Smoking, Use of Moist Snuff, and Risk of Chronic Inflammatory Diseases

Carlens, Cecilia; Hergens, Maria-Pia; Grünewald, Johan; Ekbom, Anders; Eklúnd, Anders; Höglund, Caroline Olgart; Askling, Johan

doi:10.1164/rccm.200909-1338oc

Cited by 178 publications

(135 citation statements)

References 51 publications

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“…It does, however, carry the risk of exposure to nicotine, heavy metals, and contaminating microorganisms and their products, with the levels of blood and urine nicotine/cotinine being comparable to those of smokers [81][82][83][84][85]. Although studies to date are somewhat limited, those that have been reported did not, however, detect an association between usage of snuff and risk of development of either ACPApositive or ACPA-negative RA, or for increased disease severity [86][87][88]. All of these studies were performed in Sweden and involved users of orally-applied moist snuff.…”

Section: Smokeless Tobacco (Snuff)mentioning

confidence: 97%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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Smoking is now well recognised not only as a risk factor for rheumatoid arthritis (RA), but also as a determinant of disease activity, severity, response to therapy, and possibly mortality. Recent studies have provided significant insights into the molecular and cellular mechanisms which underpin the pathogenesis of smokingrelated RA. These involve release of the enzymes, peptidylarginine deiminases (PADs) 2 and 4 from smoke-activated, resident and infiltrating pulmonary phagocytes. PADs, in turn, mediate the conversion of various endogenous proteins to putative citrullinated autoantigens. In genetically susceptible individuals, these autoantigens trigger the production of anti-citrullinated peptide/protein pathogenic autoantibodies (ACPA), an event which precedes the development of RA. This review is focused primarily on smoking-mediated harmful chronic inflammatory responses, both local and systemic, which promote the formation of ACPA, as well as the possible involvement of other types of outdoor and indoor pollution in the pathogenesis of RA. This is preceded by a brief overview of the evidence implicating smoking as a risk factor for development of ACPA-positive RA.Keywords: Anti-citrullinated peptide/protein antibodies; airway microbiota; atmospheric pollution; heavy metals; peptidylarginine deiminases; smoking cessation strategies. ImplicationsChronic inflammatory mechanisms operative in the lungs of smokers lead to the production of anti-citrullinated protein antibodies which, in turn, drive the development of rheumatoid arthritis. These mechanistic insights not only reinforce the association between smoking and risk for rheumatoid arthritis, but also the necessity to increase the level of awareness in those at highest risk.

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Section: Smokeless Tobacco (Snuff)mentioning

confidence: 97%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

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“…The biological mechanisms that would link smoking to the pathogenesis MS are elusive. Nicotine, however, might not be the sole culprit since studies have shown that use of tobacco snuff does not increase the risk of MS [83,84].…”

Section: Smokingmentioning

confidence: 99%

Environmental triggers of multiple sclerosis

Kakalacheva

Lünemann

2011

FEBS Letters

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a b s t r a c tMultiple sclerosis is a chronic immune-mediated disease of the central nervous system that develops in young adults with a complex genetic predisposition. Similar to other autoimmune disease, HLA-DR and -DQ alleles within the HLA class II region on chromosome 6p21 are by far the strongest risk-conferring genes. Less robust susceptibility effects have been reported for non-MHC related genetic variants. Improvements in the design of epidemiological studies helped to identify consistent environmental risk-associations such as the increased susceptibility for MS in individuals with a history of infectious mononucleosis, a symptomatic primary infection with the human c-herpesvirus Epstein-Barr virus (EBV). Sun exposure and serum vitamin D levels are emerging non-infectious environmental risk factors that may have independent roles. The analysis of environmental effects will likely expand in the next few years and will allow for the generation of testable hypotheses as to how environmental insults interact with genetic factors to jointly determine the susceptibility to MS. Insights gained from these studies might facilitate the development of prevention strategies and more effective treatments for MS.

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“…It is thus possible to assume that smoking plays a role in the development of NC, even when smoking appears to cause multiple sclerosis in other ways than through the mediation of nicotine (Carlens et al, 2010).…”

Section: )mentioning

confidence: 99%

“…Some studies report that NC is associated with higher levels of impulsiveness and the so-called sensation-seeking behaviour in this condition (Dimitrova et al, 2011), which might explain increased tendency to smoke. Smoking is a risk factor for development and progression of multiple sclerosis (Carlens et al, 2010;Wingerchuk, 2012;Hedstrom et al, 2013) and other inflammatory diseases such as rheumatoid arthritis, Crohn's disease, ulcerative colitis, and…”

Section: Introductionmentioning

confidence: 99%

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

et al. 2016

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Narcolepsy-cataplexy (NC) is a chronic neurological disease with suggested autoimmune etiopathogenesis. Nicotine stimulates central nervous system and smoking increases the risk of autoimmune diseases. Assessment of smoking habits and its correlation to clinical parameters among 87 adult NC patients (38 male, 49 female) included night polysomnography and multiple sleep latency test. In our sample, 43.7% NC patients were regular smokers, and 19.5% former smokers compared to 22.2%, and 12.6%, respectively, in the general population. Patients started to smoke in the mean age of 20.0 (SD ±6.0) years. 72.2% of NC smokers started to smoke before the onset of NC and the mean of the delay between smoking onset and NC onset was 9.1 (±5. Report / Vol. 117 (2016) No. 2-3, p. 81-89 a direct correlation between smoking duration and the number of awakenings, duration of N1 sleep, REM sleep latency, and apnoea/hypopnoea index (AHI), and, on the contrary, indirect correlation between smoking duration and N3 sleep duration, showing that smoking duration consistently correlates with sleep macrostructure. Smoking is highly prevalent in NC and has relationship with clinical features of NC. 82) Prague Medical

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Smoking, Use of Moist Snuff, and Risk of Chronic Inflammatory Diseases

Abstract: Smokeless tobacco does not increase the risk of chronic inflammatory diseases, suggesting that inhaled nonnicotinic components of cigarette smoke are more important than nicotine itself in the etiology of these diseases.

Cited by 178 publications

References 51 publications

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Environmental triggers of multiple sclerosis

Smoking Prevalence and Its Clinical Correlations in Patients with Narcolepsy-cataplexy

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