Zhongzheng Niu, Lina Mu, Stephen L Buka, Eric B Loucks, Meng Wang, Lili Tian, Xiaozhong Wen
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引用次数: 0
Abstract
Few population studies have sufficient follow-up period to examine early-life exposures with later life diseases. A critical question is whether involuntary exposure to tobacco smoke from conception to adulthood increases the risk of cardiometabolic diseases (CMD) in midlife. In the Collaborative Perinatal Project, serum-validated maternal smoking during pregnancy (MSP) was assessed in the 1960s. At a mean age of 39 years, 1623 offspring were followed-up for the age at first physician-diagnoses of any CMDs, including diabetes, heart disease, hypertension, or hyperlipidemia. Detailed information on their exposure to environmental tobacco smoke (ETS) in childhood and adolescence was collected with a validated questionnaire. Cox regression was used to examine associations of in utero exposure to MSP and exposure to ETS from birth to 18 years with lifetime incidence of CMD, adjusting for potential confounders. We calculated midlife cumulative incidences of hyperlipidemia (25.2%), hypertension (14.9%), diabetes (3.9%), and heart disease (1.5%). Lifetime risk of hypertension increased by the 2nd -trimester exposure to MSP (adjusted hazard ratio: 1.29, 95% confidence interval: 1.01-1.65), ETS in childhood (1.11, 0.99-1.23) and adolescence (1.22, 1.04-1.44). Lifetime risk of diabetes increased by joint exposures to MSP and ETS in childhood (1.23, 1.01-1.50) or adolescence (1.47, 1.02-2.10). These associations were stronger in males than females, in never-daily smokers than lifetime ever smokers. In conclusion, early-life involuntary exposure to tobacco smoke increases midlife risk of hypertension and diabetes in midlife.
期刊介绍:
JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions.
JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts.
The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.