healthcarebriefing.com

Author: admin

Preeclampsia Linked to Neurologic Disease in Full-Term Babies

You don’t have permission to access “http://www.medpagetoday.com/psychiatry/generalpsychiatry/85756” on this server.

Reference #18.30f2da17.1792073476.12dfc5d

https://errors.edgesuite.net/18.30f2da17.1792073476.12dfc5d

April 1, 2020
COVID-19 Workers Get Training to Protect Their Own Health

Today, the National Institutes of Health will launch a new website with important educational resources for Coronavirus workers dealing with the spread of COVID-19. The initiative got underway after Congress passed a supplemental appropriation of $10 million on March 6 “for worker-based training to prevent and reduce exposure of hospital employees, emergency first responders, and other workers who are at risk of exposure to coronavirus through their work duties.” The law provided a total of $8.3 billion in emergency funding for certain Federal agencies to respond to the coronavirus outbreak.

The worker-based training initiative is being led by NIH’s National Institute of Environmental Health Sciences (NIEHS), which has a long-established Worker Training Program (WTP). The program awards grants for training and development of educational resources for employees in high risk occupations who serve the public during emergencies and who need skills to protect their own health as they are potentially exposed to dangerous pathogens, contaminated materials, or infected people. As a part of this effort the Worker Training Program also acts as a clearinghouse among grant recipients to broadly share the training and educational resources developed with the grant money.

Joseph “Chip” Hughes, who has led the NIEHS Worker Training Program for 31 years, said, “These men and women are so dedicated and as they work so hard to serve and protect the public during this COVID-19 pandemic, I want to make sure they know how to protect their own health too. We don’t need them getting sick or taking the virus back to their families or their communities.”

With this new supplemental funding from Congress, the NIEHS Worker Training Program is creating a COVID-19 virtual safety training initiative for frontline responders including emergency medical personnel, firefighters, law enforcement officers, environmental cleanup workers, high-risk custodial service workers, food processing and delivery workers, water and sewage treatment workers, sanitation workers, and health care facility employees.

The initial focus is to build a virtual safety training delivery platform in partnership with private sector e-learning companies with the capability to deliver synchronized just-in-time web-based training across the country in targeted high-risk industrial sectors. Additionally, a cadre of COVID-19 safety trainers and virtual safety advisors is being created to leverage the delivery of advanced training technology to frontline responders.

After learning of the special appropriation, NIEHS moved quickly to convene a national workshop in partnership with Emory Health Sciences Center on March 17. The workshop titled, “Protecting Infectious Disease Responders During the COVID-19 Outbreak,” used virtual meeting technology to bring together hundreds of the country’s infectious disease experts, nurses and health care providers, emergency response organizations and academic training centers to map out a web-based, technology-assisted training strategy to respond to the escalating need to ensure protections for COVID-19 responders, particularly in health care and emergency response services.

During a recent Congressional hearing on COVID-19 response, NIH Director Francis Collins, M.D., testified that “NIEHS has played a very critical role in training people who can deal with outbreaks.” He noted the NIEHS Worker Training Program previously helped with the Ebola response.

NIEHS Worker Training Program grant recipients provided occupational safety training to workers during the anthrax attacks in 2001, the H5N1 outbreak in 2007, and the H1N1 avian influenza outbreak in 2009; mold remediation training following Hurricanes Katrina in 2005 and Hurricane Sandy in 2012; and Ebola virus disease preparedness training 2013-2015. A list of program grantees is available.

This COVID-19 virtual safety training program will be administered by NIEHS and was developed in collaboration with the Centers for Disease Control and Prevention, the U.S. Department of Health and Human Services Office of the Assistant Secretary for Preparedness and Response, the Occupational Safety and Health Administration, and the National Institute for Occupational Safety and Health.

Press Resources:

Demonstration Video

March 23, 2020
Using “organs-on-a-chip” to Model Complicated Diseases

MIT biological engineers have created a multitissue model that lets them study the relationships between different organs and the immune system, on a specialized microfluidic platform seeded with human cells.

Using this type of model, sometimes called “organs-on-a-chip” or “physiome on-a-chip,” the research team was able to explore the role of circulating immune cells in ulcerative colitis and other inflammatory diseases. They also discovered that a metabolic byproduct generated by bacteria living in the human gut plays an important role under these inflammatory conditions.

“We’ve shown that now you can start to attack some of these really thorny, chronic inflammatory diseases by designing experiments in these organs on chips,” says Linda Griffith, the School of Engineering Professor of Teaching Innovation, a professor of biological engineering and mechanical engineering, and the senior author of the study.

This approach, described today in the journal Cell Systems, could also lend itself to studying many other complex diseases, the researchers say.

“Now we have options to really decrease or increase the level of disease complexity, under controlled and systematic conditions,” says Martin Trapecar, an MIT postdoc and the lead author of the paper.

Complex models

Nearly 20 years ago, Griffith’s lab first began working on a model of the human liver known as the “liver chip.” This system, which consists of engineered human liver tissue grown on a specialized scaffold, can be used to test drug toxicity. More recently, she has been working on small-scale replicas of many interconnected organs, also known as microphysiological systems (MPS). In 2018, she reported the development of a platform that could be used to model interactions between up to 10 organs at a time.

