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A breakthrough in a Harvard lab led to a new cancer drug. Could it save a man with six months to live?

A breakthrough in a Harvard lab led to a new cancer drug. Could it save a man with six months to live?

Boston Globe17 hours ago
'You'll want to call hospice,' the surgeon told Sehy's wife, Jean, before her husband even woke from anesthesia.
At the time, about 70,000 Americans were diagnosed with melanoma every year. When the disease tipped into the advanced stages, it was pretty much a death sentence —only about 5 percent of patients might go into remission. Sehy's doctors estimated he had six months to live, though chemotherapy might stretch that a little longer if he could tolerate the side effects.
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Jean was quiet and numb on the drive back to rural Illinois, mulling over the prognosis. They'd been married 40 years and raised four children. Sehy owned a marketing supply company for veterinarians and the couple had been hoping to travel and spend more time with their two grandchildren. All those dreams were crumbling.
At home in the tiny farming and manufacturing town of
(pop. 1,587), Sehy held onto a last-ditch suggestion from his oncologist:
Sehy mowed his lawn at home in Teutopolis.
Kate Munsch for The Boston Globe
He began to methodically email every researcher his doctor pointed him toward, though the early responses were disappointing. Some weren't studying his type of cancer, others didn't have any room left in their trials. Finally, after months, one doctor 300 miles away in Nashville said he had an opening in his medical center's
drug. It was called
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MDX-1106, later known as Opdivo, would take more than five years of research and testing to become one of the key early successes of immunotherapy, arguably the most important advance in cancer treatment in a generation. Joined by similar drugs such as Keytruda that enlist the body's immune system to fight cancer, it would add years to the lives of millions of patients. Without it, they might only have expected months.
The story of Opdivo leads all the way back to
President Trump's administration has cut nearly $3 billion in research funding to Harvard, affecting
awarded to scores of universities and hospitals by the NIH — a
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The Harvard Medical School complex in Boston.
David L. Ryan/Globe Staff
Liberal bias has supplanted America's scientific enterprise, the administration said, and the country needs
MDX-1106 is the story of what happens when the time-honored paradigm works — and what risks being lost in its disruption. To get to 2009, when Sehy joined the clinical trial, took years of discovery at Harvard and elsewhere, aided by federal funding. It would be years more work before federal regulators deemed the drug safe and effective for patients. Interrupt any step in that process, and cancer patients like Sehy didn't stand a chance.
The twisting road of research
The public outcry to the biomedical research cuts has been loud but not as fierce as many scientists expected, considering that the federal government has been essential to developing medical treatments. A recent review looked at 356 drugs approved by federal regulators between 2010 and 2019. NIH funding
But 'this message is not getting through,' said Dr. Benjamin Miller, chair of the aging and metabolism research program at the Oklahoma Medical Research Foundation. His Oklahoma City-based nonprofit has helped usher three new drugs into the world, among other advances, and is now seeing its federal grants cut.
'For many years as scientists, we just sort of thought that people understood why this money was important,' Miller said, 'and we didn't spend enough time engaging in these conversations to connect those dots for people.'
Truly connecting the dots would show that defunding basic research today threatens to block the advances not of tomorrow, but those that might come five or ten or twenty years in the future.
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It's easy to imagine that the process of biomedical research is like building a bridge: Design the blueprint, then simply start connecting beams and bolts until you get to the other side. In reality, though, moving from a breakthrough in a lab to a drug for patients — the journey from bench to bedside, as scientists call it — is more like traveling a road full of twists, turns, and detours.
Cholesterol-fighting statins, the most widely prescribed drugs in the world,
It took
A breakthrough at Harvard
Dr. Arlene Sharpe, head of the immunology department at Harvard Medical School, grew up in Gary, Ind. In elementary school, she labored over an experiment on lima bean germination for her science fair. She won a blue ribbon.
