Social ecological system framework as a decision-making tool for risk mitigation: A superfund site case study.

Several studies have reported vapor intrusion (VI) occurring when volatile organic compound (VOC) vapors are transported through subsurface piping systems into building spaces (e.g. conduit VI).

Bystander chemical exposures and injuries associated with nearby plastic sewer pipe manufacture: public health practice and lessons.

Cured-in-place pipes (CIPPs) are plastic liners manufactured inside existing damaged sanitary sewer, storm sewer, and water pipes that extend the service life of host pipes. This process often is conducted in neighborhoods and near roadways. Before, during, and after plastic manufacture, waste materials that include volatile materials are released into the air.

A proposed FAIR approach for disseminating geospatial information system maps.

We present a draft Minimum Information About Geospatial Information System (MIAGIS) standard for facilitating public deposition of geospatial information system (GIS) datasets that follows the FAIR (Findable, Accessible, Interoperable and Reusable) principles. The draft MIAGIS standard includes a deposition directory structure and a minimum javascript object notation (JSON) metadata formatted file that is designed to capture critical metadata describing GIS layers and maps as well as their sources of data and methods of generation. The associated miagis Python package facilitates the creation of this MIAGIS metadata file and directly supports metadata extraction from both Esri JSON and GEOJSON GIS data formats plus options for extraction from user-specified JSON formats.

Identifying and sharing per-and polyfluoroalkyl substances hot-spot areas and exposures in drinking water.

Exposure to per- and polyfluoroalkyl substances (PFAS) in drinking water is widely recognized as a public health concern. Decision-makers who are responsible for managing PFAS drinking water risks lack the tools to acquire the information they need. In response to this need, we provide a detailed description of a Kentucky dataset that allows decision-makers to visualize potential hot-spot areas and evaluate drinking water systems that may be susceptible to PFAS contamination.

A geospatial and binomial logistic regression model to prioritize sampling for per- and polyfluorinated alkyl substances in public water systems.

As health-based drinking water standards for per- and polyfluorinated alkyl substances (PFAS) continue to evolve, public health and environmental protection decision-makers must assess exposure risks associated with all public drinking water systems in the United States (US). Unfortunately, current knowledge regarding the presence of PFAS in environmental systems is limited. In this study, a screening approach was established to: (1) identify and direct attention toward potential PFAS hot spots in drinking water sources, (2) prioritize sampling locations, and (3) provide insights regarding the potential PFAS sources that contaminate groundwater and surface water.

PCB 126 induces monocyte/macrophage polarization and inflammation through AhR and NF-κB pathways.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that contribute to inflammatory diseases such as atherosclerosis, and macrophages play a key role in the overall inflammatory response. Depending on specific environmental stimuli, macrophages can be polarized either to pro-inflammatory (e.g.

The role of nutrition in influencing mechanisms involved in environmentally mediated diseases.

Human exposure to environmental contaminants such as persistent chlorinated organics, heavy metals, pesticides, phthalates, flame retardants, electronic waste and airborne pollutants around the world, and especially in Southeast Asian regions, are significant and require urgent attention. Given this widespread contamination and abundance of such toxins as persistent organic pollutants (POPs) in the ecosystem, it is unlikely that remediation alone will be sufficient to address the health impacts associated with this exposure. Furthermore, we must assume that the impact on health of some of these contaminants results in populations with extraordinary vulnerabilities to disease risks.

Editor's Highlight: PCB126 Exposure Increases Risk for Peripheral Vascular Diseases in a Liver Injury Mouse Model.

The liver is vital for xenobiotic and endobiotic metabolism. Previously, we demonstrated that a compromised liver worsened toxicity associated with exposure to polychlorinated biphenyls (PCBs), through disruption of energy homeostasis. However, the role of a compromised liver in defining dioxin-like PCB126 toxicity on the peripheral vasculature and associated inflammatory diseases is yet to be studied.

Polychlorinated biphenyls disrupt hepatic epidermal growth factor receptor signaling.

1. Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that disrupt hepatic xenobiotic and intermediary metabolism, leading to metabolic syndrome and nonalcoholic steatohepatitis (NASH). 2.

Exercise protects against PCB-induced inflammation and associated cardiovascular risk factors.

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that contribute to the initiation of cardiovascular disease. Exercise has been shown to reduce the risk of cardiovascular disease; however, whether exercise can modulate PCB-induced vascular endothelial dysfunction and associated cardiovascular risk factors is unknown. We examined the effects of exercise on coplanar PCB-induced cardiovascular risk factors including oxidative stress, inflammation, impaired glucose tolerance, hypercholesteremia, and endothelium-dependent relaxation.

PCB 126 toxicity is modulated by cross-talk between caveolae and Nrf2 signaling.

Environmental toxicants such as polychlorinated biphenyls (PCBs) have been implicated in the promotion of multiple inflammatory disorders including cardiovascular disease, but information regarding mechanisms of toxicity and cross-talk between relevant cell signaling pathways is lacking. To examine the hypothesis that cross-talk between membrane domains called caveolae and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathways alters PCB-induced inflammation, caveolin-1 was silenced in vascular endothelial cells, resulting in a decreased PCB-induced inflammatory response. Cav-1 silencing (siRNA treatment) also increased levels of Nrf2-ARE transcriptional binding, resulting in higher mRNA levels of the antioxidant genes glutathione s-transferase and NADPH dehydrogenase quinone-1 in both vehicle and PCB-treated systems.