Pulmonary Fibrosis Foundation in the News!

Fighting for breath Published: January 30, 2005 Alone during the day at his Bend home, Kamasz works through a 20-minute walk on a treadmill with the help of an accessory oxygen bottle. His disease forced him into long-term disability from his job as a deputy with the Deschutes County Sheriff's Office. Rob Kerr / The Bulletin By Kayley Mendenhall On a March day almost seven years ago, Matt Kamasz stepped out of the shower and nearly fell to the bathroom floor. He thought his chest would explode as what he believed was a heart attack gripped him in pain and he lost his breath. It was an off-duty day from the Deschutes County Sheriff's Office for the young deputy and he drove himself to the hospital. He learned his right lung had collapsed. Doctors reinflated his lung and performed a lung biopsy. They sent some of Matt's tissue to an out-of-state lab for diagnosis. When the results came nearly two weeks later, then 26-year-old Matt Kamasz's life was forever changed. He was diagnosed with idiopathic pulmonary fibrosis and told there was neither an effective treatment nor a cure for the problem. The disease, according to medical experts, has no known cause. It is slowly turning the air sacks in Kamasz's lungs to scar tissue, causing his lungs to stiffen and reducing the amount of oxygen transferred to his blood. His lung capacity is 32 percent of normal. The damage already done cannot be reversed, and his only hope, at this point, is a double lung transplant. "It's pretty depressing," Kamasz, now 33, said. "The ultimate death thing." But, he and his wife, Sarah Kamasz, are not giving up hope. The Bend couple are working to have Matt placed on the lung transplant list, and, with any luck, he'll have a new set of lungs within a year. If Kamasz receives new lungs, his doctors believe the disease will be gone and the new lungs will be safe from damage caused by idiopathic pulmonary fibrosis. "There's no other option at this point," Sarah Kamasz, 32, said. The Bend couple are working to have Matt placed on the lung transplant list, and, with any luck, he'll have a new set of lungs within a year. "There's no other option at this point," Sarah Kamasz, 32, said. A life spent running Matt Kamasz grew up in Portland where he attended Columbia Christian High School and was a long-distance track and cross-country runner. After high school he decided to go into law enforcement, attended the Los Angeles Police Academy and began working there as a bike patrolman in 1994. "I ran eight miles every day," he said. "I wasn't keeping up as much as I should. Something was weird at the time, but it didn't dawn on me." An evaluation of Kamasz's job performance from the Los Angeles Police Department in 1996 shows that he received low marks for his poor physical condition. Kamasz said he remembers receiving the report and asking his commanding officer what more he could do in addition to running every day and lifting weights. "The last thing you're thinking is lung disease," he said. "It took a lung collapse for me to realize that." After a few years in Los Angeles, Kamasz decided he wanted to be closer to home. He applied for a job with the Deschutes County Sheriff's Office and moved to Bend, where he continued to work as a deputy for several years even after his initial diagnosis of the terminal idiopathic pulmonary fibrosis. The disease progresses at a different rate in different people, said Michael Rosenzweig, executive director and founder of the Pulmonary Fibrosis Foundation based in Chicago. "Some people will die a week after they are diagnosed. I've had it for 12 years," Rosenzweig said. "Nobody can really predict the longevity for any individual, not with any accuracy." He explained that in patients with idiopathic pulmonary fibrosis, tiny cells within the lungs become scarred, depleting the person's ability to breathe. There are approximately 200,000 people currently living with the disease in the United States. Idiopathic pulmonary fibrosis typically affects people between the ages of 50 and 70, Rosenzweig said, making Matt Kamasz a very young case. The disease can sometimes run in families as, Rosenzweig said, he lost both a brother and a sister to it. But, in Matt Kamasz's case, he is the only member of his family to show any signs of the disease so far. He has been living with it since his diagnosis for almost seven years — longer than the average given by most medical experts that patients live about five years after they are diagnosed. He and Sarah talked about the disease when they first began dating about four years ago and before they were married in August 2003. It was in the back of their minds, but, they said, they didn't want the disease to be the focus of their decisions. "We didn't know how quickly it would progress," Sarah Kamasz said. About a year ago, Matt Kamasz was taken off patrol and put on light duty at the