Posts
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
In addition to genomic instability and the bystander effect, there are other biological phenomena not adequately represented in the ICRP model of the health effects of radiation. For instance, cells vary in their sensitivity to radiation at different times throughout their lifespan. In an experiment conducted in 1966 on Chinese hamster cells, a 600-fold variation was observed in cell radiation sensitivity throughout the entire cell cycle [1]. At any one time during the life of an organism, most cells inhabit a phase commonly referred to as Gap 0 (G0). In this phase, the cell is in a non-replication mode of stasis. It is living out its life while contributing to the normal living processes of the system of which it is a part. While in this phase, the cell is relatively insensitive to radiation damage. At some point, as a result of such factors as tissue growth, damage, or senescence, a signal is generated to initiate cell replication and the cell moves into Gap 1 (G1) phase. At this point in the cell cycle, preparations are initiated for the replication of the chromosomes. The cell increases in size, produces RNA, and synthesizes proteins. Also, an important cell-cycle control mechanism is activated. A process of proofreading of the integrity of the DNA gets underway where complementary strands are compared and damage is repaired. During G1, the cell is in an intermediate state of sensitivity. If the cell is damaged at this point by radiation, a period of delay is introduced into the process of cell replication while any newly incurred damage is repaired. In this controlled sequence of preprogrammed operations, the cell then moves on to Synthesis (S) phase where the chromosomes replicate. From there, Gap 2 (G2) phase follows. During this gap between DNA synthesis and cell division, the cell continues to grow and produce new proteins. Late in G2, a last checkpoint is reached in the cell cycle to verify that the cell is ready to enter mitosis and divide. Once this transition point (TP) is passed, the cell has reached a point of no return in the sequence of events and it will undergo mitosis. At this transition point, the cell is at its most sensitive point for radiation damage. If a sublethal hit is incurred at this time and damage is introduced into a chromosome, repair is not possible. The damage will be copied and replicated in the two daughter cells regardless of the amount of damage.
The ICRP model makes no allowance for the varied sensitivity of cells throughout their lifetime. Yet again ignoring radiation effects on the cellular level, the model is out of touch with basic biological realities. This gross inconsistency, however, does serve one important purpose. It bolsters the archaic and inappropriate concept of dose which averages energy over large volumes of undifferentiated, noncellular, masses. By this means, low-level radiation effects to individual cells is afforded no room for consideration within the current paradigm of radiation safety. The hazard posed by internal emitters is thus conveniently sidestepped. The enhanced sensitivity of cells to radiation damage at the time of replication suggests that the energy/particle flux from internal emitters, even at low doses, may represent an enhanced hazard to radiation injury when compared to photons impinging on the body from the outside from naturally occurring background radiation due to ionization density. It has been determined that, as a result of the natural radiation from the environment impinging on the body externally, each cell receives on average one hit per year. In contrast to this low-level external radiation, low-level radiation emitted by radioactive particles embedded within the body have a greater likelihood (dependent, of course, on quantity and activity) of hitting cells in their immediate proximity during the period of heightened sensitivity of cell replication.
Bibliography
[1] Sinclair W.K., Morton R.A. X-ray Sensitivity during the Cell Generation Cycle of Culture Chinese Hamster Cells. Radiation Research. 1966; 29:450-474.
