Publisher Health

When a routine blood test shows high levels of a protein called SerpinB3, it often alerts doctors that something is seriously wrong. Elevated SerpinB3 can be associated with difficult-to-treat cancers or severe inflammatory diseases.
SerpinB3 is known as a key protein that helps reveal when the body’s barrier tissues, such as the skin and lungs, are under intense strain from cancer or long-term illness. It has typically been viewed as a sign that these protective surfaces are in trouble.
Recent work from scientists at Arizona State University adds an unexpected twist. Their research shows that SerpinB3, long regarded mainly as a disease marker, also plays a natural part in helping the body repair itself by supporting wound healing.
Chronic Wounds, High Costs
Skin wounds remain a major medical challenge. Each year in the U.S., an estimated 6 million wounds occur, and many are slow to heal or difficult to manage. These hard-to-treat injuries are frequently linked with diabetes, burns, infection or older age, and together they are thought to cost about $20 billion annually.
In a new study, coauthors Jordan Yaron, Kaushal Rege and their colleagues at the Biodesign Center for Biomaterials Innovation and Translation found that SerpinB3 is one of the body’s own wound-healing tools. Their results indicate that the protein helps damaged skin recover after injury.
The work opens the door to new medical strategies. Increasing SerpinB3 activity might one day speed wound repair, while limiting its activity could become a way to slow or control aggressive cancers. The research may also shed light on how SerpinB3 contributes to inflammatory diseases, ranging from skin disorders to asthma.

The findings are reported in Proceedings of the National Academy of Sciences.
Linking Biomaterials, Serpins and Tissue Repair
This study emerged from the intersection of two major efforts in the team’s lab: their broader research on bioactive materials that promote wound repair and their expertise in a family of proteins known as serpins (short for serine protease inhibitors). Serpins help regulate many processes in the body, including blood clotting and immune responses, and several members of this family appear to help keep tissue breakdown and tissue repair in balance.
“When we looked deeper into how our bioactive nanomaterials were helping tissue repair, SerpinB3, a protein originally implicated in cancer, jumped at us as a key factor that correlated with nanomaterial-driven wound healing,” Rege said. “This journey, which started from use-inspired research on biomaterials for tissue repair to uncovering the fundamental role of this protein as an injury-response mechanism in skin, has been truly fascinating. We are now building on this basic finding and investigating the role of SerpinB3 in other pathological conditions.”
Rege is a professor of chemical engineering and director of the Biodesign Center for Biomaterials Innovation and Translation. Yaron serves as an assistant professor of chemical engineering and is also part of the center’s faculty. Both researchers hold academic appointments in the School for Engineering of Matter, Transport and Energy at ASU.
A Protein With a Double Life: Cancer and Healing
Many serpins are associated with disease when their levels in the body fall out of balance, contributing to inflammation, fibrosis and cancer. SerpinB3, one member of this family, has been widely used in cancer diagnostics as a marker of particularly aggressive forms of the disease.

SerpinB3 — also known as squamous cell carcinoma antigen-1 — was first identified in cervical cancer tissue in 1977. Since then, it has been routinely used as a biomarker for aggressive cancers of the lung, liver and skin, where high concentrations often signal a poorer prognosis.
“For more than four decades, SerpinB3 has been recognized as a driver of cancer growth and metastasis — so much so that it became a clinical diagnostic. Yet after all this time, its normal role in the body remained a mystery,” Yaron said. “But when we looked at injured, healing skin, we found that cells moving into the wound bed were producing enormous amounts of this protein. It became clear that this is part of the machinery humans evolved to heal epithelial injuries, a process that cancer cells have learned to exploit to spread. This now opens the doors to understanding how this protein is involved in many more diseases.”
How SerpinB3 Speeds Skin Repair
By monitoring which genes become active during the healing process, the researchers discovered that SerpinB3 levels rose sharply in wounded skin. This increase was even greater in wounds covered with advanced biomaterial dressings, confirming earlier work from the group that showed how these materials can amplify the body’s own repair signals.
In laboratory experiments, supplying additional SerpinB3 caused skin cells to move more quickly and cover wounds more rapidly. It proved to be about as effective as Epidermal Growth Factor, a well-known molecule that promotes healing. SerpinB3 acts by stimulating keratinocytes — the skin cells that normally migrate to repair damage. When activated, these cells become less tightly attached to their surroundings and more able to move, allowing them to slide into the wound area and rebuild tissue.
The protein also supports the body’s broader repair networks, helping to coordinate healing and the growth of new tissue. Wounds treated in this way showed collagen fibers that were more orderly and better organized, creating a stronger support framework that helps the skin regain its strength and integrity.
Future Treatments for Wounds and Cancer
The scientists emphasize that additional research is needed to understand how SerpinB3 fits into the body’s overall healing systems. Because it appears to accelerate repair, SerpinB3 could eventually be developed into a therapy for chronic, hard-to-heal wounds, such as pressure sores and other ulcers that close only very slowly over time.
By uncovering SerpinB3’s double role in both cancer and tissue repair, the study suggests that learning more about the body’s own healing machinery could lead to improved treatments for persistent wounds and new approaches to controlling cancer.

