Faculty Bibliography

In developing and developed countries, urban gardening has increasingly become an integral part of local food systems for good quality produce, for enhanced urban health and sustainability. There are few gardens with naturally perfect soils for growing plants. However, the soils with poor texture and fewer nutrients can be improved by different types of organic amendments such as composts, garden soils and organic potting mixes that are commercially available in the consumer markets worldwide to promote healthy plant growth. In this study, we assessed 19 different commercially available composts, garden soils, and potting mixes for the presence of 38 per- and polyfluoroalkyl substances (PFAS). The total (Æ©38) PFAS in the samples ranged between 1.26 to 11.84 µg kg^−1 (dry weight). The total concentration of perfluorinated carboxylic acids (Æ©PFCAs) was higher than that of perfluoroalkyl sulfonic acids (PFSAs) in all products. The total oxidizable precursor assay (TOPA) was applied in the analysis of composts and potting mixes, which revealed an increase in short-chain Æ©PFCAs concentrations ranging from 0.48 to 7.63 µg kg^−1, which suggested the transformation of PFCAs precursors to short-chain PFCAs. The measured concentrations of short-chain PFCAs after TOPA in the soil substrates have the potential to contribute to plant uptake and food chain transfer of PFAS to humans due to their high mobility.

BACKGROUND:Fetal exposure to endocrine-disrupting chemicals such as phthalates and bisphenols might lead to fetal cardiovascular developmental adaptations and predispose individuals to cardiovascular disease in later life. OBJECTIVES/OBJECTIVE:We examined the associations of maternal urinary bisphenol and phthalate concentrations in pregnancy with offspring carotid intima-media thickness and distensibility at the age of 10 y. METHODS:In a population-based, prospective cohort study of 935 mother-child pairs, we measured maternal urinary phthalate and bisphenol concentrations at each trimester. Later, we measured child carotid intima-media thickness and distensibility in the children at age 10 y using ultrasound. RESULTS: DISCUSSION/CONCLUSIONS:In this large prospective cohort, higher maternal urinary bisphenols concentrations were associated with smaller childhood carotid intima-media thickness. Further studies are needed to replicate this association and to identify potential underlying mechanisms. https://doi.org/10.1289/EHP10293.

BACKGROUND:In utero exposure to bisphenols, widely used in consumer products, may alter lung development and increase the risk of respiratory morbidity in the offspring. However, evidence is scarce and mostly focused on bisphenol A (BPA) only. OBJECTIVE:To examine the associations of in utero exposure to BPA, bisphenol F (BPF), and bisphenol S (BPS) with asthma, wheeze, and lung function in school-age children, and whether these associations differ by sex. METHODS:We included 3,007 mother-child pairs from eight European birth cohorts. Bisphenol concentrations were determined in maternal urine samples collected during pregnancy (1999-2010). Between 7 and 11 years of age, current asthma and wheeze were assessed from questionnaires and lung function by spirometry. Wheezing patterns were constructed from questionnaires from early to mid-childhood. We performed adjusted random-effects meta-analysis on individual participant data. RESULTS:Exposure to BPA was prevalent with 90% of maternal samples containing concentrations above detection limits. BPF and BPS were found in 27% and 49% of samples. In utero exposure to BPA was associated with higher odds of current asthma (OR = 1.13, 95% CI = 1.01, 1.27) and wheeze (OR = 1.14, 95% CI = 1.01, 1.30) (p-interaction sex = 0.01) among girls, but not with wheezing patterns nor lung function neither in overall nor among boys. We observed inconsistent associations of BPF and BPS with the respiratory outcomes assessed in overall and sex-stratified analyses. CONCLUSION:This study suggests that in utero BPA exposure may be associated with higher odds of asthma and wheeze among school-age girls.

Previous studies have provided data on determinants of phthalates in pregnant women, but results were disparate across regions. We aimed to identify the food groups and demographic factors that predict phthalate exposure in an urban contemporary pregnancy cohort in the US. The study included 450 pregnant women from the New York University Children's Health and Environment Study in New York City. Urinary concentrations of 22 phthalate metabolites, including metabolites of di-2-ethylhexylphthalate (DEHP), were determined at three time points across pregnancy by liquid chromatography coupled with tandem mass spectrometry. The Diet History Questionnaire II was completed by pregnant women at mid-pregnancy to assess dietary information. Linear mixed models were fitted to examine determinants of urinary phthalate metabolite concentrations. Using partial-linear single-index (PLSI) models, we assessed the major contributors, among ten food groups, to phthalate exposure. Metabolites of DEHP and its ortho-phthalate replacement, diisononyl phthalate (DiNP), were found in >90% of the samples. The sum of creatinine-adjusted DiNP metabolite concentrations was higher in older and single women and in samples collected in summer. Hispanic and non-Hispanic Black women had lower urinary concentrations of summed metabolites of di-n-octyl phthalate (DnOP), but higher concentrations of low molecular weight phthalates compared with non-Hispanic White women. Each doubling of grain products consumed was associated with a 20.9% increase in ∑DiNP concentrations (95%CI: 4.5, 39.9). PLSI models revealed that intake of dried beans and peas was the main dietary factor contributing to urinary ∑DEHP, ∑DiNP, and ∑DnOP levels, with contribution proportions of 76.3%, 35.8%, and 27.4%, respectively. Urinary metabolite levels of phthalates in pregnant women in NYC varied by age, marital status, seasonality, race/ethnicity, and diet. These results lend insight into the major determinants of phthalates levels, and may be used to identify exposure sources and guide interventions to reduce exposures in susceptible populations.

