Adopted January 1996; Revised July 2010, May 2016, February 2019
The Health Physics Society1 advises against estimating health risks to people from exposures to ionizing radiation that are near or less than natural background levels because statistical uncertainties at these low levels are great.
The average annual effective dose2 from natural background radiation in the United States is about 3 mSv.3 A person might accumulate an effective dose from natural background radiation of about 50 mSv in the first 17 y of life and about 250 mSv during an average 80-y lifetime (NCRP 2009).
Substantial and convincing scientific data show evidence of health effects following high-dose exposures (many multiples of natural background). However, below levels of about 100 mSv above background from all sources combined, the observed radiation effects in people are not statistically different from zero.4
Scientists evaluate and estimate radiation risk using several assumptions that, taken together, may lead to a range of hypothetical health risk estimates for any given exposure scenario.
For radiation protection purposes and for setting radiation exposure limits, current standards and practices are based on the questionable premise that any radiation dose, no matter how small, could result in detrimental health effects such as cancer or heritable genetic damage. Implicit in this linear no-threshold (LNT) hypothesis is the core assumption that detrimental effects occur proportionately with radiation dose received (NA/NRC 2006). However, because of statistical uncertainties in biological response at or near background levels, the LNT hypothesis cannot provide reliable projections of future cancer incidence from low-level radiation exposures (NCRP 2001).
Molecular-level radiation effects are nonlinear
Studies show that dose-response relationships are typically nonlinear (Tubiana and Aurengo 2006; Tubiana et al. 2006). Substantial scientific data indicate that the LNT model of radiation effects oversimplifies the relationship between dose and response. Linearity at low dose may be rejected for a number of specific cancers, such as bone cancer, lymphoma, and chronic lymphocytic leukemia. Heritable genetic damage has not been observed in human studies.
Recent low-dose research indicates that biological response mechanisms such as DNA repair, bystander effects, and adaptive response modulate radiation-induced changes at the molecular level. Cellular transformation leading to carcinogenesis by mutation of genetic material appears to be a complicated, multistep process that is not reflected in the LNT model.
Radiogenic health effects have not been consistently demonstrated below 100 mSv
Due to large statistical uncertainties, epidemiological studies have not provided consistent estimates of radiation risk for effective doses less than 100 mSv. Underlying dose-response relationships at molecular levels appear mainly nonlinear. The low incidence of biological effects from exposure to radiation compared to the natural background incidence of the same effects limits the applicability of radiation risk coefficients at effective doses less than 100 mSv (NCRP 2012).
The references to 100 mSv in this position statement should not be construed as implying that health effects are well established for doses exceeding 100 mSv. Considerable uncertainties remain for stochastic effects of radiation exposure between 100 mSv and 1,000 mSv, depending upon the population exposed, the rate of exposure, the organs and tissues affected, and other variables. In addition, it is worth noting that epidemiological studies generally do not take into account the dose that occupationally or medically exposed persons incur as natural background; thus, the references to 100 mSv in this position statement should generally be interpreted as 100 mSv above natural background dose.
Risk estimates commonly used to predict health effects in exposed individuals or populations are based primarily on epidemiological studies of Japanese atomic bomb survivors and other populations exposed to relatively high doses delivered at high dose rates. Animal, cellular, and molecular studies demonstrate that at any level of biological organization, the responses following low-dose-rate exposure are less than observed after the same dose delivered at a high dose rate (Dauer et al. 2010). Epidemiological studies have not consistently demonstrated adverse health effects in persons exposed to small (less than 100 mSv) doses protracted over a period of many years.
Collective dose and radiation protection planning
A common approach in many circles, not recommended here, involves extrapolating the calculated risk derived at high doses to low-dose levels. Extrapolation may be convenient for setting radiation protection guidelines. However, when used prospectively to predict future risk to an exposed population, the multiplication of small risk coefficients by large population numbers leads inevitably to unsupportable claims of cancer risk from ionizing radiation (NCRP 1997, 2012).
Significant dosimetry uncertainties for individual subjects characterize most epidemiological studies. Actual doses and individual responses to radiation may be highly variable. It follows, therefore, that the collective population dose (the sum of individual effective doses expressed in units of person-Sievert) is a highly uncertain number. Since the risk coefficient at low effective dose is uncertain, and the individual contributors to population effective dose are also uncertain, the resultant uncertainty is greater than each of the individual contributions—and should not be used with confidence to predict cancer incidence in an exposed population.
Effective dose is not defined for short-term deterministic effects
The concept of effective dose applies only to reference persons for radiation protection purposes and not to biological risk for individual subjects. Since the radiation-weighting factors used to derive effective dose were developed only for stochastic effects, the effective dose is not applicable to deterministic biological effects. Therefore, effective dose should not be used for evaluating organ or tissue toxicity from radiation.
Dauer LT, Brooks AL, Hoel DG, Morgan WF, Stram D, Tran P. Review and evaluation of updated research on the health effects associated with low-dose ionising radiation. Radiat Protect Dosim 140:103–136; 2010.
International Commission on Radiological Protection. The 2007 recommendations of the International Commission on Radiological Protection. Amsterdam: Elsevier; ICRP Publication 103; 2007.
National Academies/National Research Council. BEIR VII Phase 2: health risks from exposure to low levels of ionizing radiation. Washington, DC: National Academies Press; 2006.
National Council on Radiation Protection and Measurements. Limitation of exposure to ionizing radiation. Bethesda, MD: NCRP; NCRP Report 116; 1993.
National Council on Radiation Protection and Measurements. Uncertainties in fatal cancer risk estimates used in radiation protection. Bethesda, MD: NCRP; NCRP Report 126; 1997.
National Council on Radiation Protection and Measurements. Evaluation of the linear-nonthreshold dose response model for ionizing radiation. Bethesda, MD: NCRP; NCRP Report 136; 2001.
National Council on Radiation Protection and Measurements. Ionizing radiation exposure of the population of the United States. Bethesda, MD: NCRP; NCRP Report 160; 2009.
National Council on Radiation Protection and Measurements. Uncertainties in the estimation of radiation risks and probability of disease causation. Bethesda, MD: NCRP; NCRP Report 171; 2012.
Tubiana M, Aurengo A. Dose-effect relationship and estimation of the carcinogenic effects of low doses of ionizing radiation: the joint report of the Académie des Sciences (Paris) and of the Académie Nationale de Médecine. Int J Low Radiat 2(3/4); 2006.
Tubiana M, Aurengo A, Averbeck D, Masse R. Recent reports on the effect of low doses of ionizing radiation and its dose-effect relationship. Rad Environ Biophys 44:245–251; 2006.