Publisher Health

Your body is made of close to 100 trillion cells that keep you healthy and alive. Each cell has billions of parts of its own, all of them working in tandem to keep life’s processes moving.
One vital component of a cell is called a nuclear pore, which acts like the doors and windows in a house — they allow important things, like RNA and proteins, to enter and exit a cell’s nucleus. Without nuclear pores, your cells, and everything else in your body, would shut down. Until now, scientists have not seen exactly how nuclear pores are built and how their many parts function.
Enter a team of researchers from the California Institute of Technology (Caltech), led by André Hoelz, professor of chemistry and biochemistry and faculty scholar of the Howard Hughes Medical Institute (HHMI). After almost two decades of persistence, researchers successfully mapped the atomic structure of the nuclear pore complex (NPC) by determining the structures of its many components and fitting them together. Seeing how the NPC fits together in cells furthers our understanding about how cells work and will potentially lead to new treatments for certain cancers, autoimmune and neurodegenerative diseases, and certain heart conditions.
Unraveling the NPC took time because it’s not a simple puzzle like the ones that wait in pieces in a box. It contains more than 1,000 individual proteins, and it can take scientists years to map a single one before they can even begin to put them together. The entire process is akin to a gigantic three-dimensional jigsaw puzzle, but one that is made from pieces so tiny that you cannot see them with your naked eyes or even with the best light microscope.
To make this milestone possible, the Caltech team turned to high-energy X-rays generated by the Stanford Synchrotron Radiation Lightsource (SSRL) at the Department of Energy’s (DOE) SLAC National Accelerator Laboratory, the Advanced Photon Source at the DOE’s Argonne National Laboratory, and National Synchrotron Light Source II at the DOE’s Brookhaven National Laboratory. In many experiments over the years, they zapped crystallized NPC protein samples with X-ray light, illuminating the samples’ atomic structure and overall shape. They published their findings this month in two papers in Science. The first paper reported the architecture of the face that lies at the outside of the nucleus, and the second paper revealed how the many pieces of the NPC are held together by “glue” proteins.
“X-ray crystallography provided atomic details of the individual protein components,” Aina Cohen, SLAC senior scientist, said. “As technologies have been improving, including at SLAC’s SSRL, researchers have been able to see the nuclear pore complex in clearer ways, so that they could fit the different proteins together to complete this complex puzzle.”
Without SSRL’s upgraded technology over the years, such as its microfocus capabilities and a pixel array detector (PAD), installed in 2009, the research could not have happened, Hoelz said. SSRL had one of the country’s first PADs, and the detector generated much better X-ray diffraction data than previously possible, helping the Caltech researchers map the NPC’s protein structures. Determining the crystal structure of a large six-protein piece and identifying its arrangement in the nuclear pore in 2015 showed that, with patience and diligence, the researchers could eventually provide a complete picture of the entire NPC.
“SSRL was the facility where most of the initial structural work occurred due to the ample access we had through Caltech’s Molecular Observatory, an X-ray crystallography facility with access to SSRL’s Beam Line 12-2,” Hoelz said. “This regular access allowed for the systematic improvement of various aspects of the X-ray diffraction experiments, which allowed us to solve even the most challenging nucleoporin structure determination problems. We had multiple structures that we worked on for over a decade before we solved them.”
The completed human NPC puzzle will provide a framework on which a lot of important experiments can now be done, said Christopher Bley, a senior postdoctoral scholar research associate in chemistry at Caltech and also co-first author of the studies.
“We have this composite structure now, and it enables and informs future experiments on NPC function, or even diseases,” Bley said. “There are a lot of mutations in the NPC that are associated with terrible diseases, and knowing where they are in the structure and how they come together can help design the next set of experiments to try and answer the questions of what these mutations are doing.”
Having determined the human NPC structure, scientists can now focus on working out the molecular basis for various enigmatic functions of NPCs, such as how mRNA gets exported, the underlying causes for the many NPC-associated diseases, and the targeting of NPC function by many viruses, including SARS-CoV-2 and monkeypox virus, with the goal of developing novel therapies, Hoelz said.
SSRL, APS and NSLS-II are DOE Office of Science user facilities. The research was funded by the HHMI, National Institutes of Health, and the Heritage Medical Research Institute.

Patients identified by nuclear stress testing as having severe stress-induced myocardial ischemia (lack of blood flow to the heart) are likely to benefit from heart bypass surgery or angioplasty, while those with mild or no ischemia are not, according to a new study from the Icahn School of Medicine at Mount Sinai.
