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Researchers from North Carolina State University have discovered that a particular molecular signaling pathway plays an important role in producing osteoarthritis (OA) pain. Using a mouse model of painful osteoarthritis, they show that blocking this signaling pathway eliminates pain and results in a return to normal limb use. This work is the first to find an association between this pathway and OA pain, and could lead to the development of new, effective pain treatments for human OA sufferers.
Over 32.5 million U.S. adults suffer from painful OA, making it the most common joint disorder in the country. The incidence of OA is increasing, and while it can range in severity, OA can be associated with pain which limits mobility and function.
“There are currently very few effective and safe long-term ways to manage OA pain, which is chronic and often very debilitating,” says Duncan Lascelles, professor of translational pain research and management at NC State and co-corresponding author of the research.
Previously, Lascelles, an expert in companion animal pain management, and his colleague, NC State neurobiologist Santosh Mishra, observed increased levels (or upregulation) of the components of this signaling pathway in the joint fluid, blood and sensory nerves of dogs with naturally occurring OA. The components in question — the ligand, or binding molecule artemin, and its receptor GFRα3 — were known to pain researchers, but had not been associated with OA pain signaling.
“When you feel pain, that’s the result of a molecule at the painful site interacting with a receptor on a sensory nerve, setting off a cascade of events within the nerve that lead to a signal being produced,” Lascelles says. “This signal travels along the nerve, and is interpreted as painful by the brain.”
“For acute pain, the artemin/GFRα3 system has been known to play a role, particularly in situations like cold hypersensitivity,” says Mishra, assistant professor of neuroscience at NC State and co-corresponding author of the work. “However it had not been associated with pain in a chronic condition like OA. Observing upregulation of a particular molecule doesn’t necessarily mean it’s relevant in a particular condition, so we decided to explore whether this pathway was functionally involved in pain signaling in OA — that is, explore whether this signaling pathway was actually contributing to OA pain.”
In a mouse model of chemically induced OA the researchers found that GFRα3 was upregulated in the sensory nerves — just as it was in dogs with naturally occurring OA — versus a control group of healthy mice. A subset of the OA mice were then treated with monoclonal antibodies designed to bind to GFRα3, preventing artemin from binding to GFRα3 and effectively blocking the pain signaling pathway.
Within two hours post-treatment with the antibodies, limb function had returned to normal levels in the treated mice, indicating that the artemin/GFRα3 pathway most likely plays an important role in OA pain.
“While this is a proof-of-concept study, the findings are encouraging and we hope to continue working to understand this pathway and its involvement in OA pain,” Mishra says.
“Although the work here is in a mouse model, it was based on robust observations in dogs with naturally occurring OA pain,” Lascelles says. “Because OA in dogs and humans is so similar, we believe our findings are highly relevant to both. Hopefully this work can lead to targeted drug therapies to relieve pain in both canine and human OA patients. While we cannot reverse the joint damage, we can hopefully alleviate suffering caused by pain, decreased mobility and decreased ability to function.”
The research appears in Frontiers in Neuroscience, and was supported by funding from NC State’s Translational Research in Pain Program. Former NC State graduate student Laura Minnema, and current NC State graduate student, Ankita Gupta, are co-first authors.
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Materials provided by North Carolina State University. Original written by Tracey Peake. Note: Content may be edited for style and length.

Pharmaceutical researchers speak of a hit when they come across a promising substance with a desired effect in early drug discovery. Unfortunately, hits are rarely bull’s-eyes, often showing undesirable side effects that not only complicate the search for new hits, but also the subsequent development into a drug. A new study by Slava Ziegler and Herbert Waldmann from the Max Planck Institute of Molecular Physiology in Dortmund could now help to better identify one of the most frequently observed side effects already in early drug discovery, but also to find new bioactivities.
The most commonly used cancer drugs contain active substances that manipulate the cell’s cytoskeleton by binding to microtubules. This can disrupt cell division as well as impair other essential processes, and leads to cell death. Such an effect is of course not desirable for other therapies. However, microtubules’ surface has many deep binding pockets that makes them particularly susceptible to modulation by a wide variety of chemical substances with diverse chemical scaffolds.
Drug discovery is biased
In the search for and development of new active substances, the study of known side effects plays a crucial role, especially when one considers that about 13 years and more than one billion US dollars are needed to develop a new drug. Although there are already standardized test procedures (screens) for identifying undesirable side effects, they by far do not cover all targets in cells, often do not correctly reflect the cellular context or targets could be overlooked, e.g. binding to tubulin. Thus, drug search is always biased to a certain extent.
