Smoking and Respiratory Diseases

Tomatoes may restore lung damage caused by smoking

Smoking and Respiratory Diseases | Johns Hopkins Medicine

From cutting skin cancer risk in half to supporting the immune system, a diet rich in tomatoes and fruits imparts many health benefits. Now, researchers have found that these foods may restore lung function in ex-smokers and slow lung function decline in all adults.

Share on PinterestA tomato-rich diet may slow smoking- and age-related lung function decline.

The Johns Hopkins Bloomberg School of Public Health in Baltimore, MD, conducted the study. The findings were published in the European Respiratory Journal.

Around 36.5 million adults in the United States smoke cigarettes, according to the Centers for Disease Control and Prevention (CDC), and the practice causes more than 480,000 deaths per year.

Every year, around 55.4 percent of all adult smokers attempt to quit smoking. Smoking cessation dramatically reduces the risk of disease, including lung diseases such as chronic obstructive pulmonary disease (COPD) and lung cancer, as well as early death.

Lung health after stopping smoking has been a topic that has garnered interest among ex-smokers and health professionals a.

The lungs begin to heal as soon as smoking is ceased. While the response is quick to start, lung improvement is incremental and can take many years. Furthermore, quitting smoking alone does not entirely erase the risk of developing a smoking-related lung disease.

Another factor to consider is that the lungs are fully mature by 20–25 years of age. After 35 years old, lung function begins to decline, and breathing becomes gradually more difficult.

In a nutshell: the diaphragm weakens, which decreases the ability to breathe in and out; muscles that keep airways open lose elasticity; alveoli lose their shape; and the area of the brain that regulates breathing sends weaker signals to the lungs.

Previous research published by The BMJ has demonstrated that a diet rich in fruits and vegetables may reduce the risk of COPD in current and former smokers. In fact, each extra daily serving was linked to a 4–8 percent lower risk.

The new study goes one step further to suggest that consuming a diet high in fruits and vegetables — particularly tomatoes and apples — slows down the decline in lung function among ex-smokers over the duration of 10 years.

Compared with adults who consumed fewer than one serving of fruit or one tomato per day, those who ate more than three portions of fruit or more than two tomatoes experienced slower lung function decline.

The scientists asked questions about other dietary and processed sources of fruits and vegetables, such as tomato sauce, but the protective effect was only apparent among those who ate fresh fruits and vegetables.

This finding suggests that there may be particular components in fresh tomatoes and apples that help to repair the lung damage that results from smoking.

What is more, a slower deterioration in lung function was observed in all adults in the study who ate a tomato-rich diet — including those who had never smoked.

“This study,” says lead study author Vanessa Garcia-Larsen, who works as an assistant professor in the Bloomberg School’s Department of International Health, “shows that diet might help repair lung damage in people who have stopped smoking. It also suggests that a diet rich in fruits can slow down the lung’s natural aging process even if you have never smoked.”

“The findings,” she adds, “support the need for dietary recommendations, especially for people at risk of developing respiratory diseases such as COPD.”

Garcia-Larsen and her team evaluated diet and performed lung function tests, including spirometry, among more than 650 adults from Germany, Norway, and the United Kingdom in 2002 and again 10 years later.

The connection between diet and lung function was most pronounced among ex-smokers. When the volume of air they could inhale was measured, former smokers who consumed a tomato- and fruit-rich diet had around 80 milliliter slower decline in lung function over 10 years. This indicates that specific nutrients could be playing a role in healing the damage caused by smoking.

“Our study suggests that eating more fruits on a regular basis can help attenuate the decline as people age, and might even help repair damage caused by smoking. Diet could become one way of combating rising diagnosis of COPD around the world.”

Vanessa Garcia-Larsen

The study controlled for factors such as age, sex, height, body mass index (BMI), total energy intake, and physical activity to ensure that the results were not skewed.

Source: https://www.medicalnewstoday.com/articles/320434

Exposure to Ozone Pollution or Wood Smoke Worsens Lung Health of Smokers and Former Smokers

Smoking and Respiratory Diseases | Johns Hopkins Medicine

Newswise — Over many years, exposure to the levels of ozone and other forms of pollution found in most U.S. cities and some rural communities can take a toll on a person’s health. Two studies led by Johns Hopkins researchers describe the impact of pollution on lung disease, particularly chronic obstructive pulmonary disease (COPD), in the U.S.

In one study, published Dec. 9 in JAMA Internal Medicine, Johns Hopkins researchers found that, among other effects, long-term ozone exposure increases the risk of lung disease — and the severity of that disease — among both former and current smokers. In another study, published Oct.

23 in American Journal of Respiratory and Critical Care Medicine, Johns Hopkins researchers also found that increased neighborhood use of wood as a primary heating source — which releases fine particles into the air — is associated with higher prevalence of lung disease among never-smokers in the community.

“Even if you spend very little time outside, the cumulative effect of pollution over many years seems adequate to have a negative impact on respiratory health,” says Nadia Hansel, M.D., M.P.H., director of the pulmonary and critical care division, professor of medicine and associate dean for research at the Johns Hopkins University School of Medicine and author of both studies.

