室內空氣污染對心血管血流動力學之影響:24 小時同步監測

Abstract

背景:由於大部分時間人們會待在室內環境中，而室內空氣污染對心血管疾病的影響 為近年來全球關注的議題。本研究主要目的是研究室內空氣污染對心血管血流動力學 的影響。 方法:在 2017 及 2018 年間，我們在台北市及新北市總共從 60 個家戶中招募 73 位受 測者，每位受測者皆要配戴 24 小時監測的血流動力學儀器(DynaPulse 5000A, Pulse Metric Inc., San Diego, CA)，以及於家戶的客廳配置 24 小時室內空氣污染監測儀器， 包括:測量一氧化碳、二氧化碳濃度、溫度及相對濕度、懸浮微粒濃度、揮發性有機 物質濃度、以及甲醛濃度。而我們應用時間序列分析來評估當暴露到每四分位距 (Interquartile range, IQR))之室內空氣污染物時，心血管動力學所受到的影響。而混合 效果模型被應用在控制年齡、性別、身體質量指數、高膽固醇血症、糖尿病、抽菸習 慣、受測者活動、室內溫度及相對濕度。另外，次分組分析如年齡、性別、抽菸習慣、 燒香習慣及通風狀態。 結果及討論:在此研究中，從 24 小時同步監測室內空氣污染時，可以發現臂動脈及 中心動脈收縮壓、以及心輸出量會顯著上升，而系統性血管之順應性會下降。當暴露 到每增加一個 IQR 之懸浮微粒(懸浮微粒粒徑小於 1、2.5、10 微米(PM1.0, PM2.5, PM10))， 收縮壓會分別增加 0.369 (0.096, 0.641)、0.319 (0.082, 0.5556)及 0.478(0.124, 0.833)毫米 汞柱。而當有人暴露到較高濃度的室內污染物時，心血管功能也會變弱。每增加暴露到一個 IQR 的一氧化碳及二氧化碳時，心跳會分別增加 0.881 (0.388, 1.374) 和 0.838 (0.319, 1.358) 每分鐘之心跳數，而當暴露到每增加一個 IQR 之懸浮微粒(PM1.0, PM2.5, PM10)，心跳會分別增加 0.279 (0.090, 0.468)、0.241 (0.077, 0.405)及 0.359 (0.113, 0.604) 每分鐘之心跳數。而每增加一個 IQR 之一氧化碳及二氧化碳時，體血管彈性分別會減 少 -0.011(-0.018, -0.003) 和 -0.007 (-0.017, -0.0005) 毫升/毫米汞柱。而暴露到每增加 一個 IQR 之懸浮微粒(PM1.0, PM2.5, PM10)，則會分別減少-0.008 (-0.012, -0.005)、- 0.005 (-0.009, -0.002)及-0.011 (-0.015, -0.007) 毫升/毫米汞柱。次分組分析則顯示居住 在二氧化碳濃度高於 600 ppm 濃度之較差通風環境下，其室內空氣汙染較嚴重，而且 相較於較佳通風環境(室內二氧化碳 < 600 ppm)之受測者，有較不好之心血管效應且 更明顯。而有抽菸習慣之受測者相較於無抽菸習慣之受測者，當暴露到一氧化碳及甲 醛時，會有較顯著的心跳數及心臟輸出量。另外，燒香習慣會造成一氧化碳、二氧化 碳、懸浮微粒及甲醛濃度的增加，而且會增加血壓及心臟之負荷量。 結論:室內空氣污染和血壓、心跳、及心臟負擔成正相關，且有可能造成全身血管彈 性變差，因此，為預防心血管疾病應積極改善居家的空氣品質。

Backgrounds: Since people spend the majority of their lifetime staying in indoor environments, the contribution of indoor air pollution to human health deserves to be investigated. This study aims to investigate the concurrent real-time monitoring of indoor air quality and cardiovascular function. Methods: During 2017 to 2018, 73 subjects from 60 families in both Taipei and New Taipei city, Taiwan, were recruited. Concurrent 24-h real-time monitoring of indoor air quality, including carbon monoxide (CO), carbon dioxide (CO2), particulate matter (PM), total volatile organic compound (TVOC), and formaldehyde, were set up in the living room and cardiovascular hemodynamics were performed for each participant. Time series analysis was applied to estimate the change of cardiovascular hemodynamics for every one interquartile range (IQR) increase in concentration of indoor air pollutants. The linear mixed effect models were applied to estimate the effects of indoor air pollution on cardiovascular hemodynamics after controlling age, gender, body mass index, hypercholesterolemia, diabetes, smoking habits, subject’s activity, indoor temperature, and relative humidity. Further subgroup analysis was stratified by age, gender, smoking status, incense burning habits, and ventilation status. Results: Concurrent 24-h real-time monitoring of indoor air pollution significantly increase brachial and central systolic blood pressure (SBP), cardiac output, and reduce systemic vascular compliance in 73 participants. Concurrent indoor CO2 exposure significantly increases brachial and central blood pressure. Per IQR increase in exposure to particulate matter (PM1.0, PM2.5 and PM10) also significantly increase SBP by estimated change (95% confidence intervals) of 0.369 (0.096, 0.641), 0.319 (0.082, 0.556), 0.478 (0.124, 0.833) mmHg, respectively. Furthermore, cardiac functions appear worsened among those who are exposed to higher concentration of indoor air pollution. Per IQR increase in CO and CO2 exposure can increase heart rate by 0.881 (0.388, 1.374) and 0.838 (0.319, 1.358) bpm, respectively. Per IQR increase in particulate matter (PM1.0, PM2.5 and PM10) exposure can increase heart rate by 0.279 (0.090, 0.468), 0.241 (0.077, 0.405), 0.359 (0.113, 0.604) bpm, respectively. A significant decrease in vascular function also was shown. Per IQR increase in CO and CO2 exposure can decrease SVC by -0.011(-0.018, -0.003) and -0.007 (-0.017, -0.0005) mL/mmHg, respectively. As for PM, per IQR increase in PM1.0, PM2.5, and PM10 exposure, SVC would decrease by -0.008 (-0.012, -0.005), -0.005 (-0.009, -0.002), and -0.011 (-0.015, -0.007) mL/mmHg, respectively. Subgroup analysis shows subjects with poor indoor ventilation, defined by indoor CO2 greater than 600 ppm, significantly impairs indoor air quality and subjects of living in poor ventilation environment would have worsen cardiac hemodynamics than living in good ventilation environment. Subjects with smoking habits experienced more significant effects on heart rate and cardiac output while increasing in exposure to CO and formaldehyde compared to those of non-smoking habits. In addition, habitual incense burning increased indoor CO, CO2, PM and formaldehyde levels and the increase may modify the association between indoor air pollution and blood pressure and cardiac workload. Conclusions: Indoor air pollution is associated with increased blood pressure, heart rate, and cardiac workload, and impaired vascular compliance in personized 24-h real-time monitoring of cardiovascular hemodynamics. Improving indoor air quality should be one of main focus of proactive prevention of cardiovascular diseases.