More than half of the calories people consume in the United States come from ultra-processed foods (UPFs), which include items such as fast food and packaged snacks that tend to contain large amounts of sodium, added sugars and unhealthy fats. While studies in adults have firmly connected these foods to type 2 diabetes and other chronic conditions, far less is known about how UPFs affect younger populations.
Researchers at the Keck School of Medicine of USC have now completed one of the earliest studies to examine how UPF intake relates to the body’s ability to manage glucose, a key factor for predicting diabetes. By monitoring changes over several years, the team gained a clearer picture of how long-term food choices can influence important metabolic functions.
Tracking Young Adults Over Time
The study followed 85 young adults for four years. During this period, the researchers found that higher consumption of UPFs was tied to an increased likelihood of developing prediabetes, an early stage of elevated blood sugar that can progress to diabetes. Young adults who ate more UPFs also showed signs of insulin resistance, a condition in which the body becomes less efficient at using insulin to manage blood sugar. The findings, published in the journal Nutrition and Metabolism, were supported in part by the National Institutes of Health.
“Our findings show that even modest increases in ultra-processed food intake can disrupt glucose regulation in young adults at risk for obesity. These results point to diet as a modifiable driver of early metabolic disease, and an urgent target for prevention strategies among young people,” said Vaia Lida Chatzi, MD, PhD, a professor of population and public health sciences and pediatrics and director of the Southern California Superfund Research and Training Program for PFAS Assessment, Remediation and Prevention (ShARP) Center at the Keck School of Medicine, who is the study’s senior author.
Why Early Adulthood Matters
Early adulthood represents a period when individuals have reached physical maturity and are forming routines that may continue for decades. Replacing heavily processed meals with whole foods such as fruits, vegetables and whole grains can lower the chance of developing type 2 diabetes in the future.

“Young adulthood is a critical window for shaping long-term health,” Chatzi said. “By focusing on young adults, we have an opportunity to intervene early, before prediabetes and other risk factors become lifelong conditions.”
Identifying Early Signs of Prediabetes
The participants in the study were part of the Metabolic and Asthma Incidence Research (Meta-AIR) study, itself a segment of the larger Southern California Children’s Health Study. The 85 volunteers, aged 17-22, provided dietary and health information during one visit between 2014 and 2018 and again roughly four years later.
At each appointment, participants listed everything they had eaten on a recent weekday and weekend day. Researchers grouped each food into one of two categories: UPFs (such as candy, soda, cereal, packaged spreads, flavored yogurts and many restaurant meals) or foods that were not ultra-processed. They then calculated the percentage of each person’s total daily calories that came from UPFs.
Blood samples were collected before and after participants drank a sugary beverage so the researchers could evaluate how effectively their bodies produced insulin in response to rising blood sugar. Statistical analyses were used to compare dietary shifts with markers of prediabetes while accounting for differences in age, sex, ethnicity and physical activity.
Between the baseline and follow-up visits, a 10% rise in UPF intake was linked to a 64% higher risk of prediabetes and a 56% higher likelihood of impaired glucose regulation. Participants who consumed more UPFs at the start of the study were also more likely to show elevated insulin at the follow-up visit — an early indicator of insulin resistance, when the body compensates for reduced insulin effectiveness by producing more of it.