The procedures, known as coronary revascularization, restore blood flow to blocked arteries following stress testing. For patients with severe ischemia, early revascularization was associated with a more than 30 percent reduction in mortality compared to patients with severe ischemia who were treated with medication, but no benefit was shown for the other groups.
The research, published July 11 in the Journal of the American College of Cardiology, is the first large-scale study to look at the impact of stress testing on patient management when applied to the full spectrum of patients who have both varying degrees of myocardial ischemia and heart function. This new study can help guide physicians on how to manage caring for patients with suspected heart disease.
Physicians order stress tests when they suspect that a patient’s chest pain or other clinical symptoms are from coronary artery disease (CAD), or plaque build-up inside the coronary arteries. These help determine if a patient has obstructive CAD which leads to significant ischemia. If the ischemia due to obstructive CAD is severe, physicians can restore adequate blood flow to the heart by performing coronary artery bypass grafting surgery or percutaneous coronary intervention (PCI), a less invasive procedure in which interventional cardiologists use a catheter to place stents in the blocked coronary arteries to restore the blood flow. Nuclear stress testing is the most common stress test used to detect myocardial ischemia.
“There is keen interest in assessing how measurement of myocardial ischemia during stress testing can help shape physicians’ decision to refer patients for coronary revascularization procedures, but this issue has not been well studied among patients who have underlying heart damage,” explains lead author Alan Rozanski, MD, Professor of Medicine (Cardiology) at the Icahn School of Medicine at Mount Sinai, and Director of Nuclear Cardiology and Cardiac Stress Testing and Chief Academic Officer for the Department of Cardiology at Mount Sinai Morningside. “Our study, which evaluated a large number of patients with pre-existing heart damage who underwent cardiac stress testing, finally addresses this clinical void.”
The researchers analyzed records of more than 43,000 patients who underwent nuclear stress testing with suspected CAD between 1998 and 2017 at Cedars Sinai Medical Center in Los Angeles with a median 11-year follow-up for mortality/survival. The investigators grouped patients according to both their level of myocardial ischemia during stress testing as well as their left ventricular ejection fraction (or “LVEF”), which measures the percent of blood volume pumped out of the heart’s main chamber during each heartbeat. Low LVEF measurements indicate prior heart damage that could be from scarring of the heart due to a prior heart attack.
The study provides two important clinical insights. First, the study showed that the frequency of myocardial ischemia during stress testing varies according to patients’ heart function. Of the 39,883 patients with normal heart function (LVEF above 55 percent), fewer than 8 percent of them had ischemia. However, among the 3,560 patients with reduced heart function (LVEF less than 45 percent, which indicates prior heart damage), more than 40 percent of them had myocardial ischemia. The study also showed that the presence of myocardial ischemia increases the risk of death in patients with normal and reduced heart function. Among both groups of patients, performing bypass or PCI procedures was not associated with improved survival among the large percentage of patients who had either no or only mild ischemia during the cardiac stress test. Among patients with severe ischemia, coronary procedures were associated with more than 30 percent higher survival rates compared to those managed with medication only. This was the case for patients with and without heart damage.
“These results confirm the benefits of stress testing for clinical management. What you want from any test when considering coronary revascularization procedures is that the test will identify a large percentage of patients who are at low clinical risk and do so correctly, while identifying only a small percentage of patients who are at high clinical risk and do so correctly. That is what we found with nuclear stress testing in this study,” explains Dr. Rozanski. “Importantly, the presence of severe ischemia does not necessarily mean that coronary revascularization should be applied. New data from a large clinical trial suggests that when medical therapy is optimized it may be as effective as coronary revascularization in such patients. But regardless, the presence of severe ischemia indicates high clinical risk which then requires aggressive management to reduce clinical risk.”

During sperm production, an enormous amount of DNA has to be packed into a very small space without breaking anything. A central role is played by certain proteins around which the DNA thread is wrapped — the protamines. A recent study by the University of Bonn provides new insights into this important mechanism. The results have been published in the journal PLoS Genetics.
If you are moaning once again about your suitcase being far too small as your vacation approaches, you should take human sperm cells as an inspiration. During their production, they are faced with an almost insoluble task. They have to pack 23 DNA threads with a total length of one meter into a head with a diameter of just three thousandths of a millimeter. And in the process, the delicate threads must not become entangled in an inextricable knot, nor must they tear.
