Acute Effects Of Passive Smoking Research Articles

The Acute Effects of Passive Smoking on Mean Platelet Volume in Healthy Volunteers

Mean platelet volume (MPV) is an indicator of platelet activation. We investigated the acute effect of passive smoking on MPV in healthy volunteers. Healthy nonsmoker volunteers (n = 90) spent 120 minutes in a smoke-free room. Then they were exposed to passive smoking in 3 groups consisting of 30 volunteers each in group A (carbon monoxide [CO] < 7.5 ppm), group B (CO = 7.5-15 ppm), and group C (CO > 15 ppm) for 120 minutes in a smoking room. Mean platelet volume did not change in group A and in the smoke-free room. Mean platelet volume increased significantly at the 60th minute and continued to increase at the 90th and 120th minute in group B. Mean platelet volume increased significantly at the 30th minute and continued to increase at the 60th, 90th, and 120th minute in group C. In conclusion, acute exposure to passive smoking affected MPV according to the duration and intensity of smoke.

Effect of brief secondhand smoke exposure on endothelial function and circulating markers of inflammation

ObjectiveIn contrast to the well defined detrimental consequences of long-term secondhand smoke (SHS) exposure, little is known about the acute effects of passive smoking on endothelial function and inflammation. The aim of the present study was to assess the acute effects of short-term SHS exposure on endothelial function and circulating markers of inflammation. MethodsPeripheral microvascular endothelial function assessed by reactive hyperemia peripheral arterial tonometry (RH-PAT) index, circulating markers of endothelial function (von Willebrand factor antigen, Thrombomodulin, E-selectin) and circulating inflammatory markers (high sensitivity C-reactive protein (hsCRP), Interleukin-6 (IL-6)) were measured in eighteen male, non-smoking volunteers before and 12h after a 1-h SHS exposure. ResultsTwelve hours after passive smoking, average RH-PAT index was significantly lower than before SHS exposure (1.54±0.49 vs 2.01±0.55 (mean±SD), p=0.01) indicating deterioration of peripheral microvascular endothelial function. von Willebrand factor antigen as a marker of endothelial activation was significantly increased after SHS exposure (93.0±25.5% vs 78.4±17.9%, p=0.03). Levels of Thrombomodulin, E-selectin, hsCRP, and IL-6 were unaffected by SHS exposure. ConclusionShort-term SHS exposure leads to a measurable disturbance of endothelial function. However, 1h of passive smoking appears to be too short to elicit a significant inflammatory response.

Acute Effects of Passive Smoking on Left Ventricular Systolic and Diastolic Function in Healthy Volunteers

The aim of this study was to investigate the acute effects of passive smoking on left ventricular (LV) function in healthy volunteers. Sixty-one healthy nonsmoking volunteers were enrolled in this study. LV M-mode, two-dimensional, conventional Doppler, and color tissue Doppler echocardiography were performed, and carboxyhemoglobin (COHb) levels were obtained from subjects before and immediately after exposure to passive smoking for 30 min in a smoking room. The differences between baseline and post-smoke exposure measurements of transmitral E and mitral annular Em velocities, heart rate, systolic blood pressure, diastolic blood pressure, and COHb levels were assessed. Mean COHb levels were statistically higher after exposure. There were no changes in LV systolic function and volumes. LV diastolic function changed significantly immediately after passive smoking. The transmitral E wave (0.89 ± 0.12 vs 0.70 ± 0.14 m/sec, P = .001), the pulmonary venous D wave (0.52 ± 0.12 vs 0.49 ± 0.13 m/sec, P = .01), and the transmitral E/A ratio 1.79 ± 0.48 vs 1.47 ± 0.32, P = .001) decreased, while the transmitral A wave did not change. The mitral annular Em velocity decreased (12.5 ± 2.1 vs 11.7 ± 1.9 cm/sec, P = .001), the Am velocity increased (6.3 ± 2.1 vs 6.8 ± 1.6 cm/sec, P = .001), and the Em/Am ratio decreased (2.28 ± 0.82 vs 1.78 ± 0.42, P = .001). Color Doppler echocardiography determined diastolic impairment in only women, whereas color tissue Doppler echocardiography demonstrated diastolic dysfunction in both genders. Acute deleterious effects of passive smoking on color Doppler echocardiographic parameters were more prominent in women. Change in E was related to changes in heart rate and systolic blood pressure and with COHb levels, while change in Em was related only to COHb levels. Acute exposure to passive smoking impairs LV diastolic function in healthy volunteers. The mechanism whereby passive smoking affects diastolic function is probably complex; however, carbon monoxide exposure and an increment in COHb level may be among the causes.

