Maternal and Umbilical Cord Blood Lead Levels: An Istanbul Study
INCREASED LEAD BODY BURDEN is a notorious problem associated with environmental lead contamination. Smelters, industrial emissions, food, tap water, pottery dishes, gasoline, and paint are potential sources of lead intake.[1-6] In particular, combustion of lead-containing gasoline has been a common and pervasive source of lead pollution in urban environments. This source was greatly moderated in 1989-1990, during which time the average lead content in gasoline in Turkey was lowered from 0.80 g/l to approximately 0.24 g/l. In Istanbul, where gasoline consumption accounts for approximately 30% of the country’s sales, annual lead emissions from exhaust gases decreased from 750 tons to about 280 tons during 1989-1990. Although the average lead level in gasoline is currently 0.21 g/l, the amount of lead emitted in Istanbul in 1998 by motor vehicles rose to approximately 410 tons.
There are no data regarding blood lead levels in Istanbul for the period of time that high-lead gasoline was used. Only a few studies have been undertaken subsequent to the lowering of lead levels in gasoline in Istanbul. In a 1992 study, Emis et al. reported a mean blood lead level of 8.15 [micro]g/dl (standard deviation [SD] = 5.215 [micro]g/dl); in a 1994 study, Ozek et al. reported a mean blood lead level of 8.76 [micro]g/dl (SD = 5.80 [micro]g/dl). In both studies, investigators measured lead levels in umbilical cord blood. In the most recent study–conducted in 1998–the mean blood lead level in Istanbul was 3.64 [micro]g/dl (SD: 1.36 [micro]g/dl). We linked this decrease to the long-term effect of reducing lead additives in gasoline. It should be noted, however, that our study did not include data regarding newborns and their mothers.
Although mean blood lead levels have declined in Istanbul during recent years, there is concern that fetal lead exposure may continue in utero from the mobilization of lead in bone that accumulates from previous environmental exposures. Given that approximately 90% of all lead body burden in adults is deposited in bones–where the half-life of lead is particularly long–a new equilibrium between body compartments is reached only after many years. Exposure to lead during pregnancy is particularly ominous because even low lead levels in maternal blood have been associated with prematurity, distorted postnatal neurobehavioral development, and altered fetal growth.[12-15]
In this article, we report current lead levels in umbilical cords and in maternal blood in Istanbul. We compared our results with the results of two previous studies in hopes that we would confirm the reported decrease in blood lead levels. We also sought to determine which of two indicators (i.e., average lead content in gasoline or growing levels of lead emitted in exhaust gases) provided the better measure for determining lead contribution from motor vehicle emissions in the city.
Subjects and Method
In this study, we included 104 umbilical cord blood samples and 65 maternal intravenous blood samples. all of which were collected at the University Hospital of the Marmara School of Medicine in Istanbul. Eligible; subjects included all women who were hospitalized for delivery in April and May of 1998. None of the subjects who participated in the study reported that they had been exposed to unusual lead sources.
The discrepancy in numbers between umbilical cord and maternal blood samples arose because, initially, we planned to measure blood lead only in umbilical cords (i.e., as was done in previous studies). We abandoned this unnecessary restriction after the first 39 cord blood samples and the succeeding 65 samples were compared with maternal blood. We found a much higher lead content (i.e., [is greater than] 6 [micro]g/dl) for 1 pair than for the remainder of samples. In addition, we found that in this pair cord blood lead level was higher than the maternal blood lead level. Both of these outcomes directed us to the possibility that external contamination had occurred. This high-lead pair, therefore, was not considered in further analysis.
The blood samples were stored in metal-free Vacutainers[R] that contained ethylenediaminetetraacetic acid, and they were kept cold until analysis. Lead content was analyzed with a Perkin-Elmer SIMAA 6000 atomic absorption spectrophotometer (AAS) equipped with a graphite furnace and Zeeman background correction (Perkin-Elmer [Norwalk, Connecticut]). The calibration curve for blood samples was standardized against matrix-matched certified aqueous lead solutions. The blood lead standardization curve was linear and ranged between 0.50 [micro]g/dl and 10.00 [micro]g/dl; the reliable detection limit was 0.01 [micro]g/dl. All measurements were done in certified Duzen clinical chemistry laboratories.
In the study conducted by Ozek et al. (i.e., study against which we compared our results), the investigators collected umbilical blood samples at the same hospital as did we, and the AAS measurements by Ozek et al. were performed in the same laboratory we used.
The mean lead concentration in umbilical cord blood was 1.69 [+ or -] 0.91 [micro]g/dl, and the range was 0.11-4.07 [micro]g/dl. The mean blood lead concentration in maternal blood samples was 2.37 [+ or -] 0.89 [micro]g/dl, and the range was 0.65-5.15 [micro]g/dl. The frequency distribution of lead in maternal and cord blood is presented in Figure 1. Birth weights and birth lengths of newborns did not correlate significantly with blood lead levels.
