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Costan G Magnussen - One of the best experts on this subject based on the ideXlab platform.
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exposure to Parental Smoking in childhood is associated with high c reactive protein in adulthood the cardiovascular risk in young finns study
Journal of Atherosclerosis and Thrombosis, 2017Co-Authors: Markus Juonala, Costan G Magnussen, Jorma Viikari, Nina Hutrikahonen, Di Wang, Olli T RaitakariAbstract:AIM Children exposed to Parental Smoking are at increased long-term risk of subclinical atherosclerosis in adulthood. However, it has not been quantified if exposure to Parental Smoking in childhood is associated with adult systemic inflammation. This study aimed to determine if childhood exposure to Parental Smoking was associated with high-sensitivity C-reactive protein (hsCRP) in adulthood. METHODS This longitudinal analysis of 2,511 participants used data from the Cardiovascular Risk in Young Finns Study, a prospective cohort of Finnish children. In 1980 or 1983, parents self-reported their Smoking status and serum hsCRP was collected up to 31 years later in adulthood. RESULTS Compared with children with non-Smoking parents, the relative risk of developing high hsCRP (＞3 mg/L) in adulthood increased among those with 1 or both parents who smoked [relative risk (RR), 1.3; 95%confidence interval (CI), 1.0-1.8] after adjustment for socioeconomic status, cardiovascular risk factors, and Smoking status in childhood and adulthood. Moreover, children exposed to mother Smoking [RR, 2.4; 95% CI, 1.3-4.2] had highest risk of developing high hsCRP in adulthood compared with those exposed to father Smoking [RR, 1.6; 95% CI, 1.2-2.3] and both parents Smoking [RR, 1.4; 95% CI, 0.9-2.0]. CONCLUSION Our findings suggest that children exposed to Parental Smoking are at increased risk of having high hsCRP in adulthood. Limiting children's exposure to passive Smoking may have long-term benefits on general low-grade inflammation.
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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Circulation, 2015Co-Authors: Henry W West, Markus Juonala, Seana L Gall, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Olli T Raitakari, Costan G MagnussenAbstract: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 if 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=2,448). Information on childhood exposure to Parental Smoking was collected in 1980 and 1983. Carotid ultrasound data was collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (N=1,578). The proportion of children with non-detectable cotinine levels was highest among households where neither parent smoked (84%), decreased in households where one parent smoked (62%), and was lowest among households where both parents smoked (43%). Irrespective of adjustment for potential confounding and mediating variables, the relative risk (RR) of developing carotid plaque in adulthood increased among those where one or both parents smoked (RR=1.7, 95%CI=1.0-2.8, P=0.04). Although children whose parents exercised good "Smoking hygiene" (Smoking parents whose children had non-detectable cotinine levels) had increased risk of carotid plaque compared with non-Smoking parents (RR=1.6, 95%CI=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 (RR=4.0, 95%CI=1.7-9.8, P=0.002). Conclusions —Children of parents that 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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exposure to Parental Smoking in childhood or adolescence is associated with increased carotid intima media thickness in young adults evidence from the cardiovascular risk in young finns study and the childhood determinants of adult health study
European Heart Journal, 2014Co-Authors: Seana L Gall, Markus Juonala, Costan G Magnussen, Mika Kahonen, Jorma Viikari, Olli T Raitakari, Quan Long Huynh, Terence Dwyer, Alison VennAbstract:Aim Recent evidence suggests that the exposure of children to their parents' Smoking adversely effects endothelial function in adulthood. We investigated whether the association was also present with carotid intima-media thickness (IMT) up to 25 years later. Methods and results The study comprised participants from the Cardiovascular Risk in Young Finns Study (YFS, n = 2401) and the Childhood Determinants of Adult Health (CDAH, n = 1375) study. Exposure to Parental Smoking (none, one, or both) was assessed at baseline by questionnaire. B-mode ultrasound of the carotid artery determined IMT in adulthood. Linear regression on a pooled dataset accounting for the hierarchical data and potential confounders including age, sex, Parental education, participant Smoking, education, and adult cardiovascular risk factors was conducted. Carotid IMT in adulthood was greater in those exposed to both parents Smoking than in those whose parents did not smoke [adjusted marginal means: 0.647 mm ± 0.022 (mean ± SE) vs. 0.632 mm ± 0.021, P = 0.004]. Having both parents smoke was associated with vascular age 3.3 years greater at follow-up than having neither parent smoke. The effect was independent of participant Smoking at baseline and follow-up and other confounders and was uniform across categories of age, sex, adult Smoking status, and cohort. Conclusions These results show the pervasive effect of exposure to Parental Smoking on children's vascular health up to 25 years later. There must be continued efforts to reduce Smoking among adults to protect young people and to reduce the burden of cardiovascular disease across the population.
