Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults

Celermajer, David S.; Adams, Mark; Clarkson, Patrick; Robinson, JH; McCredie, Robyn J.; Donald, Ann; Deanfield, John

doi:10.1056/nejm199601183340303

Cited by 838 publications

(551 citation statements)

References 29 publications

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“…Participants consumed no food or fluid during their time inside the chamber and until after each of the follow-up measurements. To ensure that the comparatively long half-life of specific indexeses (e.g., cotinine and fT 4) did not influence our results, a randomly chosen 50% of the men and the women participants (i.e., 7 men and 7 women) underwent the experimental trial first in sequence, while the remaining participants performed the experimental trial second in sequence. All participants were instructed to refrain from strenuous physical activity and other excessive stressors for 72 h before the first trial but also during the 2 assessment days, particularly during the period between awakening and experimentation and during transit from home to the laboratory.…”

Section: Experimental Designmentioning

confidence: 99%

“…Given the effect of sex on systolic blood pressure after the SHS exposure (see RESULTS), the same regression procedure was also used to model the effect of cotinine levels, gonadal and thyroid hormone secretion, as well as cytokine levels (independent variables) on systolic blood pressure (dependent variable). To ensure that the comparatively long half-life of specific indexes (e.g., cotinine and fT 4) did not influence our results, ANOVA was used to detect differences between the group of participants (n ϭ 14) performing the experimental trial first in sequence and those (n ϭ 14) performing the experimental trial second in sequence. The sample size calculations were conducted with PASS 2000 (Hintze J.…”

Section: Statistical Analysesmentioning

confidence: 99%

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Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Flouris

Metsios²,

Jamurtas³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Flouris AD, Metsios GS, Jamurtas AZ, Koutedakis Y. Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function. Am J Physiol Endocrinol Metab 294: E456-E462, 2008. First published December 11, 2007 doi:10.1152/ajpendo.00699.2007.-Experimental evidence for the physiological effects of secondhand smoke (SHS) is limited, although it affects millions of people globally and its prevalence is increasing, despite currently adopted antismoking measures. Also, scarce evidence suggests that the effects of SHS may be more pronounced in men. We conducted a randomized single-blind crossover study to investigate the sex-specific SHS effects in a controlled simulated bar/restaurant environment on gonadal and thyroid hormones, inflammatory cytokines, and vascular function. Twentyeight (women ϭ 14) nonsmoking adults underwent a 1-h exposure to moderate SHS and a 1-h control trial. Serum and urine cotinine, gonadal and thyroid hormones, inflammatory cytokines, heart rate, and arterial blood pressure were assessed before exposure and immediately after in both trials. Results showed that testosterone (P ϭ 0.019) and progesterone (P Ͻ 0.001) in men and 17␤-estradiol (P ϭ 0.001) and progesterone (P Ͻ 0.001) in women were significantly decreased after SHS. In men, SHS was accompanied by increased free thyroxine (P Ͻ 0.001), triiodothyronine (P ϭ 0.020), and decreased the triiodothyronine-to-free thyroxine ratio (P ϭ 0.033). In women, significant SHS-induced change was observed only in free thyroxine (P ϭ 0.010), with considerable sex variation in free thyroxine and triiodothyronine and a decrease in luteinizing hormone (P ϭ 0.026) and follicle-stimulating hormone (P Ͻ 0.001). After SHS, IL-1␤ (P ϭ 0.001) and systolic blood pressure (P ϭ 0.040) were increased in men but not women. We concluded that a 1-h SHS exposure at bar/ restaurant levels is accompanied by decrements in gonadal hormones in both sexes and marked increases in thyroid hormone secretion, IL-1␤ production, and systolic blood pressure in men.environmental tobacco smoke; cotinine; estrogen; cytokines MORE THAN 126 MILLION AMERICAN and 130 million Chinese adult nonsmokers are currently exposed to secondhand smoke (SHS) on a daily basis, while global estimates include 700 million children and 50 million pregnant women (31). These figures generate major concerns given the overwhelming evidence on the adverse health effects of SHS (26) together with recent reports showing that, despite currently adopted measures, the prevalence rates of smoking are increasing (30). Experimental data from our (17) and other (14,18,19,26) laboratories suggest that even brief exposures to SHS cause marked changes in thyroid hormone secretion, platelet aggregation, endothelial function, arterial pressure waveform, inflammatory markers, as well as other hemodynamic alterations involved in the development of ischemic heart disease. At least some of these effects appear to be more pronounced in men compared with women (14, 20),...

