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綠色通勤族之交通空氣污染暴露評估

為了解決MS279WG PTT的問題，作者吳宗鋼 這樣論述：

苯（benzene）、甲苯（toluene）、二甲苯（ethylbenzene）與鄰間對二甲苯（xylenes）這類合稱為BTEX的揮發性有機污染物和細懸浮微粒（PM2.5）為常見的交通空氣污染物（traffic-related air pollutant, TRAP），為了降低車輛排放，許多人們開始選擇成為綠色通勤族—透過騎乘腳踏車或電動機車來通勤。儘管如此，這些通勤族也因為接近路上的車輛排放源，而較其他通勤族（如轎車駕駛、捷運通勤族）有較高的空氣污染物（TRAP）濃度暴露量。為進行綠色通勤族的暴露評估，政府的空品測站或是低階微型感測器的監測方式不失為一種方法。但因為空品測站的密度與位置或

是低階感測器的量測精準度與架設位置的不確定性，使得兩者的量測值代表性受到限制。因此，在本研究中，使用直接量測的方式評估綠色通勤族的暴露。此外，亦以現場的量測結果為基礎進行暴露濃度模式的建立，模擬與評估最低暴露濃度路徑與最短通勤路徑的暴露濃度差異。本研究分成三階段的實驗。在第一階段，於自行車道架設固定式監測儀器設備以監測污染物暴露濃度，並藉由監測值結合模式分析以鑑別影響暴露濃度的環境因子與各類車輛種類的貢獻程度。在監測儀器方面，PM2.5以連續監測儀器，而BTEX則以近連續監測儀器進行暴露濃度評估。在第二階段，則是在規定的騎乘路線上，藉由綠色通勤族所攜帶監測設備，以移動監測的方式評估個人暴露，且

評估與鑑別影響暴露濃度的環境因子與各類車輛種類的貢獻程度。此階段亦使用連續監測儀器進行PM2.5的暴露濃度評估，BTEX因儀器技術的限制，只能使用時間累積式的方法來評估。資料分析方面，第一與第二階段皆以廣義線性回歸模式（generalized linear model），包含混合模式（mixed-effect model）評估影響暴露濃度的環境因子與各類車輛種類的貢獻程度。而在第二階段，亦使用健康衝擊模式（Health Impact Modelling, HIM）的方式評估自行車與電動機車通勤族的全因死亡率（All-cause mortality, ACM）風險差異。在第三階段，於亞洲三城市（

台北、大阪與首爾）藉由自行車騎士配戴PM2.5低階採樣器，以移動監測的方式評估個人暴露濃度。以個人暴露濃度為基礎，結合路徑上之土地利用特性以及機械學習演算法中的隨機森林演算法（Random Forest），建立城市PM2.5濃度分布推估模式。並以空間交叉驗證（Spatial cross-validation）方法驗證模式表現，避免模式評估過程因為空間自相關性（Sptail Autocorrelation, SAC）的狀況而有過度優化模式表現的假象。最後，以QGIS（Quantum geographic information system）之的最短路徑工具（shortest path）模擬最低

暴露濃度路徑與最短通勤路徑，並評估兩種路徑的暴露濃度差異。實驗結果顯示，主要影響綠色通勤族的交通污染物濃度暴露的因子與來源多數與交通有關，如路徑的種類、通勤的時間點、通勤工具、與交通有關的土地利用特徵、車輛數（如機車）。另外，BTEX與PM2.5的暴露濃度相比，有較高的空間變異特性。因此，BTEX可以成為評估都市土地利用規劃差異的空氣品質指標物。而第二階段的模式分析結果也顯示，透過替代通勤路徑可以有效降低空氣污染物的暴露濃度。在第二階段，HIM的結果顯示，自行車通勤族可因通勤的時間點、通勤的時間在替代通勤路徑，降低全因死亡率（ACM）的風險。在第三階段，在完成建立暴露濃度地圖後，透過模擬路徑的

比較，所有的低暴露濃度路徑的累積暴露濃度都比最短路徑的暴露濃度低。儘管有些路徑比較的結果顯示暴露濃度差異百分比不大，但每天通勤的暴露差異量，透過每日的積累，長遠來看是有其效益之存在。總結來說，避開交通量大或是有許多交通相關的土地利用特徵的路徑或時間，是可以有效降低通勤所累積的暴露濃度。而騎乘腳踏車所帶來的效益，除了降低暴露濃度外，透過騎車這項運動所產生的健康效益，有機會可以克服暴露於空氣污染物所帶來的風險。對於政策推行者，可以考慮建立以空氣污染物暴露濃度為基礎的路徑規劃的平台，供綠色通勤族使用。

Association of air pollution and body composition in obstructive sleep apnea

為了解決MS279WG PTT的問題，作者NGUYEN THANH TUNG 這樣論述：

A relationship between exposure to ambient air pollution and obstructive sleep apnea (OSA) severity was reported in epidemiological studies. Exposure to air pollution may result in increased oxidative stress, inflammation, epithelial barrier disruption, and permeability in the upper airway, which c

ould all predispose to OSA. However, there is paucity of data on the biological mechanism of this hyperpermeability. Furthermore, the overnight changes in body composition after exposure to air pollution and how they affected the severity of OSA is still unclear.To investigate the associations of bo

dy composition changes with OSA, pre- and post-sleep body composition of 1584 patients with OSA were collected. We observed that increases in limb fat deposition and visceral fat level were associated with increased OSA severity. Each increase in total fat deposition and segmental fat deposition was

associated with increased odds ratio of positional OSA. In patients with positional OSA, an increase in the fat distribution of the limbs was associated with increases in the total arousal index, especially in the non-rapid eye movement (NREM) stage.To examine the association of air pollutant expos

ure with nocturnal body composition changes and OSA, we measured pre- and post-sleep body composition of 197 subjects from a sleep center and their individual air pollution exposure (particulate matter (PM) less than 2.5 µm in aerodynamic diameter (PM2.5), ozone (O3), and nitric dioxide (NO2)). We o

bserved that exposure to air pollutants was associated with total muscle mass and leg fat percentage changes. We found an association between PM deposition in lung regions, especially in the alveolar region, and body fat accumulation in OSA. The leg fat deposition and total muscle mass changes was f

ound to be associated with the apnea-hypopnea index (AHI). These findings implied that air pollution was associated with increases in the leg fat percentage and total muscle mass changes, thus aggravating OSA severity.We then collected road dust PM2.5 from 20 cities in China and treated to human pha

ryngeal epithelial (FaDu) cells. We observed that road dust PM2.5 exposure led to declines in cell viability and increases in lactate dehydrogenase (LDH) and interleukin (IL)-6. PM2.5, especially the inorganic elemental components, led to decreases in E-cadherin and occludin and increases in EGFR an

d phosphorylated (p)-EGFR on FaDu cells, later confirmed by the knockdown of E-cadherin. The findings indicate that PM2.5 may induce the inflammation, disrupt the epithelial barrier integrity, and increase the permeability in human upper airway through the regulation of occludin, E-cadherin, EGFR, a

nd p-EGFR.Together, the air pollution-induced hyperpermeability could increase overnight fluid shift and body composition changes, thus aggravating OSA. Air pollution, particularly the PM2.5, had the potential to increase the severity of OSA through body composition changes and upper airway hyperper

meability. Our study shed light on the etiology of OSA and positional OSA. Decreasing the total fat mass and fat percentage may reduce OSA severity. Finally, measures to decrease air pollution in urban areas could be beneficial for OSA patients.