Lung Disease in WV

Ozone pollution amplifies risk of fatal respiratory illnesses

2009-03-12T10:21:00.001-04:00

By Liz Szabo, USA TODAY

For the first time, a large study shows the deadly effects of chronic exposure to ozone, one of the most widespread pollutants in the world and a key component of smog, according to a study in today's New England Journal of Medicine.
Doctors have long known that ground-level ozone — which is formed when sunlight interacts with pollution from tailpipes and coal-burning power plants — can make asthma worse. This study, which followed nearly 450,000 Americans in 96 metropolitan areas for two decades, also shows that ozone increases deaths from respiratory diseases.

HIGHEST LEVELS: Cities' ozone rankings

This ground-level ozone has very different effects than the ozone layer high above the Earth, which helps filter out harmful ultraviolet radiation, says lead author Michael Jerrett, an associate professor of environmental health sciences at the University of California-Berkeley.

Although Jerrett found there was no safe level of ground-level ozone, some cities fare worse than others. People in Riverside, Calif., the highest ozone city, were 32% more likely to die in a given year of respiratory diseases compared with people in San Francisco, the city with lowest average annual ozone concentrations.

Ozone pollution likely translates into thousands of additional deaths every year across the USA, Jerrett says. About 240,000 Americans a year die of respiratory illnesses.

Controlling ozone — one of the main greenhouse gases involved in global warming — may both save lives and also fight global climate change, Jerrett says.

The study shows yet another way that air pollution can harm public health, says Janice Nolen, assistant vice president of national policy and advocacy for the American Lung Association.

"It doesn't have to be a peak ozone day to be a problem," says Nolen, who wasn't involved with the new study. "If you're breathing it day in and day out over a longer period of time, the risk of premature death increases."

The study also suggests the Environmental Protection Agency may need to reconsider its safety standard for ozone, Nolen says. Instead of just looking at the effect of being exposed to peak ozone levels, the agency may need to look at long-term exposure to lower levels of the gas.

Last year, the EPA changed its air quality standards for ground-level ozone from an average of 84 parts per billion to 75 parts per billion over an eight-hour period, although the agency's scientific advisers had urged an even tougher standard of 60 to 70 parts per billion.

One in three Americans lives in a city that's in violation of the EPA's current ozone standard, Jerrett says.

President Obama's new EPA chief, Lisa Jackson, told USA TODAY last month that the agency should reconsider the ozone standard. "We need to go back to the basics here: science and the law," she said.

Contributing: Traci Watson

Body's Defenses May Worsen Chronic Lung Diseases In Smokers

2009-02-18T13:37:00.000-05:00

ScienceDaily (Feb. 18, 2009) — Although the immune system is designed to protect the body from harm, it may actually worsen one of the most difficult-to-treat respiratory diseases: chronic obstructive pulmonary disorder (COPD), according to new University of Cincinnati (UC) research.

In a preclinical research study, UC environmental health scientists have identified a link between cigarette smoke and activation of a specific cellular receptor (NKG2D) critical to immune system activation. They say the finding is key to understanding COPD disease progression and developing future interventional drug therapies.

“People have historically believed that if you smoke, you suppress the immune system. We’ve shown that you actually activate certain parts of the immune system and it could potentially work against you,” explains Michael Borchers, PhD, lead investigator of the study and UC assistant professor of environmental health.

Borchers and his team report their findings in the March 2009 issue of the Journal of Clinical Investigation. The study appears online ahead of print Feb. 9, 2009. It is the first study to report data defining a link between the immune system and COPD disease progression and severity.

COPD is a progressive pulmonary disease believed to be caused by long-term cigarette smoking. The irreversible and incurable condition is characterized by emphysema and severe inflammation of the lung tissue.

Previous research had suggested that immune cells (lymphocytes) contributed to chronic inflammation, a key indicator of COPD; however, it was unclear whether this caused extensive cellular damage.

For this study, Borchers’ team developed a transgenic mouse model to further examine how the immune system responds to chronic inflammation indicative of COPD. His team hypothesized that when tissue was damaged, the cells would send signals to the immune system indicating they are transformed—similar to cancer or virally infected cells—and must be destroyed.

Scientists examined molecular signaling pathways in lung tissue exposed to cigarette smoke and found a strong correlation between cellular stress signals, activation of the immune system and development of COPD-like disease.