Sharpe's parents encouraged her curiosity and, as gardeners themselves, were particularly delighted by her interest in hydroponics. 'They let me set up these aquaria in our house; I'd have the chicken wire, and I'd have the plants I was trying to grow,' Sharpe recalled, smiling at the memory. 'All I ever grew then was mold.'
In 1969, when Sharpe was 15, her mother died of leukemia. At the time, people only whispered the word 'cancer' and treatment options were limited. That seemed wrong to Sharpe. She thought scientists should be able to do something.
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Sharpe headed to Harvard for college in the early 1970s. There she met Gordon Freeman, a lanky, soft-spoken Texan, and they clicked over a shared passion for the endless possibilities of biology. The two married in 1978, had two children, and eventually began collaborating on research.
They focused on the immune system, a complex network of cells and organs that defends the body from disease and infection. With significant financial support from federal research grants, they wanted to better understand what happened when the system faced problems, such as asthma and cancer.
Dr. Arlene Sharpe, with her husband and co-investigator Gordon Freeman, at the Sharpe Laboratory at Harvard Medical School.
Jonathan Wiggs/Globe Staff
In the lab, Sharpe and Freeman offered complementary strengths that combined to make a formidable team. Freeman had a talent for identifying new molecules to explore. Sharpe was adept at removing those molecules from mice, then measuring whether the change strengthened the rodents' immune defenses or weakened them.
In 1995 they had a breakthrough. When they deleted a certain molecule on a type of white blood cell called a T cell, they noticed the rodent's immune system shifted into overdrive. Intrigued by the potential of regulating the immune response, Sharpe and her colleagues
The next year,
Berkeley researcher, showed for the first time that blocking the same molecule, CTLA-4, could eliminate tumors in mice. That flung open the door to a potential new way of treating cancer in humans, by unleashing the immune system to fight the disease.
A display of vital molecules in cancer immunotherapy that Sharpe and Freeman co-discovered.
Jonathan Wiggs/Globe Staff
The race was on to find other molecules that could prime the body to attack tumors. In 2000, Freeman and colleagues
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How immunotherapy drugs work to activate T cells, a type of white blood cell, to target and destroy cancer.
Proteins called T cell receptors detect cancer antigens (substances on the surface of cancer cells. ) But the T-cell is unable to attack the cancer because another T cell protein, PD-1, is bound to a protein on the cancer cell, called PD-L1, that's putting the brakes on the immune system.
Immunotherapy cancer drugs, anti-PD-1 medicines, release the brakes on the immune system and allow T cells to attack the cancer.
SOURCE: Gordon Freeman, and program Biorender. RYAN HUDDLE/GLOBE STAFF and Adobe Shutterstock
In a way, PD-L1 tricked the body's defenses into ignoring tumors, allowing them to grow and spread unchecked. Just when the immune system should be speeding ahead to fight cancer, PD-L1 slammed on the brakes. Sharpe and Freeman also took another step, demonstrating how the body could recognize cancer as dangerous and then release the immune system's brakes.
They knew it was an important insight. Translating it from the lab setting into a treatment for patients, however, wasn't going to be easy.
From bench to bedside
Despite the promise of immunotherapy in the early 2000s, many cancer specialists remained skeptical. Chemotherapy was long-studied and widely used, even though using it was like dropping a bomb that obliterated cancer cells and healthy ones alike. Could immunotherapy, which sought to marshal the body's own defenses, really work?
'We thought we were at the vanguard of a whole new approach to treating cancer,' recalled Dr. Israel Lowy,
then director of clinical science at Medarex,
a small biopharmaceutical company in New Jersey. 'But no one took us seriously.'
Lowy had been watching Sharpe and Freeman's breakthroughs closely, as Medarex developed an investigational cancer drug. In 2006, his team filed an application with federal regulators for MDX-1106, inspired by research from several scientists, including Sharpe and Freeman's work blocking the PD-L1 protein.
Two years later, at a May 2008 conference, the team proudly
With results like that, 'We were like kids in a candy store,' recalled Lowy, now a senior vice president at Regeneron, a biotech company. Cancer specialists weren't skeptical any longer.