These kinds of devices are well-suited for analyzing complex diseases, including those that involve multiple organs, are influenced by the immune system, or cannot be accounted for by a single gene or small number of genes.

“We wanted to build technologies that would let you connect several organ systems together, so that we could start to develop new tools to combat chronic inflammatory diseases,” Griffith says. “In drug development, the field really struggles with anything that’s not a single-gene disease.”

In the new Cell Systems study, she and Trapecar set out to model interactions between two organs, the colon and the liver. They also wanted to study how the immune system, especially T cells, influences those organs. It is already known that up to 80 percent of patients with a chronic liver autoimmune disease called primary sclerosing cholangitis also suffer from inflammatory bowel disease (IBD). And, patients with IBD have a much greater chance of developing autoimmune disorders of the liver.

The new system contains colon cells taken from patients with ulcerative colitis, along with healthy liver cells. The researchers found that when these tissues were connected, their physiological behavior completely changed as compared to when they are isolated. Inflammation in ulcerative colitis gut tissue decreased when the tissue was exposed to healthy liver cells. At the same time, genes and cellular pathways involved in metabolism and immune function became more active in both organs.

The researchers then added two types of T cells to the system: CD4+ T regulatory cells, which suppress other immune cells, and TH17 cells, which stimulate inflammation. Adding these T cells to the gut-liver interaction quickly increased inflammation and recreated certain features of both IBD and autoimmune liver diseases.

Lastly, the researchers decided to investigate the potential role of molecules called short-chain fatty acids (SCFAs) in inflammatory disease. These molecules are produced by microbes in the human gut as they feast on undigested fiber. SCFAs, which include butyrate, propionate, and acetate, are produced in large quantities and account for about 10 percent of our daily energy needs.

While these compounds have many beneficial effects in the human body, including reducing inflammation, a few studies in recent years have suggested that SCFAs can also cause harm by stimulating inflammation. The new MIT study found that adding SCFAs to the ulcerative colitis model greatly exacerbated inflammation throughout the liver and gut, but only if T cells were already present.

“The hypothesis we formed, based on these studies, is that the role of short chain fatty acids seems to depend on how much the adaptive immune system (which includes T cells) is involved,” Trapecar says.

That is, in early stages of inflammation, when T cells are not heavily involved, SCFAs can help reduce inflammation. But when many effector T cells are recruited, SCFAs stimulate them to be even more inflammatory. This could be useful in cases of infection, to help the body to fend off invaders, but it can also accelerate autoimmune disorders.

Modeling brain disorders

This study grew out of a related project in which the researchers planned to look at interactions between the gut, liver, and brain. A recent study from Sarkis Mazmanian, a professor of microbiology at Caltech, showed that in a mouse model of Parkinson’s, germ-free mice developed signs of the disease later than those housed under regular conditions. The study suggested that SCFAs produced by microbes might contribute to the observed phenomena and progression of the disease.

Griffith’s lab is now working to use the MPS system to shed light on the connection between SCFAs and Parkinson’s disease. The researchers also plan to study other complex diseases, in hopes that their results will help guide the development of new treatments for disorders that are currently difficult to treat.

“You really need very complex models,” Griffith says. “You can certainly get hypotheses from animal models, but to really go forward in drug development, you need better ways to identify targets that build on samples from human patients.”

The research was funded by the U.S. Defense Advanced Research Projects Agency, the National Institutes of Health, the National Institute of Biomedical Imaging and Bioengineering, the National Institute of Environmental Health Sciences, the Koch Institute Support (core) Grant from the National Cancer Institute, and the Pew-Stewart Trust Foundation.

March 18, 2020
Health Benefits for Kids Outweigh Risks of Eating Fish During Pregnancy
To eat or not to eat fish is a question that has long concerned pregnant women. Now, a new USC study shows that children whose mothers ate fish from one to three times a week during pregnancy were more likely to have a better metabolic profile as they grow — despite the risk of exposure to mercury — than children whose mothers ate fish rarely (less than once a week).

The findings appear today in JAMA Network Open.

“Fish is an important source of nutrients, and its consumption should not be avoided,” said Leda Chatzi, MD, PhD, associate professor of Population and Public Health Sciences at the Keck School of Medicine at USC, and the senior investigator on the study. “But pregnant women should stick to one to three servings of fish a week as recommended, and not eat more, because of the potential contamination of fish by mercury and other persistent organic pollutants.”

Fish is a major source of omega-3 long-chain polyunsaturated fatty acids, which are important for the developing fetus. However, some types, such as swordfish, shark and mackerel, can contain high levels of mercury — a potent toxin that can cause permanent neurological damage. Mercury contamination is also found in soil, air, water and plants.

Researchers looked at 805 mother-and-child pairs from five European countries participating in a collaborative research project known as the HELIX study, which is following women and their children from pregnancy onward.