Ground-level, or tropospheric, ozone is formed when industrial pollutants interact with sunlight, and it is the main ingredient in the smog found around major cities. Ozone is known to irritate the lungs by increasing inflammation, and spikes of very high ozone levels — such as those that occur on hot, sunny days with heavy traffic — can exacerbate lung diseases such as asthma.

Former and current smokers are at high risk of chronic lung diseases and are particularly susceptible to environmental triggers for lung disease flare-ups. Smokers are particularly prone to COPD, a group of diseases including emphysema and chronic bronchitis, characterized by chronic and progressive lung inflammation that leads to shortness of breath and coughing.

In the new JAMA Internal Medicine study, Hansel and her collaborators around the country used data collected from people in several U.S. cities as part of the SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) air pollution study. Participants in SPIROMICS were former and current smokers ages 40–80.

The new analysis included a subset of SPIROMICS participants for whom there was available data on the previous 10 years of ozone exposure — where people lived.

These 1,874 participants were 54% male, 79% white, 37% current smokers and had smoked an average of 50 pack-years — the equivalent of 25 cigarettes a day for two years, or five cigarettes a day for 10 years.

After adjusting for demographic and socioeconomic factors as well as smoking status and pack-years, the researchers found that people who had been exposed to higher levels of ozone over the previous 10 years were more ly to have COPD.

For every 5-parts-per-billion increase in a person’s 10-year ozone exposure, they were 16% more ly to have COPD and 37% more ly to have had a severe exacerbation of the disease in the year prior to study enrollment.

The same 5-parts-per-billion increase in ozone exposure was also associated with an increase in the percentage of people with emphysema and a worsening score of the St. George’s Respiratory Questionnaire, which reflects health impairment affecting quality of life.

“What really stood out was that the effect was apparent even among current heavy smokers,” says Hansel. “This means that active smoking doesn’t outweigh this effect of ozone.”

In other words, even people already at the highest risk of COPD had an increased risk with ozone exposure.

Moreover, Hansel says, the effect of increasing ozone was apparent even when ozone exposure was at the low end of the spectrum, such as among people living in northeastern cities where dark winters lead to an annual ozone exposure that’s relatively low compared with that of many southwestern locales. 

“I think this adds to increasing evidence that there is probably no healthy level of ozone,” she says. “There are policies that suggest we just need to reach certain targets and everything will be OK, but in my mind that is probably not enough.” Policymakers must develop ways to get ozone as low as possible, she adds, rather than aiming for a particular target number. 

The Centers for Disease Control and Prevention reports that COPD costs the U.S.

health care system more than $32 billion, and that there are approximately 7 million COPD-related emergency room visits in the U.S. each year.

Hansel and her colleagues calculated that a 5-parts-per-billion decrease in 10-year ozone levels could reduce emergency room visits by 27%, saving a substantial amount of money on COPD care.

While the JAMA Internal Medicine study only measured lung health, previous research has suggested that high levels of ozone can affect cardiovascular health. So Hansel hypothesizes that long-term exposure to ambient levels of ozone may have similar effects on heart disease as it does to lung disease.

“The adverse health effects of ozone ly go beyond what we’ve identified here,” says Hansel. “And we need to keep building evidence of these effects so that it’s not debatable anymore that we need to do more to clean the air.”

In the second paper, researchers including Hansel, associate professor of medicine Meredith McCormack, M.D., M.H.S., and pulmonary and critical care medicine fellow Sarath Raju, M.D.

, studied data on 8,500 adults enrolled in the National Health and Nutrition Examination Surveys (NHANES), 2007–2012. Of the participants, 19.5% resided in rural areas and 29.6% in urban areas. Rural areas, with a 12.

0% prevalence of COPD, had more than double the disease burden seen in urban communities, with a 5.9% prevalence.

By analyzing differences between urban and rural communities that might affect COPD risk, the team discovered that communities with a high rate of solid fuel use — either coal or wood for primary heating — were associated with COPD prevalence.

A 1% increase in the number of homes using wood as the primary heating source was linked to 12% higher odds of COPD among people who have never smoked. In rural areas, 4.1% of people used wood as their primary heating source, as opposed to 0.

6% in urban areas.

“Wood smoke is a household source of pollution that is associated with high levels of particulate matter and toxic gases,” says Raju, first author of the American Journal of Respiratory and Critical Care Medicine paper. “We hope that this paper raises awareness of the growing epidemic of rural COPD.”

The researchers are now launching further studies that aim to collect individual level — rather than community level — data on environmental exposures that might contribute to COPD. They’re also partnering with other institutions to study COPD rates and risks in rural Appalachia.

