Secondhand tobacco smoke exposure and heart rate variability and inflammation among non-smoking construction workers: a repeated measures study

Abstract

BackgroundAlthough it has been well recognized that exposure to secondhand tobacco smoke (SHS) is associated with cardiovascular mortality, the mechanisms and time course by which SHS exposure may lead to cardiovascular effects are still being explored.MethodsNon-smoking workers were recruited from a local union and monitored inside a union hall while exposed to SHS over approximately 6 hours. Participants were fitted with a continuous electrocardiographic monitor upon enrollment which was removed at the end of a 24-hr monitoring period. A repeated measures study design was used where resting ECGs and blood samples were taken from individuals before SHS exposure (baseline), immediately following SHS exposure (post) and the morning following SHS exposure (next-morning).Inflammatory markers, including high sensitivity C-reactive protein (CRP) and white blood cell count (WBC) were analyzed. Heart rate variability (HRV) was analyzed from the ECG recordings in time (SDNN, rMSSD) and frequency (LF, HF) domain parameters over 5-minute periods. SHS exposure was quantified using a personal fine particulate matter (PM2.5) monitor.Linear mixed effects regression models were used to examine within-person changes in inflammatory and HRV parameters across the 3 time periods. Exposure-response relationships with PM2.5 were examined using mixed effects models. All models were adjusted for age, BMI and circadian variation.ResultsA total of 32 male non-smokers were monitored between June 2010 and June 2012. The mean PM2.5 from SHS exposure was 132 μg/m3. Immediately following SHS exposure, a 100 μg/m3 increase in PM2.5 was associated with declines in HRV (7.8% [standard error (SE) =3%] SDNN, 8.0% (SE = 3.9%) rMSSD, 17.2% (SE = 6.3%) LF, 29.0% (SE = 10.1%) HF) and increases in WBC count 0.42 (SE = 0.14) k/μl. Eighteen hours following SHS exposure, a 100 μg/m3 increase in PM2.5 was associated with 24.2% higher CRP levels.ConclusionsOur study suggest that short-term SHS exposure is associated with significantly lower HRV and higher levels of inflammatory markers. Exposure-associated declines in HRV were observed immediately following exposure while higher levels of CRP were not observed until 18 hours following exposure. Cardiovascular autonomic and inflammation responses may contribute to the pathophysiologic pathways that link SHS exposure with adverse cardiovascular outcomes.

Are the Associations of Cardiac Acceleration and Deceleration Capacities With Fine Metal Particulate in Welders Mediated by Inflammation?

“…We did not find significant differences between baseline and post-shift levels in the levels of any of CRP, IL-6, IL-8, and IL-10. This finding is in contrast to what was previously independently documented by Zhang and Bruno in this study population 26, 27 . Whereas Zhang et al and Bruno et al had used paired samples from these participants on a non-weld day at baseline and next morning as post-exposure samples in assessing the effect of secondhand smoke exposure, we restricted our samples to the weld day because we were interested in determining the effect of weld fume exposure.…”

“…We may therefore be missing the right time window to capture observable differences between baseline and post-exposure mediator levels. Next-morning samples have been shown to capture better changes in inflammatory markers following injurious stimuli 26, 27 .…”

“…CRP, IL-6, IL-8, and IL-10 were log-transformed to approximate a normal distribution. Based on our previous work using this study population, we had planned a priori to adjust for age, active smoking status, secondhand smoke exposure, time of day when ECG was obtained, season of study, previous weld exposure (last weld day), presence of heart problems, and baseline cardiac autonomic function (baseline AC or DC for AC and DC models respectively) 11, 26, 27 . These were the relevant covariates considered in the study of the acute association of PM 2.5 exposure on AC and DC using lagged hourly models.…”

The effect of workplace smoking bans on heart rate variability and pulse wave velocity of non-smoking hospitality workers

“…Our findings are also supported by other studies that looked at acute effects of SHS on HRV and found consistent decreases in SDNN as soon as subjects were exposed (Pope et al 2001) or right after exposure (Zhang et al 2013; Wilson et al 2010). The effect of active smoking on heart rate variability has been studied extensively.…”

Mechanistic data support protecting non-smokers from the lethal effects of second-hand smoke

“…Acute effects of exposure to SHS on HRV, a marker of autonomic tone, have been shown in previous studies using cross-sectional approaches (Pope 2001; Wilson et al 2010; Zhang et al 2013), but Rajkumar et al present results of the first prospective study to examine effects of reducing SHS exposure on HRV, with addition of a dose-response in a real-world setting. Alterations in HRV have been linked to changes in particulate matter air pollution in a number of studies, but the results have not always been consistent, perhaps due to differences in methods and host factors (age, sex, comorbidities, etc) between studies (Pieters et al 2012).…”