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News Article | May 2, 2017
Site: www.eurekalert.org

WASHINGTON (May 2, 2017) - Some scientific reports have a profound impact on government policy. Sometimes, however, there are significant shortcomings in the research - yet the policy impact continues. Critically analyzing scientific research that underlies regulatory decision making and generating new information to ensure decisions are based on sound science are crucial. A recent analysis by Checkoway et al. has been awarded the Kammer Merit in Authorship Award for its review of the data from a critical epidemiological study used by scientific agencies to assess health risk from formaldehyde exposure. The findings from Checkoway et al call into question the original study's conclusions; the analysis further demonstrates the importance of data availability, research reproducibility and adherence to study design when drawing scientific conclusions. The Kammer Merit in Authorship Award recognizes an outstanding scientific contribution published in the American College of Occupational and Environmental Medicine (ACOEM's) Journal of Occupational and Environmental Medicine (JOEM) during a given year. The winning paper, titled Formaldehyde Exposure and Mortality Risks from Acute Myeloid Leukemia and Other Lymphohematopoietic Malignancies in the US National Cancer Institute Cohort Study of Workers in Formaldehyde Industries, concluded that there is no epidemiological evidence from the National Cancer Institute (NCI) cohort supporting an association between formaldehyde exposure and acute myeloid leukemia (AML). The award was announced late last week. "The findings from this analysis do not support a finding that formaldehyde exposure is a cause of leukemia," said Harvey Checkoway, Ph.D., lead author of the reanalysis and Professor of Family Medicine & Public Health at the University of California, San Diego. "This reanalysis identifies how critical data interpretation is, given that the risk assessments that rely on these analyses ultimately set occupational and environmental exposure standards." Checkoway and his colleagues performed analyses of raw data in an attempt to replicate findings reported from a NCI cohort mortality study of workers from 10 US plants producing or using formaldehyde. The NCI study has been influential in the classification of formaldehyde as a human leukemogen by the International Agency for Research on Cancer (IARC) and the National Institute of Environmental Health Sciences (NIEHS) National Toxicology Program (NTP). In the original analysis NCI investigators defined "peak" exposure to formaldehyde on a relative basis with respect to individual workers' exposures histories. This complicates data interpretations. Using this definition, analyses of updated mortality data for the NCI cohort reported tentative associations of "peak" exposures with myeloid leukemia (ML) and Hodgkin lymphoma (HL) that are inconsistent with other studies. The new research found no association between acute myeloid leukemia (AML) and cumulative, average or frequency of "peak" exposures. This became clear in the new analysis where AML and chronic myeloid leukemia (CML) were evaluated separately, as two types of leukemia are different diseases and have different risk factors. The award-winning Checkoway et al. study conducted more comprehensive analyses of associations of specific lymphohematopoietic malignancies (LHM), especially AML, with peak exposure, using a standard definition of peak exposure. Peak was defined in terms of absolute exposure dose and duration, which permitted direct comparisons among similar studies, strengthening the analysis. Checkoway et al. concluded that no clear associations for peak or cumulative formaldehyde exposures were observed in this cohort for any of the specific LHM, including AML The result of this analysis adds to the weight of evidence that formaldehyde exposure in the workplace does not cause AML, the LHM of greatest concern. It also underscores the need to ensure new information is effectively considered and incorporated into chemical assessments by IARC, NTP and other agencies. "Having this work recognized by ACOEM as a significant contribution in occupational medicine shows how important these findings are to understanding and interpreting the formaldehyde science," said Kimberly White, Ph.D., Senior Director of the American Chemistry Council Formaldehyde Panel. To learn more, view this fact sheet or visit americanchemistry.com/formaldehyde. The American Chemistry Council (ACC) represents the leading companies engaged in the business of chemistry. ACC members apply the science of chemistry to make innovative products and services that make people's lives better, healthier and safer. ACC is committed to improved environmental, health and safety performance through Responsible Care®, common sense advocacy designed to address major public policy issues, and health and environmental research and product testing. The business of chemistry is a $797 billion enterprise and a key element of the nation's economy. It is the nation's largest exporter, accounting for fourteen percent of all U.S. exports. Chemistry companies are among the largest investors in research and development. Safety and security have always been primary concerns of ACC members, and they have intensified their efforts, working closely with government agencies to improve security and to defend against any threat to the nation's critical infrastructure.


