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Hoepner, Lori
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Biography
Dr. Lori Hoepner received her DrPH in Environmental Health Sciences from Columbia University Mailman School of Public Health (2015), her MPH in Maternal and Child Health from Tulane University School of Public Health and Tropical Medicine (1995), and her BA in Biology from Barnard College (1994). With over 80 co-authored publications, her research is primarily at the intersection of environmental effects and prenatal/early childhood development. In 2015, Dr. Hoepner received Columbia University’s I. Bernard Weinstein Award for Academic Excellence in Environmental Health Sciences for the DrPH. Her doctoral dissertation focused on the ubiquitous plasticizer bisphenol A (BPA): both its effects on a) adipogenesis in human umbilical cord mesenchymal stem cells in a laboratory setting and b) childhood obesity in an urban minority birth cohort using a molecular epidemiological study design. She has extensive research experience in exposures including BPA, polycyclic aromatic hydrocarbons (PAHs), phthalates, and pesticides, as well as the outcomes of asthma, neurodevelopment, and obesity. Her research efforts have included studies of the World Trade Center tragedy and HIV/AIDS behavioral research. In addition, Dr. Hoepner has over 20 years of organizational and analytical data management expertise involving complex health assessment and public health research datasets. With her background in health disparities research, Dr. Hoepner has the goal of understanding the intricacies of race/ethnicity, sex and socioeconomics as they pertain to environmental health from a global perspective, as well as from a community-wide perspective.
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Publication Open Access Relationships among polycyclic aromatic hydrocarbon-DNA adducts, proximity to the World Trade Center, and effects on fetal growth.Perera, Frederica P; Tang, Deliang; Rauh, Virginia; Lester, Kristin; Tsai, Wei Yann; Tu, Yi Hsuan; Weiss, Lisa; Hoepner, Lori; King, Jeffrey; Del Priore, Giuseppe; Lederman, Sally AnnPolycyclic 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. PAH-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.Publication Open Access Asthma, allergy, and IgE levels in NYC head start children.(2009-11-13) Rotsides, Demetra Z; Goldstein, Inge F; Canfield, Stephen M; Perzanowski, Matthew; Mellins, Robert B; Hoepner, Lori; Ashby-Thompson, Maxine; Jacobson, Judith SBackground: Among preschool-age children in New York City neighborhoods with high asthma hospitalization rates, we analyzed the associations of total immunoglobulin E (IgE), specific IgE to common indoor allergens, and allergy symptoms with asthma. Methods: Parents of children in New York City Head Start programs were asked to complete a questionnaire covering demographic factors, health history (including respiratory conditions), lifestyle, and home environment. Children's serum samples were analyzed for total IgE and specific IgE antibodies to cockroach, dust mite, mouse, and cat allergens by immunoassay. Logistic regression was used to model the association between asthma and IgE, controlling for age, gender, ethnicity/national origin, BMI, parental asthma, smokers in the household, and allergy symptoms (e.g., runny nose, rash). Results: Among 453 participating children (mean age 4.0+/-0.5 years), 150 (33%) met our criteria for asthma. In our multivariable logistic regression models, children with asthma were more likely than other children to be sensitized to each allergen, to be sensitized to any of the four allergens (OR=1.6, 95% CI 1.0-2.6), or to be in the highest quartile of total IgE (OR=3.1, 95% CI 1.5-6.4). Allergy symptoms based on questionnaire responses were independently associated with asthma (OR=3.7, 95% CI 2.3-5.9). Conclusions: Among preschool-aged urban children, asthma was associated with total IgE and sensitization to cat, mouse, cockroach, and dust mite allergens. However, allergy symptoms were more prevalent and more strongly associated with asthma than was any allergen-specific IgE; such symptoms may precede elevated specific IgE or represent a different pathway to