Sheriff's Office. Last June, he went on long-term disability, but he says, he's not retiring from law enforcement forever. "I'm going to apply at the first police agency that will hire me," he said. "Let's go and get this (transplant) done so I can work again." Finding a new set of lungs The need for a lung transplant didn't hit Matt Kamasz overnight. He tried various medical therapies including prednisone — a steroid thought to sometimes slow the progression of idiopathic pulmonary fibrosis. Nothing really worked. As his lung capacity has continued to decline, his physical abilities have become more limited. He can't walk from his front door to his car without having to sit for several minutes and catch his breath. Sarah Kamasz said she doesn't let him push a vacuum and they hired a service to mow their lawn. "It's all those silly little things people don't think about," she said. When his health started deteriorating fast last year, Matt Kamasz went to the University of Washington Medical Center in Seattle to seek expert advice from Dr. Ganesh Raghu, a leading expert on lung diseases and lung transplants. Raghu started him on a different drug last March, but, coordinating nurse Carolyn Spada said, it hasn't helped enough. "The therapy hasn't stalled it as much as we would have liked," she said. "That's why Dr. Raghu is recommending the transplant." Matt Kamasz went through a battery of blood tests a couple of weeks ago to determine if he's physically healthy enough to undergo the surgery. The tests show that, other than his lung disease, he is in good shape.Raghu suggested Kamasz start working out regularly again, because the better physical condition he is in, the easier the recovery will be. He started walking on the treadmill for 20 minutes, two or three days a week and lifting a minimum amount of weight. "I walk on the treadmill for 20 minutes and I'm exhausted," Kamasz said. "Walking outside is harder for me." But the physical activity helps fill his days while he waits to hear back from Pacific Health Source, his insurance provider, about what will be covered. The transplant alone will cost about $250,000 not including the hospital stay and post-surgery care, Sarah Kamasz said. The Kamaszes hope Matt can have the transplant in Seattle where they already know Raghu and are familiar with the city, but the insurance company may insist the operation take place in San Francisco — a facility already approved by Pacific Health Source — instead. Once the insurance company gives the go-ahead, Spada explained, more physical and psychological tests will be conducted and a transplant committee will decide if Matt Kamasz is a good candidate. "He needs to go through a tremendous amount of evaluations. They do a total body evaluation to make sure there is nothing else that would preclude him getting a transplant. No cancer, no heart disease nothing else that might make it so a transplant won't work," she said. "There are a lot of   people who will be there to support you. That's a big aspect. It's so important in getting better." With any luck, Sarah Kamasz said, he'll be on the transplant list by June. Waiting for the call If he's accepted and put on the list, Matt Kamasz will move to either Seattle or San Francisco to wait for his new lungs. Sarah Kamasz, an elementary school teacher in Bend, will have to stay behind. "When he gets on the list and has to move, I have to stay and work because I'm the insurance carrier and the paycheck for now," Sarah Kamasz said. "When he gets the official page, I'll be on the first plane." The University of Washington asks that patients be able to reach the hospital within three hours of being called when a match comes up, said Kim Hoffman, lung transplant clinical nurse specialist. The average waiting time for lung transplant recipients was 140 days in 2003 at the Seattle facility, which is shorter than the national average of 18 months to two years. To make a match, physicians look at blood type and the height of both the patient and the lung donor, Hoffman said. Lungs are a very fragile organ and can not be transplanted if they have been damaged by illness or injury — meaning most lung donors are people who die from traumatic head injuries. "Lungs are so delicate," she said. "It's important to make sure they haven't been injured or their function compromised." According to the United Network for Organ Sharing Web site, 3,918 people are currently waiting for lung transplants nationwide and in 2004 only 901 lungs were harvested from deceased donors. After a transplant, about 80 percent of patients survive the first year and about 50 percent survive the next five years. For Matt and Sarah Kamasz, just the thought of him recovering is enough to make all the tests, the waiting and the expense worth the risks. "It's exhilarating looking toward the transplant," Sarah Kamasz said. "I want to be able to run through the park together."

