Association between secondhand smoke exposure and new-onset hypertension in self-reported never smokers verified by cotinine
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
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.
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.
참고문헌 (26)
- "Korean Health Statistics 2017: Korean National Health and Nutrition Examination Survey (KNHANES VII-2)" (2015)[URL]
- Kim BJ, "Association between cotinine-verified smoking status and hypertension in 167, 868 Korean adults", Blood Press, 26, pp.303~310 (2017)
- Kim BJ, "Relationship of cotinine-verified and self-reported smoking status with metabolic syndrome in 116, 094 Korean adults", J Clin Lipidol, 11, pp.638~645 (2017)
- Kim JH, "Association between cigarette smoking and diabetes mellitus using two different smoking stratifications in 145 040 Korean individuals : self-reported questionnaire and urine cotinine concentrations", J Diabetes, 11, pp.232~241 (2019)
- Li N, "Effects of passive smoking on hypertension in rural Chinese nonsmoking women", J Hypertens, 33, pp.2210~2214 (2015)
- Seki M, "Association of environmental tobacco smoke exposure with elevated home blood pressure in Japanese women : the Ohasama study", J Hypertens, 28, pp.1814~1820 (2010)
- Wu L, "Association between passive smoking and hypertension in Chinese non-smoking elderly women", Hypertens Res, 40, pp.399~404 (2017)
- Yang Y, "Association of husband smoking with wife’s hypertension status in over 5 million chinese females aged 20 to 49 years", J Am Heart Assoc, 6, pp.e004924~ (2017)
- Park YS, "Association between secondhand smoke exposure and hypertension in never smokers : a cross-sectional survey using data from Korean National Health and Nutritional Examination Survey V, 2010-2012", BMJ Open, 8, pp.e021217~ (2018)
- Freire AP, "Influence of time and frequency of passive smoking exposure on mucociliary clearance and the autonomic nervous system", Respir Care, 61, pp.453~461 (2016)
- Felber Dietrich D, "Effects of passive smoking on heart rate variability, heart rate and blood pressure : an observational study", Int J Epidemiol, 36, pp.834~840 (2007)
- Kim BJ, "Association between secondhand smoke exposure and hypertension in 106, 268Korean self-reported never-smokers verified by cotinine", J Clin Med, 8, pp.1238~ (2019)
- SRNT Subcommittee on Biochemical Verification, "Biochemical verification of tobacco use and cessation", Nicotine Tob Res, 4, pp.149~159 (2002)
- Messner B, "Smoking and cardiovascular disease : mechanisms of endothelial dysfunction and early atherogenesis", Arterioscler Thromb Vasc Biol, 34, pp.509~515 (2014)
- Narkiewicz K, "Cigarette smoking increases sympathetic outflow in humans", Circulation, 98, pp.528~534 (1998)
- Hering D, "Smoking is associated with chronic sympathetic activation in hypertension", Blood Press, 19, pp.152~155 (2010)
- Grassi G, "Mechanisms responsible for sympathetic activation by cigarette smoking in humans", Circulation, 90, pp.248~253 (1994)
- Johnson RA, "A heme oxygenase product, presumably carbon monoxide, mediates a vasodepressor function in rats", Hypertension, 25, pp.166~169 (1995)
- Hausberg M, "Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers", Circulation, 96, pp.282~287 (1997)
- Kato M, "The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation", J Hypertens, 17, pp.1395~1401 (1999)
- Argacha JF, "Acute effects of passive smoking on peripheral vascular function", Hypertension, 51, pp.1506~1511 (2008)
- Kim BJ, "Relationship between cotinine-verified smoking status and incidence of hypertension in 74, 743 Korean adults", Circ J, 82, pp.1659~1665 (2018)
- Wang W, "A longitudinal study of hypertension risk factors and their relation to cardiovascular disease : the Strong Heart Study", Hypertension, 47, pp.403~409 (2006)
- Dochi M, "Smoking as an independent risk factor for hypertension : a 14-year longitudinal study in male Japanese workers", Tohoku J Exp Med, 217, pp.37~43 (2009)
- Bowman TS, "A prospective study of cigarette smoking and risk of incident hypertension in women", J Am Coll Cardiol, 50, pp.2085~2092 (2007)
- Tamura T, "Association of exposure level to passive smoking with hypertension among lifetime nonsmokers in Japan : a cross-sectional study", Medicine (Baltimore), 97, pp.e13241~ (2018)