It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Wednesday, August 06, 2025
Air purifiers may reduce heart risks for people exposed to traffic pollution
Study finds in-home HEPA air filters significantly lowered systolic blood pressure in adults with elevated readings
WASHINGTON (August 6, 2025) — Usingportable high-efficiency particulate air (HEPA) purifiers at home can significantly lower systolic blood pressure (SBP) in adults with elevated baseline readings — even in areas with relatively low overall air pollution levels, according to a study published today in JACC, the flagship journal of the American College of Cardiology.
Particulate matter (PM) is a major contributor to air pollution and is strongly associated with cardiovascular disease (CVD). People living near high-traffic roadways are frequently exposed to elevated levels of PM from vehicle emissions as well as tire and brake wear. These fine particles can infiltrate homes and affect residents, increasing the risk of hypertension and elevated blood pressure—both major CVD risk factors.
“High blood pressure remains one of the most important modifiable risk factors for cardiovascular disease,” said Douglas Brugge, Ph.D., M.S., Professor and Chair of the Department of Public Health Sciences at UConn Health and lead author of the study. “This research adds to growing evidence that simple interventions, like in-home air filtration, may help improve heart health for people at risk.”
In this randomized crossover trial of 154 adults living near highways, participants were randomly assigned to receive one month of either HEPA or sham filtration (the same HEPA units with the filter removed) in their homes, followed by a one-month “washout” period with no filtration and then the alternate treatment. Blood pressure measurements and participant questionnaires were collected at the start and end of each period.
Researchers found that participants with elevated SBP (>120 mmHg) experienced an average 2.8 mmHg reduction in SBP after one month of HEPA filtration. In comparison, SBP increased slightly (0.2 mmHg) during a sham filtration period, resulting in a significant 3.0 mmHg difference in favor of HEPA filtration. There was no significant impact on diastolic blood pressure or among participants with normal SBP (<120 mmHg).
"Overwhelming evidence shows the harmful health effects of PM2.5 exposure, even at levels below current U.S. standards,” said Jonathan Newman, M.D, M.P.H., Associate Professor in the Department of Medicine, the Leon H. Charney Division of Cardiology at NYU Grossman School of Medicine, and lead author of the accompanying editorial comment. “As healthcare professionals, we must educate the public and support policies that protect clean air and improve the health of all Americans."
Harlan M. Krumholz, M.D., S.M., Editor-in-Chief of JACC, noted that the study raises the possibility that even modest improvements in indoor air quality could have a meaningful impact on blood pressure for people at risk.
“While more research is needed, these results suggest that what we breathe at home may matter for our cardiovascular health,” Krumholz said.
Study limitations include limited generalizability due to a predominantly White, higher-income participant pool, exclusion of people on blood pressure medications, potential variation in purifier use and a lack of data during hotter summer months or at times of higher indoor pollution.
For an embargoed copy of the study “Effect of HEPA Filtration Air Purifiers on Blood Pressure: A Pragmatic Randomized Crossover Trial” and its Editorial Comment, contact JACC Media Relations Manager Olivia Walther at owalther@acc.org.
The American College of Cardiology (ACC) is a global leader dedicated to transforming cardiovascular care and improving heart health for all. For more than 75 years, the ACC has empowered a community of over 60,000 cardiovascular professionals across more than 140 countries with cutting-edge education and advocacy, rigorous professional credentials, and trusted clinical guidance. From its world-class JACC Journals and NCDR registries to its Accreditation Services, global network of Chapters and Sections, and CardioSmart patient initiatives, the College is committed to creating a world where science, knowledge and innovation optimize patient care and outcomes. Learn more at www.ACC.org or connect on social media at @ACCinTouch.
The ACC’s JACC Journals rank among the top cardiovascular journals in the world for scientific impact. The flagship journal, the Journal of the American College of Cardiology (JACC) — and specialty journals consisting of JACC: Advances, JACC: Asia, JACC: Basic to Translational Science, JACC: CardioOncology, JACC: Cardiovascular Imaging, JACC: Cardiovascular Interventions, JACC: Case Reports, JACC: Clinical Electrophysiology and JACC: Heart Failure — pride themselves on publishing the top peer-reviewed research on all aspects of cardiovascular disease. Learn more at JACC.org.