Obituaries published October 30

Frank Arseneau of Bend died Thursday, October 28, 2004 of respiratory failure. He was 81. A visitation will be held at 11:00 a.m., Monday, Nov. 1, at the Deschutes Memorial Chapel in Bend. Mr. Arseneau was born May 9, 1923, in Menominee, Mich., to Alfred and Lillian (Boisvert) Arseneau. He married Irene Arseneau on May 10, 1948, in Portland. Mr. Arseneau served in the Air Force for 31 years. He served in World War II, the Berlin Airlift, the Korean Conflict and the Vietnam War. He retired in 1982. He was a member of the Home Owner's Association of Nottingham Square.Mr. Arseneau enjoyed photography, aircrafts, helping friends and neighbors, horses and reading. He is survived by his daughter, Barbara La Follette of Lancaster, Calif., two grandchildren and one great-grandchild. He was preceded in death by his wife. Memorial contributions may be made to the Pulmonary Fibrosis Foundation, 1332 N. Halsted St. Suite 201, Chicago, IL 60622

Basketball

MU assistant will meet with alumni

Trey Schwab, a special assistant basketball coach at Marquette University, will visit Green Bay on 
Oct. 26 to meet with MU alumni. Last February, Schwab had a double-lung transplant to combat 
idiopathic pulmonary fibrosis, a life-threatening lung disorder. Twelve days later, he went into 
cardiac arrest and had emergency surgery to remove a huge clot in his lungs. Three weeks after that, 
he left the hospital.

The lunch session will be at 11:45 a.m. at Titletown Brewing Co., 200 Dousman St.

To register, call Kristen Ramirez at (800) 344-7544 or e-mail her at kristen.ramirez@ marquette.edu

Many lively marchers in gray brigade

By Bard Lindeman
For the Poughkeepsie Journal

Monday, October 4, 2004 -- Question -- Excuse me, but don't all of us grow duller and blander as we age? Most old folks I know have little to say, and not much to contribute.

Answer -- Wrong. My viewpoint is that members of the Great Gray Legion form a handsome, variegated tapestry, an invaluable resource to a nation that, oddly, is inattentive or apathetic to this treasure. "Old people are certainly not bland," writes Thomas Gass in "Nobody's Home" (Cornell University Press, 2004). "Time imprints character in the wrinkles and folds of age-worn flesh. A beautiful person does not always wear beautiful skin. Often the opposite is true." Now, listen please to the voices of three disparate veteran citizens, each with a message worth recording:

- From small-town Haskell, Texas, Paul Clayton writes how he's got more time to read these days. Understand that Paul has been diagnosed with incurable pulmonary fibrosis. In summary, his lungs are so scarred by disease he cannot breathe. "I'm no martyr," he begins, adding, "The longest any of us live, after diagnosis, is two and a half years. This firstborn son of a Baptist preacher was sent home from an Abilene hospital last March, told that he was terminal. "You must immediately enroll in a Hospice program," a doctor directed. "There is nothing more we can do for you." How does invalid Clayton, tethered to an oxygen dispenser, spend his days? "I'm an advocate for my secret illness," he responds, beginning to recite the litany on pulmonary fibrosis (www. pulmonaryfibrosis.org), which some regard as a new anomaly. "I feel good in this role; it makes me productive, and so I must thank you, Mr. Columnist, for listening."

- Next up is George Sturman, of San Diego, Calif., who on Oct. 18 will achieve 90 years of age. He plans to celebrate "by ascending in a balloon." When gentleman George is not a high flyer, he's a down-to-earth guy. Indeed, he volunteers to regularly show up at the Sunrise Remington Club Retirement Home as a Professional Listener. "Got a gripe? Or an ache or an ill? Is someone bugging you? Well, tell it all to George," he says. The grateful long-term care home celebrated George for being a willing listener "with an open mind and heart." He was named Volunteer of the Year.

- Lastly, this acknowledgement to longtime correspondent Jane Poston, of Tucson, Ariz., who, following years of minding homes, plants, cats and dogs for traveling residents, moved into a retirement village. A conscientious and committed poet, journal writer and original thinker (she directed her male friend to live in her guest cottage out back; the concept worked so well, they later married!), Jane enclosed a poem. The last lines read: "When I become a writer one day, you'll know why/ It'll be because of you/ And, when people congratulate me, I'll say,/ Don't congratulate or thank me,/ Thank my inspiration."

Dare anyone hang a "bland" or "empty-headed" label on any of these three? I think not. Further, it says here that across this fractured nation there are many more equally keen and creative marchers among the Great Gray Legion. 

Write Bard Lindeman, c/o Poughkeepsie Journal, 5428 Oxbow Road, Stone Mountain, Ga. 30087-1228. Fax to Lindeman at 1-404-815-5787 or send e-mail to belindeman@earthlink.net.  

