Key result
Short-term secondhand smoke exposure was associated with immediate declines in heart rate variability, including a 7.8% decrease in SDNN per 100 μg/m3 increase in PM2.5, and increased inflammation.
Why the study?
Does acute secondhand tobacco smoke exposure reduce heart rate variability and increase inflammation in non-smoking construction workers?
Observational (n=32)
No
Does acute secondhand tobacco smoke exposure reduce heart rate variability and increase inflammation in non-smoking construction workers?
Effect estimate: -7.8% change
p-value: p=0.012
Short-term secondhand smoke exposure in non-smokers is associated with rapid declines in heart rate variability and delayed increases in systemic inflammation, suggesting potential mechanisms for acute cardiovascular risk.
May signal acute CV vulnerability in SHS-exposed non-smokers; leaves open causal effects and whether exposure reduction improves outcomes.
BACKGROUND: Although 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. METHODS: Non-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. RESULTS: A 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. CONCLUSIONS: Our 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.
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Zhang et al. (2013) conducted an observational in Healthy non-smokers (n=32). Secondhand tobacco smoke (SHS) exposure vs. Baseline (pre-exposure) was evaluated on Change in heart rate variability (SDNN) immediately following exposure per 100 μg/m3 increase in PM2.5 (-7.8% change, p=0.012). Short-term secondhand smoke exposure was associated with immediate declines in heart rate variability, including a 7.8% decrease in SDNN per 100 μg/m3 increase in PM2.5, and increased inflammation.
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