Painting in cells
A team led by Slava Ziegler and Herbert Waldmann used a new strategy to reliably detect side effects, such as the disruption of microtubules, at an early stage of the search for bioactive compounds. To do this, the researchers employed the so-called “Cell painting” approach. Here, several functional areas of the cell are stained and then examined microscopically for changes after the addition of chemical substances. This enables recording hundreds of cellular parameters in a single morphological fingerprint. If one detects similarity of this fingerprint to those of known reference substances, conclusions about the effect of the unknown substance can be drawn. The value of this approach lies in the possibility of creating fingerprints for thousands of substances in a high-throughput process. This way, the researchers revealed that more than 1% of about 15,000 studied substances had a tubulin-modulating effect. Among them was also a large number of known reference substances for which an influence on tubulin was previously unknown.
Useful add-on for drug development
“Reference substances play an essential role in the interpretation of a screen, so they should be carefully evaluated and tested. The compounds identified by the Cell painting show a wide variety of chemical scaffolds and even small chemical modifications can have a dramatic impact on the tubulin-binding properties of a compound. This risk is ubiquitous, especially during the compound optimization phase, where existing atoms are exchanged or removed and new atoms are added in order to improve the pharmacological properties. Additional morphological profiling during the search for hits and their optimisation could not only help unmask side effects such as tubulin modulation early on, but also identify desired and new bioactivities,” says Slava Ziegler. “Moreover, this approach could save time and money as it helps to early assess whether a promising substance has what it takes to become a useful compound or not.”
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Eating more meat, having less of certain bacteria in the gut, and more of certain immune cells in the blood, all link with multiple sclerosis, reports a team of researchers led by UConn Health and Washington University School of Medicine. The work, published in the 27 January issue of EBioMedicine, teased out subtle connections that could lead to a better understanding of the causes of the disease.
Multiple sclerosis (MS) is an autoimmune disease affecting fewer than 3 million people worldwide but costing $28 billion annually in the US alone — and untold suffering. MS is more prevalent in specific regions, particularly the northern mid-latitudes, suggesting that geography is somehow linked to the disease, perhaps involving diet. But teasing out the exact relationships between diet, immune response and MS has been difficult. MS is most obviously an autoimmune disease in which the body attacks the insulation surrounding its nerves. When the insulation is damaged enough, the nerves begin to misfire and malfunction like wires with frayed insulation. But what triggers the body to attack the insulation in the nervous system in the first place is unknown.
More and more evidence has suggested that bacteria might be involved. The bacteria living in our guts can affect our immune system. And what we eat can affect the bacteria in our guts. Dr. Yanjiao Zhou at UConn Health School of Medicine collaborated with Dr. Laura Piccio from Washington University and now at the University of Sydney to study the gut microbiome, immune systems, diet, and blood metabolites in 49 volunteers — 25 MS patients and 24 healthy controls — to look for correlations that might be subtle but important.
“We found a number of gut bacteria associated with MS and severity of disability of MS patients. We also found increased autoimmune markers and signature metabolites in MS. But what is really interesting is how these systems connect with each other, and how diet is involved in these connections. Using multi-OMICS approaches, we try to close the loop and show the associations between multiple systems,” says Zhou.
“This is the first study using an integrated approach to analyze the interplay between diet, gut microbiome, the immune system and metabolism and their contribution to disease pathogenesis and progression in people with MS. It opens a new modality to address future scientific questions by not looking at one individual factor, but at their complex interactions. This approach can lead to the identification of relevant networks that could be manipulated for disease prevention or therapeutic intervention,” says Piccio.
The strongest systemic linkage the researchers found involved eating meat. Their analysis linked higher meat consumption to a decrease in the population of Bacteroides thetaiotaomicron in people’s gut ecology. B. thetaiotaomicron is associated with digesting carbohydrates from vegetables.
Higher meat consumption, which was observed in the MS patients, was also linked to an increase in T-helper 17 cells in the immune system, and an increase in S-adenosyl-L-methionine (SAM) in their blood.
The relationship between meat eating and disability and the other factors was not deterministic; some healthy people eat a lot of meat. But the pattern of all the factors was suggestive that, in MS, something goes wrong with people’s gut bacteria that dissociates them from the immune system, leading to heightened T-helper 17 cells and autoimmune attacks on the nervous system. And it tends to be associated with meat eating.
