SHORT REPORT
The effects of Secondhand Smoke (SHS) exposure on microvascular endothelial function among healthy women
| 1 | Central Research Laboratory, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia |
| 2 | Department of Family Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia |
| 3 | Department of Pharmacology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Malaysia |
| 4 | Faculty of Medicine, Universiti Sultan Zainal Abidin, City Campus, Kuala Terengganu, Malaysia |
CORRESPONDING AUTHOR
Harmy Mohamed Yusoff
Department of Family Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
Department of Family Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
Publish date: 2015-09-03
Tobacco Induced Diseases 2015;13(September):32
KEYWORDS
hair samplemicrovascular perfusionmicrovascular endothelial functioncardiac microvascular endothelial celldigital blood pressure monitor
ABSTRACT
Background:
We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.
Methods:
We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.
Conclusions:
In this study, generally healthy non-smoking women who have higher, lower and non-detected hair nicotine levels did not show significant differences in their microvascular endothelial function. Low levels of SHS exposure among generally healthy non-smoking women may not significantly impair their microvascular endothelial function.
We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.
Methods:
We studied 127 women; and based on their hair nicotine levels measured using gas chromatography-mass spectrometry, 25 of them were categorized as having higher hair nicotine levels, 25 were grouped as having lower hair nicotine and 77 women were grouped into the non-detected group. The non-detected group did not have detectable levels of hair nicotine. Anthropometry, blood pressure (BP), lipid profile and high-sensitivity C-reactive protein (hsCRP) were measured accordingly. Microvascular endothelial function was assessed non-invasively using laser Doppler fluximetry and the process of iontophoresis involving acetylcholine and sodium nitroprusside as endothelium-dependent and endothelium-independent vasodilators respectively. The mean hair nicotine levels for higher and lower hair nicotine groups were 0.74 (1.04) and 0.05 (0.01) ng/mg respectively. There were no significant differences in anthropometry, BP, lipid profile and hsCRP between these groups. There were also no significant differences in the microvascular perfusion and endothelial function between these groups.
Conclusions:
In this study, generally healthy non-smoking women who have higher, lower and non-detected hair nicotine levels did not show significant differences in their microvascular endothelial function. Low levels of SHS exposure among generally healthy non-smoking women may not significantly impair their microvascular endothelial function.
REFERENCES (25)
1.
Abularrage CJ, Sidawy AN, Aidinian G, Singh N, Weiswasser JM, Arora S. Evaluation of the microcirculation in vascular disease. J Vasc Surg. 2005;42:574–81.
2.
Shimokawa H. Primary endothelial dysfunction: atherosclerosis. J Mol Cell Cardiol. 1999;31:23–37.
3.
Hornig B, Landmesser U, Kohler C, Ahlersmann D, Spiekermann S, Christoph A, et al. Comparative effect of ace inhibition and angiotensin II type 1 receptor antagonism on bioavailability of nitric oxide in patients with coronary artery disease: role of superoxide dismutase. Circulation. 2001;103:799–805.
4.
Masumoto A, Hirooka Y, Hironaga K, Eshima K, Setoguchi S, Egashira K, et al. Effect of pravastatin on endothelial function in patients with coronary artery disease (cholesterol-independent effect of pravastatin). Am J Cardiol. 2001;88:1291–4.
5.
Mather KJ, Verma S, Anderson TJ. Improved endothelial function with metformin in type 2 diabetes mellitus. J Am Coll Cardiol. 2001;37:1344–50.
6.
Brodsky SV, Zhang F, Nasjletti A, Goligorsky MS. Endothelium-derived microparticles impair endothelial function in vitro. Am J Physiol Heart Circ Physiol. 2004;286:H1910–5.
7.
Damaske A, Muxel S, Fasola F, Radmacher MC, Schaefer S, Jabs A, et al. Peripheral hemorheological and vascular correlates of coronary blood flow. Clin Hemorheol Microcirc. 2011;49:261–9.
8.
U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease, A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2010.
9.
