\t\t\tA Note on Radiation Damage<\/p>\n
“There is no safe level of radiation exposure. So the question is not: What
\n is a safe level? The question is: How great is the risk?”<\/p>\n
\t\t\t\t\t\tKarl Z. Morgan<\/p>\n
There have been three major theories as to how radiation damages living
\ntissue, all set by physicians. All are approximations, and based on broad
\nassumptions.<\/p>\n
(1) The threshold hypothesis: asserts that there exists a safe level of
\nradiation. The idea behind this thinking is that if the does is low, then
\nthe cell repair rate is of the order of the damage rate. Hence you get
\nno resultant damage.<\/p>\n
(2) The linear hypothesis: under this theory, you would expect 1 malignant
\ncancer for 1000 person-rems. For example, you would find one cancerous
\npatient if you exposed 500 people to 2 rems, or 10000 people to 0.1 rems.<\/p>\n
(3) The supralinear hypothesis: the main result here is that for low doses
\nyou get more cancers\/person-rem than at high doses. Here they not saying you
\nget more radiation; instead, you get more damaged surviving cells.<\/p>\n
\t\t\t\tSome Facts<\/p>\n
There are 4 types of ionising radiation. These are alphas
\n(fast moving helium nuclei),
\nbetas (electrons), gammas (high energy EM radiation), and neutrons (highly
\npenetrating).<\/p>\n
How does damage occur? In other words, how does radiation cause cancer? <\/p>\n
A typical cell is around 0.02mm across, a cell nucleus is about 0.001mm.<\/p>\n
When radiation, say a gamma, enters your body, there is a chance it will
\nintersect with one of your cells. Inside any cell is a nucleus, which
\ncontains chromosomes. These are essentially DNA helixes. DNA looks like
\ntwo entwined strings of nucleotides – the amino acids A, T, C, and G. Across
\nstrands they are paired A-T and C-G. A portion of DNA (a series of these
\nacids) is called a gene. Genes exist along chromosomes, and they contain
\nthe data for proteins.<\/p>\n
If the radiation happens to pass into the cell nucleus (which is a relatively
\nlarge entity compared to the rest of the cell), one of 4 things can happen.<\/p>\n
All exposure subjects cells to risk. In order of decreasing probability:<\/p>\n
\t\t(1) radiation goes right thru, no interaction.
\n\t\t(2) radiation does irrepairable destruction, and cell dies.
\n\t\t(3) radiation does damage to nucleus. Cell survives in
\n\t\t this damaged state. After it repetitively divides, it
\n\t\t grows into a solid tumour after 30 odd years – cancer.
\n\t\t(4) radiation does repairable damage, and cell returns to
\n\t\t normal state. (Very low probability).<\/p>\n
Possibility (3) is the one to watch out for. During division, the DNA
\nstrands stretch out, and it is during this time which your cells are most
\nsusceptible to damage.<\/p>\n
It is also possible for the radiation to ionise the water in the cell
\ncytoplasm, leading to the formation of free radicals, which can travel
\nsome distance. They can react chemically with the DNA in the nucleus,
\ninterfering with the chemical bonding along the helix. <\/p>\n
Two types of damaging interaction can occur with the amino acids.<\/p>\n
\t\t(a) point mutations
\n\t\t\t– deletion
\n\t\t\t– substitution
\n\t\t\t– inversion
\n\t\t\t– addition<\/p>\n
\t\t(b) large scale mutations (chromosome aberrations)
\n\t\t\t– deletion e.g. retinoblastoma
\n\t\t\t– amplification
\n\t\t\t– translocation<\/p>\n
It is also possible to have compound breaks along the DNA, which is not
\neasy for the cell to repair, unlike single strand or double strand breaks.<\/p>\n
The cell and nuclear membranes are also susceptible to damage. This could
\nbe due to alterations in permeability\/osmosis in the membrane due to the
\nradiation-induced imbalance of ionised particles.<\/p>\n
Once a certain threshold is exceeded, you will start saturating the cells.
