California has identified 600 cases of deadly silicosis among its workers who have fabricated engineered stone countertops in the past year, according to a recent public health report.
California Department of Public Health released the results on Wednesday, noting 592 cases including 31 deaths and 65 people who had undergone lung transplants.
According to the report, “Silicosis” is an incurable lung disease that progresses due to inhalation. Over the last two decades, there has been a rising risk among those who fabricate engineered stones countertops that contain crystalline silica.
The report stated that engineered-stone slabs sold as quartz countertops can contain up to 90% crystalline silicon. The report states that workers can be exposed to silica when they are cutting or finishing counters.
Health officials noted that the cases from January 2019 to June 2026 are notable because of their relatively young patients, brief exposure period, and rapid disease progression.
According to the department, workers diagnosed with silicosis at a median of 46 years old died by silicosis.
According to the report, almost all the patients diagnosed with the disease were Latino men.
California expanded its surveillance program after identifying the first case in 2019. The report states that the worker was a counter fabrication worker. The report stated that the worker had been diagnosed at 32 and passed away from respiratory failure when he turned 38.
Report said California has strengthened silica regulation and increased surveillance, however regulators are still having difficulty enforcing the workplace rules.
The report states that “despite these interventions, dangerous worker exposures continue in California.” California’s surveillance of silicosis has been expanded. However, the real burden of the disease is still underestimated because it relies on the passive reporting of diseases diagnosed. Active screening of workers and doctors has improved case detection, but screening remains inconsistent and misdiagnosis is common.

Listen to music and turn it up: According to a recent study, older adults who listen or play regular music are at a lower risk for developing dementia.
Researchers from Monash University, Australia, analyzed data of more than 10,000 adults aged 70 or older and discovered that people who listen to music every day have a lower risk of dementia. This is compared to those who only occasionally, never or rarely listen to music.
One hobby that is great for an aging brain, according to a study
The frequent music listeners also had higher scores in cognitive tests and better memory for episodic events (which is used to recall everyday, specific events).
Singing and playing an instrument were both associated with a reduction of 35% in the risk for dementia. Regularly listening to music and playing it also reduced dementia risk by 33% and cognitive impairment risk by 22%.
Music is a low-effort, easy way for older adults to reduce their anxiety about dementia. This disease affects seven million people worldwide and becomes more prevalent as the life expectancy rises.
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The study’s authors have some hypotheses about the possible benefits of music on the brain. These are backed up by previous research.
Emma Jaffa is a Monash Honors Biomedical Science student and co-author of the study. She worked with Joanne Ryan a Monash professor of biological neuroscience.
The new study revealed that this highly enjoyable activity could lower your dementia risk
She told HuffPost that “previous studies have shown it increases processing speed, language and memory.” Plus, socialization with other people helps to protect brain health.
Jaffa was particularly interested in the results because she is a singer and bassist.
She is also a fan of research which can be used to help people. I think this is what attracted me to the topic. She said that it was a combination of her hobby and the opportunity to share actionable insight with others.
The most common question Jaffa gets about this study is “Are there some types of music that are more beneficial than others?” Coltrane and Clapton, for example, have a superior cognitive function.
She said that while she does not have an answer, (participants were never asked what music they were listening too), it is something she would like to investigate in the future. It would be interesting to see if music listening can reduce the cognitive decline of those under 70.
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Researchers like Ryan and Jaffa have no reason to be surprised that they are researching this subject, considering how debilitating dementia symptoms can often be. The condition can cause speech problems, memory loss and mood swings.
A study published in the American Journal of Geriatric Psychiatry in October found that having a strong sense of purpose can protect you from dementia. It makes the brain stronger and reduces the risk of it developing. What are other ways that research has shown to help support resilience in the brain during aging? Exercise, especially moderate to vigorous activity and spending time with friends — ideally while listening to good music — are all ways to support cognitive resilience as we age.
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A study says that you can reduce your risk of dementia by almost 30% with this one thing.
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Can a drug that is notorious for causing addiction be the key to extending life?
Dave Asprey is the founder of biohacking and he has highlighted research which suggests that it might be.
Afrin is a nasal spray that can be purchased over-the-counter at any drug store. This nasal spray can be purchased at most drug stores and is a lifesaver. It opens up the airways, allowing you to breathe more easily.
