Parental smoking during pregnancy and offspring bone mass at age 10 years: findings from a prospective birth cohort.
We investigated an intrauterine influence of maternal smoking during pregnancy on childhood bone mass. Daughters, but not sons, of mothers who smoked had higher bone mass at age 10years. This appears to be due to familial factors related to parental smoking influencing increased offspring adiposity rather than a direct intrauterine effect.


BACKGROUND
Neonatal studies have demonstrated an adverse relationship between maternal smoking in pregnancy and foetal bone mineral accrual. We aimed to investigate an intrauterine influence of maternal smoking during pregnancy on offspring bone mass at mean age 9.9 years.


METHODS
We compared associations of maternal and paternal smoking in pregnancy with offspring total body less head (TBLH) and spine bone mineral content (BMC), bone area (BA), bone mineral density (BMD) and area-adjusted BMC (ABMC) in 7,121 children in the Avon Longitudinal Study of Parents and Children.


RESULTS
Maternal smoking in any trimester was associated with increased TBLH BMC, BA and BMD in girls (mean difference [95% CI] (sex-specific SD scores), 0.13 [0.05-0.22], 0.13 [0.04-0.21], 0.13 [0.04-0.22], respectively) but not boys (0.01 [-0.07-0.09], 0.00 [-0.08-0.08], 0.04 [-0.05-0.12]), and also with spine BMC, BA and BMD in girls (0.13 [0.03-0.23], 0.12 [0.03-0.22], 0.10 [0.00-0.21]) but not boys (0.03 [-0.06-0.12], 0.00 [-0.09-0.09], 0.05 [-0.04-0.14]), but not with ABMC. Paternal smoking associations were similar, with no statistical evidence for a difference between maternal and paternal effects. Maternal associations increased on adjustment for offspring birth weight and gestational age, but attenuated to the null after adjustment for current height and weight.


CONCLUSIONS
We found little evidence that maternal smoking was related to bone mass in boys. In girls, maternal smoking associations were similar to those of paternal smoking, suggesting that these were attributable to shared familial characteristics, not intrauterine mechanisms.
Macdonald-Wallis
C
C
MRC Centre for Causal Analyses in Translational Epidemiology, Department of Social Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK. C.Macdonald-Wallis@bristol.ac.uk
Tobias
J H
JH
Davey Smith
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G
Lawlor
D A
DA
D015502:Absorptiometry, Photon / Q000379:methods; D015519:Bone Density / Q000502:physiology*; D002648:Child; D004522:Educational Status; D004739:England / Q000453:epidemiology; D005220:Fathers / Q000523:psychology; D005260:Female; D006801:Humans; D008297:Male; D009035:Mothers / Q000523:psychology; D010290:Parents / Q000523:psychology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology*; D011446:Prospective Studies; D012737:Sex Factors; D012907:Smoking / Q000453:epidemiology*; D012923:Social Class