Reducing Ultra-Processed Foods for Better Health
The results underscore that UPFs pose significant risks for young adults, a demographic rarely examined in previous work.
“These findings indicate that ultra-processed food consumption increases the risk for pre-diabetes and type 2 diabetes among young adults — and that limiting consumption of those foods can help prevent disease,” said the study’s first author, Yiping Li, a doctoral student in quantitative biomedical sciences at Dartmouth College who previously worked as a researcher at the Keck School of Medicine.
The researchers noted that larger studies with more detailed food tracking could help pinpoint which specific UPFs are most harmful for young adults. They also aim to explore how nutrients in these foods may influence insulin function and blood sugar control.
Study Contributors and Funding
In addition to Li and Chatzi, the study’s authors include Elizabeth Costello, Sarah Rock, Zhanghua Chen, Frank Gilliland, Michael I. Goren, Jesse A. Goodrich and David V. Conti from the Department of Population and Public Health Sciences, Keck School of Medicine of USC, University of Southern California; William B. Patterson from the University of Colorado School of Medicine; Tanya L. Alderete from the Bloomberg School of Public Health, Johns Hopkins University; and Nikos Stratakis from the Barcelona Institute for Global Health (ISGlobal).
This work was primarily supported by the National Institute of Environmental Health Sciences (NIEHS) of the National Institutes of Health [P42ES036506, P30ES007048]. Funding for the Meta-AIR study came from the Southern California Children’s Environmental Health Center grants funded by NIEHS [5P01ES022845-03, P30ES007048, 5P01ES011627]; the U.S. Environmental Protection Agency [RD83544101]; and the Hastings Foundation. Additional funding came from NIEHS [R01ES036253, R01ES029944, R01ES030364, U01HG013288, T32ES013678, U01HG013288, R01ES035035 and R01ES035056]; the European Union [The Advancing Tools for Human Early Lifecourse Exposome Research and Translation (ATHLETE) project: 874583]; the National Institute on Minority Health and Health Disparities [P50MD017344]; and the Horizon Europe Research and Innovation Program [Marie Skłodowska-Curie Actions Postdoctoral Fellowships: 101059245]. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Across the globe, a wide range of animals, including household pets, livestock, and marine species, are developing serious health problems such as cancer, obesity, diabetes, and degenerative joint disease. These non-communicable diseases (NCDs) chronic diseases are becoming increasingly common, yet the scientific community still lacks broad, interdisciplinary research that explains why they are rising in so many species. Understanding these trends is essential because the same factors influencing animal health often affect people as well.
A recent study in Risk Analysis introduces a new conceptual approach designed to improve monitoring and management of chronic diseases in animals. Led by animal scientist Antonia Mataragka of the Agricultural University of Athens, the research offers an evidence-based risk assessment model. The framework not only supports veterinary health but also provides insights relevant to public health, since humans and animals are experiencing similar increases in chronic illnesses.
Genetic and Environmental Drivers of Disease
After reviewing existing research on NCDs in animals, Mataragka’s study highlights multiple contributing factors.
Genetic predisposition increases disease risk in certain populations. Dogs and cats that have been selectively bred for appearance and livestock bred for productivity show higher rates of conditions such as diabetes and mitral valve disease.
Environmental influences, including poor diet, limited physical activity, and long-term stress, also shape how and when these diseases appear across species.
Examples of these patterns are found in many environments. Obesity is widespread among domestic cats and dogs, with recent surveys estimating that 50-60% fall into the overweight category, which has contributed to yearly increases in feline diabetes. In agricultural settings, about 20% of intensively raised pigs develop osteoarthritis. Marine animals face similar challenges: beluga whales have documented gastrointestinal cancers, while farmed Atlantic salmon experience cardiomyopathy syndrome. Wildlife living in polluted estuaries contaminated with industrial chemicals such as polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs) show liver tumor rates as high as 15-25%.

Environmental Change Intensifies Disease Risk
Human-driven ecological transformation is amplifying these threats. Urbanization, climate disruption, land conversion, and loss of biodiversity increase the frequency and severity of harmful exposures. Warming oceans and the decline of coral ecosystems correlate with higher tumor rates in marine turtles and fish. In cities, rising temperatures and poor air quality contribute to obesity, diabetes, and immune disorders in companion animals, while chemical runoff and airborne pollution influence endocrine function in birds and mammals.
“As environmental changes accelerate disease emergence, the absence of early diagnostic systems further delays the detection of NCDs in animals,” says Mataragka. “While organizations like the World Health Organization provide extensive data on NCD mortality in humans, similar detailed statistics for animals are scarce. This indicates the need for more comprehensive research and enhanced surveillance in veterinary health to better understand and address these issues.”
Understanding Disease Patterns Across Species
The study assesses NCD prevalence among different animal groups and examines how specific risk factors contribute to disease development. It proposes mitigation strategies at four levels: individual, population (herd), ecosystem, and policy. The findings highlight climate change, habitat degradation, pollution, and dietary imbalance as major forces increasing vulnerability among pets, livestock, and wildlife.
Linking One Health and Ecohealth Approaches
Mataragka’s model blends One Health and Ecohealth frameworks, both of which emphasize the connections between human, animal, and environmental well-being (but typically operate independently). By bringing these perspectives together, the model shows how biological susceptibility (genetic predisposition) intersects with environmental and socio-ecological pressures to drive disease.
She hopes this integrated approach will support more coordinated monitoring of animals, people, and ecosystems and help identify early warning signs of rising NCDs. By recognizing shared drivers of chronic illness, researchers and policymakers may be better equipped to reduce disease risks across species.

