studies of timing of menarche would need to consider the potential effect of area-level deprivation. Supported by: This work was supported by the National Research Founda- tion of Korea, grant number NRF-2016R1D1A1B03933410. P-162 Tuesday, October 9, 2018 6:30 AM BISPHENOL A EXPOSURE NEGATIVELY IMPACTS EMBRYO DEVELOPMENT THROUGH A MECHA- NISM THAT INVOLVES ZINC DEPLETION, REACTIVE OXYGEN SPECIES OVERPRODUCTION AND INDUC- TION OF APOPTOSIS. C. Chatzicharalampous, R. Jeelani, K. Ghoniem, S. Najeemuddin, N. Joshi, R. T. Morris, A. Awonuga, H. M. Abu-Soud. Obstetrics and Gynecology, Wayne State University, De- troit, MI. OBJECTIVE: Background: Bisphenol A (BPA) is a ubiquitous xenoes- trogen utilized during the manufacturing of plastic products, including food containers, paper products, water pipes, toys, medical equipment, and electronics. Females exposed to BPA may be susceptible to its detrimental effects including infertility. Recent studies have shown that BPA exposure at levels as low as 100 mg/kg/day can impair embryo implantation in the mouse model 1 . BPA can also interfere with the endocrine function of hypo- thalamic-pituitary axis and affect fertility 2 . It can accumulate in reproductive organs and act as an endocrine disruptor due to its structural similarity to es- trogen. No known study investigated the mechanism on how BPA affects em- bryo development. Potential mechanisms may involve induction of apoptosis, reactive oxygen species (ROS) overproduction 3 and zinc deple- tion. Zinc supports embryo development and is important in egg activation 4 . Even minimal exposure to toxins is thought to result in changes to zinc ho- meostasis leading to embryo impairment. OBJECTIVE: In this study we hypothesize that BPA exposure affects em- bryo development and survival through a mechanism that involves induction of apoptosis, intracellular zinc depletion and ROS overproduction. DESIGN: A case-control study of mouse pronuclear embryos pre-exposed in vitro to increasing BPA concentrations for 18 hours and then followed through day 5 of development. They were photographed, graded and treated to examine ROS generation, zinc depletion and induction of apoptosis. MATERIALS AND METHODS: Mice oocytes were retrieved from 8-10 weeks female mice and were fertilized using IVF. The embryos were subse- quently divided in 4 groups that were exposed to increasing concentrations of BPA (10 - 100 mM) for 18 hours and one group that were untreated controls (n ¼ 20 / group). The embryos were photographed and graded daily based on their appearance and development. A subgroup of the treated embryos (n ¼ 10 / group) were further evaluated for induction of apoptosis, overproduc- tion of ROS and zinc depletion using commercially available assays. Confocal microscopy was used to assess the embryos. Statistical analysis was performed using ANOVA repeated measures, chi-square and survival curves. P < 0.05 was considered statistically significant. RESULTS: Day 5 embryos that were exposed to BPA concentrations > 50mM had fewer progressions to blasts, lower blast grades and more were ar- rested compared to controls (p<0.05). Enhancement of ROS production as well as increased apoptosis was observed in the treated groups compared to controls (p<0.05). Zinc depletion was evident in embryos treated with BPA at concentrations > 50 mM (p<0.05). CONCLUSIONS: Exposure to BPA, may negatively affect embryo devel- opment through mechanisms that involve alteration of the redox potential and increased oxidative stress, induction of apoptosis and intracellular zinc depletion. References: 1. Huo, X. et al. Int J Environ Res Public Health. 2015 Sep 7;12(9):11101-16. 2. Yuan, M. et al. Fertil Steril 2018;109:735-44. 3. Jeelani R, et al. Free Radic Biol Med. 2017 Sep;110:11-18. 4. Zhang N. et al. Sci Rep. 2016; 6: 22772. Supported by: None. P-163 Tuesday, October 9, 2018 6:30 AM WORK RELATED EXPOSURES: IMPACTS ON HOR- MONE LEVELS, ANOVULATION AND THE MEN- STRUAL CYCLE. J. Pilgrim, a K. Kim, b M. J. Hill, c S. Mumford, b L. Sjaarda, d N. Perkins, b A. H. DeCherney, b R. Silver, e E. Schisterman. b a NIH, Bethesda, MD; b NICHD, Bethesda, MD; c NIH, Germantown, MD; d Epidemiology Branch, DIPHR, NIH, Be- thesda, MD; e Univ of Utah, Salt Lake City, UT. OBJECTIVE: Work related exposures may influence health, but few data are available about routine day-to-day work activities and reproduction. The goal of this study was to examine impacts of environmental work exposures on hormone levels, risk