Other authors on the JAMA Internal Medicine paper were Han Woo, Roger Peng, Ashraf Fawzy, Nirupama Putcha and Patrick Breysse of Johns Hopkins; Laura Paulin of Dartmouth-Hitchcock Medical Center; Amanda Gassett, Kipruto Kirwa and Joel Kaufman of University of Washington; Neil Alexis of University of North Carolina at Chapel Hill; Richard Kanner, Robert Paine III and Cheryl Pirozzi of University of Utah; Stephen Peters of Wake Forest University; Jerry Krishnan of University of Illinois at Chicago; Mark Dransfield of University of Alabama, Birmingham; Prescott Woodruff of University of California, San Francisco; Christopher Cooper of University of California, Los Angeles; Graham Barr of Columbia University Medical Center; Alejandro Comellas and Eric Hoffman of University of Iowa; MeiLan Han of University of Michigan, Ann Arbor; and Fernando Martinez of Weill Cornell Medicine.

The work described in the JAMA Internal Medicine paper, part of the broader SPIROMICS study, was supported by the National Institutes of Health (HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C, U01 HL137880, R01ES023500, K23ES025781), AstraZeneca/MedImmune, Bayer, Bellerophon Therapeutics, Boehringer Ingelheim Pharmaceuticals Inc., Chiesi Farmaceutici S.P.A., Forest Research Institute Inc., GlaxoSmithKline, Grifols Therapeutics Inc., Inkaria Inc., Novartis Pharmaceuticals Corporation, Nycomed GmbH, ProterixBio, Regeneron Pharmaceuticals Inc., Sanofi, Sunovion, Takeda Pharmaceutical Company, Theravance Biopharma, and Mylan.

Other authors of the American Journal of Respiratory and Critical Care Medicine paper are Emily Brigham, Nirupama Putcha and Aparna Balasubramanian of Johns Hopkins and Laura Paulin of Dartmouth-Hitchcock Medical Center. The AJRCCM paper was supported by the National Institutes of Health (P50MD010431, F32 ES029786-01, R21ES025840, T32 HL007534-36) and the Environmental Protection Agency (R836150).

Source: https://www.newswise.com/articles/exposure-to-ozone-pollution-or-wood-smoke-worsens-lung-health-of-smokers-and-former-smokers

M. Bradley Drummond, MD, MHS | Department of Medicine

Smoking and Respiratory Diseases | Johns Hopkins Medicine

Speciality Areas: COPD, alpha-1 antitrypsin deficiency, asthma, smoking cessation, HIV-related lung diseases

Chronology: BS Biology: Emory University, 1997; MD: University of Texas Southwestern Medical School, 2001; Resident: Johns Hopkins Hospital, 2001-2004; Pulmonary and Critical Care Fellow: Johns Hopkins Hospital, 2004-2010; Chief Resident, Osler Medical Residency Program: Johns Hopkins Hospital, 2005-2006; Clinical Instructor: Johns Hopkins Hospital, 2010-2011; Assistant Professor of Medicine: Johns Hopkins Hospital, 2011-2015; Associated Professor of Medicine: Johns Hopkins Hospital, 2015-2016; Associate Professor of Medicine, University of North Carolina, 2016-Present. Director, UNC Obstructive Lung Diseases Clinical and Translational Research Center, 2016-Present.

Dr. Drummond is a board-certified pulmonary and critical care physician. His clinical expertise includes chronic obstructive lung disease (COPD), alpha-1 antitrypsin deficiency, and smoking cessation.

He is also a clinical and translational researcher whose research focus includes characterizing the mechanisms for development of chronic lung disease in individuals at-risk or with chronic obstructive pulmonary disease (COPD).

He has expertise in epidemiology and clinical trials design, and has applied these skills to understand the pattern and risk factors for lung function progression in smokers as well as HIV-infected individuals.

His primary project is an NHLBI-funded study of a novel biomarker in the blood and lungs of individuals with or at-risk for COPD, and examining the role of vitamin D on levels of this biomarker. Additionally, Dr.

Drummond is involved in characterizing the longitudinal impact of smoking, HIV infection and tobacco dependence on long-term outcomes related to chronic obstructive pulmonary disease. He is the director of the UNC Obstructive Lung Diseases Clinical and Translational Research Center, where he oversees clinical research studies supported by NIH and industry sponsors.

Selected Bibliography (reverse chronological order):

Burkes RM, Astemborski J, Lambert AA, Brown TT, Wise RA, Kirk GD, Drummond MB. Plasma cathelicidin and longitudinal lung function in current and former smokers. PLoS One. 2019 Feb 72;14(2):e0212628. PMID 30811465

Ghosh S, Pleasants RA, Ohar JA, Donohue JF, Drummond MB. Prevalence and factors associated with suboptimal peak inspiratory flow rates in COPD. International J COPD. 2019:14:585-595.

Ghosh S, Anderson WH, Putcha N, Han MK, Curtis JL, Criner GJ, Dransfield MT, Barr RG, Krishnan JA, Lazarus SC, Cooper CB, Paine R, Peters SP, Hansel NN, Martinez FJ, Drummond MB. Alignment of Inhaled COPD Therapies with Published Strategies: Analysis of the GOLD Recommendations in SPIROMICS.  Annals Am Thor Soc.2019:16(2):200-208. PMID 30216731

Pleasants RA, Wang T, Xu K, Beiko T, Bei H, Suodi Z, Drummond MB. Effect of nebulized corticosteroids on lung function in the treatment of chronic obstructive pulmonary disease exacerbations: Systematic review, meta-analysis and clinical perspective. Respiratory Care. 2018:63(10):1302-1310.