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Journal
Journal of the American College of Cardiology
Subject of Research
People
Article Title
Effect of HEPA Filtration Air Purifiers on Blood Pressure: A Pragmatic Randomized Crossover Trial
Article Publication Date
6-Aug-2025
WHITE MAN'S MEDICINE
Effective therapy for MDS is vastly underused, especially in female and non-white patients
Over half of eligible patients do not receive recommended therapies or complete the full course of treatment; white males are most likely to get the right treatment at the right dose
(WASHINGTON – August 6, 2025) – Most patients with high-risk myelodysplastic syndromes (MDS) do not receive guideline-recommended treatment with hypomethylating agents (HMAs), according to results published inBlood Neoplasia. The findings suggest that underuse of these drugs may help explain why MDS outcomes have not improved over the past two decades since these life-extending medications became available.
The study is the largest analysis of MDS treatment patterns in the United States to date and the most comprehensive study of real-world use of HMAs, which are highly effective in improving outcomes. HMAs are the best available treatment option for the majority of older people with high-risk disease who cannot get a curative bone marrow transplant. According to the study findings, about half of patients who should be started on an HMA are not receiving these drugs, and even among those who do start treatment, many do not complete the recommended therapy. The results also showed that women and non-white patients were significantly less likely to receive the treatment than white males.
“The disparities we found based on gender, race, and ethnicity were really striking,” said the study’s lead author, Sudipto Mukherjee, MD, PhD, MPH, a physician in the department of hematology and medical oncology at Cleveland Clinic. “Given the absence of newly approved therapies over the last two decades, the most impactful way to improve outcomes in newly diagnosed high-risk MDS requires that we do better with the available therapies. Making changes with these therapies and how they are given (that is, when to treat and how to treat) is a key intervention that can have a huge impact.”
MDS, a group of blood cancers in which the bone marrow does not produce enough healthy blood cells, causes debilitating fatigue and increased susceptibility to infections and bleeding. Without treatment, MDS can progress to acute myeloid leukemia. MDS is most common in adults over the age of 70, most of whom cannot get a bone marrow transplant – the only known cure for MDS – due to frailty, comorbidities, or cost.
HMAs modify the genes involved in blood formation in a way that boosts the production of healthy blood cells and slows the progression of MDS. Although these drugs do not cure the disease, clinical trials have shown that they help patients live longer and improve quality of life. However, real-world outcomes have shown little improvement since the U.S. Food and Drug Administration approved two HMAs, azacitidine and decitabine, for high-risk MDS about 20 years ago.
The researchers analyzed Medicare claims data from more than 49,000 U.S. adults to assess which patients received HMAs and whether the drugs were being administered according to guidelines. They assessed clinical factors such as blood counts, transfusions, frailty, and comorbidities, as well as demographic factors such as population density, neighborhood education and poverty levels, and the concentration of physicians and specialists where patients live.
According to the findings, just 16% of newly diagnosed patients with MDS on Medicare received HMAs during the period analyzed (2011-2014). This is about half of the estimated 30-40% of patients who fall into the high-risk category at the time of diagnosis for which HMAs are recommended. People who were older than 85, female, or non-white were significantly less likely to start HMA treatment. Although men and women are diagnosed with MDS at roughly the same rate, the study found women were 19% less likely to start HMAs. Black patients were 30% less likely to start HMAs, and patients of other races were 22% less likely to start HMAs compared to white patients.
Researchers suggested that the lower rate of HMA uptake among people over age 85 may be explained by a tendency for older patients to decline treatment. However, they could not identify any obvious reason why women or non-white patients would be less likely to receive the treatment, suggesting that implicit bias may be a factor.
The dosing and duration of treatment strongly influence HMA outcomes, with the best response to treatment typically achieved after four to six one-month cycles. However, the study revealed that most patients who received HMAs did not complete the treatment as recommended. Over one-third of patients discontinued the treatment by the end of the fourth cycle, and half discontinued by the end of the sixth cycle. Fewer than half (30-40%) received the full guideline-directed dose of their drug in each of the first four cycles.