9 hours agoShareSaveShivani ChaudhariEssexShareSaveSuppliedWhen Alex Allan was diagnosed with polycystic ovary syndrome (PCOS) aged 22 her GP told her the symptoms could only be managed and to come back when she wanted to have a baby. Thirty years on, she says women are still being given the same advice. PCOS is a hormonal disorder where ovaries produce large amounts of male sex hormones that interfere with the development and release of the eggs, which can affect periods and fertility.Mrs Allan, 51, is from Leigh-on-Sea, Essex, and works as a nutritionist.She says her PCOS symptoms included hair loss, facial hair, feeling low and gaining weight. “When I have calls with women who are young and they are given the same advice I was given 30 years ago, [it] makes me feel so sad that we haven’t moved forward,” she says. One in eight women in the UK are affected by PCOS, according to the charity Verity. At the time of her diagnosis Mrs Allan was living in London and working in the children’s book industry. When she went to her GP about her condition she says she felt blamed for her symptoms because of her weight.”There is nothing we can do – go on the pill and come back and see me when you want to have a baby,” she says the doctor told her. After that appointment, she says the GP surgery offered no further information.”One of the symptoms of PCOS can be fertility, but not every woman has that and not every person with PCOS wants to have a baby,” she says.The now mother-of-two said she was not thinking about having children at 22. “Once their diagnosis is confirmed, [patients with PCOS] are generally offered the contraceptive pill.”It’s not really getting to the root cause of your condition. “I don’t think it should be a bog standard – one-size-fits-all approach,” she says. At the time the internet was still in its infancy, so Mrs Allan said she turned to dieting groups as a way to manage her symptoms on the understanding that they were due to her weight.Verity found only 3% of PCOS patients felt informed by their healthcare provider and 28% felt like their symptoms were not taken seriously. “The lack of public awareness delays diagnosis and leaves many patients struggling alone with symptoms they don’t understand,” the report stated. SuppliedCharlotte Notley, 34, from Norwich, was diagnosed with insulin resistance PCOS in 2021 and says the GP offered her the pill and would only refer her to a gynaecologist if she wanted to have a baby.She says living with PCOS has made her feel like she is not normal, adding: “I don’t know what it is like to wake up and not have a horrendous migraine or have pain in my ovaries or my uterus.”Mrs Notley says the lack of information led her to turn to social media and Chat GPT to find out more about her symptoms. “Social media, as scary as it is, has been my doctor for the past 18 months. “I shouldn’t have to use social media and use advice of others and what they’ve tried and tested in order to manage a condition that isn’t curable. “I should be able to go to my GP and ask what are the best things I can do,” she says. In 2024, Mrs Notley says she stopped seeking help from the GP over the condition. “I just wasn’t getting anywhere and I was tired of being told that I was too fat all the time,” she says. SuppliedRahat Khan, 50, a NHS consultant obstetrician and gynaecologist at Phoenix Hospital Chelmsford, says: “PCOS is a condition, it is not a disease, it can affect periods and fertility.”It is a difficult condition to diagnose and there is no cure for it. “It is not appropriate to blame anyone for being overweight or for having PCOS because that can affect their mental wellbeing in an adverse manner. “It is important to touch base with your GP or gynaecologist rather than self-treating yourself or trying to find solutions because that might not be very helpful.” Chand Kaur, 27, the founder of PCOS Relief, said the charity supports 2,500 people worldwide and that although she felt there had been research into the condition internationally, there has not been enough to make “a huge breakthrough”. “A lot of research now has come from Australia, so Australia is now leading the way in terms of PCOS,” she says. “I think medicine has advanced but in terms of the diagnosis and the terminology [around PCOS] – I think that it is very much the same,” she says. Mrs Kaur says a PCOS diagnosis often comes with the stigma of being infertile. She adds, however, that once pregnant 65% of women with PCOS carry to full term, though they may face higher risks of complications such as gestational diabetes or preeclampsia.Sue Mann, the national clinical director for women’s health at NHS England, said: “We are acutely aware that too many women with conditions like polycystic ovary syndrome have struggled to get the help they need.”That’s why we’re taking action to improve services and experiences for women, including rolling out women’s health hubs across the country.”With so much content circulating online, it is so important that women get clear, personalised advice from trusted NHS professionals.”A spokesperson from the Department of Health and Social Care said: “Women with polycystic ovary syndrome have been failed for too long.”We’re updating guidance for clinicians, improving training, tackling medical misogyny and have renewed our Women’s Health Strategy to make sure every woman gets the care they deserve.”More on this story

