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在对缺铁啮齿动物的铅代谢研究中发现,伴随着铁吸收的增加,铅的吸收也相应增加(Six K M,1972;Ra-gan H A,1977;Barton J C,1978;Hamilon D L,1978;Flanagan P R,1979;Barton J C,1981)。在人类研究中也发现,饮食低铁增加铅的毒性或铅的吸收(Watson W S,1980;Yip R,1981;Flanagan P R,1982)。美国NHANES Ⅱ的调查资料进一步证实,血铁浓度与EP呈负相关关系,缺铁合并高血铅导致的EP升高程度较单纯高血铅为高,儿童合并发生铁缺乏性高血铅的机会要比铁合适儿童高3倍(Dallman P R,1984;Mahaffey K R,1986;Marcus AH,1987)。
In studies of lead metabolism in iron-deficient rodents, lead absorption was also found to increase with increasing iron absorption (Six KM, 1972; Ra-gan HA, 1977; Barton JC, 1978; Hamilon DL, 1978; Flanagan PR, 1979; Barton JC, 1981). In human studies, it was also found that dietary low iron increases lead toxicity or lead absorption (Watson W S, 1980; Yip R, 1981; Flanagan P R, 1982). American NHANES Ⅱ survey data further confirmed that there is a negative correlation between serum iron concentration and EP, iron deficiency combined with elevated blood lead-induced elevated EP levels higher than pure high blood lead, children with iron deficiency lead synthesis high blood lead 3 times higher than iron-eligible children (Dallman PR, 1984; Mahaffey KR, 1986; Marcus AH, 1987).