Burkes RM, Gassett AJ, Anderson W, O’Neal WK, Woodruff PG, Krishnan JA, Barr RG, Han MK, Martinez FJ, Comellas AP, Lambert AA, Kaufman JD, Dransfield MT, Wells JM, Kanner RA, Paine R, Bleecker ER, Paulin LM, Hansel NN, Drummond MB. Rural residence is associated with COPD exacerbations: Analysis of the SPIROMICS cohort. Annals Am Thor Soc.2018:15(7):808-816. PMID 29584453

Morris MA, Jacobson SR, Tashkin DP, Woodruff PG, Hoffman EA, Kanner RE, Kinnery GL, Cooper CB, Drummond MB, Barr RG, Oelner EC, Make BJ, Han MK, Hansel NN, O’Neal WK, Bowler RP. Cannabis use associations with pulmonary symptoms and function in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS). Chronic Obstructive Pulm Dis. 2018;5(1):46-56.

Bowler R, Hansel N, Jacobson S, Barr G, Make B, Han M, O’Neal W, Oelsner E, Casaburi R, Barjaktarevi I, Cooper C, Foreman M, Wise R, DeMeo D, Silverman E, Bailey W, Harrington K, Woodruff P, Drummond MB. Electronic cigarette use in adults at-risk or with COPD. J Gen Int Med. 2017:32(12):1315-1322. PMID 28884423

Drummond MB, Lambert AA, Hussien AF, Lin CT, Merlo CA, Wise RA, Kirk GD, Brown RH. HIV infection is independently associated with increased CT scan lung density. Acad Radiol. 2017;24:137-145. PMID 27876271

Drummond MB, Popescu I, Gama L, Lambert AA, Hoji A, Coon T, Merlo CA, Wise RA, Keruly J, Clements JE, Kirk GD, McDyer JF. HIV Suppression Restores Lung Mucosal CD4+ T-Cell Viral Immunity and Resolves CD8+ Alveolitis in Patients at Risk for HIV-associated COPD. J Infectious Diseases. 2016;214(10):1520-1530. PMID 27613775

Leader JK, Crothers K, Huang L, King MA, Morris A, Thompson BW, Flores SC, Drummond MB, Rom WN, Diaz PT. Risk Factors Associated With Quantitative Evidence of Lung Emphysema and Fibrosis in an HIV-Infected Cohort. J Acquir Immune Defic Syndr. 2016:71:420-427.

Drummond MB, Huang L, Diaz PT, Kirk GD, Kleerup EC, Morris A, Rom W, Weiden MD, Zhao E, Thompson B, Crothers K. Factors associated with abnormal spirometry among HIV-infected individuals. AIDS. 2015;29(13):1691-1700.

Brown RH, Wise RA, Kirk G, Drummond MB, Mitzner W. Lung density changes with growth and inflation. Chest. 2015;148(4):995-1002.

Lambert AA, Kirk GD, Astemborski J, Mehta SH, Wise RA, Drummond MB. HIV Infection is Associated with Increased Risk for Acute Exacerbation of COPD. JAIDS. 2015;69(1):68-74.

Drummond MB, Popescu I, Gama L, Coon T, Merlo CA, Wise RA, Clements JE, Kirk GD, McDyer JF. Activation-induced cell death drives profound lung CD4+ T cell depletion in HIV-associated COPD. Am J Resp Crit Care Med. 2014;190(7):744-755.

Drummond MB, Astemborski J, Lambert AA, Goldberg S, Stitzer ML, Merlo CA, Rand CS, Wise RA, Kirk GD. A Randomized Study of Contingency Management and Spirometric Lung Age for Motivating Smoking Cessation among Injection Drug Users. BMC Public Health. 2014;14:761.

Lambert AA, Drummond MB, Mehta SH, Brown TT, Lucas GM, Kirk GD, Estrella MM. Risk Factors for Vitamin D Deficiency among HIV-infected and Uninfected Injection Drug Users. PLoSOne. 2014;9(4):e95802.

Lambert AA, Kirk GD, Astemborski J, Neptune ER, Mehta SH, Wise RA, Drummond MB. A cross sectional analysis of the role of the antimicrobial peptide cathelicidin in lung function impairment with the ALIVE cohort. PLoSOne. 2014;9(4):e95099.

Putcha N, Drummond MB, Connett JE, Scanlon PD, Tashkin DP, Hansel NN, Wise RA. Chronic productive cough is associated with death in smokers with early COPD. COPD. 2014;11(4):451-458.

Fischer WA, Drummond MB, Merlo CA, Thomas DL, Brown R, Mehta SH, Wise RA, Kirk GD. Hepatitis C infection is not an independent risk factor for obstructive lung disease. COPD. 2014;11(1):10-16.

