The hours you work earlier in life may be associated with worse health years later, according to a study published April 3, 2024 in the open-access journal PLOS ONE by Wen-Jui Han from New York University.
Studies have consistently shown that nonstandard work schedules — working outside the traditional nine-to-five workday — can negatively impact physical and mental health as well as social and family life. The current study uses a life-course approach to provide a longer-term perspective on how work schedule patterns throughout a person’s working life impact their health in middle age.
Han used data from The National Longitudinal Survey of Youth-1979 (NLSY79), which includes data on more than 7,000 people in the US over 30 years, to see whether employment patterns in younger adulthood were associated with sleep, physical health, and mental health at age 50.
Han found that around a quarter of participants (26%) worked stable standard hours, with a further third (35%) working mostly standard hours. 17 percent initially worked standard hours in their 20s, later transitioning into volatile working patterns — a combination of evening, night, and variable hours. 12 percent initially worked standard hours and then switched to variable hours. A final ten percent were mostly not working over this period.
Compared to individuals who mostly worked during traditional daytime hours throughout their working career, those whose careers featured more volatile work schedules slept less, had lower sleep quality, and were more likely to report depressive symptoms at age 50. The most striking results were seen in those who had stable work hours in their 20s and then transitioned to more volatile work hours in their 30s. This effect size was significant and similar to that of being educated only to below high school level.
Han also found racial and gender-related trends. For example, Black Americans were more likely to have volatile work schedules associated with poorer health, highlighting how some groups may disproportionately shoulder the adverse consequences of such employment patterns.
Han suggests that volatile work schedules are associated with poor sleep, physical fatigue, and emotional exhaustion, which may make us vulnerable to an unhealthy life. The study also suggests that positive and negative impacts of work schedules on health can accumulate over one’s lifetime while highlighting how employment patterns can contribute to health inequities.
Han adds: “Work that is supposed to bring resources to help us sustain a decent life has now become a vulnerability to a healthy life due to the increasing precarity in our work arrangements in this increasingly unequal society. People with vulnerable social positions (e.g., females, Blacks, low-education) disproportionately shoulder these health consequences.”

Alzheimer’s disease starts with a sticky protein called amyloid beta that builds up into plaques in the brain, setting off a chain of events that results in brain atrophy and cognitive decline. The new generation of Alzheimer’s drugs — the first proven to change the course of the disease — work by tagging amyloid for clearance by the brain’s immune cells.
Now, researchers at Washington University School of Medicine in St. Louis have found a different and promising way to remove the noxious plaques: by directly mobilizing immune cells to consume them.
In a study published April 3 in Science Translational Medicine, the researchers showed that activating immune cells called microglia with an antibody reduces amyloid plaques in the brain and mitigates behavioral abnormalities in mice with Alzheimer’s-like disease.
The approach could have implications beyond Alzheimer’s. Toxic clumps of brain proteins are features of many neurodegenerative conditions, including Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and Huntington’s disease. Encouraged by the study results, researchers are exploring other potential immunotherapies — drugs that harness the immune system — to remove junk proteins from the brain that are believed to advance other diseases.
“By activating microglia generally, our antibody can remove amyloid beta plaques in mice, and it could potentially clear other damaging proteins in other neurodegenerative diseases, including Parkinson’s disease,” explained the study’s senior author, Marco Colonna, MD, the Robert Rock Belliveau, MD, Professor of Pathology.
Microglia surround plaques to create a barrier that controls the damaging protein’s spread. They also can engulf and destroy the plaque proteins, but in Alzheimer’s disease they usually do not. The source of their passivity could result from a protein called APOE that is a component of amyloid plaques. The APOE proteins in the plaque bind to a receptor — LILRB4 — on the microglia surrounding the plaques, inactivating them, Yun Chen, co-first author on the study, explained.
For reasons that are still unknown, the researchers found that, in mice and people with Alzheimer’s disease, microglia that surround plaques produce and position LILRB4 on their cell surface, which inhibits their ability to control damaging plaque formation upon binding to APOE. The other co-first author Jinchao Hou, PhD, now a faculty member at Children’s Hospital of Zhejiang University School of Medicine in Zhejiang Province, China, treated mice that had amyloid beta plaques in the brain with a homemade antibody that blocked APOE from binding to LILRB4. After working with Yongjian Liu, PhD, a professor of radiology in Washington University’s Mallinckrodt Institute of Radiology, to confirm that the antibody reached the brain, the researchers found that activated microglia were able to engulf and clear the amyloid beta plaques.

