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Objective: This study was designed to determine whether prenatal mercury exposure, including potential releases from the World Trade Center (WTC) disaster, adversely affects fetal growth and child development. Methods: We determined maternal and umbilical cord blood total mercury of nonsmoking women who delivered at term in lower Manhattan after 11 September 2001, and measured birth outcomes and child development. Results: Levels of total mercury in cord and maternal blood were not significantly higher for women who resided or worked within 1 or 2 miles of the WTC in the month after 11 September, compared with women who lived and worked farther away. Average cord mercury levels were more than twice maternal levels, and both were elevated in women who reported eating fish/seafood during pregnancy. Regression analyses showed no significant association between (ln) cord or maternal blood total mercury and birth outcomes. Log cord mercury was inversely associated with the Bayley Scales of Infant Development psychomotor score [Psychomotor Development Index (PDI)] at 36 months (b = -4.2, p = 0.007) and with Performance (b = -3.4, p = 0.023), Verbal (b = -2.9, p = 0.023), and Full IQ scores (b = -3.8, p = 0.002) on the Wechsler Preschool and Primary Scale of Intelligence, Revised (WPPSI-R), at 48 months, after controlling for fish/seafood consumption and other confounders. Fish/seafood consumption during pregnancy was significantly associated with a 5.6- to 9.9-point increase in 36-month PDI, and 48-month Verbal and Full IQ scores. Conclusions: Blood mercury was not significantly raised in women living or working close to the WTC site in the weeks after 11 September 2001. Higher cord blood mercury was associated with reductions in developmental scores at 36 and 48 months, after adjusting for the positive effects of fish/seafood consumption during pregnancy.

The effects of prenatal exposure to pollutants from the World Trade Center (WTC) disaster on fetal growth and subsequent health and development of exposed children remain a source of concern. We assessed the impact of gestational timing of the disaster and distance from the WTC in the 4 weeks after 11 September on the birth outcomes of 300 nonsmoking women who were pregnant at the time of the event. They were recruited at delivery between December 2001 and June 2002 from three hospitals close to the WTC site. Residential and work addresses of all participants for each of the 4 weeks after 11 September 2001 were geocoded for classification by place and timing of exposure. Average daily hours spent at each location were based on the women's reports for each week. Biomedical pregnancy and delivery data extracted from the medical records of each mother and newborn included medical complications, type of delivery, length of gestation, birth weight, birth length, and head circumference. Term infants born to women who were pregnant on 11 September 2001 and who were living within a 2-mile radius of the WTC during the month after the event showed significant decrements in term birth weight (-149 g) and birth length (-0.82 cm), compared with infants born to the other pregnant women studied, after controlling for sociodemographic and biomedical risk factors. The decrements remained significant with adjustment for gestational duration (-122 g and -0.74 cm, respectively). Women in the first trimester of pregnancy at the time of the WTC event delivered infants with significantly shorter gestation (-3.6 days) and a smaller head circumference (-0.48 cm), compared with women at later stages of pregnancy, regardless of the distance of their residence or work sites from the WTC. The observed adverse effects suggest an impact of pollutants and/or stress related to the WTC disaster and have implications for the health and development of exposed children.

Background: Polycyclic aromatic hydrocarbons (PAHs), including benzo[a]pyrene (BaP), are air pollutants released by the World Trade Center (WTC) fires and urban combustion sources. BaP-DNA adducts provide a measure of PAH-specific genetic damage, which has been associated with increased risk of adverse birth outcomes and cancer. We previously reported that levels of BaP-DNA adducts in maternal and umbilical cord blood obtained at delivery were elevated among subjects who had resided within 1 mile of the WTC site during the month after 9/11; and that elevated blood adducts in combination with in utero exposure to environmental tobacco smoke (ETS) were significantly associated with decreased fetal growth. Objective: Our aim was to assess possible effects of prenatal exposure to WTC pollutants on child development. Methods: After 11 September 2001, we enrolled a cohort of nonsmoking pregnant women who delivered at three lower Manhattan hospitals. We have followed a subset of children through their third birthdays and measured cognitive and motor development using the Bayley-II Scales of Child Development (BSID-II). Results: In multivariate analyses, we found a significant interaction between cord blood adducts and in utero exposure to ETS on mental development index score at 3 years of age (p = 0.02, n = 98) whereas neither adducts nor ETS alone was a significant predictor of (BSID-II) cognitive development. Conclusion: Although limited by small numbers, these results suggest that exposure to elevated levels of PAHs in conjunction with prenatal ETS exposure may have contributed to a modest reduction in cognitive development among cohort children.