We often sit on the suitcase to close it. The body resorts to a similar trick during spermatogenesis. Normally, DNA forms a comparatively loose tangle. In sperm cells, however, it is enormously compressed. “If DNA were to take up as much space as a watermelon under normal circumstances, sperm cells would then only be as big as a tennis ball,” says Prof. Dr. Hubert Schorle from the Institute of Pathology at the University Hospital Bonn.
DNA must be enormously compressed
Biologists call this process hypercondensation. In their loose state, DNA threads are wrapped around numerous spherical protein molecules, the histones. In this state, they resemble 23 tiny strings of pearls. During hypercondensation, the histones are first exchanged for transition proteins. In a subsequent step, these are replaced by so-called protamines. Due to their chemical composition, protamines exert a very strong attraction on DNA. The thread therefore wraps itself in very firm and tightly loops around the protamine
“Most mammals seem to produce only one type of protamine, PRM1,” explains Dr. Lena Arévalo, a postdoctoral researcher in Schorle’s group. “In humans, but also rodents like mice, it’s different — they have a second type, PRM2.” Exactly what this second protamine is needed for was not known until now. However, it was known that some parts of it are successively cut off during sperm development.
And it is precisely these cut-off parts that appear to be immensely important, according to the new study. When mice produce only a truncated PRM2 molecule that lacks the cut-off snippets, they are infertile. “The removal of transition proteins during hypercondensation is impaired,” Arévalo says. “In addition, the condensation seems to proceed too quickly, causing the DNA strands to break.”
Hope for therapies against male infertility
It is possible that a defective protamine 2 can also lead to infertility in males of our own species. The team now plans to investigate this hypothesis further. “There are only a few research groups that analyze the role of protamines in hypercondensation,” says Schorle, who is also a member of the Transdisciplinary Research Area (TRA) “Life and Health” at the University of Bonn. “We are the only laboratory in the world to date that has succeeded in generation and breeding of both PRM1 and PRM2 deficient mouse lines which are now used to study the role of these proteins in spermatogenesis.” In the medium term, this could also lead to new therapies against male infertility, the researcher hopes.
Funding
The study was supported by the German Research Foundation (DFG) and the FEMHABIL program of the University Hospital Bonn.
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Using UT Southwestern’s Cryo-Electron Microscopy Facility, researchers for the first time have captured images of an autoantibody bound to a nerve cell surface receptor, revealing the physical mechanism behind a neurological autoimmune disease. The findings, published in Cell, could lead to new ways to diagnose and treat autoimmune conditions, the study authors said.
“We’re entering a new era of understanding how autoimmune disease works in the central nervous system,” said Colleen M. Noviello, Ph.D., Assistant Professor of Neuroscience at UTSW who specializes in obtaining cryo-electron microscopy (cryo-EM) images down to an atomic level of resolution. Dr. Noviello co-led the study with Ryan Hibbs, Ph.D., Associate Professor of Neuroscience and Biophysics, an Effie Marie Cain Scholar in Medical Research, and an Investigator in the Peter O’Donnell Jr. Brain Institute and Harald Prüss of Universitätsmedizin Berlin.
Researchers have studied autoimmune diseases — a class of conditions in which the immune system attacks healthy parts of the body — for decades. However, the first autoimmune disease targeting a neuronal receptor protein was discovered just 15 years ago, Dr. Noviello explained. Since then, researchers have reported the existence of a handful of other diseases that fall into this category. These include autoimmune encephalitis, a condition characterized by the sudden onset of severe symptoms including psychosis, seizures, movement disorders, impaired consciousness, and problems with the autonomic nervous system, which controls involuntary bodily functions.
Researchers in Germany recently identified a patient, then 8 years old, whose autoimmune encephalitis appeared to be caused by antibodies that attack the GABAA receptor, a protein that sits on the surface of synapses — specialized structures that connect brain cells. This receptor’s role is to inhibit neuronal firing, balancing the electrical signals prompted by excitatory receptors to maintain healthy signaling between nerve cells.
After confirming that two kinds of antibodies derived from this young patient’s immune cells readily bound to the GABAA receptor, Drs. Noviello, Hibbs, and their colleagues in the Hibbs lab performed cryo-EM — a technique that freezes proteins in place to get high-resolution microscopic images — for each antibody bound to the receptor. UTSW’s cryo-EM facility, opened in 2016 with support from the Cancer Prevention and Research Institute of Texas (CPRIT), provides 3D images of biological molecules up to atomic resolution.
