Sooyong Kim1, Arielle Selya2, Lauren S Wakschlag3, Lisa Dierker4, Jennifer S Rose4, Don Hedeker5, Robin J Mermelstein6. 1. Behavioral Sciences Group, Sanford Research, Sioux Falls, SD, United States; PinneyAssociates, Inc., Pittsburgh, PA, United States. 2. Behavioral Sciences Group, Sanford Research, Sioux Falls, SD, United States; PinneyAssociates, Inc., Pittsburgh, PA, United States; Department of Pediatrics, University of South Dakota Sanford School of Medicine, Sioux Falls, SD, United States. Electronic address: Arielle.Selya@SanfordHealth.org. 3. Department of Medical Social Sciences, Feinberg School of Medicine and Institute for Innovations in Developmental Sciences, Northwestern University Chicago, IL, United States. 4. Department of Psychology, Wesleyan University, Middletown, CT, United States. 5. Department of Public Health Sciences, University of Chicago, Chicago, IL, United States. 6. Institute for Health Research and Policy, University of Illinois-Chicago, Chicago, IL, United States.
Abstract
INTRODUCTION: Maternal smoking is a well-known risk factor for youth smoking, yet whether this relationship is causal remains unresolved. This study utilizes propensity score methods for causal inference to robustly account for shared risk factors between maternal and offspring smoking. METHODS: An 8-year longitudinal cohort of 900 adolescents in the Chicago area were followed starting from approximately age 15.6. The effects of maternal lifetime smoking (MLS) and prenatal tobacco exposure (PTE) (among participants reporting MLS) on offspring's past 30-day smoking, daily smoking status and smoking frequency were examined using logistic regression and Poisson regression after nearest-neighbor propensity matching. Age dependency of this relationship was then examined across the age range of 15-25 using time-varying effect modeling. RESULTS: Propensity matching yielded 438 and 132 pairs for MLS and PTE study samples, respectively. MLS demonstrated significant associations with past 30-day smoking (RR 1.09; 95% CI 1.04-1.14), daily smoking (RR 1.08; 95% CI 1.05-1.12), and smoking frequency of offspring (RR 1.32; 95% CI 1.15-1.52), with stable effects across age. Among participants reporting MLS, having PTE showed significant additional effects on daily smoking (RR 1.09; 95% CI 1.02-1.17) and age-dependency that showed significance during young adulthood but not adolescence. CONCLUSION: The relationship between maternal and offspring smoking was not fully accounted for by shared risk factors, suggesting possible causation with PTE having a delayed effect across age. Targeted prevention efforts should be made on maternal smoking-exposed adolescents to mitigate their risks of developing heavy smoking habits in adulthood.
INTRODUCTION: Maternal smoking is a well-known risk factor for youth smoking, yet whether this relationship is causal remains unresolved. This study utilizes propensity score methods for causal inference to robustly account for shared risk factors between maternal and offspring smoking. METHODS: An 8-year longitudinal cohort of 900 adolescents in the Chicago area were followed starting from approximately age 15.6. The effects of maternal lifetime smoking (MLS) and prenatal tobacco exposure (PTE) (among participants reporting MLS) on offspring's past 30-day smoking, daily smoking status and smoking frequency were examined using logistic regression and Poisson regression after nearest-neighbor propensity matching. Age dependency of this relationship was then examined across the age range of 15-25 using time-varying effect modeling. RESULTS: Propensity matching yielded 438 and 132 pairs for MLS and PTE study samples, respectively. MLS demonstrated significant associations with past 30-day smoking (RR 1.09; 95% CI 1.04-1.14), daily smoking (RR 1.08; 95% CI 1.05-1.12), and smoking frequency of offspring (RR 1.32; 95% CI 1.15-1.52), with stable effects across age. Among participants reporting MLS, having PTE showed significant additional effects on daily smoking (RR 1.09; 95% CI 1.02-1.17) and age-dependency that showed significance during young adulthood but not adolescence. CONCLUSION: The relationship between maternal and offspring smoking was not fully accounted for by shared risk factors, suggesting possible causation with PTE having a delayed effect across age. Targeted prevention efforts should be made on maternal smoking-exposed adolescents to mitigate their risks of developing heavy smoking habits in adulthood.
Authors: Allison N Kurti; Ryan Redner; Alexa A Lopez; Diana R Keith; Andrea C Villanti; Cassandra A Stanton; Diann E Gaalema; Janice Y Bunn; Nathan J Doogan; Antonio Cepeda-Benito; Megan E Roberts; Julie Phillips; Stephen T Higgins Journal: Prev Med Date: 2017-08-05 Impact factor: 4.018