Despite their known carcinogenic potential, primary aromatic amines (AAs) continue to be used in various consumer products. Human exposure to AAs is a subject of current concern. Although urinary measurements are used in the assessment of exposure, little is known about within- and between-individual temporal variability in urinary concentrations of AAs. In this study, we determined the concentrations of 30 AAs, nicotine and cotinine in 213 first morning void (FMV) urine samples collected longitudinally for over a five-week period from 15 participants residing in the Albany area of New York State, USA. Eight AAs, namely, aniline, 2-naphthylamine (2-NA), p-cresidine (p-CD), p-toluidine (p-TD), o/m-toluidine (o/m-TD), 4-chloroaniline (4-CA), 4,4'-methylenedi-o-toluidine (4,4'-MDA), and 2,6-dimethylaniline (2,6-DMA) were found in urine at a detection frequency (DF) in the range of 68-100%. Aniline and 2,6-DMA were the predominant compounds found at median concentrations of 6.0 and 3.81 ng/mL, respectively. Intraclass correlation coefficients (ICCs) of all urinary AA concentrations, except for 4-CA, showed moderate to poor predictability (ICC values ranged 0.248-0.697). Gender and ethnicity-related variations in ∑₈AA concentrations were significant. Spearman's correlations among AA concentrations suggested that the sources of exposure were not related to tobacco smoke. No significant correlations existed between AAs concentrations and oxidative stress biomarkers (OSBs). The estimated daily intakes of AAs calculated based on urinary concentrations were several orders of magnitude below the tolerable daily intakes.

Environmental chemical exposures have been associated with cancer, diabetes, hormonal and immunological disorders, and cardiovascular diseases. Some direct effects of chemical exposure that are precursors to adverse health outcomes, including oxidative stress, nitrative stress, hormonal imbalance, neutrophilia, and eosinophilia, can be assessed through the analysis of biomarkers in urine. In this study, we describe a novel methodology for the determination of 19 biomarkers of health effects: malondialdehyde (MDA), 8-isoprostaglandin-F_2α (8-PGF_2α), 11-β-prostaglandin-F_2α (11-PGF_2α), 15-prostaglandin-F_2α (15-PGF_2α), 8-iso-15-prostaglandin-F_2α (8,15-PGF_2α), 8-hydroxy-2'-deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8-HdG), 8-hydroxyguanine (8-HG), dityrosine (diY), allantoin (Alla), and two metabolic products of 4-hydroxynonenal (HNE), namely 4-hydroxy-2-nonenal glutathione (HNE-GSH) and 4-hydroxy-2-nonenal mercapturic acid (HNE-MA) (in total, 12 oxidative stress biomarkers, OSBs); 8-nitroguanosine (8-NdG), 8-nitroguanine (8-NG), and 3-nitrotyrosine (NY) (3 nitrative stress biomarkers, NSBs); chlorotyrosine (CY) and bromotyrosine (BY) (2 inflammatory biomarkers); and the advanced glycation end-products (AGEs) N^ε-carboxymethyllysine (CML) and N^ε-carboxyethyllysine (CEL) (2 metabolic disorder biomarkers). Since these biomarkers are trigged by a variety of environmental insults and produced by different biomolecular pathways, their selective and sensitive determination in urine would help broadly elucidate the pathogenesis of diseases mediated by environmental factors.

Our previous studies demonstrated that prenatal bisphenol A (BPA) exposure affected the hepatic transcriptome and lipidome in rat offspring in a sex- and age-dependent manner. In this study, we investigated the effects of gestational exposure to BPA on the rat dams, after weaning period, and compared them with those of their offspring. Our results showed alterations in hepatic transcriptome related to insulin signaling, circadian rhythm, and infectious disease pathways in BPA-treated dams even 4 weeks after the exposure, whereas slight modifications on the lipid profile were found. Alterations in lipid and transcriptome profiles were more prominent in the prenatally BPA-exposed offspring at postnatal day (PND) 1 and 21 than those in the dams, suggesting that in utero exposure to BPA is more serious than exposure in the adulthood. Cryptochrome-1 (Cry1) and peroxisome proliferator-activated receptor delta (Ppard) were commonly altered in both dams and offspring. Nevertheless, the results of DIABLO (Data Integration Analysis for Biomarker discovery using Latent cOmponents), showed that multi-omics data successfully distinguished the exposed dams from the corresponding controls and their offspring with a high level of accuracy. The accuracy rates in BPA50 models (including control and 50 μg BPA/kg bw/day exposed groups) were smaller than those in BPA5000 models (control and 5000 μg BPA/kg bw/day exposed groups), suggesting dose-dependent severity in BPA effects. Palmitic acid and genes related to circadian rhythm, insulin responses, and lipid metabolism (e.g., 1-acylglycerol-3-phosphate O-acyltransferase 2 (Agpat2), B-cell CLL/lymphoma 10 (Bcl10), Cry1, Harvey rat sarcoma virus oncogene (Hras), and NLR family member X1 (Nlrx1)) were identified through DIABLO models as novel biomarkers of effects of BPA across two generations.

