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Human Pathogens Abundant in the Bacterial Metagenome of Cigarettes 

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• Cigarettes harbor many pathogenic bacteria 

Cigarettes are "widely contaminated" with bacteria, including some known to cause disease in people, concludes a new international study conducted by a University of Maryland environmental health researcher and microbial ecologists at the Ecole Centrale de Lyon in France.

The research team describes the study as the first to show that "cigarettes themselves could be the direct source of exposure to a wide array of potentially pathogenic microbes among smokers and other people exposed to secondhand smoke." Still, the researchers caution that the public health implications are unclear and urge further research.

"We were quite surprised to identify such a wide variety of human bacterial pathogens in these products," says lead researcher Amy R. Sapkota, an assistant professor in the University of Maryland's School of Public Health.

"The commercially-available cigarettes that we tested were chock full of bacteria, as we had hypothesized, but we didn't think we'd find so many that are infectious in humans," explains Sapkota, who holds a joint appointment with the University's Maryland Institute for Applied Environmental Health and the department of epidemiology and biostatistics.

"If these organisms can survive the smoking process -- and we believe they can -- then they could possibly go on to contribute to both infectious and chronic illnesses in both smokers and individuals who are exposed to environmental tobacco smoke," . . .

The study will appear in an upcoming edition of the journal Environmental Health Perspectives. . . .

Sapkota's team took a more holistic approach using DNA microarray analysis to estimate the so-called bacterial metagenome, the totality of bacterial genetic material present in the tested cigarettes.

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The commercially-available cigarettes that we tested were chock full of bacteria, as we had hypothesized, but we didn't think we'd find so many that are infectious in humans. If these organisms can survive the smoking process -- and we believe they can -- then they could possibly go on to contribute to both infectious and chronic illnesses in both smokers and individuals who are exposed to environmental tobacco smoke.
Lead researcher Amy R. Sapkota, an assistant professor in the University of Maryland's School of Public Health, on the study that will appear in an upcoming edition of the journal Environmental Health Perspectives.

Smoking cessation toolbox for allergists  

Objectives: To review nicotine addiction, to examine how tobacco use has a direct negative impact on common disorders seen in allergy practice, and to provide a summary of the national guidelines for treating tobacco use and dependence. . . .

Conclusions: Allergists know the significant impact that smoking has and will make on the lives and health of patients. It is important for these specialists to make an impact on the chronic disease of tobacco addiction because it directly affects the care rendered. By using the standardized tobacco use treatment concept of the 5 A's (ask, advise, assess, assist, and arrange), allergists can make a positive impact on reducing US smoking rates and improve patient health. Screening, providing brief counseling, and prescribing first-line smoking cessation medications will help the United States get closer to achieving the national goal laid out in Healthy People 2010 of smoking rates of 12% or less.

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In H1N1 Flu Battle, Electronic Cigarettes Could be a Surprising Ally 

"Dr. Robertson placed groups of mice in a chamber and sprayed its air first with propylene glycol, then with influenza virus. All the mice lived. Then he sprayed the chamber with virus alone. All the mice died."

This quote is from a TIME magazine article entitled "Medicine: Air Germicide" which dates back to November 16, 1942 (time.com/time/magazine/article/0,9171,932876,00.html). The article has renewed relevance today because propylene glycol is the main ingredient in e cigarette cartridges.

An electronic cigarette (or e-cigarette) looks like a standard cigarette, but doesn’t burn tobacco or release toxic smoke. Instead, each puff vaporizes a small amount of nicotine dissolved in water and propylene glycol. Early studies on the benefits of switching from regular to electronic cigarettes have been promising enough to earn this October 2009 policy statement from Action on Smoking and Health (ASH), a UK public health charity that works to eliminate the harm caused by tobacco: . . .

With current and inevitable future outbreaks of respiratory illnesses such as swine flu, avian flu, SARS and antibiotic-resistant pneumonia, updated and comprehensive research into this topic deserves to be given a high priority in the medical research community.