In the future, the team would like to expand the research to include more people, including those with a more severe form of MS. Eventually they hope to understand more of the cause-and-effect between diet, bacterial ecosystems in the gut, and immune response, and potentially help prevent or mitigate MS symptoms in people suffering from the disease.
This research was funded by Strategic Pharma-Academic Research Consortium (SPARC) Awards.
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Materials provided by University of Connecticut. Original written by Kim Krieger. Note: Content may be edited for style and length.

Thenumber of people hospitalized for a hypertensive crisis — when blood pressure increases so much it can cause a heart attack, stroke or other sudden cardiovascular event — more than doubled from 2002 to 2014, according to Cedars-Sinai investigators.
The increase occurred during a period when some studies reported overall progress in blood pressure control and a decline in related cardiovascular events in the U.S. The findings are published in the Journal of the American Heart Association.
“Although more people have been able to manage their blood pressure over the last few years, we’re not seeing this improvement translate into fewer hospitalizations for hypertensive crisis,” said Joseph E. Ebinger, MD, a clinical cardiologist and director of clinical analytics at the Smidt Heart Institute and first author of the study.
Ebinger said there could be various explanations for why a growing number of people are being hospitalized for dangerously high blood pressure. It could be that an increasing number may be unable to afford medications to control hypertension or are seeing their blood pressure rise after taking inadequate doses of these drugs. Socioeconomic factors may also make it difficult for people to avoid a high-salt diet, inactivity, smoking or other unhealthy behaviors that can contribute to hypertension. These factors may include limited access to health care, financial insecurity, or work and family demands.
“We need more research to understand why this is happening and how clinicians can help patients stay out of the hospital,” Ebinger said.
To conduct their study, the investigators analyzed data from the National Inpatient Sample, a publicly available database. The data include a subset of all hospitalizations across the U.S., providing a picture of nationwide trends. They found that annual hospitalizations for hypertensive crises more than doubled over a 13-year period. Hospitalizations related to hypertensive crises represented 0.17% of all admissions for men in 2002 but 0.39% in 2014. Hospitalizations related to hypertensive crisis represented 0.16% of all admissions for women in 2002 but 0.34% in 2014.
The investigators estimated that from 2002 to 2014, there were 918,392 hospitalizations and 4,377 in-hospital deaths related to hypertensive crisis across the U.S.
The risk of dying from a hypertensive crisis, however, did decrease slightly overall during the studied time period. Women died at the same rate as men, even though they had fewer health issues than men who also were hospitalized for a hypertensive crisis.
“These findings raise the question: Are there sex-specific biologic mechanisms that place women at greater risk for dying during a hypertensive crisis?” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the Department of Cardiology at the Smidt Heart Institute and senior author of the study. “By understanding these processes, we could prevent more deaths among women,” added Dr. Cheng, who is also the Erika J. Glazer Chair in Women’s Cardiovascular Health and Population Science and professor of cardiology.
Other Cedars-Sinai researchers who worked on this study are Yunxian Liu, PhD, MS; Matthew Driver, MPH; C. Noel Bairey Merz, MD; Florian Rader, MD, MSc; and Christine M. Albert, MD, MPH.
Funding: The research reported in this study was funded in part by National Institutes of Health under awardnumbers R01-HL134168, R01-HL131532, R01-HL143227, R01-HL142983, R01-HL146158, K23-HL153888, and U54-AG065141; the National Center for Advancing Translational Sciences under award number UL1TR000124; the Edythe L. Broad and the Constance Austin Women’s Heart Research Fellowships; the Barbra Streisand Women’s Cardiovascular Research and Education Program; the Linda Joy Pollin Women’s Heart Health Program; the Erika Glazer Women’s Heart Health Project; and the Adelson Family Foundation; and Cedars Sinai Medical Center.
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The severity of Covid-19 pneumonia can be difficult to assess in people from different ethnic groups, due to inaccurate readings from a device that measures the level of oxygen in the blood of patients.
The findings of the research, published in the European Respiratory Journal, show that pulse oximeters gave false readings of nearly 7% higher in a group of patients of Mixed ethnicity with Covid-19, compared to White patients at just over 3%. There were also falsely high readings in patients with both Black and Asian ethnicity, which could delay patients receiving the best and most timely treatment for the virus.
