biostudies-literatureYoshida KNational Institute of Arthritis and Musculoskeletal and Skin DiseasesRheumatology Research FoundationNHLBI NIH HHSNational Heart, Lung, and Blood InstituteNational Institute of HealthNHGRI NIH HHSNational Cancer InstituteNCI NIH HHSNIAMS NIH HHSNIH HHS2219-2228https://www.ebi.ac.uk/biostudies/studies/S-EPMC8976916biostudies-literatureUnknown73(12)<h4>Objective</h4>To investigate passive smoking throughout the life course and the risk of rheumatoid arthritis (RA), while accounting for personal smoking.<h4>Methods</h4>We analyzed the Nurses' Health Study II prospective cohort, using information collected via biennial questionnaires. We assessed the influence of 1) maternal smoking during pregnancy (in utero exposure), 2) childhood parental smoking, and 3) years lived with smokers since age 18. Incident RA and serostatus were determined by medical record review. Using the marginal structural model framework, we estimated the controlled direct effect of each passive smoking exposure on adult incident RA risk by serologic phenotype, controlling for early-life factors and time-updated adulthood factors including personal smoking.<h4>Results</h4>Among 90,923 women, we identified 532 incident RA cases (66% seropositive) during a median of 27.7 years of follow-up. Maternal smoking during pregnancy was associated with RA after adjustment for confounders, with a hazard ratio (HR) of 1.25 (95% confidence interval [95% CI] 1.03-1.52), but not after accounting for subsequent smoking exposures. Childhood parental smoking was associated with seropositive RA after adjustment for confounders (HR 1.41 [95% CI 1.08-1.83]). In the controlled direct effect analyses, childhood parental smoking was associated with seropositive RA (HR 1.75 [95% CI 1.03-2.98]) after controlling for adulthood personal smoking, and the association was accentuated among ever smokers (HR 2.18 [95% CI 1.23-3.88]). There was no significant association of adulthood passive smoking with RA (HR 1.30 for ≥20 years of living with a smoker versus none [95% CI 0.97-1.74]).<h4>Conclusion</h4>We found a potential direct influence of childhood parental smoking on adult-onset incident seropositive RA even after controlling for adulthood personal smoking.Arthritis & rheumatology (Hoboken, N.J.)Passive Smoking Throughout the Life Course and the Risk of Incident Rheumatoid Arthritis in Adulthood Among Women.PMC89769161OT2OD026553R01 AR119246P30 AR069625K23 AR069688U01 CA176726L30 AR066953R01 AR049880K24 AR052403R01 CA067262OT2 OD026553R03 AR075886K23 AR076453R01 HL034594U01 HG008685P30 AR072577U01 HL145386R01 AR057327P30 AR070253UM1 CA186107Sparks JACostenbader KHMarchand NPrisco LCKarlson EWMartin LWWang JMalspeis SYoshida KFord JALu BfalsePassive Smoking Throughout the Life Course and the Risk of Incident Rheumatoid Arthritis in Adulthood Among Women.<h4>Objective</h4>To investigate passive smoking throughout the life course and the risk of rheumatoid arthritis (RA), while accounting for personal smoking.<h4>Methods</h4>We analyzed the Nurses' Health Study II prospective cohort, using information collected via biennial questionnaires. We assessed the influence of 1) maternal smoking during pregnancy (in utero exposure), 2) childhood parental smoking, and 3) years lived with smokers since age 18. Incident RA and serostatus were determined by medical record review. Using the marginal structural model framework, we estimated the controlled direct effect of each passive smoking exposure on adult incident RA risk by serologic phenotype, controlling for early-life factors and time-updated adulthood factors including personal smoking.<h4>Results</h4>Among 90,923 women, we identified 532 incident RA cases (66% seropositive) during a median of 27.7 years of follow-up. Maternal smoking during pregnancy was associated with RA after adjustment for confounders, with a hazard ratio (HR) of 1.25 (95% confidence interval [95% CI] 1.03-1.52), but not after accounting for subsequent smoking exposures. Childhood parental smoking was associated with seropositive RA after adjustment for confounders (HR 1.41 [95% CI 1.08-1.83]). In the controlled direct effect analyses, childhood parental smoking was associated with seropositive RA (HR 1.75 [95% CI 1.03-2.98]) after controlling for adulthood personal smoking, and the association was accentuated among ever smokers (HR 2.18 [95% CI 1.23-3.88]). There was no significant association of adulthood passive smoking with RA (HR 1.30 for ≥20 years of living with a smoker versus none [95% CI 0.97-1.74]).<h4>Conclusion</h4>We found a potential direct influence of childhood parental smoking on adult-onset incident seropositive RA even after controlling for adulthood personal smoking.2021-01-01T00:00:00Z2021 Dec2025-04-05T09:43:24.445Z2025-04-05T09:43:24.445ZS-EPMC89769163440670910.1002/art.41939