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Parental Smoking in childhood and brachial artery flow mediated dilatation in young adults the cardiovascular risk in young finns study and the childhood determinants of adult health study
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Markus Juonala, Costan G Magnussen, Alison Venn, Seana L Gall, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Terho Lehtimaki, Eero Jokinen, Cong SunAbstract:Objective— Passive Smoking has been associated with increased cardiovascular morbidity. The present study aimed to examine the long-term effects of childhood exposure to tobacco smoke on endothelium-dependent vasodilation in adults. Methods and Results— The analyses were based on 2171 participants in the population-based Cardiovascular Risk in Young Finns (N=2067) and Childhood Determinants of Adult Health (N=104) studies who had measures of conventional risk factors (lipids, blood pressure, adiposity, socioeconomic status) and self-reported Parental Smoking status when aged 3 to 18 years at baseline. They were re-examined 19 to 27 years later when aged 28 to 45 years. Brachial artery flow-mediated dilatation was measured at follow-up with ultrasound. In analyses adjusting for age, sex, and childhood risk factors, flow-mediated dilatation was reduced among participants who had parents that smoked in youth compared to those whose parents did not smoke (Young Finns: 9.2±0.1% (mean±SEM) versus 8.6±0.1%, P =0.001; Childhood Determinants of Adult Health: 7.4±0.6% versus 4.9±0.9%, P =0.04). These effects remained after adjustment for adult risk factors including own Smoking status (Young Finns, P =0.003; Childhood Determinants of Adult Health, P =0.03). Conclusion— Parental Smoking in youth is associated with reduced flow-mediated dilatation in young adulthood measured over 20 years later. These findings suggest that passive exposure to cigarette smoke among children might cause irreversible impairment in endothelium-dependent vasodilation.
Markus Juonala - One of the best experts on this subject based on the ideXlab platform.
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childhood exposure to Parental Smoking and life course overweight and central obesity
Annals of Medicine, 2021Co-Authors: Johanna M Jaakkola, Markus Juonala, Suvi P Rovio, Katja Pahkala, Jorma Viikari, Tapani Ronnemaa, Antti Jula, Harri Niinikoski, Juha Mykkanen, Nina HutrikahonenAbstract:To evaluate the association between childhood Parental Smoking exposure and the risk of overweight/obesity from childhood to adulthood. This study leverages the data from two longitudinal populatio...
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childhood exposure to passive Smoking and bone health in adulthood the cardiovascular risk in young finns study
The Journal of Clinical Endocrinology and Metabolism, 2019Co-Authors: Markus Juonala, Tomi Laitinen, Eero Jokinen, Nina Hutrikahonen, Niina Pitkanen, Sanna Tolonen, Marika Laaksonen, Harri Sievanen, Matthew A Sabin, Terho LehtimakiAbstract: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.
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exposure to Parental Smoking in childhood is associated with high c reactive protein in adulthood the cardiovascular risk in young finns study
Journal of Atherosclerosis and Thrombosis, 2017Co-Authors: Markus Juonala, Costan G Magnussen, Jorma Viikari, Nina Hutrikahonen, Di Wang, Olli T RaitakariAbstract:AIM Children exposed to Parental Smoking are at increased long-term risk of subclinical atherosclerosis in adulthood. However, it has not been quantified if exposure to Parental Smoking in childhood is associated with adult systemic inflammation. This study aimed to determine if childhood exposure to Parental Smoking was associated with high-sensitivity C-reactive protein (hsCRP) in adulthood. METHODS This longitudinal analysis of 2,511 participants used data from the Cardiovascular Risk in Young Finns Study, a prospective cohort of Finnish children. In 1980 or 1983, parents self-reported their Smoking status and serum hsCRP was collected up to 31 years later in adulthood. RESULTS Compared with children with non-Smoking parents, the relative risk of developing high hsCRP (＞3 mg/L) in adulthood increased among those with 1 or both parents who smoked [relative risk (RR), 1.3; 95%confidence interval (CI), 1.0-1.8] after adjustment for socioeconomic status, cardiovascular risk factors, and Smoking status in childhood and adulthood. Moreover, children exposed to mother Smoking [RR, 2.4; 95% CI, 1.3-4.2] had highest risk of developing high hsCRP in adulthood compared with those exposed to father Smoking [RR, 1.6; 95% CI, 1.2-2.3] and both parents Smoking [RR, 1.4; 95% CI, 0.9-2.0]. CONCLUSION Our findings suggest that children exposed to Parental Smoking are at increased risk of having high hsCRP in adulthood. Limiting children's exposure to passive Smoking may have long-term benefits on general low-grade inflammation.
