| Summary: | 碩士 === 國立臺灣大學 === 職業醫學與工業衛生研究所 === 90 === Objective: To evaluate whether air pollution will affect susceptible population heart rate variability (HRV) and blood pressures.
Methods: We conducted a panel study on 10 susceptible adults and 1 healthy control. Three of susceptible adults are chronic obstructive pulmonary diseases (COPD) patients and seven are obstructive sleep apnea syndromes (OSAS) patients. In order to evaluate whether air pollution will affect heart rate variability (HRV) and blood pressures. We measured continuously each subject’s 24-hour electrocardiographics by PacerCorder, blood pressures by DynaPulse, carbon monoxide exposure by CO compact portable analyzer and submicron particle exposures (PM1, particulates ≦ 1 μm in diameter) by P-Trak twice during the study. We used linear mixed-effects models to estimate the relationship between particle exposures and their physiological response, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR) and the time-domain measures of HRV, such as standard deviation of normal-to-normal (NN) intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent NN intervals (r-MSSD), and the frequency domain measures of HRV, such as low frequency (LF, 0.04-0.15 Hz), and high frequency (HF, 0.15-0.40 Hz). The response variables include SDNN, r-MSSD, LF, HF were log10-transformed.
Results: After adjusting for age, body mass index, tobacco exposure and disease. We found significant association between particle exposures and blood pressure, HRV parameters of time and frequency domains among susceptible adults. During wake period, 4-hour moving PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN, r-MSSD, LF, HF were —0.033, -0.050, -0.090, -0.125. During sleep period, 5-minute PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN, r-MSSD, LF, HF were —0.035, -0.036, -0.075, -0.70. 4-hour PM1 average increased 10,000 particles/cm3, the β coefficients of LF, HF, DBP were -0.136, -0.109, 2.730. We further adjusted for SpO2 during sleep period, the 5-minute PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN, r-MSSD, LF, HF were —0.036, -0.043, -0.066, -0.74. 4-hour PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN r-MSSD, LF, HF, SBP, DBP MAP were -0.098, -0.144, -0.371, -0.169, 4.03, 3.44, 3.29. We also investigated the relationship of blood pressure, HRV parameter with moving PM1 averages among OSAS subjects and found that during wake period, 4-hour moving PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN, r-MSSD, LF, HF were —0.047, -0.068, -0.112, -0.153. During Sleep period that adjusted for SpO2, age, body mass index, tobacco exposure and disease. The 5-minute PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN, r-MSSD, LF, HF were —0.034, -0.042, -0.065, -0.062. 4-hour PM1 average increased 10,000 particles/cm3, the β coefficients of SDNN r-MSSD, LF, HF, DBP MAP were -0.085、-0.127、-0.202、-0.171、3.72, 3.21. We didn’t find any significant association between particle exposures and blood pressure, HRV parameters of time and frequency domains among healthy control.
Conclusions: Our findings suggested that submicron particles might have short-term effects and long-term effects on OSAS and COPD patients’ time and frequency domains of HRV as well as blood pressures in wake and sleep periods. The decrease in HRV became larger as the exposure metric increased. The mechanism of such effects was related to either immediate autonomic stress or delayed cytokines production after exposures.
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