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Passive tobacco exposure early in life linked to heightened RA risk in women

Jairia Dela Cruz
06 Sep 2018

Passive exposure to tobacco in childhood contributes to an increased risk of developing rheumatoid arthritis (RA) in women, a study suggests.

Therefore, it is important to protect children from any environmental tobacco smoke exposure, especially those with a family history of RA, the investigators said. Also, parents should be aware of the risk and ensure that their children avoid passive exposure at home.

The study included 71,248 women (mean age 49.5 years) from the French E3N cohort, among whom 371 developed RA during a mean follow-up of 23.8 years. Among RA patients, 172 (46.4 percent) reported that they were never smokers during baseline evaluation, 69 (18.6 percent) were current smokers and 130 (35.0 percent) were previous smokers.

Age-adjusted Cox proportional hazards models showed that compared with never smokers, current and previous smokers had an elevated risk of developing RA (adjusted hazard ratios [aHRs], 1.54; 95 percent CI, 1.10–2.14 and 1.31; 1.05–1.63, respectively). Notably, additional exposure to tobacco early in life, through passive smoking, further increased the risk of RA. [Rheumatology 2018;doi:10.1093/rheumatology/key219]

Childhood passive smoking was associated with a significant risk increase among ever-smokers (current and previous; aHR, 1.67; 1.17–2.39) and a borderline increase among those who were never smokers (aHR, 1.43; 0.97–2.11) relative to never-exposed women. The HR for incident RA in ever-smokers not exposed to passive smoking during childhood was 1.38 (1.10–1.74).

Finally, RA occurred earlier in ever-smokers with childhood passive smoking exposure (mean age, 60.2 years). In contrast, mean age at RA onset was 64.1 years in the never-exposed group.

“Our findings perfectly fit with the preclinical scheme of RA where an external event occurs at an early stage to promote emergence of autoimmunity, followed years after by clinical RA,” the investigators noted. “Indeed, in our study, passive exposure to smoking during adulthood only was not associated with any increase in RA risk either in smokers or in nonsmokers.”

Tobacco induces protein citrullination in lung alveoli, where immunity against citrullinated antigens may be triggered in individuals carrying certain HLA (human leukocyte antigen) genotypes, as reported in previous studies. [Arthritis Rheum 2006;54:38-46; Arthritis Res Ther 2012;14:R89]

“In favour of the hypothesis that the priming of autoimmunity occurs in the lungs, it has been shown that other kinds of exposure to tobacco (ie, nonairway exposure such as moist snuff) is not associated with an increased risk of RA. However, maternal exposure during pregnancy has been found to be associated with an increased risk of RA. This observation emphasizes the fact that very early exposure to tobacco might have an influence on future development of RA,” the investigators pointed out.

Despite its strengths, the study has several limitations. First, the diagnoses of RA were self-reported, and misdiagnoses could not be excluded. Also, study was not able to analyse a potential gene–environment interaction or to separately examine ACPA-positive vs -negative RA.

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