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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Circulation, 2015Co-Authors: Henry W West, Markus Juonala, Seana L Gall, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Olli T Raitakari, Costan G MagnussenAbstract: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 if 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=2,448). Information on childhood exposure to Parental Smoking was collected in 1980 and 1983. Carotid ultrasound data was collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (N=1,578). The proportion of children with non-detectable cotinine levels was highest among households where neither parent smoked (84%), decreased in households where one parent smoked (62%), and was lowest among households where both parents smoked (43%). Irrespective of adjustment for potential confounding and mediating variables, the relative risk (RR) of developing carotid plaque in adulthood increased among those where one or both parents smoked (RR=1.7, 95%CI=1.0-2.8, P=0.04). Although children whose parents exercised good "Smoking hygiene" (Smoking parents whose children had non-detectable cotinine levels) had increased risk of carotid plaque compared with non-Smoking parents (RR=1.6, 95%CI=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 (RR=4.0, 95%CI=1.7-9.8, P=0.002). Conclusions —Children of parents that 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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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Heart Lung and Circulation, 2015Co-Authors: H West, Markus Juonala, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Seana Gall, Olli T RaitakariAbstract: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 carot...
Derek G Cook - One of the best experts on this subject based on the ideXlab platform.
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health effects of passive Smoking 10 summary of effects of Parental Smoking on the respiratory health of children and implications for research
Thorax, 1999Co-Authors: Derek G Cook, David P StrachanAbstract:BACKGROUND—Two recent reviews have assessed the effect of Parental Smoking on respiratory disease in children. METHODS—The results of the systematic quantitative review published as a series in Thorax are summarised and brought up to date by considering papers appearing on Embase or Medline up to June 1998.The findings are compared with those of the review published recently by the Californian Environmental Protection Agency (EPA). Areas requiring further research are identified. RESULTS—Overall there is a very consistent picture with odds ratios for respiratory illnesses and symptoms and middle ear disease of between 1.2 and 1.6 for either parent Smoking, the odds usually being higher in pre-school than in school aged children. For sudden infant death syndrome the odds ratio for maternal Smoking is about 2. Significant effects from paternal Smoking suggest a role for postnatal exposure to environmental tobacco smoke. Recent publications do not lead us to alter the conclusions of our earlier reviews. While essentially narrative rather than systematic and quantitative, the findings of the Californian EPA review are broadly similar. In addition they have reviewed studies of the effects of environmental tobacco smoke on children with cystic fibrosis and conclude from the limited evidence that there is a strong case for a relationship between Parental Smoking and admissions to hospital. They also review data from adults of the effects of acute exposure to environmental tobacco smoke under laboratory conditions which suggest acute effects on spirometric parameters rather than on bronchial hyperresponsiveness. It seems likely that such effects are also present in children. CONCLUSIONS—Substantial benefits to children would arise if parents stopped Smoking after birth, even if the mother smoked during pregnancy. Policies need to be developed which reduce Smoking amongst parents and protect infants and young children from exposure to environmental tobacco smoke. The weight of evidence is such that new prevalence studies are no longer justified. What are needed are studies which allow comparison of the effects of critical periods of exposure to cigarette smoke, particularly in utero, early infancy, and later childhood. Where longitudinal studies are carried out they should be analysed to look at the way in which changes in exposure are related to changes in outcome. Better still would be studies demonstrating reversibility of adverse effects, especially in asthmatic subjects or children with cystic fibrosis.
