人體呼出微粒監測系統之應用

Abstract

傳統上，認為呼吸道疾病的傳播方式是經由病患咳嗽或打噴嚏所產生的生物氣膠所引起，事實上，咳嗽及打噴嚏的動作是易引起周遭人群注意及迴避的，因這兩種傳播方式會引起較大聲響，且產生之液滴為高濃度及粒徑亦較大。然而，近幾年許多研究發現，人體在「安靜的」正常呼吸下亦能產生微粒，因此，認為正常呼吸在呼吸道疾病傳播上亦扮演重要的角色，特別是在較擁擠的公共場所及醫療場所。目前研究發現人體呼出微粒(Exhaled Breath Aerosol, EBA)的產生機制有兩種，一為因呼吸道中的紊流將呼吸道管壁上的黏液捲起而產生氣懸膠隨後被呼出(Turbulence induced aerosolization)；另一種機制為細支氣管液體薄膜破裂模式(Bronchiole Fluid Film Burst, BFFB)。本研究之目的是利用已建置完成之人體呼出微粒監測系統以達到：(1) 驗證過去文獻提出之肺部產生微粒之機制。(2) 探討呼出微粒濃度與呼吸型態及肺功能參數間之相關性。(3) 比較受試者在健康及感冒狀態下，呼出微粒濃度之變化情形。 以閉氣方式證實一般呼吸產生的微粒主要是因收縮的小支氣管再次打開所形成，且產生於吸氣階段。每口呼氣的微粒數隨潮氣容積增加而增加，但呼吸頻率無明顯影響，推論是因潮氣容積增加時，會使收縮及再打開的細支氣管數量增加，而此現象與頻率無關；在相同呼吸條件下，不同受試者間每口呼氣的微粒數有顯著差異，但同一受試者在相同呼吸條件且不同時間下，每口呼氣的微粒數的再現性高，可能因個體間的氣管中黏液特性及呼吸道構造不同所致。粒徑分佈眾數為0.3微米，有高達90%的微粒為次微米的粒徑，且不同受試者間無明顯差異。另外，在健康與感冒狀態下的呼出微粒濃度比較方面，同一受試者在相同條件下，感冒時會呼出較高濃度的微粒，約高出20~50%，認為可能與呼吸道中的黏液特性發生變化有關，而此狀況的產生對於醫療院所的照護者是一大威脅。

Coughing and sneezing are known to spread respiratory diseases. The aerosol outputs by coughing and sneezing are visible because of the high number concentration and large micro-metered size. Coughing and sneezing can be loud and irritating to people around, which is good because it alerts people to stay away. In contrast to these audible and visible aerosol generation mechanisms, several recent studies reported that “silent” tidal breathing can also generate aerosols. This might play a more important role in disease transmission, especially in intensive care and emergency care units. Two aerosol generation mechanisms were proposed in previous studies: the turbulence induced aerosolization and the Bronchiole Fluid Film Burst (BFFB). The main objectives of the present study were (1) to verify the proposed lung aerosol generation mechanisms, (2) to study the dependency of exhaled breath aerosol on breathing pattern and other lung function variables, and (3) to characterize the differences in exhaled breath aerosols between healthy and sick conditions of the same subjects. The results supported the hypothesis of BFFB through a breath-holding technique. The EBA (Exhaled Breath Aerosol) count per breath increased with increasing tidal volume. However, breathing frequency did not affect EBA generation. We speculated that this is due the number of closing-up and re-opening terminal bronchioles increased with increasing tidal volume. This number apparently is independent of breathing frequency. The between-subject variation is much higher than the within-subject variation, indicating that the mucus properties and the respiratory tract structure vary more significantly among subjects. The EBA of all tested subjects showed similar size distribution, with a count median diameter of 0.3 micrometer and GSD of 2.4. When subjects were sick, they tended to generate more exhaled breath aerosols, showing 20 to 50% increase in count per breath, a bad news to health-care workers.