Philip Morris stop-smoking campaign attacked as a PR stunt

Marlboro cigarette maker Philip Morris International (PM.N) drew accusations of hypocrisy after using a four-page newspaper advertisement to urge smokers to quit cigarettes.

The wraparound advertisement covering Monday’s Daily Mirror tabloid is part of Philip Morris’s 2 million pound ($2.61 million) “Hold My Light” campaign, in which the world’s biggest international tobacco company is pushing a 30-day challenge for people to give up smoking.

The campaign also features a video and a website where smokers can sign up for the challenge and gain information to help them to kick the habit.

Cigarettes account for the vast majority of Philip Morris’s revenue, but the company has repeatedly stated a longer-term vision to replace cigarette sales with products such as its IQOS tobacco-heating device, which it says is less dangerous.

“This is staggering hypocrisy from a tobacco company to promote its own smoking-cessation products in the UK while continuing to promote tobacco cigarettes across the world,” Cancer Research UK said. 

“The best way Philip Morris could help people to stop smoking is to stop making cigarettes.”

Philip Morris has said that Britain, where advertising and marketing of cigarettes is prohibited, could eradicate cigarettes in coming years. British health regulators have also endorsed e-cigarettes as a way to help people to quit.

“This campaign is simply PR puff,” said Hazel Cheeseman, director of policy for Action on Smoking and Health.

“If they were serious about a smoke-free world they wouldn’t challenge tobacco legislation around the world but instead support regulations that will really help smokers quit and prevent children from taking up smoking.”

Last year Reuters published a special report on efforts by Philip Morris to subvert the World Health Organization’s global tobacco treaty, which is aimed at reducing smoking worldwide.


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Triple Therapy Improves COPD Exacerbations Regardless of Reversibility Status

Single-inhaler triple therapy fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI; Trelegy Ellipta) continues to boast positive findings from the Informing the Pathway of COPD Treatment (IMPACT) study.

In new data to be presented at the 2018 CHEST Annual Meeting in San Antonio, TX, GlaxoSmithKline (GSK) has reported their first-of-its-kind triple therapy inhaler significantly reduced the annual rate of moderate-to-severe and severe exacerbations, improved lung function, and boosted overall quality of life in patients with chronic obstructive pulmonary disease (COPD)—regardless of baseline reversibility.

The IMPACT trial—a 52-week, randomized, double-blind, parallel-group, global analysis involving 10,355 symptomatic patients with COPD who have a history of moderate-to-severe exacerbations—compared Trelegy Ellipta to combination therapies inhaled corticoid steroid/long-acting beta agonist (ICS/LABA) and long-acting muscarinic agonist/long-acting beta agonist (LAMA/LABA).

Trelegy Ellipta, the first triple therapy approved by the US Food and Drug Administration (FDA) for the treatment of patients with COPD on fixed-dose treatment in September 2017, is itself a ICS/LAMA/LABA combination therapy. The original intent of the IMPACT trial was to understand the benefits and risks of the triple combination therapy in treating COPD, in addition to improving the understand of what particular patients need ICS therapy or maximal bronchodilation.

In this newest analyses, led by Robert Wise, MD, of the Johns Hopkins University School of Medicine, patients who were reversible were defined through different between pre- and post-albuterol assessments of forced expiratory volume in 1 second (FEV1) of at least 12% and 200 mL.

Investigators also assessed for the effect of baseline reversibility on treatment response across the 3 treatment arms. Lung function and quality of life were measured by patient responders on the St George Respiratory Questionnaire (SGRQ).

Investigators reported that 18% of patients demonstrated reversibility, with a significant reduction in the rate of moderate and severe exacerbation in both reversible and nonreversible patients administered FF/UMEC/VI versus those administered UMEC/VI. Severe exacerbation reduction rates were 44% (95% CI: 14 – 63) in reversible patients, and 31% (95% CI: 17-44) in nonreversible patients.

Lung function, as measured by change from baseline in trough FEV1 at week 52, was markedly...