of anovulation and menstrual cycle changes. DESIGN: Prospective cohort study of 1,184 women enrolled in the EAGeR (Effects of Aspirin in Gestation and Reproduction) Trial, a random- ized clinical trial of preconception-initiated low dose aspirin on live birth, with information on work exposures. MATERIALS AND METHODS: Women aged 18-40 years and attempt- ing pregnancy completed an occupational exposure questionnaire focused on employment status and job-related exposures (night work, rotating shift, whole body vibration, loud noise, extreme heat, heavy exertion, and pro- longed standing). Urinary reproductive hormones including pregnanediol glucuronide (PdG), follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estrone-3-glucuronide (E1G) were measured up to 5 times per cy- cle during the first 2 cycles of study participation. Anovulation was assessed using fertility monitors and luteal phase urinary PdG levels for up to 6 cycles. Mixed models estimated associations between work exposures and urinary hormones and cycle length; generalized linear mixed models were used for outcomes of anovulation. Models were weighted for the number of contrib- uted cycles per woman and adjusted for age, BMI, race, physical activity, in- come, education, and treatment assignment. RESULTS: Overall, 76.5% of participants were working while attempting pregnancy. There were no associations between employment status and uri- nary hormone concentrations. However, lower levels of urinary PdG were found among night workers compared to non-exposed women (b¼-0.18 ng/mL, 95% confidence interval [CI] -0.31, -0.05), though no associations were observed with cycle length or risk of anovulation. Though exposure to loud noise was associated with longer follicular phase length (b ¼1.11 days, 95% CI 0.03, 2.19), no associations were found with hormones or an- ovulation. Exposures to other work exposures were not associated with reproductive hormones, cycle length, or anovulation. CONCLUSIONS: Though night shift work was linked to lower urinary PdG and loud noise exposure was associated with longer follicular phase length, no work-related exposures were associated with anovulation. These data suggest that the exposures studied here are likely not harmful to men- strual cycle function. Supported by: Supported by the Intramural Research Program of the Eu- nice Kennedy Shriver, National Institute of Child Health and Human Devel- opment (NICHD). P-164 Tuesday, October 9, 2018 6:30 AM NICKEL EXPOSURE IN VITRO PREVENTS HATCH- ING IN MOUSE EMBRYOS BY DOWN-REGULATING PLURIPOTENT GENES AND REPRESSING TROPHEC- TODERM CDX2 EXPRESSION. F. Wang, a S. M. Maxwell, b A. K. Masbou, b F. M. Bourroul, a D. L. Keefe. a,b a Depart- ment of Obstetrics and Gynecology, NYU LangoneHealth, New York, NY; b New York University Langone FertilityCenter, New York, NY. OBJECTIVE: To evaluate the effect of exposure to the environmental toxi- cant Nickel on preimplantation embryo development in vitro using a mouse model. DESIGN: Prospective Laboratory Study. MATERIALS AND METHODS: Mouse zygotes (Embryotech) were thawed in M2 medium and randomly treated with 0mM (control group), 50mM or 100mM (exposure groups) of Nickel(II) chloride (Sigma) in Global medium (Lifeglobal) supplemented with 0.4% BSA until blastocyst stage. The rates of embryo development to 2-Cell, 4-Cell, Blastocyst or hatching stages were recorded by imaging. Relative gene expression of 4-Cell em- bryos and Blastocysts were analyzed by RT-qPCR in SYBR green system. Statistical analysis used GraphPad Prism software. RESULTS: Nickel at 100mM completed eliminated hatching, which was significantly different from controls (P ¼ 0.0032, Fisher’s exact test). The rate of hatching under 50mM of Nickel exposure (22%) was lower than that of controls (78%), a difference which almost reached significance (P ¼ 0.0567, Fisher’s exact test). Development (%) to 2-Cell, 4-Cell and blas- tocyst stages (see table) under exposure to Nickel did not differ from controls (P > 0.05, Fisher’s exact test). Pluripotent gene (Nanog, Oct4, Sox2 and Klf4) expression levels in blastocysts exposed to Nickel were down-regu- lated in a dose-depend manner compared to controls (P < 0.05, One-way ANOVA). Relative mRNA levels of the trophectoderm gene Cdx2 in blasto- cysts exposed to 50mM and 100mM Nickel were significantly down-regulated compared to controls (139.598 Æ 9.794 and 1.003 Æ 0.118 respectively vs. e172 ASRM Abstracts Vol. 110, No.4, Supplement, September 2018