UMass Researcher: Cancer-risk Assessment Is Based on Flawed Science

AMHERST — In a new paper, UMass Amherst environmental toxicologist Edward Calabrese continues his campaign to cast doubt on the legitimacy of the linear no threshold (LNT) single-hit model for risk assessment for exposure to ionizing radiation and, by extension, other chemicals and compounds.

He asserts that the scientific foundations used in support of the LNT single-hit model contains “fundamental scientific flaws that undermine not only the seminal recommendation of the 1956 Biological Effects of Atomic Radiation (BEAR) I Genetics Panel to adopt the LNT single-hit model for risk assessment but also any rationale for its continued use in the present day.” His new exploration of the issue appears in the journal Environmental Research.

As in his earlier assessments of the historical origins of the LNT single-hit model, Calabrese lays much of the blame for its now-near-global acceptance at the feet of one of the fathers of radiation genetics, Hermann Muller, who was awarded the Nobel Prize in medicine in 1946 for his apparent discovery that X-rays induce gene mutations in fruit flies. Calabrese challenges the claim that Muller had induced gene mutation and offers a detailed documentation of objections initially raised at the time by USDA plant geneticist Lewis Stadler.

Calabrese says Muller and others, notably those on the U.S. National Academy of Sciences 1956 genetics panel, who favored the LNT single-hit model, were successful in “obfuscating, deceiving, and misrepresenting the scientific record” and that these “ideologically-based” actions “infected and affected the highest levels of regulatory policy in the U.S. government where they still remain in place today.”

Calabrese writes that Stadler, a “well-known and respected geneticist at the time, strongly disagreed with and challenged Muller’s claims. Detailed evaluations by Stadler over a prolonged series of investigations revealed that Muller’s experiments had induced gross heritable chromosomal damage instead of specific gene mutations, as had been claimed by Muller at his Nobel lecture. These X-ray-induced alterations became progressively more frequent and were of larger magnitude, more destructive, with increasing doses. Thus, Muller’s claim of having induced discrete gene mutations represented a substantial speculative overreach and was, in fact, without proof.”

Further, he adds, “the post hoc arguments of Muller to support his gene-mutation hypothesis were significantly challenged and weakened by a series of new findings in the areas of cytogenetics, reverse mutation, adaptive and repair processes, and modern molecular methods for estimating induced genetic damage. These findings represented critical and substantial limitations to Muller’s hypothesis of X-ray-induced gene mutations.”

Calabrese argues that Muller had a larger-than-life influence with Curt Stern of the University of Rochester and others who performed key experiments and served on the National Academy of Sciences’ BEAR committee, and that they deliberately manipulated the scientific record to ensure that the LNT single-hit model was adopted by the regulatory community in the 1950s.

“The scientific community and regulatory agencies such as the EPA uncritically accepted what was handed to them by a band of prestigious geneticists who were ideologically motivated,” Calabrese claims. “They had great authority and used this authority to greatly exaggerate risks, and were thus able to manipulate the regulatory process. This U.S. National Academy of Sciences, Biological Effects of Atomic Radiation (BEAR) Committee, as led by Hermann Muller, created the ‘fake’ science world of cancer-risk assessment, which needs to be corrected to better serve society.”