\nThis lethal threshold serves to define two categories of radiation.<\/p>\n
\t\t\t\tEffects<\/p>\n
EFFECT\t\tNATURE\t\t\tTHRESHOLD?\tDOSE DEPENDENCE<\/p>\n
Stochastic\tNon-lethal mutations\tNo\t\tProbability of
\n(somatic or\taffecting single cells \t\t\teffect increases
\ngenetic)\t\t\t\t\t\twith dose<\/p>\n
Deterministic\tLethal mutations\tYes\t\tSeverity of
\n\t\taffecting large number\t\t\teffect increases
\n\t\tof cells\t\t\t\twith dose<\/p>\n
\t\t\t\tCancer<\/p>\n
Stem cells are ones which are able to undergo mitosis when the human body
\nhas reached full maturity. Examples are blood cells, and the cells lining
\nyour intestines. During normal functioning of your body, cell replacement
\nbalances cell loss.<\/p>\n
In cancer, a stem fails to stop its mitosis. It and its descendants divide
\nuncontrolled, forming a tumour. A bit like a binary tree in cell
\nmultiplicity.<\/p>\n
Oncogenes are genes which interfere with the cell division process. They
\nare mutations of proto-oncogenes, whose role are to control cell growth
\nand mitosis. It is thought radiation promotes creation of oncogenes.<\/p>\n
There are also cancer-suppressing genes, which inhibit oncogene formation.
\nThe best known example is the Rb gene, which inhibits retinoblastoma.<\/p>\n
After all of this, let me add a fourth idea on radiation damage:<\/p>\n
(4) probability of hereditary genetic damage or cancer is a function of:<\/p>\n
type of radiation (a,b,g,n) x energy of radiation x dose rate<\/p>\n
Here you have 4 discrete degrees of freedom, and 2 continuous degrees: rate &
\nenergy. Assume that there is a cut-off energy for a unit of a particular type
\nof radiation, E_max, such that if E > E_max a cell will die, and E < E_max
\nthe cell will survive (either in damaged or undamaged state). We are worried
\nabout the E E_max then you get radiation poisoning and
\nyou will definitely die if you get a large enough dose.<\/p>\n
The probability of nucleus intersection is a function of radiation type. (The
\nsize of radiation varies considerably.)<\/p>\n
The probability of a nucleus being hit twice or more is very low, unless
\nthe number of incident radiation approaches the sample size. In which case
\nyou get radiation poisoning and die anyway.<\/p>\n
You get a 6D phase space of statistical mechanics. Supplement this with an
\naction in path integral form. Plotted, you’d have a 6D graph, unlike your
\nnormal 3D graphs. It’s worse than the 4D spacetime of general relativity.
\nNo wonder the physicicans only plot projections! You can trace out a person’s
\nhistory in this phase space, and then give them a final probability of
\ncancer\/hereditary damage.<\/p>\n
============================================================================<\/p>\n
Plutonium’s Risk to Human Health Depend On Its Form<\/p>\n
In a nuclear explosium, plutonium-239 fissions and releases a huge amount of
\nenergy and radiation. But plutonium itself is a highly toxic element that requires
\na great deal of care in handling.<\/p>\n
Experts agree that the silvery, unstable metal plutonium-239, with a half-life of
\n24,000 years, is hazardous and sould be isolated from the biosphere. However, the
\nrisks posed to workers and communities by stored plutonium depend on the route of
\nexposure as well as the particle size, isotope, and chemical form.<\/p>\n
Weapons-grade plutonium outside the body presents little risk unless exposures are
\nfrequent and extensive. It emits primarily alpha particles, which cannot penetrate
\nskin, clothing, or even paper. Nearly all the energy from plutonium is deposited
\non the outer, nonliving layer of the skin, where it causes no damage. The neutrons
\nand the relatively weak gamma photons it emits can penetrate the body, but large
\namounts of weapons-grade plutonium would be needed to yield substantial doses.<\/p>\n
Workers wearing only lead aprons can handle steel drums containing solid plutonium
\nmetal with no immediate untoward effects. However, as weapons-grade plutonium
