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Human Health Risks from Low-Level Environmental Exposures: No Apparent Safety Thresholds

PLoS Medicine
Public Library of Science
Publication Date
DOI: 10.1371/journal.pmed.0020350
  • Policy Forum
  • Other
  • Epidemiology/Public Health
  • Health Policy
  • Pediatrics
  • Toxicology/Environmental Health
  • Public Health
  • Environmental Health
  • Biology
  • Chemistry
  • Ecology
  • Geography
  • Medicine
  • Pharmacology


PLME0212_1232-1234.indd PLoS Medicine | 1232 Policy Forum Open access, freely available online December 2005 | Volume 2 | Issue 12 | e350 Recent developments in environmental epidemiology offer the promise of strengthening human health protection. Regulatory agencies responsible for protecting human health from environmental hazards assess data on relationships between exposure levels and adverse health effects to develop limits for contaminant levels in air, water, food, soil, house dust, and consumer products. Most regulatory agencies assume that there is no safe level of exposure to carcinogens and use linear dose-response models to estimate human health risks at low exposure levels. In contrast, regulators usually assume that a threshold, or “safe,” exposure level exists for noncarcinogens. Risk Assessment In conducting risk assessments to characterize potential adverse health effects of human exposures to environmental hazards [1], regulators depend on experimental animal studies in the absence of adequate epidemiologic data. These studies are critical to uncover health effects before human exposure occurs (e.g., premarket testing of a new chemical) whereas epidemiologic studies can be used to directly evaluate health effects among exposed persons. The diffi culty of directly measuring health risks at very low exposure levels can be an important limitation of both epidemiologic and toxicologic studies. Sources of uncertainty in conventional animal studies include: (1) the much shorter exposure period compared to humans, (2) testing is often limited to adult (but not pregnant, newborn, or sexually immature) animals, (3) use of genetically homogeneous animals (with loss of the ability to detect potentially heightened risks among genetically diverse subgroups, such as exist in human populations), (4) the use of very high doses of test chemicals (e.g., administration of high doses of a teratogeni

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