Drummond MB, Merlo CA, Astemborski J, Kalmin MM, Kisalu A, McDyer JF, Mehta SH, Brown RH, Wise R, Kirk GK. The effect of HIV infection on longitudinal lung function decline among injection drug users: A prospective cohort. AIDS. 2013;27(8):1303-1311.

Putcha N, Puhan MA, Hansel NN, Drummond MB, Boyd CM. Impact of comorbidities on self-rated health in self-reported COPD: an analysis of NHANES 2001-2008. J COPD. 2013;10(3):324-332.

Drummond MB, Hansel NH, Connett JE, Scanlon PD, Tashkin DP, Wise RA. Spirometric predictors of lung function decline and mortality in early COPD. Am J Respir Crit Care Med. 2012;185(12):1301-1306.

Drummond MB, Kirk GD, Astemborksi J, Marshall MM, Mehta SH, McDyer JF, Brown RH, Wise RA and Merlo CA. Association between obstructive lung disease and markers of HIV infection in a high risk cohort. Thorax. 2012;67:309-314.

Drummond MB, Peters SP, Castro M, Holbrook JT, Irvin CG, Smith LJ, Wise RA and Sugar EA. Risk factors for montelukast treatment failure in step-down therapy for controlled asthma. Journal of Asthma. 2011;48:1051-1057.

Drummond MB, Kirk GD, Astemborski J, McCormack MC, Marshall MM, Mehta SH, Wise RA, Merlo CA. Prevalence and risk factors for unrecognized obstructive lung disease among urban drug users. Int J Chron Obstruct Pulmon Dis. 2011;6:89-95.

Drummond MB, Kirk GD, McCormack MC, Marshall MM, Ricketts EP, Mehta SH, Wise RA, Merlo CA. HIV and COPD: impact of risk behaviors and diseases on quality of life. Qual Life Res. 2010;19(9):1295-1302.

Drummond MB, Wise RA, John M, Zvarich MT, McGarvey LP. Accuracy of death certificates in COPD: analysis from the TORCH trial. COPD. 2010;7(3):179-185.

Drummond MB, Kirk GD, Ricketts EP, McCormack MC, Hague JC, McDyer JF, Mehta SH, Engels EA, Wise RA, Merlo CA. Cross sectional analysis of respiratory symptoms in an injection drug user cohort: the impact of obstructive lung disease and HIV. BMC Pulm Med. 2010; 10:27.

Drummond MB, Dasenbrook EC, Pitz MW, Murphy DJ, Fan E. Inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease. JAMA. 2008;300(20):2407-2416.

Drummond MB, Blackford AL, Benditt JO, Make BJ, Sciurba FC, McCormack MC, Martinez FJ, Fessler HE, Fishman AP, Wise RA; NETT Investigators. Continuous oxygen use in nonhypoxemic emphysema patients identifies a high-risk subset of patients: retrospective analysis of the National Emphysema Treatment Trial. Chest. 2008;134(3):497-506.

Drummond MB, Schwartz PF, Duggan WT, Teeter JG, Riese RJ, Ahrens RC, Crapo RO, England RD, Macintyre NR, Jensen RL, Wise RA. Intersession variability in single-breath diffusing capacity in diabetics without overt lung disease. Am J Respir Crit Care Med. 2008;178(3):225-232.

A complete list of Dr. Drummond’s publications can be found here.

Source: https://www.med.unc.edu/medicine/directory/m-bradley-drummond-md-mhs/

Drug shields lungs from smoking damage

Smoking and Respiratory Diseases | Johns Hopkins Medicine

JOHNS HOPKINS (US) — A common blood pressure medicine appears to help prevent the lung damage associated with cigarette smoke, according to a study with mice.

Administering the drug, losartan (also known by the brand name Cozaar) to mice improved or prevented lung tissue breakdown, airway wall thickening, inflammation, and lung overexpansion associated with two months of exposure to cigarette smoke.

[sources]

“The results … suggest that losartan or similar drugs could serve as an effective treatment for smoking-related lung diseases in humans,” says senior investigator Enid Neptune, assistant professor of medicine at Johns Hopkins University.

“And because these drugs are already approved for use in the United States as safe and effective treatments for hypertension, incorporating them into our treatment regimen for COPD would be quite rapid.”

The next step, the researchers say, is a clinical trial of the drug in people with smoking-related chronic obstructive pulmonary disease (COPD), the long-term consequence of smoking. At present, there is no known treatment to prevent or repair the lung damage resulting from COPD.

Existing medication

COPD is the third-leading cause of death in the United States, mostly in people with either chronic bronchitis or emphysema, or both; some 12 million Americans have been diagnosed with COPD.

The mouse study, published in the Journal of Clinical Investigation, is considered a breakthrough, the research team says, because it is the first to show that a drug already in clinical use can prevent most the serious consequences of smoking in an animal test model, by preserving both lung structure and function.