Gleevec for lung disease 7/18/2004 3:00 PM By: Ivanhoe Broadcast News According to the Pulmonary Fibrosis Foundation, more than 200,000 people in the United States suffer from pulmonary fibrosis. Pulmonary fibrosis is a progressive disease that involves scarring of the lung. Gradually, the air sacs of the lungs become replaced by fibrotic tissue. When scars form, the tissue becomes thicker -- causing an irreversible loss of the ability to transfer oxygen into the bloodstream. Symptoms of pulmonary fibrosis include shortness of breath, chronic cough, fatigue and weakness, discomfort in the chest, loss of appetite, and rapid weight loss. Typically, patients are diagnosed with pulmonary fibrosis between ages 40 and 70 years. About 40,000 patients with the disease die each year. There are currently no treatments that have proven to be effective for pulmonary fibrosis patients. Some medications that are used to treat patients with pulmonary fibrosis include corticosteroids such as prednisone, cyclophosphamide -- an anti-cancer drug, and a drug called azathioprine. Researchers from Tulane University in New Orleans are testing the cancer drug Gleevec on patients with idiopathic pulmonary fibrosis. Gleevec has received national attention for its success in treating leukemia, and doctors believe it may also benefit patients with pulmonary fibrosis. "Because fibrosis and cancer share some of the mechanisms of the development of the disease, we thought this [Gleevec] may be of some benefit for the patients who have fibrosis," Dr. Joseph Lasky, from Tulane University, said. Based on lab studies, Lasky said Gleevec should stop the scarring from progressing. "At best, we hope to stop the progression of the disease. We don't think that, at present, we're able to make the scars that are presently there go away. So, we're very much interested in getting patients who have the earlier symptoms of shortness of breath, so that we can, at any given time, point when they have more lung function still preserved," he said. Other than Tulane, the sites participating in the study include the Mayo Clinic in Rochester, Yale University, Loyola University in Chicago, University of Chicago, the INOVA Institute, Vanderbilt University, University of Miami, the Cleveland Clinic, University of Mexico in Mexico City, and the University of Southern California. For more information, contact: Fran Simon Public Relations Director Tulane University Health Sciences Center (504) 588-5221 or Chodie Gabor, R.N. (504) 585-6966

New Light Shed on Deadly Lung Disease

Study finds traveling cells contribute to pulmonary fibrosis

By Amanda Gardner
HealthDay Reporter  

TUESDAY, Aug. 3 (HealthDayNews) -- New research holds out hope for people suffering from pulmonary fibrosis, a deadly lung disease, by discovering that cells that travel to the organ to repair damage end up doing more harm than good. The study found these biological repairmen, which experts had thought originally resided in the lungs, were actually adult stem cells that migrated there from the patient's bone marrow -- and this migration can be halted.

The discovery may help people suffering from other conditions that, like pulmonary fibrosis, involve the excessive formation of scar tissue, experts said. As it stands now, however, the research is still in its infancy. "It's certainly very exciting research, but the information is obviously very preliminary," said Dr. Alfred Munzer, a lung specialist from Maryland and past president of the American Lung Association. "We have to see what meaning it holds."

Pulmonary fibrosis is a chronic and often fatal disorder that is characterized by extra scar tissue in the lungs. The disease, which affects some 80,000 individuals in the United States , has traditionally been treated with steroids and other immunosuppressive therapies, but with little effect. About 70 percent of people die within five years of diagnosis. "At the moment, there is no effective treatment for pulmonary disease, and it is not that uncommon a disease," Munzer said.

Scientists had believed the condition was caused by cells called fibroblasts and myofibroblasts that were already located in the lung. "The classical concept of repair is that you have cells within the local environment which can migrate into the site of the injury and which have the ability to contract the wound and increase the amount of material that repairs that wound like collagen," said study author Dr. Robert M. Strieter, chief of pulmonary and critical care medicine at the University of California at Los Angeles David Geffen School of Medicine.

Later on, scientists realized that cells in circulation in the bloodstream actually migrated to the injury to help repair it. The only problem was that the repairs themselves ended up being destructive. "The lung is an organ that likes to be filled with air, not scar tissue, so the lung doesn't function very well," Strieter said. Now Strieter and his colleagues, reporting in the Aug. 2 issue of the Journal of Clinical Investigation, have identified these traveling cells as adult stem cells from the bone marrow. In a mouse model, they have also managed to stop them from traveling to the lung where they contribute to the onset of the disease.