This method was repeated and cross-referenced in tissue samples from a human cohort that included non-smokers, smokers with COPD and smokers who did not develop COPD. In patients who had never smoked, there was a complete absence of the NKG2D signal. Current and former smokers who developed the disease expressed signals that correlated with severe COPD disease.

By combining both sets of data, they determined that cigarette smoke set off a molecular chain of events resulting in activation of a specific receptor—NKG2D—in lung cells, causing the immune system to attack stressed (damaged) lung tissue.

“Our study is evidence that when the lungs are exposed to chronic damage from cigarette smoke, at some point that damage exceeds the body’s natural ability to repair tissue and can start to contribute to COPD instead of protecting against it,” Borchers says.

Borchers intends to expand this research using other genetically altered mouse models to explore the relationship between the NKG2D receptor and other immune pathways involved in of alterations in the immune system of COPD patients.

Funding for the multi-institutional study comes from the National Institute of Environmental Health Sciences. UC thoracic surgeons Michael Reed, MD, and Sandra Starnes, MD, and investigators at the Institut Municipal d’Investigació Mèdica in Barcelona, Spain, provided tissue samples for the study.

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Adapted from materials provided by University of Cincinnati.

COPD raises risk of depression: study

2009-01-31T21:22:00.001-05:00

By Megan Rauscher

NEW YORK (Reuters Health) - Patients with the chronic breathing disorder COPD appear to have a significantly higher risk of becoming clinically depressed than healthy individuals and patients with another common chronic condition - diabetes.

"The relationship between depression and COPD was described before, but what this study adds is that we found a temporal relationship. In other words, COPD did lead to a higher risk for a diagnosis of depression," said Lisette van den Bemt from Radboud University Nijmegen Medical Center, The Netherlands.

"It seems that the increased risk of depression is not the result from having a chronic disease in general but is specific for COPD," she and her colleagues note in the current issue of the medical journal Chest.

COPD, or chronic obstructive pulmonary disease, is a progressive disease that makes it hard to breathe. COPD can cause coughing that produces large amounts of mucus, wheezing, shortness of breath, chest tightness, and other symptoms. Cigarette smoking is the leading cause of COPD.

In their study, van den Bemt's team compared the risk of an initial diagnosis of depression in 999 patients with COPD, 978 with diabetes, and 2494 matched control subjects without chronic health conditions.

In total, 5.5 percent of the overall population of patients with COPD or diabetes could not be included in the study because of an existing history of depression.

According to the investigators, the risk of a first diagnosis of depression was significantly higher in the COPD patients than in the control patients.

Co-existing illness, they note, "is a well-established phenomenon that was found in 85 percent of the patients with COPD in this study but did not result in higher risk for depression in patients with COPD compared to healthy control subjects and diabetes mellitus patients."

"Patients with COPD have a higher probability of a first episode of depression at any time...compared to patients with diabetes mellitus and control subjects," the researchers note.

Doctors, van den Bemt told Reuters Health, need to be aware of the higher risk of depression in patients with COPD. "Especially since there are treatment options for depression, and reduced mood and emotional functioning can enhance dyspnea (difficulty breathing) -- one of the key symptoms of COPD," she said.

SOURCE: Chest, January 2009.

Drug Shields Mice From Emphysema

2009-01-08T19:40:00.000-05:00

Drug Shields Mice From Emphysema

By Steven Reinberg
HealthDay Reporter
Monday, December 22, 2008; 12:00 AM

MONDAY, Dec. 22 (HealthDay News) -- In experiments in mice, scientists have shown that a new drug may protect the animals from the respiratory damage caused by cigarettes.

The finding holds out hope for patients with chronic obstructive pulmonary disease (COPD) -- a chronic progressive lung disease involving both emphysema and chronic obstructive bronchitis.

COPD, most commonly linked to smoking, is the fourth leading cause of death in the United States and there are no effective treatments.

"Our previous studies have shown that there is a defect in Nrf2 -- a master regulator of antioxidant and detoxifying pathways -- in the lungs of COPD patients that may be involved in the severity of this disease," explained lead researcher Shyam Biswal, an associate professor at the Johns Hopkins Bloomberg School of Public Health in Baltimore.

In this study, the researchers used a novel drug molecule called CDDO-imidazole (CDDO-Im) to curb the progression of the disease by targeting the Nrf2 pathway.

"The result demonstrates that this strategy is effective in the preclinical model of emphysema," Biswal said.