News Article | May 2, 2017
Site: www.prnewswire.com

"The findings from this analysis do not support a finding that formaldehyde exposure is a cause of leukemia," said Harvey Checkoway, Ph.D., lead author of the reanalysis and Professor of Family Medicine & Public Health at the University of California, San Diego. "This reanalysis identifies how critical data interpretation is, given that the risk assessments that rely on these analyses ultimately set occupational and environmental exposure standards." Checkoway and his colleagues performed analyses of raw data in an attempt to replicate findings reported from a NCI cohort mortality study of workers from 10 US plants producing or using formaldehyde. The NCI study has been influential in the classification of formaldehyde as a human leukemogen by the International Agency for Research on Cancer (IARC) and the National Institute of Environmental Health Sciences (NIEHS) National Toxicology Program (NTP). In the original analysis NCI investigators defined "peak" exposure to formaldehyde on a relative basis with respect to individual workers' exposures histories. This complicates data interpretations. Using this definition, analyses of updated mortality data for the NCI cohort reported tentative associations of "peak" exposures with myeloid leukemia (ML) and Hodgkin lymphoma (HL) that are inconsistent with other studies. The new research found no association between acute myeloid leukemia (AML) and cumulative, average or frequency of "peak" exposures. This became clear in the new analysis where AML and chronic myeloid leukemia (CML) were evaluated separately, as two types of leukemia are different diseases and have different risk factors. The award-winning Checkoway et al. study conducted more comprehensive analyses of associations of specific lymphohematopoietic malignancies (LHM), especially AML, with peak exposure, using a standard definition of peak exposure. Peak was defined in terms of absolute exposure dose and duration, which permitted direct comparisons among similar studies, strengthening the analysis. Checkoway et al. concluded that no clear associations for peak or cumulative formaldehyde exposures were observed in this cohort for any of the specific LHM, including AML. The result of this analysis adds to the weight of evidence that formaldehyde exposure in the workplace does not cause AML, the LHM of greatest concern. It also underscores the need to ensure new information is effectively considered and incorporated into chemical assessments by IARC, NTP and other agencies. "Having this work recognized by ACOEM as a significant contribution in occupational medicine shows how important these findings are to understanding and interpreting the formaldehyde science," said Kimberly White, Ph.D., Senior Director of the American Chemistry Council Formaldehyde Panel. To learn more, view this fact sheet or visit americanchemistry.com/formaldehyde. The American Chemistry Council (ACC) represents the leading companies engaged in the business of chemistry. ACC members apply the science of chemistry to make innovative products and services that make people's lives better, healthier and safer. ACC is committed to improved environmental, health and safety performance through Responsible Care®, common sense advocacy designed to address major public policy issues, and health and environmental research and product testing. The business of chemistry is a $797 billion enterprise and a key element of the nation's economy. It is the nation's largest exporter, accounting for fourteen percent of all U.S. exports. Chemistry companies are among the largest investors in research and development. Safety and security have always been primary concerns of ACC members, and they have intensified their efforts, working closely with government agencies to improve security and to defend against any threat to the nation's critical infrastructure. To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/acc-research-shows-no-link-between-formaldehyde-and-leukemia-300449140.html