Clearing the amyloid beta plaques in mice also alleviates risk-taking behavior. Individuals with AD may lack memory of past experiences to inform their decisions. They may engage in risky behavior, making them vulnerable to becoming victims of fraud or financial abuse. Treating mice with an antibody to clear the plaques showed promise in altering the behavior.
After amyloid beta plaques form in the brain, another brain protein — tau — becomes tangled inside neurons. In this second stage of the disease, neurons die and cognitive symptoms arise. High levels of LILRB4 and APOE have been observed in AD patients in this later stage, Chen explained. It is possible that blocking the proteins from interacting and activating microglia could alter later stages of the disease. In future studies, the researchers will test the antibody in mice with tau tangles.
Drugs that target amyloid plaques directly can cause a potentially serious side effect. In Alzheimer’s patients, amyloid proteins build up on the walls of the arteries in the brain as well as other parts of brain tissue. Removing plaques from brain blood vessels can induce swelling and bleeding, a side effect known as ARIA. This side effect is seen in some patients receiving lecanemab, a drug approved by the Food and Drug Administration to treat Alzheimer’s. The mice used in this study lacked amyloid plaques on blood vessels, so the researchers could not evaluate what happens when blood vessel plaques are removed.
They are working with a different mouse model — one that does have plaques on brain arteries — to understand if this new approach also carries a risk of ARIA.
“Lecanemab, as the first therapeutic antibody that has been able to modify the course of the disease, confirmed the importance of amyloid beta protein in Alzheimer’s disease progression,” said author David Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology. “And it opened new opportunities for developing other immunotherapies that use different methods of removing damaging proteins from the brain.”
Senior medical sciences writer Tamara Schneider contributed to this story.

Ever want to scream during a particularly bad day, but then manage not to? Thank the human brain and how it regulates emotions, which can be critical for navigating everyday life. As we perceive events unfolding around us, the ability to be flexible and reframe a situation impacts not only how we feel, but also our behavior and decision-making.
In fact, some of the problems associated with mental health relate to individuals’ inability to be flexible, such as when persistent negative thoughts make it hard to perceive a situation differently.
To help address such issues, a new Dartmouth-led study is among the first of its kind to separate activity relating to emotion generation from emotion regulation in the human brain. The findings are published in Nature Neuroscience.
“As a former biomedical engineer, it was exciting to identify some brain regions that are purely unique to regulating emotions,” says lead author Ke Bo, a postdoctoral researcher in the Cognitive and Affective Neuroscience Lab (CANlab) at Dartmouth. “Our results provide new insight into how emotion regulation works by identifying targets which could have clinical applications.”
For example, the systems the researchers identified could be good targets for brain stimulation to enhance the regulation of emotion.
Using computational methods, the researchers examined two independent datasets of fMRI studies obtained earlier by co-author Peter Gianaros at the University of Pittsburgh. Participants’ brain activity was recorded in an fMRI scanner as they viewed images that were likely to draw a negative reaction such as a bloody scene or scary- looking animals.
The participants were then asked to recontextualize the stimulus by generating new kinds of thoughts about an image to make it less aversive, before a neutral image was presented followed by another dislikable image.