Acute effects of passive smoking on blood pressure and heart rate in healthy females

Carbon monoxide (CO) is suspected of playing a major role in cigarette smoke-induced cardiovascular diseases. Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. We aimed to investigate the immediate effects of passive smoking on blood pressure and heart rate during and after exposure in healthy females. In addition, we examined that whether carboxyhemoglobin (COHb) levels were correlated with heart rate and blood pressure measurements. Thirty healthy nonsmoker female volunteers (mean age: 26±5 years) were prospectively enrolled in the study. Systolic and diastolic blood pressure and heart rate were obtained at baseline, 5th, 10th, 15th, 30th minute of exposure and at 5th, 15th, and 30th minute after exposure. Blood samples for measuring COHb were taken at baseline and after spending 30 min in the smoking room from all volunteers. Difference between baseline and second measurements of COHb were described as ΔCOHb. Mean COHb level was significantly higher at the end of exposure when compared with baseline values (COHb 0.5±0.1 vs. 1.8±0.4%, P<0.05). Heart rate and systolic blood pressure measurements at 15th and 30th minute of exposure were higher than at baseline and 5th minute of exposure (88±3.2 and 90±3.7 vs. 76±3.9 and 78±4.5 beats/min, P<0.05; 135±1.1 and 136±4.0 vs. 113±5.7 and 115±3.5 mmHg, P<0.05). They elevated significantly at the same time interval. Diastolic blood pressure was significantly increased at 30th minute of exposure when compared with earlier measurements (90±5.1 vs. 74±2.2, 72±3.2 vs. 71±4.5 mmHg, P<0.05). Heart rate and systolic blood pressure decreased notably at 15th minute and returned to baseline values at 30th minute after exposure (80±1.2 and 76±3.2 vs. 88±4.5 beats/min, P<0.05; 120±4.4 and 115±1.9 vs. 135±2.2 mmHg, P<0.05). Diastolic blood pressure decreased significantly at 30th minute and returned to baseline values at 60th minute after exposure (75±3.6 and 70±2.5 vs. 89±4.3 mmHg, P<0.05). Heart rate and diastolic blood pressure measurements were moderately correlated and systolic blood pressure measurements were closely correlated with ΔCOHb values at the end of the exposure. Our results suggested that passive smoking has remarkable acute effect on heart rate and blood pressure in young healthy females. Beside this, we found that ΔCOHb level is closely correlated with systolic blood pressure and moderately correlated with heart rate and diastolic blood pressure measurements.

Acute Effects of Passive Smoking on Endothelial Function

Impairment of endothelial functions has been shown to occur after acute and chronic exposure to passive smoking (PS), as assessed by flow-mediated dilatation (FMD) of the brachial artery. A total of 61 participants, 30 male and 31 female, mean ages 26 (18-36) were enrolled in the study. All were clinically well and nonsmokers. All participants stayed for 30 minutes in the smoking room. Carbon monoxide (CO) level was 7.42 ± 0.98 ppm (4.71-10.50). Mean carboxyhemoglobin (COHb) levels of participants were significantly elevated after PS. Mean FMD was 18.6% ± 9% and decreased to 12.4% ± 7% after PS (P < .001). In the current study, with more number of participants at lower CO concentrations (7.42 ppm) and with smaller increase in COHb (51%) significant reduction (33%, P < .001) in FMD was observed.

Acute Effects of Passive Smoking on Asthma in Childhood

Although evidence-based asthma guidelines report passive smoke exposure as one of the triggers of asthma symptoms and exacerbations, its prevelance is still high among children with asthma especially in those coming from low income families. Passive smoke exposure affects different aspects of asthma control not only diurnal and nocturnal symptoms and exacerbations but also rescue medication use and lung functions as well as bronchial hyperreactivity, school absenteeism and quality of life. Immediate effects of passive smoke exposure in all these asthma parameters seem to be additive to those of chronic exposure. Smoking cessation interventions therefore play a pivotal role for a better asthma control.