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• Tobacco smoke linked with respiratory diseases 

Tobacco smoke is involved in uncontrolled asthma, a diminished response to anti-asthma drugs, rhinitis, nasal obstruction, and deregulation of the immune system according to an international expert at the annual meeting of the American College of Allergy, Asthma and Immunology (ACAAI) in Miami Beach, Fla.

Tobacco smoking has been mainly associated with chronic obstructive pulmonary disease (COPD), and is attributed to being one of the main reasons that COPD disease is the fourth leading cause of death in the United States.

"Recent studies have shown that smoking can be linked with other respiratory diseases such as asthma exacerbations and rhinitis," said Carlos Baena-Cagnani, M.D., faculty of medicine, at Catholic University of Cordoba in Argentina. "Both active and passive smoking has been shown to be involved in uncontrolled asthma and associated with asthma exacerbations in children and adolescents."

According to Dr. Baena-Cagnani, active smoking also causes changes in inflammation in asthma patients, diminishes their response to anti-asthma drugs, and has been found to induce nasal obstruction and decreased mucociliary clearance.

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Risk Of Skin Damage Increases In Smokers With Autoimmune Disorder 

Reports say researchers have come up with another reason to stay away from cigarettes after linking smoking to skin problems in people with systemic lupus erythematosus (SLE).

Experts at the Research Institute of the McGill University Health Centre (RI-MUHC) found that smokers with the long-term autoimmune disorder faced an increased risk for skin damage and rashes.

The study's lead author Dr. Christian A Pineau, Co-Director of the Lupus and Vasculitis clinic at the MUHC, said: "Up to 85 per cent of people with SLE develop skin involvement at some point.

"Our study shows that the risk of skin damage such as permanent hair loss and scarring from skin inflammation is significantly increased in smokers. So is the rate of active lupus rash."

Dr. Sasha Bernatsky, study co-author and physician in the MUHC's Rheumatology Division, added: "However, smoking may interfere with the effectiveness of some medications used to control skin disease in SLE.

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New research discovers link between smoking and brain damage 

New research which suggests a direct link between smoking and brain damage will be published in the July issue of the Journal of Neurochemistry. Researchers, led by Debapriya Ghosh and Dr Anirban Basu from the Indian National Brain Research Center (NBRC), have found that a compound in tobacco provokes white blood cells in the central nervous system to attack healthy cells, leading to severe neurological damage.

The research centers on a compound known as NNK, which is common in tobacco. NNK is a procarinogen, a chemical substance which becomes carcinogenic when it is altered by the metabolic process of the body.

Unlike alcohol or drug abuse NNK does not appear to harm brain cells directly, however, the research team believe it may cause neuroinflamation, a condition which leads to disorders such as Multiple Sclerosis.

"Considering the extreme economical and disease burden of neuroinflammation related disorders, it is extremely important from a medical, social and economic point of view to discover if NNK in tobacco causes neuroinflammation" said Ghosh.

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Cigarette Smoking and Cutaneous Damage in Systemic Lupus Erythematosus 

Conclusion Current cigarette smoking may be associated with cutaneous damage and active lupus rash in SLE, suggesting another reason to emphasize smoking cessation in patients with SLE.

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• Smokers With Common Autoimmune Disorder At Higher Risk For Skin Damage 

a team of researchers at the Research Institute of the McGill University Health Centre (RI-MUHC) have just found another. A study led by Dr. Christian A Pineau, Co-Director of the Lupus and Vasculitis clinic at the MUHC, has clearly linked skin damage and rashes to smoking in people with systemic lupus erythematosus (SLE). The study was published in a recent issue of the Journal of Rheumatology.

SLE is a long-term autoimmune disorder affecting about one in every 2000 people. About 90 per cent of SLE patients are women, many of them young. Symptoms are caused by an overactive immune system, and the disease can cause inflammation and damage in almost any organ system, including the skin.