News Article | June 1, 2017
Site: www.eurekalert.org

Baby teeth from children with autism contain more toxic lead and less of the essential nutrients zinc and manganese, compared to teeth from children without autism, according to an innovative study funded by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. The researchers studied twins to control genetic influences and focus on possible environmental contributors to the disease. The findings, published June 1 in the journal Nature Communications, suggest that differences in early-life exposure to metals, or more importantly how a child's body processes them, may affect the risk of autism. The differences in metal uptake between children with and without autism were especially notable during the months just before and after the children were born. The scientists determined this by using lasers to map the growth rings in baby teeth generated during different developmental periods. The researchers observed higher levels of lead in children with autism throughout development, with the greatest disparity observed during the period following birth. They also observed lower uptake of manganese in children with autism, both before and after birth. The pattern was more complex for zinc. Children with autism had lower zinc levels earlier in the womb, but these levels then increased after birth, compared to children without autism. The researchers note that replication in larger studies is needed to confirm the connection between metal uptake and autism. "We think autism begins very early, most likely in the womb, and research suggests that our environment can increase a child's risk. But by the time children are diagnosed at age 3 or 4, it's hard to go back and know what the moms were exposed to," said Cindy Lawler, Ph.D., head of the NIEHS Genes, Environment, and Health Branch. "With baby teeth, we can actually do that." Patterns of metal uptake were compared using teeth from 32 pairs of twins and 12 individual twins. The researchers compared patterns in twins where only one had autism, as well as in twins where both or neither had autism. Smaller differences in the patterns of metal uptake occurred when both twins had autism. Larger differences occurred in twins where only one sibling had autism. The findings build on prior research showing that exposure to toxic metals, such as lead, and deficiencies of essential nutrients, like manganese, may harm brain development while in the womb or during early childhood. Although manganese is an essential nutrient, it can also be toxic at high doses. Exposure to both lead and high levels of manganese has been associated with autism traits and severity. The study was led by Manish Arora, Ph.D., an environmental scientist and dentist at the Icahn School of Medicine at Mount Sinai in New York. With support from NIEHS, Arora and colleagues had previously developed a method that used naturally shed baby teeth to measure children's exposure to lead and other metals while in the womb and during early childhood. The researchers use lasers to extract precise layers of dentine, the hard substance beneath tooth enamel, for metal analysis. The team previously showed that the amount of lead in different layers of dentine corresponds to lead exposure during different developmental periods. Arora said that autism is a condition where both genes and environment play a role, but figuring out which environmental exposures may increase risk has been difficult. "What is needed is a window into our fetal life," he said. "Unlike genes, our environment is constantly changing, and our body's response to environmental stressors not only depends on just how much we were exposed to, but at what age we experienced that exposure." Prior studies relating toxic metals and essential nutrients to autism have faced key limitations, such as estimating exposure based on blood levels after autism diagnosis rather than before, or not being able to control for differences that could be due to genetic factors. "A lot of studies have compared current lead levels in kids that are already diagnosed," said Lawler. "Being able to measure something the children were exposed to long before diagnosis is a major advantage." The method of using baby teeth to measure past exposure to metals also holds promise for other disorders, such as attention deficit hyperactivity disorder. "There is growing excitement about the potential of baby teeth as a rich record of a child's early life exposure to both helpful and harmful factors in the environment," said David Balshaw, Ph.D., head of the NIEHS Exposure, Response, and Technology Branch, which supported the development of the tooth method. Reference: Arora M, Reichenberg A, Willfors C, Austin C, Gennings C, Berggren S, Lichtenstein P, Anckarsater H, Tammimies K, Bolte S. 2017. Fetal and postnatal metal dysregulation in autism. Nat Commun; doi: 10.1038/NCOMMS15493 [Online 1 June 2017]. NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit http://www. . Subscribe to one or more of the NIEHS news lists to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications. The Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the National Institute of Mental Health, also provided funding for the study. About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www. .


