Relation between sources of particulate air pollution and biological effect parameters in samples from four European cities: an exploratory study

Inhal Toxicol. 2006 May;18(5):333-46. doi: 10.1080/08958370500515913.

Abstract

Given that there are widely different prevalence rates of respiratory allergies and asthma between the countries of Europe and that exposure to ambient particulate matter (PM) is substantial in urban environments throughout Europe, an EU project entitled "Respiratory Allergy and Inflammation Due to Ambient Particles" (RAIAP) was set up. The project focused on the role of physical and chemical composition of PM on release of cytokines of cells in vitro, on respiratory inflammation in vivo, and on adjuvant potency in allergy animal models. Coarse (2.5-10 microm) and fine (0.15-2.5 microm) particles were collected during the spring, summer and winter in Rome (I), Oslo (N), Lodz (PL), and Amsterdam (NL). Markers within the same model were often well correlated. Markers of inflammation in the in vitro and in vivo models also showed a high degree of correlation. In contrast, correlation between parameters in the different allergy models and between allergy and inflammation markers was generally poor. This suggests that various bioassays are needed to assess the potential hazard of PM. The present study also showed that by clustering chemical constituents of PM based on the overall response pattern in the bioassays, five distinct groups could be identified. The clusters of traffic, industrial combustion and/or incinerators (TICI), and combustion of black and brown coal/wood smoke (BBCW) were associated primarily with adjuvant activity for respiratory allergy, whereas clusters of crustal of material (CM) and sea spray (SS) are predominantly associated with measures for inflammation and acute toxicity. The cluster of secondary inorganic aerosol and long-range transport aerosol (SIALT) was exclusive associated with systemic allergy. The present study has shown that biological effect of PM can be linked to one or more PM emission sources and that this linkage requires a wide range of bioassays.

MeSH terms

  • Air Pollutants / analysis
  • Air Pollutants / toxicity*
  • Air Pollution*
  • Animals
  • Cell Line
  • Cluster Analysis
  • Humans
  • Immunoglobulin E / blood
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Particle Size
  • Rats
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Uteroglobin / biosynthesis

Substances

  • Air Pollutants
  • SCGB1A1 protein, human
  • Scgb1a1 protein, mouse
  • Tumor Necrosis Factor-alpha
  • Immunoglobulin E
  • Uteroglobin