“If you are not even treating the patients for the recommended duration of time, you will not see a response,” said Dr. Mukherjee. “When starting these treatments, blood counts and transfusion needs may initially get worse before they improve, and you have to plow through it. That is not the time to discontinue, but that is what the data is saying.”
It is normal for patients’ blood cell counts to decrease in the first few cycles of HMA treatment, which can lead to increased fatigue and a greater need for blood transfusions. Based on the data, Dr. Mukherjee suggested that doctors and patients may be too quick to skip doses or stop treatment in response to these effects. While this can be understandable in cases where patients have less support, or access to care, or are in poorer health overall, failing to deliver the full course of treatment as recommended undermines patients’ ability to fully benefit from these medications.
One way to address this gap could be for community health clinics to partner with larger tertiary care centers to guide HMA treatment, Dr. Mukherjee suggested. For example, patients could visit a hospital with more expertise in HMA treatment for a one-time consultation to formulate a treatment plan, and then return to their local community clinic where doctors would follow through on that recommended course of treatment, referring back to the tertiary care center as needed for guidance on handling side effects or altering the dosage.
As the study was a retrospective analysis based on Medicare claims data, the researchers noted that they did not have access to data on disease markers necessary to comprehensively assess the appropriateness of the decision of whether or not to start HMA treatment in all patients, nor did the data specify why HMA treatment was stopped early in each case. Despite these limitations, using Medicare claims data provided a large, nationally representative study cohort in older adults, a demographic with the highest prevalence of MDS.
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Blood Neoplasia (www.bloodneoplasia.org) is an online only, open access journal of the American Society of Hematology (www.hematology.org), the world’s largest professional society concerned with the causes and treatment of blood disorders.
URBANA, Ill. — Imagine moving into a new house just to discover it has no insulation. That’s what life can be like for a bat box resident.
Bat boxes, a kind of artificial roost, are a simple and cost-effective way to increase habitat for these flying mammals. They’re a preferred spot for mother bats to raise pups if their favorite housing option, large dead trees, are hard to come by. But if improperly designed, bat boxes can end up hurting more than helping, Illinois bat researcher Joy O’Keefe says.
Bat box design might seem straightforward at first glance. Bats need habitat, and boxes can provide shelter. But the reality is much more complicated, O’Keefe said.
“Bats can’t really evaluate the key characteristics that could dictate how healthy or safe these boxes are,” O’Keefe said. “So it’s incumbent upon us to put out good habitat for them.”
One such important characteristic is temperature. As ambient temperature and sunlight fluctuate throughout the day, bat boxes might get dangerously hot or cold. But bats can’t predict this before choosing the box to roost in, O’Keefe said, and are unlikely to leave boxes during the day due to fear of predation. The results can be deadly, as entire bat families have died in poorly designed boxes.
Improving these boxes is critical as bats face habitat loss and epidemic disease. Midwestern bats are threatened by white nose syndrome, a widespread illness caused by fungal infection, but face an even greater threat from the destruction of forests, where they live.
Insulation simulations
O’Keefe and Bakken simulated different bat box designs, varying color, dimensions, orientations, heat storage, and insulation. The team tried out pine, foam, water, and air to insulate the boxes and keep temperatures stable throughout the day. They then ran the simulations for three “days” to see how temperatures might vary.
“We’re trying to save people the energy and expense of building novel boxes with no idea how they’ll perform,” O’Keefe said. “The simulations are a good preliminary step to give you a sense of how designs will differ. The relative differences between designs should be the same in practicality as they are in the simulation.”
In the simulation, the unmodified bat box reached lethal temperatures of over 113°F (45°C) within the first day. Boxes with a heat storage layer, such as water, externally surrounded by an insulator, like foam, were cooler and retained the most stable temperature over the three days. Lighter colors and thoughtful orientation could also make the boxes safer. For instance, at low latitudes, the most effective method to provide optimal daytime temperatures was to orient the box so that its longer sides faced north and south, in addition to painting the south and west sides white and the north and east sides black.
