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研究生：	周晏如 Chou, Yen-Ju
論文名稱：	食用油重覆油炸後之酸價與油品內含PAHs之變化情形及其對勞工呼吸道暴露之影響 Assessing Variations of Acid Values and Polycyclic Aromatic Hydrocarbon (PAH) Contents of Cooking Oils and Their Effects on Worker’s Inhalatory Exposure after Repeated Frying Processes
指導教授：	蔡朋枝 Tsai, Perng-Jy
學位類別：	碩士 Master
系所名稱：	醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health
論文出版年：	2011
畢業學年度：	99
語文別：	英文
論文頁數：	55
中文關鍵詞：	食用油、油炸、酸價、多環芳香烴化合物、Microtox毒性
外文關鍵詞：	Soybean oil, Frying process, Acid value, Polycyclic aromatic hydrocarbons (PAHs), Microtox acute toxicity
相關次數：	點閱：185 下載：11
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本研究探討食用油重覆油炸後其油品內之酸價值（acid value; AV）與逸散至空氣中之多環芳香烴化合物（polycyclic aromatic hydrocarbons; PAHs）濃度及毒性之變異情形。本研究選取市面上用量最多之一種食用油（沙拉油）及一種食物（雞肉），進行重覆油炸。油炸前後油品利用滴定法量測其酸價值，並以PS-1高流量採樣器與微孔均勻沈積衝擊器（Micro-Orifice uniform deposit impactor; MOUDI）進行空氣樣本採樣，以瞭解勞工作業環境暴露濃度與區域粒徑之分佈。所獲得之樣本並以氣相層析儀/質譜儀（Gas Chromatography/Mass Spectrometry; GC/MS）及螢光檢測儀（Microtox Analyzer），分別分析油炸後逸散至空氣中及其油霧滴之急毒性。
研究發現沙拉油每日油炸四小時，連續油炸七天之全部AV值並未超過我國衛生署食品衛生處訂定之標準值（2 mg KOH/g）。AV值會隨著油炸時間增加而增加，且油炸時間足以預測油品內之AV值。另作業環境Total-PAHs濃度隨油炸時間增加而增加，total benzo[a]pyrene equivalent （Total-BaPeq）濃度亦隨油炸時間增加而增加，由此得知食用油因重覆油炸使用，人體暴露之慢毒性亦隨之提高，亦可推論油炸時間足以預測食用油重覆油炸後其逸散至空氣中Total-PAHs濃度。另因食用油之黏滯度與油炸溫度不變，油炸作業環境第一天、第四天及第七天之PAHs粒徑分佈並未隨油炸時間增加而改變，其氣動粒徑質量中位數（mass median aerodynamic diameter; MMAD）分別為0.70 μm、0.66μm及0.84 μm，粒徑之幾何標準偏差（geometric standard deviation; GSD）分別為2.38、2.07及2.49。油霧滴濃度雖未隨油炸時間增加而增加，但PAHs濃度卻隨油炸時間增加而增加，其主要原因為單位油霧滴之PAHs含量上升所致。油炸第一天、第四天及第七天勞工PAHs平均暴露濃度：肺泡區（461、587及855 ng/m3）＞氣管與支氣管區（76.8、150及209 ng/m3）＞頭區（48.3、87.6及87.4 ng/m3）。產生之粒狀PAHs大部分會到達勞工呼吸道肺泡區。由螢光檢測儀之急毒性結果得知，油霧滴未隨油炸時間增加而增加，但其內含PAHs所造成之慢毒性卻隨油炸時間增加而增加，由此證明油炸環境造成作業人員之健康危害，應以慢毒性為主。油品重覆油炸AV值上升至標準值之天數，較PAHs達容許濃度之天數為少，故可利用油品AV值重覆測定來保護作業勞工之PAHs暴露。然食用油油炸過程產生之PAHs大部分會到達勞工呼吸道肺泡區，故應針對細粒徑部分之PAHs採取適當之控制方法，如裝設有效之局部排氣裝置。唯當局部排氣未裝置前，可要求勞工於油炸過程全程配戴合適之呼吸防護具（例如R或P系列之防油性粒狀物之呼吸防護具）。

This study is set out to assess the variation of acid values (AV) and contents of polycyclic aromatic hydrocarbons (PAHs) in repeatedly used frying oils and their effects on workers’ inhalatory PAH exposures. Deep frying chicken processes were conducted for 4 hours per day continuously 7 days by using one of the market most used frying oils (soybean oil). Pre- and post soybean oil bulk samples were collected and analyzed by titration analysis to determine their AVs. Air samples were collected by a PS-1 sampler and a Micro-Orifice uniform deposit impactor (MOUDI). Collected air samples were analyzed by Gas Chromatography/Mass Spectrometry (GC/MS) to determine the contents of 22 PAH compounds, and also analyzed by Microtox Analyzer to determine their acute toxicities.
In this study, we found that all measured AVs (0.29-1.22 mg KOH/g) were consistently less than the current standard value (2 mg KOH/g) set by Department of Health in Taiwan after the 7-day repeated frying process. AV increased as the frying time increased, and hence the frying time could be used to predict AV in frying oil. Total PAH concentrations and total benzo[a]pyrene equivalent (Total-BaPeq) concentrations increased as the frying time increased indicating that repeated deep-frying processes would result in the increased in the chronic toxicity of emitted PAHs. The above results also infer that the emitted total PAH emission concentrations could be predicted by the frying time. Because viscosity and temperature of cooking oil remained constant, PAH-containing particle size distributions obtained from the frying workplace atmospheres were cinsistently in a unimodal form. But the increase in the frying time would not result in the increase in oil mist concentrations. The fractions of emitted PAHs mainly exposed to the alveolar region. For all collected PAH samples, their Microtox acute toxicity results remained unchanged as the frying time increased, but increased in their corresponding Total-BaPeq concentrations. The above results indicate that the increase in the frying time would result in the health effect of the chronic toxicity rather than the acute toxicity. Our results also showed that the predicted frying time for AV to reach its limit value was shorter than that of measured PAH concentrations to reach the corresponding occupational exposure limit. The above result suugests that periodical observations of AV could be a suitable approach for protecting workers’ from PAH exposures. An appropriate control measure, such as the installation of a local exhaust ventilation system, is suggested to be taken to reduce workers’ exposures to the PAHs of the respirable fraction. But the respiratory protection equipment (R or P-series filters) could also be adopted if the above mentioned engineering control measures were not available.