With approval to expand, researchers eventually launched a bigger clinical trial at 13 medical centers around the country, including three in Boston. This time, 306 cancer patients would receive infusions of the experimental drug every two weeks for nearly two years.
One of those patients would be Stephen Sehy.
The trials of a cancer patient
By the winter of 2009, Sehy was getting sicker. It had been eight months since his diagnosis, but the melanoma tumors on his face and liver had overtaken the cocktail of chemotherapy drugs he'd been receiving. Still, from the beginning, Sehy had been determined to enjoy whatever time he had left.
'He would say to me, 'OK Jeanie, if I have only six months to live, you are not going to be crying around,'' Jean recalled.
Sehy's first infusion of MDX-1106 was scheduled for December 21, 2009. When the couple returned from the 300 mile drive to Vanderbilt University Medical Center in Tennessee, Sehy sat down at a computer to type out a Christmas email. 'Have a great holiday, and enjoy each day,' he wrote to friends and family. 'All the little things in life add up to a big deal!'
After that first infusion, he and Jean would not have to wait long for a positive sign.
At Sehy's next appointment, just two weeks later, a doctor at Vanderbilt confirmed what the couple feared they'd only been imagining: the tumor near his right ear had shrunk by more than a tenth of an inch. They should know that happens sometimes, the doctor gently explained, and then the tumor comes charging back.
The couple let themselves quietly start dreaming anyway, about a trip to Hawaii, maybe one to Alaska. They didn't know if Sehy would live long enough. But they could hope.
'Steve didn't want me to write this, because it may get everyone's hopes up, but I thought, so what?' Jean wrote to their loved ones at one point. 'That's what it's about. HOPE, isn't it?'
Over time, the tumors on Sehy's face kept shrinking. They waited for him to suffer side effects, but none came. In 2011, the couple made it to Hawaii for one of their dream trips.
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Timeline: What a trail-blazing discovery meant to Stephen Sehy
Nov. 1995
Harvard Medical School researcher Dr. Arlene Sharpe and colleagues show for the first time that knocking out a protein, CTLA-4, on T cells in mice can over-stimulate their immune system, suggesting a way to regulate the system.
Oct. 2000
Harvard Medical School/Dana-Farber Cancer Institute researcher Gordon Freeman and colleagues show how cancer cells disable immune defenses, and how this cell process, known as PD1/PD-L1, could be blocked. Sharpe and Freeman's research is critical in the design of anti-PD-1 immunotherapies for cancer that restore the immune system's ability to spot and destroy tumors.
April 2009
Stephen Sehy is given six months to live after a surgeon discovers melanoma has spread to his liver and spine.
Dec. 2009
Sehy enrolls in the Phase One clinical trial of MDX1106, an experimental PD-1 antibody for the treatment of cancer, based on the research from Sharpe and Freeman. The treatment would become the cancer drug Opdivo, approved by FDA in 2014.
Jan. - Sept. 2010
The first nine months of 2010 were busy for the Sehys; they welcomed four more grandchildren from January through September.
Jan. 2011
Stephen and Jean Sehy take a trip to Hawaii.
Oct. 2011
Stephen completes the clinical trial of MDX1106.
Nov. & Dec. 2011
The Sehys welcome two more grandchildren, a girl and a boy.
Dec. 2011
Scans show the tumors on Stephen Sehy's liver and spine are gone. Here, Sehy is pictured in a Christmas card photo.
Aug. 2012
Stephen and Jean vacation in Alaska, where they try the Zip line.
Jan. 2013
The couple's ninth grandchild, a grandson, is born.
June 2014
Their fifth grandson is born. Later that year FDA approves Keytruda, a drug similar to Opdivo, and soon after approves Opdivo. The drugs enter wide circulation.
Feb. 2015
Their sixth grandson, the 11th grandchild, is born.
June 2016
A 70th birthday party for Stephen with 100 invited friends and family.
July 2019
Stephen and Jean celebrate their 50th wedding anniversary with a party, dinner and dancing.
July 2024
The couple vacation in Branson, Missouri with all four of their children and 11 grandkids.
That December, two years after he was accepted into the MDX-1106 trial, Sehy received an early holiday gift: Two separate scans showed the tumors on his liver and spine were gone.
Not slowing in their growth. Not shrinking. Gone.
And Sehy wasn't alone. Word was trickling in from other MDX-1106 trial sites that tumors were also disappearing in other patients.
The immunotherapy treatment was working.
The age of immunotherapy