\nages, it becomes more dangerous because some of the contaminating plutonium-241 is
\nconverted via beta decay to americium-241, which emits far stronger gamma
\nradiation.<\/p>\n
On the other hand, plutonium inside the body is highly toxi. Solid plutonium metal
\nis neither easily dispersed nor easily inhaled or absorbed into the body. But if
\nplutonium metal is exposed to air to any degree, it slowly oxidizes to plutonium
\noxide (PuO2), which is a powdery, much more dispersable substance. Depending on
\nthe particle size, plutonium-239 oxide may lodge deep in the alveoli of the lung
\nwhere it has a biological half-life of 500 days, and alpha particles from the
\nopxide can cause cancer. Also, fractions of the inhaled plutonium oxide can slowly
\ndissolve, enter the bloodstream, and end up primarily in bone or liver.<\/p>\n
Plutonium oxide is weakly soluble in water. If it is ingested in food or water,
\nonly a small fraction (4 parts per 10,000) is absorbed into the gastrointestinal
\ntract. However, it may take just a few millionths of a gram to cause cancer over
\ntime. In animals, small doses induce cancer, especially in lung and bone.<\/p>\n
In published studies of plutonium’s effects on humans, most subjects were exposed
\nto multiple sources of radiation. Some researchers say the available health data
\non plutonium workers have not yet been used to do careful epidemiological studies,
\nbecause researchers have been denied access to much of the data on workers and
\nmilitary personnel exposed to plutonium. In the studies done so far, plutonium
\nworkers do not show major excesses of any type of cancer.<\/p>\n
Becuase of the relative lack of human data, the risks of chronic exposure to
\nplutonium are uncertain. Exposure standards in the U.S. are based partly on
\nstudies of survivors of Hiroshima and Nagasaki and partly on animal experiments. A
\n1991 White House Office of Science & Technology Policy studye says that
\n“sufficient human data are not available to provide accurate risk assessment of
\nexposure.”<\/p>\n
============================================================================<\/p>\n
\t\t\tNuclear Blast Effects<\/p>\n
The first thing bomb victims experience is the intense flux of photons from
\nthe blast, which releases 70-80% of the bomb’s energy. See the Hiroshima-
\nNagasaki file for first hand accounts. The effects go up to third degree
\nthermal burns, and are not a pretty sight. Initial deaths are due to this
\neffect.<\/p>\n
Then next phenomenon is the supersonic blast front. You see it before you
\nhear it. The pressure front has the effect of blowing away anything in its
\npath. Heavy steel girders were found bent at 90 degree angles after the
\nJapanese bombings. <\/p>\n
After the front comes the overpressure phase. It would feel like being under
\nwater a few hundred metres. At a few thousand metres under the sea, pressurised
\nhulls implode. The pressure gradually dies off, and there is a negative
\noverpressure phase, with a reversed blast wind. This reversal is due to
\nair rushing back to fill the void left by the explosion.<\/p>\n
The air gradually returns to room pressure. At this stage, fires caused by
\nelectrical destruction and ignited debris, turn the place into a firestorm.
\nJust like Dresden in WWII. It is estimated over fifty thousand died in the
\nfirst few days of the Hiroshima bombing.<\/p>\n
Then come the middle term effects such as keloid formation and retinal
\nblastoma.<\/p>\n
Genetic or hereditary damage can show up up to forty years after initial
\nirradiation.<\/p>\n
The following diagram is of blast zone radii, courtesy of Outlaw Labs.
\nNote that damage from blast pressure falls off as a function of 1\/r^3.<\/p>\n
============================================================================<\/p>\n
– Breakdown of the Atomic Bomb’s Blast Zones –
\n ———————————————-<\/p>\n
.
\n . .<\/p>\n
. . .
\n . .
\n [5] [4] [5]
\n .
\n . . . .<\/p>\n
. . . .<\/p>\n
. [3] _ [3] .
\n . . [2] . .
\n . _._ .
\n . .~ ~. .
\n . . [4] . .[2]. [1] .[2]. . [4] . .
