Prenatal lead exposure measures

In any case, it s estimated that the human fetus is ten to a hundred times more sensitive to ambient lead than children or adults, such that the so-called national averages are almost certainly dangerous for the fetus. In 2006, researchers reported a study of 146 pregnant women in Mexico City.13 It s one of the few studies to measure maternal lead values during each trimester of pregnancy. The researchers examined the impact of prenatal lead exposure on fetal neurodevelopment by measuring whole blood and plasma levels of lead in the pregnant mothers at each trimester and then in umbilical cord blood at delivery. When the infants were at 12 and 24 months of age, the researchers measured their BLL and also evaluated their neural development with a standard method (the Spanish version of the Bayley Scales of Infant Development). From the evidence,... 

The Cincinnati study also has found an effect of prenatal lead exposure on gestational age, measured in weeks as a continuous variable. One analysis (Dietrich et al, 1986) indicated that gestational age was reduced by approximately 0.6 week for each natural log unit of prenatal maternal blood lead (PbB measurements were transformed to natural logarithms for these analyses to better approximate a normal distribution). Also related to these findings is the cross-sectional study by Moore et al (1982), which has shown a significant relationship between pre-term delivery and either maternal or cord PbB levels in Glasgow, Scotland. This relationship held even after adjustment for a number of possible confounders. 

Evidence from several recent prospective and retrospective studies indicates that lead may be psychoteratogenic at relatively low levels of foetal exposure. In the present interim study, lead measured in whole blood during the prenatal (maternal blood lead) and neonatal periods was found to be inversely related to a complex of sensorimotor developmental indices at 6 and 12 months. Prenatal blood lead was also related to lower birth weight, which in turn was related to poorer sensorimotor performance in infants during the first year. These adverse effects were observed at levels of lead exposure common in pregnant women in the United States, Europe, and other developed areas. 

Minor anomalies were related to lead level in the Boston study (Needleman et al, 1984) but not in the Port Pirie (McMichael et al, 1986) or the Cleveland (Ernhart et al, 1986) studies. While there were a number of methodological differences between the Boston and the Cleveland studies, one discrepancy in findings that may be meaningful is that the Boston group failed to find an association between their alcohol-use measure and neonatal anomalies. This is notable, since it has been estimated that 5% of anatomic congenital defects may be attributable to prenatal alcohol exposure (Sokol, 1981). 

As to other prenatal effects, lead certainly appears toxic to the fetus, although intrauterine exposure is generally believed to be at a low level. In a study by Barltrop (1969) only about 300/tg of lead was found in the fetus at term. Measurements of lead in amniotic fluid show a concentration of less than 20 ng/100 ml, i.e. below the limits of detection for the analytical method used (Kubasik and Volosin, 1972). However, lead is shown to be present in the fetus at all stages of development, and this may be of greater importance than the presence of a given load at term. The distribution of radiolabelled lead in embryonic animals indicates that all major organ systems are exposed (Carpenter, 1974). 

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