Dr. Douglas Johnson had helped enroll participants in the MDX-1106 trial at Vanderbilt while he was training in oncology. Even then, he knew all about 'the conversation,' the time doctors had to advise melanoma patients to get their affairs in order. But after the arrival of immunotherapy, he said, that conversation 'changed almost overnight.'
In 2011,federal regulators approved Yervoy,
Three years later, MDX-1106 — the drug based on Sharpe and Freeman's research at Harvard and now named Opdivo — was approved for cancer patients, as was a similar drug called Keytruda. Today, these immunotherapies are used to treat at least 20 types of cancer and have provided additional years of life for millions of patients. (Last year alone, they also generated more than $23 billion in US sales, according to
'I fell in love with taking care of patients with melanoma in large part because of these drugs coming on board,' said Johnson, now an oncology professor at Vanderbilt who leads a melanoma research program. 'It's such a paradigm shift to be able to offer this to patients who previously didn't have many options.'
Before immunotherapy drugs, survival rates for people with metastatic skin cancer were often dismal, Johnson said, with maybe up to 5 percent experiencing remission. Today, advanced melanoma patients treated with a combination of immunotherapies can have a 50 percent or higher survival rate. The number can be around 30 percent for people with bladder or lung cancers treated by immunotherapy.
Experts now believe immunotherapy may also train the immune system, through its memory T cells, to recognize cancer if it recurs and keep fighting back, even after treatments have ended.
'In some cases, patients can now live for years with a durable response even after they stop therapy, and we never had anything like that before,' said Dr. Arnold Baskies,
former chair of the American Cancer Society's National Board of Directors.
Sehy pushed grandson Victor, 10, on a swing in his backyard.
Kate Munsch for The Boston Globe
That's the way it has gone for Sehy. Sixteen years after he was given six months to live, he remains cancer free.
Sehy is now 79, with a shock of white hair and a serious pickleball hobby. The only visible mark of his place in immunotherapy history is a patch of discolored skin in front of his right ear, where doctors removed the last of his tumors months after his final MDX-1106 treatment.
He and Jean made it on their trip to Alaska and many other places around the world, too. The two young grandchildren he thought of when he first heard his diagnosis are now 17 years old and have been joined by nine others.
A portrait of Stephen and Jean Sehy's family above their fireplace includes their four children and 11 grandchildren.
Kate Munsch for The Boston Globe
'There was a time I thought I would never see another grandkid,' Sehy said. 'Now, I'm thinking I just want to see one of them graduate college. And then I'll want to see them get married.'
In search of new breakthroughs
Whenever she sees advertisements for immunotherapy drugs, Arlene Sharpe does a double-take, remembering her early discovery at Harvard. Even more powerful is meeting cancer survivors who, thanks to treatments that followed, have lived years past their doctors' initial expectations.
'People will come up to me at different meetings and thank me, and they'll tell me that they received either Keytruda or Opdivo a decade ago,' she said. 'And every time, it's just chilling.'
But Sharpe, now 71, spends most of her time looking forward, not back. Some patients' tumors don't respond to immunotherapy, and others struggle with significant
'We see that there can be success, and now we want to build on the success,' she said.
In recent months, she's had to do that work without federal support. The Trump administration has choked off nearly all government funding to Harvard, including for her research and that of 12 other faculty in her department. She's now searching for private funding sources to keep everything afloat. But that's no guarantee, either.
'Private foundations often want to fund things at a later stage, they don't want to fund the discovery work,' she said. 'It's really the fundamental discovery science that [the government] funds.'
Dr. Arlene Sharpe at Harvard Medical School.
Jonathan Wiggs/Globe Staff
Harvard is challenging the federal cuts, though it has already had to lay off staff and institute hiring freezes. The university has also
Sharpe knows the road to a scientific breakthrough is long and twisting, but slowing down is out of the question. About
'There's an urgency here,' Sharpe said. 'Patients and their families don't have the time to wait.'
Kay Lazar can be reached at
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Ritz Peanut Butter Cracker Recall Sparks Nationwide Warning
Ritz Peanut Butter Cracker Recall Sparks Nationwide Warning

