Distinguishing potential sources of genotoxic exposure via HPRT mutations

Radiats Biol Radioecol. 2000 Sep-Oct;40(5):529-34.

Abstract

We utilize T-cell HPRT mutations to monitor exposure to environmental mutagens in siblings of children who have developed cancer at a persistently high rate in Toms River, New Jersey, U.S.A. A preliminary epidemiological study has found a statistically-significant association between drinking public water (by pregnant mother or infant) and subsequent risk for childhood cancer. Three potential sources of mutagenic exposures in Toms River may have increased the rate of carcinogenic initiation significantly in children: 1. Benzidine-based, other azo dye and anthraquinone dye wastes released by Ciba-Geigy, 2. Styrene-acrylonitrile (SAN) trimer and other plastic wastes of Union Carbide, and 3. Radium-224, present in unusually high concentrations in the Cohansey aquifer. Specific patterns of HPRT mutations are utilized to distinguish these various potential sources of carcinogenic exposures in the drinking water of families with childhood cancer and to differentiate chemically or radiologically induced cancers from those which occur spontaneously.

MeSH terms

  • Child
  • Environmental Monitoring
  • Epidemiological Monitoring
  • Female
  • Genetic Markers
  • Humans
  • Hypoxanthine Phosphoribosyltransferase / genetics*
  • Neoplasms / chemically induced*
  • Neoplasms / epidemiology
  • Neoplasms / genetics
  • Neoplasms, Radiation-Induced / genetics
  • New Jersey / epidemiology
  • Pregnancy
  • Radium / toxicity
  • Water Pollutants, Chemical / toxicity*
  • Water Pollutants, Radioactive / toxicity
  • Water Supply / standards*

Substances

  • Genetic Markers
  • Water Pollutants, Chemical
  • Water Pollutants, Radioactive
  • Hypoxanthine Phosphoribosyltransferase
  • Radium