Every label will warn you not to use the product for longer than three consecutive days.
When the body adapts quickly to a drug, it becomes dependent on that medication to maintain airways. When you stop taking the medication, you may find that your sinuses swell up much more than they did before. You may be tempted to reach for another spray of Afrin for relief.
I’m taking Afrin to prolong my life. Asprey joked in an Instagram message. That’s not a good idea.
Researchers are seeing signs that the active ingredient of the drug, oxymetazoline could be used in the future for keeping our cells functional and young.
Asprey claims that a simple solution, which is available and familiar to most people, could lead to the “next breakthrough in longevity.”
He wrote: “Some of our biggest gains in longevity will be from drugs that are already on the shelf. Not from new molecules.” I’ve said this for many years.
What is the ageing effect of Afrin?
Researchers at Northeastern University examined 6,442 different drugs in order to determine how they could impact on 11 biological processes known as “hallmarks for aging.”
This includes changes in whether genes are “on” and “off”, (called epigenetic alteration), as well as cells that lose the ability to remove proteins from within, which allows them to build up.
Afrin’s active ingredient, oxymetazoline (also known as Afrin), was found to help in one of the “hallmarks”, cell-to-cell communications.
The aging process affects the way cells transmit, receive and process chemical signals across the entire body. It can have a variety of adverse effects, ranging from a weakened immune system to muscle loss and bone loss.
The Oxymetazoline found in Sinex eyedrops, nasal sprays and creams to treat redness could also be used in this way.
Harvard researchers are currently conducting research on the possible effects of this drug on cells. Researchers at Harvard are currently researching how oxymetazoline can improve communication between cells.
For the time being, there is no human research. The authors also noted that this is not a cure for aging, but rather “a roadmap” that can be tested on cells, animals, and ultimately, human beings.
Bnaya gross, the lead author of this book, said: “I don’t think we have reached that point yet.” We are “moving toward an era of precision.”
Can Aspirin also be used as an anti-aging remedy?
This study identified a variety of drugs that may help slow down aging.
Intercellular communication is one of the five signs of aging that Aspirin affects, and it’s also affected by oxymetazoline.
The nutrient sensor can also help with cell senescence, which is when cells stop growing but don’t actually die.
As with oxymetazoline in humans, no anti-aging effects have been proven.

Charlotte Touzalin, a teenager at the time, began to struggle with unwanted facial hair and weight gain. These symptoms had plagued Charlotte’s mother for years and no one could figure out what was wrong.
Touzalin is an 18 year old college student in Colorado. “I couldn’t figure out why I was gaining weight or why some of my friends did not have to shave.
Touzalin Schultz and her mother, Anne Schultz were both diagnosed with polyendocrine ovarian metabolic syndrome. This hormonal disorder affects 1 in 8 women around the world. Touzalin, unlike her mother, is starting young adulthood full of hope. She took part in a research study that tested blockbuster GLP-1 medications as a possible treatment.
These medications for obesity may work to treat PMOS, not just by helping with weight loss. They also improve insulin resistance and hormone balance. This is the key to this disease. It was previously called polycystic Ovarian Syndrome, but it has been renamed to PMOS earlier this year in order to focus on the ovaries instead of cysts.
Touzalin said, “We have to be better at managing it.” Dr. Melanie Cree has been leading three studies that tested GLP-1 medications for PMOS. We are finding that they’re incredibly effective, and this is really exciting in terms of improving the symptoms for women who have PMOS.
PMOS can be a strange and frustrating disease
Touzalin’s and her mother’s frustrating, long journey with PMOS are common.
Doctors may dismiss symptoms that overlap or vary with others, and doctors can take years to diagnose the condition. This disorder runs in families and affects many women, but not all. There is no specific cause for this disorder, and there aren’t any known treatments. Instead, the symptoms can be managed by taking birth-control pills to control periods or exercising and eating healthy.
PMOS is primarily caused by two hormones: testosterone and insulin. Testosterone, for example, helps to maintain muscle mass, sexual desire and bone density.