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Parental Smoking and spirometric indices in children
Thorax, 1998Co-Authors: Derek G Cook, David P Strachan, Iain M CareyAbstract:BACKGROUND—A systematic quantitative review was conducted of the evidence relating Parental Smoking to spirometric indices in children. METHODS—An electronic search of the Embase and Medline databases was completed in April 1997 and identified 692 articles from which we included four studies in neonates, 42 cross-sectional studies in school aged children (22 were included in a meta-analysis), and six longitudinal studies of lung function development. RESULTS—In a pooled analyses of 21 surveys of school aged children the percentage reduction in forced expiratory volume in one second (FEV1) in children exposed to Parental Smoking compared with those not exposed was 1.4% (95% CI 1.0 to 1.9). Effects were greater on mid expiratory flow rates (5.0% reduction, 95% CI 3.3 to 6.6) and end expiratory flow rates (4.3% reduction, 95% CI 3.1 to 5.5). Adjustment for potential confounding variables had little effect on the estimates. A number of studies reported clear evidence of exposure response. Where exposure was explicitly identified it was usually maternal Smoking. Two studies in neonates have reported effects of prenatal exposure to maternal Smoking. Of five cross sectional studies that compared effects of perinatal exposure (retrospectively assessed) with current exposure to maternal Smoking in later childhood, the three largest concluded that the major effect was in utero or neonatal exposure. Longitudinal studies suggest a small effect of current exposure on growth in lung function, but with some heterogeneity between studies. CONCLUSIONS—Maternal Smoking is associated with small but statistically significant deficits in FEV1 and other spirometric indices in school aged children. This is almost certainly a causal relationship. Much of the effect may be due to maternal Smoking during pregnancy.
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Parental Smoking and childhood asthma longitudinal and case control studies
Thorax, 1998Co-Authors: David P Strachan, Derek G CookAbstract:BACKGROUND The relation of Parental Smoking to wheezing and asthma occurring after the first year of life was assessed by a systematic quantitative review of case-control and longitudinal studies, complementing earlier reviews of cross sectional surveys and wheezing in early childhood. METHODS Fifty one relevant publications were identified after consideration of 1593 abstracts selected by electronic search of the Embase and Medline databases using keywords relevant to passive Smoking in children. The search was completed in April 1997 and identified six studies of asthma incidence, seven of prognosis, 22 case-control studies, and 10 case series addressing disease severity. RESULTS Maternal Smoking was associated with an increased incidence of wheezing illness up to age 6 (pooled odds ratio 1.31, 95% CI 1.22 to 1.41), but less strongly thereafter (1.13, 95% CI 1.04 to 1.22). The long term prognosis of early wheezing illness was better if the mother smoked. The pooled odds ratio for asthma prevalence from 14 case-control studies was 1.37 (95% CI 1.15 to 1.64) if either parent smoked. Four studies suggest that Parental Smoking is more strongly associated with wheezing among non-atopic children. Indicators of disease severity including symptom scores, attack frequency, medication use, hospital attendance, and life threatening bronchospasm were in general positively related to household smoke exposure. CONCLUSIONS The excess incidence of wheezing in Smoking households appears to be largely non-atopic “wheezy bronchitis” with a relatively benign prognosis, but among children with established asthma, Parental Smoking is associated with more severe disease. This apparent paradox may be reconciled if environmental tobacco smoke is considered a co-factor provoking wheezing attacks, rather than a cause of the underlying asthmatic tendency.
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health effects of passive Smoking 5 Parental Smoking and allergic sensitisation in children
Thorax, 1998Co-Authors: David P Strachan, Derek G CookAbstract:BACKGROUND: A systematic review was conducted of the effects of Parental Smoking on immunoglobulin (IgE) levels, skin prick positivity, and allergic rhinitis or eczema in children. Asthma was excluded in order to distinguish more clearly the effect of passive smoke exposure on allergic sensitisation. METHODS: Thirty six relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive Smoking in children. The search was completed in April 1997 and identified nine studies of IgE in neonates, eight of IgE in older children, 12 which included skin prick tests, and 10 describing symptoms of allergic disease other than asthma or wheezing. A quantitative meta-analysis was possible only for the studies reporting skin prick tests. RESULTS: Several large studies failed to confirm early reports of a substantial or statistically significant association of maternal Smoking with concentrations of total serum IgE in neonates or in older children. No consistent association emerged between Parental Smoking and allergic rhinitis or eczema. Few of these studies adjusted for potential confounding variables. The quantity and quality of evidence was greatest for skin prick tests, and studies of Parental Smoking during pregnancy or infancy were broadly consistent in showing no adverse effect on prick positivity (pooled odds ratio 0.87, 95% confidence interval 0.62 to 1.24). There was much greater and statistically significant (p = 0.002) heterogeneity of odds ratios relating current Parental Smoking to skin prick positivity. CONCLUSIONS: Parental Smoking, either before or immediately after birth, is unlikely to increase the risk of allergic sensitisation in children.