By examining the neural activity, researchers could identify the brain areas that are more active when emotions are regulated versus when emotions are generated.
The new study reveals that emotion regulation, also known in neuroscience as “reappraisal,” involves particular areas of the anterior prefrontal cortex and other higher-level cortical hierarchies whose role in emotion regulation had not previously been isolated with this level of precision. These regions are involved in other high-level cognitive functions and are important for abstract thought and long-term representations of the future.
The more people are able to activate these emotion regulation-selective brain regions, the more resilient they are to experiencing something negative without letting it affect them personally. These findings build on other research linking these areas to better mental health and the ability to resist temptations and avoid drug addiction.
The results also demonstrated that the amygdala, which is known as the threat-related brain region responsible for negative emotion and has long been considered an ancient subcortical threat center, responds to aversive experiences the same way, whether people are using their thoughts to self-regulate down-regulate negative emotion or not. “It’s really the cortex that is responsible for generating people’s emotional responses, by changing the way we see and attach meaning to events in our environments,” says Bo.
The researchers were also interested in identifying the neurochemicals that interact with emotion regulation systems. Neurotransmitters like dopamine and serotonin shape how networks of neurons communicate and are targets for both illicit drugs and therapeutic treatments alike. Some neurotransmitters may be important for enabling the ability to self-regulate or “down-regulate.”
The team compared the emotion regulation brain maps from the two datasets to neurotransmitter binding maps from 36 other studies. The systems involved in regulating negative emotion overlapped with particular neurotransmitter systems.

“Our results showed that receptors for cannabinoids, opioids, and serotonin, including 5H2A, were especially rich in areas that are involved in emotion regulation,” says senior author Tor Wager, the Diana L. Taylor Distinguished Professor in Neuroscience and director of the Dartmouth Brain Imaging Center at Dartmouth. “When drugs that bind to these receptors are taken, they are preferentially affecting the emotion regulation system, which raises questions about their potential for long-term effects on our capacity to self-regulate.”
Serotonin is well-known for its role in depression, as the most widely used antidepressant drugs inhibit its reuptake in synapses, which transmit signals from one neuron to another.
5H2A is the serotonin receptor most strongly affected by another exciting new type of treatment for mental health — psychedelic drugs. The study’s findings suggest that the effects of drugs on depression and other mental health disorders may work in part by altering how we think about life events and our ability to self-regulate. This may help explain why drugs, particularly psychedelics, are likely to be ineffective without the right kind of psychological support. The study could help improve therapeutic approaches by increasing our understanding of why and how psychological and pharmaceutical approaches need to be combined into integrated treatments.
“It’s important to consider these types of connections that come from basic science,” says Wager. “Understanding drug effects requires understanding the brain systems involved and what they’re doing at a cognitive level.”

The trial lasted only one year but offered embers of hope to some experts.In 1817, James Parkinson expressed a hope about the disease that is named after him. He thought that at some point there would be a discovery and “the progress of the disease may be stopped.”Now, nearly 200 years since Parkinson expressed his hope, and after four decades of unsuccessful clinical trials, a group of French researchers reports the first glimmer of success — a modest slowing of the disease in a one-year study.And the drug they used? A so-called GLP-1 receptor agonist, similar to the wildly popular drugs Ozempic, for diabetes, and Wegovy, for obesity.As many as half a million Americans have been diagnosed with Parkinson’s disease, a degenerative brain illness second only to Alzheimer’s in prevalence.Symptoms include tremors, slowness and stiffness, and difficulty with balance. That can lead to difficulty walking, talking and swallowing. Many patients develop dementia.But there are drugs and treatments, like deep brain stimulation, that help, said Dr. David Standaert, a Parkinson’s expert at the University of Alabama at Birmingham.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Richard Slayman, 62, is the first patient to receive a kidney from a genetically modified pig. Two weeks after the procedure, he was well enough to be discharged, doctors said.The first patient to receive a kidney transplanted from a genetically modified pig has fared so well that he has been discharged from the hospital on Wednesday, just two weeks after the groundbreaking surgery.The transplant and its encouraging outcome represent a remarkable moment in medicine, scientists say, possibly heralding an era of cross-species organ transplantation.Two previous organ transplants from genetically modified pigs failed. Both patients received hearts, and both died a few weeks later. In one patient, there were signs that the immune system had rejected the organ, a constant risk.But the kidney transplanted into Richard Slayman, 62, is producing urine, removing waste products from the blood, balancing the body’s fluids and carrying out other key functions, according to his doctors at Massachusetts General Hospital.“This moment — leaving the hospital today with one of the cleanest bills of health I’ve had in a long time — is one I wished would come for many years,” he said in a statement issued by the hospital. “Now it’s a reality.”He said he had received “exceptional care” and thanked his physicians and nurses, as well as the well-wishers who reached out to him, including kidney patients who were waiting for an organ.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A collaboration between research groups at the University of California, TU Dresden in Germany and Cedars-Sinai Guerin Children’s in Los Angeles has identified a mechanism by which embryonic cells organize themselves to send signals to surrounding cells, telling them where to go and what to do. While these signaling centers have been known to science for a while, how individual cells turn into organizers has been something of a mystery.
Until now. In a paper published in the journal Nature Cell Biology, the researchers find that cells are literally pressed into becoming organizers.
“We were able to usemicrodroplet techniquesto figure out how the buildup of mechanical pressure affects organ formation,” said co-corresponding authorOtger Campàs, former associate professor of mechanical engineering at UC Santa Barbara, who is currently managing director, professor and chair of tissue dynamics at thePhysics of Life Excellence Cluster of TU Dresden.
Peer pressure
Finding out how cells decide to become organizers during the formation of organs remains a central challenge in the study of embryogenesis, and is key to understanding embryonic development.
“By understanding how an embryo forms organs, we can start to ask questions about what goes wrong in children born with congenital malformations,” said fellow co-authorOphir Klein, MD, executive director of Cedars-Sinai Guerin Children’s, where he is also the David and Meredith Kaplan Distinguished Chair in Children’s Health.
Building on techniques previously developed by Campàs, in which minute droplets inserted between developing embryonic cells sense the forces exerted by cells on each other, and through observations of an embryonic incisor tooth, the researchers found that pressure influences a cell’s fate — they feel the squeeze and use this information to organize themselves.