The report is published in this week's online edition of the Proceedings of the National Academy of Sciences.

For the study, Biswal's team exposed mice to cigarette smoke for six months. Half the mice were treated with CDDO-Im while the other animals were not.

The researchers found that mice treated with CDDO-Im did not develop heart and lung damage while their untreated counterparts did.

Dr. Norman Edelman, chief medical officer of the American Lung Association, believes the new approach to treating COPD could be effective.

"There have been several studies identifying disrupted oxidant defense systems in COPD," Edelman said. "What's different about this one is that a control point for a whole group of oxidant defenses has been identified in rather elegant studies. Thus, if a therapy up-regulating this site were developed it would be more likely to be effective in COPD," he said.

This study provides hope that strategies aimed at targeting the Nrf2 pathway might be effective in inhibiting the development of emphysema, Biswal said.

"Future studies will be done in COPD patients to test the strategy of targeting Nrf2, to test the efficacy in reducing the burden of this debilitating disease," Biswal said.

However, Dr. Bartolome R. Celli, chief of pulmonary care at St. Elizabeth's Medical Center in Boston, said the jury is still out on the effectiveness of this approach.

"It is an interesting and intriguing study," Celli said. "However, from the experiments in mice to reality in humans there usually is a great distance," he said.

There is consensus that oxidative stress associated with cigarette smoking is important in COPD, so balancing oxidative stress with antioxidants makes sense, Celli said.

"This study takes it one step further by testing the hypothesis in vivo [animals]," according to Celli. "Let's wait for the translation into humans," he said.

For more information on emphysema, visit the U.S. National Library of Medicine .

World COPD Day in Canada

2008-11-19T19:51:00.003-05:00

WV has highest COPD death rate in the nation

2008-10-06T20:17:00.002-04:00

Link: http://www.mountainmessenger.com

Lisa Richardson can tell you how important it is to understand COPD (Chronic Obstructive Pulmonary Disease)—she has it. This former three-pack a day smoker, who hasn’t smoked since Apr. 14 of this year, still battles for breath. “I was at least three packs a day and thought nothing of it. Now that’s an addiction.”

COPD is a combination of chronic lung diseases that obstruct breathing, including emphysema, pneumonia and bronchitis. Approximately 90 percent of all cases of COPD are caused by long-term smoking. COPD often goes untreated or even undiagnosed.

West Virginia ranks first in the nation for deaths caused by COPD, and the number in the US is rising according to West Virginia University’s Center for Respiratory Biology and Lung Disease.

About five years ago, Richardson was told that she had chronic bronchitis, but she was given no management or treatment information. She wasn’t told that she had COPD until this year.

“COPD is misleading to people like me, because it’s a new phrase. Emphysema I know, and I know that it’s bad. But COPD? It’s a new fancy name for why I can’t breathe. I don’t think people put the two together. It’s the same thing.”

When asked how she felt about having COPD, she simply said “I’m scared to death.”

She says that she does feel better now that she doesn’t smoke anymore, but she still has trouble with shortness of breath. “I waited too long to quit smoking.”

When asked what she would say to anyone just diagnosed with COPD, her answer is quick and to-the-point. “Quit smoking.”

“COPD will never go away. You are not indestructible. You can quit smoking. You will recover in some ways. You will get better. But you will never, ever be the same as you were as a nonsmoker. Don’t kid yourself.” She admits that quitting was hard, but says that it’s not impossible. “If I can quit, anybody can quit. Trust me.”

“It’s not the nicotine withdraw that was so hard. That was gone in a short amount of time, and you can control that with the gum or patches. The problem is the habit. That’s what’s hard to break. You got to have the habit. If you can redirect your energy, that’s what’s hard to break.“

Lisa completed the Freedom From Smoking program—an eight session smoking cessation program—at Saint Francis Hospital.
“If it had not been for the class, I wouldn’t have been able to do it.”

“We need the community to understand the importance and prevalence of this disease in our state,” says Kelli Caseman , Program Manager, American Lung Association of West Virginia.

For more information contact Kelli Caseman at (304) 342-6600 or e-mail kcaseman@lunginfo.org.

American Lung Association to Host Respiratory Rally

2008-09-29T11:30:00.003-04:00

Bev Davis
Register-Herald Senior Editor

Anyone with chronic obstructive pulmonary disease, more commonly referred to as COPD, or their family members might be interested in the state’s first Respiratory Rally to be held from 9 a.m. to 4 p.m. Sept. 6 at the Charleston Civic Center. The event is sponsored by the American Lung Association.