Newsweek

timean hour ago

  • Newsweek

Ritz Peanut Butter Cracker Recall Sparks Nationwide Warning

Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources. Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content. Mondelēz Global LLC is recalling multiple carton sizes of Ritz peanut butter cracker sandwiches due to fears the product may be mislabeled. Newsweek reached out to the company via email Tuesday for comment. Why It Matters Numerous recalls have been initiated in 2025 due to the potential of damaged products, foodborne illness, contamination and undeclared food allergens. Millions of Americans experience food sensitivities or allergies every year. According to the Food and Drug Administration (FDA), the nine "major" food allergens in the U.S. are eggs, milk, fish, wheat, soybeans, Crustacean shellfish, sesame, tree nuts and peanuts. People with a sensitivity or allergy to peanuts may experience "serious or life-threatening allergic reactions" if they consume the recalled product, the FDA warns. Accidental ingestion can lead to anaphylaxis, a rapid and life-threatening allergic reaction that requires immediate medical intervention. Even trace amounts of peanuts can cause symptoms from hives and swelling to difficulty breathing and shock. What To Know In the alert, the FDA says the products were manufactured in the United States and sold nationwide. The Ritz Peanut Butter Cracker Sandwiches in eight-pack, 20-pack and 40-pack cartons as well as the 20-pack Ritz Filled Cracker Sandwich Variety Pack cartons are being recalled due to the possibility of the individually wrapped packages inside the carton potentially being labeled cheese, the FDA says. "All outer cartons affected are labeled correctly and provide an allergen advisory statement indicating that the product 'contains peanuts,'" the FDA notes. No other Mondelēz Global LLC products or Ritz products are impacted by the recall. In the alert, the FDA posted a chart with corresponding best if used by dates along with retail UPC numbers. The alert also has pictures of the affected products. Ritz cheese cracker sandwiches, peanut butter cracker sandwiches and Ritz filled cracker sandwich variety packs with different best by dates and UPC numbers are also not affected by the recall. There have been no reported illnesses or injuries as of Tuesday, the alert says. Mondelēz Global LLC reaffirms the recall was initiated as a precaution. A grocery store aisle in Brooklyn is pictured on May 13 in New York City. (Photo by) A grocery store aisle in Brooklyn is pictured on May 13 in New York City. (Photo by) What People Are Saying The FDA in its alert, in part: "The recall was initiated after Mondelēz Global LLC discovered that film packaging rolls used to package individually wrapped products containing peanut butter may contain defects due to a supplier error. Corrective actions are being taken to help ensure this issue does not recur." What Happens Next Customers with questions or concerns may contact the company around the clock via phone at 1-844-366-1171.

Women are twice as likely to suffer from Alzheimer's as men. Scientists have figured out why
Women are twice as likely to suffer from Alzheimer's as men. Scientists have figured out why

Yahoo

time2 hours ago

  • Yahoo

Women are twice as likely to suffer from Alzheimer's as men. Scientists have figured out why

Experts have long known that women are at a greater risk of developing Alzheimer's disease. They're twice as likely to be affected as men. Now scientists say they may be on their way to understanding why that's the case - pinpointing two stark differences between men and women. Firstly, women have different chromosomes than men. They also undergo menopause: a process that occurs when a woman's reproductive hormones naturally decline starting in her 40s and 50s. One in three older Americans dies with Alzheimer's, or another dementia, according to the Alzheimer's Association. Almost two-thirds of Americans with Alzheimer's disease are women. 'Epidemiologically, we see that for almost all neurological diseases, there are differences in how many biological women and men are affected,' Anna Bonkhoff, resident and research fellow in neurology at Harvard Medical School and Mass General Brigham, explained in a recent interview. 'There's a tendency, for example, in [multiple sclerosis] and migraine for more females to be affected, while it's the contrary for brain tumors and Parkinson's.' 'Just based on these numbers, you get the feeling that something needs to underlie these differences in terms of the biology,' she added. Looking inside the body, while women have two 'X' chromosomes, men have an 'X' and a 'Y.' Chromosomes are thread-like structures of DNA inside our cells that carry hundreds or even thousands of genes. Genes determine a person's physical characteristics. Differences between genes held on the X and Y chromosomes may give women an increased chance of developing Alzheimer's disease. Recent research has shown that genes on the X chromosome are related to Alzheimer's disease, including that women with Alzheimer's live longer than men with the disease due to their second X chromosome. 'A lot of genes for the immune system and regulating brain structure are located on the X chromosome, so the dosages differ to certain degrees between men and women. That seems to have an effect,' said Bonkhoff. Women's different dominant hormones — such as estrogen, which acts on the brain — could also play a role. 'Menopause is part of the puzzle, probably one of the bigger ones,' Bonkhoff said. 'I'm not saying it's the only one — aging is relevant by itself, and there's a lot of interesting research looking at what aging does to the immune system that seems to have implications for cognitive changes.' During menopause, when ovaries stop producing estrogen and progesterone, some women turn to hormone replacement therapy. The practice offers relief for symptoms of lower hormone levels in menopause such as hot flashes. But for some women it may increase their risk of dangerous medical conditions, including heart attacks, strokes, breast cancer, blood clots and gall bladder disease, according to the Centers for Disease Control and Prevention. Women who received hormone replacement after age 70 also have significantly higher levels of the protein known as 'tau,' according to Rachel Buckley, associate professor of neurology at Harvard Medical School. The accumulation of tau is a hallmark of Alzheimer's disease. They also suffered higher cognitive decline. Buckley published those findings last March in the journal Science Advances. But further research is needed to understand these associations. 'We work with a lot of secondary data that already exists, and that's great but there are limitations to what we can do with it,' Buckley said. 'We're trying to see if we can set up a new study design where we can really look at the time of menopause, what is changing in the blood, what is changing in the brain, what is changing in cognition, and how that might be associated with later life risk.'

