estimates instead of actual counts for local traffic volumes, and lack of personal pollution exposure data. In addition, these cases represent circumstances in just one city and one period of time. Nonetheless, the study offers some of the first evidence that long-term exposure to vehicle emissions may be an important contributor to heart attacks.

Pregnant women often receive confusing information about whether or not they should consume fish and fish oils. Protein and unsaturated fatty acids in fish confer health benefits. Yet numerous studies have suggested that fish consumption is a major source of mercury exposure, and scientists have raised concerns that mercury levels safe for adults could pose a hazard to the developing fetus. Now a new study suggests another possible hazard associated with mercury exposure during pregnancy: preterm delivery [EHP 115:42 47; Xue et al.]. Predictor of preemies? Measures of mercury in maternal hair may predict risk for preterm delivery. image credit: Millanovic/iStockPhoto The Pregnancy Outcomes and Community Health study, conducted by researchers at Michigan State University, is the first large, community-based study to examine the risk of preterm birth in relation to mercury concentrations among women with low to moderate exposure to the contaminant. This study is also the largest in the United States to correlate fish consumption and maternal hair mercury. Hair levels of total mercury reflect a longer window of contaminant exposure (for example, across the first half of pregnancy) than blood levels, which reflect recent exposure. The researchers examined maternal hair mercury levels during mid-pregnancy (between weeks 15 and 27) in 1,024 women from 52 prenatal clinics in five Michigan communities. This state borders on four of the five Great Lakes, giving the women easy access to sport-caught fish, which can be relatively high in mercury. Each community included urban, suburban, and rural areas. The women reported the amount and category of fish they consumed from the beginning of the current pregnancy through the time of the interview. Canned fish was the most frequently eaten fish category during the first six months of pregnancy, followed by fish bought at a store or restaurant. Only 9.2% of women reported consuming sport-caught fish during the first six months of pregnancy, and almost none ate shellfish. These women's levels of reported fish consumption would be considered moderate to low when compared to populations that subsist on fish. The researchers took hair samples from close to the scalp to approximate exposure during the pregnancy to date, then assessed them for total mercury levels. They found that total fish consumption correlated positively with mercury levels in hair. Women who delivered before 35 weeks had three times the odds of having hair mercury levels at or above the 90th percentile (0.55 2.5 microg/g), compared with women delivering at term (37 weeks or later). Although the study sample was large, the small number of women delivering before 35 weeks (44) means more studies are needed to test this association.

Urinary biomarkers are useful measures of environmental agents in the body. However, little is known about levels of such biomarkers in children and how they may vary by race, age, body mass index, and sex. A three-city pilot study reported this month used urinary biomarkers to better characterize a number of exposures in young girls [EHP 115:116 121; Wolff et al.]. The discovery of detectable urine levels of a range of hormonally active substances in the children may shed light on how various biomarkers relate to pubertal development. Chemicals in kids. Scientists have identified useful biomarkers of girls' exposure to chemicals including agents found in antimicrobial soaps, shampoos, and other personal products. image credit: Robert Gubbins/Shutterstock The study authors measured parent compounds and metabolites of phytoestrogens, phthalates, and phenols in the urine of girls aged 6 to 9. They tested for 25 biomarkers from 22 agents including triclosan (an antimicrobial agent found in many household products), enterolactone (a micronutrient from seeds and grains), and monoethyl phthalate (a metabolite of phthalates used in shampoos, soaps, and cosmetics). The chemical classes studied were chosen because of their suspected hormonal activity and because they have been widely detected in the general population. The 90 girls in the pilot study were recruited in New York, Cincinnati, and San Francisco, and included members of four racial/ethnic groups. The pilot study sampled a relatively small population to determine whether urinary biomarkers of the chemicals of concern would be detectable and variable enough for meaningful comparisons of their concentrations in relation to outcomes of female growth and development. Most of the markers analyzed were found in more than 94% of the participants. Nine of them including metabolites of isoflavones found in foods containing soy and of di(2-ethylhexyl) phthalate, a softening agent used in plastics were found in all of the girls. The team established that urinary metabolites of phenols, phthalates, and phytoestrogens in children are detectable and variable enough to make meaningful comparisons. And though the number of subjects was small, preliminary results point to variations in concentrations of some metabolites between girls of different races, as well as variation according to body mass index, and seasonal variation during the year all factors that will be useful in dissecting the roles of the studied chemical classes in breast cancer and other diseases.