scholarly journals Maternal smoking during pregnancy and fractures in offspring: national register based sibling comparison study

BMJ ◽  
2020 ◽  
pp. l7057 ◽  
Author(s):  
Judith S Brand ◽  
Ayako Hiyoshi ◽  
Yang Cao ◽  
Deborah A Lawlor ◽  
Sven Cnattingius ◽  
...  

Abstract Objective To study the impact of maternal smoking during pregnancy on fractures in offspring during different developmental stages of life. Design National register based birth cohort study with a sibling comparison design. Setting Sweden. Participants 1 680 307 people born in Sweden between 1983 and 2000 to women who smoked (n=377 367, 22.5%) and did not smoke (n=1 302 940) in early pregnancy. Follow-up was until 31 December 2014. Main outcome measure Fractures by attained age up to 32 years. Results During a median follow-up of 21.1 years, 377 970 fractures were observed (the overall incidence rate for fracture standardised by calendar year of birth was 11.8 per 1000 person years). The association between maternal smoking during pregnancy and risk of fracture in offspring differed by attained age. Maternal smoking was associated with a higher rate of fractures in offspring before 1 year of age in the entire cohort (birth year standardised fracture rates in those exposed and unexposed to maternal smoking were 1.59 and 1.28 per 1000 person years, respectively). After adjustment for potential confounders the hazard ratio for maternal smoking compared with no smoking was 1.27 (95% confidence interval 1.12 to 1.45). This association followed a dose dependent pattern (compared with no smoking, hazard ratios for 1-9 cigarettes/day and ≥10 cigarettes/day were 1.20 (95% confidence interval 1.03 to 1.39) and 1.41 (1.18 to 1.69), respectively) and persisted in within-sibship comparisons although with wider confidence intervals (compared with no smoking, 1.58 (1.01 to 2.46)). Maternal smoking during pregnancy was also associated with an increased fracture incidence in offspring from age 5 to 32 years in whole cohort analyses, but these associations did not follow a dose dependent gradient. In within-sibship analyses, which controls for confounding by measured and unmeasured shared familial factors, corresponding point estimates were all close to null. Maternal smoking was not associated with risk of fracture in offspring between the ages of 1 and 5 years in any of the models. Conclusion Prenatal exposure to maternal smoking is associated with an increased rate of fracture during the first year of life but does not seem to have a long lasting biological influence on fractures later in childhood and up to early adulthood.

2006 ◽  
Vol 155 (2) ◽  
pp. 347-354 ◽  
Author(s):  
K B Lundin ◽  
Y L Giwercman ◽  
L Rylander ◽  
L Hagmar ◽  
A Giwercman

Background: The human androgen receptor (AR) gene contains two polymorphisms of CAG and GGN repeats respectively. The GGN repeat function is still largely unknown and to date there are no in vivo data on this segment with respect to the general population. Methods: We investigated the impact of CAG and GGN repeats on male reproductive function, one by one and in interaction with each other, in 220 adolescent men from the general Swedish population. Physical examination and semen analysis, including accessory sex gland markers and measurement of reproductive hormone levels, were performed. Lifestyle-associated factors, including maternal smoking during pregnancy, were recorded. GGN and CAG repeat lengths were determined by sequencing. Results: GGN<23 was associated with lower semen volume when compared to GGN=23 (mean difference −0.6 ml, P=0.02) and GGN>23 (mean difference −0.9 ml, P=0.002). Men with GGN<23, exposed to maternal smoking during pregnancy, had higher body mass index compared to men with other GGN lengths, no matter whether their mother had smoked or not during pregnancy (mean difference 4.8 kg/m2, P<0.001). Conclusions: Short GGN repeats seem to be associated with decreased semen volume, possibly due to suboptimal AR activity. Body composition may be influenced by the combination of fetal exposure to maternal smoking and certain AR genotypes.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tadashi Shiohama ◽  
Aya Hisada ◽  
Midori Yamamoto ◽  
Kenichi Sakurai ◽  
Rieko Takatani ◽  
...  

AbstractMaternal tobacco smoke exposure during pregnancy impairs fetal body size, including head circumference (HC) at birth; however, the mechanism still remains unclear. This analysis using a large prospective cohort study evaluated the impact of maternal tobacco exposure on their offspring’s HC and the relationship with placental weight ratio (PWR) and placental abnormalities. Parents-children pairs (n = 84,856) were included from the 104,065 records of the Japan Environmental and Children’s Study. Maternal perinatal clinical and social information by self-administered questionnaires, offspring’s body size, and placental information were collected. Data were analyzed with binominal logistic regression analysis and path analysis. Logistic regression showed significantly elevated adjusted odds ratio (aOR) (1.653, 95% CI 1.387–1.969) for the impact of maternal smoking during pregnancy on their offspring’s smaller HC at birth. Maternal exposure to environmental tobacco smoke in the non-smoking group did not increase aOR for the smaller HC. Path analysis showed that maternal smoking during pregnancy decreased the offspring’s HC directly, but not indirectly via PWR or placental abnormalities. The quitting smoking during pregnancy group did not increase aOR for the smaller HC than the non-smoking group, suggesting that quitting smoking may reduce their offspring’s neurological impairment even after pregnancy.


