Pregnancy and Infant Development (PRIDE)—a preliminary observational study of maternal adversity and infant development

Background Children from socioeconomically disadvantaged families have a markedly elevated risk for impaired cognitive and social-emotional development. Children in poverty experience have a high risk for developmental delays. Poverty engenders disproportionate exposure to psychological adversity which may contribute to impaired offspring development; however the effect may be mitigated by social support and other aspects of resilience. Our objective was to determine the association between maternal stress, adversity and social support and early infant neurobehavior and child behavior at two and three years. Methods We conducted a longitudinal mother-infant cohort study nested within a regional home visiting program in Cincinnati, Ohio. Four home study visits were completed to collect measures of maternal stress, adversity and social support and infant and child behavior. A measure of infant neurobehavior (‘high-arousal’ infant) was derived from the NICU Network Neurobehavioral Scale (NNNS) at 1 month and externalizing and internalizing symptoms were measured by the Child Behavior Checklist (CBCL) at 24 and 36 months. Linear and logistic regression identified associations between maternal risk/protective factors and infant and child behavioral measures. We used stratification and multiplicative interaction terms to examine potential interactions. Results We enrolled n = 55 pregnant mothers and follow 53 mother–offspring dyads at 1 month, 40 dyads at 24 months and 27 dyads at 36 months. Maternal adversity and protective factors were not associated with neurobehavior at one month. However, maternal depression and measures of distress in pregnancy were significantly associated with internalizing and externalizing symptoms at 24 and 36 months. Conclusions This pilot study established the feasibility of conducting longitudinal research within a community intervention program. In addition, although there were no statistically significant associations between maternal psychosocial factors in pregnancy and infant neurobehavior, there were several associations at 24 months, primarily internalizing symptoms, which persisted through 36 months. Future work will replicate findings within a larger study as well as explore mediators and modifiers of these associations

Environ Int

An increasing amount of evidence suggests ultrafine particles (UFPs) are linked to adverse health effects, especially in those with chronic conditions such as asthma, due to their small size and physicochemical characteristics. Toxicological and experimental studies have demonstrated these properties, and the mechanisms by which they deposit and translocate in the body result in increased toxicity in comparison to other air pollutants. However, current epidemiological literature is limited due to exposure misclassification and thus identifying health outcomes associated with UFPs. The objective of this study was to investigate the association between weekly personal UFP exposure with lung function and respiratory symptoms in 117 asthmatic and non-asthmatic adolescents between 13 and 17\ua0years of age in the Cincinnati area. Between 2017 and 2019, participants collected weekly UFP concentrations by sampling for 3\ua0h a day in their home, school, and during transit. In addition, pulmonary function was evaluated at the end of the sampling week, and respiratory symptoms were logged on a mobile phone application. Multivariable linear regression and zero-inflated Poisson (ZIP) models were used to estimate the association between personal UFP and respiratory outcomes. The average median weekly UFP exposure of all participants was 4340 particles/cm| (p/cc). Results of fully adjusted regression models revealed a negative association between UFPs and percent predicted forced expiratory volume/forced vital capacity ratio (%FEV|/FVC) (\u3b2:-0.03, 95% CI [-0.07, 0.02]). Prediction models estimated an association between UFPs and respiratory symptoms, which was greater in asthmatics compared to non-asthmatics. Our results indicate an interaction between asthma status and the likelihood of experiencing respiratory symptoms when exposed to UFPs, indicating an exacerbation of this chronic condition. More research is needed to determine the magnitude of the role UFPs play on respiratory health.R33 ES024713/ES/NIEHS NIH HHSUnited States/T42 OH008432/OH/NIOSH CDC HHSUnited States/2022-11-01T00:00:00Z34237487PMC83807341205

The Children's Respiratory and Environmental Workgroup (CREW) birth cohort consortium: design, methods, and study population