During their pregnancy, the women were asked about their weekly fish consumption and tested for mercury exposure. When the children were between 6 and 12 years old, they underwent a clinical examination with various measurements, including waist circumference, blood pressure, high-density lipoprotein cholesterol, triglyceride levels and insulin levels. These measures were combined to calculate a metabolic syndrome score.

More fish is not better

The children of women who ate fish from one to three times a week had lower metabolic syndrome scores than the children of women who ate fish less than once a week. (A lower score is better for health outcomes.) But the benefit declined if women ate fish more than three times a week.

“Fish can be a common route of exposure to certain chemical pollutants, which can exert adverse effects,“ said Nikos Stratakis, PhD, a USC postdoctoral scholar who was one of the study’s authors. “It is possible that when women eat fish more than three times a week, that pollutant exposure may counterbalance the beneficial effects of fish consumption seen at lower intake levels.”

The study found that higher mercury concentration in a woman’s blood was associated with a higher metabolic syndrome score in her child.

The study also examined how fish consumption by the mother affected the levels of cytokines and adipokines in her child. These biomarkers are related to inflammation, a contributor to metabolic syndrome. Compared with low fish intake, moderate and high fish consumption during pregnancy were associated with reduced levels of proinflammatory cytokines and adipokines in the children.

This is the first human study to show that reduction in these inflammation biomarkers could be the underlying mechanism explaining why maternal fish consumption is associated with improved child metabolic health.

Next, the researchers plan to look at the effects of consuming different types of fish with different nutrients and mercury levels. The goal is to follow up on these children until the age of 14-15 years.

About this study

In addition to Dr. Chatzi and Stratakis, the studies’ additional authors are David Conti, Shohreh F. Farzan and Rob McConnell from the Department of Population and Public Health Sciences, Keck School of Medicine, USC; Eva Borras and Eduardo Sabido from the CRG/UPF Proteomics Unit, Barcelona, Spain; Xavier Basagana, Mariona Bustamante, Maribel Casas, Dr. Serena Fossati, Juan R. Gonzalez, Lea Maitre, Jose Urquiza and Martine Vrijheid from the ISGlobal Institute, Barcelona, Spain; Theano Roumeliotaki and Marina Vafeiadi from the Department of Social Medicine, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece; Eleni Papadopoulou, Anne-Lise Brantsaeter, and Helle-Margrete Meltzer from the Department of Environmental Health, Norwegian Institute of Public Health, Oslo, Norway; Lydiane Agier from the Team of Environmental Epidemiology Applied to Reproduction and Respiratory Health, Inserm, CNRS, University Grenoble Alpes, Institute for Advanced Biosciences, U1209 Joint Research Center, La Tronche, Grenoble, France; Regina Grazuleviciene, the department of Environmental Sciences, Vytautas Magnus University, Kaunas, Lithuania; Barbara Heude, from Centre of Research in Epidemiology and Statistics, Inserm, Institut National de la Recherche Agronomique, Universite de Paris, Paris, France; Rosemary R. C. McEachan, Jane West and John Wright from the Bradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK; and Ioannis Theologidis from the Foundation for Research and Technology, Institute of Molecular Biology and Biotechnology, Heraklion, Greece.

This study was supported by the European Community Seventh Framework Program (Human Early Life Exposome Project, grant ID: 308333) and by the National Institute of Environmental Health Science (R01 ES029944, R21 ES029681, R21 ES028903, P30 ES007048-23, P01CA196569).

— Laura LeBlanc

Related:
March 16, 2020
Texas A&M Researchers Develop New Tool to Help Communities Access Environmental Risk Data

nginx

March 16, 2020
The Complex Biology Behind Your Love (or Hatred) of Coffee

(Credit: Marina Keremkhanova/Shutterstock)

Why do some people feel like they need three cups of coffee just to get through the day when others are happy with only one? Why do some people abstain entirely? New research suggests that our intake of coffee – the most popular beverage in America, above bottled water, sodas, tea, and beer – is affected by a positive feedback loop between genetics and the environment.

This phenomenon, known as “quantile-specific heritability,” is also associated with cholesterol levels and body weight, and is thought to play a role in other human physiological and behavioral traits that defy simple explanation.

“It appears that environmental factors sort of set the groundwork in which your genes start to have an effect,” said Paul Williams, a statistician at Lawrence Berkeley National Laboratory (Berkeley Lab). “So, if your surroundings predispose you to drinking more coffee – like your coworkers or spouse drink a lot, or you live in an area with a lot of cafes – then the genes you possess that predispose you to like coffee will have a bigger impact. These two effects are synergistic.”

Williams’ findings, published in the journal Behavioral Genetics, came from an analysis of 4,788 child–parent pairs and 2,380 siblings from the Framingham Study – a famous, ongoing study launched by the National Institutes of Health in 1948 to investigate how lifestyle and genetics affect rates of cardiovascular disease. Participants, who are all related to an original group from Framingham, Massachusetts, submit detailed information about diet, exercise, medication use, and medical history every three to five years. Data from the study have been used in thousands of investigations into many facets of human health.