Instead of giving out uniform recommendations — telling everyone to use pine- and water-insulated bat boxes, for example — O’Keefe and Bakken made their simulation code public, so everyone could use it. Bat conservationists can enter their latitude, box dimensions, and box color, then play around with designs until they find one that works for them. This allows practitioners to tailor their solutions to their particular climate.
Safer roosts for better harvests
Bat boxes are more than just homes for mother and baby bats. They’re an important puzzle piece in strengthening Midwestern ecosystems and reducing the pest burden faced by farmers.
Bats are insectivores — they can’t get enough bugs. They love flies, including mosquitoes. O’Keefe says we want these bug eaters around to get rid of the insects that bite us and our food, but bats need quality habitat to do that. They won’t stick around residential and agricultural areas if there’s nowhere for them to live.
O’Keefe primarily studies the Indiana bat. “It’s been endangered since the inception of the Endangered Species Act, and it relies on large dead trees,” O’Keefe said. “In one area I study, an Indiana bat population is essentially 100% reliant on bat boxes now, because there are no big dead trees on this landscape. If we hadn’t put up boxes, this colony would have moved somewhere else.”
By improving bat boxes, O’Keefe hopes to provide needed habitat for these endangered bats and other bat species. Doing so will ensure bats are foraging over our agricultural and natural ecosystems for years to come.
The study, “Simple design modifications can tailor bat box thermal conditions to life history requirements in different habitats,” is published in the Ecological Solutions and Evidence [DOI: 10.1002/2688-8319.70057]. Authors include George Bakken and Joy O’Keefe.
Top row: In a mouse model of Alzheimer’s disease, lithium deficiency (right) dramatically increased amyloid beta deposits in the brain compared with mice that had normal physiological levels of lithium (left). Bottom row: The same was true for the Alzheimer’s neurofibrillary tangle protein tau.
Alt text: One pair of boxes shows fewer green amyloid clusters on the left and more on the right. Another pair of boxes shows a dim arc of purple and red tau on the left and a brighter arc on the right.
Study shows for the first time that lithium plays an essential role in normal brain function and can confer resistance to brain aging and Alzheimer’s disease.
Scientists discovered that lithium is depleted in the brain by binding to toxic amyloid plaques — revealing a new way Alzheimer’s may begin.
A new class of lithium-based compounds avoids plaque binding and reverses Alzheimer’s and brain aging in mice, without toxicity.
What is the earliest spark that ignites the memory-robbing march of Alzheimer’s disease? Why do some people with Alzheimer’s-like changes in the brain never go on to develop dementia? These questions have bedeviled neuroscientists for decades.
Now, a team of researchers at Harvard Medical School may have found an answer: lithium deficiency in the brain.
The work, published Aug. 6 in Nature, shows for the first time that lithium occurs naturally in the brain, shields it from neurodegeneration, and maintains the normal function of all major brain cell types. The findings — 10 years in the making — are based on a series of experiments in mice and on analyses of human brain tissue and blood samples from individuals in various stages of cognitive health.
The scientists found that lithium loss in the human brain is one of the earliest changes leading to Alzheimer’s, while in mice, similar lithium depletion accelerated brain pathology and memory decline. The team further found that reduced lithium levels stemmed from binding to amyloid plaques and impaired uptake in the brain. In a final set of experiments, the team found that a novel lithium compound that avoids capture by amyloid plaques restored memory in mice.
The results unify decades-long observations in patients, providing a new theory of the disease and a new strategy for early diagnosis, prevention, and treatment.
Affecting an estimated 400 million people worldwide, Alzheimer’s disease involves an array of brain abnormalities — such as clumps of the protein amyloid beta, neurofibrillary tangles of the protein tau, and loss of a protective protein called REST — but these never explained the full story of the disease. For instance, some people with such abnormalities show no signs of cognitive decline. And recently developed treatments that target amyloid beta typically don’t reverse memory loss and only modestly reduce the rate of decline.
It’s also clear that genetic and environmental factors affect risk of Alzheimer’s, but scientists haven’t figured out why some people with the same risk factors develop the disease while others don’t.
