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The MIT Center for Environmental Health Sciences (CEHS), an interdisciplinary research center, funded by the National Institute of Environmental Health Sciences (NIEHS), invites MIT junior faculty and research staff with principal investigator privileges to submit applications for funding of pilot projects related to environmental health, to support either basic or translational research. Please see the NIEHS strategic plan to gain understanding of the types of projects center plans to fund. Preference is given to projects that address the NIEHS Strategic Goals. The center anticipates funding of $25,000 (direct costs) for each project. The center encourages junior faculty to apply, especially those who are involved in interdisciplinary environmental health collaborations, for example between engineers and scientists. Projects can be anywhere on the spectrum between basic sciences and clinical translation. In all cases, the trajectory to human application must be clear and feasible. Translational Pilot Projects will be evaluated separately from those in the basic sciences. These projects are funded through the generosity of Vilma and Lionel Kinney, and are named in honor of Theron G. Randolph, a pioneer in the fields of environmental and natural products medicine. Applicants should submit a four-page research plan that outlines the specific aims and research strategy (i.e. significant, innovation, and approach). In the project title, please add a parenthesis indicating (Basic Research) or (Translational Research). Applications should also include a detailed budget form (Form Page 4), budget justification, and a biographical sketch using the NIH PHS398 forms. Please note that travel for scientific conferences/meetings are not allowed with these funds. Questions regarding the application process or proposal ideas should be directed to Professor Bevin P. Engelward, deputy director. Deadline for this call is May 31 with an anticipated start date of July 1. Completed applications should be submitted via email to: Amanda Tat, administrative officer of the CEHS.


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 | November 29, 2016
Site: www.eurekalert.org

In a small study of young or recently retired NFL players, researchers at Johns Hopkins report finding evidence of brain injury and repair that is visible on imaging from the players compared to a control group of men without a history of concussion. In a report on the study that used positron emission tomography (PET) and MRI, published in JAMA Neurology on Nov. 28, the researchers highlighted the value of PET imaging to monitor a marker of injury and repair in the brains of NFL players and athletes in other contact sports. The new research builds on a rising tide of anecdotal evidence and a few scientific studies suggesting that people with repeated concussive head injuries incurred while playing football, hockey or boxing are at higher-than-normal risk of developing the neurodegenerative disease called chronic traumatic encephalopathy (CTE). CTE is associated with memory deficits, confusion, poor decision-making and later onset of dementia. However, because CTE is often only diagnosed at autopsy, and because similar symptoms may occur in people without repeated head injuries, researchers, including those at Johns Hopkins Medicine, have been developing methods to better visualize tissue damage in the living brain to demonstrate better cause and effect. "The exciting part of our new findings is that we now believe we have a useful tool to monitor the brains of NFL players and athletes in other contact sports," says Jennifer Coughlin, M.D., assistant professor of psychiatry and behavioral sciences at Johns Hopkins. "We can measure TSPO, a PET biomarker of brain injury, in these younger players, and we can now begin to follow it over time to see if the brain is repairing itself or not." In early 2015, the Johns Hopkins research team published PET imaging results showing higher levels of this same biomarker in the brains of nine elderly former NFL players compared to control participants. However, since they initially studied elderly players who were many years from play, the researchers were unable to tell if the findings were also linked to aging and vascular disease, independent of past NFL play. For the new study, the researchers collected PET imaging data from 11 men without a history of concussion and compared the scans to those of 12 young NFL players, all of whom were still active or had retired within the past 12 years. All players had a self-reported history of at least one concussion. These players were an average age of 31 years old. About 80 percent were Caucasian and 20 percent were African-American. The control participants were matched to the players by body mass index, age and education level. The PET imaging was acquired using a radioactive chemical that binds to translocator protein 18 kDa (TSPO), which is normally found at low levels in healthy brain tissue. Since TSPO is increased during cellular response to brain injury, high levels of the TSPO signal on each PET scan can indicate where injury and reparative processes occur. The researchers found higher radiotracer binding to TSPO in players compared to control participants in eight of the 12 brain regions studied. These regions included the hippocampus, a region functionally involved in memory. Separately, the researchers examined data from MRI scans to look for structural changes in the brains of the study participants. They found no evidence of brain tissue loss in players compared to control participants in any of the brain regions examined, yet they did find some evidence of white matter changes in the players' brains. "We suspect that when the brain moves during a hard hit, it causes a shearing injury of the white matter fibers that travel across the brain," says Coughlin. Coughlin cautioned that there are some limitations to the imaging technique. For example, the radiotracer used in the PET scans doesn't work well in people with a specific variation in the gene that codes for TSPO protein, which occurs in about one in 10 people of European descent. Also, the researchers observed that use of creatine supplements -- taken by athletes to improve performance -- may interfere with the imaging results, necessitating further study of this effect before including participants taking creatine. "With further research using this technology, we may better understand the relationship between concussion and brain damage," says Coughlin. "Further understanding may help inform players of associated risk, and will allow us to test preventive and therapeutic interventions that may improve the lives of players." According to Centers for Disease Control and Prevention estimates, anywhere from 1.6 to 3.8 million concussions happen each year in the U.S. because of sports or recreational activities. Other researchers contributing to the study include Yuchuan Wang, Il Minn, Nicholas Bienko, Emily Ambinder, Xin Xu, Matthew Peters, John Dougherty, Melin Vranesic, Soo Min Koo, Hye-Hyun Ahn, Merton Lee, Chris Cottrell, Haris Sair, Akira Sawa, Cynthia Munro, Robert Dannals, Constantine Lyketsos, Gwenn Smith, Brian Caffo, Susumu Mori and Martin Pomper of The Johns Hopkins University; Christopher Nowinski of Boston University; Michael Kassiou of the University of Sydney; and Tomas Guilarte of Florida International University. The study was funded by the Brain and Behavior Research Foundation, the Alexander Wilson Schweizer Fellowship, the National Institute of Environmental Health Sciences (NIEHS-ES007062) and the GE/NFL Head Health Challenge. The funders had no role in designing, conducting or reporting on the study results.