A dose of statistics

Paul T. Williams. (Credit: Roy Kaldschmidt/Berkeley Lab)

Williams used a statistical approach called quantile regression to calculate what proportion of participants’ coffee drinking could be explained by genetics – as the study follows families – and what must be influenced by external factors. Past research shows that the most significant environmental factors influencing coffee drinking are culture and geographic location, age, sex, and whether or not one smokes tobacco; with older male smokers of European ancestry drinking the most, overall.

The analysis indicated that between 36% and 58% of coffee intake is genetically determined (although the exact causative genes remain unknown). However, confirming Williams’ hypothesis that coffee drinking is a quantile-specific trait, the correlation between a parent’s coffee drinking and an offspring’s coffee drinking got increasingly stronger for each offspring’s coffee consumption quantile, or bracket (for example, zero cups per day, one to two cups, two to four cups, and five or more cups).

“When we started to decode the human genome, we thought we’d be able to read the DNA and understand how genes translate into behavior, medical conditions, and such. But that’s not the way it’s worked out,” said Williams, who is a staff scientist in Berkeley Lab’s Molecular Biophysics & Integrated Bioimaging (MBIB) Division. “For many traits, like coffee drinking, we know that they have a strong genetic component – we’ve known coffee drinking runs in families since the 1960s. But, when we actually start looking at the DNA itself, we usually find a very small percentage of the traits’ variation can be attributed to genes alone.”

The traditional assumption in genetic research has been that one’s surroundings and lifestyle alter gene expression levels in consistent and measurable ways, ultimately creating the outward manifestation – called a phenotype – of a trait. Williams’ statistics work shows that the situation is more complex, which helps explain the diversity of traits we see in the real world.

MBIB Division Director Paul Adams commented, “Paul’s statistical studies complement the genomics research that Berkeley Lab bioscientists conduct to learn more about the relationship between genes and the environment.”

Next, Williams plans to assess whether quantile-specific heritability plays a role in alcohol consumption and pulmonary function. “This is a whole new area of exploration that is just now opening up,” he said. “I think it will change, in a very fundamental way, how we think genes influence a person’s traits.”

This research was funded by a grant from the National Institute of Environmental Health Sciences and a gift from HOKA ONE ONE. The Framingham Study Data were made available through the Biologic Specimen and Data Repository Information Coordinating Center of the National Heart, Lung, and Blood Institute.

# # #

Founded in 1931 on the belief that the biggest scientific challenges are best addressed by teams, Lawrence Berkeley National Laboratory and its scientists have been recognized with 13 Nobel Prizes. Today, Berkeley Lab researchers develop sustainable energy and environmental solutions, create useful new materials, advance the frontiers of computing, and probe the mysteries of life, matter, and the universe. Scientists from around the world rely on the Lab’s facilities for their own discovery science. Berkeley Lab is a multiprogram national laboratory, managed by the University of California for the U.S. Department of Energy’s Office of Science.

DOE’s Office of Science is the single largest supporter of basic research in the physical sciences in the United States, and is working to address some of the most pressing challenges of our time. For more information, please visit energy.gov/science.

March 5, 2020
Women Firefighters Face High Exposure to Toxic ‘Forever Chemicals’

Study is part of a larger investigation into female firefighters’ risk of breast cancer

By Kara Manke

Maiko Bristow, a firefighter and EMT with the San Francisco Fire Department, is part of a long-term investigation into breast cancer risks experienced by women firefighters. (UC Berkeley photo by Brittany Hosea-Small)

February 26, 2020

Maiko Bristow, a firefighter and EMT with the San Francisco Fire Department, is part of a long-term investigation into female firefighter’s risk of breast cancer. (UC Berkeley photo by Brittany Hosea-Small)

San Francisco’s women firefighters are exposed to higher levels of certain toxic PFAS chemicals than women working in downtown San Francisco offices, shows a new study led by researchers at the University of California, Berkeley, the University of California, San Francisco, and Silent Spring Institute.

Per- and polyfluoroalkyl substances (PFAS) are used in grease- and water-resistant coatings and can be found in fabrics, furniture and food packaging, but also notably in firefighting foam and turnout gear. These “forever chemicals,” which don’t easily break down in the environment, have been linked to a variety of cancers and are known to interfere with immune function, endocrine function and breast development.

The study, which appears online today (Wednesday, Feb. 26) in the journal Environmental Science and Technology, is one of the first published results from the Women Firefighter Biomonitoring Collaborative, a long-term investigation into the chemical exposures faced by women firefighters. Partners in the collaboration include the United Fire Service Women, the San Francisco Cancer Prevention Foundation, Commonweal and Breast Cancer Prevention Partners.

“Women firefighters actually raised concern about what they have perceived as elevated rates of breast cancer among their cohort in San Francisco,” said Jessica Trowbridge, a graduate student at UC Berkeley and lead author of the paper. “As a team, we decided to conduct an exposure study looking at chemicals that are potential breast carcinogens.”

While studies are beginning to document higher rates of cancer among firefighters and higher PFAS exposures, in particular, these studies have primarily focused on men. Documenting the risks faced specifically by women firefighters is critical to ensuring that they receive the protections they need, both for cancer prevention and for compensation if they get sick.