PEDIATRICS ◽  
1996 ◽  
Vol 97 (4) ◽  
pp. 547-553
Author(s):  
Carolyn D. Drews ◽  
Catherine C. Murphy ◽  
Marshalyn Yeargin-Allsopp ◽  
Pierre Decouflé

Objectives. Smoking has been linked to small cognitive, achievement, and behavioral deficits but has not been associated with more severe cognitive impairments. This investigation evaluated the relationship between maternal smoking during pregnancy and idiopathic mental retardation (MR). Methods. Data on maternal smoking during pregnancy were obtained during face-to-face interviews with the mothers of 221 children with idiopathic MR and the mothers of 400 children attending public school. All children had been born in the five-county metropolitan Atlanta area in 1975 or 1976 and were living in the area when they were 10 years of age. We used exposure odds ratios (ORs) to assess the relationship between maternal smoking and MR, controlling for sex, maternal age at delivery, race, maternal education, economic status, parity, and alcohol use. Results. Maternal smoking during pregnancy was associated with slightly more than a 50% increase in the prevalence of idiopathic MR (adjusted OR, 1.6; 95% confidence interval, 1.0-2.4), and children whose mothers smoked at least one pack a day during pregnancy had more than a 75% increase in the occurrence of idiopathic MR (OR, 1.9;95% confidence interval, 1.0-3.4). This increase was neither accounted for by other sociodemographic risk factors for MR nor explained by an increase in the prevalence of low birth weight among the children of smokers. Conclusions. Our data suggest that maternal smoking may be a preventable cause of mental retardation.


2012 ◽  
Vol 27 (12) ◽  
pp. 3593-3600 ◽  
Author(s):  
A. Ernst ◽  
S.L. Kristensen ◽  
G. Toft ◽  
A.M. Thulstrup ◽  
L.B. Håkonsen ◽  
...  

2019 ◽  
Vol 22 (8) ◽  
pp. 1330-1338 ◽  
Author(s):  
Mikael O Ekblad ◽  
Emily Rolan ◽  
Kristine Marceau ◽  
Rohan Palmer ◽  
Alexandre Todorov ◽  
...  

Abstract Introduction Maternal smoking during pregnancy (SDP) is associated with disruptive behavior. However, there is debate whether the SDP-disruptive behavior association is a potentially causal pathway or rather a spurious effect confounded by shared genetic and environmental factors. Aims and Methods The Missouri Mothers and Their Children Study is a sibling comparison study that includes families (n = 173) selected for sibling pairs (aged 7–16 years) discordant for SDP. Critically, the sibling comparison design is used to disentangle the effects of SDP from familial confounds on disruptive behavior. An SDP severity score was created for each child using a combination of SDP indicators (timing, duration, and amount of SDP). Multiple informants (parents and teachers) reported on disruptive behavior (i.e., DSM-IV semi-structured interview, the Child Behavior Checklist, and Teacher Report Form). Results The variability in disruptive behavior was primarily a function of within-family differences (66%–100%). Consistent with prior genetically informed approaches, the SDP–disruptive behavior association was primarily explained by familial confounds (genetic and environmental). However, when using a multi-rater approach (parents and teachers), results suggest a potentially causal effect of SDP on disruptive behavior (b = 0.09, SE = 0.04, p = 0.03). The potentially causal effect of SDP remained significant in sensitivity analyses. Discussion These findings suggest that familial confounding likely plays a complex role in the SDP–disruptive behavior association when examining both parent and teacher reports of behavior. Importantly, the current study highlights the importance of multiple raters, reflecting a more comprehensive measure of complex behaviors (e.g., disruptive behavior) to examine the teratogenic effects of SDP. Implications Our study provides additional evidence that controlling for genetic and family factors is essential when examining the effect of SDP on later behavioral problems, as it explains a portion of the association between SDP and later behavioral problems. However, we found a significant association between SDP and disruptive behavior when using a multi-rater approach that capitalizes on both parent and teacher report, suggesting that parent and teacher ratings capture a unique perspective that is important to consider when examining SDP–behavior associations.


2005 ◽  
Vol 35 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Aimin Chen ◽  
Michael L Pennell ◽  
Mark A Klebanoff ◽  
Walter J Rogan ◽  
Matthew P Longnecker

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