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health effects of passive Smoking 4 Parental Smoking middle ear disease and adenotonsillectomy in children
Thorax, 1998Co-Authors: David P Strachan, Derek G CookAbstract:BACKGROUND: A systematic quantitative review was conducted of evidence relating Parental Smoking to acute otitis media, recurrent otitis media, middle ear effusion, and adenoidectomy and/or tonsillectomy. METHODS: Forty five relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive Smoking in children. The search was completed in April 1997 and identified 13 studies of acute otitis media, nine of recurrent otitis media, five of middle ear effusion, nine of glue ear surgery, and four of adenotonsillectomy. A quantitative meta-analysis was possible for all outcomes except acute otitis media, using random effects modelling where appropriate to pool odds ratios from each study. RESULTS: Evidence for middle ear disease is remarkably consistent, with pooled odds ratios if either parent smoked of 1.48 (95% CI 1.08 to 2.04) for recurrent otitis media, 1.38 (1.23 to 1.55) for middle ear effusion, and 1.21 (0.95 to 1.53) for outpatient or inpatient referral for glue ear. Odds ratios for acute otitis media are in the range 1.0 to 1.6. No single study simultaneously addresses selection bias, information bias and confounding, but where these have been investigated or excluded in the design or analysis, the associations with Parental Smoking persist virtually unchanged. Large French and British studies are inconsistent with regard to the association of Parental Smoking and tonsillectomy. CONCLUSIONS: There is likely to be a causal relationship between Parental Smoking and both acute and chronic middle ear disease in children.
Jorma Viikari - One of the best experts on this subject based on the ideXlab platform.
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childhood exposure to Parental Smoking and life course overweight and central obesity
Annals of Medicine, 2021Co-Authors: Johanna M Jaakkola, Markus Juonala, Suvi P Rovio, Katja Pahkala, Jorma Viikari, Tapani Ronnemaa, Antti Jula, Harri Niinikoski, Juha Mykkanen, Nina HutrikahonenAbstract:To evaluate the association between childhood Parental Smoking exposure and the risk of overweight/obesity from childhood to adulthood. This study leverages the data from two longitudinal populatio...
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exposure to Parental Smoking in childhood is associated with high c reactive protein in adulthood the cardiovascular risk in young finns study
Journal of Atherosclerosis and Thrombosis, 2017Co-Authors: Markus Juonala, Costan G Magnussen, Jorma Viikari, Nina Hutrikahonen, Di Wang, Olli T RaitakariAbstract:AIM Children exposed to Parental Smoking are at increased long-term risk of subclinical atherosclerosis in adulthood. However, it has not been quantified if exposure to Parental Smoking in childhood is associated with adult systemic inflammation. This study aimed to determine if childhood exposure to Parental Smoking was associated with high-sensitivity C-reactive protein (hsCRP) in adulthood. METHODS This longitudinal analysis of 2,511 participants used data from the Cardiovascular Risk in Young Finns Study, a prospective cohort of Finnish children. In 1980 or 1983, parents self-reported their Smoking status and serum hsCRP was collected up to 31 years later in adulthood. RESULTS Compared with children with non-Smoking parents, the relative risk of developing high hsCRP (＞3 mg/L) in adulthood increased among those with 1 or both parents who smoked [relative risk (RR), 1.3; 95%confidence interval (CI), 1.0-1.8] after adjustment for socioeconomic status, cardiovascular risk factors, and Smoking status in childhood and adulthood. Moreover, children exposed to mother Smoking [RR, 2.4; 95% CI, 1.3-4.2] had highest risk of developing high hsCRP in adulthood compared with those exposed to father Smoking [RR, 1.6; 95% CI, 1.2-2.3] and both parents Smoking [RR, 1.4; 95% CI, 0.9-2.0]. CONCLUSION Our findings suggest that children exposed to Parental Smoking are at increased risk of having high hsCRP in adulthood. Limiting children's exposure to passive Smoking may have long-term benefits on general low-grade inflammation.