Pulse oximetry is a non-invasive test that measures the oxygen saturation level of the blood. It can rapidly detect even small changes in oxygen levels. These levels show how efficiently blood is carrying oxygen to the extremities furthest from the heart, including the arms and legs. Medical professionals routinely use them in primary care and critical care settings like emergency rooms or hospitals to monitor the clinical status of their patients.
The light wave transmission that this technology uses is modified by skin pigmentation and may vary by skin colour. A recent study reported different outputs in patients with Black skin compared to patients with White skin, which has the potential to adversely affect patient care. This led to the Food and Drink Administration in the USA releasing an expression of concern about the accuracy of pulse oximeters in 2021, which led to the current study.
The study was delivered by a consortium of multidisciplinary teams from the University of Nottingham and Nottingham University Hospitals NHS Trust. They made use of the electronic datasets that are collected for clinical use in real time, but archived and available to answer important clinical questions and improve both patient care and patient safety in the future. The NUH Covid-19 Patient Safety Database is anonymised to allow lessons to be learned without compromising individual patient confidentiality. The team included clinicians, managers, statisticians, computer analysts, software coders and data warehouse archivists.
The team of experts from Nottingham used data from patients with Covid-19 infection to look at the difference in blood oxygen levels as measured by pulse oximetry and arterial blood gas tests, spilt into different ethnic groups over a wide range of oxygen saturations. Arterial blood gas tests measure the levels of oxygen in the blood from an artery, and represent the gold standard measurement for oxygen levels.
The team used electronic data for patients admitted to Nottingham University Hospitals NHS Trust between February 2020 and September 2021 with Covid-19 infection. Pulse oximetry measurements with a paired blood gas measurement within a half an hour window were compared.
Mean differences between pulse oximetry and blood gas oxygen saturations were recorded by ethnicity of White, Mixed, Asian, and Black patients, and were also split up by level of oxygen saturation as measured by arterial blood gases.
There were differences in oxygen saturations (amounts of oxygen in the blood), between the pulse oximetry arterial blood gas readings in all groups. The highest difference was in the Mixed ethnicity group which was nearly 7% higher in the oximetry reading, with the lowest in the White group at 3.2% higher than the true measurement from arterial blood gases. A reading of 5.4% higher using pulse oximetry was found in the Black group of participants and 5.1% higher in the Asian population.
The difference between the readings also increased in the clinically important range of 85 to 89%, when many clinical decisions are made. Mean values as measured by pulse oximeter were higher than reality in individuals with a recorded Black and Asian ethnicity, compared to those of a White ethnicity.
The findings of the research are important as high levels of skin pigmentation are associated with ethnic groups who have a poorer outcome from Covid-19 infection, and would require the most accurate oxygen measurements available in order to deliver the most appropriate and timely treatment.
Dr Andrew Fogarty, from the School of Medicine at the University and the lead author of the study, said: “This data builds on what we know, which is that patients with darker skin have less accurate oxygen measurements using the pulse oximeters. Any error of measurement of oxygen levels will make assessing the severity of Covid-19 infection more difficult, and may delay delivery of timely medical care. We are now exploring the impact of this on clinical outcomes to see if it may have led to any issues in escalating treatment intensity for our patients.”
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Materials provided by University of Nottingham. Note: Content may be edited for style and length.

By analyzing disease mechanisms in human neurons, researchers led by the University of California San Diego developed a new method to screen drugs for treating Alzheimer’s disease. Their work sheds light on why Alzheimer’s drugs so far have been ineffective at curing or reversing the disease and identifies new targets for drug development.
The findings, reported in a paper published Jan. 27 in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, could help pave the way for radically new therapeutic approaches to treating Alzheimer’s.
Drug development for Alzheimer’s has long been driven by the hypothesis that amyloid plaques — formed by the buildup of amyloid-beta proteins in the brain — are what kill neurons and cause Alzheimer’s. As a result, many research efforts have focused on designing drugs that clear out these plaques.
“But this approach has not led to a cure or improved dementia in patients. Sometimes it has made the disease worse,” said senior author Shankar Subramaniam, a professor of bioengineering at the UC San Diego Jacobs School of Engineering.
To understand why, Subramaniam and his collaborators developed a drug screening method that looks at what disease mechanisms, or endotypes, change in patients’ neurons as a result of treatment. The most widely studied Alzheimer’s endotype is amyloid plaque formation. But there are other endotypes — reported for the first time by Subramaniam and colleagues in a previous study — that also warrant attention. These include de-differentiation of neurons to an earlier “non-neuron” cell state; suppression of neuronal genes; and loss of synaptic connections.