The researchers injected these human stem cells into an immunodeficient mouse and demonstrated that the cells traveled to the lungs when there was an injury. Next, they demonstrated that mouse cells did the same thing. "They could actually traffic and hone to the lung under conditions of injury and contribute to the fibrotic process," Strieter said. How did they make the lung their destination? A specific receptor on the cells interacted with a specific ligand (which binds to the receptor) to pull the cells towards the lungs. "It's a way to target these cells to a specific area," Strieter explained.

The next step was to use an antibody to target the ligand, thus blocking "recruitment" of the cells and also the development of fibrosis. While the technique holds promise for pulmonary fibrosis, it also holds hope for people suffering from connective-tissue diseases such as rheumatoid arthritis and liver cirrhosis. "These cells are not unique to the lung," Strieter said.

Although more research needs to be done, results may come sooner than expected, as there are already drugs that target this receptor-ligand pair. The particular receptor under investigation here (CXCR4) is also involved in HIV. Specifically, "HIV strains that target T-cells use this receptor as a co-receptor to infect T-cells," Strieter said. "The discovery of its association with AIDS has propelled the pharmaceutical field to make discoveries that may be useful not to treat AIDS, but to treat this."

More information

For more on pulmonary fibrosis, visit the Pulmonary Fibrosis Foundation (www.pulmonaryfibrosis.org ).  

About 200,000 are living with pulmonary fibrosis. "It's very difficult to diagnose, and very few pulmonary 
physicians have been knowledgeable enough to pick it up in the early stages," Dr. Rosenzweig said.

This story appeared on Page A1 of The Standard-Times on January 6, 2004.

Interferon a No Go for Pulmonary Fibrosis

By Amanda Gardner
HealthDay Reporter

WEDNESDAY, Jan. 7 (HealthDayNews) -- A once hopeful treatment for pulmonary fibrosis, a fatal disease of the lungs, appears to have little or no effect on progression of the disease or on quality of life, a new study has found. There remains some optimism, however, that the treatment, interferon gamma-1b, might benefit patients with mild to moderate symptoms of the disease. The authors of the study, which appears in the Jan. 8 issue of the New England Journal of Medicine, are launching a new trial to test this hypothesis.

The median survival time for patients diagnosed with pulmonary fibrosis is only two to three years. The disease results in a scarring of the lungs that eventually prevents the lungs from fulfilling their primary mission of delivering oxygen to the body. The only effective treatment is lung transplantation, although many people are treated with anti-inflammatory and immunosuppressive drugs, both of which have side effects. "There are some medicines which have anecdotally improved patients, [but] for the vast majority of patients this is a devastating illness," says Dr. Alvin S. Tierstein, a professor of medicine at Mount Sinai School of Medicine in New York City and author of an accompanying editorial in the journal.

"It just progresses and progresses, and nothing that we have helps," he adds. "A huge number of patients are on the transplant list waiting for lung transplants, which usually take about two years to come through, and most of the patients die on the list waiting." A study published in 1999 reported that nine patients treated with interferon gamma-1b and prednisolone did experience improvements. Those results essentially provided the impetus for the current study, which was funded by InterMune Pharmaceuticals Inc., maker of interferon gamma-1b. Dr. David Schwartz, one of the principal investigators on the new study and chairman of the pulmonary allergy and critical care division at Duke University Medical Center , has been a paid consultant for InterMune since 2000.

Scientists thought interferon might have an effect by decreasing the production of collagen, which is a key component of the scarring, Schwartz says. "The concept was that interferon gamma would down regulate the disease-causing factors that perpetuate this process in the lungs," he explains. Schwartz and his colleagues randomly assigned 330 patients with idiopathic pulmonary fibrosis -- whose cause is unknown -- to receive either interferon gamma treatment or a placebo. The participants were located at medical centers in the United States , Europe and South Africa . Treatment was administered three times a week for just over a year.

The interferon treatment did not slow the progression of the disease, nor did it have a significant effect on lung function or quality of life. "There was no change at all. So in those terms this is a negative study and it has to be represented that way," Tierstein says. "I don't think we should fool anybody and say this medicine makes you better." Still, there are some potential silver linings in this cloud. For one thing, over the course of the study, only 10 percent of the patients in the interferon gamma group died, compared to 17 percent in the placebo group.

"It is conceivable that interferon is affecting other things," Tierstein says. "We know that interferon is important in the control of infections and it may be that we're preventing infections from carrying these patients off." Also, patients with milder symptoms lived longer when receiving interferon gamma than similar patients in the placebo group. Among participants with mild pulmonary fibrosis, 3.5 percent receiving the drug treatment died versus 12.5 percent in the placebo group.