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Mouse Study: Lung Inflammation from Childhood Asthma May Be Linked to Later Anxiety

Research has shown that childhood asthma is associated with a two to three times higher chance of developing an internalizing disorder such as anxiety or depression, but the exact reasons for this have remained a mystery.

In a new mouse study at Pennsylvania State University, the researchers suggest that persistent lung inflammation may be one possible explanation for an increased risk of anxiety. They discovered that exposure to allergens early in life was linked with persistent lung inflammation and also tied to changes in gene expression related to stress and serotonin function. They also found that females were more likely to have inflamed lungs for a longer period of time.

“The idea of studying this link between asthma and anxiety is a pretty new area, and right now we don’t know what the connection is,” said Dr. Sonia Cavigelli, associate professor of biobehavioral health. “What we saw in the mice was that attacks of labored breathing may cause short-term anxiety, but that long-term effects may be due to lasting lung inflammation.”

The researchers say that finding the root cause of this connection is difficult because in addition to the biological aspects of asthma, there are also several social and environmental factors that could contribute to anxiety in humans. For example, air pollution or a parent’s anxiety about their child’s asthma could also influence the child’s risk for anxiety.

“With the mice, we can look at the different components of asthma, like the lung inflammation or the airway constriction,” said Jasmine Caulfield, graduate student in neuroscience and lead author on the study.

“A person who’s having an asthma attack may have inflammation in their lungs and labored breathing at the same time, so you can’t separate which is contributing to later outcomes. But in mice, we can isolate these variables and try to see what is causing these anxiety symptoms.”

To help differentiate between these potential causes, the researchers studied a total of 98 mice, divided into four groups: one with airway inflammation due to dust mite exposure; one that experienced episodes of labored breathing; one that experienced both conditions; and one that experienced neither, as a control.

The findings reveal that three months after being exposed to the allergen, the mice still had lung inflammation and mucus, suggesting that even when allergy triggers are removed, there are lasting effects in the lungs long...

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Putting the Brake on E-Cigarettes

The FDA has launched strong regulatory and enforcement moves against the industry, branding the use of e-cigarettes among teens and ‘epidemic.’

In a pronouncement, Food and Drug Administration Commissioner Scott Gottlieb on Sept. 12 declared e-cigarette use "epidemic" among teens, signaled a possible ban on flavored e-cigarette liquids and launched sweeping enforcement efforts against retailers who sell e-cigarettes to minors.

"I use the word epidemic with great care," Gottlieb said in a statement. "The FDA won't tolerate a whole generation of young people becoming addicted to nicotine as a tradeoff for enabling adults to have unfettered access to these same products."

The enforcement action against nearly 1,300 retailers is the largest organized crackdown of its kind in FDA history, Gottlieb said. The agency issued warning letters and imposed fines ranging from $279 to $11,182 on 130 repeat offenders. A ban on flavorings could put the brakes on a fast-growing market. Average monthly sales grew 132 percent between 2012 and 2016, according to a study published in August by the Centers for Disease Control and Prevention.

Joanna Cohen is the Bloomberg professor of disease prevention and director of the Institute for Global Tobacco Control at the Johns Hopkins Bloomberg School of Public Health.


Gottlieb hinted at preliminary FDA data, not yet published, indicating that e-cigarette use is soaring among high school students. In August, the CDC reported that e-cigarette use increased 900 percent among U.S. high schoolers from 2011 to 2015, making them the most commonly used source of nicotine in this group, driven by aggressive marketing and appealing flavors.

Officials say that e-cigarettes may be a safer way to deliver nicotine and may help smokers reduce their risk of smoking-related illnesses and death, but they worry about the rapid rise of e-cigarettes among teens and young adults.

The Vapor Technology Association, a trade group representing more than 600 members, accused the FDA in a statement of "kowtowing to hysterical public health groups," taking a "giant step backwards" in smoking prevention and reinvigorating "Big Tobacco."