“This is the first study, to our knowledge, that’s been done on women firefighters,” said Rachel Morello-Frosch, a professor of public health and of environmental science, policy and management at UC Berkeley and senior author of the paper. “The idea of characterizing women’s workplace exposures is something that few people are paying any attention to, and here, we are using the newest available technologies to start to do that.”

San Francisco is ideal location for this investigation because it has more women firefighters than any other urban fire department in the country. Women make up approximately 15% of the San Francisco fire force, compared to about 5% nationwide. This is due, in part, to 1980s litigation and a consent decree that encouraged the department to hire more women and people of color.

“Women firefighters have benefitted from these well-paid, very honorable professions and now are facing similar concerns about the impacts on their health that studies have demonstrated in men,” Morello-Frosch said.

Firefighting foam and turnout gear, such as helmets, boots, and jackets, can be sources of PFAS exposure. UC Berkeley photo by Brittany Hosea-Small

‘Is our job causing cancer?’

In 2012, Lt. Heather Buren, along with colleagues form the San Francisco Firefighters Cancer Prevention Foundation (SFFCPF) noticed an alarming trend: In that year alone, five female firefighters were diagnosed with breast cancer.

“We started asking questions, wondering what was up,” said Buren, co-author of the paper. “Cancer wasn’t new to our profession, but for the first time, I was thinking about cancer as an occupational disease: Was fighting fire somehow a contributing factor in my friends getting sick? Were our repeated exposures to toxic burning chemicals on the fire ground a factor to the high breast cancer rates among SFFD women firefighters?”

Heather Buren (center), a lieutenant with the San Francisco Fire Department, is a principal investigator of the Women Firefighters Biomonitoring Collaborative. She is pictured here with Julie Mau (left) and Dawn Dewitt (right). (Photo courtesy Heather Buren)

Through a series of discussions and community meetings with Commonweal and Breast Cancer Prevention Partners, Buren was introduced to Morello-Frosch. Together, the two began the steps that would eventually launch the biomonitoring collaborative.

Since beginning the study, Buren and a small group of other women firefighters have teamed up with the Bluegreen Alliance to create a training program to help other firefighters take steps to reduce their exposures to PFAS and other toxic chemicals. These steps include many basic measures, like immediately wiping down exposed areas of skin and removing and cleaning turnout gear — a firefighter’s coat, boots and helmet — after an incident.

“There’s also a lot of interest in having firefighters use foams that don’t contain PFAS, not just to protect the firefighters, but also because the PFAS foams have contaminated a lot of groundwater and drinking water across the U.S.,” said study co-author Ruthann Rudel, research director at Silent Spring Institute.

Because many manufacturers do not disclose the ingredients contained in firefighting foam, the project GreenScreen has recently launched a certification program to identify PFAS-free foams, Rudel pointed out.

‘We’re here, and our health is important’

To conduct the study, the researchers collected blood samples from 86 women firefighters and 84 women who work in offices in downtown San Francisco. They also conducted hour-long interviews with each participant, asking about workplace activities, eating habits and consumer product use to tease out possible sources of PFAS exposure.

Of the 12 types of PFAS chemicals the researchers tested for, seven were found in detectable amounts in most participants’ blood samples, and four were found at detectable amounts in all participants’ samples. Three of the seven — PFHxS, PFUnDA, and PFNA — were detected at significantly higher amounts in firefighters’ blood, compared to office workers’ blood.

Each participant received a digital report generated by Silent Spring, detailing their individual results and providing information and concrete steps for reducing their PFAS exposure.

In a companion paper, which also appeared online this month in Environmental Science and Technology, the team detailed a new method that will allow researchers to rapidly screen blood samples for the presence of a variety of different toxic compounds. This method could help identify what else these women firefighters are exposed to that might be harmful. A future study, currently in preparation, will also report on the levels of flame-retardants in the blood samples of the women firefighters and office workers.

“We are here, and our health is important,” Buren said. “In many occupations, women are often overlooked and understudied. Firefighting is no different. The SFFD has more women firefighters than any other metropolitan fire department in the U.S. The strength in numbers, coupled with the continued and strong support from our administration and union, has allowed us to focus on the health of our women, which we hope will benefit all firefighters nationally.”

Co-authors of the paper include Roy Gerona of UCSF and Vincent Bessonneau of Silent Spring Institute.

This work is supported by the California Breast Cancer Research Program (19BB-2900), the National Institute of Environmental Health Sciences (R01ES027051), the National Institute for Occupational Safety and Health, the Targeted Research Training Program (T42 OH008429), the San Francisco Firefighter Cancer Prevention Foundation and the International Association of Firefighters-Local 798.

UC Berkeley photo by Brittany Hosea-Small

February 26, 2020
Think All BPA-free Products Are Safe? Not so Fast, Scientists Warn

News Release | Research

MU scientists find BPA alternative, bisphenol S, could negatively affect both a mother’s placenta and potentially a developing baby’s brain.