Cree, PMOS Clinic Director at Children’s Hospital Colorado, explained that most women who have PMOS are insulin resistant, meaning their hormones don’t function as they should. The high insulin levels can directly affect the ovaries of many women. This causes them to produce more testosterone, causing problems such as skipped periods and severe acne.
Schultz (43), didn’t know that the disorder existed until she began experiencing irregular periods at age 18 and noticed bloating. She also suffered from the same symptoms that her daughter did, as well as ovaries problems and miscarriages. PMOS is more common.
Schultz was given several diagnoses, before she learned that PMOS affected her around the time when her daughter also faced similar issues.
Schultz remembered discussing Touzalin’s symptoms with her pediatrician, who had been treating Touzalin for binge-eating and ADHD.
Schultz said to the doctor, “There has got to be another thing going on.”
Touzalin says she “felt heard for the first” time when a nurse-practitioner began putting things together several years ago. Cree diagnosed her definitively last year.
It was like an angel appeared to Schultz. We finally found an answer, and a way forward for her.
Touzalin took semaglutide every week for 10 months in Cree’s research. Her periods returned to normal and the abnormal hair growth stopped. She stopped constantly gaining weight and felt satisfied after meals for the first time.
She said, “I was a happier person.” “I felt like a normal person.”
Insurance companies continue to put barriers up while research continues on GLP-1s and PMOS.
Touzalin’s results were not unique. The study was published in Fertility and Sterility in June. Early results showed that eight out of eleven participants who completed the test lost more than 10% of their weight. Median weight loss was 42 pounds, and testosterone levels dropped by 52%. Six of the women experienced more than one period, and four went on to monthly cycles.
Cree conducted three studies in which women taking GLP-1s shed more pounds than their control group counterparts, while testosterone levels, blood sugar, and insulin also dropped. The study with Touzalin focuses on semaglutide injections, while the two other studies looked at exenatide pills and semaglutide tablets.
Similar positive findings have been reported in other studies around the world. Despite the small size of these studies, researchers believe GLP-1s have already shown promising results in treating metabolic problems associated with PMOS. Some researchers say that the research is still uncertain and further studies are being conducted.
While research is ongoing, increasing numbers of doctors are prescribing drugs for PMOS “off-label” and observing improvements among their patients. Insurance coverage can be a challenge because these drugs have not been approved for treating the condition.
Endocrinologist Dr. Rana Malek of the University of Maryland’s Medical System said, “I take these medications a lot.”
She said that she uses these pills to aid in weight loss among patients who have insulin resistance.
The results can vary. GLP-1s are not for everyone, and they can cause side effects like nausea or constipation. Weight can come back if people stop taking GLP-1s.
Malek says that they are still a great help to many PMOS sufferers, but it is frustrating for them not to be available due insurance problems. They are not only unapproved by PMOS but some insurance companies also don’t pay for them to lose weight.
Touzalin herself recently encountered this obstacle. She no longer receives free GLP-1s after finishing her participation in the study and was forced to stop taking them by June.
Schultz wants to be able to take her medications again. Schultz is fighting her insurance company and also has a plan B to obtain medications via a pharmaceutical company’s program. Although she would like to use GLP-1s on her own, her daughter is her priority.
Touzalin dreams of a time when every PMOS sufferer can receive the necessary treatment.
She said, “It could be very helpful to a number of people.”
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This story was contributed by Brittany Peterson, a video journalist with AP in Denver.
___
Robert Wood Johnson Foundation and Howard Hughes Medical Institute Department of Science Education provide support to the Associated Press Health and Science Department. All content is the sole responsibility of The Associated Press.

I felt like a character from a Western movie, dancing around, dodging tumbleweeds, and avoiding trouble. Our neurosurgeon appeared behind the doors with a big grin and said: “It is time to perform the surgery!”
“We’re still not ready!” I shouted. In a state of panic, I was lying in an hospital bed in New York City when I awoke. My 6-year-old Riaan was lying next to me, with his EEG cables falling from his head and his fragile body drowned in a hospital gown. He remained sleeping, which was a blessing. After I was awoken, I ran over to the nursing station to beg them to cool down our room. It felt as if I was unable to breathe.
Riaan, the next day on April 21st, 2026 was to be the first human to ever receive the gene therapy to treat Cockayne Syndrome.
