Search

Background: Prenatal exposure to phthalates, a group of synthetic chemicals widely used in consumer products, has previously been associated with adverse infant and child development. Studies also suggest that maternal depression and anxiety, may amplify the harmful effects of phthalates on infant and child neurodevelopment. Study design: Our analysis included a subset of dyads enrolled in the Atlanta African American Maternal-Child Cohort (N = 81). We measured eight phthalate metabolites in first and second trimester (8–14 weeks and 24–32 weeks gestation) maternal urine samples to estimate prenatal exposures. Phthalate metabolite concentrations were averaged across visits and natural log-transformed for analysis. Maternal symptoms of depression and anxiety were assessed using validated questionnaires (Edinberg Postnatal Depression Scale and State Trait Anxiety Inventory, respectively) and the total score on each scale was averaged across study visits. The NICU Network Neurobehavioral Scale (NNNS) was administered at two weeks of age. Our primary outcomes included two composite NNNS scores reflecting newborn attention and arousal. Linear regression was used to estimate associations between individual phthalate exposures and newborn attention and arousal. We assessed effect modification by maternal depression and anxiety. Results: Higher levels of urinary phthalate metabolites were not associated with higher levels of infant attention and arousal, but true associations may still exist given the limited power of this analysis. In models examining effect modification by maternal depression, we observed that an interquartile range increase in mono (2-ethlyhexyl) phthalate (MEHP), mono (2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) was associated with a significant increase in newborn arousal only among those with high depressive symptoms (MEHP: β = 0.71, 95% confidence interval [CI] = 0.10, 1.32 for high, β = −0.30, 95% CI = −0.73, 0.12 for low; MEOHP: β = 0.60, 95% CI = −0.03, 1.23 for high, β = −0.12, 95% CI = −0.58, 0.33 for low; MEHHP: β = 0.54, 95% CI = −0.04, 1.11 for high, β = −0.11, 95% CI = −0.54, 0.32 for low). Similar patterns were observed in models stratified by maternal anxiety, although CIs were wide. Conclusion: Our results suggest maternal anxiety and depression symptoms may exacerbate the effect of phthalates on infant neurodevelopment. Future studies are needed to determine the optimal levels of attention and arousal in early infancy.

Background: Obstetric hemorrhage is the leading cause of maternal mortality and severe maternal morbidity (SMM) in Maryland and nationally. Currently, through a quality collaborative, the state is implementing the Alliance for Innovation on Maternal Health (AIM) patient safety bundle on obstetric hemorrhage., Objective: To describe SMM events contributed by obstetric hemorrhage and their preventability in Maryland., Study Design: This cross-sectional study used data from hospital-based SMM surveillance and review program in Maryland. Hospital-based SMM criteria include admission to an intensive care unit and/or transfusion of 4 or more units of blood products (of any type) during pregnancy or within 42 days postpartum. A total of 193 obstetric hemorrhage events that met the surveillance definition were identified in hospitals participating in SMM surveillance since inception on August 1, 2020 until December 31, 2022. We compared patient and delivery characteristics, practices done well, and recommendations for care improvement among patients with severe obstetric hemorrhage deemed preventable and non-preventable by hospital-based review committees. For obstetric hemorrhage events deemed preventable, we further identified factors that contributed to the SMM outcome at the provider, system, and patient levels., Results: Uterine atony was the leading cause of obstetric hemorrhage events (37.8%), followed by uterine rupture, laceration and intra-abdominal bleeding (23.8%). Sixty-six (34.2%) obstetric hemorrhage events were preventable. Patients with preventable obstetric hemorrhage were significantly more likely to have an emergency than planned cesarean delivery and less likely to have a placental complication or >1500 mL blood loss volume. Hospital-based review committees determined that 81.8%, 30.3%, and 22.7% of preventable events could have been prevented or made less severe through changes to provider, system, or patient factors, respectively. Recommendations following event reviews aligned with the Alliance for Innovation on Maternal Health Obstetric Hemorrhage Patient Safety Bundle, particularly regarding elements in the Recognition and Prevention and Response domains., Conclusion: About one-third of SMM events contributed by obstetric hemorrhages were deemed preventable. Of AIM bundle elements, assessing hemorrhage risk on admission to labor and delivery, peripartum, and upon transition to postpartum care together with rapid, unit-standardized management of hemorrhage are likely to benefit more than half of patients with preventable SMM contributed by obstetric hemorrhage., (Copyright © 2025 Elsevier Inc. All rights reserved.)