Joanna Cohen, the Bloomberg professor of disease prevention at the Johns Hopkins Bloomberg School of Public Health and director of the Institute for Global Tobacco Control, spoke to U.S. News about the FDA's growing authority to rein in e-cigarette manufacturers and...

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Testosterone Replacement Therapy Can Slow Men’s COPD, Study Finds

Testosterone replacement therapy can help slow the progression of chronic obstructive pulmonary disease (COPD) in men, a new study shows.

Men with COPD tend to experience shortness of breath, leading physicians to prescribe them long-term steroid-based medications. While these medications help treat pulmonary symptoms, they are also associated with testosterone dysfunction.

Accordingly, previous studies have shown that men with COPD have low testosterone levels, which could lead to a worsening of the condition.

“Previous studies have suggested that testosterone replacement therapy may have a positive effect on lung function in men with COPD,” Jacques Baillargeon, the study’s author and a professor in preventive medicine and community health at University of Texas Medical Branch at Galveston, said in a press release.

The study, set to be published in the journal Chronic Respiratory Disease, was designed to determine whether testosterone replacement therapy (in which patients are prescribed testosterone) could help reduce the risk of hospitalization due to respiratory disease in middle-aged and older men with COPD.

Baillargeon noted that “we are the first to conduct a large-scale, nationally representative study on this association.”

Baillargeon and his colleagues used the Clinformatics Data Mart dataset, which comprises one of the largest commercially insured populations in the United States. They examined data from 450 men ages 40-63 with COPD who began testosterone replacement therapy between 2005 and 2014.

Researchers also used the national Medicare database to study data from 253 men age 66 and up with COPD, and who initiated testosterone replacement therapy between 2008 and 2013.

Researchers found that patients who underwent testosterone replacement therapy had a greater reduction in respiratory hospitalizations when compared to patients who did not receive the therapy.

“Specifically, middle-aged testosterone replacement therapy users had a 4.2 percent greater decrease in respiratory hospitalizations compared with non-users,” Baillargeon said. “Older testosterone replacement therapy users had a 9.1 percent greater decrease in respiratory hospitalizations compared with non-users.”


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Research Suggests New Mechanism at Play in Some Severe Asthma Cases

A newly published study offers a better understanding of the mechanisms at play in a subset of patients with severe asthma. Scientists hope the new insights will help direct the development of more tailored approaches to asthma therapy.

For the study, a team of investigators from several US academic research hospitals set out to better understand the pathogenesis of severe asthma, which does not respond to treatment with corticosteroids and which affects about 10% of the 24 million Americans with asthma.

Some of those patients with severe asthma have substantial neutrophilia, and the investigators hypothesized that the presence of neutrophilia is indicative of mechanisms distinct from other types of inflammation.

To test their hypothesis, the team mimicked allergic lung inflammation by exposing a mouse model to house dust mites and endotoxin. When exposed to both the allergen and endotoxin, the mice showed an increase in lung neutrophils and neutrophil extracellular traps (NETs). NETs help defend a host by immobilizing invading microorganisms; however, they can also cause inflammation and injure organs. NETs are activated and released through NETosis. During vital NETosis, neutrophils eject their nuclear material to form NETs, then re-seal themselves, forming cytoplasts.

The animal model findings suggest NETosis and cytoplasts play an important role in sparking and amplifying the allergen-initiated neutrophilic immune responses in lung inflammation. To confirm the insights, the investigators analyzed fluid samples from the lungs of human patients with severe asthma. Indeed, a group of those patients also had high neutrophil counts as well as NETs and cytoplasts.

Lead author Bruce Levy, MD, chief of the division of pulmonary and critical care medicine at Brigham and Women’s Hospital, told MD Magazine® that the findings suggest potential therapeutic pathways for investigators working on asthma.

“There are many reasons why patients can develop an increased neutrophil count,” he said. “If a patient has severe asthma with an increased lung neutrophil count, our findings have uncovered a new immunological mechanism for this type of inflammation that we hope will inform new (yet-to-be-developed) treatment.”