“It’s like those toys that absorb water and grow in size,” said Neha Pincha Shroff, a postdoctoral scholar in the School of Dentistry at UCSF, and co-lead author of the study. “Just imagine that happening in a confined space. What happens in the incisor knot is that the cells multiply in number in a fixed space and this causes a pressure to build up at the center, which then becomes a cluster of specialized cells.” The researchers found that the cells feeling the stronger pressure stop growing and start sending signals to organize the other surrounding cells in the tooth.
Embryos use several of these signaling centers to guide cells as they form tissues and organs. Cells around these centers receive stronger or weaker signals depending on their location, and they make decisions accordingly. Like building skyscrapers or bridges, sculpting our organs involves tight planning, a lot of coordination and the right structural mechanics. Failure in any of these processes can be catastrophic when it comes to building a bridge, and it can also be damaging for us when growing in the womb.
“This work may lead to additional research into how birth defects are formed and can be prevented,” Klein remarked.
Seeing how pressure works in embryonic development opens up further research possibilities, according to Campàs.
“It is really exciting that pressure has a role in establishing signaling centers,” he said. “It will be interesting to see if or how mechanical pressure affects other important developmental processes.”
Investigators Pengfei Xu (co-first author), Sangwoo Kim, Elijah Shelton, Ben Gross, Yucen Liu, Carlos Gomez, Qianlin Ye, Tingsheng Yu Drennon, Jimmy Hu, and Jeremy Green also participated in the study.

