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| Fig. 1: Excess Relative Risk (ERR) as a function of radiation dose for colon cancer. [9] ERR is a convoluted scale that corresponds to the increased percentage chance of developing cancer over one's lifetime. 1 ERR is a 10% increase and 0.5 is a 5% increase. The horizontal scale is in grays (Gy). (After Preston et al. [9]) |
A recent spate of cancer outbreaks among Latin and South American presidents has prompted some to accuse the United States of developing a way to weaponize cancer. A "caner gun" could be used to target a country's political adversaries while affording that country with a reasonable degree of deniability since determining the direct cause of cancer is currently beyond our scientific reach. Additionally, a significant portion of the population will develop cancer anyway (about 40% in the United States according to the National Cancer Institute's SEER program). Credibility for this kind of conspiracy theory was bolstered by Alexander Litvinenko's 2007 assassination in London by polonium 210 poisoning and the myriad cases of Acute Radiation Poisoning (ARP). The following short essay aims to provide a simple framework to address the issue of inducing cancer using the products of nuclear decay: gamma radiation, beta particles, alpha particles, and neutrons.
There is a subtle distinction here between radiation poisoning and radiation-caused cancer. Radiation exposure of 1 gray (absorption of 1 joule of energy per 1 kilogram of matter) corresponds to about a 5% increased chance of developing cancer over 30 years (Fig. 1), exposure to 2 grays is enough to induce Acute Radiation Sickness, and 3.5 grays has a 50% mortality rate within 60 days of exposure. [1,2] There is a fine line between increasing someone's chance of developing cancer, and killing that person with radiation poisoning. We are discussing the former. The latter is relatively easy to do, if you have access to nuclear waste, and is relatively easy to detect with modern laboratory techniques.
The human body has many mechanisms that ensure its survival. Several of these mechanisms must fail for a person to eventually succumb to cancer. The following is a list of requisite genetic mutations needed for normal cells to develop into cancerous cells and ultimately kill their human host. [3]
Sustaining Proliferative Signaling: The human body regulates cell growth. Cells need to receive mitogenic growth signals from surrounding tissue in order to divide and proliferate. Therefore, tumor cells must generate many of their own growth signals. It is suspected that the growth signaling pathways in all human tumors have suffered deregulation. In addition to growth signals, cells also have antigrowth signals. These signals inhibit cell growth when surrounding tissue determines it is appropriate. Cancer cells must develop a genetic insensitivity to these antiproliferative signals.
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| Fig. 2: Once DNA is damaged by radiation, repair mechanisms are activated. If these mechanisms fail, then the damaged cell has three possible fates: cancer, apoptosis (triggered cell death), or senescence (cell stops dividing). Source: Harold Brenner at Wikimedia Commons) |
Resisting Cell Death: Cells are preprogramed to disintegrate and die after a certain lapse of time or at the development of certain abnormalities. The cell dies, disintegrates, and gets engulfed by neighboring cells. This process is called apoptosis and tumor cells have the unique ability to resist it.
Enabling Replicative Immortality: Despite the complete uncoupling of cancerous cell growth from the various environmental signals that attempt to regulate that growth, cancerous cells also have to overcome an intrinsic cellular program that places limits on cell reproduction. Cells have a finite replicative potential -- after a certain number of cell divisions, cells stop reproducing (called senescence). Small errors compound after each cell division ultimately rendering the cell incapable of further reproduction. Tumor cells have the ability to correct these genetic errors after each division.
Inducing Angiogenesis: Cells need oxygen and nutrients to survive. In order to obtain this needed sustenance, cells must reside within 100 microns of a capillary blood vessel. Cancer cells must induce the growth of new blood vessels (called angiogenesis) to sustain any macroscopic growth. Normal cells do not have the ability to induce angiogenesis on their own behalf.
Activating Invasion and Metastasis: Tumor masses must spawn clusters of pioneer cells to leave their current location and invade adjacent cells and tissue to form new colonies of cancer cells. This process of metastasis is the overwhelming cause of cancer deaths.
Damage of Tumor Suppressor Genes: The above cancer cell characteristics are acquired either directly or indirectly through genetic mutation; but, in a cell there exists a complex array of DNA monitoring and repairing enzymes that strive to maintain the integrity of the DNA. Since it is highly unlikely that all the mutations needed for cancer could occur in a person's lifetime and any mutation that does occur can be corrected, cancer cells must possess the ability to inhibit these tumor suppressor genes or they must be damaged by some other process.
So in order to induce cancer, the above mechanisms must be actively realized through genetic mutations. There are roughly two ways for radiation from nuclear decay to induce these genetic mutations. Firstly, free radicals created from ionizing radiation can interact with DNA and cause mutations. Radiation with enough energy can liberate an electron bound to an atom or molecule. That atom or molecule will then have an unpaired valence electron that could covalently bond with neighboring DNA to introduce a genetic error that could be passed on in reproduction (Fig. 2). Secondly, radiation with enough kinetic energy can damage the physical structure of DNA and cause Single Strand Breaks (SSB) or Double Strand Breaks (DSB). When the repair mechanisms in DNA attempt to correct this damage, mutations can be introduced.