A Scripps Institution of Oceanography at the University of California San Diego-led research team discovered for the first time that a common marine sponge hosts bacteria that specialize in the production of toxic compounds nearly identical to man-made fire retardants. The new findings put the research team one step closer to unraveling the mystery of this powerful group of chemical compounds, known as polybrominated diphenyl ethers (PBDEs), in the marine environment. PBDEs are a subgroup of brominated flame retardants that are combined into foam, textiles, and electronics to raise the temperature at which the products will burn. These man-made industrial chemicals are powerful endocrine disruptors that mimic the activity of the human body's most active thyroid hormone. Vinayak Agarwal, a postdoctoral researcher at Scripps, picked up a cold case first started nearly 50 years ago by Scripps chemist John Faulkner, an early pioneer in the study of natural products from the sea, to continue the investigation into the source of these toxic compounds that are found in large quantities in the world’s oceans. “For the first time we were able to conclusively show that genes and enzymes produced in bacteria from sponges are responsible for the production of these compounds toxic to humans,” said Agarwal, co-first author of the paper along with Scripps PhD student Jessica Blanton. The study was part of the National Science Foundation (NSF)/ National Institute of Environmental Health Sciences (NIEHS)-funded Center for Oceans and Human Health research being conducted at Scripps. In 2014, Agarwal and colleagues at Scripps Oceanography were the first to discover that unrelated free-living marine bacteria produce these fire retardant compounds naturally, albeit in very small quantities. In this new study, the researchers employed two modern-day techniques—genome “mining” pioneered by Scripps marine chemist Brad Moore and an environmental DNA sequencing approach pioneered by Scripps biologist Eric Allen—to take the investigation a step further and identify the specific genes and enzymes involved in the overproduction of the toxic molecules in sponges. Marine sponges obtain food and oxygen by filtering seawater through the pores and channels in their bodies. This constant water flow means that these immobile animals host many bacteria, viruses, and fungi in their complex microbiomes. The research team collected 18 sponge samples for the study during two research expeditions to Guam. They then isolated the various components of this complex mixture of organisms from the sponge’s tissues to identify the specific genes and enzymes that code for the production of PBDEs. “For many years scientists were finding clues that suggested nature was making these compounds,” said Bradley Moore, a professor at the Scripps Center of Marine Biotechnology and Biomedicine and the Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego, and a senior author of the study. “Now that we understand how they are produced in the marine environment, we are exploring why they exist, and the human health concerns associated with them.” Moore’s genome "mining" approach along with Allen’s metagenomic sequencing gives scientists a way to connect the natural chemicals produced by organisms back to the enzymes that construct them. The study, which appears on the cover of the May issue of the journal Nature Chemical Biology, was a unique collaboration among chemists and biologists at UC San Diego and elsewhere. “This study is a powerful combination of chemical, biological and environmental research,” said Henrietta Edmonds of the NSF’s Division of Ocean Sciences, which supported the research. “It has the potential to help us understand the production, fate and health consequences of natural and pollutant compounds in the marine environment.” “We care about naturally produced PBDEs because they end up in the food chain,” said Frederick Tyson, Ph.D., of the NIEHS, which helped to fund the research. “Preliminary data from this research team suggest that some naturally occurring PDBEs may be even more toxic than those that are man-made, so we need to develop a better understanding of these compounds.” These ocean-dwelling microbes have been found in habitats as diverse as sea grasses, corals and whales. The next step of the investigation for the researchers is to mine the genes and enzymes in other marine hosts to find out what other organisms are making similar toxic compounds and why. Co-authors from Scripps Oceanography include Sheila Podell, Michelle Schorn, Julia Busch, and Paul Jensen. Researchers Arnaud Taton and James Golden from UC San Diego’s Division of Biological Sciences, Jason Biggs from University of Guam’s Marine Laboratory, Zhenjian Lin and Eric Schmidt from the University of Utah, and Valerie Paul from the Smithsonian Marine Station also contributed to the study. Funding for the research was provided through: National Science Foundation grants OCE-1313747, DGE-1144086, IOS-1120113, MCB-1149552; National Institutes of Health grants P01-ES021921, K99-ES026620, R01-GM107557, R01-CA172310, S10-OD010640; the U.S. Department of Energy grant DE-EE0003373; and a Helen Hay Whitney Foundation postdoctoral fellowship.