Background: Single birth cohort studies have been the basis for many discoveries about early life risk factors for childhood asthma but are limited in scope by sample size and characteristics of the local environment and population. The Children’s Respiratory and Environmental Workgroup (CREW) was established to integrate multiple established asthma birth cohorts and to investigate asthma phenotypes and associated causal pathways (endotypes), focusing on how they are influenced by interactions between genetics, lifestyle, and environmental exposures during the prenatal period and early childhood. Methods and results: CREW is funded by the NIH Environmental influences on Child Health Outcomes (ECHO) program, and consists of 12 individual cohorts and three additional scientific centers. The CREW study population is diverse in terms of race, ethnicity, geographical distribution, and year of recruitment. We hypothesize that there are phenotypes in childhood asthma that differ based on clinical characteristics and underlying molecular mechanisms. Furthermore, we propose that asthma endotypes and their defining biomarkers can be identified based on personal and early life environmental risk factors. CREW has three phases: 1) to pool and harmonize existing data from each cohort, 2) to collect new data using standardized procedures, and 3) to enroll new families during the prenatal period to supplement and enrich extant data and enable unified systems approaches for identifying asthma phenotypes and endotypes. Conclusions: The overall goal of CREW program is to develop a better understanding of how early life environmental exposures and host factors interact to promote the development of specific asthma endotypes.HHS/NIH [5UG3OD023282]; Columbia University [P01ES09600, R01 ES008977, P30ES09089, R01 ES013163, R827027]; Tucson Children's Respiratory Study (TCRS) [NHLBI 132523]; Infant Immune Study (IIS) [HL-56177]; Childhood Origins of Asthma Study (COAST) [P01 HL070831, U10 HL064305, R01 HL061879]; Wayne County Health, Environment, Allergy and Asthma Longitudinal Study (WHEALS) [R01 AI050681, R56 AI050681, R01 AI061774, R21 AI059415, K01 AI070606, R21 AI069271, R01 HL113010, R21 ES022321, P01 AI089473, R21 AI080066, R01 AI110450, R01 HD082147]; Fund for Henry Ford Health System; Childhood Allergy Study (CAS) [R01 AI024156, R03 HL067427, R01 AI051598]; Blue Cross Foundation Johnson; Fund for Henry Ford Hospital; Microbes, Allergy, Asthma and Pets (MAAP) [P01 AI089473]; Infant Susceptibility to Pulmonary Infections and Asthma following RSV Exposure (INSPIRE) [NIH/NIAID U19 AI 095227, NIH/NCATS UL1 TR 002243, NIH/NIAID K24 AI 077930, NIH/NHLBI R21 HD 087864, NIH/NHLBI X01 HL 134583]; Wisconsin Infant Study Cohort (WISC) [U19 AI104317, NCATS UL1TR000427]; Upper Midwest Agricultural Safety and Health Center (UMASH) [U54 OH010170]; RTI International, Research Triangle Park, North Carolina, USA; NIH [U24OD023382]; Urban Environment and Childhood Asthma Study (URECA) [NO1-AI-25482, HHSN272200900052C, HHSN272201000052I, NCRR/NIH RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, UL1TR001079, 5UL1RR024992-02, NCATS/NIH UL1TR000040]; Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) [R01 ES11170, R01 ES019890]; Epidemiology of Home Allergens and Asthma Study (EHAAS) [R01 AI035786]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

An Evaluation of the Use of a Clinical Research Data Warehouse and I2b2 Infrastructure to Facilitate Replication of Research

Replication of clinical research is requisite for forming effective clinical decisions and guidelines. While rerunning a clinical trial may be unethical and prohibitively expensive, the adoption of EHRs and the infrastructure for distributed research networks provide access to clinical data for observational and retrospective studies. Herein I demonstrate a means of using these tools to validate existing results and extend the findings to novel populations. I describe the process of evaluating published risk models as well as local data and infrastructure to assess the replicability of the study. I use an example of a risk model unable to be replicated as well as a study of in-hospital mortality risk I replicated using UNMC’s clinical research data warehouse. In these examples and other studies we have participated in, some elements are commonly missing or under-developed. One such missing element is a consistent and computable phenotype for pregnancy status based on data recorded in the EHR. I survey local clinical data and identify a number of variables correlated with pregnancy as well as demonstrate the data required to identify the temporal bounds of a pregnancy episode. Next, another common obstacle to replicating risk models is the necessity of linking to alternative data sources while maintaining data in a de-identified database. I demonstrate a pipeline for linking clinical data to socioeconomic variables and indices obtained from the American Community Survey (ACS). While these data are location-based, I provide a method for storing them in a HIPAA compliant fashion so as not to identify a patient’s location. While full and efficient replication of all clinical studies is still a future goal, the demonstration of replication as well as beginning the development of a computable phenotype for pregnancy and the incorporation of location based data in a de-identified data warehouse demonstrate how the EHR data and a research infrastructure may be used to facilitate this effort

Anthropogenic impacts on pathogen outcomes of our wild neighbors and closest companions

The rapid global conversion of natural habitat to built environments create corridors that facilitate cross-species transmission at the human–domestic animal–wildlife interface. Understanding pathogen outcomes of animals that live directly at this interface will provide insight into the transmission dynamics of pathogens that pose risk to companion animals, wildlife, and humans. This dissertation is comprised of two sections where I study pathogen outcomes in two groups of animals that live directly alongside humans: wildlife that live in anthropogenic structures (e.g., buildings, bridges, homes, and tunnels, etc.) and companion animals. In the first section, I create a novel database of anthropogenic roosting ecology in bats to identify ecological and evolutionary determinants of anthropogenic roosting ability. I then assess the importance of this ability in predicting viral outcomes using a machine learning approach. In the second section of this dissertation, I utilize veterinary diagnostic reports to evaluate the influence of climactic and land use factors on vector-borne pathogen exposure risk in canines.Ecology, Evolution and Behavio