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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Circulation, 2015Co-Authors: Henry W West, Markus Juonala, Seana L Gall, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Olli T Raitakari, Costan G MagnussenAbstract: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 if 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=2,448). Information on childhood exposure to Parental Smoking was collected in 1980 and 1983. Carotid ultrasound data was collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (N=1,578). The proportion of children with non-detectable cotinine levels was highest among households where neither parent smoked (84%), decreased in households where one parent smoked (62%), and was lowest among households where both parents smoked (43%). Irrespective of adjustment for potential confounding and mediating variables, the relative risk (RR) of developing carotid plaque in adulthood increased among those where one or both parents smoked (RR=1.7, 95%CI=1.0-2.8, P=0.04). Although children whose parents exercised good "Smoking hygiene" (Smoking parents whose children had non-detectable cotinine levels) had increased risk of carotid plaque compared with non-Smoking parents (RR=1.6, 95%CI=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 (RR=4.0, 95%CI=1.7-9.8, P=0.002). Conclusions —Children of parents that 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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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Heart Lung and Circulation, 2015Co-Authors: H West, Markus Juonala, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Seana Gall, Olli T RaitakariAbstract: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 carot...
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exposure to Parental Smoking in childhood or adolescence is associated with increased carotid intima media thickness in young adults evidence from the cardiovascular risk in young finns study and the childhood determinants of adult health study
European Heart Journal, 2014Co-Authors: Seana L Gall, Markus Juonala, Costan G Magnussen, Mika Kahonen, Jorma Viikari, Olli T Raitakari, Quan Long Huynh, Terence Dwyer, Alison VennAbstract:Aim Recent evidence suggests that the exposure of children to their parents' Smoking adversely effects endothelial function in adulthood. We investigated whether the association was also present with carotid intima-media thickness (IMT) up to 25 years later. Methods and results The study comprised participants from the Cardiovascular Risk in Young Finns Study (YFS, n = 2401) and the Childhood Determinants of Adult Health (CDAH, n = 1375) study. Exposure to Parental Smoking (none, one, or both) was assessed at baseline by questionnaire. B-mode ultrasound of the carotid artery determined IMT in adulthood. Linear regression on a pooled dataset accounting for the hierarchical data and potential confounders including age, sex, Parental education, participant Smoking, education, and adult cardiovascular risk factors was conducted. Carotid IMT in adulthood was greater in those exposed to both parents Smoking than in those whose parents did not smoke [adjusted marginal means: 0.647 mm ± 0.022 (mean ± SE) vs. 0.632 mm ± 0.021, P = 0.004]. Having both parents smoke was associated with vascular age 3.3 years greater at follow-up than having neither parent smoke. The effect was independent of participant Smoking at baseline and follow-up and other confounders and was uniform across categories of age, sex, adult Smoking status, and cohort. Conclusions These results show the pervasive effect of exposure to Parental Smoking on children's vascular health up to 25 years later. There must be continued efforts to reduce Smoking among adults to protect young people and to reduce the burden of cardiovascular disease across the population.
Olli T Raitakari - One of the best experts on this subject based on the ideXlab platform.