In smoking-related COPD, breathing becomes difficult and progressively worsens, as the small airways and airspaces that conduct oxygen through the lungs and into the bloodstream become damaged. Airway walls thicken and are more readily obstructed by mucus, and the airspaces lose their elasticity.

“It is very exciting that an existing medication has proven capable in an animal model of not only treating the problems of COPD, but also disrupting the biological pathway that precipitated them,” says pulmonologist Robert A. Wise, who is piloting the clinical studies.

“If our tests in people prove successful, we could help restore lung health to millions of people who have suffered from tobacco addiction.”

Wise says existing remedies for smoking-related COPD consist mainly of providing relief of symptoms, such as shortness of breath, coughing, and mucus production. Drugs that lower blood pressure also help, and surgery can be done to remove damaged portions of the lung or transplant new lungs.

Wise and Neptune began their investigation of losartan after a Johns Hopkins colleague, Harry (Hal) Dietz, discovered it could potentially treat Marfan syndrome, which results from a single genetic mutation and weakens arteries, affecting all major organs, including the lungs.

The pulmonary researchers wanted to know if the medication had the same reparative effects on the lungs in other more complex and common respiratory diseases, such as COPD.

Previous research on losartan, by Dietz and others, had shown that the drug blocked the action of a key signaling protein called transforming growth factor beta, or TGF-beta.

Neptune’s research showed that TGF-beta levels were elevated in lung tissue samples from smokers with COPD and in the lung tissue of mice with Marfan syndrome. Neptune and Dietz had also shown in 2003 that TGF-beta neutralizing antibodies prevented developmental emphysema in Marfan mice.

Early tests

In the new experiments, the team first confirmed elevated levels of TGF-beta in the lungs of mice exposed to cigarette smoke and in lung tissue samples of smokers with COPD.

Biochemical analyses showed that smoke-exposed mice had a fourfold increase in TGF-beta signaling in their lungs than mice exposed to indoor air only; in people, TGF-beta signaling in the COPD sufferers’ lungs was 25 percent greater than in those of nearly a dozen smokers without COPD.

While continuing exposure to tobacco smoke, the researchers treated some mice with either a low or high dose of losartan. Another set of smoke-exposed mice was given a neutralizing antibody to TGF-beta signaling, the same treatment that had been used in Marfan mice.

Researchers found major improvements in more than a half-dozen measures of lung damage. In untreated mice exposed to smoke, airway wall thickness had doubled. The thickening was 50 percent less in mice treated with either dose of losartan or with TGF-beta antibodies.

Losartan-treated mice showed no signs of lung overexpansion and no signs of increased collagen deposition, a gauge of TGF-beta activity, and had normal levels of elastin-metabolizing enzymes and protein fragments in their air sac walls. Measures of oxidative stress, inflammation and cell death were also better in mice given the blood pressure medication.

Funding support for the mouse study was provided by the National Heart, Lung and Blood Institute (NHLBI), one of the National Institutes of Health, and by the Grace Anne Dorney Fund for Tobacco-related Research.

Funding for the clinical trial is from NHLBI and the drug’s manufacturer, Merck & Co.

More news from Johns Hopkins University: http://releases.jhu.edu

Source: https://www.futurity.org/drug-shields-lungs-from-smoking-damage/

Diet rich in apples and tomatoes may help repair lungs of ex-smokers, study suggests

Smoking and Respiratory Diseases | Johns Hopkins Medicine

A study from the Johns Hopkins Bloomberg School of Public Health found the natural decline in lung function over a 10-year period was slower among former smokers with a diet high in tomatoes and fruits, especially apples, suggesting certain components in these foods might help restore lung damage caused by smoking.

The researchers found that adults who on average ate more than two tomatoes or more than three portions of fresh fruit a day had a slower decline in lung function compared to those who ate less than one tomato or less than one portion of fruit a day, respectively. The researchers inquired about other dietary sources such as dishes and processed foods containing fruits and vegetables (e.g. tomato sauce) but the protective effect was only observed in fresh fruit and vegetables.

The paper, which is part of the Ageing Lungs in European Cohorts (ALEC) Study, funded by the European Commission and led by Imperial College London, also found a slower decline in lung function among all adults, including those who had never or had stopped smoking, with the highest tomato consumption. Poor lung function has been linked with mortality risks from all diseases, including chronic obstructive pulmonary disease (COPD), heart disease, and lung cancer.

The findings appear in the December issue of the European Respiratory Journal.

“This study shows that diet might help repair lung damage in people who have stopped smoking.

It also suggests that a diet rich in fruits can slow down the lung's natural aging process even if you have never smoked,” says Vanessa Garcia-Larsen, assistant professor in the Bloomberg School's Department of International Health and the study's lead author. “The findings support the need for dietary recommendations, especially for people at risk of developing respiratory diseases such as COPD.”

For the study, the research team assessed diet and lung function of more than 650 adults in 2002, and then repeated lung function tests on the same group of participants 10 years later.

Participants from three European countries — Germany, Norway and the United Kingdom — completed questionnaires assessing their diets and overall nutritional intake.