The findings are important because current clinical trials for new moderate and severe asthma therapies don’t distinguish between patients with high neutrophil counts.

Levy said these findings might also pave the way...

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Smoking Banned in Public Housing Nationwide

Smokers can no longer light up in or near public housing facilities in the U.S. due to a new rule that went into effect July 31. The nationwide ban on smoking in public housing was implemented nearly two years after the rule was passed by the Obama administration in 2016.

The Department of Housing and Urban Development (HUD) now prohibits the use of cigarettes, cigars and pipes in all public housing units and common areas, as well as any outdoor areas up to 25 feet from public housing and administrative office buildings. The ban does not apply to e-cigarettes, snuff and chewing tobacco, although there may be restrictions on those in some areas.

HUD says about 228,000 public housing units under more than 600 local agencies were already smoke-free, and the new rule wipes out smoking in more than 940,000 other units. The ban is expected to save government housing agencies $153 million a year in repairs and health care costs, including $16 million for costs tied to smoking-related fires, the Centers for Disease Control and Prevention estimated in 2014.

HUD said the new policy would reduce health hazards from secondhand smoke and encourage residents to quit smoking

The ban on smoking products must be included in public housing tenants' leases, HUD says. Tenants will not be evicted for a single instance of smoking but could face eviction after several smoking violations.

Reach out to MD Spiro for information on Smoking Cessation and the products we offer to help your patients QUIT once and for all!

Additionally, for more information to quit smoking, officials recommend calling 1-800-QUIT-NOW (1-800-784-8669) toll-free to talk to a trained coach or go to


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Unraveling the Relationship Between COPD and Stroke

Emerging evidence suggests that chronic obstructive pulmonary disease (COPD) could be a risk factor for stroke.1,2 COPD is the fourth leading cause of death worldwide, and up to 80% of patients with the disease have at least one comorbidity.2 Many of the commonalities between COPD and stroke portend poor outcomes for patients with both diseases: age, indoor and outdoor pollution exposure, tobacco smoke, asthma and airway hyper-reactivity, and lower socioeconomic status.2

One of the preventable confounders for COPD and stroke risk is smoking, which contributes to fatal events and stroke.2 Indeed, in a systematic review of 30 studies, Ann D. Morgan, MSc, of the National Heart and Lung Institute at the Imperial College London, and colleagues, found that COPD increased the prevalence and incidence of stroke. Even when the researchers adjusted for smoking, COPD was still a risk factor for stroke.1

In a recent interview with Pulmonology Advisor, coauthor Jennifer Quint, MD, clinical senior lecturer in respiratory epidemiology at the National Heart and Lung Institute in London, United Kingdom, explained, “Independently of COPD, smoking increases the risk of having a stroke. There is something about having COPD, too, though, that also increases the risk. This may be linked to inflammation that occurs as a result of having COPD.”

“Tobacco smoking is a risk factor both for ischemic stroke and COPD. Patients who are hospitalized for either condition should receive intensive tobacco cessation education and support both during the hospital and as they make the transition to their post-discharge residence,” neurologist Dawn M. Bravata, MD, of Indiana University School of Medicine and the Richard L. Roudebush VA Medical Center in Indianapolis, told Pulmonology Advisor.

Exacerbations and Comorbidities That Increase Stroke Risk

Current and former smokers with a 10-pack-year history were included in a cohort study of 16,485 patients with COPD (age range, 40-80 years) with cardiovascular disease (CVD) or multiple CVD risk factors to determine whether acute exacerbations of COPD (AECOPD) increased the risk for CV events.3 Kunisaki and colleagues found that when people with COPD needed additional antibiotics or corticosteroids, they were at higher risk of having a CV event, including CV death, myocardial infarction (MI), unstable angina, transient ischemic attack, or stroke 30 days after the exacerbation (hazard ratio, 3.8; 95% CI, 2.7-5.5). For those...

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