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Long-term exposure to secondhand smoke (SHS) is associated with impaired vascular function. The authors investigated the vascular and blood pressure (BP) reactions to acute SHS exposure. Twenty-five healthy nonsmoking adults underwent a 1-hour exposure to SHS (mean fine particulate matter <2.5 μm level=315±116 μg/m3). Microvascular endothelial-dependent vasodilatation (EDV) (EndoPAT, Itamar Medical, Caesarea, Israel) and aortic hemodynamics/compliance (SphygmoCor, AtCor Medical, West Ryde, Australia) were measured before and after the SHS exposure with BP measured every 15 minutes during and for a 24-hour period before and after the exposure. SHS exposure did not change EDV, aortic hemodynamics, arterial compliance, or 24-hour BP. However, diastolic BP significantly increased during the SHS exposure period by 3.4±5.6 mm Hg. Our brief SHS exposure did not impair microvascular endothelial function or arterial compliance in healthy nonsmoking adults, but brachial diastolic BP increased.
Prev Cardiol. 2010;13:175–179.©2010 Wiley Periodicals, Inc.
Exposure to secondhand smoke (SHS) increases cardiovascular (CV) risk.1,2 Several studies have shown that a ban on indoor smoking in public venues reduces CV events within only months.3,4 Thus, it is possible that even short-term exposure (or repeated brief contacts with) SHS can rapidly impart clinically meaningful health risks.2
Among several potential biologic mechanisms explaining this association, the most recent Surgeon General’s Report states that the evidence is sufficient to infer a causal relationship between SHS and endothelial cell dysfunction.5 Although long-term exposure is consistently linked to impaired vascular function,1 the few studies reporting the effects of brief exposure are inconsistent.2 In addition, the acute effect of SHS on systemic hemodynamics also remains controversial.2 Avoidance of SHS is proven to reduce CV risk and should be recommended to all high-risk patients.3,4 Nonetheless, many individuals may be involuntarily exposed.
The aims of this study were therefore to specifically determine whether short-term SHS exposure impairs vascular function and/or alters systemic hemodynamics. Since most previous reports have focused on only one vascular territory (thereby missing the entirety of potentially discordant CV responses),1,2 we investigated the effect of SHS on both microvascular endothelial-dependent vasodilatation (EDV) and large arterial compliance and central aortic hemodynamics.
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The study protocol was approved by the University of Michigan institutional review board. We recruited 25 healthy nonsmoking adults aged 18 to 50 years who lived in a nonsmoking household and were not exposed to SHS on a routine basis. All participants were free of known CV disease or risk factors (fasting glucose <126 mg/dL, low-density lipoprotein cholesterol <160 mg/dL, blood pressure [BP] <140/90 mm Hg) and taking no medications known to alter vascular function. All female participants had a negative urine pregnancy test result upon enrollment.
Participants were fasting >8 hours prior to each study visit. They underwent a 1-hour exposure to SHS in a smoking research laboratory between 8 and 9 am. All vascular studies and systemic hemodynamic measurements were done on-site before and after each exposure by the same technician using the same equipment. Participants wore an ambulatory BP monitor (90207 ABP Monitor; Spacelabs Healthcare, Inc., Issaquah, WA) for 24 hours before and after the exposure.
Exposures occurred in a ventilated room where participants remained resting in a seated position throughout the study. We generated mainstream and sidestream SHS because both are toxicologically important.1,2 One cigarette was actively smoked within 2 m of the participant, while we left a second cigarette lit on an ashtray within 1 m of the participant. Our smoker smoked at a rate of 1 cigarette every 15 minutes, and the cigarette in the ashtray was replaced every 15 minutes. Carbon monoxide (CO) levels were continuously monitored (Thermo Environmental Franklin, MA), which always remained <10 PPM to assure CV effects were not attributed to CO. Fine particulate matter <2.5 μm (PM2.5) levels were continuously measured during exposures by a laser-based light scattering instrument (nephelometer, MIE Inc, Bedford, MA) that was placed at the level of the head within 1 m of the participant. Each participant had his or her dominant arm brachial BP measured in triplicate at the start and every 15 minutes throughout the exposure. The BP results were blinded to the participants and recorded in the memory of the automated oscillometric device (Omron HEM-712C, Omron, Schaumburg, IL). The mean of the second and third BP and heart rate were recorded for analyses.
Participants lay supine for 10 minutes prior to all vascular studies. First, central aortic BP waveform and hemodynamic analyses were performed by right arm radial artery tonometer. Second, arterial compliance was measured by determining pulse wave velocity (carotid and femoral artery tonometer positions). Both methods were performed using the SphygmoCor system (AtCor Medical, West Ryde, Australia), as we have previously described.6 Third, participants remained supine for 5 minutes, and then finger EDV was measured by determining the reactive hyperemia index (RHI) using the EndoPAT2000 system.7 Last, endothelial-independent vasodilatation was determined by the finger nitroglycerin index, as previously described.7
Data were collected and analyzed using SPSS 15.0 for Windows. All pre-exposure vs post-exposure parameters were compared by 2-tailed paired t tests. The slopes of the changes of the intra-exposure BP and heart rate were compared vs a slope of zero by a linear mixed model analysis. The 5 time points for BP and heart rate were compared by a mixed model analysis. Significance was defined as a P<.05.
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All participants were healthy and without CV risk factors (Table I). PM2.5 levels during exposure were high (315±116 μg/m3; range 158–565 μg/m3), yet at environmentally relevant concentrations, as found in public smoking areas in restaurants and bars.8 SHS exposure did not significantly impair EDV (RHI), arterial compliance (pulse wave velocity), or central aortic or 24-hour ambulatory brachial BP (Table II).
Table I. Participant Characteristics
| ||Entire Cohort (N=25)|
| Age, y||32±9|
| BMI, kg/m2||25.5±3.8|
|Blood laboratory values|
| Total cholesterol, mg/dL||178±31|
| LDL-C, mg/dL||110±30|
| HDL-C, mg/dL||52±13|
| Triglycerides, mg/dL||85±51|
Table II. Vascular and Hemodynamic Responses Before and After Secondhand Smoke Exposure
| ||Pre-Exposure||Post-Exposure||24 Hours Post|
| Reactive hyperemia index||1.76±0.57||1.76±0.42||–|
| Nitroglycerin index||1.44±0.75||1.40±0.51||–|
|Arterial compliance and hemodynamics|
| Central systolic blood pressure, mm Hg||105±10||101±8||–|
| Pulse pressure, mm Hg||33±6||27±5||–|
| Augmentation pressure, mm Hg||4±5||4±5||–|
| Augmentation index, %@ HR 75||7±13||5±19||–|
| Ejection duration, %||35±5||33±5||–|
| Subendocardial viability ratio, %||166±41||184±36||–|
| Pulse wave velocity, m/s||7±1||7±1||–|
|Ambulatory blood pressure monitoring|
| Systolic blood pressure, mm Hg||112±8||–||112±8|
| Diastolic blood pressure, mm Hg||67±6||–||68±7|
| Heart rate, beats/min||72±12||–||73±15|
Table III shows the exposure BP and heart rate responses; systolic BP and heart rate did not change. However, diastolic BP significantly increased (P<.05) during the SHS exposure (Figure), and it increased in 19 participants (76%).
Table III. Blood Pressure and Heart Rate During Secondhand Smoke Exposures
|Time, min||Systolic Blood Pressure, mm Hg||Diastolic Blood Pressure, mm Hg||Heart Rate, beats/min|