New historical perspectives as to how/why EPA adopted the Linear-Non-Threshold (LNT) Model

This article [see attached] is the latest historical analysis — in a long series by Ed Calabrese — on details surrounding acceptance of the Linear Non-Threshold (LNT) Model in 1975 by the U.S. Environmental Protection Agency (EPA). In 1956, the US National Academy of Sciences (NAS) Biological Effects of Atomic Radiation (BEAR) I Genetics Panel recommended that risk assessment for ionizing radiation (for germ-cell mutation) be switched from a threshold model to a linear dose response model. This was a precipitous moment in risk assessment history that was long anticipated and highly publicized (e.g. it became a prominent paper in the journal Science, front page stories in the New York Times and Washington Post, and other major outlets, with the report sent to all public libraries in the United States). The NAS BEAR I Genetics Panel was considered the “1950s equivalent of a genetics Dream Team,” having great influence and standing — within the scientific, legislative, regulatory, news media, and general public communities.

Their report was followed by Congressional Hearings in 1957 and it influenced advisory groups — such as the National Council on Radiation Protection and Measurements (NCRPM) to adopt a linear dose response for cancer risk assessment in December 1958. This NCRPM position was based on the assumption that radiation-induced genetic damage is “completely cumulative and that the effect is independent of the rate at which the radiation is delivered” (this statement embraced the geneticists’ mantra of the 1950s and the position of the 1956 NAS BEAR Genetics Panel Report). However, in contrast to the scientific beliefs of the 1956 BEAR Genetics Panel, the 1960 NCRPM statement did not accept these assumptions and conclusions as established facts; the NCRPM specifically stated that they “were adopted as prudent public health policy” — reflecting, in effect, a Precautionary Principle.

The timing of the 1958 NCRPM policy meeting (Dec. 29/30, 1958) was remarkable — appearing about 2 weeks after the seminal publication of Russell et al. in the journal Science on December 19, 1958 — demonstrating that radiation-induced mutation frequency was explained by

dose rate, NOT total dose, and that such mutations could be readily repaired. There has been no record yet obtained that clarifies why the

decision to adopt a linear dose response policy by the NCRPM was not affected by the Russell et al. findings, because James F Crow and Edwin B Lewis (both prominent figures in the radiation geneticist community) were members of the NCRPM Committee. In other words, why didn’t NCRPM delay their decision — pending a review of the Russell findings?

Of particular relevance to the LNT issue is that the 1956 BEAR Medical/Pathology Panel, which met concurrently with the BEAR Genetics Panel, offered a different perspective/evaluation of ionizing radiation-induced mutation, and its relationship to cancer — as did the Genetics Panel. The Medical/Pathology Panel downplayed and even questioned the role of somatic mutation in cancer. These developments had the potential to suggest that a threshold model may be biologically more plausible than the LNT. Thus, while the statements of the 1960 BEAR Panels seemed to provide a type of quiet cover (or support) to the NCRPM policy statement, this veiled support in the form of uncertainty was no longer sufficient (i.e. not convincing enough). It is suggested here that the new Congressionally mandated environmental agency, the EPA, created in 1970, needed something better than regulation by uncertainty. The 1972 BEIR Report provided EPA a basis (i.e. male mouse mutagenicity data) to support a linearity approach — with the Russell data providing the Gold Standard and could be promoted in public as being based on studies using nearly two million mice.

The 1972 BEIR Report had the prerequisite caveats of some uncertainty — and erring to some extent on the side of protection. However, the critical point was that now there was sufficient information for a science-supported EPA linearity risk assessment policy that would soon have the apparent exacting precision of biostatistical model estimates of cancer risks in the low-dose zone via the LNT approach. This historical evaluation thus suggests that the EPA did not want to have its hands tied, or its scientific image affected, by statements from the 1960 BEAR Genetics and Medicine Panels that “there was too much uncertainty to estimate cancer risk in the low-dose zone.” Their comments were simply ignored and swept under the regulatory rug. ☹


Chem-Biol Interactions May 2o19; 308: 110–112

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