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                  鉛可通過胎盤侵襲胎兒(英)

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                  Transplacental Exposure and Lead

                  ---- The prevalence among pregnant women is high.


                       Lead crosses the placenta, and the blood lead concentration of the infant is similar to that of the mother(Graziano et al., 1990).  The source of fetal exposure to lead can be endogenous, from internal stores, or exogenous, from dietary, cultural, environmental or occupational sources.  The main endogenous source of lead is the skeleton.  Lead that enters the body is redistributed to virtually every tissue and is released over time at a rate that is determined by several factors, some of which are dependent on the unique physiology of that organ.  Lead in bone has a half-life of years to decades and can be released at an increased rate during times of physiological stress, such as the body’s increased need for calcium during pregnancy or lactation (Gulson, ????).  Therefore, lead stored in bone as a result of childhood exposures can be passed on to the developing fetus exerting a similar effect on development seen in postnatal exposures (Schnass et al., 2006).  Cultural sources of lead exposure include that use of traditional medications, lead containing cosmetics, pica behavior (the culturally accepted practice of eating soil or crushed pottery), contaminated food and lead-glazed ceramics (Graber et al., 2004).  Lead exposed fetuses are more likely to be born prematurely (Falcon et al. 2003; Torres-Sanchez et al. 1999; Baghurst et al. 1991).  The mothers are at an increased risk for spontaneous abortion(Borja-Aburto et al., 1999) and increased blood pressure during pregnancy (Sower et al., 2002; Rothenberg et al. 2002).  These effects have been demonstrated at maternal blood lead levels as low 5 µg/dL.  The prevalence of women of child bearing age with these levels may be remarkably high, if not universal, in some communities.  In New York City, 37% of Bangladeshi born women, 21% of Mexican born women and 11% of all women had blood lead levels in the first trimester which were ≥ 5 µg/dL (Graber, 2006). 

                   

                   

                   

                   

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