asthma.Publication Open Access Prenatal and postnatal bisphenol A exposure and asthma development among inner-city children.Donohue, Kathleen M; Miller, Rachel L; Perzanowski, Matthew S; Just, Allan C; Hoepner, Lori A; Arunajadai, Srikesh; Canfield, Stephen; Resnick, David; Calafat, Antonia M; Perera, Frederica P; Whyatt, Robin MBackground: Bisphenol A (BPA) is used widely to manufacture food container linings. Mouse models suggest exposure to BPA might increase allergic inflammation. Objectives: We hypothesized that BPA exposure, as assessed based on urinary BPA concentrations, would be associated with increased odds of wheeze and asthma and increased fraction of exhaled nitric oxide (Feno) values in children. Methods: The Columbia Center for Children's Environmental Health recruited pregnant women for a prospective birth cohort study (n = 568). Mothers during the third trimester and children at ages 3, 5, and 7 years provided spot urine samples. Total urinary BPA concentrations were measured by using online solid-phase extraction, high-performance liquid chromatography, isotope-dilution tandem mass spectrometry. Wheeze in the last 12 months was measured by using questionnaires at ages 5, 6, and 7 years. Asthma was determined by a physician once between ages 5 and 12 years. Feno values were measured at ages 7 to 11 years. Results: Prenatal urinary BPA concentrations were associated inversely with wheeze at age 5 years (odds ratio [OR], 0.7; 95% CI, 0.5-0.9; P = .02). Urinary BPA concentrations at age 3 years were associated positively with wheeze at ages 5 years (OR, 1.4; 95% CI, 1.1-1.8; P = .02) and 6 years (OR, 1.4; 95% CI, 1.0-1.9; P = .03). BPA concentrations at age 7 years were associated with wheeze at age 7 years (OR, 1.4; 95% CI, 1.0-1.9; P = .04) and Feno values (β = 0.1; 95% CI, 0.02-0.2; P = .02). BPA concentrations at ages 3, 5, and 7 years were associated with asthma (OR, 1.5 [95% CI, 1.1-2.0], P = .005; OR, 1.4 [95% CI, 1.0-1.9], P = .03; and OR, 1.5 [95% CI, 1.0-2.1], P = .04, respectively). Conclusions: This is the first report of an association between postnatal urinary BPA concentrations and asthma in children.Publication Open Access Physical activity and asthma symptoms among New York City Head Start Children.Rundle, Andrew; Goldstein, Inge F; Mellins, Robert B; Ashby-Thompson, Maxine; Hoepner, Lori; Jacobson, Judith SThe coincidence of both an obesity epidemic and an asthma epidemic among children in the United States has suggested that childhood overweight and sedentary lifestyles may be risk factors for asthma development. We therefore conducted a study of those factors among children enrolled in Head Start Centers located in areas of New York City with high asthma hospitalization rates. Data were gathered from 547 children through an intensive home visit, and physical activity was measured on 463 children using the Actiwatch accelerometer. Data on allergy and asthma symptoms and demographic variables were obtained from parents' responses to a questionnaire and complete data were available from 433 children. Overall physical activity was highest in warmer months, among boys, among children whose mothers did not work or attend school, and among children of mothers born in the United States. Activity was also positively associated with the number of rooms in the home. The season in which the activity data were collected modified many of the associations between demographic predictor variables and activity levels. Nearly half the children were above the range considered healthy weight. In cross-sectional analyses, before and after control for demographic correlates of physical activity, asthma symptoms were not associated with physical activity in this age group. Comparing the highest quartile of activity to the lowest, the odds ratio for asthma was 0.91 (95% CI = 0.46, 1.80). However, the novel associations with physical activity that we have observed may be relevant to the obesity epidemic and useful for planning interventions to increase physical activity among preschool children living in cities in the northern United States.Publication Open Access Neighborhood differences in exposure and sensitization to cockroach, mouse, dust mite, cat, and dog allergens in New York City.