The MIT Center for Environmental Health Sciences (CEHS), an interdisciplinary research center funded by the National Institute of Environmental Health Sciences (NIEHS), invites MIT faculty and research staff with principal investigator privileges to submit applications for funding of pilot projects related to environmental health, to support either basic or translational research. Please see the NIEHS strategic plan to gain understanding of the types of projects the center plans to fund. Preference is given to projects that address the NIEHS Strategic Goals. The center anticipates funding of $25,000 in direct costs for each project. The center encourages proposals from junior faculty, any faculty member wishing to branch into new areas of environmental health research, and faculty who are involved in interdisciplinary environmental health collaborations — for example between engineers and scientists.  Projects can be anywhere on the spectrum between basic sciences and clinical translation. In all cases, the trajectory to human application must be clear and feasible. Translational pilot projects will be evaluated separately from those in the basic sciences. These projects are funded through the generosity of Vilma and Lionel Kinney, and are named in honor of Theron G. Randolph, a pioneer in the fields of environmental and natural products medicine. Applicants should submit a four-page research plan that outlines the specific aims and research strategy (i.e. significant, innovation, and approach). In the project title, please add a parenthesis indicating (Basic Research) or (Translational Research). Applications should also include a detailed budget form (Form Page 4), budget justification, and a biographical sketch using the NIH PHS398 forms. Completed applications should be submitted via email to Amanda Tat, administrative officer of the CEHS at atat@mit.edu. Questions regarding the application process should be directed to Professor John M. Essigmann at jessig@mit.edu or Professor Bevin P. Engelward at bevin@mit.edu. Deadline for this call is June 30, with an anticipated start date of Sept. 1. Please visit the program website for more information.