News Article | May 11, 2017
Site: www.eurekalert.org

A Scripps Institution of Oceanography at the University of California San Diego-led research team discovered for the first time that a common marine sponge hosts bacteria that specialize in the production of toxic compounds nearly identical to man-made fire retardants. The new findings put the research team one step closer to unraveling the mystery of this powerful group of chemical compounds, known as polybrominated diphenyl ethers (PBDEs), in the marine environment. PBDEs are a subgroup of brominated flame retardants that are combined into foam, textiles, and electronics to raise the temperature at which the products will burn. These man-made industrial chemicals are powerful endocrine disruptors that mimic the activity of the human body's most active thyroid hormone. Vinayak Agarwal, a postdoctoral researcher at Scripps, picked up a cold case first started nearly 50 years ago by Scripps chemist John Faulkner, an early pioneer in the study of natural products from the sea, to continue the investigation into the source of these toxic compounds that are found in large quantities in the world's oceans. "For the first time we were able to conclusively show that genes and enzymes produced in bacteria from sponges are responsible for the production of these compounds toxic to humans," said Agarwal, co-first author of the paper along with Scripps PhD student Jessica Blanton. The study was part of the National Science Foundation (NSF)/ National Institute of Environmental Health Sciences (NIEHS)-funded Center for Oceans and Human Health research being conducted at Scripps. In 2014, Agarwal and colleagues at Scripps Oceanography were the first to discover that unrelated free-living marine bacteria produce these fire retardant compounds naturally, albeit in very small quantities. In this new study, the researchers employed two modern-day techniques--genome "mining" pioneered by Scripps marine chemist Brad Moore and an environmental DNA sequencing approach pioneered by Scripps biologist Eric Allen--to take the investigation a step further and identify the specific genes and enzymes involved in the overproduction of the toxic molecules in sponges. Marine sponges obtain food and oxygen by filtering seawater through the pores and channels in their bodies. This constant water flow means that these immobile animals host many bacteria, viruses, and fungi in their complex microbiomes. The research team collected 18 sponge samples for the study during two research expeditions to Guam. They then isolated the various components of this complex mixture of organisms from the sponge's tissues to identify the specific genes and enzymes that code for the production of PBDEs. "For many years scientists were finding clues that suggested nature was making these compounds," said Bradley Moore, a professor at the Scripps Center of Marine Biotechnology and Biomedicine and the Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego, and a senior author of the study. "Now that we understand how they are produced in the marine environment, we are exploring why they exist, and the human health concerns associated with them." Moore's genome "mining" approach along with Allen's metagenomic sequencing gives scientists a way to connect the natural chemicals produced by organisms back to the enzymes that construct them. The study, which appears on the cover of the May issue of the journal Nature Chemical Biology, was a unique collaboration among chemists and biologists at UC San Diego and elsewhere. "This study is a powerful combination of chemical, biological and environmental research," said Henrietta Edmonds of the NSF's Division of Ocean Sciences, which supported the research. "It has the potential to help us understand the production, fate and health consequences of natural and pollutant compounds in the marine environment." "We care about naturally produced PBDEs because they end up in the food chain," said Frederick Tyson, Ph.D., of the NIEHS, which helped to fund the research. "Preliminary data from this research team suggest that some naturally occurring PDBEs may be even more toxic than those that are man-made, so we need to develop a better understanding of these compounds." These ocean-dwelling microbes have been found in habitats as diverse as sea grasses, corals and whales. The next step of the investigation for the researchers is to mine the genes and enzymes in other marine hosts to find out what other organisms are making similar toxic compounds and why. Co-authors from Scripps Oceanography include Sheila Podell, Michelle Schorn, Julia Busch, and Paul Jensen. Researchers Arnaud Taton and James Golden from UC San Diego's Division of Biological Sciences, Jason Biggs from University of Guam's Marine Laboratory, Zhenjian Lin and Eric Schmidt from the University of Utah, and Valerie Paul from the Smithsonian Marine Station also contributed to the study. Funding for the research was provided through: National Science Foundation grants OCE-1313747, DGE-1144086, IOS-1120113, MCB-1149552; National Institutes of Health grants P01-ES021921, K99-ES026620, R01-GM107557, R01-CA172310, S10-OD010640; the U.S. Department of Energy grant DE-EE0003373; and a Helen Hay Whitney Foundation postdoctoral fellowship. Scripps Institution of Oceanography at the University of California, San Diego, is one of the oldest, largest, and most important centers for global science research and education in the world. Now in its second century of discovery, the scientific scope of the institution has grown to include biological, physical, chemical, geological, geophysical, and atmospheric studies of the earth as a system. Hundreds of research programs covering a wide range of scientific areas are under way today on every continent and in every ocean. The institution has a staff of more than 1,400 and annual expenditures of approximately $195 million from federal, state, and private sources. Scripps operates oceanographic research vessels recognized worldwide for their outstanding capabilities. Equipped with innovative instruments for ocean exploration, these ships constitute mobile laboratories and observatories that serve students and researchers from institutions throughout the world. Birch Aquarium at Scripps serves as the interpretive center of the institution and showcases Scripps research and a diverse array of marine life through exhibits and programming for more than 430,000 visitors each year. Learn more at scripps.ucsd.edu and follow us at: Facebook | Twitter | Instagram. At the University of California San Diego, we constantly push boundaries and challenge expectations. Established in 1960, UC San Diego has been shaped by exceptional scholars who aren't afraid to take risks and redefine conventional wisdom. Today, as one of the top 15 research universities in the world, we are driving innovation and change to advance society, propel economic growth, and make our world a better place. Learn more at http://www. .