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Section: Experimental Designmentioning

confidence: 99%

Section: Statistical Analysesmentioning

confidence: 99%

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Flouris

Metsios²,

Jamurtas³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

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“…This study was among the first in humans to demonstrate the important role of endothelial dysfunction early in the course of atherosclerosis. Similarly, abnormal vasomotion occurs in subjects with uncomplicated hypertension (71), diabetes (72)(73)(74)(75), cigarette smoking (76,77) and low levels of high density lipoprotein (78,79). Oxidized low density lipoprotein plays an important role in abnormal endothelial vasorelaxation, leukocyte adhesion and endothelin production (80)(81)(82)(83).…”

Section: Relationship Of Endothelial Function To Risk Factors and Thementioning

confidence: 99%

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Anderson

2006

Canadian Journal of Cardiology

148

112

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T he understanding of the pathophysiology of atherosclerosis and its vascular complications has increased dramatically over the past decade. Numerous measurable biomarkers play a role in the atherosclerosis process, and are associated with clinically important vascular events. Not only has their evaluation advanced our knowledge of the atherosclerotic process but it has also accelerated a search for new diagnostic tools to aid in risk stratification. Putative factors include soluble biomarkers and imaging assessments of vascular structure and function. The endothelium plays a key role in vascular homeostasis through the release of a variety of paracrine factors that interact with platelets, inflammatory cells and the vessel wall. The endothelium's central location allows it to sense and respond to a variety of perturbations. Endothelial dysfunction is an early marker of disease. Risk factors can also affect mechanical properties such as arterial stiffness, which is now recognized as a major contributor to systolic hypertension in elderly people. Methods of assessing endothelial function and arterial stiffness are available for clinical research and recent evidence suggests that these measures may provide important prognostic information. ATTRIBUTES OF A SURROGATE BIOMARKEREpidemiological studies, such as Framingham, have allowed longitudinal assessment of cardiovascular events and the development of simple scoring tables for risk calculation (1,2). These factors involved include blood pressure, lipid profile, smoking status and age. More recently, many factors thought to be associated with the atherosclerotic process have been studied. Some of these have been shown to correlate with clinical outcomes and have been deemed biomarkers (3,4). However, association does not necessarily imply causation and, due to a variety of limitations, most of these markers will not be useful for the clinical evaluation of risk or drug therapy (5). To become clinically important, a biomarker must fulfill the criteria for a surrogate marker. A surrogate substitutes for clinically important end points with respect to how an individual feels, functions or survives. Classic examples include blood pressure and low density lipoprotein cholesterol. These are targets of treatment. A surrogate should meet the following criteria:• Adds independent information above currently used criteria;• Is reliably and reproducibly measured;• Accounts for a significant proportion of disease risk;• Provides good predictive value;• Is reasonably associated with the underlying pathophysiology;• If it is to be used in risk prevention, is present before the clinical appearance of the outcome; and• Is available and practical for widespread application (5-8). ADVANCES IN VASCULAR BIOLOGY

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“…We measured FMD of the brachial artery, a non-invasive technique using ultrasound, as set up by Celermajer et al (1996). The ultrasound images were made with a linear array transducer (range 8 -14 MHz) of an Esaote AU5 scanner (Pie Medical Benelux B.V., Maastricht, The Netherlands).…”

Section: Flow-mediated Vasodilation Of the Brachial Arterymentioning

confidence: 99%

Trans monounsaturated fatty acids and saturated fatty acids have similar effects on postprandial flow-mediated vasodilation

et al. 2002

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Objective: Several studies suggest that a fatty meal impairs flow-mediated vasodilation (FMD), a measure of endothelial function. We tested whether the impairment was greater for trans fats than for saturated fats. We did this because we previously showed that replacement of saturated fats by trans fats in a controlled diet decreased FMD after 4 weeks. Design: We fed 21 healthy men two different test meals with 0.9 -1.0 g fat=kg body weight in random order: one rich in saturated fatty acids (Sat), mainly from palm kernel fat, and one rich in trans fatty acids (Trans) from partially hydrogenated soy bean oil. The study was performed in our metabolic ward. We had complete data for both diets of 21 men. Results: FMD increased from a fasting value of 2.3 AE 2.0% of the baseline diameter to 3.0 AE 1.7% after the Sat test meal (95% CI for change 7 0.33, 1.70) and from 2.7 AE 2.3 to 3.1 AE 2.0% after the Trans test meal (95% CI for change 7 0.57, 1.29). The increase after the Sat meal was 0.22 ( 7 1.18 -1.61) FMD% higher than after the Trans meal. Serum triacylglycerols increased by 0.46 AE 0.36 mmol=l after the Sat test meal and by 0.68 AE 0.59 mmol=l after the Trans test meal; a difference of 0.23 (0.07, 0.39) mmol=l. Serum HDL-cholesterol was hardly affected by the test meals. The activity of serum paraoxonase, an esterase bound to HDL, increased slightly after the two test meals but the difference between meals was not significant. Conclusion: FMD was not impaired and not different after test meals with saturated or trans fatty acids. Thus, differences in long-term effects of these fats are not caused by differences in acute effects on the vascular wall.

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Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults

Abstract: Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.

Cited by 838 publications

References 29 publications

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Sexual dimorphism in the acute effects of secondhand smoke on thyroid hormone secretion, inflammatory markers and vascular function

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Trans monounsaturated fatty acids and saturated fatty acids have similar effects on postprandial flow-mediated vasodilation

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