"It may be, since all the medicines we have are toxic, we tend not to treat until we have no choice and pulmonary function is really bad," Tierstein says. "Maybe we're waiting too long. Maybe we should treat earlier." Adds Schwartz: "There is some hope that it [interferon gamma] still will work. In fact, we're in the process of launching a major study to look at the effect of this drug in individuals with mild to moderate disease. If anything, it looks like we focused on everyone with pulmonary fibrosis when we should have focused on those with mild to moderate disease."

That study, which will follow participants for up to four years, will be looking primarily at survival rates.

More information

For more on this disease, visit the Pulmonary Fibrosis Foundation

(SOURCES: David Schwartz, M.D., professor, medicine and genetics, and chairman, pulmonary allergy and critical care division, Duke University Medical Center, Durham, N.C.; Alvin S. Tierstein, M.D., professor, medicine, Mount Sinai School of Medicine, New York City; Jan. 8, 2004, New England Journal of Medicine)  

  GREENVILLE , MAINE - A Farmington teenager who suffers from lung disease plans to swim 32.4 miles of Moosehead Lake on Sunday to raise funds for research of a lung disease that took the life of his grandfather.Although Joseph Fowler, 17, has never seen Moosehead Lake , he plans to take his plunge into the cold water at Seboomook and end in Greenville Junction.

Fowler, who has asthma, hopes to raise more than $1,000 for the Pulmonary Fibrosis Foundation in memory of his grandfather, the late Vincent L. Oliver. Oliver died of the lung disease in June 2002. Fowler's effort is being hailed by the Pulmonary Fibrosis
Foundation. "Joseph Fowler is an outstanding young man and a great role model for the young people of this country," Michael Rosenzweig, foundation executive, said this week.

Pulmonary fibrosis affects 200,000 people in the United States , including Jerry Lewis, and more than 40,000 die from it annually,
said Rosenzweig, who also has the disease. At this time there are no effective treatments for the illness.

Knowing that prompted Fowler to take action.

"I'm very enthusiastic about doing this Moosehead swim, Fowler said this week. The honor student, who has been a competitive swimmer since seventh grade, said he selected Moosehead because it is the largest lake in the state and because its conditions are the
fiercest. "I wanted to set a goal that was seemingly unrealistic -one that was far beyond what others expect me to complete," Fowler said. The swim will be a physical test for his mind as well as his body. He believes the worst problems he will encounter will not be the cold, but perhaps the harsh winds and mental fatigue. "I'm more worried about losing things to think about while I swim. If I start to think about what I'm doing ... I 'm done for."

To prepare for the roughly 15-hour trip, Fowler has been increasing his swim distances. He swims a regular 5-mile loop around Clearwater Lake in Industry, and on Fridays the busy teenager swims longer. Three weeks ago, he made two laps around the 5-mile loop and two weeks ago, he swam 15 miles from Madison to Skowhegan down the Kennebec River under the guidance of his coach, Craig Taylor. In the interim, the Mt. Blue High School senior teaches swim lessons part time at the University of Maine at Farmington Health and Fitness Center , and works full time during the summer as a lifeguard at Mount Blue State Park in Weld. Fowler has prepared his body for the swim by eating as many carbohydrates as possible. Pasta, potatoes, breads and rice have been his staples, as well has plenty of fluids. While swimming Moosehead Lake , he will be provided an electrolyte drink every 15
minutes. "This keeps me going strong and with 70 calories a cup, [it] provides plenty of calories to keep my body fueled to swim," he said.

Abiding by marathon swimmers' rules, Fowler does not plan to wear any sort of a wet suit or dive suit, but he does plan to wear a swim cap and earplugs to help prevent hypothermia. Following the teenager's journey in a pontoon boat will be his parents, Fenwick and Fran Fowler; his 15-year-old sister, Mattie; Taylor; and Dan Delucca, who swam the entire distance of Moosehead
Lake several years ago.

Anyone wishing to help Fowler meet his fund-raising goal should send contributions to the Pulmonary Fibrosis Foundation, 1332 N. Halsted St. Suite 201, Chicago, IL 60622

UPDATE...........

Greenville - Joseph Fowler, 17, became the second swimmer on record to cross New England 's largest lake, and the fastest by more than five hours. It took him 16 hours, 46 minutes to cross Moosehead Lake . He swam as a fundraiser for pulmonary fibrosis, which took the life of his grandfather last year.