12 hours agoShareSaveHelen BushbyCulture reporterShareSave

3 hours agoShareSaveMartin HeathHertfordshire political reporterShareSaveGetty ImagesA county’s health officials have warned more children and young people could become infected with a severe strain of flu than usual at this time of year.Public health bosses in Hertfordshire said hospital admissions were low at the moment but were expected to rise over the next few weeks.They advised anyone with symptoms to wear a face mask and avoid contact with other people.The county council’s executive member for public health, Ajanta Hilton, has called for a national awareness campaign.Experts in Hertfordshire and across the country were watching the situation in Australia with growing alarm.The southern hemisphere country has seen its worst flu season on record, with 1,544 cases per 100,000 people – a 10.8% increase on the 2024 record.Hertfordshire’s director of public health, Sarah Perman, said: “Australia experiences its flu season a few months before we do [and] we’re beginning to see with some concern that case rates are rising in this country.”Cases among the under-5s in Australia accounted for almost 11% of all infections (more than More than 44,500 cases) and more than a third of the infections were recorded in children below the age of 15.Ms Perman said a similar trend was now being seen in the UK, but other groups were also at risk.Hertfordshire County CouncilMs Perman added: “We are seeing the dominant virus being a strain of influenza A, which is associated with more severe illness and higher mortality, particularly in older people, than some of the other viruses that we commonly see during the flu season.”She urged children, older people, pregnant women and people with certain health conditions to take advantage of a free vaccination.”It is also really important,” she added, “that as many people as possible who may not be eligible for the free vaccination get their own vaccination, and you can purchase it privately at many pharmacies across Hertfordshire.”Hertfordshire County CouncilThe most common symptoms are fever, chills, headache, aching joints and extreme tiredness.Ms Perman said anyone with these symptoms should “try to limit your contact with others, especially those who might be more vulnerable.”People with symptoms who need to leave the house “should wear a face mask where possible, wash your hands regularly and use dispose of tissues hygienically.”Hilton said: “What I would love to see is a national campaign to really promote the message, coming alongside our local one that goes out to all our GPs surgeries.More on this storyRelated internet links

Three new Cochrane reviews report that GLP-1 drugs can lead to meaningful weight loss, although the strong involvement of pharmaceutical companies in many studies raises concerns. The World Health Organization (WHO) requested these reviews to help shape upcoming recommendations on using these medications for obesity treatment.
The analyses evaluated three GLP-1 receptor agonists used for weight management and found that each one produced clinically important weight loss when compared with placebo. Even so, there is still limited or uncertain evidence about their long-term safety, possible side effects, and how financial ties might influence study results.
Glucagon-like peptide-1 (GLP-1) receptor agonists were first introduced in the mid-2000s to help people with type 2 diabetes. In that setting, particularly among those with underlying heart or kidney disease, the drugs helped improve blood sugar levels, lowered the risk of related complications, aided weight reduction, and reduced the likelihood of early death.
More recently, researchers have been testing GLP-1 receptor agonists in people with obesity. These medications work by imitating a natural hormone that slows digestion and helps individuals feel full for longer. In the United Kingdom, they are approved for weight management when combined with a reduced calorie diet and physical activity for people with obesity or for those who are overweight with related health issues.
GLP-1 drugs show promise for weight management
Across the reviewed studies, tirzepatide, semaglutide, and liraglutide consistently led to significant weight loss over one to two years compared with placebo, and the benefits appeared to continue during ongoing treatment. Tirzepatide (administered once weekly) produced about a 16% reduction in body weight after 12 to 18 months. Results from 8 randomized controlled trials (6 361 participants) indicated that these effects might last up to 3.5 years, although long-term safety data remain limited. Semaglutide (also injected weekly) was associated with an average weight loss of around 11% after 24 to 68 weeks, with evidence suggesting the effect can persist for up to two years, based on 18 randomized controlled trials (27 949 participants). More people achieved at least a 5% weight reduction, but the drug caused higher rates of mild-to-moderate gastrointestinal issues. Liraglutide (a daily injection) resulted in an average 4-5% weight loss in 24 trials (9 937 participants), still outperforming placebo. Evidence on benefits beyond two years was more limited.The reviews found little to no difference between the drugs and placebo when looking at major cardiovascular events, mortality, or quality of life. However, nausea and digestive discomfort appeared more often among people taking GLP-1 drugs, and some participants discontinued treatment because of these side effects.