The images show that, both together and separately, the antibodies prevent the GABAA receptor from inhibiting neuronal signaling, causing neurons to become too electrically excited and leading to brain inflammation, cell death, and seizures characteristic of autoimmune encephalitis. Screening for these antibodies could lead to better diagnosis of this condition, said Dr. Noviello; likewise, finding ways to block the interaction between these antibodies and their target could lead to better ways to treat it.
As understanding of autoimmune nervous system diseases is still in its infancy, Dr. Hibbs said that he, Dr. Noviello, and their colleagues plan to make the study of these disorders using cryo-EM a focus of the Hibbs lab’s research into the future. The team is already collaborating with Steven Vernino, M.D., Ph.D., Professor of Neurology, Vice Chair for Education and Faculty Affairs, and Distinguished Teaching Professor; and Nancy Monson, Ph.D., Associate Professor of Neurology and Immunology, to study more autoimmune conditions that affect the central nervous system.
Dr. Vernino holds the Rex Griswold Distinguished Professorship in Multiple System Atrophy and the Dr. Bob and Jean Smith Foundation Distinguished Chair in Neuromuscular Disease Research.
Other UTSW researchers who contributed to this study include Jinfeng Teng.
This study was supported by grants from The Welch Foundation (I-1812), the National Institutes of Health (DA047325), the German Research Foundation (FOR3004, PR 1274/3-1, and PR 1274/5-1), the Helmholtz Association (HIL-A03), and the German Federal Ministry of Education and Research (Connect-Generate 01GM1908D). Single-particle cryo-EM data were collected at UTSW’s Cryo-Electron Microscopy Facility, which is supported by the CPRIT Core Facility Support Award RP170644.

Antibiotic resistant bacterial pathogens are increasingly playing a role in rising illness and preventing wound healing, especially in hospitals. While more and more pathogens have developed biofilms that protect them from being eradicated by antibiotics, fewer classes of antibiotics are being developed. Researchers from Ben-Gurion University of the Negev decided to go in a different direction and investigated a phytochemical derived from cruciferous vegetables such as broccoli that breaks down the biofilm.
The phytochemical 3,3′-diindolylmethane (DIM) successfully broke down the biofilms protecting two different pathogens including Acinetobacter baumannii and Pseudomonas aeruginosa- enabling their eradication 65% and 70% of the time, respectively. Combined with antibiotics, that number jumped to 94%.
Prof. Ariel Kushmaro, Dr. Karina Golberg and his team together with Prof. Robert Marks, all of them members of the Avram and Stella Goldstein-Goren Department of Biotechnology Engineering at BGU chronicled their findings in the peer-reviewed journal Pharmaceutics recently.
Additionally, when they introduced DIM into an infected wound, it sped up the healing process significantly, the team found.
“Our findings show promise for other avenues of research in addition to known classes of antibiotics,” says Prof. Kushmaro.
Further development and commercialization of the technology is currently being done at the startup company LifeMatters (http://lifematters.co.il).
Additional researchers from Prof. Kushmaro’s lab included: Bat-el Kagan, Sigalit Barzanizan, Dr. Karin Yaniv and Dr. Esti Kramarsky-Winter. They collaborated with researchers from Near East University and Girne American University in Cyprus.
The research was supported by the National Institute for Biotechnology in the Negev and Israel’s Ministry of Science and Technology.
Prof. Kushmaro is also a member of the Goldman Sonnenfeldt School of Sustainability and Climate Change, and the Ilse Katz Center for Nanoscale Science and Technology.
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Using four unrelated strains of the microscopic nematode C. elegans originating from different parts of the world, a group of worm biologists have developed a model system to study individual differences in metabolism. The use of C. elegans, a widely studied model organism, allowed the team to study the unique and complex interplay between genetics, diet, microbiota and other environmental factors that can affect fundamental metabolic processes in different individuals. This advancement represents a potentially important step toward “personalized” or “precision” medicine, a relatively new discipline that tailors dietary advice and disease treatment to an individual’s own genome sequence.
The research, by Marian Walhout, PhD, the Maroun Semaan Chair in Biomedical Research and chair and professor of systems biology at UMass Chan Medical School and collaborators Erik Andersen, PhD, from Northwestern University and Frank Schroeder, PhD, from Cornell University, published in Nature, identifies a novel metabolic condition linked to variation in the hphd-1 gene of a strain of C. elegans found on the Big Island in Hawaii. The strain, known as DL238, has an abnormal accumulation and secretion of the metabolite 3-hydroxypropionate (3HP). Moreover, this strain was found to generate a set of novel metabolites that have 3HP conjugated to several amino acids. These novel metabolites are not found in the laboratory strain that has been used for decades to make seminal biological discoveries. By conjugating 3HP to amino acids, DL238 is removing 3HP, which is toxic at high concentrations.