Perchlorate (ClO₄

OBJECTIVE:To determine if higher exposures measured in early childhood to environmental phenols, phthalates, pesticides, and/or trace elements, are associated with increased odds of having a diagnosis of Autism Spectrum Disorder (ASD), Developmental Delay (DD), or Other Early Concerns (OEC) compared to typically developing children (TD). METHODS:This study included 627 children between the ages of 2-5 who participated in the Childhood Autism Risks from Genetics and Environment (CHARGE) study. Urine samples were collected at the same study visit where diagnostic assessments to confirm diagnosis indicated during the recruitment process were performed. Adjusted multinomial regression models of each chemical with diagnosis as the outcome were conducted. Additionally, two methods were used to analyze mixtures: repeated holdout multinomial weighted quantile sum (WQS) regression for each chemical class; and a total urinary mixture effect was assessed with repeated holdout random subset WQS. RESULTS:Many urinary chemicals were associated with increased odds of ASD, DD or OEC compared to TD; however, most did not remain significant after false discovery rate adjustment. Repeated holdout WQS indices provided evidence for associations of both a phenol/paraben mixture effect and a trace element mixture effect on DD independently. In analyses adjusted for confounders and other exposures, results suggested an association of a pesticide mixture effect with increased risk for ASD. Results also suggested associations of a total urinary mixture with greater odds of both ASD and DD separately. CONCLUSION/CONCLUSIONS:Higher concentrations of urinary biomarkers were associated with ASD, DD, and OEC compared to TD, with consistency of the results comparing single chemical analyses and mixture analyses. Given that the biospecimens used for chemical analysis were generally collected many months after diagnoses were made, the direction of any causal association is unknown. Hence findings may reflect higher exposures among children with non-typical development than TD children due to differences in behaviors, metabolism, or toxicokinetics.

CONTEXT/BACKGROUND:Phthalates may disrupt maternal-fetal-placental endocrine pathways, affecting pregnancy outcomes and child development. Placental corticotropin releasing hormone (pCRH) is critical for healthy pregnancy and child development, but understudied as a target of endocrine disruption. OBJECTIVE:To examine phthalate metabolite concentrations (as mixtures and individually) in relation to pCRH. DESIGN/METHODS:Secondary data analysis from a prospective cohort study. SETTING/METHODS:Prenatal clinics in Tennessee, USA. PATIENTS/METHODS:1018 pregnant women (61.4% non-Hispanic Black, 32% non-Hispanic White, 6.6% other) participated in the CANDLE study and provided data. Inclusion criteria included: low-medical-risk singleton pregnancy, age 16-40, and gestational weeks 16-29. INTERVENTION/METHODS:None. MAIN OUTCOME MEASURES/METHODS:Plasma pCRH at two visits (mean gestational ages 23.0 and 31.8 weeks) and change in pCRH between visits (ΔpCRH). RESULTS:In weighted quantile sums (WQS) regression models, phthalate mixtures were associated with higher pCRH at Visit 1 (β = 0.07, 95 %CI: 0.02, 0.11) but lower pCRH at Visit 2 (β = -0.08, 95 %CI: -0.14, -0.02). In stratified analyses, among women with gestational diabetes (n = 59), phthalate mixtures were associated with lower pCRH at Visit 1 (β = -0.17, 95 %CI: -0.35, 0.0006) and Visit 2 (β = -0.35, 95 %CI: -0.50, -0.19), as well as greater ΔpCRH (β = 0.16, 95 %CI: 0.07, 0.25). Among women with gestational hypertension (n = 102), phthalate mixtures were associated with higher pCRH at Visit 1 (β = 0.20, 95 %CI: 0.03, 0.36) and Visit 2 (β = 0.42; 95 %CI: 0.19, 0.64) and lower ΔpCRH (β = -0.17, 95 %CI: -0.29, -0.06). Significant interactions between individual phthalate metabolites and pregnancy complications were observed. CONCLUSIONS:Phthalates may impact placental CRH secretion, with differing effects across pregnancy. Differences in results between women with and without gestational diabetes and gestational hypertension suggest a need for further research examining whether women with pregnancy complications may be more vulnerable to endocrine-disrupting effects of phthalates.