“These drugs have the potential to bring about substantial weight loss, particularly in the first year,” says Juan Franco, co-lead researcher from Heinrich Heine University Düsseldorf, Germany. “It’s an exciting moment after decades of unsuccessful attempts to find effective treatments for people living with obesity.”
Independent research and equitable access are key
Most of the studies included in the reviews were funded by the companies that manufacture the drugs and were shaped by those companies in terms of design, analysis, and reporting. This has raised questions about potential conflicts of interest and highlights the importance of independent research.
The authors also stressed that the use of these medications should be viewed in a broader health context, including issues such as access, affordability, and insurance coverage, so that existing health inequities are not made worse. Costs remain a major barrier, particularly for semaglutide and tirzepatide, while liraglutide has become more affordable since its patent expired. Semaglutide’s patent is set to expire in 2026.
Most of the trials were conducted in middle- and high-income countries, with little or no representation from regions such as Africa, Central America, and Southeast Asia. Because body composition, eating patterns, and health behaviors differ around the world, the authors emphasized the need to understand how these drugs work in more diverse populations.
“We need more data on the long-term effects and other outcomes related to cardiovascular health, particularly in lower-risk individuals,” says Eva Madrid, co-lead researcher from the Universidad de Valparaíso, Chile. “Weight regain after stopping treatment may affect the long-term sustainability of the observed benefits. More independent studies from a public health perspective are needed.”
The reviews highlight the need for long-term, independent investigations to guide clinical and policy decisions and to better define the role of GLP-1 receptor agonists in lasting weight management.
Commissioned by the World Health Organization, the reviews will contribute to upcoming WHO guidelines on the use of GLP-1 receptor agonists for treating obesity.

Counties in Pennsylvania that contain or sit close to cultivated cropland show notably higher melanoma rates than other parts of the state, according to new research led by scientists at Penn State.
Researchers at the Penn State Cancer Institute reviewed cancer registry data collected from 2017 through 2021 and discovered that adults over age 50 living in a 15-county area of South Central Pennsylvania were 57% more likely to be diagnosed with melanoma, the deadliest form of skin cancer, compared to residents elsewhere in the state. The team reported these results on Nov. 14 in the journal JCO Clinical Cancer Informatics.
Charlene Lam, associate professor of dermatology at Penn State Health and co-author of the study, noted that the elevated cases appear in both rural and urban counties. She explained that the higher risk is not limited to isolated locations or people who spend much of their time outdoors.
Agricultural Environments Linked to Elevated Risk
“Melanoma is often associated with beaches and sunbathing, but our findings suggest that agricultural environments may also play a role,” she said. “And this isn’t just about farmers. Entire communities living near agriculture, people who never set foot in a field, may still be at risk.”
The usual suspect — sunlight — was included in the analysis. Yet even after adjusting for ultraviolet radiation levels in Pennsylvania and considering socioeconomic factors, two consistent associations emerged. Counties with more cultivated acreage and counties with greater herbicide use displayed significantly higher melanoma rates.
Herbicides, Biological Effects, and Melanoma Patterns
“Pesticides and herbicides are designed to alter biological systems,” said Eugene Lengerich, emeritus professor of public health sciences at Penn State and senior author on the paper. “Some of those same mechanisms, like increasing photosensitivity or causing oxidative stress, could theoretically contribute to melanoma development.”

According to the analysis, a 10% increase in cultivated land was linked to a 14% rise in melanoma cases across the region. Herbicide exposure showed a similar pattern: a 9% increase in herbicide-treated land corresponded to a 13% increase in melanoma incidence.
Lam emphasized that exposure is not restricted to those handling agricultural chemicals. She explained that these substances can drift on air currents, settle in household dust and enter water sources.
Chemical Drift and Community-Wide Exposure
“Our findings suggest that melanoma risk could extend beyond occupational settings to entire communities,” she said. “This is relevant for people living near farmland. You don’t have to be a farmer to face environmental exposure.”
The study also referenced earlier research showing links between pesticide and herbicide exposure and melanoma, citing evidence that these chemicals can heighten sensitivity to sunlight, interfere with immune responses and damage DNA in non-human animals and plants.
Study Shows Associations, Not Proof of Cause
Benjamin Marks, first author on the paper and a medical and public health student at the Penn State College of Medicine, cautioned that while higher melanoma rates appear in areas with more cropland and herbicide use, the findings do not prove that chemicals used on crops such as corn, soybeans and grains directly cause cancer. Instead, he said the patterns point to a connection that deserves further study.