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Cockayne Syndrome is a rare genetic disorder that leads to progressive diseases and premature death. Our prenatal screenings did not include it. Riaan’s 15-month diagnosis was the first we heard about it. Riaan has a defective gene, CSA. This is a critical one for DNA repair, transcription and cellular health. In order to restore protein production in his brain and stop disease progression, the gene therapy aimed to inject a healthy version of CSA.
We were initially told that Riaan’s disease would only last five years. Born small (only 5 pounds 6 ounces), he developed cataracts both in eyes and did not reach developmental milestones. It took him a full year to gain control of his head and eat. It took up to an hour just to give him two ounces. He still wears onesies that are meant for 18-month olds.
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The first time I heard Riaan’s diagnosis, I wasn’t devastated that he might be disabled. I was distraught because I had been told Riaan was going to die soon. The grief and shock I felt that first night were overwhelming. My body was not sure how it would survive. When I woke up the next morning, my parents’ Florida house was ablaze with sunshine. It felt like a slap in the face.
Riaan was always happy, social and mischievous. He is full of energy. At 15 months, Riaan didn’t seem like a young child with a limited time. I was disturbed that my love for Richie and myself had caused a deadly disease to our firstborn.
Our reality was too much to bear after the diagnosis. Riaan was my first love and I wanted to give him a better life.
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This love is what propelled me to the world of unknown drug development. Riaan Research Initiative was launched and we connected with scientists that understood the urgency. We raised $4M through relentless storytelling, public activism, fundraising campaigns and the generosity of donors. We climbed the mountain that seemed insurmountable.
The drug development process isn’t a nine-to-five job. Years of night and day work were spent with our manufacturing, regulatory, scientific, clinical and clinical teams. The review period that followed the submission of the Investigational New Drug Application to the U.S. Food and Drug Administration was my favorite. The FDA will send clarification questions during this time, but we only have a few days to answer. A clinical hold can be imposed if the answer is incorrect or not satisfactory. The process was stressful, exciting, and high stakes for me as a lawyer. We were given the go-ahead to move forward. When I thanked the team for their work, I quoted the Count of Monte Cristo, “All wisdom in the world is found here: Wait and Hope.” After so many years waiting and hoping the moment finally arrived.
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The idea of being involved in the development of a new drug and funding it is quite strange. It didn’t make it easier for us to determine whether or not we should give it to him.
Richie, my husband and I were struggling with the decision of how to move forward and our agony at seeing this dream become a reality. Riaan’s disease was advanced, so the prospects of recovery were less sure. Riaan was happy, stable and never had been in the hospital before. It was wrong to make him endure a weeklong hospital stay and immunosuppression, even though children with this disease are more susceptible to the side effects of anesthesia and medications. It was wrong to expose him to unknown side effects of a gene therapy that is the first in humans.
The risks of gene therapy are not insignificant: from liver failure, to a catastrophic response to cerebral edema. The immunosuppression required to stop the body attacking gene therapy, or causing a harmful response, can also be a challenge.
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This was a chance that would never come again, both for Riaan as well as for us. If we were able to prove it safe in Riaan’s case, then we believed it might be a proof-of-concept for future administrations of the drug on other children. There was nothing else. It was the only hope.
The gene therapy improved the quality of life and extended lifespan for neonatal mice models suffering from Cockayne Syndrome. Riaan, however, was not a baby mouse. Riaan weighed 22 pounds, could not sit, stand, eat himself or speak. Was it possible to make the leap from a mouse to a child in terms of science?
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Richie spent many nights with me on the couch. We would sometimes argue, and we felt the pressure of making this difficult parenting decision.
Why couldn’t there be more choices for parents?
We’re one of only a few parents with access to treatment for a rare illness in their child. This is a great privilege that we should not take for granted.
What if he dies?
They were very helpful. No one told me not to do it.
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Riaan is not verbal and could therefore not give his consent. He is our shining star, and we have shared six intensely joyful years with him. He enjoys pulling Jivan’s little hair and taking his toys. Nani Ji also loves to video-chat with him. He had a blast in Bermuda. Infinity pools, pink beaches, and swimming were all part of the fun. He was just perfect the way he is.
