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Objective: Parental smoking and residential secondhand tobacco smoke exposure in the perinatal period and childhood has been associated with risk for asthma and reduced lung function in adolescence (Dia et al., 2017; Milanzi et al., 2020). Among adults, forced expiratory volume in one second (FEV1) has been found to be moderately heritable (.55-.65; e.g., Ingebrigtsen et al., 2011; Sillanpää et al., 2017; Tian et al., 2017); less is known about the heritability of FEV1 in childhood. The extent to which caregiver smoking behaviors impacts the genetic and environmental influences on lung function in childhood is largely unknown. The current study examined if past caregiver smoking behaviors moderated the heritability of lung function (assessed by FEV1) among twins in middle childhood.
Methods: Participants included 485 twin children (48.9% female; 60.1% non-Hispanic White, 28.8% Hispanic) and their caregivers (244 families; 29.7% MZ, 36.5% same-sex DZ, 33.8% opposite-sex DZ) from an ongoing, longitudinal twin study. When the twins were approximately eight years (M=8.33 SD=0.62), both the primary and secondary (if applicable, 62.7%) caregivers completed a series of questionnaires including the Global Adult Tobacco Survey (Global Adult Tobacco Survey Collaborative Group, 2010). This questionnaire included an item assessing if they ever smoked in the past, during the twins’ lives. A year later, twins completed a lung function assessment (M=9.36, SD=0.74). Three maneuvers were completed with digital peak flow meters that yielded estimates of FEV1. The highest value from the three maneuvers was retained. A mean composite of primary and secondary caregivers’ past smoking behaviors was calculated for analyses. Child sex, age, height, and waist circumference were regressed out from FEV1 values prior to analyses.
Results: Approximately 23% of families had at least one caregiver that reported past smoking behaviors (daily or less than daily). Univariate ACE models indicated that child lung function assessed by FEV1 was highly heritable (74%). As indicated by a significant worsening of fit when comparing the full moderated model to the non-moderated model, we found that past caregiver smoking moderated the heritability of FEV1. Specifically, caregiver past smoking moderated the unique environmental influence (E) on FEV1, such that there were less unique environmental influences at increased levels of smoking behaviors (Δ-2LL=1.159, Δdf=2, p=0.56).
Conclusions: Findings indicate that caregivers’ past smoking behaviors moderated the heritability of FEV1 in twins in middle childhood. At greater reports of caregiver smoking in the past, the unique environmental influences on FEV1 decreased. Given that FEV1 is primarily influenced by genetic and unique environmental factors at this age, this allows for greater genetic influences when there are higher endorsements of past smoking. Findings are consistent with the diathesis-stress model, where genetic influences are more prominent in ‘riskier’ environments. This study highlights the importance of prior smoking behaviors on children’s lung function and suggests the need to focus on smoking cessation among caregivers.