“If you’re like me and you have COPD, you know that sometimes it’s hard to find a good doctor, useful information, adequate resources, etc.,” said Steve James, who’s helping coordinate the event. “If you’re a health care professional who treats folks like me with COPD, you know that there’s a definite lack of information, up-to-date programming and community resources available to patients.”

Two national keynote speakers will provide some of the latest information available about COPD.

Keynote speaker Steven D. Nathan, M.D., is the director of the advanced lung disease program and the medical director of the lung transplant program at Inova Fairfax Hospital in Falls Church, Va. He is also an affiliate professor of biomedical sciences at George Mason University.

The second speaker, Len Geiger, was diagnosed as Alpha-1 (Alpha-1 antitrypsin deficiency) lung affected in 1994 and has been involved in the Alpha-1 community ever since. He received a life-saving double lung transplant in 2002. Since then, he has been featured in Runner’s World magazine and Sports Illustrated as well as a number of other newspaper articles and publications.

Having been a guest or subject of documentaries on CNN, the “Today” show, Discovery Health Channel, HBO’s “Real Sports with Bryant Gumbel” and most recently ABC's “World News Tonight with Charles Gibson,” Geiger continues to raise awareness for Alpha-1 and the importance of early detection.

As director of Alpha-1 Patient Advocacy for Centric Health Resources, the distributor of Prolastin, Geiger maintains his commitment to raising awareness of Alpha-1 and serves as a resource for medical professionals, newly diagnosed patients and their families.

For those living with COPD, attendance is free. Lunch will be provided, and those with COPD can bring two friends or family members to assist them.

There will be free oxygen refills for those who need them. There will be door prizes awarded throughout the day that will benefit those coping with lung disease.

Information will be provided about a genetic cause of COPD, James said. “Up to 3 percent of those with COPD — me being one of them — have a genetic disorder called Alpha-1 as an underlying cause.” Free Alpha-1 testing will be available at the rally.

“A lot of people who have COPD are smokers, but there are a lot of us who got it genetically and we’re trying to get the word out about that,” James said.

COPD, also referred to as emphysema and bronchitis, is the fourth-leading cause of death in the United States, killing more than 120,000 Americans each year, James said.

“In West Virginia, COPD is the third most common cause of death. In fact, according to WVU’s Center for Respiratory Biology and Lung Disease, our state ranks first in the nation for rates of death due to COPD.”

James said he expects the rally to beneficial for anyone with the disease or those who have a loved one affected by COPD.

“If you have COPD, if you know someone who does, of if you are a health care professional who wants to see your patients learn better management skills and could use both information and inspiration to live with their disease, I strongly encourage you to attend. After all, it’s free and I think you will enjoy the day,” James said.

For more information or to register, call toll-free at 1-800-586-4872 or 304-342-6600.

COPD? Eat Your Veggies

2008-09-28T14:31:00.001-04:00

ScienceDaily (Sep. 18, 2008) — You know it's good for you in other ways, but could eating your broccoli also help patients with chronic lung disease? It just might.

According to recent research from Johns Hopkins Medical School, a decrease in lung concentrations of NRF2-dependent antioxidants, key components of the lung's defense system against inflammatory injury, is linked to the severity of chronic obstructive pulmonary disease (COPD) in smokers. Broccoli is known to contain a compound that prevents the degradation of NFRP.

COPD is the fourth-leading cause of death in the U.S. and affects more than 16 million Americans.

In this study, researchers examined tissue samples from the lungs of smokers with and without COPD to determine if there were differences in measured levels of NRF2 expression and the level of its biochemical regulators, including KEAP1, which inhibits NRF2, and DJ-1, which stabilizes it. Dr. Biswal had previously shown that disruption in NRF2 expression in mice exposed to cigarette smoke caused early onset of severe emphysema.

When compared to non-COPD lungs, the lungs of patients with COPD showed markedly decreased levels of NRF2-dependent antioxidants, increased oxidative stress markers, a significant decrease in NRF2 protein with no change in NRF2 mRNA levels (indicating that it was expressed, but subsequently degraded), and similar KEAP1 levels, but a marked decrease in the level of DJ-1.