A recent breakthrough sheds light on how the malaria parasite, Plasmodium falciparum, invades human red blood cells. The study, led by the Swiss Tropical and Public Health Institute (Swiss TPH) and Griffith University’s Institute for Glycomics, reveals the role of a sugar called sialic acid in this invasion process. The findings, published yesterday in Cell Reports, have major implications for malaria vaccine and drug development.
With 249 million cases of malaria and 608,000 deaths in 2022, malaria has remained an intractable global health threat. The malaria parasite Plasmodium falciparum is the leading cause of severe malariaand is responsible for the largest portion of malaria deaths. All clinical symptoms of malaria are caused by the multiplication of malaria parasites in the red blood cells.
Key component found for malaria invasion
P. falciparum is known to invade human red blood cells, but the precise details of the targets that the parasite binds to has not been known to date. Although we know that the malaria protein, cystein-rich protective antigen (CyRPA), is essential for the invasion of red blood cells, its precise role in this process was not understood.
A multidisciplinary, collaborative research team from six institutions, led by investigators at Swiss TPH in Switzerland and Institute for Glycomics in Australia examined the binding properties of CyPRA. The researchers discovered that a sugar called sialic acid is a key component of the red blood cell surface that is recognized by the malaria parasite, and which is essential for the invasion process. The findings were published in the peer-reviewed journal Cell Reports.
“We are now demonstrating that P. falciparum CyRPA binds to a specific carbohydrate structure (glycan) present on the red blood cell surface. The CyRPA protein is highly adapted to bind to a glycan terminating with a sialic acid. The discovery of the key function of CyRPA in host cell invasion provides an explanation for the parasite inhibitory activity of CyRPA-specific antibodies” said Gerd Pluschke, Group Leader of Molecular Immunology at Swiss TPH, and co-corresponding author of the publication.
Malaria parasite adapted to humans
“Humans differ from other primates because they can only produce one type of sialic acid, called Neu5Ac. This genetic difference between humans and closely related primates has long been proposed to contribute to the species-specific targeting of malaria parasites. In this study, we show that the human form of sialic acid, Neu5Ac, is strongly preferred by the human-specific malaria parasite P. falciparum, and may explain the adaptation of this parasite to humans,” said Michael Jennings, Acting Director of the Institute for Glycomics, and co-corresponding author of the paper.

Implications for vaccine and drug development
Vaccines targeting the P. falciparum pre-erythrocytic stages are registered for use. However, they only show moderate levels of efficacy. There is no registered vaccine against the blood stage of malaria, but there is intensive research on blood stage vaccines. “The discovery of the key function of CyRPA in host cell invasion strongly supports the concept to clinically test CyRPA as a blood stage vaccine target,” said Pluschke.
Moreover, as the emergence of drug resistance in the parasites that cause malaria is a major health threat, the study’s findings offer hope for new antimalarial drugs that are urgently needed. “The essential binding activity of CyRPA to a specific glycan also validates CyRPA as drug target, and we demonstrate that small molecule inhibitors that interfered with this function can inhibit malaria replication in our study,” said Jennings.

To better understand COVID-19’s spread during the pandemic, public health officials expanded wastewater surveillance. These efforts track SARS-CoV-2 levels and health risks among most people, but they miss people who live without shelter, a population particularly vulnerable to severe infection. To fill this information gap, researchers reporting in ACS’ Environmental Science & Technology Letters tested flood-control waterways near unsheltered encampments, finding similar transmission patterns as in the broader community and identifying previously unseen viral mutations.
In recent years, testing untreated wastewater for SARS-CoV-2 incidence and dominant viral variants, as well as other pathogens, has been vital to helping public health officials determine infectious disease transmission in local communities. Yet, this monitoring only captures information on viruses shed from human feces and urine in buildings that are connected to local sewage infrastructure. Beyond the pandemic’s impact on human health, it also exacerbated socioeconomic difficulties and increased the number of people experiencing homelessness and living in open-air encampments without access to indoor bathrooms. To understand the prevalence of COVID-19 among people who live unsheltered, Edwin Oh and colleagues tested for SARS-CoV-2 in waterways near encampments outside Las Vegas from December 2021 through July 2022.
Using quantitative polymerase chain reaction, the researchers identified SARS-CoV-2 RNA in more than 25% of the samples tested from two flood-control channels. The highest detection frequency over the study period aligned with Las Vegas’ first wave of omicron variant infections, as confirmed through parallel testing at a local wastewater treatment plant. The researchers say these results suggest a similar level of transmission was occurring within the unsheltered community as it was among the general population. Then the researchers conducted whole genome sequencing to identify the SARS-CoV-2 variants in the waterways. These samples largely contained the same variants identified in the broader community. Deeper computational analysis of the viral sequences identified three novel viral spike protein mutations in some waterway samples, but the researchers have not yet examined what impact these mutations might have on viral function or clinical outcomes. Regardless, the ability to detect and identify SARS-CoV-2 in environmental water samples could help improve public health measures for a community that is often underrepresented in current surveillance methods. The researchers also say monitoring waterways could warn health officials of unexpected variants circulating in the community.
The authors acknowledge funding from the National Institutes of Health, the Nevada Governor’s Office of Economic Development, the Centers for Disease Control and Prevention, and the Water Resources Research Institute of the United States Geological Survey.