Barnoya J, Glantz SA. Cardiovascular effects of secondhand smoke: nearly as large as smoking. Circulation. 2005;111:2684–98.
10.
Xu CB, Pessah-Rasmussen H, Stavenow L. Interactions between cultured bovine arterial endothelial and smooth muscle cells: effects of injury on the release of growth stimulating and growth inhibiting substances. Pharmacol Toxicol. 1991;69:195–200.
11.
Zhang JY, Cao YX, Xu CB, Edvinsson L. Lipid-soluble smoke particles damage endothelial cells and reduce endothelium-dependent dilatation in rat and man. BMC Cardiovasc Disord. 2006;6:3.
12.
Ministry of Health Malaysia. Clinical practice guidelines on treatment of tobacco use and dependence. 2003. p. 1–39.
13.
Man CN, Ismail S, Harn GL, Lajis R, Awang R. Determination of hair nicotine by gas chromatography–mass spectrometry. J Chromatogr B Analyt Technol Biomed Life Sci. 2009;877:339–42.
14.
Al-Tahami BA, Yvonne-Tee GB, Halim AS, Ismail AA, Rasool AHG. Reproducibility of Laser Doppler fluximetry and the process of iontophoresis in assessing microvascular endothelial function using low current strength. Methods Find Exp Clin Pharmacol. 2010;32:181–5.
15.
Al-Tahami BA, Yvonne-Tee GB, Halim AS, Ismail AA, Rasool AHG. Method optimization on the process of iontophoresis with laser Doppler fluximetry in the assessment of microvascular endothelial function. Malaysian J Med Health Sci. 2011;7:35–40.
16.
Celermajer DS. Endothelial dysfunction: does it matter? is it reversible? J Am Coll Cardiol. 1997;30:325–33.
17.
Bard RL, Dvonch JT, Kaciroti N, Lustig SA, Brook RD. Is acute high-dose secondhand smoke exposure always harmful to microvascular function in healthy adults? Prev Cardiol. 2010;13:175–9.
18.
Bonetti PO, Lardi E, Geissmann C, Kuhn MU, Brüesch H, Reinhart WH. Effect of brief secondhand smoke exposure on endothelial function and circulating markers of inflammation. Atherosclerosis. 2011;215:218–22.
19.
Argacha JF, Adamopoulos D, Gujic M, Fontaine D, Amyai N, Berkenboom G, et al. Acute effects of passive smoking on peripheral vascular function. Hypertension. 2008;51:1506–211.
20.
Celermajer DS, Adam MR, Clarkson P, Robinson J, McCredie R, Donald A, et al. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. N Engl J Med. 1996;334:150–4.
21.
Sumida H, Watanabe H, Kugiyama K, Ohgushi M, Matsumura T, Yasue H. Does passive smoking impair endothelium-dependent coronary artery dilatation in women? J Am Coll Cardiol. 1998;31:811–5.
22.
Gräfe M, Auch-Schwelk W, Hertel H, Terbeek D, Steinheider G, Loebe M, et al. Human cardiac microvascular and macrovascular endothelial cells respond differently to oxidatively modified LDL. Atherosclerosis. 1998;137:87–95.
23.
Bapat M, Musikantow D, Khmara K, Chokshi P, Khanna N, Galligan S, et al. Comparison of passive leg raising and hyperemia on macrovascular and microvascular responses. Microvasc Res. 2013;86:30–3.
24.
Sandoo A, Carrol D, Metsios GS, Kitas GD, van Zanten JJCS V. The association between microvascular and macrovascular endothelial function in patients with rheumatoid arthritis: a cross-sectional study. Arthritis Res Ther. 2011;13:R99.
25.
Kim S, Wipfli H, Navas-Acien A, Dominici F, Avila-Tang E, Onicescu G, et al. Determinants of hair nicotine concentrations in nonsmoking women and children: a multicountry study of secondhand smoke exposure in homes. Cancer Epidemiol Biomarkers Prev. 2009;18:3407–14.