[Figure 1 ILLUSTRATION OMITTED]
Umbilical blood lead levels, which correlated significantly with maternal blood lead levels (r = .71; p [is less than] .001 [n = 64]), were approximately 70% of the maternal levels. Regression analysis revealed that cord blood lead level was dependent upon the blood lead level of the mother at delivery, in accordance with the equation: y = 0.64x + 0.10 ([R.sup.2] = .50; p [is less than] .001).
Umbilical cord blood lead levels among babies born at the University Hospital of Marmara School of Medicine in Istanbul declined considerably during the 4 y between 1994 and 1998. The mean blood lead levels decreased by 81%–from 8.76 [+ or -] 5.80 [micro]g/dl in 1994 (reported by Ozek et al.) to 1.69 [+ or -] 0.91 [micro]g/dl in 1998. The umbilical cord blood lead levels in our study were also lower than the mean level of 8.15 [+ or -] 5.25 [micro]g/dl reported by Emis et al. in another hospital in Istanbul in 1992. Therefore, the observed reduction in blood lead levels allows for decreased concern about the possibility that fetal lead exposure occurs via mobilization of previously accumulated lead in bone. Although a comparison of our results with studies performed in other countries was not possible because of differences, among others, in lead sources, nutrition status, and study designs, we point out that there was a similarity between the current low blood levels in Istanbul and the levels reported recently by Hu et al. (1.1 9 [micro]g/dl) in Boston and by Rhainds et al. (1.58 [micro]g/dl) in Quebec.
The mean lead concentration in maternal blood found in our study (2.37 [micro]g/dl) is in good agreement with that reported in the 1998 screening study in Istanbul: 3.64 [+ or -] 1.36 [micro]g/dl. Although low blood lead levels in our subjects might point to a decreased mean blood lead concentration during pregnancy (as has been observed in some studies[17,18]), small sample size and differences in sampling design thwart this conclusion. In our study, lead levels in maternal blood were also lower than levels reported from other developing countries.
Lead concentrations in umbilical cord blood are significantly correlated with, and are lower than, concentrations in maternal venous blood. This finding is consistent with the findings of other studies.[1,20-22] In fact, blood lead levels in umbilical cords are approximately 70% of levels found in maternal blood; this finding supports the conclusion that the placenta is not a very effective biological barrier and it does not hinder much of the lead transport.
In or near Istanbul, there are neither smelters nor heavy industry; in addition, use of lead-glazed pottery for cooking is uncommon, and lead-based paint is used only rarely because it is so expensive. Therefore, the drastic decrease in blood lead levels reported herein likely occurred as a long-term consequence of the reduction (in 1989) of tetraalkyl lead in gasoline. Substantial decreases in blood lead levels, during the years that followed the reduction of lead in gasoline, were also reported in studies from other countries.[23-27]
Although the average lead content in gasoline has remained approximately constant in Istanbul during the past 8 y, the amount of lead emitted in exhaust gases has grown from approximately 280 tons/y in 1992 to 340 tons/y in 1994 to 410 tons/y in 1998. (There has been a concomitant increase in the numbers of motor vehicles in the city.)The increase in lead emitted in exhaust gases, however, is not reflected in changes in lead blood levels. As the population of Istanbul has grown, the city area has also expanded considerably; perhaps local exposures to exhaust gases have not changed appreciably. Therefore, the average lead content in gasoline appears to be a better measure of the contribution that motor vehicles in the city make to lead pollution than measuring the total amount of lead emitted by gasoline combustion. The small size of our sample and the scant data from the previous years, however, render these comparisons tentative; further confirmation is needed.
Finally, despite low blood lead levels reported here, lead may nonetheless pose a health hazard to mothers and newborns in some other city districts. Our results should be repeated with a larger sample size before we can generalize them to Istanbul. As the numbers of vehicles increase–and as gasoline consumption continues to rise–a reduction in the average lead content in gasoline might be required. To assure that blood lead levels remain low, investigators should establish a blood-lead monitoring program in the near future.
The authors thank Duzen Laboratories for affording them with the opportunity to use atomic absorption spectrophotometry.
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ANDRZEJ FURMAN Institute of Environmental Sciences Bogazici University Istanbul, Turkey
MEHMET LALELI Diizen Clinical Chemistry Laboratories Ankara, Turkey
This study was supported by grant 98Y02 front the Research Fund of the Bogazici University in Istanbul.
Submitted for publication August 13, 1999; revised; accepted for publication June 15, 2000.
Requests for reprints should be sent to Dr. Andrzej Furman, Institute
of Environmental Sciences, Bogazici University, Bebek 80815, Istanbul, Turkey.
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