He added that research of this kind is useful for spotting broad trends, even though it cannot identify individual risk.
“Think of this as a signal, not a verdict,” Marks said. “The data suggest that areas with more cultivated land and herbicide use tend to have higher melanoma rates, but many other factors could be at play like genetics, behavior or access to health care. Understanding these patterns helps us protect not just farmers, but entire communities living near farmland.”
Implications Beyond Pennsylvania
Lam said she hopes to better understand how agricultural practices relate to public health, especially since similar trends have been identified in farming regions of Utah, Poland and Italy. She encouraged anyone concerned about risk to perform routine skin checks and use sun-protective clothing and sunscreen. As part of the next phase of research, she is leading studies in rural communities within the affected area to learn more about farming practices and potential exposure pathways.
“Cancer prevention can’t happen in isolation,” Lengerich said. “This study demonstrates the importance of a ‘One Health’ approach, an understanding that human health is deeply connected to our environment and agricultural systems. If herbicides and farming practices are contributing to melanoma risk, then solutions must involve not just doctors, but farmers, environmental scientists, policymakers and communities working together.”
Other co-authors include Jiangang Liao, professor of public health sciences at Penn State College of Medicine, and Camille Moeckel, a fourth-year medical student and research associate at Penn State College of Medicine.
This work was supported by the MPH Capstone Program and the Medical Student Research Project at the Penn State College of Medicine, along with the University’s Algin B. Garrett Professorship.

A major international research effort is reshaping the long-held belief that lead exposure is primarily a modern problem. The new findings show that early human ancestors encountered lead repeatedly for more than two million years, suggesting that this toxic metal may have played an unexpected role in shaping the evolution of hominid brains, behavior, and possibly language.
The study — published in Science Advances — also offers a new angle on why modern humans ultimately surpassed Neanderthals. Lab-grown brain organoids with Neanderthal genetic variants reacted more strongly to lead than organoids with human genetics, hinting that Neanderthals may have been more vulnerable to lead’s neurological effects.
Researchers from the Geoarchaeology and Archaeometry Research Group (GARG) at Southern Cross University (Australia), the Department of Environmental Medicine at the Icahn School of Medicine at Mount Sinai Hospital (New York, USA), and the School of Medicine at the University of California San Diego (UCSD, USA) combined fossil chemistry, brain organoid experiments, and evolutionary genetics to uncover how lead factored into hominid history.
Evidence of Ancient Lead Exposure in Fossil Teeth
For many years, lead toxicity was assumed to be closely tied to human industry, including smelting, mining, and the use of leaded petrol and paint. That view shifted when researchers analysed 51 fossil teeth from a range of hominids and great apes, including Australopithecus africanus, Paranthropus robustus, early Homo, Neanderthals, and Homo sapiens. The teeth showed clear chemical traces of intermittent lead exposure that stretch back nearly two million years.
High-precision laser-ablation geochemistry performed at Southern Cross University’s GARG Facility (located in Lismore, NSW) and at Mount Sinai’s Exposomics laboratories revealed distinct ‘lead bands’ in the enamel and dentine. These bands formed during childhood and indicate recurring periods of lead intake from environmental sources (such as polluted water, soil, or volcanic activity) or from lead stored in the body’s bones and released during times of stress or illness.
“Our data show that lead exposure wasn’t just a product of the Industrial Revolution — it was part of our evolutionary landscape,” said Professor Renaud Joannes-Boyau, Head of the GARG research group at Southern Cross University.

“This means that the brains of our ancestors developed under the influence of a potent toxic metal, which may have shaped their social behavior and cognitive abilities over millennia.”
How Lead Interacted With Early Brain Development
To understand the functional impact of this exposure, the team studied human brain organoids, which serve as simplified, lab-grown models of early brain development. They tested how lead affected two versions of a key developmental gene known as NOVA1, which regulates gene expression under lead exposure during neurodevelopment. The modern human version of NOVA1 differs from the variant seen in Neanderthals and other extinct hominids, although the reason for this evolutionary change was previously unclear.
Organoids carrying the Neanderthal-like NOVA1 variant showed substantial disruptions in FOXP2-expressing neurons in the cortex and thalamus when exposed to lead. These brain regions are essential for language and speech development. Organoids with the modern human NOVA1 gene showed far less disruption.
“These results suggest that our NOVA1 variant may have offered protection against the harmful neurological effects of lead,” said Professor Alysson Muotri, Professor of Pediatrics/Cellular & Molecular Medicine and Director of the UC San Diego Sanford Stem Cell Institute Integrated Space Stem Cell Orbital Research Center.
“It’s an extraordinary example of how an environmental pressure, in this case, lead toxicity, could have driven genetic changes that improved survival and our ability to communicate using language, but which now also influence our vulnerability to modern lead exposure.”
Genetic Insights Into the Rise of Modern Humans

