摘要: | 目的:本研究利用回溯性世代研究的設計,評估航空製造業勞工作業環境噪音及揮發性有機溶劑暴露情形,並探討不同暴露族群(噪音暴露、有機溶劑暴露及噪音與有機溶劑共同暴露)及不同噪音頻率與高血壓發生率之關係。
方法:本研究以台灣某航空製造業2652名員工作為研究族群,進行全廠區之現場訪視及基本資料之收集。我們針對不同製程之工作點利用TES-1358八音度音頻分析儀、ENTECH不銹鋼採樣筒、活性碳吸附管與氣相層析火焰離子偵測器,分別進行環境噪音及揮發性有機物之測量;並對噪音平均值≧80分貝之工作區域,進行8小時時量均能音量測定,其中噪音平均值≧90分貝之工作區域,則進行63 Hz、125 Hz、250 Hz、0.5k Hz、1k、2k Hz、4k Hz及8k Hz的頻譜分析。我們徵求1412名自願者填寫生活習慣問卷及收集勞工健檢資料,排除37名配戴耳塞的行政人員,最終使用1377名自願者之健檢與問卷資料進行健康狀況分析。本研究利用Cox proportional hazards regressions分析不同暴露組之高血壓相對危險比及95%的信賴區間,並校正干擾因子。
結果:在噪音與高血壓發生率方面,本研究發現噪音暴露強度與高血壓發生率沒有相關,但是僱用時間為3-10年勞工的噪音暴露強度與高血壓風險呈顯著的劑量反應關係,而僱用時間超過15年勞工的噪音暴露強度與高血壓風險呈相反的關係。在溶劑與高血壓發生率方面,本研究發現丁酮暴露濃度與高血壓發生率沒有相關,但是暴露於丁酮濃度≧2 ppm勞工的高血壓風險會隨著僱用時間的增加而降低;且僱用時間為3-15年勞工有顯著較高的高血壓風險,而僱用時間超過15年勞工有較低的高血壓風險。在噪音及溶劑共同暴露與高血壓發生率方面,本研究發現噪音與丁酮的共同暴露對高血壓發生率沒有影響,但是暴露於噪音≧80 dBA與丁酮濃度≧2 ppm且僱用時間在3-15年勞工有顯著較高的高血壓風險;共同暴露且僱用時間在3-15年勞工的高血壓風險(RR=3.35, 95%CI=1.19-9.41)會些微高於噪音暴露組或溶劑暴露且僱用時間在3-15年的風險(RR=3.13, 95%CI=1.65-5.93; RR=3.32, 95%CI=1.04-10.58),但是噪音與溶劑共同暴露並沒有發現顯著的相加效應。在噪音頻率與高血壓發生率方面,暴露於頻率為0.5k Hz≧68 dBA(RR=10.73, 95%CI=3.06-37.68)及1k Hz≧70 dBA (RR=10.73, 95%CI=3.06-37.68)且僱用時間為3-10年相較於其他頻率噪音有顯著較高的高血壓風險。
結論:本研究顯示僱用時間為3-15年勞工的噪音暴露強度及丁酮暴露濃度與高血壓風險呈劑量反應關係,而噪音與溶劑的共同暴露對高血壓發生率沒有相加效應,且暴露於頻率0.5k Hz或1k Hz噪音有較高的高血壓風險。
Objectives: The retrospective cohort study aimed to investigate effects of exposure to noise and/or organic solvents and noise exposure at different frequencies on the incidence of hypertension among aviation industry workers.
Methods: We selected an aircraft manufacturing company with 2625 employees as the studying population to perform the walk-through survey. Octave-band analyzers (TES-1358), ENTECH canisters, charcoal tubes and GC/FID were used to determine the environmental levels of noise and VOCs in the workplace. We measured the time weighted average sound level at workstations with occupational noise levels above 80 dBA and performed frequency analyses of noise levels at 63 Hz, 125 Hz, 250 Hz, 0.5k Hz, 1k Hz, 2k Hz, 4k Hz and 8k Hz for workstations ≥ 90 dBA. We collected health checkups and a standardized questionnaire from 1377 volunteers as study subjects. The Cox proportional hazard regressions were conducted to estimate relative risks (RRs) and 95% confidence intervals (CI) for comparing between-group differences in hypertension by controlling for potential confounders.
Results: We found no relationship between noise intensity and the incidence of hypertension. There was a significant exposure-response trend increasing with noise exposure during 3-10 years of employments. Such relationship did not exist during other periods of employments. In addition, no relationship existed between VOCs exposure and the incidence of hypertension. Field workers exposed to methyl ethyl ketone (MEK) above 2 ppm during 3-15 years of employments had a significantly higher risk of hypertension than those employed less than 3 years. Co-exposure to noise levels ≥ 80 dBA and MEK ≥ 2 ppm during 3-15 years of employments was significantly associated with the risk of hypertension. For field workers employed 3-15 year of duration, co-exposure to noise and MEK had the highest risk of hypertension (RR=3.35, 95%CI=1.19-9.41) than noise exposure or MEK exposure (RR=3.13, 95%CI=1.65-5.93; RR=3.32, 95%CI=1.04-10.58). Field workers exposed to noise level ≥ 68 dBA at 0.5k Hz (RR=10.73, 95%CI=3.06-37.68) and those exposed to noise level ≥ 70 dBA at 1k Hz (RR=10.73, 95%CI=3.06-37.68) had the highest risk of hypertension than other groups with different frequencies of noise exposure.
Conclusion: Our findings suggest that exposure to noise and/or MEK during 3-15 years of employments was significantly associated with the incidence of hypertension. There were no interactive effects of co-exposure to noise and MEK on the risk of hypertension. Exposure to noise at 0.5k Hz and 1k Hz might have the greatest impact on the development of hypertension. |