Lithium, the study authors said, may be a critical missing link.
“The idea that lithium deficiency could be a cause of Alzheimer’s disease is new and suggests a different therapeutic approach,” said senior author Bruce Yankner, professor of genetics and neurology in the Blavatnik Institute at HMS, who in the 1990s was the first to demonstrate that amyloid beta is toxic.
The study raises hopes that researchers could one day use lithium to treat the disease in its entirety rather than focusing on a single facet such as amyloid beta or tau, he said.
One of the main discoveries in the study is that as amyloid beta begins to form deposits in the early stages of dementia in both humans and mouse models, it binds to lithium, reducing lithium’s function in the brain. The lower lithium levels affect all major brain cell types and, in mice, give rise to changes recapitulating Alzheimer’s disease, including memory loss.
The authors identified a class of lithium compounds that can evade capture by amyloid beta. Treating mice with the most potent amyloid-evading compound, called lithium orotate, reversed Alzheimer’s disease pathology, prevented brain cell damage, and restored memory.
Although the findings need to be confirmed in humans through clinical trials, they suggest that measuring lithium levels could help screen for early Alzheimer’s. Moreover, the findings point to the importance of testing amyloid-evading lithium compounds for treatment or prevention.
Other lithium compounds are already used to treat bipolar disorder and major depressive disorder, but they are given at much higher concentrations that can be toxic, especially to older people. Yankner’s team found that lithium orotate is effective at one-thousandth that dose — enough to mimic the natural level of lithium in the brain. Mice treated for nearly their entire adult lives showed no evidence of toxicity.
“You have to be careful about extrapolating from mouse models, and you never know until you try it in a controlled human clinical trial,” Yankner said. “But so far the results are very encouraging.”
Lithium depletion is an early sign of Alzheimer’s
Yankner became interested in lithium while using it to study the neuroprotective protein REST. Finding out whether lithium is found in the human brain and whether its levels change as neurodegeneration develops and progresses, however, required access to brain tissue, which generally can’t be accessed in living people.
So the lab partnered with the Rush Memory and Aging Project in Chicago, which has a bank of postmortem brain tissue donated by thousands of study participants across the full spectrum of cognitive health and disease.
Having that range was critical because trying to study the brain in the late stages of Alzheimer’s is like looking at a battlefield after a war, said Yankner; there’s a lot of damage and it’s hard to tell how it all started. But in the early stages, “before the brain is badly damaged, you can get important clues,” he said.
Led by first author Liviu Aron, senior research associate in the Yankner Lab, the team used an advanced type of mass spectroscopy to measure trace levels of about 30 different metals in the brain and blood of cognitively healthy people, those in an early stage of dementia called mild cognitive impairment, and those with advanced Alzheimer’s.
Lithium was the only metal that had markedly different levels across groups and changed at the earliest stages of memory loss. Its levels were high in the cognitively healthy donors but greatly diminished in those with mild impairment or full-blown Alzheimer’s.
The team replicated its findings in samples obtained from multiple brain banks nationwide.
The observation aligned with previous population studies showing that higher lithium levels in the environment, including in drinking water, tracked with lower rates of dementia.
But the new study went beyond by directly observing lithium in the brains of people who hadn’t received lithium as a treatment, establishing a range that constitutes normal levels, and demonstrating that lithium plays an essential role in brain physiology.
“Lithium turns out to be like other nutrients we get from the environment, such as iron and vitamin C,” Yankner said. “It’s the first time anyone’s shown that lithium exists at a natural level that’s biologically meaningful without giving it as a drug.”
Then Yankner and colleagues took things a step further. They demonstrated in mice that lithium depletion isn’t merely linked to Alzheimer’s disease — it helps drive it.
Loss of lithium causes the range of Alzheimer’s-related changes
The researchers found that feeding healthy mice a lithium-restricted diet brought their brain lithium levels down to a level similar to that in patients with Alzheimer’s disease. This appeared to accelerate the aging process, giving rise to brain inflammation, loss of synaptic connections between neurons, and cognitive decline.