More than half of East Coast beaches tested positive for fecal contamination, shocking new study reveals — how did your vacation spot do?
More than half of East Coast beaches tested positive for fecal contamination, shocking new study reveals — how did your vacation spot do?

New York Post

time3 hours ago

  • New York Post

More than half of East Coast beaches tested positive for fecal contamination, shocking new study reveals — how did your vacation spot do?

Hold your nose — and maybe hold off on that beach day. More than 60% of U.S. beaches tested in 2024 had at least one day where the water was so full of fecal bacteria that it failed federal safety standards, according to a new report by Environment America's Research & Policy Center. That's 1,930 beaches out of 3,187 that were dirtier than your dog after a mud run. Advertisement The top offenders? The Gulf Coast, where a whopping 84% of beaches had at least one 'poo-lution' problem day, followed by the West Coast (79%) and the Great Lakes (71%). The East Coast didn't exactly sparkle — 54% were flagged for contamination. Only Alaska and Hawaii offered a relatively clean sweep, with just 10% of beaches testing unsafe. Advertisement 3 So much for West Coast beaches being cleaner than the East Coast. Christopher Sadowski How bad is it? Nearly 1 in 7 beaches showed potentially dangerous levels of fecal contamination on a quarter of all testing days, the report found. And the fun doesn't stop at dirty data. Swimming in these murky waters could bring a not-so-sunny side of summer — think gastrointestinal illnesses, respiratory issues, ear infections, and skin rashes. The report estimates 57 million related cases hit Americans each year, most of which go unreported — or unremembered once the vacation tan fades. 'Enjoying the fresh sea breeze and splash of waves at the beach is a highlight of the summer for many Americans,' said John Rumpler, clean water director for Environment America Research & Policy Center. 'But pollution still plagues too many of the places where we swim.' Advertisement As previously reported by The Post, New York's own Windmill Beach in Sag Harbor made national headlines for being one of the top 10 most bacteria-ridden beaches in the country — with a stomach-churning 43% contamination rate. It's not the Hamptons souvenir you want to bring home. 3 Nearly 1 in 7 beaches tested dirty on at least 25% of the days sampled — meaning swimmers had a 1-in-4 shot of wading into a bacterial brew. Christopher Sadowski In fact, over half of New York's beaches were found to be contaminated with poop or sewage last year, according to a previous Environment America report. Déjà poo, anyone? Advertisement Adding insult to injury? Federal funding to fix this mess is circling the drain. The Clean Water State Revolving Fund, which helps communities upgrade aging sewer and stormwater systems, needs $630 billion over the next two decades, per the EPA. But the White House's 2026 budget proposal would slash it. 'Now is not the time to slash the water infrastructure funding that communities sorely need to stop the flow of nasty bacteria and pollution to our beaches,' Rumpler warned. And it's not just the infrastructure getting flushed — beachgoers themselves aren't helping. 3 Beachgoers aren't helping this gross situation by peeing in the ocean. NurPhoto via Getty Images As The Post previously dished, a staggering 70% of Americans admit to peeing in the ocean, and 1 in 4 admit to littering, even though 82% say it's the most annoying beach behavior. So before you cannonball into your local shoreline this summer, maybe check if it's a splash zone — or a crap trap.

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