They also underwent spirometry, a procedure that measures the capacity of lungs to take in oxygen.

The test collects two standard measurements of lung function: Forced Exhaled Volume in 1 second (FEV1), which measures how much air a person can expel from their lungs in one second; and Forced Vital Capacity (FVC), the total amount of air a person can inhale in 6 seconds. The study controlled for factors such as age, height, sex, body mass index (an indicator of obesity), socio-economic status, physical activity and total energy intake.

Among former smokers, the diet-lung-function connection was even more striking. Ex-smokers who ate a diet high in tomatoes and fruits had around 80 ml slower decline over the ten-year period. This suggests that nutrients in their diets are helping to repair damage done by smoking.

“Lung function starts to decline at around age 30 at variable speed depending on the general and specific health of individuals,” explains Garcia-Larsen “Our study suggests that eating more fruits on a regular basis can help attenuate the decline as people age, and might even help repair damage caused by smoking. Diet could become one way of combating rising diagnosis of COPD around the world.”

make a difference: sponsored opportunity

Story Source:

Materials provided by Johns Hopkins University Bloomberg School of Public Health. Note: Content may be edited for style and length.

Journal Reference:

  1. Vanessa Garcia-Larsen, James F. Potts, Ernst Omenaas, Joachim Heinrich, Cecilie Svanes, Judith Garcia-Aymerich, Peter G. Burney, Deborah L. Jarvis. Dietary antioxidants and ten-year lung function decline in adults from the ECRHS survey. European Respiratory Journal, December 2017 DOI: 10.1183/13993003.02286-2016

Source: https://www.sciencedaily.com/releases/2017/12/171221101347.htm

Diet Rich in Apples and Tomatoes May Help Repair Lungs of Ex-Smokers, Study Suggests

Smoking and Respiratory Diseases | Johns Hopkins Medicine

Home > News > News Releases > 2017 > Diet Rich in Apples and Tomatoes May Help Repair Lungs of Ex-Smokers, Study Suggests

December 21, 2017

Study also found that regular intake of tomatoes may also help slow the natural decline in lung function among all adults

A study from the Johns Hopkins Bloomberg School of Public Health found the natural decline in lung function over a 10-year period was slower among former smokers with a diet high in tomatoes and fruits, especially apples, suggesting certain components in these foods might help restore lung damage caused by smoking.

The researchers found that adults who on average ate more than two tomatoes or more than three portions of fresh fruit a day had a slower decline in lung function compared to those who ate less than one tomato or less than one portion of fruit a day, respectively. The researchers inquired about other dietary sources such as dishes and processed foods containing fruits and vegetables (e.g. tomato sauce) but the protective effect was only observed in fresh fruit and vegetables.

The paper, which is part of the Ageing Lungs in European Cohorts (ALEC) Study, funded by the European Commission and led by Imperial College London, also found a slower decline in lung function among all adults, including those who had never smoked or had stopped smoking, with the highest tomato consumption. Poor lung function has been linked with mortality risks from all diseases, including chronic obstructive pulmonary disease (COPD), heart disease, and lung cancer.

The findings appear in the December issue of the European Respiratory Journal.  

“This study shows that diet might help repair lung damage in people who have stopped smoking.

It also suggests that a diet rich in fruits can slow down the lung’s natural aging process even if you have never smoked,” says Vanessa Garcia-Larsen, assistant professor in the Bloomberg School’s Department of International Health and the study’s lead author. “The findings support the need for dietary recommendations, especially for people at risk of developing respiratory diseases such as COPD.”

For the study, the research team assessed diet and lung function of more than 650 adults in 2002, and then repeated lung function tests on the same group of participants 10 years later.

Participants from three European countries — Germany, Norway and the United Kingdom — completed questionnaires assessing their diets and overall nutritional intake.

They also underwent spirometry, a procedure that measures the capacity of lungs to take in oxygen.

The test collects two standard measurements of lung function: Forced Exhaled Volume in one second (FEV1), which measures how much air a person can expel from their lungs in one second; and Forced Vital Capacity (FVC), the total amount of air a person can inhale in six seconds. The study controlled for factors such as age, height, sex, body mass index (an indicator of obesity), socio-economic status, physical activity and total energy intake.

Among former smokers, the diet-lung-function connection was even more striking. Ex-smokers who ate a diet high in tomatoes and fruits had around 80 ml slower decline over the 10-year period. This suggests that nutrients in their diets are helping to repair damage done by smoking.  

”Lung function starts to decline at around age 30 at variable speed depending on the general and specific health of individuals,” explains Garcia-Larsen “Our study suggests that eating more fruits on a regular basis can help attenuate the decline as people age, and might even help repair damage caused by smoking. Diet could become one way of combating rising diagnosis of COPD around the world.”

“Dietary antioxidants and 10-year lung function decline in adults from the ECRHS survey” was written by Vanessa Garcia-Larsen, James F. Potts, Ernst Omenaas, Joachim Heinrich, Cecilie Svanes, Judith Garcia-Aymerich, Peter G. Burney, and Deborah L. Jarvis 

The ALEC Study is funded by the European Union's Horizon 2020 Research and Innovation programme under grant agreement No. 633212.