Choosing paint for your home brings a lot of options: What kind of paint, what type of finish and what color? Water-based paints have emerged as “greener” and less smelly than solvent-based options. And they are often advertised as containing little-to-no volatile organic compounds (VOCs). But, according to research published in ACS’ Environmental Science & Technology Letters, some of these paints do contain compounds that are consideredVOCs, along with other chemicals of emerging concern.
Paint consists of four ingredients: pigments, binders, additives and a liquid. If the liquid is water — as in latex and some acrylic paints — it’s classified as a water-based paint, rather than solvent-based. Historically, solvent-based paints were easy to apply and durable, though they released foul-smelling VOCs into the air both during and after application, stinking up a newly painted room. These airborne VOCs can cause respiratory irritation and headaches, among other potential health problems, especially in high concentrations or over long periods of time. Despite water-based paints sporting labels with “zero-” or “low-VOC,” their formulations could contain potentially dangerous chemicals of their own. So, Ying Xu and colleagues wanted to understand more about these paints’ formulations. The team notes that there are differing definitions of what constitutes a VOC, some of which are stricter than others, including the World Health Organization’s definition used in this research.
The team collected 40 water-based paints from around the world, all ranked among the top 70 most-sold brands, and many labelled as zero- or low-VOC. Both dry and wet samples were analyzed by gas chromatography-mass spectrometry to determine their composition. Twenty semi-volatile organic compounds were identified in concentrations ranging from 10 to 35,000 parts per million. While less likely to be in a gaseous form, these can still persist indoors for years, often incorporated into dust. Endocrine-disrupting phthalates, which act as binders, were largely absent in the tested paints. However, several phthalate-replacement chemicals were detected — their toxicities are still being assessed. Nearly half the analyzed samples contained measurable amounts of isothiazolinones — preservatives that have been linked to skin irritation and asthmatic symptoms. In 24 of the wet paint samples advertised as either zero- or low-VOC, 11 different VOCs were detected at concentrations up to 20,000 parts per million.These concentrations represent the chemical composition within the paint, not the air. Further studies are required to understand how much of these potentially hazardous compounds become airborne as painted surfaces are drying. The researchers say that this work could allow for the design of safer paint products in the future.
The authors acknowledge funding from the National Natural Science Foundation of China.

The crack of a gunshot ringing out in the night is all too familiar to many Americans. A new study captures just how common — and potentially disruptive — nighttime gunshots can be in American cities. In a cross-institutional collaboration from Mass General Brigham’s founding members, Brigham and Women’s Hospital and Massachusetts General Hospital, researchers examined the number of nights and people potentially affected by the sound of nighttime versus daytime gunshots and the relationship between the sound of nighttime gunshots and median household income in the United States. The team found gunshots are twice as likely to occur at night, and that low-income communities are disproportionately affected by them. Their results are published in the Journal of General Internal Medicine.
“A nighttime gunshot likely disrupts the sleep of nearby community residents due to the sheer sound of the shot, which is then followed by a cacophony of sirens from police vehicles and ambulances,” said corresponding author Rebecca Robbins, MMSc, PhD, MS, of the Division of Sleep and Circadian Disorders at Brigham and Women’s Hospital. “The findings from our study shed light on this potentially significant and underexplored social determinant of sleep and population health.”
Minimizing disruptions during the sleep cycle is critical to achieving quality sleep and improving overall health. Various factors, including jetlag from traveling or the onset of hunger during the late hours of the night, can interrupt sleep and lead to metabolic, cardiovascular, and mental health diseases and conditions. Other disruptions, such as nighttime gunshots, warrant further exploration.
Gun violence is a public health threat and the leading cause of death among children and adolescents in the United States. The number of gun deaths due to gun violence in America is staggering. According to the Centers for Disease Control and Prevention, there were more than 48,000 gun-related deaths in the United States in 2022.
Additionally, researchers note that there is potential for an exponentially broader community impact of gunshots beyond those that result in casualties. The current study focuses on the impact of the sounds of guns on surrounding communities; previous studies from the authors have focused on mental and behavioral health consequences from gun violence.
“The traumatic ripple effects from gunshots can extend across families and entire communities. Our work helps to broaden how we think about who is impacted by these events,” said co-last author Chana A. Sacks, MD, MPH, of the Division of General Internal Medicine and Mongan Institute at Massachusetts General Hospital.
The team gathered 72,236 publicly available records on the time and location of gunshots in six major cities in the United States, including Baltimore, Boston, Washington, DC, New York, Philadelphia, and Portland, Ore., from 2015-2021. Using those data, investigators compared the prevalence of gunshots during the day versus the night. In addition, they created maps to visualize nighttime gunshot density across the cities. To identify communities potentially impacted by the sound of the gunshot, they estimated the number of those residing near to the location where gunshots took place. The team also examined the association between the number of nighttime gunshots and median household income.