“This work provides an important step toward the development of metabolic network models that capture individual-specific differences of metabolism and more closely represent the diversity that is found over entire species,” said Walhout. “Employing this system, we can begin studying interindividual metabolism and the unique interplay of metabolites, diets and environments on an individual level.”
When the human genome was sequenced, clinical researchers envisioned an era when our personal genomic information could be used to tailor medical treatments to fit the needs of each individual, explained Walhout. Despite the completion of the Human Genome Project in 2003, and advancements in genomics and deep sequencing technologies, personalized medicine remains more promise than reality.
Part of the challenge in developing personalized medicine is that our DNA makes up only a portion of human health; an individual’s diet and environment both profoundly impact metabolic processes. And because no two individuals have the same exact diet, unraveling the complex interplay of genetics, diet and environment and connecting these to variations in metabolism is cumbersome. In addition to sequencing individual genomes, scientists would need to replicate metabolic measurements in people of the same age and gender, who ideally would also consume the same exact diet and experience identical environments.
To address this challenge, Walhout, a leader in metabolism and gene expression research, teamed up with Dr. Andersen, an expert in quantitative genetics, and Dr. Schroeder, a chemist, to develop a comparative system for studying interindividual variations in metabolism.

Silents are potentially golden in the search for antibiotics to slow the ongoing crisis of resistance in the treatment of disease.
Rice University bioscientists have designed novel on and off switches to control the “silent” genes in a strain of bacteria. Their strategy could boost the perpetual search for new antibiotics.
The researchers customized CRISPR tools to control the expression of genes in Streptomyces bacteria that, in nature, are only expressed when necessary. Until now, those genes have been challenging for synthetic biologists to access.
“As labs started to sequence the genomes of these organisms that were known to produce one or a few antibiotics, we realized that the pathways responsible for the production of antibiotic and other molecules of interest are much more abundant than previously thought,” said James Chappell, an assistant professor of biosciences whose lab studies bacteria and ways to engineer them.
“Each Streptomyces strain is now predicted to be able to produce up to 40 different molecules of interest, including antibiotics, on average,” he said.
The work led by Chappell and graduate student Andrea Ameruoso may allow labs to quickly develop libraries of possible antibiotics to test on pathogens. Significantly, they said that while CRISPR-Cas9 has been used to create a platform to activate genes in organisms like Escherichia coli, this is the first time it’s been applied to Streptomyces.

Adults with abnormal heart metabolism are up to three times more likely to experience life-threatening arrhythmias (an irregular heart rhythm), and MRI techniques could be used to detect the condition and predict future sudden cardiac death (SCD), according to a small, but rigorous study led by Johns Hopkins Medicine researchers.
The findings were published June 22 in JCI Insight.
“We believe this is the first time that impaired cardiac metabolism in people has been linked to an increased risk of life-threatening arrhythmias or sudden cardiac death,” says study senior author Robert Weiss, M.D., professor of medicine at the Johns Hopkins University School of Medicine. “This could open a window for a whole new approach, a metabolic approach for treating or preventing severe arrhythmias, which is something that is not currently available in cardiology.”
Sudden cardiac death accounts for 50% of all cardiovascular deaths in the United States, claiming more than 300,000 American lives annually, according to the American Heart Association. Currently, an implantable cardioverter-defibrillator (ICD) — a small, battery-powered device placed in the chest to detect and stop irregular heart rhythms — is the primary means of preventing SCD in high-risk patients. The device continuously monitors the heart rhythm and delivers electric shocks, when needed, to restore a regular heart rhythm. The battery life of an ICD is typically between five to seven years.
“Over seven years, 60%-70% of these devices never discharge to save a life,” says T. Jake Samuel, Ph.D., first author of the study and fellow in cardiology at Johns Hopkins Medicine. “We’re spending billions of dollars a year on ICDs that are implanted and have procedural and postprocedural risks. There is a need for noninvasive approaches to better assess risk for who needs or doesn’t need an ICD to prevent sudden cardiac death in people.”