# # #

Media contacts for the Johns Hopkins Bloomberg School of Public Health: Brandon Howard at 410-502-9059 at brandonhoward@jhu.edu and Barbara Benham at 410-614-6029 or bbenham1@jhu.edu.

Source: https://www.jhsph.edu/news/news-releases/2017/diet-rich-in-apples-and-tomatoes-may-help-repair-lungs-of-ex-smokers-study-suggests.html

Smoking and Respiratory Diseases | Johns Hopkins Medicine

By Serena Gordon
HealthDay Reporter

TUESDAY, Jan. 14, 2020 (HealthDay News) — Lung illnesses and deaths from vaping have been grabbing headlines for months, and now two new studies offer fresh evidence pointing to long-term respiratory concerns.

The studies link the use of electronic cigarettes to asthma and chronic obstructive pulmonary disease (COPD).

“These studies add to the body of evidence on the relationship between electronic cigarette use and lung conditions,” said Dr. Albert Osei, a postdoctoral fellow at Johns Hopkins University School of Medicine in Baltimore. He's lead author of a study published earlier this month in the American Journal of Preventive Medicine.

The studies cannot definitely prove a cause-and-effect link, he noted, adding: “We believe this warrants further longitudinal studies.”

Introduced to the U.S. market more than a decade ago, e-cigarettes are marketed as less harmful than traditional tobacco cigarettes, and as a way to help quit smoking. In 2016, almost 11 million American adults used e-cigarettes.

Most have a vaporization chamber, a nicotine cartridge that can include flavoring and a rechargeable battery. The vapor they produce is inhaled into the lungs — a process called vaping.

Past studies have suggested the vapor may irritate airway cells, impair their ability to fight infection, and lead to destruction of lung tissue. A study just published in December found that e-cigarette users are also at significantly higher risk of chronic lung diseases such as asthma, bronchitis, emphysema and COPD.

Vaping been linked to a nationwide outbreak of serious lung illness. As of Jan. 7, there have been more than 2,600 illnesses and 57 deaths — many linked to vaping products with THC, the component in marijuana that produces a high. An additive called Vitamin E acetate that makes the THC last longer may be the culprit, according to U.S. Centers for Disease Control and Prevention.

Osei's study looked at a database of more than 705,000 adults.

Almost 65,000 smoked regular cigarettes. More than 25,000 smoked e-cigarettes; their average age: 30 to 34. More than 200,000 were former traditional smokers.

About 2% of smokers reported using both traditional and e-cigarettes. More than 53,000 in the group said they had COPD, chronic bronchitis or emphysema.

In people who had never smoked regular cigarettes, e-cigarette use was associated with 75% higher odds of COPD, the study found. Daily users of e-cigarettes had 2.6 times higher odds of COPD than people who never smoked regular cigarettes.

The second study — published recently in the journal BMC Pulmonary Medicine — included more than 400,000 adults who never smoked regular cigarettes. More than 34,000 had asthma. Just 3,100 people currently used e-cigarettes. Their average age: 18 to 24.

The risk of asthma was 39% higher in current e-cigarette users than in people who had never vaped. And the more people vaped, the higher their asthma odds, the study reported.

Osei, the head of a pro-vaping advocacy group noted that these studies don't prove that e-cigarettes was responsible for either condition.

It's possible that people with asthma or COPD might have had their conditions before using e-cigarettes, said Greg Conley, president of the American Vaping Association.

“There is no plausible mechanism by which vaping, which exposes users to far fewer toxins than cigarette smoking, could cause COPD in a period of a few years,” he said. “Even among heavy smokers, several decades are required for COPD to develop.”

Dr. Len Horovitz is a pulmonary specialist at Lenox Hill Hospital in New York City who also reviewed the findings.

“Long gone are the days when makers of e-cigarettes could claim that this form of nicotine use was not harmful,” he said. There is no safe smoking or vaping.”

Study author Osei agreed, pointing out that both combustible and e-cigarettes contain nicotine.

“The majority of people using electronic cigarettes are young people. Over time, we will have a generation who becomes nicotine-dependent from using electronic cigarettes,” Osei said. “As a public health physician, I cannot say that electronic cigarettes are without risk.”

SOURCES: Albert Osei, M.D., M.P.H., postdoctoral fellow, Johns Hopkins University School of Medicine, Ciccarone Center for the Prevention of Cardiovascular Disease, Baltimore; Greg Conley, president, American Vaping Association; Len Horovitz, M.D., pulmonary specialist, Lenox Hill Hospital, New York City;American Journal of Preventive Medicine, Jan. 2, 2020;BMC Pulmonary Medicine,Oct. 16, 2019 Copyright © 2013-2020 HealthDay. All rights reserved.

Source: https://www.webmd.com/lung/news/20200114/more-studies-link-vaping-to-asthma-copd