Polycyclic aromatic hydrocarbons (PAHs) are toxic pollutants released by the World Trade Center (WTC) fires and various urban combustion sources. Benzo[a]pyrene (BaP) is a representative member of the class of PAHs. PHA-DNA adducts, or BaP-DNA adducts as their proxy, provide a measure of chemical-specific genetic damage that has been associated with increased risk of adverse birth outcomes and cancer. To learn whether PAHs from the WTC disaster increased levels of genetic damage in pregnant women and their newborns, we analyzed BaP-DNA adducts in maternal (n = 170) and umbilical cord blood (n = 203) obtained at delivery from nonsmoking women who were pregnant on 11 September 2001 and were enrolled at delivery at three downtown Manhattan hospitals. The mean adduct levels in cord and maternal blood were highest among newborns and mothers who resided within 1 mi of the WTC site during the month after 11 September, intermediate among those who worked but did not live within this area, and lowest in those who neither worked nor lived within 1 mi (reference group). Among newborns of mothers living within 1 mi of the WTC site during this period, levels of cord blood adducts were inversely correlated with linear distance from the WTC site (p = 0.02). To learn whether PAHs from the WTC disaster may have affected birth outcomes, we analyzed the relationship between these outcomes and DNA adducts in umbilical cord blood, excluding preterm births to reduce variability. There were no independent fetal growth effects of either PAH-DNA adducts or environmental tobacco smoke (ETS), but adducts in combination with in utero exposure to ETS were associated with decreased fetal growth. Specifically, a doubling of adducts among ETS-exposed subjects corresponded to an estimated average 276-g (8%) reduction in birth weight (p = 0.03) and a 1.3-cm (3%) reduction in head circumference (p = 0.04). The findings suggest that exposure to elevated levels of PAHs, indicated by PAH-DNA adducts in cord blood, may have contributed to reduced fetal growth in women exposed to the WTC event.

Abstract Introduction Perfluoroalkyl substances (PFAS) were among various persistent organic pollutants suspected to have been released during the collapse of the World Trade Center (WTC) on 9/11/2001. Evidence suggests that PFAS may have cardiometabolic effects, including alterations in lipid profiles. This study evaluated the association between cord blood PFAS and lipids in a population prenatally exposed to the WTC disaster. Study Population 222 pregnant women in the Columbia University WTC birth cohort enrolled between December 13, 2001 and June 26, 2002 at hospitals located near the WTC site: Beth Israel, St. Vincent’s, and New York University Downtown. Methods We evaluated the association between 5 cord blood PFAS—perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA), perfluorodecane sulfonate (PFDS)—and cord blood lipids (total lipids, total cholesterol, triglycerides). Results Median (interquartile range [IQR]) concentrations of PFAS were 6.32 (4.58–8.57), 2.46 (1.77–3.24), 0.38 (0.25–0.74), 0.66 (0.48–0.95) and 0.11 (0.09–0.16) ng/mL for PFOS, PFOA, PFNA, PFHxS, and PFDS, respectively. Median (IQR) for lipids were 59.0 (51.5–68.5) mg/dL for total cholesterol, 196.5 (170.5–221.2) mg/dL for total lipids and 33.1 (24.2–43.9) mg/dL for triglycerides. In fully adjusted models, several PFAS were associated with higher lipid levels, including evidence of a strong linear trend between triglycerides and both PFOA and PFHxS. Conclusions Findings support previous evidence of an association between PFAS exposure and altered lipid profiles and add novel information on this relationship in cord blood, as well as for an understudied PFAS, PFDS (J Clin Endocrinol Metab 105: 43–54, 2020).

Maternal weight homeostasis during lactation depends on the management of energy resources. Studies indicate that regulatory processes allow for successful lactation in varied conditions of food availability. These processes involve mobilizing fat, increasing food intake, reducing energy expenditure, and changing the composition or volume of milk. Changes in energy efficiency do not seem important. Early in lactation, fat mobilization appears to be physiologic and gradual, even when food is readily available. Later in lactation, dietary intake may decline even though that allows continued loss of body fat when fat has already lowered. Where increasing dietary intake is less possible, or dietary restriction is imposed, reductions in energy expenditure seem to take precedence over an increase in the rate of fat mobilization. The findings reviewed indicate that for lactation to play a major role in the reduction of body fat in the postpartum period, women have to breastfeed fully for a substantial period.

We examined whether data obtained by maternal report could be used for research in clinical settings in place of abstraction of the clinical record. Reported prepregnancy weight, delivery type, and infant's birth date, birth weight, and length were compared to the same information from the clinical record. Reported data, obtained from 198 women, were more complete than data in the 168 clinical records obtained. Prepregnancy weight from the clinical record was highly correlated with weight measured by us in early pregnancy, and with the value reported by the mother (differing significantly only in underweight women, who overreported by 2.4 lbs). There was complete concordance on birth date and method of delivery, and no significant differences in mean birth weight or length, between the reported and recorded information. The mother's report is a satisfactory substitute for clinical record data, being consistent with the record, and more complete, yet easier to obtain for clinical studies.

To determine weight gain during pregnancy and weight changes postpartum in first-time mothers delivering at or near term. At about 2 weeks after delivery, 47 adult, Black and Hispanic women provided information on their prepregnancy weight and height and maximum pregnancy weight. Women reinterviewed at 2 and 6 months after delivery reported their most recent weight measurement and the date of that measurement. This information was used to compute each woman's prepregnancy body mass index, pregnancy weight gain, and weight loss postpartum. Information on infant feeding was also collected at each postpartum visit. About 2/3 of the women and 100% of the overweight and obese women gained excessive weight during pregnancy. Weight gain was most marked in women who started pregnancy overweight or obese. At 2 months postpartum, women were on average almost 18 lb above their prepregnancy weight. No additional maternal weight was lost by 6 months postpartum. Most infants were started on formula by 2 weeks of age. At 2 months of age, 85% were fed formula only and 91% of the infants were on WIC. Our results demonstrate a need for interventions to help women avoid obesity by regulating their pregnancy weight gain, losing weight for a longer period postpartum, and initiating and maintaining exclusive breast-feeding.