Passive Smoking, Asthma and Allergy in Children

Despite the recent campaigns to eliminate smoking and hinder the detrimental effects of passive smoking (PS), actual smoking rates still increase worldwide. Several physiological systems, with the respiratory being the primary, are disrupted by PS and progressively deteriorate through chronic exposures. This is of particular importance in children, given that respiratory complications during childhood can be transferred to adulthood, lead to significantly inferior health profiles. Hence, it is no surprise that children that are exposed to PS either in utero or during their adulthood may have an increased prevalence of allergies and asthma. However, investigating the acute effects of PS in children is inherently limited by complexities pertaining mainly to ethical constrains. Knowledge of the acute effects could be very important as it is the dose-dependant acute effects of passive smoking that lead to the long-term adaptations linked with the development of allergy and asthma. Current available data show that the chemical and carcinogenic constituents of tobacco have profound effects on children's health as they may disrupt normal biological development. PS appears to have pronounced effects on respiratory parameters that promote asthma development and persistent wheezing rather than other allergies. As such, PS exposure has to be eliminated and researchers have to develop interventions for supporting smoking cessation as well as minimised PS exposure either this is in utero or during childhood.

Lead, Smoking, and Peripheral Vascular Function

To the Editor: We read with interest the article by Argacha et al1 dealing with acute effects of passive smoking on peripheral vascular function. The authors presented data concluding that passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. …

Acute Effects of Passive Smoking on Peripheral Vascular Function

Environmental tobacco smoke (ETS) acutely affects peripheral and coronary vascular tone. Whether ETS exerts specific deleterious effects on aortic wave reflection through nicotine exposure, whether they persist after ETS cessation, and whether the smoke environment impairs microvascular function and increases asymmetrical dimethyl-arginine levels are not known. We tested these hypotheses in a randomized, crossover study design in 11 healthy male nonsmokers. The effects of 1 hour of exposure to ETS, as compared with a nontobacco smoke and normal air, on augmentation index corrected for heart rate and skin microvascular hyperemia to local heating were examined. Augmentation index increased both during (P=0.01) and after (P<0.01) the ETS session but remained unchanged in the nontobacco smoke session when compared with normal air. Nicotine levels after the exposure were related to the peak rise in augmentation index (r=0.84; P<0.01), denoting a predominant role of nicotine in ETS vascular effects. This was confirmed in a second set of experiments (n=14), where the sublingual administration of nicotine was associated with an acute impairment in wave reflection as compared with placebo (P=0.001). Both ETS and nontobacco smokes increased plasma asymmetrical dimethyl-arginine levels (P<0.001), but only ETS reduced the late rise in skin blood flow in response to heating (P=0.03). In conclusion, passive smoking specifically increases aortic wave reflection through a nicotine-dependent pathway and impairs microvascular function, even after the end of the exposure. However, both tobacco and nontobacco passive smoking inhalation increase plasma asymmetrical dimethyl-arginine levels.

Acute Effects of Passive Smoking on Peripheral Vascular Function

Acute Effects of Passive Smoking on Peripheral Vascular Function

Resting Energy Expenditure Response Following Environmental Tobacco Smoke Exposure

It has been well-established that active smoking increases the levels of energy metabolism. Specifically, in active smokers resting energy expenditure (REE), exhibits increases equal to 7.2%, when pre - and post - smoking values are compared. Nevertheless, no studies have investigated the effects of passive smoking on energy expenditure. PUrPose: The purpose of this study was to investigate the acute effects of passive smoking on REE. METHODS: The REE of 18 healthy adult non-smokers (9 male; 9 female; age:25.3±3.1 years; height:172.4±10.1 cm; weight: 65±13.7 kg) was evaluated four consecutive times, via indirect calorimetry. The first two REE measurements - separated with a one-hour resting period - were reserved for the control measurements (CREE1 andCREE2). The other two REE assessments were separated by a one-hour resting period while exposed to passive smoke (XREE1 andXREE2) in carbon monoxide concentrations of 15 ppm. Carbon monoxide (CO) concentrations were determined via a gas mixture in a sample chamber using a Horiba (Mexa 311 GE) CO analyzer. Serum cotinine concentrations were obtained before all REE assessments and analyzed via blood chromatography. Analysis of variance (ANOVA) with Bonferroni adjustment was utilized to detect mean differences among REE measurements and adjust for multiple comparisons. RESULTS: Means±standard deviation forCREE1 andCREE2 were 1489.2±285.3 kcal/ day and 1504.3±286.2 kcal/day, whereas forXREE1 andXREE2, 1495.9±291 kcal/day and 1584.9±296.8 kcal/day, respectively. No significant differences were detected betweenCREE1 vs.CREE2 (p > 0.05), andCREE1 vs.XREE1 (p > 0.05), whereas this was not the case forXREE1 vs.XREE2 (p < 0.001) andXREE2 vs.CREE2 (p < 0.05). Serum cotinine concentrations beforeCREE1 andCREE2 were 6.9±3.8 and 6.9±3.6 (p > 0.05) respectively whereas forXREE1 andXREE2 the cotinine concentrations revealed significant differences (7.3±3.6 and 34.0±19.1 respectively, p < 0.001). CONCLUSION: The observed differences betweenXREE1 vs.XREE2 suggest that passive smoking significantly increases energy metabolism in healthy adult nonsmokers. This may be due to immediate immune and or hormonal responses, as exactly clarified in smokers. Further research is required to establish the mechanisms which underline the cause of this increase in REE after passive smoking. This research was supported by the Research Committee of the University of Thessaly.