(2011-05-04) Olmedo, Omar; Goldstein, Inge F; Acosta, Luis; Divjan, Adnan; Rundle, Andrew G; Chew, Ginger L; Mellins, Robert B; Hoepner, Lori; Andrews, Howard; Lopez-Pintado, Sara; Quinn, James W; Perera, Frederica P; Miller, Rachel L; Jacobson, Judith S; Perzanowski, Matthew SBackground: Prior research has linked maternal prenatal and postnatal mental health with the subsequent development of asthma in children. However, this relationship has not been examined in inner-city African Americans and Hispanics, populations at high risk for asthma. Objective: To determine the relationship of maternal demoralization with wheeze, specific wheeze phenotypes, and seroatopy among children living in a low-income, urban community. Methods: African American and Dominican women aged 18 to 35 years residing in New York City (the Bronx and Northern Manhattan) were recruited during pregnancy (n = 279). Maternal demoralization (ie, psychological distress) was measured both prenatally and postnatally by validated questionnaire. Outcomes included wheeze, transient (birth to 2.5 years of age), late onset (3-5 years), and persistent (birth to 5 years of age), evaluated via questionnaire and total and indoor allergen specific IgE (at birth and ages 2, 3, and 5 years). Logistic regression with generalized estimating equations assessed the association of demoralization with wheeze and atopy. Multinomial regression explored associations between demoralization and specific wheeze phenotypes. Results: Prenatal demoralization significantly predicted overall wheeze (adjusted odds ratio OR, 1.66; 95% confidence interval [CI], 1.29-2.14), transient wheeze (OR, 2.25; 95% CI, 1.34-3.76), and persistent wheeze (OR, 2.69; 95% CI, 1.52-4.77). No association was found between demoralization and IgE after adjustment (total IgE: OR, 1.04; 95% CI, 0.74-1.45; any specific IgE: OR, 0.96; 95% CI, 0.57-1.60). Conclusions: In this inner-city cohort, prenatal demoralization was associated with transient and persistent wheeze. Understanding how maternal demoralization influences children's respiratory health may be important for developing effective interventions among disadvantaged populations.Publication Open Access Urinary concentrations of bisphenol A in an urban minority birth cohort in New York City, prenatal through age 7 years.(2013-01-08) Hoepner, Lori A; Whyatt, Robin M; Just, Allan C; Calafat, Antonia M; Perera, Frederica P; Rundle, Andrew GBackground: Despite growing concern over potential health effects associated with exposures to the endocrine disruptor, bisphenol A (BPA), insufficient information is available on determinants of BPA concentrations among minority populations in the US. Objectives: To describe concentrations and predictors of BPA in an inner-city longitudinal birth cohort. Methods: We analyzed spot urines for total BPA collected during pregnancy and child ages 3, 5, and 7 years from African Americans and Dominicans (n=568) enrolled in the Columbia Center for Children's Environmental Health birth cohort and residing in Northern Manhattan and the South Bronx. Adjusting for specific gravity, generalized estimating equations were used to compare BPA concentrations across paired samples and linear regression analyses were used to determine relationships between BPA, season of sample collection, socio-demographic variables and urinary concentrations of phthalate metabolites. Results: BPA was detected in ≥ 94% of samples. Prenatal concentrations were significantly lower than postnatal concentrations. Geometric means were higher among African Americans compared to Dominicans in prenatal (p=0.008), 5 year (p<0.001) and 7 year (p=0.017) samples. Geometric means at 5 and 7 years were higher (p=0.021, p=0.041 respectively) for children of mothers never married compared to mothers ever married at enrollment. BPA concentrations were correlated with phthalate metabolite concentrations at prenatal, 3, 5 and 7 years (p-values <0.05). Postnatal BPA concentrations were higher in samples collected during the summer. Conclusions: This study shows widespread BPA exposure in an inner-city minority population. BPA concentration variations were associated with socio-demographic characteristics and other xenobiotics.Publication Open Access