On one occasion, I asked him to feel my nose if, indeed, he was interested in the treatment. My nose was immediately touched. He usually took a long time or ignored my request. This was a clear sign.
The team that was around me, from scientists and doctors at UMass Chan Medical School and Weill Cornell to so many others who were committed to Riaan and felt part of the mission. Our physician-scientist adviser, known as Batman in the genetherapy world, was always available to answer our questions, even at odd times. He had a wealth of scientific knowledge and was able to provide us with regulatory information.
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I asked the researcher who I most trust if he’d do it if Riaan was his son. He agreed, saying that he couldn’t guarantee anything and no one else could. But he was willing to do so.
The decision was made to move forward. After we agreed, we stopped wondering “what if” and focused on the positive outcome of the procedure.
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It was not an easy day. Riaan hadn’t eaten or drank anything by mouth for the entire day because of the delay. As he finally entered the operating room that evening, I wondered if it had been written in the stars. We felt like shepherds as we gave our firstborn to the surgeons. We finally realized the importance of that moment when we saw Riaan’s AAV9 dosage in the ziplock bag we made.
Riaan clung to us, crying.
Richie placed him gently on the table and then the team of anesthesiologists put a mask over him. He looked fierce and peaceful in the Simba sweater as our brave lion went into anesthesia. We told him that we love him and were proud of his accomplishments. I said a quick prayer.
Richie (my friend) and I went back into our rooms like zombies. It was impossible to move, talk or look each other in the eye. The heavy burden of responsibility fell on me as the parent that had led the effort to treat my child. We had tried everything to help our child, but this diagnosis was beyond us.
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As soon as I heard that the surgery was completed, I sprinted to the Pediatrics Intensive Care Unit. The surgical team informed me in the hall that Riaan did extremely well. Our gifted neurosurgeon was in my arms. Then I heard Riaan scream from his room. It was a noise I’d never heard before. “What is wrong with him?” I yelled at the doctors, terrified. “What happened?” They all told me that he’s fine and just needed to be seen by you.
Riaan’s first appearance reminded me when Frankenstein gains consciousness. The wires were coming from every part of my beautiful boy. His mouth was open and he gasped for water. He had gauze loosely placed on his head, covering his incision. Tylenol and some time were needed to calm him.
He slept in my arms that night — an uneasy sleep with neuro tests every two hours. Even when I had to fight back a vicious cough, I did not dare move. The next morning, he looked much healthier, and was even smiling as he played balloon volleyball with me. He was fine physically, but the team closely monitored him. We left the hospital a few days after the initial visit and went to a hotel nearby during this critical period of monitoring. We finally made it home three weeks after we left Queens.
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The gene therapy may take months or even years to show if it has helped him. We are thankful for the close monitoring he receives via blood tests and exams, but it can be challenging at times. We don’t yet know the duration of any clinical benefits.
Riaan is still clinically stable, even after three months of treatment. He wakes up with a smile, demanding “The Circle of Life”, his morning favorite. This is his way of starting the day. Riaan is back to his happy self, although it’s still early. We’ve already seen some encouraging signs. He will still have Cockayne’s syndrome and his future is unknown.
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The FDA approved the treatment of other Cockayne Syndrome children. We are looking forward to engaging with them again in the months ahead to get approval for the drug to be manufactured to treat more children. Our goal is to raise money to pay for the costs of clinical trials.
We were lucky, but parents shouldn’t have to be drug developers, because the disease of their child is rare and not profitable for pharmaceutical companies. Families shouldn’t have to spend millions of dollars, attend manufacturing meetings and learn about regulatory strategies before they can decide if their child will receive a drug that was developed by them. We would, out of love for Riaan as well as for any children that may follow him, do it all over again.
Riaan’s first birth, I promised him that I would do everything I could to protect and care for him. It’s my way of saying I love him.
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Jo Kaur, a former civil rights lawyer turned drug developer, is an expert in the field of human rights. She founded Riaan Research Initiative (a patient advocacy group that works to develop gene therapies for Cockayne Syndrome, a fatal and rare pediatric genetic disorder). Jo founded the Riaan Research Initiative in 2021, after Riaan’s diagnosis. She lives with her husband Richie, her children Riaan, Jivan and their two sons in New York City.