“This is a new test for measuring whether an Alzheimer’s drug works,” said Subramaniam. “The key here is that we are using the endotypes that we discovered to see how current drugs fail. When drugs interact with human neurons, what endotypes do the drugs fix, and what endotypes do they not fix in the process?”
What’s also special about this method is that it screens drugs on actual patient cells. “The power of this is that you can do precision medicine and have a good model system to study Alzheimer’s,” said Subramaniam.

A new study in mice from University of Maryland School of Medicine researchers showed that an unhealthy vaginal microbiome in pregnant mothers in combination with an unhealthy diet contributed to increased pup deaths and altered development in the surviving babies.
The researchers offset these deaths from the unhealthy vaginal microbiome by giving the mothers a healthier diet. The researchers say their findings could imply that simple interventions, such as access to a diet rich in fiber-containing fruits and vegetables, may help counteract some of the harmful effects on human babies that an unhealthy microbiome may impart — particularly in vulnerable populations.
Their findings were published on November 1, 2021, in Nature Communications.
When babies pass through the birth canal, they are exposed to their mother’s vaginal microbiome, where their skin is coated and they ingest their first microbes outside the sterile womb.
Women with certain chronic diseases, such as diabetes or high blood pressure, and those in low-resourced neighborhoods with limited access to healthcare and nutrition, are more at risk of having an unhealthy vaginal microbiome. These unhealthy vagina microbiomes have too many different kinds of bacteria, viruses, or yeast which, unlike diversity in the gut, is a bad thing in the vagina, increasing the likelihood for infections.
According to the U.S. Department of Health and Human Services, Black women in the U.S. have infant mortality rates 2.3 times higher than white women, and this is independent of education and income levels.

Even slight exposure to light can prompt the critical sleep-promoting hormone melatonin to plummet in preschoolers in the hour before bedtime, potentially disrupting slumber long after the light goes out, according to new CU Boulder research.
The study, published this month, is the latest in a series, funded by the National Institutes of Health, examining how the central body clock of young children is unique. It suggests that preschoolers are highly susceptible to the physiological impacts of light at night, and some children may be even more sensitive than others.
“Our previous work showed that one, fairly high intensity of bright light before bedtime dampens melatonin levels by about 90% in young children,” said first author Lauren Hartstein, a postdoctoral fellow in the Sleep and Development Lab at CU Boulder. “With this study, we were very surprised to find high melatonin suppression across all intensities of light, even dim ones.”
Light: The body’s strongest time cue
Light is the body’s primary time cue, influencing circadian rhythms that regulate everything from when we feel tired or hungry to what our body temperature is throughout the day.
When light hits the retina, a signal transmits to a part of the brain called the suprachiasmatic nucleus, which coordinates rhythms throughout the body, including nightly production of melatonin. If this exposure happens in the evening as melatonin is naturally increasing, it can slow or halt it, delaying the body’s ability to transition into biological nighttime.

Researchers from the University of California, Irvine have discovered that the absence of Adiponectin receptor 1 protein (AdipoR1), one of the principal enzymes regulating ceramide homeostasis in the retina, leads to an accumulation of ceramides in the retina, resulting in progressive photoreceptor cell death and ultimately vision loss. The team also found that a combination of desipramine and L-cycloserine reduced lowered ceramide levels, which protected photoreceptors, helped preserve the retina’s structure and function, and improved vision.
The study, titled “Inhibition of ceramide accumulation in AdipoR1-/- mice increases photoreceptor survival and improves vision,” was published this month in the Journal of Clinical Investigation Insight.
Study findings show that ceramide imbalance damages the neural retina and retinal pigmented epithelium, accompanied by a significant reduction of electroretinogram amplitudes, decreased retinoid content in the retina, reduced cone opsin expression and massive inflammatory response. A buildup of ceramides in the retina, likely due to insufficient ceramidase activity, led to photoreceptor death. When treated with the desipramine and L-cycloserine combination, ceramide levels were lowered, which helped preserve photoreceptors in mice. The team also observed improved daylight vision in the L-cycloserine treated mice, and that prolonged treatment significantly improved electrical responses of the primary visual cortex to visual stimuli.
“Although AdipoR1 is found in multiple organs, the highest levels are found in the eye and brain, suggesting its critical importance in these neural tissues. Our study results highlight the significance of AdipoR1 ceramides in the retina, and show that pharmacological inhibition of ceramide generation can provide a therapeutic strategy for patients suffering from retinitis pigmentosa or AdipoR1-related retinopathies,” said Krzysztof Palczewski, PhD, Donald Bren Professor of Ophthalmology at the UCI School of Medicine and co-corresponding author.