Feb. 18, 2020
Contact: Eric Stann, 573-882-3346, StannE@missouri.edu

Using “BPA-free” plastic products could be as harmful to human health — including a developing brain — as those products that contain the controversial chemical, suggest scientists in a new study led by the University of Missouri and published in the Proceedings of the National Academy of Sciences.

For decades, scientists have studied BPA extensively in animal models with results indicating the chemical plays a role in early pregnancy loss, placental diseases and various negative health outcomes after birth. As these adverse health effects have become more widely known, companies have turned to using alternative chemicals to develop plastic products — namely water bottles and food containers — and often labeling them “BPA-free.” However, MU scientist Cheryl Rosenfeld warns these chemical alternatives, such as bisphenol S (BPS), still aren’t safe for people to use.

As adverse health effects of BPA have become more widely known, companies have turned to using alternative chemicals to develop plastic products — namely water bottles and food containers — and often labeling them “BPA-free.”

In the study, Rosenfeld and her colleagues focused on examining the effects of BPS on a mouse’s placenta. She said the placenta serves as a historical record of what an unborn child faces while in the womb; the placenta also can transfer whatever the mother might be exposed to in her blood, such as harmful chemicals, into the developing child.

“Synthetic chemicals like BPS can penetrate through the maternal placenta, so whatever is circulating in the mother’s blood can easily be transferred to the developing child,” said Rosenfeld, a professor of biomedical sciences in the College of Veterinary Medicine, investigator in the Bond Life Sciences Center, and research faculty member for the Thompson Center for Autism and Neurobehavioral Disorders at MU. “This mouse model is the best model we have now to simulate the possible effects of BPS during human pregnancy, because the placenta has a similar structure in both mice and humans.”

Cheryl Rosenfeld

Rosenfeld adds that the placenta serves as a primary source of serotonin for fetal brain development in both mice and humans. Serotonin, while commonly associated with the feeling of happiness, is a natural chemical that can impact a person’s functions, including their emotions and physical activities such as sleeping, eating and digesting food.

“The placenta responds to both natural chemicals as well as synthetic chemicals that the body misinterprets as natural chemicals, but the body doesn’t have the ability to mitigate the detrimental effects of such industrial-made chemicals,” Rosenfeld said. “More importantly, these chemicals have the ability to lower the placenta’s serotonin production. Lower levels of serotonin can compromise fetal brain development because during this critical time in development the brain relies on the placenta to produce serotonin. Thus, developmental exposure to BPA or even its substitute, BPS, can lead to longstanding health consequences.”

Rosenfeld’s research is an example of an early step in translational medicine, or research that aims to improve human health by determining the relevance of animal science discoveries to people. This research can provide the foundation for precision medicine, or personalized human health care. Precision medicine will be a key component of the NextGen Precision Health Initiative — the University of Missouri System’s top priority — by helping to accelerate medical breakthroughs for both patients in Missouri and beyond.

The study, “Bisphenol A and bisphenol S disruptions of the mouse placenta and potential effects on the placenta-brain axis,” was published in the journal Proceedings of the National Academy of Sciences. Co-corresponding authors include R. Michael Roberts at MU and Geetu Tuteja at Iowa State University. Other authors include Jiude Mao, Saurav Sarma, Barbara Sumner, Zhentian Lei, Lloyd Sumner and Nathan Bivens at MU; Ashish Jain at Iowa State University; and Nancy Denslow, Mohammad Zaman Nouri, Sixue Chen, Tingting Wang, Ning Zhu and Jin Koh at University of Florida.

Funding was provided by grants from the National Institutes of Health, National Institute of Environmental Health Sciences and the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies.

Oct. 14, 2026

Mizzou astronomer leads global team on NASA mission to create unprecedented view of the early universe

The international team of 130 researchers will be among the first to use NASA’s Nancy Grace Roman Space Telescope, capturing one of the deepest and widest views of the early universe ever made.

Oct. 13, 2026

MURR announces availability of Terbium-161

Oct. 11, 2026

CAFNR celebrates state-of-the-art facilities to benefit Missouri agriculture

The four projects resulted from strong collaborations and investment in Missouri agriculture across agronomy, beef production, meat science and vinology.

Oct. 6, 2026

At Mizzou, a scientist is rewriting the rules for how researchers study plant stress

Rather than isolating individual factors one at a time, Ron Mittler studies how organisms respond to multiple stressors simultaneously, paving the way for better crops and potentially better medical treatments.

Stay up-to-date with the latest news by subscribing to the Show Me Mizzou newsletter.

Subscribe

February 20, 2020
Cancer-causing Culprits Could Be Caught by Their DNA Fingerprints

Causes of cancer are being catalogued through an international study revealing the genetic fingerprints of DNA-damaging processes that drive cancer development. Researchers from University of California San Diego School of Medicine, Wellcome Sanger Institute, Duke-NUS Medical School Singapore, the Broad Institute of MIT and Harvard, with collaborators around the world, have created the most detailed list yet of these genetic fingerprints, providing clues to how each cancer develops.

These fingerprints will allow scientists to search for previously unknown chemicals, biological pathways and environmental agents responsible for causing cancer.

