Markus Juonala1,2, Niina Pitkänen3, Sanna Tolonen4, Marika Laaksonen4, Harri Sievänen5, Eero Jokinen6, Tomi Laitinen7, Matthew A Sabin2,8, Nina Hutri-Kähönen9, Terho Lehtimäki10, Leena Taittonen11, Antti Jula12, Britt-Marie Loo12,13, Olli Impivaara12, Mika Kähönen14, Costan G Magnussen3,15, Jorma S A Viikari1, Olli T Raitakari3,16. 1. Department of Medicine, University of Turku and Division of Medicine, Turku University Hospital, Turku, Finland. 2. Murdoch Childrens Research Institute, Parkville, Victoria, Australia. 3. Research Center of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. 4. Department of Food and Nutrition, University of Helsinki, Helsinki, Finland. 5. UKK-institute, Tampere, Finland. 6. Department of Pediatric Cardiology, Hospital for Children and Adolescents, University of Helsinki, Helsinki, Finland. 7. Department of Clinical Physiology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland. 8. Royal Children's Hospital, Parkville, Victoria, Australia. 9. Department of Pediatrics, Tampere University and Tampere University Hospital, Tampere, Finland. 10. Department of Clinical Chemistry, Fimlab Laboratories and Faculty of Medicine and Health Technology, Finnish Cardiovascular Research Center- Tampere, Tampere University, Tampere, Finland. 11. Vaasa Central Hospital, Vaasa, Finland. 12. Department of Chronic Disease Prevention, National Institute for Health and Welfare, Turku, Finland. 13. Joint Clinical Biochemistry Laboratory of University of Turku and Turku University Hospital, Turku, Finland. 14. Department of Clinical Physiology, Tampere University Hospital and Tampere University, Tampere, Finland. 15. Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia. 16. Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland.
Abstract
CONTEXT: Passive smoke exposure has been linked to the risk of osteoporosis in adults. OBJECTIVE: We examined the independent effects of childhood passive smoke exposure on adult bone health. DESIGN/ SETTING: Longitudinal, the Cardiovascular Risk in Young Finns Study. PARTICIPANTS: The study cohort included 1422 individuals followed for 28 years since baseline in 1980 (age 3 to 18 years). Exposure to passive smoking was determined in childhood. In adulthood, peripheral bone traits were assessed with peripheral quantitative CT (pQCT) at the tibia and radius, and calcaneal mineral density was estimated with quantitative ultrasound. Fracture data were 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, body mass index, 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 (OR, 1.28; 95% CI, 1.01 to 1.62). Individuals with elevated cotinine levels (3 to 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 to 20 ng/mL) had significantly lower pQCT-derived bone sum index compared with those with smoking parents but had low cotinine levels (<3 ng/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.
CONTEXT: Passive smoke exposure has been linked to the risk of osteoporosis in adults. OBJECTIVE: We examined the independent effects of childhood passive smoke exposure on adult bone health. DESIGN/ SETTING: Longitudinal, the Cardiovascular Risk in Young Finns Study. PARTICIPANTS: The study cohort included 1422 individuals followed for 28 years since baseline in 1980 (age 3 to 18 years). Exposure to passive smoking was determined in childhood. In adulthood, peripheral bone traits were assessed with peripheral quantitative CT (pQCT) at the tibia and radius, and calcaneal mineral density was estimated with quantitative ultrasound. Fracture data were 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, body mass index, 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 (OR, 1.28; 95% CI, 1.01 to 1.62). Individuals with elevated cotinine levels (3 to 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 to 20 ng/mL) had significantly lower pQCT-derived bone sum index compared with those with smoking parents but had low cotinine levels (<3 ng/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.
Authors: Johanna M Jaakkola; Suvi P Rovio; Katja Pahkala; Jorma Viikari; Tapani Rönnemaa; Antti Jula; Harri Niinikoski; Juha Mykkänen; Markus Juonala; Nina Hutri-Kähönen; Mika Kähönen; Terho Lehtimäki; Olli T Raitakari Journal: Ann Med Date: 2021-12 Impact factor: 4.709
Authors: S Tolonen; M Juonala; M Fogelholm; K Pahkala; M Laaksonen; M Kähönen; H Sievänen; J Viikari; O Raitakari Journal: Calcif Tissue Int Date: 2022-07-27 Impact factor: 4.000