Degeneration of photoreceptor cells and retinal pigment epithelium is the underlying cause of several progressive retinal diseases. Many of these conditions have only minimally effective or no treatment options. New therapeutic approaches are urgently needed to combat these disorders and reduce vision loss.
Ceramides are essential for eukaryotic cell membrane stability and act as potent signaling molecules in inflammation, cell cycle arrest, cell death and heat shock response pathways. Ceramide imbalance has also been found in cancer, Alzheimer’s disease, type 2 diabetes, multiple sclerosis, cardiovascular disease and non-alcoholic fatty liver disease.
“Noninvasive pharmacological treatment is more easily achieved in humans than gene therapy,” said first and co-corresponding author Dominik Lewandowski, PhD, postdoctoral scholar at the UCI School of Medicine. “Our proposed pharmacological strategy might become broadly applicable to other neurodegenerative conditions related to high ceramide levels.”
This work was supported by by funding from the National Institutes of Health under grants R24EY027283, NEI: F30 EY031566, and T32GM007250; and the Audacious Goals Initiative for Regenerative Medicine, a National Eye Institute program to push the boundaries of vision science and restore vision through regeneration of the retina, under grants P30 014195, and 1S10OD021815-01, and the Helmsley Center for Genomic Medicine.
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New research shows that chemical reactivity, seasonality and distribution of airborne particulate matter are critical metrics when considering air pollution’s impact on human health. Current environmental regulations focus on the mass of pollutant particles, and researchers at the University of Illinois Urbana-Champaign are pushing to refocus regulatory efforts on more regional and health-relevant factors.
A new study of air quality in the Midwestern U.S. found that measuring the mass concentration of PM2.5 — particles that are 2.5 micrometers in diameter or smaller — does not correspond well with current methods for classifying particle toxicity. Additionally, the researchers found that PM2.5 exposure may be just as hazardous in rural areas as in urban areas — evidence that challenges a common misconception that air pollution is more toxic in urban areas than in than rural areas, the researchers said.
The findings of the study, led by civil and environmental engineering professor Vishal Verma, are published in the Journal of Hazardous Materials.
“The EPA classification of PM2.5 accounts for particle diameter and mass, which are characteristics that are easy to measure,” Verma said. “However, not all particles that make up PM2.5 contribute to health equally.”
PM2.5 poses a health risk because it can become embedded in lung tissue when inhaled, the researchers said. Although chemically reactive fractions of these particles are known to be toxic, a previous study by Verma’s group shows that the exact relationship between PM2.5 mass and toxicity is unclear.
“Most air pollution studies have shifted focus from particle mass to a property called cellular oxidative potential,” Verma said. “Cellular oxidative potential describes the capability of the particles to generate reactive, oxygen-based chemicals that can lead to a variety of health problems in the cells of lung tissue.”
To examine the influence of oxidative potential more closely, the researchers collected PM2.5 samples weekly in the summer and fall of 2018 and in the winter and spring of 2019. They chose three urban localities: Chicago, Indianapolis and St. Louis; a rural location in Bondville, Illinois; and a roadside location adjacent to an interstate highway in Champaign, Illinois.
Using an automated analytical technique developed in a previous study, Verma’s team analyzed the sample composition, oxidative potential and mass. The team found that all locations shared similar levels of oxidative potental — but saw a poor correlation between oxidative potential and mass. That suggests that some of the lighter particles that make up PM2.5 contribute more to tissue damage than others, the study reports.
“Our rural samples did have less mass than those in the urban settings, but the oxidative potential was equal to samples from urban settings,” Verma said. “Additionally, the oxidative potential of the rural samples was higher in the summer than in the winter, suggesting that summertime agricultural activity can produce PM2.5 particles that are just as toxic as those from urban settings.”
The team hopes this study brings attention to these newly uncovered risks associated with PM2.5 in rural areas.
“The current methods used to measure PM2.5 oxidative potential are time-consuming and laborious, and we hope that our new methodology, combined with these study findings, makes testing for oxidative potential more appealing to environmental regulators and policymakers,” Verma said.
The National Science Foundation supported this research.
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Materials provided by University of Illinois at Urbana-Champaign, News Bureau. Original written by Lois Yoksoulian. Note: Content may be edited for style and length.