Henry W West1, Markus Juonala1, Seana L Gall1, Mika Kähönen1, Tomi Laitinen1, Leena Taittonen1, Jorma S A Viikari1, Olli T Raitakari1, Costan G Magnussen2. 1. From Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia (H.W.W., S.L.G., C.G.M.); Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, and Division of Medicine and Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Finland (M.J., J.S.A.V., O.T.R., C.G.M.); Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Finland (M.K.); Department of Clinical Physiology, University of Kuopio, Finland (T.L.); and Department of Pediatrics, Vaasa Central Hospital, Finland (L.T.). 2. From Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia (H.W.W., S.L.G., C.G.M.); Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, and Division of Medicine and Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Finland (M.J., J.S.A.V., O.T.R., C.G.M.); Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Finland (M.K.); Department of Clinical Physiology, University of Kuopio, Finland (T.L.); and Department of Pediatrics, Vaasa Central Hospital, Finland (L.T.). cmagnuss@utas.edu.au.
Abstract
BACKGROUND: The association between passive smoking exposure in childhood and adverse cardiovascular health in adulthood is not well understood. Using a 26-year follow-up study, we examined whether childhood exposure to passive smoking was associated with carotid atherosclerotic plaque in young adults. METHODS AND RESULTS: Participants were from the Cardiovascular Risk in Young Finns Study (n=2448). Information on childhood exposure to parental smoking was collected in 1980 and 1983. Carotid ultrasound data were collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (n=1578). The proportion of children with nondetectable cotinine levels was highest among households in which neither parent smoked (84%), was decreased in households in which 1 parent smoked (62%), and was lowest among households in which both parents smoked (43%). Regardless of adjustment for potential confounding and mediating variables, the relative risk of developing carotid plaque in adulthood increased among those children with 1 or both parents who smoked (relative risk, 1.7; 95% confidence interval, 1.0-2.8; P=0.04). Although children whose parents exercised good "smoking hygiene" (smoking parents whose children had nondetectable cotinine levels) had increased risk of carotid plaque compared with children with nonsmoking parents (relative risk, 1.6; 95% confidence interval, 0.6-4.0; P=0.34), children of smoking parents with poor smoking hygiene (smoking parents whose children had detectable serum cotinine levels) had substantially increased risk of plaque as adults (relative risk, 4.0; 95% confidence interval, 1.7-9.8; P=0.002). CONCLUSIONS: Children of parents who smoke have increased risk of developing carotid atherosclerotic plaque in adulthood. However, parents who exercise good smoking hygiene can lessen their child's risk of developing plaque.
BACKGROUND: The association between passive smoking exposure in childhood and adverse cardiovascular health in adulthood is not well understood. Using a 26-year follow-up study, we examined whether childhood exposure to passive smoking was associated with carotid atherosclerotic plaque in young adults. METHODS AND RESULTS:Participants were from the Cardiovascular Risk in Young Finns Study (n=2448). Information on childhood exposure to parental smoking was collected in 1980 and 1983. Carotid ultrasound data were collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (n=1578). The proportion of children with nondetectable cotinine levels was highest among households in which neither parent smoked (84%), was decreased in households in which 1 parent smoked (62%), and was lowest among households in which both parents smoked (43%). Regardless of adjustment for potential confounding and mediating variables, the relative risk of developing carotid plaque in adulthood increased among those children with 1 or both parents who smoked (relative risk, 1.7; 95% confidence interval, 1.0-2.8; P=0.04). Although children whose parents exercised good "smoking hygiene" (smoking parents whose children had nondetectable cotinine levels) had increased risk of carotid plaque compared with children with nonsmoking parents (relative risk, 1.6; 95% confidence interval, 0.6-4.0; P=0.34), children of smoking parents with poor smoking hygiene (smoking parents whose children had detectable serum cotinine levels) had substantially increased risk of plaque as adults (relative risk, 4.0; 95% confidence interval, 1.7-9.8; P=0.002). CONCLUSIONS:Children of parents who smoke have increased risk of developing carotid atherosclerotic plaque in adulthood. However, parents who exercise good smoking hygiene can lessen their child's risk of developing plaque.
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