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Parental smoking in childhood influences bone parameters in adulthood

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February 13, 2019

Children exposed to parental smoking are more likely to show evidence of impaired bone health in adulthood, including reduced bone mass, lower bone density and more low-energy fractures vs. adults not exposed to nicotine in childhood, according to findings from a longitudinal analysis.

Markus Juonala

Passive exposure to tobacco smoke in childhood may have long-term consequences on bone health,” Markus Juonala, MD, PhD, professor of internal medicine at the University of Turku, Finland, told Endocrine Today. “Every effort should be made to minimize children’s smoke exposure.”

Juonala and colleagues analyzed data from 1,422 participants from the Cardiovascular Risk in Young Finns Study, a cohort followed from childhood for 28 years beginning in 1980. Parents of participants self-reported smoking status at baseline. Researchers collected blood samples at baseline to measure serum cotinine; values between 3 ng/mL and 20 ng/mL in nonsmokers were considered indicative of positive, passive nicotine exposure. Researchers stratified participants into three groups according to level of nicotine exposure: no parental smoking and nondetectable cotinine level; parental smoking and nondetectable cotinine level (defined as hygienic smoking); and parental smoking and a detectable cotinine level (defined as nonhygienic smoking). In adulthood, researchers measured bone traits via peripheral quantitative CT at the tibia and radius and estimated calcaneal mineral density with quantitative ultrasound. Fractures were self-reported via questionnaires. Researchers used parental smoking, serum cotinine and parental smoking hygiene as exposure variables in linear regression models to examine the effects of childhood passive smoking on bone parameters.

Researchers found that passive smoking in childhood (elevated cotinine level) was inversely associated with bone sum index z score (P = .0003), bone mass (P = .003), bone density (P = .0001), bone area (P = .81) and bone strain z score (P = .003). Results persisted after adjustment for birth weight, smoking in adulthood or when active smokers in adulthood were excluded.

Participants with an elevated cotinine level in childhood also had a higher low-energy fracture rate in adulthood vs. participants with low cotinine levels (14.3% vs. 11.3%; P = .15).

In analyses stratified by parental smoking hygiene, researchers found that children whose parents smoked nonhygienically had a lower bone sum index z score vs. children whose parents smoked hygienically (P = .008).

The researchers noted that there was only a single measurement of parental smoking and of serum cotinine concentration in children; however, age interactions were not detected, indicating that a single measurement may be representative of childhood exposure.

“It is essential to know whether the passive smoke exposure is also related with osteoporotic fractures,” Juonala said. – by Regina Schaffer

For more information:

Markus Juonala, MD, PhD, can be reached at Turku University Hospital, Division of Medicine, Kiinamyllynkatu 4-8, 20520, Turku, Finland; email:

Disclosures: The authors report no relevant financial disclosures.

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