Gamma Rays: Although clinical studies have concluded that electromagnetic radiation (EMR) is a contributing cause of cancer, there is not a scientific consensus on how this occurs. [4] Non-ionizing EMR as well as ionizing EMR are both implicated. Photons with enough energy, like gamma rays, can ionize electrons to produce free radicals and even penetrate human skin to cause SSB and DSB in DNA.
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| Fig. 3: Nuclear decay products ionizing tissue. (Source: Wikimedia Commons) |
Beta Particles: A beta particle is an electron and antineutrino (or a positron and neutrino). Betas can burn the skin and penetrate skin up to 20 mm, depending on their kinetic energy. This penetration can be most effective in ionizing DNA or creating free radicals if the beta particles are produced inside the body.
Alpha Particles: Alpha particles cannot penetrate skin (or even a piece of paper), so they are only dangerous if an alpha emitter is ingested or inhaled into the body. Since alpha particles are made of two protons and two neutrons, if ingested, they represent the biggest risk to biological tissue of all the nuclear decay products because of their relatively large mass and charge. When an alpha particle strikes DNA, its positive charge can ionize constituents of DNA or deposit energy in a process called Linear Energy Transfer (LET) causing SSB or DSB of DNA. A single alpha particle can cause DNA damage that will result in a carcinogenic mutation. Alpha particles have also been linked to the damage of tumor suppressor genes. [5,6] Ingesting an emitter of alpha particles is probably the most effective way to induce Acute Radiation Poisoning; ingesting only a few hundred micrograms of alpha-emitting polonium 210 will likely be fatal. [7]
Neutrons: In comparison to alpha particles, neutrons can cause equivalent damage to DNA in much the same way, but are more effective at penetrating skin. Neutrons are only slowed down by elastic collisions with lighter atoms or molecules. Slower neutrons are then more easily captured by a nucleus. This capture might make the nucleus radioactive, which will compound the problem by emitting more radiation. A free neutron (not bound in a nucleus) will only survive for about 15 minutes until it decays into a proton by emitting a beta particle.
These four ways of inducing cancer are also used to treat cancer: radiation therapy (x-rays and gamma rays), unsealed source therapy (alphas, betas, and gammas), radiopharmaceuticals (alphas, betas, and gammas), and fast neutron therapy. The distinction is that enough radiation will not only cause mutations in DNA, but it will also destroy that DNA. For cancer therapies, enough radiation is directed at the tumor to destroy the tumor's cells and DNA, while attempting to minimize the damage to neighboring healthy cells. What causes cancer can also destroy it.
So, exposing someone to a little less than 2 grays of radiation from nuclear decay should be enough to increase someone's risk of getting cancer by 5 to 10 percent while hopefully avoiding Acute Radiation Poisoning (which would expose the attempted assassination). Even one neutron, alpha particle, or gamma ray is enough to cause a cancerous mutation in a gene that could one day develop into a metastasizing cancer. Of course, this small increase in the percentage chance of developing cancer will take 2 to 5 years for leukemia and at least 10 years for other solid cancers. [8] Fortunately however, this long incubation period and the inherently stochastic nature of cancer renders any attempt of inducing cancer with radiation impractical. Political enemies of the United States can all sleep soundly tonight knowing that they have little to fear from a cancer gun.
© Josh Francis. The author grants permission to copy, distribute and display this work in unaltered form, with attribution to the author, for noncommercial purposes only. All other rights, including commercial rights, are reserved to the author.
[1] Health Risks From Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase 2 (National Academies Press, 2006).
[2] L. F. Fajardo, Radiation Pathology (Oxford U. Press, 2001), p. 10.
[3] D. Hanahan and R. A. Weinberg, "The Hallmarks of Cancer," Cell 100, 57 (2000).
[4] D. Belpomme et al., "The Multitude and Diversity of Environmental carcinogens," Environ. Res. 105, 414 (2007).
[5] M. Hollstein et al., "p53 Gene Mutation analysis in Tumors of Patients Exposed to Alpha-Particles," Carcinogenesis 18, 511 (1997).
[6] M. Andersson et al., "Mutations in the Tumor Suppressor Gene p53 in Human Liver cancer Induced by Alpha-Particles," Cancer Epidemiol. Biomarkers Prev. 4, 756 (1995).
[7] B. R. Scott, "Health Risk Evaluations of Ingestion Exposure of Humans to Polonium-210," Dose Response 5, 94 (2007).
[8] An Evaluation of Radiation Exposure Guidance for Military Operations: Interim Report (National Academies Press, 1997).
[9] D. L. Preston et al., "Studies of Mortality of Atomic Bomb Survivors. Report 13: Solid Cancer and Noncancer Disease Mortality: 1950-1997," Radiat. Res. 160, 381 (2003).