"NRF2-dependent antioxidants and DJ-1 expression was negatively associated with severity of COPD," wrote principle investigator, Shyam Biswal, Ph.D., an associate professor in the Bloomberg School's Department of Environmental Health Sciences and Division of Pulmonary and Critical Care at the Johns Hopkins School of Medicine. "Therapy directed toward enhancing NRF2-regulated antioxidants may be a novel strategy for attenuating the effects of oxidative stress in the pathogenesis of COPD."

While clinical trials to date of antioxidants have been disappointing in improving the clinical course of patients with COPD, this study points to a possibility of benefit from restoring NRF2 levels in damaged lungs by reducing the action of KEAP1, which is an inhibitor of NRF2. "[I]ncreasing NRF2 may also restore important detoxifying enzymes to counteract other effects of tobacco smoke," wrote Peter Barnes, D.M., of the National Heart and Lung Institute in London, in the accompanying editorial. "This has been achieved in vitro and in vivo by isothiocynate compounds, such as sulforaphane, which occurs naturally in broccoli and [wasabi]."

Sulforapane has been shown to be able to restore antioxidant gene expression in human epithelial tissue in which DJ-1 has been reduced. Isothicyanate compounds such as that found in broccoli inhibit KEAP1, and thus prevent it from degrading NRF2, according to Dr. Barnes.

"Future studies should target NRF2 as a novel strategy to increase antioxidant protection in the lungs and test its ability to decrease exacerbations and improve lung function in patients with COPD," concluded Dr. Biswal.

John Heffner, MD, past president of the ATS, commented that "mounting evidence over several decades underscores the importance of oxidant-mediated damage for the development of COPD in addition to other lung diseases. This study adds greater precision to our understanding of the specific antioxidants that may protect the lung against emphysema to allow clinical trials based on valid pathophysiologic principles."

The findings were published in the second issue for September of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

Link: http://www.sciencedaily.com/releases/2008/09/080912075156.htm

COPD Medicines: Risky or Safe?

2008-09-28T14:11:00.009-04:00

Study Links 2 COPD Drugs to Risks of Heart Attack, Stroke, Death
By Kathleen Doheny

WebMD Health NewsReviewed by Louise Chang, MDSept. 23, 2008 -- Two commonly used treatments for the lung disease known as chronic obstructive pulmonary disease (COPD) boost the risk of heart attack, stroke, or death from cardiovascular causes, according to a new analysis. But the drugs' marketers sharply disagree.

The medicines under scrutiny are called inhaled anticholinergics, which work by relaxing the muscles around constricted airways and relieving symptoms such as shortness of breath.

The use of two commonly prescribed anticholinergics, Spiriva and Atrovent, for more than a month boosted the risk of heart attack, stroke, or dying of cardiovascular problems by 58%, says Sonal Singh, MD, MPH, assistant professor of internal medicine at Wake Forest University School of Medicine in Winston-Salem, N.C., and lead author of the study, which appears in The Journal of the American Medical Association.

Singh and colleagues pooled the results of 17 randomized trials that included nearly 15,000 patients who took the anticholinergics or a control treatment. "Every study points in the same direction," he tells WebMD.

Meanwhile, pharmaceutical industry spokespeople issued a statement strongly disagreeing with the conclusions of the study, issuing their own new analysis that they say confirms the safety of Spiriva.

COPD Medicines: Study Details
Singh and his colleagues looked at the 17 trials to see if the medicines increased the risk of heart attack, stroke, and death from cardiovascular disease or death from other causes.

They found that the COPD medicines increased risk of death from cardiovascular disease as well as the risk of stroke or heart attack when the three outcomes were grouped together, but the drugs did not significantly increase the risk of death from all causes.

While 1.2% of control patients had a heart attack, stroke, or died from cardiovascular disease during the follow-up (which ranged from six weeks to five years), 1.8% of those on the anticholinergics did. That accounts for the 58% increase.

When Singh looked at the individual outcomes, rather than as a group, the increased risk for stroke didn't turn out to be significant, but the risk for heart attack and death from cardiovascular disease remained so.

The latest research isn't the first to uncover the risk. Atrovent was linked with a 34% increased risk of cardiovascular death by other researchers, who published their findings in the Annals of Internal Medicine last week.

LINK: http://www.webmd.com/news/20080923/copd-medicines-risky-safe

New Guidelines for COPD

2008-09-15T16:50:00.002-04:00

American College Of Physicians Issues New COPD Guidelines - video powered by Metacafe