"Up to 85 per cent of people with SLE develop skin involvement at some point," explains Dr. Pineau. "Our study shows that the risk of skin damage such as permanent hair loss and scarring from skin inflammation is significantly increased in smokers. So is the rate of active lupus rash."

While there is no cure for SLE, symptoms can be treated with drugs. "However, smoking may interfere with the effectiveness of some medications used to control skin disease in SLE," says Dr. Sasha Bernatsky, study co-author and physician in the MUHC's Rheumatology Division. "This may be part of the reason why smoking heightens skin damage in SLE.

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• E Cigarettes May Be More Effective Than Swine Flu Vaccine  

According to the Centers for Disease Control, during 2000-2004, "An estimated 443,000 persons in the United States died prematurely each year from smoking or exposure to secondhand smoke. During 2001-2004, the average annual smoking-attributable health-care expenditures nationwide were approximately $96 billion. When combined with productivity losses of $97 billion, the total economic burden of smoking is approximately $193 billion per year."

Comparing the health risks of tobacco smoking to the Swine Flu brings out some interesting and thought provoking statistics. According to President Obama's Council of Advisors on Science and Technology on H1N1, "A plausible scenario is that the epidemic could cause between 30,000 and 90,000 deaths in the United States." That puts the comparison of real deaths of 443,000 smokers to a "war games guess" of 30,000 to 90,000 for the H1N1 influenza for which the government recently declared a Health Emergency. That declaration and the shortage of the H1N1 vaccine has caused a panic in the U.S.

No study or statistic has been offered that points to the Swine Flu as being more deadly than tobacco cigarettes in causing death, yet a disproportional effort in preventative measures are currently being channeled to defend against a lower risk health issue. Toxic tobacco smoke contains many additional chemicals, including carbon monoxide and tar which is a sticky substance that accumulates in the lungs, causing lung cancer and respiratory distress. Tobacco is the leading cause of preventable death in the world and is responsible for more than 5 million deaths each year.

What the flu vaccine is to H1N1 as a preventative, the electronic cigarette may be for the tobacco smoker. An electronic cigarette is a futuristic advancement in science

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Lung Myeloid Dendritic Cells Coordinately Induce TH1 and TH17 Responses in Human Emphysema  

Exposure to tobacco smoke activates innate and adaptive immune responses that in long-term smokers have been linked to diseases of the lungs, cardiovascular system, joints, and other organs. The destruction of lung tissue that underlies smoking-induced emphysema has been associated with T helper 1 cells that recognize the matrix protein elastin. Factors that result in the development of such autoreactive T cells in smokers remain unknown but are crucial for further understanding the pathogenesis of systemic inflammatory diseases in smokers. Here, we show that lung myeloid dendritic cells were sufficient to induce T helper 1 and T helper 17 responses in CD4 T cells. T helper 1 and 17 cells are invariably present in lungs from patients with emphysema but not in lungs from normal individuals. Interleukin-17A, a canonical T helper 17 cytokine, enhanced secretion of CCL20, a chemoattractant for dendritic cells, and matrix metalloproteinase 12, a potent elastolytic proteinase, from lung macrophages. Thus, although diverse lung factors potentially contribute to T helper effector differentiation in vivo, lung myeloid dendritic cells direct the generation of pathogenic T cells and support a feedback mechanism that sustains both inflammatory cell recruitment and lung destruction. This mechanism may underlie disease in other elastin-rich organs and tissues.

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• Dendritic Cells Spark Smoldering Inflammation In Smokers' Lungs 

Inflammation still ravages the lungs of some smokers years after they quit the habit. What sparks that smoldering destruction remained a mystery until a consortium of researchers led by Baylor College of Medicine found that certain dendritic cells in the lung - the cells that "present" a foreign antigen or protein to the immune system - provoke production of destructive T-cells that attack a key protein called elastin, leading to death of lung tissue and emphysema.