Expression quantitative trait locus fine mapping of the 17q12-21 asthma locus in African American children: a genetic association and gene expression study.Ober, Carole; McKennan, Chris G; Magnaye, Kevin M; Altman, Matthew C; Washington, Charles; Stanhope, Catherine; Naughton, Katherine A; Rosasco, Mario G; Bacharier, Leonard B; Billheimer, Dean; Gold, Diane R; Gress, Lisa; Hartert, Tina; Havstad, Suzanne; Khurana Hershey, Gurjit K; Hallmark, Brian; Hogarth, D Kyle; Jackson, Daniel J; Johnson, Christine C; Kattan, Meyer; Lemanske, Robert F; Lynch, Susan V; Mendonca, Eneida A; Miller, Rachel L; Naureckas, Edward T; O'Connor, George T; Seroogy, Christine M; Wegienka, Ganesa; White, Steven R; Wood, Robert A; Wright, Anne L; Zoratti, Edward M; Martinez, Fernando D; Ownby, Dennis; Nicolae, Dan L; Levin, Albert M; Gern, James E; Hoepner, LoriBackground: African ancestry is associated with a higher prevalence and greater severity of asthma than European ancestries, yet genetic studies of the most common locus associated with childhood-onset asthma, 17q12-21, in African Americans have been inconclusive. The aim of this study was to leverage both the phenotyping of the Children's Respiratory and Environmental Workgroup (CREW) birth cohort consortium, and the reduced linkage disequilibrium in African Americans, to fine map the 17q12-21 locus. Methods: We first did a genetic association study and meta-analysis using 17q12-21 tag single-nucleotide polymorphisms (SNPs) for childhood-onset asthma in 1613 European American and 870 African American children from the CREW consortium. Nine tag SNPs were selected based on linkage disequilibrium patterns at 17q12-21 and their association with asthma, considering the effect allele under an additive model (0, 1, or 2 effect alleles). Results were meta-analysed with publicly available summary data from the EVE consortium (on 4303 European American and 3034 African American individuals) for seven of the nine SNPs of interest. Subsequently, we tested for expression quantitative trait loci (eQTLs) among the SNPs associated with childhood-onset asthma and the expression of 17q12-21 genes in resting peripheral blood mononuclear cells (PBMCs) from 85 African American CREW children and in upper airway epithelial cells from 246 African American CREW children; and in lower airway epithelial cells from 44 European American and 72 African American adults from a case-control study of asthma genetic risk in Chicago (IL, USA). Findings: 17q12-21 SNPs were broadly associated with asthma in European Americans. Only two SNPs (rs2305480 in gasdermin-B [GSDMB] and rs8076131 in ORMDL sphingolipid biosynthesis regulator 3 [ORMDL3]) were associated with asthma in African Americans, at a Bonferroni-corrected threshold of p<0·0055 (for rs2305480_G, odds ratio [OR] 1·36 [95% CI 1·12-1·65], p=0·0014; and for rs8076131_A, OR 1·37 [1·13-1·67], p=0·0010). In upper airway epithelial cells from African American children, genotype at rs2305480 was the most significant eQTL for GSDMB (eQTL effect size [β] 1·35 [95% CI 1·25-1·46], p<0·0001), and to a lesser extent showed an eQTL effect for post-GPI attachment to proteins phospholipase 3 (β 1·15 [1·08-1·22], p<0·0001). No SNPs were eQTLs for ORMDL3. By contrast, in PBMCs, the five core SNPs were associated only with expression of GSDMB and ORMDL3. Genotype at rs12936231 (in zona pellucida binding protein 2) showed the strongest associations across both genes (for GSDMB, eQTLβ 1·24 [1·15-1·32], p<0·0001; and for ORMDL3 (β 1·19 [1·12-1·24], p<0·0001). The eQTL effects of rs2305480 on GSDMB expression were replicated in lower airway cells from African American adults (β 1·29 [1·15-1·44], p<0·0001). Interpretation: Our study suggests that SNPs regulating GSDMB expression in airway epithelial cells have a major role in childhood-onset asthma, whereas SNPs regulating the expression levels of 17q12-21 genes in resting blood cells are not central to asthma risk. Our genetic and gene expression data in African Americans and European Americans indicated GSDMB to be the leading candidate gene at this important asthma locus.Publication Open Access Prenatal phthalate and early childhood bisphenol A exposures increase asthma risk in inner-city children.