2011-08-012024-05-13https://scholars.lib.ntu.edu.tw/handle/123456789/647634摘要：環境流行病學的研究顯示在胎兒和兒童時期暴露到環境污染物，若干擾了特定時間的生長和發育過程，不僅對易感的胎兒和兒童會造成不良的健康影響，也可能導致成人時期的病痛。胎兒編程 (fetal programming)的假說，即是說明胎兒在母體子宮內的生長遲滯，除導致低出生體重外，也會使成年時期得到糖尿病和冠狀動脈疾病的機率增加。因此，暴露時期對環境毒物的研究是相當重要的量測。全氟碳化合物是由不同長度的氟化長碳鏈和帶電功能基所組成，自1950年代被合成以來，廣泛地應用於工業和商業用途;正因為其穩定的化學結構，不易被分解，而被歸類為持續性有機污染物。高劑量或重覆的暴露，會使實驗動物產生肝毒性、生長發育遲緩、免疫抑制、甲狀腺功能異常及發生腫瘤；懷孕期間的暴露不只造成子宮內生長遲滯、先天缺陷和死亡率提高，也會導致成鼠的神經行為發展遲緩；且不同懷孕妊娠周期的暴露，幼鼠的死亡率也不同。有限的人類研究顯示全氟碳化合物的體內濃度，會隨著妊娠週數增加而遞減，臍帶血和母乳的濃度也比母體低，但低劑量的子宮內暴露，仍可能對生長造成影響。利用整合型計畫的團體合作，本研究已完成Taiwan Birth Panel Study I (TBPS I)所收案之臍帶血中12種全氟碳化合物的量測，初步的分析顯示臍帶血中全氟辛磺酸 (PFOS)濃度和新生兒出生結果呈現負向相關。從妊娠時期開始的出生世代追蹤研究(Taiwan Birth Panel Study II, TBPSII)正持續進行中，收集母血、飲食習慣問卷、胎盤和臍帶血。預計利用接著一年的時間深入探討胎兒時期全氟碳化合物的暴露和嬰幼兒成長的關係，也將探討不同妊娠週期和飲食習慣之全氟碳化合物的暴露差異。本研究的最終目標是提供流行病學的證據以作為風險評估的模式和後續衛生管理的規畫。<br> Abstract: Over the decades, epidemiologic research demonstrated the vulnerability of the human fetus, child and adult to adverse health outcomes from parental or childhood exposures to environmental toxicants that disrupted time-specific growth and developmental processes. The fetal programming hypothesis proposes that exogenous maternal malnutrition during pregnancy causes a lifelong, persisting adaptation of the fetus resulting in low birth weight, increased cardiovascular risk, and non-insulin dependent diabetes in adult life. Perfluoroalkyal acids (PFAAs), consist a carbon backbone typically 4-14 in length and a charged function moiety, have been widely used in a variety of consumer and industrial applications since the production of 1950. They were classified as persistent organic pollutants due to chemical stability and general lack of biodegradation. High dose or repeat exposure of PFAAs cause a range of problems in laboratory animals, including liver damage, developmental delay, immunosuppression, imbalance of thyroid hormone, as well as tumor formation. Besides, maternal exposure might lead to intrauterine growth retardation, congenital malformation, increased infant mortality, and also cause neurobehavioral defect in adult mice later. In addition, the neonatal mortality rate varied as the exposure took place at different gestational age. Limited human epidemiological study revealed the internal dose of PFAAs would decreased as the gestational age advanced, and the concentration in cord blood and breast milk were lower compared with maternal blood. Even though, low intrauterine exposures still cause growth impairment. Through the cooperation with integrated team, we’ve complete the analysis of 12 PFAAs in cord blood of Taiwan Birth Panel Study I (TBPS I). The initial analysis had suggested inverse association between PFOS levels in umbilical cord blood plasma and birth outcomes. A new longitudinal birth cohort (Taiwan Birth Panel Study II) that begins from early pregnancy is still processing as collection of maternal blood, diet exposure questionnaires, placenta and cord blood. In the following one year, this project is proposed to investigate the association between in utero PFAAs exposure and growth from fetus to early infancy. In addition, the exposure levels between different gestational age and different diet habit would be explored. The final goal of this study is to provide epidemiological evidence for risk assessment modeling and future health management program design.全氟碳化合物早產出生體重低於妊娠周數新生兒的生長指標肝功能Perfluoroalkyal acidspretermsmall for gestational agegrowth indicators of newbornliver function