A report of their work appears in the current issue of Science Transformational Medicine. The National Heart, Lung and Blood Institute estimates that 2 million Americans have emphysema, most of them over the age of 50 years. People with emphysema find it harder and harder to breathe as the lung's air sacs or alveoli are destroyed, causing holes in the lung and blocking airways. They have difficulty exchanging oxygen as their lungs become less elastic. Cigarette smoking is the greatest risk factor for the disease that contributes to as many as 100,000 deaths each year.

In previous work, Dr. Farrah Kheradmand, associate professor of medicine - pulmonary and immunology at BCM, and colleagues had shown that T-helper cells and some enzymes in the lung destroyed tissue in the lungs of emphysema patients. . . .

When the embargo lifts, this report will be available at http://stm.sciencemag.org/

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Nontypeable Haemophilus influenzae Clearance by Alveolar Macrophages Is Impaired by Exposure to Cigarette Smoke  

We showed that alveolar macrophages clear NTHI infections by adhesion, phagocytosis, and phagolysosomal processing of the pathogen. Bacterial uptake requires host actin polymerization, the integrity of plasma membrane lipid rafts, and activation of the phosphatidylinositol 3-kinase (PI3K) signaling cascade. Parallel to bacterial clearance, macrophages secrete tumor necrosis factor alpha (TNF-) upon NTHI infection. In contrast, exposure to cigarette smoke extract (CSE) impaired alveolar macrophage phagocytosis, although NTHI-induced TNF- secretion was not abrogated. Mechanistically, our data showed that CSE reduced PI3K signaling activation triggered by NTHI. Treatment of CSE-exposed cells with the glucocorticoid dexamethasone reduced the amount of TNF- secreted upon NTHI infection but did not compensate for CSE-dependent phagocytic impairment. The deleterious effect of cigarette smoke was observed in macrophage cell lines and in human alveolar macrophages obtained from smokers and from patients with chronic obstructive pulmonary disease.

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• Ciggie smoke 'weakens lungs' natural defense against harmful pathogen 

Exposure to cigarette smoke might weaken immune cells' ability to remove bacterial infections from the lungs, specifically nontypeable Haemophilus influenzae (NTHI), a pathogen often associated with respiratory infections and the progression of respiratory disease, says a new study.

NTHI has been found to cause invasive diseases such as meningitis, sinusitis, pneumonia, and bronchitis.

It is also the pathogen most frequently isolated in the respiratory tract of patients with chronic obstructive pulmonary disease (COPD) and chronic bronchitis.

Alveolar macrophages are part of the lungs'' innate defense system and they play an essential role in the clearance of bacterial infections.

The research team has found that cigarette smoke may disrupt the capability of alveolar macrophages to clear NTHI from the lungs. . . .

The study appears in journal Infection and Immunity.

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• Smoking Raises Arthritis Risk and Makes It Harder to Treat  

Smoking cigarettes can lead to the development of rheumatic diseases and make them harder to treat, according to three new studies presented this week at the 2009 annual meeting of the American College of Rheumatology in Philadelphia.

The first study focused on what happens when people with rheumatoid arthritis light up while being treated for the disease.

Researchers looked at the medical records of 1,756 rheumatoid arthritis (RA) patients in Sweden, determined their smoking history or lack thereof and then looked at their response to methotrexate or anti-TNF therapy - two common RA treatments. . . .

Mark Fisher, MD, MPH, a rheumatologist at Massachusetts General Hospital in Boston says he found this the most impressive study of the three. "There aren't any studies that show smoking has an effect on response to methotrexate and it was a really well done study. So for those reasons I think it's significant," Dr. Fisher says.

A second study found that smoking is associated with organ damage and disease activity in people with systemic lupus erythematosus, a chronic inflammatory disease that can affect the skin, joints, kidneys, lungs, nervous system and other organs.

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