Developing intensive, short-term courses for public health-Creation and outcome evaluation of the Skills for Health and Research Professionals (SHARP) program at the Columbia University Mailman School of Public Health.

Short, intensive education programs provide an under-utilized avenue for public health professionals to learn and apply the latest methods and technologies. We report on the creation and implementation of the Skills for Health and Research Professionals (SHARP) program at the Columbia University Mailman School of Public Health. The self-sustaining, concise, intense educational format equips participants with concrete skills, better enabling them to respond to complex public health challenges.

In Utero Exposure to Caffeine and Acetaminophen, the Gut Microbiome, and Neurodevelopmental Outcomes: A Prospective Birth Cohort Study.

Pregnant individuals are exposed to acetaminophen and caffeine, but it is unknown how these exposures interact with the developing gut microbiome. We aimed to determine whether acetaminophen and/or caffeine relate to the childhood gut microbiome and whether features of the gut microbiome alter the relationship between acetaminophen/caffeine and neurodevelopment. Forty-nine and 85 participants provided meconium and stool samples at 6-7, respectively, for exposure and microbiome assessment.

Methylome-wide association study provides evidence of particulate matter air pollution-associated DNA methylation.

Background: DNA methylation (DNAm) may contribute to processes that underlie associations between air pollution and poor health. Therefore, our objective was to evaluate associations between DNAm and ambient concentrations of particulate matter (PM) ≤2.5, ≤10, and 2.

Prenatal manganese and cord blood mitochondrial DNA copy number: Effect modification by maternal anemic status.

Introduction: Manganese (Mn) is an essential nutrient but also a toxicant at high exposures, when it can induce oxidative stress (OS). Mn uptake is inversely correlated with iron status, therefore anemic individuals may be more susceptible to Mn overload induced-OS, which can manifest as changes in mitochondrial DNA copy number (mtDNA CN). Our objectives were to: 1) determine stage-specific associations of prenatal Mn exposure with cord blood MtDNA CN; and 2) investigate effect modification by maternal anemia, ferritin, and mean corpuscular volume (MCV).

Associations of prenatal exposure to polybrominated diphenyl ethers and polychlorinated biphenyls with long-term gut microbiome structure: a pilot study.

Background: The gut microbiome is influenced by early-life exposures, but-despite potentially enormous implications for child health-is understudied in environmental epidemiology. This pilot study is one of the first to explore exposures and long-term gut microbiome profiles. We examined the association between exposure to polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) during pregnancy and the mid-childhood gut microbiome.

Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort.

Introduction: Lead (Pb) crosses the placenta and can cause oxidative stress, reduced fetal growth and neurological problems. The principal source of oxidative stress in human cells is mitochondria. Therefore, disruption of normal mitochondrial function during pregnancy may represent a primary mechanism behind the adverse effects of lead.

Prenatal Metal Concentrations and Childhood Cardiometabolic Risk Using Bayesian Kernel Machine Regression to Assess Mixture and Interaction Effects.

Background: Trace metal concentrations may affect cardiometabolic risk, but the role of prenatal exposure is unclear. We examined (1) the relation between blood metal concentrations during pregnancy and child cardiometabolic risk factors; (2) overall effects of metals mixture (essential vs. nonessential); and (3) interactions between metals.

Association Between Meconium Acetaminophen and Childhood Neurocognitive Development in GESTE, a Canadian Cohort Study.

Acetaminophen is the only over-the-counter pain reliever that is not contraindicated during pregnancy, but recent studies have questioned whether acetaminophen is safe for the fetus, particularly the developing brain. This prospective birth cohort study probed the previously observed association between in utero exposure to acetaminophen and neurodevelopment by using concentrations of acetaminophen measured in meconium, which more objectively captures exposure of the fetus than maternal report. Exposure, measured by liquid chromatography coupled with tandem mass spectrometry, was categorized into nondetection, low detection, and high detection levels.

Prenatal Stress, Methylation in Inflammation-Related Genes, and Adiposity Measures in Early Childhood: the Programming Research in Obesity, Growth Environment and Social Stress Cohort Study.

Objective: Maternal stress during pregnancy may influence childhood growth and adiposity, possibly through immune/inflammatory programming. We investigated whether exposure to prenatal stress and methylation in inflammation-related genes were associated with childhood adiposity in 424 mother-child pairs in Mexico City, Mexico.

Methods: A stress index was created based on four prenatally administered stress-related scales (Exposure to Violence, Crisis in Family Systems, State-Trait Anxiety Inventory, and Edinburgh Postnatal Depression Scale).

Long-term exposure to black carbon, cognition and single nucleotide polymorphisms in microRNA processing genes in older men.

Introduction: Air pollution exposure has been linked to impaired cognitive aging, but little is known about biomarkers modifying this association. MicroRNAs (miRNAs) control gene expression and neuronal programming. miRNA levels vary due to single nucleotide polymorphisms (SNPs) in genes processing miRNAs from precursor molecules.

Traffic-Related Air Pollution, Blood Pressure, and Adaptive Response of Mitochondrial Abundance.

Background: Exposure to black carbon (BC), a tracer of vehicular-traffic pollution, is associated with increased blood pressure (BP). Identifying biological factors that attenuate BC effects on BP can inform prevention. We evaluated the role of mitochondrial abundance, an adaptive mechanism compensating for cellular-redox imbalance, in the BC-BP relationship.