Summary of project PR000326

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR000326. The data can be accessed directly via it's Project DOI: 10.21228/M8C31Q This work is supported by NIH grant, U2C- DK119886.


Project ID: PR000326
Project DOI:doi: 10.21228/M8C31Q
Project Title:Controlled Human Exposure to Particulate matter (PM) and Gaseous Co-Pollutants
Project Type:Exposome Evaluation
Project Summary:During the past decade, several epidemiological studies have reported statistically significant positive correlations between daily concentrations of ambient air particles and acutely increased mortality and morbidity. It has been estimated that 50,000 - 60,000 excess deaths in the U.S. each year may be attributable to ambient particles. Several panel studies have reported associations between fine PM and decreased heart rate variability and increased vascular markers of inflammation. In addition, recent controlled human exposure studies have reported that fine particles can increase pulmonary inflammation, decrease heart rate variability, and increase vascular factors of inflammation and blood coagulation. However, these latter studies only assessed the effects of particulate matter. In the real world, people are simultaneously exposed to both gaseous pollutants (e.g. ozone, nitrogen dioxide) and particles. Recognition of this leads the National Research Council to list studies of PM and gaseous co-pollutants as one of the ten highest priorities in PM research. One of these co-pollutants that frequently occur together with PM is nitrogen oxides (NOx), which is produced during combustion processes. NOx consists of nitric oxide (NO) and nitrogen dioxide (NO2). NO dominates near roadsides and peaks in morning rush hours while NO2 levels show less temporal and spatial variability. NO and NO2 concentrations may reach values over 1 ppm and 0.5 ppm respectively during smog situations. NO2 is an oxidant capable of oxidizing and nitrating lipids and proteins and can cause cytotoxic effects on the cell membranes of epithelial cells as well as macrophages. Controlled exposure of healthy humans to 2 ppm NO2 reduced phagocytic capacity in macrophages. At similar concentrations controlled NO2 exposure produced small changes in large airway function and increased airway reactivity to methacholine. The inflammatory effects of NO2 may thus enhance the adverse effects of PM. In this study we hypothesize that NO2 and PM2.5 affect the cardiopulmonary system beyond what either pollutant is capable of inducing by itself. Cardiopulmonay impairment will be assessed by measuring changes in bronchoalveolar lavage (BAL) neutrophils and cytokines, heart rate variability, and plasma factors involved in inflammation and coagulation.
Laboratory:National Health and Environmental Effects Research Laboratory
Last Name:Devlin
First Name:Robert
Address:109 Alexander Drive, Research Triangle Park, NC 27709

Summary of all studies in project PR000326

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)
(* : Contains raw data)
ST000417 Controlled Human Exposure to Particulate Matter (PM) and Gaseous Co-Pollutants Homo sapiens RTI International MS 2018-06-05 1 81 Uploaded data (1.8G)*