People with Parkinson's disease (PD) and their care partners frequently report cognitive decline as one of their greatest concerns. Mild cognitive impairment affects approximately 20-50% of people with PD, and longitudinal studies reveal dementia in up to 80% of PD. Through the Parkinson's Disease Foundation Community Choice Research Award Program, the PD community identified maintaining cognitive function as one of their major unmet needs. In response, a working group of experts across multiple disciplines was organized to evaluate the unmet needs, current challenges, and future opportunities related to cognitive impairment in PD. Specific conference goals included defining the current state in the field and gaps regarding cognitive issues in PD from patient, care partner, and healthcare professional viewpoints; discussing non-pharmacological interventions to help maintain cognitive function; forming recommendations for what people with PD can do at all disease stages to maintain cognitive health; and proposing ideas for how healthcare professionals can approach cognitive changes in PD. This paper summarizes the discussions of the conference, first by addressing what is currently known about cognitive dysfunction in PD and discussing several non-pharmacological interventions that are often suggested to people with PD. Second, based on the conference discussions, we provide considerations for people with PD for maintaining cognitive health and for healthcare professionals and care partners when working with people with PD experiencing cognitive impairment. Furthermore, we highlight key issues and knowledge gaps that need to be addressed in order to advance research in cognition in PD and improve clinical care., Competing Interests: J.G.G. has received consulting/advisory board honoraria from Acadia, Aptinyx, Biogen; grants/research support from Acadia, Biotie (site PI), Consolidated Anti-Aging, National Institutes of Health, National Parkinson Foundation, Michael J. Fox Foundation, Rush University; honoraria from American Academy of Neurology, International Parkinson and Movement Disorder Society, MedEdicus; and salary from Rush University Medical Center. B.A.V. has received salary from the Parkinson’s Foundation. R.C. has received research funding from the Canadian Institutes for Health Research (CIHR), Alberta Innovates Solutions, the Alzheimer Society of Canada, University of Alberta Hospital Foundation, and National Institutes of Health and is a site investigator for a pharmaceutical trial sponsored by Axovant (back up site); served on the Scientific advisory board for Michael J. Fox Foundation, the Parkinson’s Disease Foundation, Parkinson Canada, Editorial board for Frontiers in Aging Neurosciences, Dementia and Geriatric Cognitive Disorders, Parkinsonism and Related Disorders, and as safety monitor/scientific advisor for a Harvard University/Tel Aviv University trial of DCTMS and a Western University investigator initiated pharmaceutical trial. N.D. has received grant/research support from the National Institutes of Health, Parkinson’s Foundation, Michael J. Fox Foundation, Parkinson Council, Biotie, Abbvie and salary from the University of Pennsylvania. R.D. has received grant/research support from the Michael J. Fox Foundation, the Parkinson’s Unity Walk, the Veteran Affairs Administration, and the Parkinson’s Foundation; consulting fees from the Michael J. Fox Foundation and the University of Delaware; and salary from Rutgers University. T.E. has received grant/research support from the National Institutes of Health, American Parkinson Disease Association and salary support from Boston University. J.E.G. has received grant/research support from the National Institutes of Health, Florida Department of Health, the Harry T. Mangurian Foundation, and the Association for Frontotemporal Degeneration, serves as a scientific advisor for Axovant, Biogen, Eisai, and Eli Lilly; receives licensing fees from Pfizer, Lilly, Axovant, and Quintiles; conducts on-going clinical trials funded by Biogen, Axovant, and Janssen, and serves on the editorial boards of Neurodegenerative Disease Management, Alzheimer’s Disease and Associated Disorders, and Acta Neuropathologica. C.M. has received grant/research support from The Michael J. Fox Foundation, Canadian Institutes of Health Research, Movement Disorders Society; National Institutes of Health; served as a consultant to Accorda Therapeutics; received honoraria from EMD Serono, steering committee for National Parkinson Foundation; and salary from the University Health Network. J. Edwards serves on Data Safety Monitoring Boards on National Institutes of Health grants awarded to Posit Science Inc. She previously served as a limited consultant to Posit Science Inc. in 2007, and has worked as a consultant to Wilson Sonsini Goodrich & Rosati. J.F. has received grant support from the Patient Centered Outcomes Research Institute, National Institutes of Health, and salary from Mayo Clinic, Rochester, MN. J.K. serves as a site PI for clinical trials sponsored by Novartis and Lilly and as a consultant to John Hancock. L.S. has received grant/research support from the National Institutes of Health, the Michael J. Fox Foundation, and Biotie/Acorda. G.S. has received grant support from the Patient Centered Outcomes Research Institute and National Institutes of Health and the Florida Department of Health; consulting fees from Novartis, the NFL Concussion Settlement Program and book royalties; and salary from the University of Florida, Gainesville. C.T. has received grant/research support from National Institutes of Health; consulting/advisory board honoraria from UpToDate Inc., Viocare Food Intake Advisory Board; and salary from Rush University Medical Center. C.A.T. has received grant/research support from the National Institutes of Health and salary support from Boston University. E.U. has received grant/research support from Michael J. Fox Foundation, National Institutes of Health, Department of Veterans Affairs; honoraria from the American Academy of Neurology; and salary from University of Iowa and Department of Veterans Affairs. The remaing authors declare no competing interests.