Genetic and proteomic data from the study showed that lead exposure in organoids with archaic gene variants disrupted multiple pathways tied to neurodevelopment, communication, and social behavior. The FOXP2 disruptions are especially noteworthy because of FOXP2’s well-established role in speech and language. These results suggest that long-term pressure from environmental toxins may have nudged cognitive and communicative traits along different evolutionary paths in modern humans and Neanderthals.
“This study shows how our environmental exposures shaped our evolution,” said Professor Manish Arora, Professor and Vice Chairman of Environmental Medicine.
“From the perspective of inter-species competition, the observation that toxic exposures can offer an overall survival advantage offers a fresh paradigm for environmental medicine to examine the evolutionary roots of disorders linked to environmental exposures.”
What Ancient Lead Exposure Means for Us Today
Although modern lead exposure is mostly linked to industrial activities, it continues to pose a serious health threat, especially for children. The new findings show that human susceptibility to lead may be deeply rooted in our evolutionary past and shaped by interactions between genes and environmental conditions.
“Our work not only rewrites the history of lead exposure,” added Professor Joannes-Boyau, “it also reminds us that the interaction between our genes and the environment has been shaping our species for millions of years, and continues to do so.”
The research drew on fossil teeth from Africa, Asia, Europe, and Oceania, using detailed geochemical mapping to trace childhood episodes of lead intake. In parallel, brain organoids containing either modern or archaic NOVA1 genes were used to study how lead affected brain development, with particular attention to FOXP2, a gene central to language. Genetic, transcriptomic, and proteomic analyses were combined to build a broad understanding of how lead may have influenced the evolution of hominid cognition and social behavior.

Prof. Alon Monsonego of Ben-Gurion University of the Negev found that T helper lymphocytes, which are immune cells involved in regulating the body’s defenses, shift in function as people grow older. These shifts can reflect a person’s biological age, which may not match their chronological age. Within these changes, the research team (the labs of Prof. Monsonego and Prof. Esti Yeger-Lotem) identified a previously unknown group of T helper cells that become more common with age.
The significance of this discovery became clearer when a Japanese study on supercentenarians, meaning individuals who live well past 100, found that this same T helper cell subset was abundant in their immune systems. Prof. Monsonego now believes these cells may help maintain an immune response that is suitable for a person’s stage of life.
The team’s findings, led by Dr. Yehezqel Elyahu in collaboration with Prof. Valery Krizhanovsky of the Weizmann Institute of Science, were recently reported in Nature Aging.
Aging, Senescent Cells, and the Immune Response
Scientists describe aging as a process in which cells gradually lose the ability to repair routine damage. When this occurs, the body shows signs of aging. Senescence cells, which naturally appear when regulated properly, become harmful if they accumulate, since they can trigger inflammation and tissue injury.
The researchers discovered that a portion of the T helper cells that increase with age unexpectedly have killing capabilities. These cells help remove senescence cells, thereby limiting their negative effects. Prof. Monsonego’s work showed that reducing the number of these T helper cells in mice caused the animals to age more quickly and shortened their lifespan.
This unusual and highly specialized subset of T helper cells continues to rise in number with age and appears to play an important role in slowing the aging process.

Tracking Biological Age and Rethinking Immune Resetting
Because T helper cells shift as people age and appear central to how aging unfolds, Prof. Monosonego and his team suggest monitoring these immune patterns in individuals beginning in their 30s. Such tracking could reveal how quickly someone is aging biologically and help guide early steps to support healthy aging. Differences of decades can develop between biological and chronological ages.
“People say that to reverse aging and “rejuvenate,” we need to reset their immune system like the immune systems of people in their 20s. However, our research shows that this might not be the case. People don’t need a super-charged immune system; they need one that is working properly and appropriate for their stage in life. So, one of the “axioms” of how to reduce aging may be incorrect,” says Prof. Monsonego.
In addition to offering new insight into aging, the newly identified cells may also be useful in diagnostics and future treatments addressing dysregulated aging, longevity, and diseases linked to aging.
Research Team and Support
Prof. Monsonego is part of The Shraga Segal Department of Microbiology, Immunology and Genetics in the Faculty of Health Sciences at BGU, and is also affiliated with TheSchool of Brain Sciences and Cognition.
Contributors to the research included Ilana Feygin, Ekaterina Eremenko, Noa Pinkas, Alon Zemer, Amit Shicht, Omer Berner, Roni Avigdory-Meiri, Anna Nemirovsky, and Keren Reshef from BGU, along with Lior Roitman from Weizmann.
The work received support from the Israel Ministry of Science and Technology (Grant no. 3-16148) and the Litwin and Gural Foundations.