Acute effects of passive smoking on the coronary circulation in healthy young adults.

Recent studies have shown that passive smoking is a risk factor for ischemic heart disease and may be associated with vascular endothelial dysfunction. The acute effects of passive smoking on coronary circulation in nonsmokers are not known. To determine the acute effects of passive smoking on coronary circulation using coronary flow velocity reserve (CFVR), assessed by noninvasive transthoracic Doppler echocardiography. Cross-sectional study conducted from September 2000 to November 2000 among 30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 asymptomatic active smokers) without history of hypertension, diabetes mellitus, or hyperlipidemia. Coronary flow velocity reserve, calculated as the ratio of hyperemic to basal coronary flow velocity induced by intravenous infusion of adenosine triphosphate and measured in each participant before and after a 30-minute exposure to environmental tobacco smoke. Heart rate and blood pressure responses to adenosine triphosphate infusion were not affected by passive smoking exposure in either group. Passive smoking exposure had no effect on basal coronary flow velocity in either group. Mean (SD) CFVR in nonsmokers was significantly higher than that in active smokers before passive smoking exposure (4.4 [0.91] vs 3.6 [0.88], respectively; P =.02), while CFVR after passive smoking exposure did not differ between groups (P =.83). Passive smoking exposure significantly reduced mean (SD) CFVR in nonsmokers (4.4 [0.91] vs 3.4 [0.73], respectively; P<.001). Passive smoking substantially reduced CFVR in healthy nonsmokers. This finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.

Is passive smoking in the workplace hazardous to health?

Apart from evidence on the acute effects of passive smoking, there is relatively little information available on whether breathing other people's smoke at work causes disease. However, exposure does commonly occur at work, and it does not differ qualitatively from passive smoking occurring in other settings. Therefore it appears sensible to extrapolate from what is known about health risks in settings such as the home. There is too little known to quantify precisely workplace risks due to passive smoking. However, the weight and consistency of the epidemiologic evidence, backed up by the data from active smoking, favor a causal link between passive smoking and serious disease, especially lung cancer. In the light of this evidence, enough is known to justify action to reduce smoking at work.

Acute Effects of Passive Smoking on Respiratory Function in Asthmatic Patients

Fifteen asthmatic children, whose prick tests to tobacco smoke were all negative, were exposed to sidestream cigarette smoke (passive smoking) for 30 minutes in a room in which the carbon monooxide concentration was 7-8ppm. At the time of study, the patients were asymptomatic and had normal or nearly normal respiratory function. Patients showed an increase of 0.21per cent in carboxyhemoglobin as a result of the passive smoking. Passive smoking produced almost no change in the flow volume curves. However, there was a decrease in functional residual capacity (FRC), thoracic gas volume (TGV) and specific airway conductance (SGaw) More interestingly, airway resistance (Raw) showed a continuous increase, even at 6 hours after passive smoking. These findings suggest that passive smoking does not induce allergic reaction to tobacco smoke, but does stimulate bronchial hyperactivity in asthmatic children.

Acute Effects of Passive Smoking on Lung Function and Airway Reactivity in Asthmatic Subjects

We studied the acute effects of one hour of passive cigarette smoking on the lung function and airway reactivity of nine young adult asthmatic volunteers. At the time of this study, the subjects were asymptomatic and had normal or nearly normal lung function. Passive smoking produced no change in expiratory flow rates. However, there was a small decrease in nonspecific bronchial reactivity, as assessed by methacholine inhalation challenge testing (p = 0.022). Pharmacologically active substances present in cigarette smoke, such as nicotine, may explain the observed change in airway reactivity. Although the finding of decreased airway reactivity might suggest that passive smoking produces a "protective" effect on the underlying asthma, the observed change in reactivity was slight and of uncertain clinical significance. We conclude that passive smoking presents no acute respiratory risk to young asymptomatic asthmatic patients.