However, people can control what they eat, and healthful dietary choices might help the body put up a natural defense system against the adverse effects of environmental toxicants. Investigators at the University of Kentucky Superfund Research Center (UK-SRC) were the first to obtain evidence that healthy nutrients and biological components rich in plant-derived diets, as well as increased physical activity, can counteract the negative effects of environmental pollutants. Such pollutants, which include polychlorinated biphenyls (PCBs), remain in the environment for a long time and can accumulate in the body. The study, led by nutritional biochemist and UK-SRC director Bernhard Hennig, was featured this month as a National Institute of Environmental Health Science/National Institutes of Health "Story of Success." These online articles highlight NIEHS/NIH-funded scientists working in a variety of disciplines and performing groundbreaking research into how the environment influences the development and progression of disease. PCBs, which were banned from industrial uses decades ago for hazardous effects, continue to exist in soil, water, air and sediments, especially in areas designated by the Environmental Protection Agency (EPA) as Superfund sites. Researchers in the UK-SRC investigate persistent organic pollutants common at Superfund sites in Kentucky with the objective of detecting and reducing such toxic chemicals from the environment. Biomedical researchers in the UK-SRC are interested in discovering whether nutrition, or the type of food we eat, can modulate the adverse effects of environmental pollutant exposure at the molecular level, utilizing mostly cell culture and animal models. Major findings suggest that consuming healthful diets rich in nutrients with antioxidant and anti-inflammatory properties, such as green tea-derived polyphenols, can reduce the disease risk caused by exposure to PCBs. The results of a recent animal-model study, which was selected as a Research Brief for the National Institutes of Environmental Health's website, show an interaction between dioxin-like PCBs and a biomarker for cardiovascular disease. Exposure to a dioxin-like PCB was associated with increased production of a biomarker for cardiovascular disease called trimethylamine N-oxide (TMAO), which is produced when the body metabolizes animal-derived foods including dairy and meat. Several studies have shown an association between TMAO and a high risk for cardiovascular disease in animals and in humans. The UK study was the first to suggest that exposure to dioxin-like PCBs can increase the circulating level of TMAO in the body, and the researchers proposed that PCBs contribute to individual variability of a common biomarker for cardiovascular disease. The researchers observed an association of higher levels of PCB in the blood with the metabolic process that produces TMAO. The researchers believe this mechanism reveals a link between exposure to PCBs, diet and cardiovascular disease risk. Hennig said their research generated optimistic findings with evidence that people can potentially moderate the adverse effects of ubiquitous pollutants through dietary choices. Hennig said the research within the UK-SRC gives insight into how stressful chemical elements interact in the body and create a ripple effect in human cells that leads to dysfunction and disease. Understanding the interplay of diet and chemical toxicity in the development of many diseases will allow health providers to recommend healthful nutrition to fight disease risks associated with exposure to environmental pollutants and related chemical toxicants. "The idea is that healthful nutrition, and even physical activity or exercise, is helpful and it actually makes you less vulnerable to disease potential that is a result of exposure to these pollutants," Hennig said. Hennig, with fellow UK-SRC scientists Andrew Morris and Michael Petriello, will continue work with researchers at the Centers for Disease Control (CDC) to explore mechanisms of diet-derived biomarkers like TMAO and leverage this knowledge for human health. They will test blood samples of individuals exposed to high levels of PCB living in Alabama to verify their findings in animals which suggest associations between PCB exposure, high circulating levels of TMAO and an increased risk for cardiovascular diseases. Hennig is hopeful that their continued research will show that healthy dietary choices, such as diets rich in fruits and vegetables, can reduce the negative impacts of chemical stressors that can contribute to heart disease, atherosclerosis and stroke. "There is a lot of opportunity throughout life for this disease to be modified," Hennig said. "Individual food components can modulate environmental stressors, and nutritional interventions may provide the most sensible means to develop primary prevention strategies of diseases associated with many environmental toxic insults." More information: Michael C. Petriello et al. Dioxin-like pollutants increase hepatic flavin containing monooxygenase (FMO3) expression to promote synthesis of the pro-atherogenic nutrient biomarker trimethylamine N-oxide from dietary precursors, The Journal of Nutritional Biochemistry (2016). DOI: 10.1016/j.jnutbio.2016.03.016