A Scripps Institution of Oceanography at the University of California San Diego-led research team discovered for the first time that a common marine sponge hosts bacteria that specialize in the production of toxic compounds nearly identical to man-made fire retardants. The new findings put the research team one step closer to unraveling the mystery of this powerful group of chemical compounds, known as polybrominated diphenyl ethers (PBDEs), in the marine environment. PBDEs are a subgroup of brominated flame retardants that are combined into foam, textiles, and electronics to raise the temperature at which the products will burn. These man-made industrial chemicals are powerful endocrine disruptors that mimic the activity of the human body's most active thyroid hormone. Vinayak Agarwal, a postdoctoral researcher at Scripps, picked up a cold case first started nearly 50 years ago by Scripps chemist John Faulkner, an early pioneer in the study of natural products from the sea, to continue the investigation into the source of these toxic compounds that are found in large quantities in the world’s oceans. “For the first time we were able to conclusively show that genes and enzymes produced in bacteria from sponges are responsible for the production of these compounds toxic to humans,” said Agarwal, co-first author of the paper along with Scripps PhD student Jessica Blanton. The study was part of the National Science Foundation (NSF)/ National Institute of Environmental Health Sciences (NIEHS)-funded Center for Oceans and Human Health research being conducted at Scripps. In 2014, Agarwal and colleagues at Scripps Oceanography were the first to discover that unrelated free-living marine bacteria produce these fire retardant compounds naturally, albeit in very small quantities. In this new study, the researchers employed two modern-day techniques—genome “mining” pioneered by Scripps marine chemist Brad Moore and an environmental DNA sequencing approach pioneered by Scripps biologist Eric Allen—to take the investigation a step further and identify the specific genes and enzymes involved in the overproduction of the toxic molecules in sponges. Marine sponges obtain food and oxygen by filtering seawater through the pores and channels in their bodies. This constant water flow means that these immobile animals host many bacteria, viruses, and fungi in their complex microbiomes. The research team collected 18 sponge samples for the study during two research expeditions to Guam. They then isolated the various components of this complex mixture of organisms from the sponge’s tissues to identify the specific genes and enzymes that code for the production of PBDEs. “For many years scientists were finding clues that suggested nature was making these compounds,” said Bradley Moore, a professor at the Scripps Center of Marine Biotechnology and Biomedicine and the Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego, and a senior author of the study. “Now that we understand how they are produced in the marine environment, we are exploring why they exist, and the human health concerns associated with them.” Moore’s genome "mining" approach along with Allen’s metagenomic sequencing gives scientists a way to connect the natural chemicals produced by organisms back to the enzymes that construct them. The study, which appears on the cover of the May issue of the journal Nature Chemical Biology, was a unique collaboration among chemists and biologists at UC San Diego and elsewhere. “This study is a powerful combination of chemical, biological and environmental research,” said Henrietta Edmonds of the NSF’s Division of Ocean Sciences, which supported the research. “It has the potential to help us understand the production, fate and health consequences of natural and pollutant compounds in the marine environment.” “We care about naturally produced PBDEs because they end up in the food chain,” said Frederick Tyson, Ph.D., of the NIEHS, which helped to fund the research. “Preliminary data from this research team suggest that some naturally occurring PDBEs may be even more toxic than those that are man-made, so we need to develop a better understanding of these compounds.” These ocean-dwelling microbes have been found in habitats as diverse as sea grasses, corals and whales. The next step of the investigation for the researchers is to mine the genes and enzymes in other marine hosts to find out what other organisms are making similar toxic compounds and why. Co-authors from Scripps Oceanography include Sheila Podell, Michelle Schorn, Julia Busch, and Paul Jensen. Researchers Arnaud Taton and James Golden from UC San Diego’s Division of Biological Sciences, Jason Biggs from University of Guam’s Marine Laboratory, Zhenjian Lin and Eric Schmidt from the University of Utah, and Valerie Paul from the Smithsonian Marine Station also contributed to the study. Funding for the research was provided through: National Science Foundation grants OCE-1313747, DGE-1144086, IOS-1120113, MCB-1149552; National Institutes of Health grants P01-ES021921, K99-ES026620, R01-GM107557, R01-CA172310, S10-OD010640; the U.S. Department of Energy grant DE-EE0003373; and a Helen Hay Whitney Foundation postdoctoral fellowship.


