Biomarkers of genotoxicity of urban air pollution. Overview and descriptive data from a molecular epidemiology study on populations exposed to moderate-to-low levels of polycyclic aromatic hydrocarbons: the AULIS project

Mutat Res. 2001 Sep 20;496(1-2):207-28. doi: 10.1016/s1383-5718(01)00222-4.

Abstract

Epidemiologic studies indicate that prolonged exposure to high pollution levels is associated with increased risk of cancer, especially lung cancer. However, under conditions of moderate or low air pollution, epidemiologic evidence does not permit reliable conclusions. Biomarker-based population studies may serve as complementary tools providing a better understanding of the relative contribution of ambient atmospheric pollution to the overall genotoxic burden suffered by city dwellers. However, past efforts to apply biomarkers to studies of low levels exposure to urban air pollution have given inconclusive results, partly because of the absence of adequate data on personal exposure, covering a time-window which is appropriate for the biomarkers being examined, as well as a battery of biomarkers reflecting different stages of the carcinogenic process. In the present paper, the potential of biomarker-based population studies to aid the assessment of the genotoxic and carcinogenic effects of urban air pollution is reviewed by reference to the achievements and limitations of earlier reported studies. The design and methodology adopted in a recently completed large-scale population study, carried out in the context of the European Union Environment and Climate Programme, known by the short name of AULIS project, is discussed and descriptive statistics of the main findings of the project are presented. These findings indicate that for cohorts suffering moderate-to-low exposures to airborne particulate-bound polycyclic aromatic hydrocarbons (PAHs), no simple correlation with biomarkers of genotoxicity existed and suggest that additional factors made a significant contribution to the overall genotoxic burden.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Air Pollutants / adverse effects*
  • Air Pollutants / blood
  • Air Pollutants / urine
  • Air Pollution / adverse effects*
  • Air Pollution / analysis
  • Biomarkers / analysis
  • DNA / analysis
  • DNA / drug effects
  • DNA Adducts / analysis
  • Environmental Illness / chemically induced
  • Environmental Illness / epidemiology
  • Female
  • Greece
  • Humans
  • Hypoxanthine Phosphoribosyltransferase / genetics
  • Hypoxanthine Phosphoribosyltransferase / metabolism
  • Inhalation Exposure / adverse effects*
  • Inhalation Exposure / analysis
  • Lung Neoplasms / chemically induced
  • Lung Neoplasms / epidemiology
  • Lymphocytes / drug effects
  • Male
  • Molecular Epidemiology
  • Mutagens / adverse effects*
  • Mutagens / analysis
  • Mutation
  • Phosphorus Radioisotopes / metabolism
  • Polycyclic Aromatic Hydrocarbons / adverse effects*
  • Polycyclic Aromatic Hydrocarbons / blood
  • Polycyclic Aromatic Hydrocarbons / urine
  • Polymorphism, Genetic
  • Sister Chromatid Exchange
  • Urban Health
  • Urban Population

Substances

  • Air Pollutants
  • Biomarkers
  • DNA Adducts
  • Mutagens
  • Phosphorus Radioisotopes
  • Polycyclic Aromatic Hydrocarbons
  • DNA
  • Hypoxanthine Phosphoribosyltransferase