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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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Risk Factors and Viruses Associated With Hospitalization Due to Lower Respiratory Tract Infections in Canadian Inuit Children: A Case-Control Study 

Conclusions: Smoking during pregnancy, place of residence, Inuit race, lack of breast-feeding, and overcrowding were all independently associated with increased risk of hospital admission for LRTI among Inuit children less than 2 years of age. Future research on the role of adoption and genetics on the health of Inuit children are required.

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Tobacco leading cause of rheumatism: Study 

PUNE: Among the 8,000 people surveyed in Pune city, about 10 per cent complained of one or the other kind of rheumatic pain. The data, which is part of an ongoing study, revealed that most of the people surveyed consumed tobacco in one form or the other.

"The study to measure burden of rheumatism on the Indian population at 17 cities/towns shows that at least 10-15 per cent of the population suffers from arthritis or some form of rheumatism. And the use of tobacco has emerged as a leading risk factor for rheumatic pains. This public health issue is yet to be recognised by the Indian medical faculty and community," said rheumatologist Arvind Chopra.

Chopra has combined his skills with that of the gram panchayat at Bhigwan village, where too 9,000 people were surveyed, to create an exemplary community model of rheumatic disease.

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Autoimmune condition, especially combined with smoking and oral contraceptive use, massively increases risk of stroke and heart attack in young women 

Autoimmune condition, especially combined with smoking and oral contraceptive use, massively increases risk of stroke and heart attack in young women

The autoimmune condition antiphospholipid syndrome mainly affects young women. An Article published Online First and in the November edition of the Lancet Neurology shows that women with a particular subtype of antibody called lupus anticoagulant (LA) have a more than 40-fold increased risk of stroke and 5-fold increased risk of heart attack compared with the general population (of young women). Smoking and oral contraceptive use increase the risk of these events even more. The Article is written by Dr Rolf Urbanus and Dr Philip de Groot, University Medical Centre Utrecht, Netherlands, together with colleagues from the Leiden University Medical Centre.

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Antiphospholipid antibodies and risk of myocardial infarction and ischaemic stroke in young women in the RATIO study: a case-control study 

Interpretation

Our results suggest that lupus anticoagulant is a major risk factor for arterial thrombotic events in young women, and the presence of other cardiovascular risk factors increases the risk even further.

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• Autoimmune Condition, Especially Combined With Smoking And Oral Contraceptive Use, Massively Increases Risk Of Stroke And Heart Attack In Young Women 

The autoimmune condition antiphospholipid syndrome mainly affects young women. An Article published Online First and in the November edition of The Lancet Neurology shows that women with a particular subtype of antibody called lupus anticoagulant (LA) have a more than 40-fold increased risk of stroke and 5-fold increased risk of heart attack compared with the general population (of young women). Smoking and oral contraceptive use increase the risk of these events even more. The Article is written by Dr Rolf Urbanus and Dr Philip de Groot, University Medical Centre Utrecht, Netherlands, together with colleagues from the Leiden University Medical Centre.

Antiphospholipid syndrome occurs when autoantibodies* bind to cell membranes, interfering with the regular clotting mechanism of the blood. Diagnosis occurs when young women (under 50 years) suffer a thrombotic event such as a stroke or heart attack, and antiphospholipid antibodies are tested. Although it is known that this condition causes thrombosis, bleeding, and repeat miscarriage in women, the extent of the increased risk for stroke and heart attack was unknown before this study. . . .

In an accompanying Reflection and Reaction, Dr Kathryn Kirchoff-Torres and Dr Steven R Levine, Stroke Center, Mount Sinai School of Medicine, New York, NY, USA, say that the most important aspect of the study is its conclusion that young women with LA need to be warned about the dangers of smoking and use of oral contraceptives.

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Second-hand smoke exposure in cars and respiratory health effects in children 

We examined potential associations of ever asthma, and symptoms of wheeze (past 12 months), hay fever, eczema and bronchitis (cough with phlegm) among school children exposed to second-hand smoke (SHS) in cars, using a modified Irish International Study of Asthma and Allergies in Childhood (ISAAC) protocol. . . .

Approximately one in seven Irish schoolchildren are exposed to SHS in cars and could have adverse respiratory health effects. Further studies are imperative to explore such associations across different population settings.

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• Passive smoking in cars linked to hayfever and wheezing in children 

Children who are regularly exposed to second-hand tobacco smoke when traveling by car have significantly higher rates of hayfever and wheezing than those without such exposure, results of an Irish study show.

Writing in the European Respiratory Journal, Luke Clancy, from the Tobacco Free Research Institute in Dublin, and team explain: “Children may be more vulnerable to second-hand smoke-induced respiratory diseases due to smaller airways and greater oxygen demand, as well as a less-mature immune system.”

But they add that “there is no evidence quantifying second-hand smoke-induced respiratory health effects in children exposed to second-hand smoke in cars.”

To address this, the team studied 2809 children, aged 13–14 years, selected randomly from schools throughout Ireland.

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