CAJ | 학술논문

、(20.8±7.4)ng/ml.中毒组与对照组比较,t=20.206,P=0.000;与锰暴露组比较,t′=13.144,P=0.000.中毒组与低、高锰暴露亚组比较,t′值分别为12.964、9.957,P=0.000].8例高锰暴露工人1年后追踪调查仅发现作业环境空气MnO2浓度中位数较1年前相比降低,差异有统计学意义(依次为0.89、0.31 mg/m3,Z=-2.142,P=0.032).结论锰暴露引起工人脑MR T1WI信号明显增强,PI可能是锰致CNS损伤的中枢暴露生物学标志.
、(20.8±7.4)ng/ml.중독조여대조조비교,t=20.206,P=0.000;여맹폭로조비교,t′=13.144,P=0.000.중독조여저、고맹폭로아조비교,t′치분별위12.964、9.957,P=0.000].8례고맹폭로공인1년후추종조사부발현작업배경공기MnO2농도중위수교1년전상비강저,차이유통계학의의(의차위0.89、0.31 mg/m3,Z=-2.142,P=0.032).결론 맹폭로인기공인뇌MR T1WI신호명현증강,PI가능시맹치CNS손상적중추폭로생물학표지.
fference was significant in statistics. Conclusion Our data suggests that SIGP of MR T1WI among workers was obviously increased by manganese-exposure. PI may be taken as the signal of CNS injury which was induced by manganese-exposure.