Childhood secondhand smoke exposure linked to increased adult rheumatoid arthritis risk
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Parental smoking during childhood is potentially associated with seropositive rheumatoid arthritis later in life, according to data published in Arthritis & Rheumatology.
“There has been intense interest in mucosal lung inflammation as a site of initiation of rheumatoid arthritis,” Jeffrey A. Sparks, MD, MMSc, of Brigham and Women’s Hospital and Harvard Medical School, in Boston, told Healio Rheumatology. “Smoking is the best-established RA risk factor, but many RA patients are non-smokers.”
To analyze the link between passive smoking exposure throughout life and the risk for RA, while accounting for personal smoking, Sparks and colleagues studied data from the Nurses’ Health Study II (NHSII) prospective cohort. According to the researchers, NHSII enrolled a total of 116,429 female nurses aged 25 to 42 years in 1989, and has prospectively followed up every 2 years through mailed questionnaires. Survey questions collect data on sociodemographics, anthropometrics, behaviors, medications, dietary intake and health conditions, with follow-up rates are reportedly greater than 90%.
For their own study, Sparks and colleagues excluded participants who self-reported prevalent RA or connective tissue diseases prior to the 1989 baseline questionnaire, as well as those missing childhood parental smoking data. This resulted in a study population of 90,923. The researchers examined maternal smoking during pregnancy, childhood parental smoking and the number years lived with smokers since the age 18 years among these participants. They determined cases of RA and serostatus by reviewing medical records.
In their analysis, Sparks and colleagues used a marginal structural model framework to estimate the controlled direct impact of each type of passive smoking exposure on adulthood RA risk by serologic phenotype, controlling for early-life and time-updated adult factors, such as personal smoking.
According to the researchers, there were 532 cases of RA — 66% seropositive — during a median 27.7 years of follow-up. Maternal smoking during pregnancy was associated with RA after confounding adjustment (HR = 1.25; 95% CI, 1.03-1.52), but not after accounting for subsequent smoking exposures. Meanwhile, childhood parental smoking was associated with seropositive RA after adjusting for confounders (HR = 1.41; 95% CI, 1.08-1.83).
After controlling for adult personal smoking in the controlled direct-effect analyses, childhood parental smoking remained associated with seropositive RA (HR = 1.75; 95% CI, 1.03-2.98). This associated was accentuated among ever smokers (HR = 2.18; 95% CI, 1.23-3.88). There was no significant association of adult passive smoking with RA, with a hazard ratio of 1.3 (95% CI, 0.97-1.74) for an individual with 20 or more years lived as a smoker, compared with 0 years.
“We found that parental smoking during childhood was associated with RA occurring in adulthood,” Sparks said. “The association was specific to seropositive RA and was not explained by personal smoking that occurred later in life. This study adds to the paradigm of mucosal inflammation of the lung as a potential initiating site for RA. Early life exposures such as passive smoking may predispose people to developing RA, and perhaps other autoimmune diseases.”
The lead author of the study, Kazuki Yoshida, MD, ScD, also of Brigham and Women’s Hospital and Harvard Medical School, added that the future development of RA was just one of many dangers associated with passive exposure to smoking during childhood.
“The prevention of childhood passive smoking is of paramount importance,” Yoshida told Healio Rheumatology. “Our advanced statistical modeling suggests a long-term immunological impact of passive smoking in addition to its known behavioral consequence: Increased smoking uptake.”
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