(2014-08-28) Whyatt, Robin M; Rundle, Andrew G; Perzanowski, Matthew S; Just, Allan C; Donohue, Kathleen M; Calafat, Antonia M; Hoepner, Lori; Perera, Frederica P; Miller, Rachel LPublication Open Access Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children.Perera, Frederica P; Rauh, Virginia; Whyatt, Robin M; Tsai, Wei-Yann; Tang, Deliang; Diaz, Diurka; Hoepner, Lori; Barr, Dana; Tu, Yi-Hsuan; Camann, David; Kinney, PatrickOur prospective cohort study of nonsmoking African-American and Dominican mothers and children in New York City is evaluating the role of prenatal exposure to urban pollutants, including polycyclic aromatic hydrocarbons (PAHs) , environmental tobacco smoke (ETS) , and pesticides, in the pathogenesis of neurobehavioral disorders. We used the Bayley Scales of Infant Development to evaluate the effects on child mental and psychomotor development of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling. Behavioral development was assessed by the Child Behavior Checklist. We adjusted for potential confounders including sociodemographic factors and prenatal exposure to ETS and chlorpyrifos. Prenatal exposure to PAHs was not associated with psychomotor development index or behavioral problems. However, high prenatal exposure to PAHs (upper quartile) was associated with lower mental development index at age 3 [beta=-5.69; 95% confidence interval (CI), -9.05 to -2.33; p<0.01]. The odds of cognitive developmental delay were also significantly greater for children with high prenatal exposure (odds ratio=2.89; 95% CI, 1.33 to 6.25; p=0.01). General estimated equation analysis showed a significant age times PAH effect on mental development (p=0.01), confirming the age-specific regression findings. Further adjustment for lead did not alter the relationships. There were no differences in effect sizes by ethnicity. The results require confirmation but suggest that environmental PAHs at levels recently encountered in New York City air may adversely affect children's cognitive development at 3 years of age, with implications for school performance.Publication Open Access Transcriptional biomarkers of steroidogenesis and trophoblast differentiation in the placenta in relation to prenatal phthalate exposure.Adibi, Jennifer J; Whyatt, Robin M; Hauser, Russ; Bhat, Hari K; Davis, Barbara J; Calafat, Antonia M; Hoepner, Lori A; Perera, Frederica P; Tang, Deliang; Williams, Paige LBackground: Phthalates can alter steroidogenesis and peroxisome proliferator-activated receptor gamma (PPARgamma)mediated transcription in rodent tissues. The placenta offers a rich source of biomarkers to study these relationships in humans. Objective: We evaluated whether gestational phthalate exposures in humans were associated with altered human placental steroidogenesis and trophoblast differentiation as measured by markers of mRNA transcription. Methods: We measured seven target genes in placentas collected from 54 Dominican and African-American women at delivery in New York City using quantitative real-time polymerase chain reaction (qPCR), normalized to 18S rRNA. qPCR results for the target genes were log-transformed, converted to Z-scores, and grouped into two functional pathways: steroidogenesis (aromatase, cholesterol side chain cleavage enzyme, 17beta-hydroxysteroid dehydrogenase type 1, and cytochrome P450 1B1) and trophoblast differentiation (PPARgamma, aryl hydrocarbon receptor, and human chorionic gonadotropin). Repeated measures models were used to evaluate the association of phthalate metabolites measured in third-trimester urine samples with each group of target genes, accounting for correlation among the genes within a pathway. Results: Higher urinary concentrations of five phthalate metabolites were associated with lower expression of the target genes reflecting trophoblast differentiation. Results were less consistent for genes in the steroidogenesis pathway and suggested a nonlinear dose-response pattern for some phthalate metabolites. Conclusions: We observed a significant association between prenatal exposure to phthalates and placental gene expression within two pathways. Further studies are warranted to understand the significance of this association with respect to fetal development and placental function.