Showing items related by title, author, creator and subject.

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  Childhood Exposure to Parental Smoking and Midlife Cognitive Function The Young Finns Study 

  Rovio, Suvi P.; Pihlman, Jukka; Pahkala, Katja; Juonala, Markus; Magnussen, Costan G.; Pitkänen, Niina; Ahola-Olli, Ari; Salo, Pia; Kähönen, Mika; Hutri-Kähönen, Nina; Lehtimäki, Terho; Jokinen, Eero; Laitinen, Tomi; Taittonen, Leena; Tossavainen, Päivi; Viikari, Jorma S. A.; Raitakari, Olli T. (2020)

  We studied whether exposure to parental smoking in childhood/adolescence is associated with midlife cognitive function, leveraging data from the Cardiovascular Risk in Young Finns Study. A population-based cohort of 3,596 children/adolescents aged 3-18 years was followed between 1980 and 2011. In 2011, cognitive testing was performed on 2,026 participants aged 34-49 years using computerized testing. Measures of secondhand smoke exposure in childhood/adolescence consisted of parental self-reports of smoking and participants' serum cotinine levels. Participants were classified into 3 exposure groups: 1) no exposure (nonsmoking parents, cotinine 1.0 ng/mL). Analyses adjusted for sex, age, family socioeconomic status, polygenic risk score for cognitive function, adolescent/adult smoking, blood pressure, and serum total cholesterol level. Compared with the nonexposed, participants exposed to nonhygienic parental smoking were at higher risk of poor (lowest quartile) midlife episodic memory and associative learning (relative risk (RR) = 1.38, 95% confidence interval (CI): 1.08, 1.75), and a weak association was found for short-term and spatial working memory (RR = 1.25, 95% CI: 0.98, 1.58). Associations for those exposed to hygienic parental smoking were nonsignificant (episodic memory and associative learning: RR = 1.19, 95% CI: 0.92, 1.54; short-term and spatial working memory: RR = 1.10, 95% CI: 0.85, 1.34). We conclude that avoiding childhood/adolescence secondhand smoke exposure promotes adulthood cognitive function.
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  The relation of environmental tobacco smoke (ETS) to chronic bronchitis and mortality over two decades 

  Pelkonen, Margit K.; Laatikainen, Tiina K.; Jousilahti, Pekka (2019)

  Introduction: Our aim was to describe how the prevalence of subjects exposed to environmental tobacco smoke (ETS) has changed from 1992 to 2012 in Finland. We also investigated the association between ETS and chronic bronchitis and cause-specific and all-cause mortality. Methods: The study population is composed of 38 494 subjects aged 25-74 years who participated in the National FINRISK Study between 1992 and 2012. Each survey included a standardized questionnaire on exposure to ETS, symptoms of chronic bronchitis, smoking habits and other risk factors, and clinical measurements at the study site. Data on mortality was obtained from the National Causes of Death Register. Results: In 2012, 5% of the participants were exposed to ETS compared to 25% in 1992. The adjusted odds ratio (OR) for ETS exposure in 2012 compared with that in 1992 was 0.27, p <0.001. Exposure to ETS was more common in men than in women and among smokers than in non-smokers. Exposure to ETS was in turn associated with chronic bronchitis, OR 1.63 (95% confidence interval 1.49-1.78),-also separately both at work (OR 1.36) and at home (OR 1.69). Subjects with exposure to ETS had significantly increased all-cause (hazard ratio=HR 1.15, 1.05-1.26) and cardiovascular mortality (HR 1.26, 1.07-1.47). However, when stratified by smoking ETS was associated with all-cause mortality only in smokers (HR 1.31, 1.15-1.48). Conclusion: The proportion of subjects exposed to ETS decreased substantially during the study. Additionally, ETS exposure was associated with chronic bronchitis throughout the study and increased all-cause and cardiovascular mortality.
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  Smoking induces coordinated DNA methylation and gene expression changes in adipose tissue with consequences for metabolic health 

  Tsai, Pei-Chien; Glastonbury, Craig A.; Eliot, Melissa N.; Bollepalli, Sailalitha; Yet, Idil; Castillo-Fernandez, Juan E.; Carnero-Montoro, Elena; Hardiman, Thomas; Martin, Tiphaine C.; Vickers, Alice; Mangino, Massimo; Ward, Kirsten; Pietilaeinen, Kirsi H.; Deloukas, Panos; Spector, Tim D.; Vinuela, Ana; Loucks, Eric B.; Ollikainen, Miina; Kelsey, Karl T.; Small, Kerrin S.; Bell, Jordana T. (2018)

  Background: Tobacco smoking is a risk factor for multiple diseases, including cardiovascular disease and diabetes. Many smoking-associated signals have been detected in the blood methylome, but the extent to which these changes are widespread to metabolically relevant tissues, and impact gene expression or metabolic health, remains unclear. Methods: We investigated smoking-associated DNA methylation and gene expression variation in adipose tissue biopsies from 542 healthy female twins. Replication, tissue specificity, and longitudinal stability of the smoking-associated effects were explored in additional adipose, blood, skin, and lung samples. We characterized the impact of adipose tissue smoking methylation and expression signals on metabolic disease risk phenotypes, including visceral fat. Results: We identified 42 smoking-methylation and 42 smoking-expression signals, where five genes (AHRR, CYP1A1, CYP1B1, CYTL1, F2RL3) were both hypo-methylated and upregulated in current smokers. CYP1A1 gene expression achieved 95% prediction performance of current smoking status. We validated and replicated a proportion of the signals in additional primary tissue samples, identifying tissue-shared effects. Smoking leaves systemic imprints on DNA methylation after smoking cessation, with stronger but shorter-lived effects on gene expression. Metabolic disease risk traits such as visceral fat and android-to-gynoid ratio showed association with methylation at smoking markers with functional impacts on expression, such as CYP1A1, and at tissue-shared smoking signals, such as NOTCH1. At smoking-signals, BHLHE40 and AHRR DNA methylation and gene expression levels in current smokers were predictive of future gain in visceral fat upon smoking cessation. Conclusions: Our results provide the first comprehensive characterization of coordinated DNA methylation arid gene expression markers of smoking in adipose tissue. The findings relate to human metabolic health and give insights into understanding the widespread health consequence of smoking outside of the lung.