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Related Experiment Videos

Human mutagens: evidence from paternal exposure?

S A Narod1, G R Douglas, E R Nestmann

  • 1Department of Community Medicine and Epidemiology, University of Ottawa, Ontario, Canada.

Environmental and Molecular Mutagenesis
|January 1, 1988
PubMed
Summary

Environmental contaminants may induce inherited mutations, increasing disease risk in offspring. Limited human data and animal models suggest a link, necessitating expanded surveillance for genetic effects.

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Area of Science:

  • Genetics
  • Environmental Health
  • Epidemiology

Background:

  • Inherited mutations cause human diseases like Down syndrome.
  • Environmental contaminants are suspected to induce mutations, increasing genetic defect risks in exposed populations.
  • Lack of direct evidence for induced inherited genetic disorders in humans hinders risk assessment.

Purpose of the Study:

  • To review evidence for induced inherited genetic effects in humans.
  • To explore methods for developing risk estimation techniques by comparing human and animal data.
  • To identify endpoints and improve surveillance for documenting associations between induced mutations and genetic disease.

Main Methods:

  • Reviewed prospective epidemiologic studies (atomic bomb survivors, chemotherapy patients).

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  • Analyzed retrospective (case-control) studies focusing on paternal exposure to minimize confounding.
  • Considered endpoints like congenital malformations and spontaneous abortion.

    • Main Results:

    • No significant elevation in inherited genetic effects detected in offspring of atomic bomb survivors or chemotherapy patients.
    • Retrospective studies with paternal exposure focus show limited, suggestive evidence for induced inherited effects.
    • Limited evidence suggests anesthetic gas exposure may induce male germ cell mutations, leading to miscarriage and congenital abnormalities.

    Conclusions:

    • Paternal exposure studies offer better resolution for detecting inherited effects.
    • Comparing human male-exposure endpoints with animal models (e.g., dominant lethal, inherited cancer) can aid risk extrapolation.
    • Expanding surveillance systems and improving data access are crucial for establishing relationships between induced mutations and genetic disease.