To measure the potential effect of the sound of nighttime gunshots, the team estimated the number of individuals within earshot and the number of nights of potentially disrupted sleep for all individuals within hearing range. The team defined this metric as “person nights” and estimated that approximately 12.5 million person nights across the six cities could be impacted annually. Among the findings was that as median household income went up, rates of nighttime gunshots went down. This highlighted a higher level of gunshot impact — and resulting potential sleep and other disruptions — for people living in low-income neighborhoods. Additionally, it was discovered that 51,789 (72%) of the gunshots occurred during the nighttime across all six cities, with most of them occurring on Saturday and Sunday nights.
The authors note that they did not directly measure sleep disruptions as part of this study. Only six of the 30 most populated cities in the U.S. had enough publicly available data to be included in the analysis. The research team plans to study sleep disturbances in response to nighttime gunshots as they work to design community-based sleep interventions to support individuals in communities with high incidences.
The authors credit their collaboration across hospitals and across areas of research expertise for the insights described in their paper.
“Working as a multidisciplinary research team across the Mass General Brigham healthcare system, with experts in sleep and gun violence, we have been able to advance our understanding of the impacts that gunshots have on communities and inform this critical national conversation,” said Robbins. “Conversations about guns often focus on the statistics on gun-related deaths, but our work draws attention to some of the less discussed impacts of gun violence.”
Authorship: Mass General Brigham of the study include Peter T. Masiakos, Cornelia Griggs and Elizabeth Klerman. Additional authors include Mahmoud Affouf and Jay M. Iyer.
Disclosures: Robbins reports receiving consulting income from by Nacht GmbH, Savoir Beds Ltd., Oura Health Oy, Castle Hot Springs, Sonesta International Hotels Corporation. Robbins has received funding from Bryte Labs. Klerman reports consulting income from the American Academy of Sleep Medicine Foundation, Circadian Therapeutics, National Sleep Foundation, Sleep Research Society Foundation, and Yale University Press; has received travel support from the European Biological Rhythms Society, EPFL Pavilion, the Santa Fe Institute, Sleep Research Society, and the World Sleep Society; and is an unpaid member of the scientific advisory board of Chronsulting. Klerman’s partner is founder, chief scientific officer of Chronsulting.
Funding: This study was supported by the MGH Gun Violence Prevention Center. Robbins has received grant support from the NIH/ NHLBI (K01HL150339). Klerman has received grant support from the NIH (R01NS099055, U01NS114001, U54AG062322, R21DA052861, R21DA052861, R01NS114526-02S1, R01-HD107064), DoD (W81XWH201076), and Leducq Foundation for Cardiovascular Research.
Paper cited: Robbins, R et al. “Estimating Community Disruption from Nighttime Gunshots in 6 U.S. Cities, 2015-2021. Journal of General Internal Medicine. DOI: 10.1007/s11606-024-08707-9