Researchers have discovered for the first time that a common marine sponge hosts bacteria that specialize in the production of toxic compounds nearly identical to man-made fire retardants, a finding that could help scientists better understand the human health implications of these common additives. The new findings, by scientists at the Scripps Institution of Oceanography (SIO) at the University of California, San Diego, moved the research team a step closer to unraveling the mysteries of this powerful group of chemical compounds, known as polybrominated diphenyl ethers (PBDEs). The National Science Foundation's (NSF) Division of Ocean Sciences and the National Institute of Environmental Health Sciences (NIEHS) of the National Institutes of Health jointly funded the research through SIO's Center for Oceans and Human Health. "For many years scientists have been finding clues that suggested nature was making these compounds," said SIO marine chemist Brad Moore, a senior author of the study. "Now that we understand how they are produced in the marine environment, we are exploring why they exist, and the human health concerns associated with them." The results, which appear in the May issue of the journal Nature Chemical Biology, came from a unique collaboration among chemists and biologists at SIO and elsewhere. "This study is a powerful combination of chemical, biological and environmental research," said Henrietta Edmonds of NSF's Division of Ocean Sciences. "It has the potential to help us understand the production, fate and health consequences of natural and pollutant compounds in the marine environment." Manufacturers add PBDEs to foam, textiles, electronics and other products to make them less flammable. These industrial chemicals are powerful endocrine disruptors that mimic the activity of the human body's most active thyroid hormone. Vinayak Agarwal, a researcher at SIO, picked up a cold case first started nearly 50 years ago by SIO chemist John Faulkner, an early pioneer in the study of natural products from the sea. Agarwal continued Faulkner's investigation into the source of toxic PDBEs, found in large quantities in the world's oceans. "For the first time we were able to conclusively show that genes and enzymes produced in bacteria from sponges are responsible for the production of these compounds toxic to humans," said Agarwal, co-first author of the paper along with Scripps researcher Jessica Blanton. In 2014, Agarwal and colleagues were the first to discover that unrelated free-living marine bacteria produce the fire retardant compounds naturally. In the new study, researchers employed two modern-day techniques -- genome "mining" and environmental DNA sequencing -- to take the investigation a step farther and identify the specific genes and enzymes involved in the overproduction of the toxic molecules in sponges. Marine sponges obtain food and oxygen by filtering seawater through the pores and channels in their bodies. This constant flow of water means that these immobile animals host many bacteria, viruses and fungi in their complex microbiomes. The research team collected 18 sponge samples for the study during two research expeditions to Guam. They then isolated the various components in the complex mixture of organisms from the sponge's tissues to identify the specific genes and enzymes that code for the production of PBDEs. The genome "mining" approach along with metagenomic sequencing gave the scientists a way to connect the natural chemicals produced by organisms back to the enzymes that constructed them. "We care about naturally produced PBDEs because they end up in the food chain," said NIEHS's Frederick Tyson. "Preliminary data from this research suggest that some naturally occurring PDBEs may be even more toxic than those that are man-made, so we need to develop a better understanding of these compounds." The next step in the investigation is to mine the genes and enzymes in other marine species to found out what other organisms are making similar toxic compounds and why. Co-authors from SIO include Sheila Podell, Michelle Schorn, Julia Busch, and Paul Jensen. Researchers Arnaud Taton and James Golden from UC San Diego's Division of Biological Sciences, Jason Biggs from the University of Guam's Marine Laboratory, Zhenjian Lin and Eric Schmidt from the University of Utah, and Valerie Paul from the Smithsonian Marine Station also contributed to the study.


News Article | August 17, 2017
Site: www.eurekalert.org

A protein called COUP-TFII determines whether a mouse embryo develops a male reproductive tract, according to researchers at the National Institutes of Health and their colleagues at Baylor College of Medicine, Houston. The discovery, which appeared August 18 in the journal Science, changes the long-standing belief that an embryo will automatically become female unless androgens, or male hormones, in the embryo make it male. Humphrey Hung-Chang Yao, Ph.D., head of the Reproductive Developmental Biology Group at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, studies how male and female mouse embryos acquire their sex-specific reproductive systems. He said all early-stage mammalian embryos, regardless of their sex, contain structures for both male and female reproductive tracts. For a mouse or human to end up with the reproductive tract of one sex after birth, the other tract has to disintegrate. "I learned in graduate school that androgens are needed to maintain the male reproductive tract, but our work finds that maintenance of the male reproductive tract can be achieved without androgen," Yao said. Since the 1950s, scientists have believed that androgens produced by embryonic testes, promote the survival of the male reproductive tract. The scientific consensus favored a female by default scenario, in which the absence of androgens in female embryos resulted in the breakdown of the male reproductive tract. However, Yao's work demonstrated that female embryos actively promote the elimination of the male tract through the action of COUP-TFII, challenging the female by default theory. The evidence comes from a mouse model created by Yao and his group. The mice lack COUP-TFII in an embryonic structure that develops into distinct male and female reproductive ducts. To the surprise of Yao and his visiting fellow Fei Zhao, Ph.D., who is also lead author on the paper, female mouse embryos without COUP-TFII displayed both male and female ducts. Control females with COUP-TFII appropriately exhibited only the female duct. Since Yao and his team did not find any evidence of androgen production in female mice without COUP-TFII, they concluded that the presence of the male reproductive tract in female embryos lacking COUP-TFII occurs without androgen. The study suggests that COUP-TFII has to be present to block the growth of male reproductive tracts. Without COUP-TFII, the mice are born intersex, or having both male and female reproductive tracts. "This work is just the beginning and many interesting questions remain unanswered," Zhao said. "We will continue to study how the embryo develops a functional reproductive system." Yao's group plans to use mouse models to examine how birth defects of the reproductive system originate. These birth defects lead to disorders of sexual development (DSD), which include common defects, such as cryptorchidism, or undescended testicles, as well as the genetic disorders Klinefelter Syndrome and Turner Syndrome. "Individuals with DSD may have developmental challenges due to the presence of intersex organ systems," said Kenneth Korach, Ph.D., head of the NIEHS Reproductive and Developmental Biology Laboratory. "With its highly novel approach and unexpected findings, Yao's research has important implications for understanding the potential causes of these conditions." NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit http://www. . Subscribe to one or more of the NIEHS news lists to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications. About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www. . Reference: Zhao F, Franco HL, Rodriguez KF, Brown PR, Tsai MJ, Tsai SY, Yao HHC. 2017. Elimination of the male reproductive tract in the female embryo is promoted by COUP-TFII in mice. Science; doi: 10.1126/science.aai9136 [18 August 2017].


