Childhood exposure to passive smoking and bone health in adulthood. The Cardiovascular Risk in Young Finns Study.

Context: Passive smoke exposure has been linked with the risk of osteoporosis in adults.

Objective: We aimed to examine the independent effects of exposure to passive smoking in childhood on adult bone health.

Design/Setting: Longitudinal, the Cardiovascular Risk in Young Finns Study.

Participants: Study cohort included 1422 individuals followed up for 28 years since baseline in 1980 (age 3-18 years). Exposure to passive smoking was determined in childhood. In adulthood, peripheral bone traits were assessed with quantitative computed tomography (pQCT) at the tibia and radius, and calcaneal mineral density was estimated with quantitative ultrasound. Fracture data was gathered by questionnaires.

Results: Parental smoking in childhood was associated with lower pQCT derived bone sum index in adulthood (β±SE -0.064±0.023 per smoking parent, P=0.004) in multivariate models adjusted for age, sex, active smoking, BMI, serum 25-OH vitamin D concentration, physical activity, and parental socioeconomic position. Similarly, parental smoking was associated with lower heel ultrasound estimated bone mineral density in adulthood (β±SE -0.097±0.041 per smoking parent, P=0.02). Parental smoking was also associated with the incidence of low-energy fractures (odds ratio 1.28, 95% confidence interval 1.01-1.62). Individuals with elevated cotinine levels (3-20 ng/ml) in childhood had lower bone sum index with pQCT (β±SE -0.206±0.057, P=0.0003). Children whose parents smoked and had high cotinine levels (3-20 ng/ml) had significantly lower pQCT derived bone sum index compared to those with smoking parents but low cotinine levels (<3ng/ml) (β±SE -0.192±0.072, P=0.008).

Conclusions and relevance: Children of parents who smoke have evidence of impaired bone health in adulthood.