Chronic smoke exposure induces rheumatoid factor and anti-heat shock protein 70 autoantibodies in susceptible mice and humans with lung disease.

The impact of cigarette smoke (CS), a risk factor for rheumatoid arthritis (RA), on sauto-antibody production was studied in humans and mice with and without chronic lung disease (LD). Rheumatoid factor (RF), anti-cyclic citrullinated peptides (CCPs), and anti-HSP70 autoantibodies were measured in several mouse strains and in cohorts of smokers and nonsmokers with and without autoimmune disease. Chronic smoking-induced RFs in AKR/J mice, which are most susceptible to LD. RFs were identified in human smokers, preferentially in those with LD. Anti-HSP70 auto-antibodies were identified in CS-exposed AKR/J mice but not in ambient air exposed AKR/J controls. Whereas inflammation could induce anti-HSP70 IgM, smoke exposure promoted the switch to anti-HSP70 IgG autoantibodies. Elevated anti-CCP autoantibodies were not detected in CS-exposed mice or smokers. AKR/J splenocytes stimulated in vitro by immune complexes (ICs) of HSP70/anti-HSP70 antibodies produced RFs. The CD91 scavenger pathway was required as anti-CD91 blocked the HSP70-IC-induced RF response. Blocking Toll-like receptors did not influence the HSP70-IC-induced RFs. These studies identify both anti-HSP70 and RFs as serological markers of smoke-related LD in humans and mice. Identification of these autoantibodies could suggest a common environmental insult, namely CS, in a number of different disease settings.

Correlates of former smoking in patients with cerebrovascular disease: a cross-sectional study.

OBJECTIVE: To identify multilevel correlates of former smoking in patients with cerebrovascular disease. DESIGN: Secondary data analysis of the Canadian Community Health Survey. METHODS: We used data from the 2007-2008 Canadian Community Health Survey (CCHS). Smoking status (former smoking vs smoker) was described by multilevel correlates of former smoking. A multilevel approach for variable selection for this study was used to understand how multiple levels in society can have an impact on former smoking. The study sample was selected from those respondents of the CCHS that reported they suffered from stroke symptoms. Logistic regression was used to predict former smoking in patients with cerebrovascular disease while controlling for multilevel confounders. Proportions were weighted to reflect the Canadian population. RESULTS: There were 172 355 respondents who reported to suffer from stroke. From this sample, 36.5% were smokers and 63.5% were former smokers. Age groups 55-69 and 70-80 and higher education (secondary education +) were positively related to former smoking. Household and vehicle smoking restrictions significantly predicted former smoking. Counselling advice from a physician and having access to a general practitioner were correlates of former smoking. Finally, the use of buproprion was positively related to former smoking. CONCLUSIONS: There are multilevel correlates of former smoking in smokers with reported stroke symptoms. These correlates include older age groups, higher education, household and vehicle smoking restrictions, pharmacotherapy use (bupropion), access to a general practitioner and counselling advice from a physician.