44,99 €
inkl. MwSt.
Versandkostenfrei*
Versandfertig in 6-10 Tagen
  • Broschiertes Buch

In this research work concentrations of airborne size specific ( 1, 1-1.8, 1.8 µm) microbial contaminants (endotoxin, -glucan) were determined using cyclone samplers in two distinctly different environments: farms and homes. Using inhalable samplers and vacuum cleaners airborne inhalable and dust contaminants from these homes were collected. This approach was used to compare PM1 microbial contaminants in a particular home with those in inhalable particles and in dust inside the same home. Samples were analyzed with Limulus Amebocyte Lysate assays for endotoxin and -glucan. Airway inflammation…mehr

Produktbeschreibung
In this research work concentrations of airborne size specific ( 1, 1-1.8, 1.8 µm) microbial contaminants (endotoxin, -glucan) were determined using cyclone samplers in two distinctly different environments: farms and homes. Using inhalable samplers and vacuum cleaners airborne inhalable and dust contaminants from these homes were collected. This approach was used to compare PM1 microbial contaminants in a particular home with those in inhalable particles and in dust inside the same home. Samples were analyzed with Limulus Amebocyte Lysate assays for endotoxin and -glucan. Airway inflammation was assessed in school-age children by measuring exhaled nitric oxide (eNO) levels with non-invasive nitric oxide monitoring system (NIOX-Flex). Results indicate that PM1 endotoxin concentration may be a better predictor of airway inflammation than inhalable or larger particles Exposures to high PM1 endotoxin may protect against airway inflammation in non-asthmatic school-age children. Whether this protection is sustained, needs to be confirmed through follow-up studies.
Autorenporträt
A medical graduate (University of Calcutta, India) and Ph.D. (Environmental Health, University of Cincinnati), currently interested in clinical research on Transient Receptor Potential (TRP) ion channels in neuronal cells for recognition of mechanistic pathways mediating health effects resulting from environmental exposures acting as irritants.