News Article | November 7, 2016
Site: www.sciencedaily.com

Today's release of the U.S. Department of Health and Human Services 14th Report on Carcinogens includes seven newly reviewed substances, bringing the cumulative total to 248 listings. The chemical trichloroethylene (TCE), and the metallic element cobalt and cobalt compounds that release cobalt ions in vivo, are being added to the list, as well as five viruses that have been linked to cancer in humans. The five viruses include human immunodeficiency virus type 1, human T-cell lymphotropic virus type 1, Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, and Merkel cell polyomavirus. "Given that approximately 12 percent of human cancers worldwide may be attributed to viruses, and there are no vaccines currently available for these five viruses, prevention strategies to reduce the infections that can lead to cancer are even more critical," said Linda Birnbaum, Ph.D., director of the National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP). "The listings in this report, particularly the viruses, bring attention to the important role that prevention can play in reducing the world's cancer burden. There are also things people can do to reduce their exposure to cobalt and TCE." The Report on Carcinogens is a congressionally mandated report prepared for the HHS Secretary by NTP. The report identifies many different types of environmental factors, collectively called substances, including chemicals; infectious agents, such as viruses; physical agents, such as X-rays and ultraviolet radiation; mixtures of chemicals; and exposure scenarios in two categories -- known to be a human carcinogen and reasonably anticipated to be a human carcinogen. It's important to note that a listing in the report indicates a cancer hazard, but does not by itself mean that a substance or a virus will cause cancer. Many factors, including an individual's susceptibility to a substance, and the amount and duration of exposure, can affect whether a person will develop cancer. In the case of viruses, a weakened immune system may also be a contributing factor. People should talk to their health care providers about decreasing their cancer risk from viruses. All five viruses are being added to the category of known to be a human carcinogen. Collectively, these viruses have been linked to more than 20 different types of cancers. Trichloroethylene (TCE) is an industrial solvent used primarily to make hydrofluorocarbon chemicals. It is being listed in the Report on Carcinogens as a known human carcinogen. Since 2000, TCE had been listed as a reasonably anticipated human carcinogen. However, numerous human studies showing a causal association between TCE exposure and an increased risk for kidney cancer have led NTP to reevaluate and reclassify TCE as known to be a human carcinogen. There are many ways people can be exposed to TCE. It can be released into the air, water, and soil at places where it is produced or used. It breaks down slowly and can move readily through soil to make its way into underground drinking water sources. Because of its widespread use as a metal degreasing agent to maintain military equipment, it has been found in the groundwater at many military and Superfund sites. Cobalt and cobalt compounds that release cobalt ions in vivo Cobalt and cobalt compounds that release cobalt ions in vivo are being listed as reasonably anticipated to be a human carcinogen. The listing for cobalt includes different types of cobalt compounds that release ions into the body. It does not include vitamin B-12, because cobalt in this essential nutrient is bound to protein and does not release cobalt ions. Cobalt is a naturally occurring element used to make metal alloys and other metal compounds, such as military and industrial equipment, and rechargeable batteries. The highest exposure occurs in the workplace and from failed surgical implants. The listing for this metal and its compounds is based largely on studies in experimental animals. The new report is available at http://ntp.niehs.nih.gov/go/roc14.


News Article | November 4, 2016
Site: www.gizmag.com

You likely already know that cigarettes and certain types of radiation cause cancer, but there are actually over 200 other substances in the U.S. National Institutes of Health (NIH) just-released 14th annual Report on Carcinogens (ROC) that are believed to lead to malignant tumors in human beings. And seven of those were just added. Five of the new substances added are actually viruses that either cause cancer directly or make it easier for other cancer-causing viruses to do their deadly work. They include: Human immunodeficiency virus type 1 (HIV-1); Human T-cell lymphotropic virus type 1 (HTLV-1); Epstein-Barr virus (EBV); Kaposi sarcoma-associated herpesvirus (KSHV); Merkel cell polyomavirus (MCV). All five of these viruses are classified as "Known to be a human carcinogen," as opposed to the agency's other category of "Reasonably anticipated to be a human carcinogen." "Given that approximately 12 percent of human cancers worldwide may be attributed to viruses, and there are no vaccines currently available for these five viruses, prevention strategies to reduce the infections that can lead to cancer are even more critical," said Linda Birnbaum, Ph.D., director of the National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP). "The listings in this report, particularly the viruses, bring attention to the important role that prevention can play in reducing the world's cancer burden." HIV-1 made the list because it serves up a double threat. It has not only been implicated in increasing the risk of cancer, including non-melanoma skin cancer, eye cancer, and possibly lung cancer, but by weakening the immune system it allows other cancer-causing viruses to move in, which can lead to "non-Hodgkin and Hodgkin lymphomas; anogenital cancers, including penile, vaginal/vulvar, cervix, and anal; Kaposi sarcoma; and possibly oral-related cancers and liver cancer," according to the agency. As for Epstein-Barr, the NIH says that 90 percent of all adults are already infected with the herpes-related virus but most of our immune systems hold it in check. It has, however been implicated in four types of lymphoma: "Burkitt, Hodgkin, immune-suppression-related non-Hodgkin, and nasal type extranodal NK/T-cell — and two types of epithelial cancer — nasopharyngeal cancer and some types of stomach cancer," says the agency. In addition to the five viruses, the industrial solvent Trichloroethylene (TCE) has received a bump in status from "reasonably anticipated human carcinogen" to "known human carcinogen" due to its role in increasing kidney cancer risk. "There are many ways people can be exposed to TCE," says the NIH. "It can be released into the air, water, and soil at places where it is produced or used. It breaks down slowly and can move readily through soil to make its way into underground drinking water sources. Because of its widespread use as a metal degreasing agent to maintain military equipment, it has been found in the groundwater at many military and Superfund sites." "Cobalt is a naturally occurring element used to make metal alloys and other metal compounds, such as military and industrial equipment, and rechargeable batteries," says the agency. "The highest exposure occurs in the workplace and from failed surgical implants. The listing for this metal and its compounds is based largely on studies in experimental animals." Cobalt is also found in Vitamin B12, but because the cobalt is bound to proteins in the vitamin, it does not release ions in the body and therefore is not considered a carcinogen. When cobalt ions are taken up in the cell, they can interfered with the DNA repair process and cause other damaging effects that could lead to cancer, although the method through which the ions can lead to tumor growth is still not thoroughly understood. Cobalt ions replace cobalt sulphate in the report, which was added to the list in 2004. Substances are reviewed for the ROC by the NIH's National Toxicology Program (NTP) after being submitted by researchers and after a period of public commentary. The full process can be seen in the infographic below. The complete 14th annual Report on Carcinogens is available to the public as a PDF from the NTP.