摘要 I
Abstract II
誌謝 III
Contents IV
List of Tables VI
List of Figures	VIII
Chapter 1 Introduction 1
1.1 Background and significance	1
1.2 Objectives 2
Chapter 2 Literature Reviews 3
2.1 Types of cooking oil 3
2.2 Consumptions of cooking oil 3
2.3 Physical and chemical changes of cooking oil after deep-frying processes 3
2.4 Determinations and qualities of cooking oil	4
2.5 PAH emissions of cooking oil 5
2.6 Biotoxicity assessment 6
2.7 Intake rate of food types 7
Chapter 3 Materials and Methods	9
3.1 Study framework 9
3.2 Sampling strategies 9
3.2.1 Frying conditions 9
3.2.2 Air samples sampling 9
3.3 Samples analysis 10
3.3.1 AV analyses 10
3.3.2 Gaseous and particulate PAHs analyses 10
3.3.3 Microtox acute toxicity test 11
3.4 Quality assurance and quality control 12
3.4.1 AV 12
3.4.2 PAHs 12
3.4.3 Microtox acute toxicity test 13
3.5 Data analysis 14
3.5.1 Calculation of PAH concentrations and their corresponding BaP equivalent concentrations 14
3.5.2 Particle size distribution of particulate PAH concentrations for frying workplace 14
3.5.3 PAH exposure concentrations to the different regions of the respiratory tract 14
Chapter 4 Results and Discussion 16
4.1 The variations of AV in cooking oil after repeated frying processes 16
4.2 PAH concentrations during repeated frying processes	16
4.3 Size distributions of particle-phase PAHs 18
4.4 PAH concentrations exposure to different regions of the respiratory tract 19
4.5 Microtox toxicities of oil mists after repeated deep-frying processes 20
4.6 The associations among AV, PAH concentrations, and toxicities after repeated deep-frying proceses 20
Chapter 5 Conclusions and Suggestions 22
5.1 Conclusions	22
5.2 Suggestions	22
References 24
 
List of Tables
Table 1 The consumption (tons) of cooking oils in Taiwan in 2006 32
Table 2 Ingredients (g) in the flour dough and flavoring used for the preparation of 1.5 kg frying chicken wings	33
Table 3 Method detection limits (MDL) of GC/MS for 22 individual PAH standards 34
Table 4 Blank tests for sampling medium (glass fiber filter, PUF cartridge, and tube-type glass fiber filter) and analysis solvent (DCM and hexane) 35
Table 5 Mean and standard deviation (SD) of the GC/MS retention time for 22 individual PAH standards 36
Table 6 The precision and accuracy of recovery efficiencies for 22 individual PAH standards	37
Table 7 PAH species and their equivalent factors (TEFs) proposed by Nisbet snd Lagoy in 1992 38
Table 8 Measured AVs of cooking oil for samples collected during different frying days 39
Table 9 PAH concentrations of the background atmosphere and that of during the combustion of fuel gas 40
Table 10 Particle phase PAH concentrations for samples collected from different frying days 41
Table 11 Gaseous phase PAH concentrations for samples collected from different frying days 42
Table 12 Total PAH and total BaPeq concentrations for samples collected from different frying days 43
Table 13 PAH concentrations for samples collected during 1st, 4th, and 7th days frying process 44
Table 14 Oil mist concentrations for samples collected during 1st, 4th, and 7th days frying process 44
Table 15 PAH contents containing in oil mist for samples collected during 1st, 4th, and 7th days frying process 45
Table 16 Mean total particle phase PAH exposure concentrations and their standard deviation to the head, tracheobronchial, and alveolar regions for different frying days 45
Table 17 The fractions PAHs exposed to head, tracheobronchial, and alveolar regions for different frying days 46
Table 18 Microtox toxicities in EC50 (1/m3) for samples from deep-frying processes, background atmosphere, and fuel gas combustion 46
 
List of Figures
Fig 1 Changes occurring during deep fat frying 47
Fig 2 The research flowchart 48
Fig 3 Illustrating the serial number of incubators 49
Fig 4 The relationship between frying time (x) and AV (y) measured from cooking oil samples 50
Fig 5 The relationship between frying time (x) and total PAH concentrations (y) for samples collected during deep-frying processes 51
Fig 6 Size distributions of particle phase PAHs	52
Fig 7 The relationship between gaseous phase PAH concentrations (x) and the corresponding Microtox toxicities (y) 53
Fig 8 The relationship between particle phase PAH concentrations (x) and the corresponding Microtox toxicities (y) 54
Fig 9 The relationships between AV (x) and total PAH concentrations (y-left axis), and total-BaPeq concentrations (y-right axis) 55


                                    

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