What follows is the continuation, in serial form, of a central chapter from my book A Primer in the Art of Deception: The Cult of Nuclearists, Uranium Weapons and Fraudulent Science.
Exhibit D continued
The varying sensitivity of the cell to radiation throughout its life cycle is a central feature of Dr. Chris Busby’s Second Event Theory. According to this theory, particular radionuclides that undergo sequential radioactive decay and “hot particles” (particles made up of a number of radioactive atoms) represent a unique hazard when immobilized in the body as compared to random hits delivered by natural background radiation. Central to Second Event Theory is the concept of time between hits to a cell, a factor not taken into account by current assessments of risk from radiation. According to Busby’s theory, certain types of sublethal radiation damage created by a single track through a cell can stimulate the cell to undergo a repair and replication sequence. This lasts for a period of between eight and fifteen hours. If the cell is hit again — the second event — while it is at the point of heightened sensitivity in the repair cycle, irreparable sublethal damage may occur in the form of a mutation that will be passed on to daughter cells. Given that natural background radiation is responsible for but one hit per year per cell, on average, only a remotely small probability exists that this source will produce two hits to the same cell within the timeframe of heightened vulnerability to irreversible genetic damage during cell replication. However, the same cannot be said for some types of internal emitters. For instance, strontium-90 has a half-life of twenty-eight years. When it undergoes radioactive decay inside the body, it will hit nearby cell(s) with its emitted beta particle. Having decayed, the atom will have been transformed into yttrium-90. Yttrium-90 has a short half-life of sixty-four hours. The possibility thus exists that this yttrium atom will undergo radioactive decay within the period of maximum susceptibility of the nearby previously hit cell and strike it a second time with its emitted beta particle. In this way, an internalized sequential emitter can be responsible for two hits to the same cell during the window of opportunity of non-reparable genetic damage. A number of other sequential emitters can be similarly hazardous. For instance, tellurium-132 has a half-life of seventy-eight hours. By beta decay, it transforms into iodine-132 that has a half-life of 2.28 hours. Similarly, barium-140 possesses a half-life of 12.8 days and decays into lanthanum-140 with a half-life of forty hours. It is crucial to emphasize that sequential emitters are not the sole source of second-event processes. A “hot” particle can produce the same effect. A particle of plutonium entering into the lung can be made up of billions of atoms. Once lodged in place, it will continue, on an ongoing basis, to shower nearby cells with alpha particles. Two hits to the same cell within the proper time period can be responsible for inducing mutations in hit cells that will be passed on to daughter cells. This is a plausible pathway for the initiation of a cancer. Not to be forgotten in the latter portion of this book is this important fact: A particle of depleted uranium has the capacity of inducing multiple hits to the same cell during that cell’s period of maximum vulnerability. Depleted uranium is quite capable of causing genetic damage and inducing mutations within cells in its immediate vicinity. Once again the propagandists are shown up as liars. Depleted uranium internalized into the human body does pose a radiological hazard.