News Article | November 3, 2016
Site: www.eurekalert.org

Today's release of the U.S. Department of Health and Human Services 14th Report on Carcinogens includes seven newly reviewed substances, bringing the cumulative total to 248 listings. The chemical trichloroethylene (TCE), and the metallic element cobalt and cobalt compounds that release cobalt ions in vivo, are being added to the list, as well as five viruses that have been linked to cancer in humans. The five viruses include human immunodeficiency virus type 1, human T-cell lymphotropic virus type 1, Epstein-Barr virus, Kaposi sarcoma-associated herpesvirus, and Merkel cell polyomavirus. "Given that approximately 12 percent of human cancers worldwide may be attributed to viruses, and there are no vaccines currently available for these five viruses, prevention strategies to reduce the infections that can lead to cancer are even more critical," said Linda Birnbaum, Ph.D., director of the National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP). "The listings in this report, particularly the viruses, bring attention to the important role that prevention can play in reducing the world's cancer burden. There are also things people can do to reduce their exposure to cobalt and TCE." The Report on Carcinogens is a congressionally mandated report prepared for the HHS Secretary by NTP. The report identifies many different types of environmental factors, collectively called substances, including chemicals; infectious agents, such as viruses; physical agents, such as X-rays and ultraviolet radiation; mixtures of chemicals; and exposure scenarios in two categories -- known to be a human carcinogen and reasonably anticipated to be a human carcinogen. The new report is available at http://ntp. . It's important to note that a listing in the report indicates a cancer hazard, but does not by itself mean that a substance or a virus will cause cancer. Many factors, including an individual's susceptibility to a substance, and the amount and duration of exposure, can affect whether a person will develop cancer. In the case of viruses, a weakened immune system may also be a contributing factor. People should talk to their health care providers about decreasing their cancer risk from viruses. All five viruses are being added to the category of known to be a human carcinogen. Collectively, these viruses have been linked to more than 20 different types of cancers. Trichloroethylene (TCE) is an industrial solvent used primarily to make hydrofluorocarbon chemicals. It is being listed in the Report on Carcinogens as a known human carcinogen. Since 2000, TCE had been listed as a reasonably anticipated human carcinogen. However, numerous human studies showing a causal association between TCE exposure and an increased risk for kidney cancer have led NTP to reevaluate and reclassify TCE as known to be a human carcinogen. There are many ways people can be exposed to TCE. It can be released into the air, water, and soil at places where it is produced or used. It breaks down slowly and can move readily through soil to make its way into underground drinking water sources. Because of its widespread use as a metal degreasing agent to maintain military equipment, it has been found in the groundwater at many military and Superfund sites. Cobalt and cobalt compounds that release cobalt ions in vivo Cobalt and cobalt compounds that release cobalt ions in vivo are being listed as reasonably anticipated to be a human carcinogen. The listing for cobalt includes different types of cobalt compounds that release ions into the body. It does not include vitamin B-12, because cobalt in this essential nutrient is bound to protein and does not release cobalt ions. Cobalt is a naturally occurring element used to make metal alloys and other metal compounds, such as military and industrial equipment, and rechargeable batteries. The highest exposure occurs in the workplace and from failed surgical implants. The listing for this metal and its compounds is based largely on studies in experimental animals. The Report on Carcinogens, 14th Edition, is prepared by the National Toxicology Program (NTP). NTP is a federal, interagency program, headquartered at the NIEHS, whose goal is to safeguard the public by identifying substances in the environment that may affect human health. For more information about NTP and its programs, visit http://ntp. . 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 (http://www. ) 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. .


