Abstract
This review focuses on the impacts of lead exposure on reproductive health and outcomes. High levels of paternal lead exposure (>40 ΞΌg/dl or >25 ΞΌg/dl for a period of years) appear to reduce fertility and to increase the risks of spontaneous abortion and reduced fetal growth (preterm delivery, low birth weight). Maternal blood lead levels of approximately 10 ΞΌg/dl have been linked to increased risks of pregnancy hypertension, spontaneous abortion, and reduced offspring neurobehavioral development. Somewhat higher maternal lead levels have been linked to reduced fetal growth. Some studies suggest a link between increased parental lead exposure and congenital malformations, although considerable uncertainty remains regarding the specific malformations and the doseβresponse relationships. Common methodological weaknesses of studies include potential exposure misclassifications due to the frequent unavailability of exposure biomarker measurements at biologically appropriate times and uncertainty regarding the best exposure biomarker(s) for the various outcomes. A special concern with regard to the pregnant woman is the possibility that a fetus might be exposed to lead mobilized from bone stores as a result of pregnancyβrelated metabolic changes, making fetal lead exposure the result of exposure to exogenous lead during pregnancy and exposure to endogenous lead accumulated by the woman prior to pregnancy. By reducing bone resorption, increased calcium intake during the second half of pregnancy might reduce the mobilization of lead from bone compartments, even at low blood lead levels. Subgroups of women who incurred substantial exposures to lead prior to pregnancy should be considered to be at increased risk. Birth Defects Research (Part A), 2005. Β© 2005 WileyβLiss, Inc.