Perchlorate is a commonly occurring environmental toxicant that may be transported across the placental barrier by the sodium-iodide symporter (NIS), possibly resulting in both increased perchlorate exposure and decreased iodide uptake by the fetus. Therefore, we measured levels of three physiologically relevant NIS-inhibitors (perchlorate, nitrate and thiocyanate) and iodide in maternal and fetal fluids collected during cesarean-section surgeries on 150 U.S. women. Geometric means of perchlorate, thiocyanate and nitrate levels in maternal urine (2.90, 947 and 47900 µg/L, respectively) were similar to previously published results, while urinary iodide levels (1420 µg/L) were significantly higher (p<0.0001), likely because of prevalent prenatal vitamin use in the study population (74%). Thiocyanate levels were higher in the maternal serum, cord serum, and amniotic fluid of smokers compared to women with environmental tobacco smoke exposure and non-smokers (p-values of 0.0006, p=0.0011, and 0.0026, respectively). Perchlorate was detected in most samples: urine (100%), maternal serum (94%), cord serum (67%), and amniotic fluid (97%). Maternal urinary perchlorate levels were positively correlated with perchlorate levels in amniotic fluid (r=0.57), indicating that maternal urine perchlorate is an effective biomarker of fetal perchlorate exposure. Maternal serum perchlorate was generally higher than cord serum perchlorate (median ratio 2.4:1 for paired samples), and maternal urine perchlorate was always higher than fetal amniotic fluid perchlorate levels (mean ratio 22:1); conversely, iodide levels were typically higher in fetal fluids compared to maternal fluids. We found no evidence of either disproportionate perchlorate accumulation or lack of iodide in the fetal compartment. In this panel of healthy infants, we found no association between cord blood levels of these anions and newborn weight, length and head circumference.
Phthalates are known reproductive and developmental toxicants in experimental animals. However, in humans, there are few data on the exposure of pregnant women that can be used to assess the potential developmental exposure experienced by the fetus. We measured several phthalate metabolites in maternal urine, maternal serum, and cord serum samples collected at the time of delivery from 150 pregnant women from central New Jersey. The urinary concentrations of most metabolites were comparable to or less than among the U.S. general population, except for mono(2-ethylhexyl) phthalate (MEHP), mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), three metabolites of di(2-ethylhexyl) phthalate (DEHP). The median urinary concentrations of MEHHP (109 μg/l) and MEOHP (95.1 μg/l) were more than 5 times their population-based concentrations, whereas the median urinary concentration of MEHP was more than 20 times higher. High concentration of MEHP may indicate a recent exposure to the parent chemical DEHP in the hospital shortly before the collection of the samples. Calculation of daily intakes using the urinary biomarker data reveals that none of the pregnant women tested had integrated exposures to DEHP greater than the NIH Public Access Author ManuscriptHum Ecol Risk Assess. Author manuscript; available in PMC 2010 August 2. Agency for Toxic Substances and Disease Registry's minimal risk levels (MRLs chronic 60, intermediate 100 μg/kg/day). No abnormal birth outcomes (e .g., birth weight, Apgar Score, and gestational age) were noted in those newborns whose mothers had relatively greater exposure to DEHP during the perinatal period than others in this study. Significantly greater concentrations and detection frequencies in maternal urine than in maternal serum and cord serum suggest that the urinary concentrations of the phthalate metabolites may be more reliable biomarkers of exposure than their concentrations in other biological specimens.
Pregnant outbred albino (CD-1) mice received (gavage, three times a day in cottonseed oil) a xylene mixture (60.2% m-xylene, 9.1% o-xylene, 13.6% p-xylene, and 17.0% ethyl benzene) on d 6-15 of gestation (d 1 being the day vaginal plugs were observed). The mice were killed on d 18, the general and reproductive health of the dams evaluated, and the fetuses examined and processed to characterize external, visceral, and skeletal malformation. At 3.6 ml/kg.d, xylene killed 12 of 38 dams and caused a significantly (p less than 0.05) smaller average weight gain during pregnancy than did the vehicle (cottonseed oil). Fetuses from dams treated with xylene at 2.4 ml/kg.d and higher doses had average fetal weights significantly lower than that of the control fetuses. However, the percent of resorptions for xylene was significantly greater than for the control only at 3.6 ml/kg-d. At 2.4, 3.0, and 3.6 ml/kg-d xylene produced a significantly (p less than 0.01) greater average percent of malformed fetuses than did the control. Cleft palate was the major malformation at all three doses. When bilateral (multiple) wavy ribs were counted as a malformation, the average percent of malformed fetuses increased from 7.8 to 10.5 at 3.0 ml/kg.d and from 9.1 to 13.4 at 3.6 ml/kg.d. It is concluded that xylene (mixed isomers) is teratogenic to the CD-1 mouse at 2.4 and 3.0 ml/kg.d, doses approaching lethal levels.
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