In Alzheimer’s mouse models, depleted lithium dramatically accelerated the formation of amyloid-beta plaques and structures that resemble neurofibrillary tangles. Lithium depletion also activated inflammatory cells in the brain called microglia, impairing their ability to degrade amyloid; caused the loss of synapses, axons, and neuron-protecting myelin; and accelerated cognitive decline and memory loss — all hallmarks of Alzheimer’s disease.
The mouse experiments further revealed that lithium altered the activity of genes known to raise or lower risk of Alzheimer's, including the most well-known, APOE.
Replenishing lithium by giving the mice lithium orotate in their water reversed the disease-related damage and restored memory function, even in older mice with advanced disease. Notably, maintaining stable lithium levels in early life prevented Alzheimer’s onset — a finding that confirmed that lithium fuels the disease process.
“What impresses me the most about lithium is the widespread effect it has on the various manifestations of Alzheimer’s. I really have not seen anything quite like it all my years of working on this disease,” said Yankner.
A promising avenue for Alzheimer’s treatment
A few limited clinical trials of lithium for Alzheimer’s disease have shown some efficacy, but the lithium compounds they used — such as the clinical standard, lithium carbonate — can be toxic to aging people at the high doses normally used in the clinic.
The new research explains why: Amyloid beta was sequestering these other lithium compounds before they could work. Yankner and colleagues found lithium orotate by developing a screening platform that searches a library of compounds for those that might bypass amyloid beta. Other researchers can now use the platform to seek additional amyloid-evading lithium compounds that might be even more effective.
“One of the most galvanizing findings for us was that there were profound effects at this exquisitely low dose,” Yankner said.
If replicated in further studies, the researchers say lithium screening through routine blood tests may one day may offer a way to identify individuals at risk for Alzheimer’s who would benefit from treatment to prevent or delay disease onset.
Studying lithium levels in people who are resistant to Alzheimer’s as they age might help scientists establish a target level that they could help patients maintain to prevent onset of the disease, Yankner said.
Since lithium has not yet been shown to be safe or effective in protecting against neurodegeneration in humans, Yankner emphasizes that people should not take lithium compounds on their own. But he expressed cautious optimism that lithium orotate or a similar compound will move forward into clinical trials in the near future and could ultimately change the story of Alzheimer’s treatment.
“My hope is that lithium will do something more fundamental than anti-amyloid or anti-tau therapies, not just lessening but reversing cognitive decline and improving patients’ lives,” he said.
Authorship, funding, disclosures
Additional authors are Zhen Kai Ngian, Chenxi Qiu, Jaejoon Choi, Marianna Liang, Derek M. Drake, Sara E. Hamplova, Ella Lacey, Perle Roche, Monlan Yuan, and Saba S. Hazaveh of HMS; Eunjung A. Lee of Boston Children’s Hospital; and David A. Bennett of the Rush Alzheimer’s Disease Center at Rush University Medical Center in Chicago.
This work was supported by the National Institutes of Health (grants R01AG046174, R01AG069042, K01AG051791, DP2AG072437, P30AG10161, P30AG72975, R01AG15819, R01AG17917, U01AG46152, and U01AG61356), the Ludwig Family Foundation, the Glenn Foundation for Medical Research, and the Aging Mind Foundation.
Lithium deficiency thinned the myelin that coats neurons (right) compared to normal mice (left). Alt text: side-by-side grayscale electron microscopy images show thicker cell borders on the left and thinner borders on the right.
Treating mice with the amyloid-evading lithium orotate (top row) reduced amyloid beta (left) and tau (right) much more effectively than lithium carbonate (bottom row).
Alt text: Stacked boxes on the left show significantly fewer green amyloid-beta clumps for mice treated with lithium orotate. Stacked boxes on the right show a similar drop in red tau tangles.
Credit
Yankner Lab
Lithium was the only metal that differed significantly between people with and without mild cognitive impairment, often a precursor to Alzheimer’s disease.
Alt text: a scatter plot of different metals shows one main cluster and then an outlier, labeled “lithium.”
Credit
Aron et al, 'Lithium deficiency and the onset of Alzheimer’s disease', Nature