“We identified almost every publically available cancer genome at the start of this project and analyzed their whole genome sequences,” said first author Ludmil B. Alexandrov, PhD, assistant professor of in the departments of Cellular and Molecular Medicine and Bioengineering at UC San Diego. “The data from these thousands of cancers allowed us to describe mutational signatures in much more detail, and we are confident that we now know most of the signatures that exist.”

The research, published on February 5, 2020 in Nature as part of the global Pan-Cancer Project, will help delineate the causes of cancer, inform prevention strategies and define new directions for cancer diagnoses and treatments.

In the United States, the National Cancer Institute estimates 1.7 million new cases of cancer were diagnosed in 2018 and more than 600,000 people died from the disease. Approximately 38 percent of men and women in this country will be diagnosed with cancer in their lifetime.

Cancer is caused by genetic changes — mutations — in the DNA of a cell, prompting the cell to divide uncontrollably. Many known causes of cancer, such as ultraviolet light and tobacco use, leave a specific fingerprint of damage in the DNA, known as a mutational signature. These fingerprints can help understand how cancers develop, and potentially how they might be prevented. However, past studies have not been large enough to identify all potential mutational signatures.

“Using our detailed catalogue of the range of mutational signatures in cancer DNA, researchers worldwide will now be able to investigate which chemicals or processes are linked to these signatures,” said co-senior author Mike Stratton, PhD, director of the Wellcome Sanger Institute. “This will increase our understanding of how cancer develops, and discover new causes of cancer, helping to inform public health strategies to prevent cancer.”

This study identified new mutational signatures that had not been seen before, from single letter typo mutations, to slightly larger insertions and deletions of genetic code. The result is the largest database of reference mutational signatures. Only about half of all mutational signatures have known causes.

“Some types of these DNA fingerprints, or mutational signatures, reflect how the cancer could respond to drugs,” said co-senior author Steven Rozen, PhD, director of the Center for Computational Biology and professor of Cancer and Stem Cell Biology at Duke-NUS Medical School. “Further research into this could help to diagnose some cancers and what drugs they might respond to.”

The global Pan-Cancer Project is the largest and most comprehensive study of whole cancer genomes. The collaboration has created a huge resource of primary cancer genomes, available to researchers worldwide to advance cancer research.

“The availability of a large number of whole genomes enabled us to apply more advanced analytical methods to discover and refine mutational signatures and expand our study into additional types of mutations,” said co-senior author Gad Getz, PhD, institute member of the Broad Institute of MIT and Harvard, professor of pathology at Harvard Medical School, and faculty member and director of bioinformatics at the Massachusetts General Hospital Cancer Center.

“Our new collection of signatures provides a more complete picture of biological and chemical processes that damage or repair DNA and will enable researchers to decipher the mutational processes that affect the genomes of newly sequenced cancers.”

UC San Diego School of Medicine

Established in 1968, University of California San Diego School of Medicine is consistently ranked among the top medical school programs in the country for primary care and research by U.S. News & World Report and among the top 10 medical schools for National Institutes of Health total funding. The school is internationally recognized as a place where discoveries are delivered — bringing breakthroughs from the research lab to patients’ bedsides. Faculty members care for patients at UC San Diego Health, where primary care is available at several convenient locations throughout San Diego County and our advanced specialty care consistently ranks among the nation’s best. For more information, visit medschool.ucsd.edu.

The Wellcome Sanger Institute

The Wellcome Sanger Institute is a world leading genomics research centre. We undertake large-scale research that forms the foundations of knowledge in biology and medicine. We are open and collaborative; our data, results, tools and technologies are shared across the globe to advance science. Our ambition is vast — we take on projects that are not possible anywhere else. We use the power of genome sequencing to understand and harness the information in DNA. Funded by Wellcome, we have the freedom and support to push the boundaries of genomics. Our findings are used to improve health and to understand life on Earth. Find out more at www.sanger.ac.uk or follow us on Twitter, Facebook, LinkedIn and on our Blog.

About Duke-NUS Medical School

Duke-NUS is Singapore’s flagship graduate entry medical school, established in 2005 with a strategic, government-led partnership between two world-class institutions: Duke University School of Medicine and the National University of Singapore (NUS). Through an innovative curriculum, students at Duke-NUS are nurtured to become multi-faceted ‘Clinicians Plus’ poised to steer the healthcare and biomedical ecosystem in Singapore and beyond. A leader in ground-breaking research and translational innovation, Duke-NUS has gained international renown through its five signature research programmes and nine centres. The enduring impact of its discoveries is amplified by its successful Academic Medicine partnership with Singapore Health Services (SingHealth), Singapore’s largest healthcare group. This strategic alliance has spawned 15 Academic Clinical Programmes, which harness multi-disciplinary research and education to transform medicine and improve lives. For more information, please visit duke-nus.edu.sg.

About the Broad Institute of MIT and Harvard

Broad Institute of MIT and Harvard was launched in 2004 to empower this generation of creative scientists to transform medicine. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods, and data openly to the entire scientific community. Founded by MIT, Harvard, Harvard-affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff, and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to www.broadinstitute.org.