PHILADELPHIA -- (Feb. 27, 2017) -- Scientists at The Wistar Institute in collaboration with Roswell Park Cancer Institute found a significant association between a rare genetic variant of the p53 gene present in African American women and their risk of developing breast cancer in premenopausal age. The study was published online by the journal NPJ Breast Cancer. TP53 is the most frequently mutated gene in human cancer. The p53 protein is a critical tumor suppressor in the cell and genetic mutations that occur in cancer cause a loss of its function in regulating proliferation arrest and cell death. In addition to these changes, there are several minor, naturally occurring genetic variants of the p53 gene, also known as polymorphisms, and some of them are associated with an increased risk of cancer. The rare p53 polymorphism analyzed in this study is found almost exclusively in populations of African descent. Wistar scientists have previously shown that this polymorphism impairs the ability of p53 to induce cell death in vitro and significantly increases cancer risk when recreated in a mouse model. The new study analyzed the statistical association of this variant with the risk of developing breast cancer in African American women. "Based on our previous studies on the functional effects of this genetic variant on the p53 protein, we sought to verify if it alters cancer risk in human carriers," said Maureen Murphy, Ph.D., professor and program leader of the Molecular and Cellular Oncogenesis Program at Wistar and senior author of the study. "This genetic variant is present exclusively in people of African descent, so our study addresses cancer disparities in African American women, a historically underrepresented group in research studies." "Our results show that the risk of developing breast cancer is increased by nearly 70 percent in premenopausal women who carry this polymorphism," Murphy said. "Because its frequency is very low in the African American population, larger studies will be needed to confirm our observations." Murphy and colleagues conducted statistical studies on a cohort of more than 14,000 women of African descent and didn't find any association of the polymorphism with increased breast cancer risk overall. However, as previously observed with other genetic variants of p53, a significant association was present in women in premenopausal age. Elucidating the effects of p53 polymorphisms on cancer risk is a challenging task, especially due to the limited availability of sample cohorts from specific populations. This study provides a strong suggestion that the genetic variant considered might be associated with a significant increase in breast cancer risk, although this association will need to be confirmed in a larger sample set. This work was supported by National Institutes of Health grants R01 CA102184, CA201430, P01 CA151135, R01 CA092447, R01 CA135288, P01 CA82707, R25-CA57726, NICHD-N01-HD-3-3175, NCO-N01-PC-67010, NIEHS-ES07084, R01 CA142996, P50 CA125183, R01 CA89085, and U01 CA161032; National Cancer Institute grant UM1CA164974 and the Intramural Research Program of the National Cancer Institute, Center for Cancer Research; grants from the Breast Cancer Research Foundation, the University Cancer Research Fund of North Carolina, the Department of Defense Breast Cancer Research Program, the Era of Hope Scholar Award Program W81XWH-08-1-0383, the Komen Foundation for the Cure, and the Stacy Goldstein Faculty Scholar Award. Core support for The Wistar Institute and the Rutgers Cancer Institute of New Jersey was provided by the Cancer Center Support Grants P30CA010815 and P30CA072720, respectively. Qin Liu is a co-author of this study from The Wistar Institute. Other co-authors include: Song Liu, Chi-Chen Hong, Qiang Hu and Christine B. Ambrosone from Roswell Park Cancer Institute; Dezheng Huo and Olufunmilayo I. Olopade from the University of Chicago; Sonia C. Dolfi and Kim M. Hirshfield from Rutgers Cancer Institute of New Jersey; Andrew F. Olshan and Sarah Nyante from University of North Carolina; Temidayo O. Ogundiran from University of Ibadan, Nigeria; Clement Adebamowo from University of Maryland; Susan M. Domchek and Katherine L. Nathanson from the University of Pennsylvania; Barbara Nemesure from Stony Brook University; Stefan Ambs and Regina G. Ziegler from National Cancer Institute; William J. Blot, Wei Zheng and Sandra L. Deming from Vanderbilt University; Ye Feng, Sue A. Ingles, Michael F. Press and Christopher A. Haiman from University of Southern California; Esther M. John from Stanford University; Leslie Bernstein from Beckman Research Institute; Jennifer J. Hu and Jorge L. Rodriguez-Gil from University of Miami; Kathryn L. Lunetta and Julie R. Palmer from Boston University. The Wistar Institute is an international leader in biomedical research with special expertise in cancer research and vaccine development. Founded in 1892 as the first independent nonprofit biomedical research institute in the United States, Wistar has held the prestigious Cancer Center designation from the National Cancer Institute since 1972. The Institute works actively to ensure that research advances move from the laboratory to the clinic as quickly as possible. wistar.org.

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