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exposure to Parental Smoking in childhood is associated with high c reactive protein in adulthood the cardiovascular risk in young finns study
Journal of Atherosclerosis and Thrombosis, 2017Co-Authors: Markus Juonala, Costan G Magnussen, Jorma Viikari, Nina Hutrikahonen, Di Wang, Olli T RaitakariAbstract:AIM Children exposed to Parental Smoking are at increased long-term risk of subclinical atherosclerosis in adulthood. However, it has not been quantified if exposure to Parental Smoking in childhood is associated with adult systemic inflammation. This study aimed to determine if childhood exposure to Parental Smoking was associated with high-sensitivity C-reactive protein (hsCRP) in adulthood. METHODS This longitudinal analysis of 2,511 participants used data from the Cardiovascular Risk in Young Finns Study, a prospective cohort of Finnish children. In 1980 or 1983, parents self-reported their Smoking status and serum hsCRP was collected up to 31 years later in adulthood. RESULTS Compared with children with non-Smoking parents, the relative risk of developing high hsCRP (＞3 mg/L) in adulthood increased among those with 1 or both parents who smoked [relative risk (RR), 1.3; 95%confidence interval (CI), 1.0-1.8] after adjustment for socioeconomic status, cardiovascular risk factors, and Smoking status in childhood and adulthood. Moreover, children exposed to mother Smoking [RR, 2.4; 95% CI, 1.3-4.2] had highest risk of developing high hsCRP in adulthood compared with those exposed to father Smoking [RR, 1.6; 95% CI, 1.2-2.3] and both parents Smoking [RR, 1.4; 95% CI, 0.9-2.0]. CONCLUSION Our findings suggest that children exposed to Parental Smoking are at increased risk of having high hsCRP in adulthood. Limiting children's exposure to passive Smoking may have long-term benefits on general low-grade inflammation.
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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Circulation, 2015Co-Authors: Henry W West, Markus Juonala, Seana L Gall, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Olli T Raitakari, Costan G MagnussenAbstract: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 if 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=2,448). Information on childhood exposure to Parental Smoking was collected in 1980 and 1983. Carotid ultrasound data was collected in adulthood in 2001 or 2007. Childhood serum cotinine levels from 1980 were measured from frozen samples in 2014 (N=1,578). The proportion of children with non-detectable cotinine levels was highest among households where neither parent smoked (84%), decreased in households where one parent smoked (62%), and was lowest among households where both parents smoked (43%). Irrespective of adjustment for potential confounding and mediating variables, the relative risk (RR) of developing carotid plaque in adulthood increased among those where one or both parents smoked (RR=1.7, 95%CI=1.0-2.8, P=0.04). Although children whose parents exercised good "Smoking hygiene" (Smoking parents whose children had non-detectable cotinine levels) had increased risk of carotid plaque compared with non-Smoking parents (RR=1.6, 95%CI=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 (RR=4.0, 95%CI=1.7-9.8, P=0.002). Conclusions —Children of parents that 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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exposure to Parental Smoking in childhood is associated with increased risk of carotid atherosclerotic plaque in adulthood the cardiovascular risk in young finns study
Heart Lung and Circulation, 2015Co-Authors: H West, Markus Juonala, Mika Kahonen, Tomi Laitinen, Leena Taittonen, Jorma Viikari, Seana Gall, Olli T RaitakariAbstract: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 carot...
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exposure to Parental Smoking in childhood or adolescence is associated with increased carotid intima media thickness in young adults evidence from the cardiovascular risk in young finns study and the childhood determinants of adult health study
European Heart Journal, 2014Co-Authors: Seana L Gall, Markus Juonala, Costan G Magnussen, Mika Kahonen, Jorma Viikari, Olli T Raitakari, Quan Long Huynh, Terence Dwyer, Alison VennAbstract:Aim Recent evidence suggests that the exposure of children to their parents' Smoking adversely effects endothelial function in adulthood. We investigated whether the association was also present with carotid intima-media thickness (IMT) up to 25 years later. Methods and results The study comprised participants from the Cardiovascular Risk in Young Finns Study (YFS, n = 2401) and the Childhood Determinants of Adult Health (CDAH, n = 1375) study. Exposure to Parental Smoking (none, one, or both) was assessed at baseline by questionnaire. B-mode ultrasound of the carotid artery determined IMT in adulthood. Linear regression on a pooled dataset accounting for the hierarchical data and potential confounders including age, sex, Parental education, participant Smoking, education, and adult cardiovascular risk factors was conducted. Carotid IMT in adulthood was greater in those exposed to both parents Smoking than in those whose parents did not smoke [adjusted marginal means: 0.647 mm ± 0.022 (mean ± SE) vs. 0.632 mm ± 0.021, P = 0.004]. Having both parents smoke was associated with vascular age 3.3 years greater at follow-up than having neither parent smoke. The effect was independent of participant Smoking at baseline and follow-up and other confounders and was uniform across categories of age, sex, adult Smoking status, and cohort. Conclusions These results show the pervasive effect of exposure to Parental Smoking on children's vascular health up to 25 years later. There must be continued efforts to reduce Smoking among adults to protect young people and to reduce the burden of cardiovascular disease across the population.