Co-authors include: Erik N. Bergstrom and S. M. Ashiqul Islam of UC San Diego; Jaegil Kim, Broad Institute of MIT and Harvard; Nicholas J. Haradhvala and Gad Getz, Broad Institute of MIT and Harvard, and Massachusetts General Hospital; Mi Ni Huang, Alvin Wei Tian Ng, Yang Wu, Arnoud Boot and John R. McPherson of Duke-NUS Medical School; Kyle R. Covington and David A. Wheeler of Baylor College of Medicine; Dmitry A. Gordenin and Leszek J. Klimczak of National Institute of Environmental Health Sciences; Nuria Lopez-Bigas, The Barcelona Institute of Science and Technology, Universitat Pompeu Fabra, and Institucio Catalana de Recerca i Estudis Avancats; Sandro Morganella, Wellcome Sanger Institute; Radhakrishnan Sabarinathan, Universitat Pompeu Fabra, Tata Institute of Fundamental Research, and Institute for Research in Biomedicine; Ville Mustonen, University of Helsinki; and the Pan-Cancer Analysis of Whole Genomes Consortium Mutational Signatures Working Group.

Funding for this research came, in part, from the Wellcome grant (206194), Singapore National Medical Research Council (NMRC/CIRG/1422/2015, MOH-000032/MOHCIRG18may-0004), Singapore Ministry of Health via the Duke-NUS Signature Research Programmes, National Institutes of Health (Z1AES103266), the European Research Council Consolidator (682398), National Cancer Institute (U24CA143843, U24CA210999, U24CA143845) and Cancer Research UK Grand Challenge Award (C98/A24032).

Disclosures: Gad Getz receives research funds from IBM and Pharmacyclics and is an inventor on patent applications related to MuTect, ABSOLUTE, MutSig, MSMuTect and POLYSOLVER.

February 6, 2020
A High-fiber Diet May Counteract the Harmful Health Effects of Pollutants

LEXINGTON, Ky. (Jan. 30, 2020) — Research from the University of Kentucky’s Superfund Research Center (UK-SRC) shows that a diet high in fiber could possibly reverse the adverse effects that environmental toxins have on cardiovascular health.

The findings are part of UK-SRC’s “Project #1,” which examines how nutrients affect toxicity caused by polychlorinated biphenyls (PCBs) in vascular tissues.

PCBs are man-made chemicals that were used in industrial and commercial applications and have been linked to a number of adverse health effects in humans and animals. Although they were banned more than 40 years ago, PCBs can still be released into the environment from poorly maintained hazardous waste sites.

Prior UK-SRC research in the lab of Bernhard Hennig, a professor in UK’s Department of Animal & Food Sciences, found a connection between PCBs and cardiovascular disease. Pan Deng, a postdoctoral researcher working in Hennig’s lab, is continuing this research with a study that found that nutrients including fiber reduced PCB toxicity in multiple organ systems, including gut microbiota, liver and vasculature.

“Using animal models, we found that eating a high-fiber diet can prevent pollutant-induced cardiovascular disease,” said Deng. “This finding may lead to nutritional and therapeutic interventions in people who are exposed to PCBs.”

Deng’s field of research is called metabolomics, and it examines how metabolites within a cell, tissue or biofluid of an organism respond to external stressors – in this case the toxic exposure from PCBs. Deng checks levels of nutrients and pollutants in the cells through liquid and gas chromatography testing. The process is called metabolic profiling.

“Metabolic profiling gave us the power to discover how environmental pollutants contribute to human disease. The very important thing is that this technology can be applied to biological samples obtained from humans,” said Deng.

The findings may be beneficial to those impacted by or residing near toxic Superfund chemicals, which include PCBs.

The Environmental Protection Agency (EPA) has designated thousands of contaminated sites in the U.S. as “Superfund” sites. They include manufacturing facilities, processing plants, landfills and mining sites where hazardous waste has been improperly managed.

Kentucky is home to 20 (13 active) EPA National Priorities List Superfund hazardous waste sites. The UK-SRC is an interdisciplinary program including researchers from several UK colleges that strives to reduce the negative health and environmental impacts of chlorinated organic compounds found at these sites across Kentucky and the U.S.

The UK-SRC is funded by the National Institutes of Health/National Institute of Environmental Health Science (NIEHS) and is one of NIEHS’s nationwide family of Superfund Research Programs. Specifically, UK-SRC biomedical research examines potential roles for nutritional components and lifestyle choices to minimize negative human health impacts related to chemical exposures.

As the state’s flagship, land-grant institution, the University of Kentucky exists to advance the Commonwealth. We do that by preparing the next generation of leaders — placing students at the heart of everything we do — and transforming the lives of Kentuckians through education, research and creative work, service and healthcare. We pride ourselves on being a catalyst for breakthroughs and a force for healing, a place where ingenuity unfolds. It’s all made possible by our people — visionaries, disruptors and pioneers — who make up 200 academic programs, a $1.02 billion research and development enterprise and a world-class medical center, all on one campus.

January 30, 2020