For their study, Samuel and colleagues measured the levels of adenosine triphosphate (ATP), the primary chemical cellular energy source, in the hearts of 46 people prior to getting an ICD for primary prevention. The cardiac ATP levels were measured on clinical magnetic resonance imaging (MRI) scanners using a magnetic resonance spectroscopy (MRS) technique developed at Johns Hopkins Medicine by Paul Bottomley, Ph.D., a co-author on the study, to determine which patients had abnormal ATP metabolism. All patients were followed up every three to six months for an average of 10 years to determine which patients had appropriate ICD firings for life-threatening arrhythmias.
Results showed that people with low cardiac ATP levels (impaired metabolism) had a three-fold higher risk of sudden cardiac death (if not saved by ICD intervention) compared to those with normal ATP metabolism. This was still the case when adjusted for low left ventricular ejection fraction, the metric currently used to determine the need for a primary prevention ICD.
“The ICD was never needed in roughly 80% of those with normal cardiac ATP levels in the 10 years during the study period,” Samuel and colleagues report. They say the study findings could complement current approaches and lead to better predictions for who’s most likely to need, or not need an ICD. However, they stress, that more studies are needed to assess different and larger populations.
“But we’re excited about these truly new findings, arguably the first in people, and believe they can be transformative on how doctors assess sudden cardiac death risk,” Weiss says. “Once we have confirmed that metabolism and SCD are linked, we hope to study which drugs preserve and improve ATP metabolism, and whether they can be used to reduce SCD risk.”
In addition to Weiss, other researchers include T. Jake Samuel, Michael Schär, Katherine Wu, Angela Steinberg, Mark Anderson, Gary Gerstenblith and Paul Bottomley from the Johns Hopkins University School of Medicine; An-Chi Wei from the National Taiwan University in Taipei, Taiwan; and Gordon Tomaselli from Albert Einstein College of Medicine in Bronx, New York.
This research was supported by the DW Reynolds Foundation, the NIH (grants HL61912, HL056882, HL103812, HL132181, HL140034) and the Russell H. Morgan and Clarence Doodeman endowments at Johns Hopkins

Pregnant women who were exposed to multiple phthalates during pregnancy had an increased risk of preterm birth, according to new research by the National Institutes of Health. Phthalates are chemicals used in personal care products, such as cosmetics, as well as in solvents, detergents, and food packaging.
After analyzing data from more than 6,000 pregnant women in the United States, researchers found that women with higher concentrations of several phthalate metabolites in their urine were more likely to deliver their babies preterm, which is delivering three or more weeks before a mother’s due date.
“Having a preterm birth can be dangerous for both baby and mom, so it is important to identify risk factors that could prevent it,” said Kelly Ferguson, Ph.D., an epidemiologist at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, and the senior author on the study published in the journal JAMA Pediatrics.
In this study, the largest study to date on this topic, Ferguson and her team pooled data from 16 studies conducted across the United States that included individual participant data on prenatal urinary phthalate metabolites (representing exposure to phthalates) as well as the timing of delivery. Researchers analyzed data from a total of 6,045 pregnant women who delivered between 1983-2018. Nine percent, or 539, of the women in the study delivered preterm. Phthalate metabolites were detected in more than 96% of urine samples.
Higher concentrations of most phthalate metabolites examined were associated with slightly higher odds of preterm birth. Exposure to four of the 11 phthalates found in the pregnant women was associated with a 14-16% greater probability of having a preterm birth. The most consistent findings were for exposure to a phthalate that is used commonly in personal care products like nail polish and cosmetics.
The researchers also used statistical models to simulate interventions that reduce phthalate exposures. They found that reducing the mixture of phthalate metabolite levels by 50% could prevent preterm births by 12% on average. Interventions targeting behaviors, such as trying to select phthalate-free personal care products (if listed on label), voluntary actions from companies to reduce phthalates in their products, or changes in standards and regulations could contribute to exposure reduction and protect pregnancies.
“It is difficult for people to completely eliminate exposure to these chemicals in everyday life, but our results show that even small reductions within a large population could have positive impacts on both mothers and their children,” said Barrett Welch, Ph.D., a postdoctoral fellow at NIEHS and first author on the study.
Eating fresh, home-cooked food, avoiding processed food that comes in plastic containers or wrapping, and selecting fragrance-free products or those labeled “phthalate-free,” are examples of things people can do that may reduce their exposures. Changes to the amount and types of products that contain phthalates could also reduce exposures.
The researchers are conducting additional studies to better understand the mechanisms by which exposure to phthalates can affect pregnancy and to determine if there are effective ways for mothers to reduce their exposures.