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      Association between secondhand smoke exposure and new-onset hypertension in self-reported never smokers verified by cotinine

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          Abstract

          Background/Aims

          There is no study assessing the effect of changes of secondhand smoke (SHS) exposure and new-onset hypertension. We investigated the effect of a change of SHS exposure status on new-onset hypertension in self-reported and cotinine-verified never smokers.

          Methods

          Out of individuals enrolled in the Kangbuk Samsung Health Study between 2011 and 2016, 87,486 self-reported and cotinine-verified never smokers without hypertension at baseline visit were included with a median follow-up of 36 months. Individuals were divided into four groups on the basis of their SHS exposure status at baseline and at follow-up: no, new, former, and sustained SHS exposure groups.

          Results

          The incidence rates per 10,000 person-year of new-onset hypertension in no, new, former, and sustained SHS exposure groups were 84.7, 113.3, 102.0, and 123.7, respectively ( p < 0.001). A multivariable Cox-hazard analyses showed that new and sustained SHS exposure groups increased their hazard ratio (HR) for new-onset hypertension compared to no SHS exposure group (HR, 1.31; 95% confidence interval [CI], 1.08 to 1.60 for new SHS exposure group; and HR, 1.24; 95% CI, 1.06 to 1.45 for sustained SHS exposure group). However, being part of the former SHS exposure group did not increase the risk of new-onset hypertension (HR, 0.91; 95% CI, 0.81 to 1.03).

          Conclusions

          This study showed that either new, or sustained SHS exposure, but not former SHS exposure, increased the risk for new-onset hypertension in self-reported never smokers verified as nonsmokers by urinary cotinine. These findings show the possibility that changing exposure to SHS even for a relatively short period can modify the risk of new-onset hypertension in self-reported and cotinine-verified never smokers.

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          Most cited references26

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          Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis.

          Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes.
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            Biochemical verification of tobacco use and cessation.

            (2002)
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              A prospective study of cigarette smoking and risk of incident hypertension in women.

              We undertook this study to prospectively evaluate whether cigarette smoking was associated with an increased risk of developing hypertension. Smoking is a well-recognized risk factor for cardiovascular disease. Few prospective cohort studies have examined the relationship between smoking and hypertension. We conducted a prospective cohort study among 28,236 women in the Women's Health Study who were initially free of hypertension, cardiovascular disease, and cancer. Detailed risk factor information, including smoking status, was collected from self-reported questionnaires. We used Cox proportional hazards survival models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of incident hypertension (defined as either new diagnosis, the initiation of antihypertensive medication, systolic blood pressure > or =140 mm Hg or diastolic blood pressure > or =90 mm Hg). At baseline, 51% of women were never smokers, 36% were former smokers, 5% smoked 1 to 14 cigarettes, and 8% smoked > or =15 cigarettes per day. During a median of 9.8 years, there were 8,571 (30.4%) cases of incident hypertension. The age-adjusted HRs of developing hypertension among never, former, and current smokers of 1 to 14 and > or =15 cigarettes per day were 1.00 (reference), 1.04 (95% CI 0.99 to 1.09), 1.00 (95% CI 0.90 to 1.10), and 1.10 (95% CI 1.01 to 1.19), respectively. In multivariable models further adjusting for lifestyle, clinical, and dietary variables, the corresponding HRs were 1.00 (reference), 1.03 (95% CI 0.98 to 1.08), 1.02 (95% CI 0.92 to 1.13), and 1.11 (95% CI 1.03 to 1.21), respectively. Among women who smoked > or =25 cigarettes per day, the multivariable HR was 1.21 (95% CI 1.06 to 1.39). In this large cohort of women, cigarette smoking was modestly associated with an increased risk of developing hypertension, with an effect that was strongest among women smoking at least 15 cigarettes per day.
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                Author and article information

                Journal
                Korean J Intern Med
                Korean J Intern Med
                KJIM
                The Korean Journal of Internal Medicine
                The Korean Association of Internal Medicine
                1226-3303
                2005-6648
                November 2021
                9 June 2021
                : 36
                : 6
                : 1377-1388
                Affiliations
                [1 ]Division of Cardiology, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
                [2 ]Center for Cohort Studies, Total Healthcare Center, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
                Author notes
                Correspondence to Byung Jin Kim, M.D. Division of Cardiology, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, 29 Saemunan-ro, Jongno-gu, Seoul 03181, Korea Tel: +82-2-2001-2401 Fax: +82-2-2001-2400 E-mail: bjjake.kim@ 123456samsung.com
                Author information
                http://orcid.org/0000-0002-9008-8506
                Article
                kjim-2021-214
                10.3904/kjim.2021.214
                8588976
                34742177
                6bd1fc7c-2c75-4f81-b5b5-54cac9978932
                Copyright © 2021 The Korean Association of Internal Medicine

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 3 May 2021
                : 8 June 2021
                : 9 June 2021
                Categories
                Original Article
                Cardiology

                Internal medicine
                epidemiology,hypertension,blood pressure,tobacco smoke pollution,smoke
                Internal medicine
                epidemiology, hypertension, blood pressure, tobacco smoke pollution, smoke

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