以結構方程模式評估出生前金屬暴露對嬰幼兒神經行為發展之影響

Abstract

背景與目的:胎兒、嬰幼兒和幼童是環境毒性化學物質暴露中最受到關注的易感受族群，因為這樣的暴露可能導致其神經行為發展出現問題。過去長久以來，針對個別金屬暴露後健康效應的研究已有廣泛的討論，但尚未有研究著重於多種重金屬的共同暴露影響。為釐清不同金屬對健康效應的表現，本篇研究利用結構方程模型評估出生前金屬暴露對嬰幼兒的出生狀態及後續神經行為發展之影響。 材料與方法: 研究對象選取自2004年4月至2005年1月間收案的台灣出生世代先驅研究，共計106名孕婦及其新生兒被納入本研究。母親血液和新生兒臍帶血液中的金屬濃度作為反映出生前暴露的指標。以嬰幼兒綜合發展測驗 (The Comprehensive Developmental Inventory for Infants and Toddlers)評估孩童兩歲大時之神經行為發展。 結果:母親血液中的總砷和總汞濃度分別為6.7 ± 2.0 ( ug/L ) and 4.6 ± 1.7 ( ug/L )，臍帶血中的總砷和總汞濃度則為13.9 ± 1.8 ( ug/L ) and 4.5 ± 1.6 ( ug/L )。結構方程模式顯示，其模型適配度卡方值為 38.12 (p值=0.12)，CFI=0.95，RMSEA=0.06。血液中的砷及汞濃度和出生狀態及神經行為發展有關。模型中的出生狀態也可被推定為出生前金屬暴露影響神經行為發展的中介因子。 結論: 比較不同的途徑後，本篇研究指出出生前的砷暴露對出生狀態和之後的神行為發展相較於汞暴露有較強的表現。懷孕期間海鮮的攝取被認為是常見的砷和汞的來源之一，對其同時所帶來的營養價值和潛在危害的綜合影響仍需後續的研究繼續探討。

Background and objectives: Fetuses, infants, and young children are the most susceptible to some of environmental toxicological chemicals which can potentially affect their neurodevelopment. The effects of single metal exposure have been widely discussed for a long time, but few studies described joint exposure of heavy metals. To evaluate the roles of various affecting metals, a structural equation model was applied to estimate the effect from prenatal metal exposure on birth outcomes and the following neurodevelopment. Methods: A prospective cohort study was conducted from April 2004 to January 2005 in Taiwan and a total of 106 delivering women and their newborns were enrolled in this study. Metal concentrations in maternal and umbilical cord blood samples were obtained to reflect prenatal metal exposure while birth outcomes were observed after delivery. The Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) was used for assessing toddler’s neurodevelopment at 2 years of age. Results: Concentration of total arsenic and total mercury were 6.7 ± 2.0 ug/L and 4.6 ± 1.7 ug/L in maternal blood samples and 13.9 ± 1.8 ug/L and 4.5 ± 1.6 ug/L in umbilical blood samples. Results of structural equation model indicated that prenatal arsenic and mercury exposure were inversely associated with birth outcomes (coefficients -0.28 (p=0.05), -0.06 (p=0.05)) and neurodevelopment with model χ2 value of 38.12 (p=0.12), CFI of 0.95 and RMSEA of 0.06 for goodness of fit. This model also indicated that fetal birth outcome could be a mediated factor for prenatal metal exposure to predict following neurodevelopment. Conclusions: By comparing different exposure pathways, this study suggested prenatal arsenic exposure might play a stronger role, as compared to mercury, affecting the birth outcomes and the following neurodevelopment. Seafood intake during pregnancy was thought as one of the exposure sources for arsenic and mercury exposure, therefore, further study to simultaneously explore to the nutritional benefits of seafood as well as the potential harms should be concerned.