News Article | May 26, 2017
Site: www.eurekalert.org

New research from the University of Cincinnati (UC) reveals that residents of the Mid-Ohio River Valley (from Evansville, Indiana, north to Huntington, West Virginia) had higher than normal levels of perfluorooctanoic acid (PFOA) based on blood samples collected over a 22-year span. The exposure source was likely from drinking water contaminated by industrial discharges upriver. The study, appearing in the latest publication of Environmental Pollution, looked at levels of PFOA and 10 other per- and polyfluoroalkyl substances (PFAS) in 931 Mid-Ohio River Valley residents, testing blood serum samples collected between 1991 and 2013, to determine whether the Ohio River and Ohio River Aquifer were sources of exposure. This is the first study of PFOA serum concentrations in U.S. residents in the 1990s. "These Mid-Ohio River Valley residents appear to have had concentrations of PFOA in their bloodstream at higher than average U.S. levels," says Susan Pinney, PhD, professor in the Department of Environmental Health at the UC College of Medicine, a member of both the Cincinnati Cancer Consortium and UC Cancer Institute and senior author of the study. Ohio River PFOA concentrations downstream were elevated, suggesting Mid-Ohio River Valley residents were exposed through drinking water, primarily contaminated by industrial discharges as far as 666 kilometers (413 miles) upstream. Industrial discharges of PFOA to the Ohio River, contaminating water systems near Parkersburg, West Virginia, were previously associated with nearby residents' serum PFOA concentrations above U.S. general population medians. The article notes that use of granular activated carbon filtration (GAC) by water treatment facilities reduced PFOA exposure by as much as 60 percent. "Where GAC has been used, the blood level concentration of PFOA was decreased significantly," says co-author Robert Herrick, a UC doctoral student in the Department of Environmental Health. Nearly all of the samples tested positive for some level of PFOA (99.9%) but 47 percent of the samples had PFOA levels higher than the 95th national percentile. The study additionally looked at information about municipal water distribution systems and the zones that were serviced by each of the water treatment plants. "We conducted statistical analyses to determine if factors such as location and years of residence, drinking water source and breast feeding were predictors of the person's serum PFC concentration," says Herrick. PFCs have had wide consumer use and industrial applications. They are surfactants used in fire-fighting foams and in the manufacture of stain and water resistant coatings, on cookware, furniture and carpeting. PFOA, or C-8, can be found as a residual impurity in some paper coatings used on containers for processed food. As a byproduct of commercial production, PFCs/PFOA are released into the environment and, although no longer used in manufacturing in the U.S., are considered persistent in the environment. Pinney points out that the primary concern with PFCs/PFOA is that they take a very long time to leave the human body, and studies indicate that exposure to PFOA and PFOS over certain levels may result in adverse health effects, including developmental effects, liver and tissue damage and immune and thyroid impacts. "Because the elimination time could be several years, it is hard to determine what impact these environmental exposures may have on our health and children's health," says Pinney. "These data from the 1990s demonstrate that that the contaminants have been in our water a long time, at unchecked levels, before anyone was paying attention to it." Pinney cites projects like this one as having the translational potential to make improvements in public health. "Studies like these provide evidence to support changes in water treatment practices." An earlier study looking at samples from girls and young women from Northern Kentucky showed that about half of the samples from the girls were much higher than the national average for U.S. children (the 95th percentile) concentration. The Northern Kentucky Water department has since then implemented the use of GAC at their plants to meet new federal regulations, and Cincinnati Water Works used the study's findings to check their treatment regulations and filtration usage. The Mid-Ohio River Valley study was conducted by researchers within the UC College of Medicine Department of Environmental Health, at Cincinnati Children's Hospital Medical Center and the National Institute of Environmental Health Sciences (NIEHS). Research was made possible by the Breast Cancer and the Environment Research Program awards U01ES012770 and U01ES019453 from the NIEHS and the National Cancer Institute; P30-ES006096, R21 ES017176 and T32-ES10957 from NIEHS; EPA-RD-83478801 from the United States Environmental Protection Agency, and CSTAUL1RR026314 from the National Center for Research Resources. Pinney cites no conflict of interest.

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