\n . . . .
\n . ~-.-~ .
\n . . [2] . .
\n . [3] – [3] .<\/p>\n
. . . .<\/p>\n
. ~ ~ .
\n ~
\n [5] . [4] . [5]
\n .
\n . .<\/p>\n
. .
\n .<\/p>\n
============================================================================<\/p>\n
– Diagram Outline –
\n ———————<\/p>\n
[1] Vaporization Point
\n ——————
\n Everything is vaporized by the atomic blast. 98% fatalities.
\n Overpress=25 psi. Wind velocity=320 mph.<\/p>\n
[2] Total Destruction
\n —————–
\n All structures above ground are destroyed. 90% fatalities.
\n Overpress=17 psi. Wind velocity=290 mph.<\/p>\n
[3] Severe Blast Damage
\n ——————-
\n Factories and other large-scale building collapse. Severe damage
\n to highway bridges. Rivers sometimes flow countercurrent.
\n 65% fatalities, 30% injured.
\n Overpress=9 psi. Wind velocity=260 mph.<\/p>\n
[4] Severe Heat Damage
\n ——————
\n Everything flammable burns. People in the area suffocate due to
\n the fact that most available oxygen is consumed by the fires.
\n 50% fatalities, 45% injured.
\n Overpress=6 psi. Wind velocity=140 mph.<\/p>\n
[5] Severe Fire & Wind Damage
\n ————————-
\n Residency structures are severely damaged. People are blown
\n around. 2nd and 3rd-degree burns suffered by most survivors.
\n 15% dead. 50% injured.
\n Overpress=3 psi. Wind velocity=98 mph.<\/p>\n
—————————————————————————-<\/p>\n
– Blast Zone Radii –
\n ———————-
\n [3 different bomb types]
\n____________________________________________________________________________
\n ______________________ ______________________ ______________________
\n | | | | | |
\n | -[10 KILOTONS]- | | -[1 MEGATON]- | | -[20 MEGATONS]- |
\n |———————-| |———————-| |———————-|
\n | Airburst – 1,980 ft | | Airburst – 8,000 ft | | Airburst – 17,500 ft |
\n |______________________| |______________________| |______________________|
\n | | | | | |
\n | [1] 0.5 miles | | [1] 2.5 miles | | [1] 8.75 miles |
\n | [2] 1 mile | | [2] 3.75 miles | | [2] 14 miles |
\n | [3] 1.75 miles | | [3] 6.5 miles | | [3] 27 miles |
\n | [4] 2.5 miles | | [4] 7.75 miles | | [4] 31 miles |
\n | [5] 3 miles | | [5] 10 miles | | [5] 35 miles |
\n | | | | | |
\n |______________________| |______________________| |______________________|
\n____________________________________________________________________________<\/p>\n
============================================================================<\/p>\n
\t\t\tAtmospheric Effects of Blasts<\/p>\n
The Mushroom Cloud<\/p>\n
The heat from fusion and fission instantaneously raises the surrounding air
\nto 10 million degrees C. This superheated air plasma gives off so much light
\nthat it looks brighter than the sun, and is visible hundreds of kms away.
\nThe resultant fireball quickly expands. It is made up of hot air, and hence
\nrises, at a rate of a few hundred metres per second. After a minute or so,
\nthe fireball has risen to a few kilometres, and has cooled off to the extent
\nthat it no longer radiates.<\/p>\n
The surrounding cooler air exerts some drag on this rising air, which slows
\ndown the outer edges of the cloud. The unimpeded inner portion rises a bit
\nmore quicker than the outer edges. A vacuum effect occurs when the outer
\nportion occupies the vacuum left by the higher inner portion. The result is
\na smoke ring. <\/p>\n
The inner material gradually expands out into a mushroom cloud, due to
\nconvection. If the explosion is on the ground, dirt and radioactive debris
\nget sucked up the stem, which sits below the fireball. <\/p>\n
Collisions and ionisation of the cloud particles result in lightning bolts
\nflickering to the ground. <\/p>\n
Initially, the cloud is orange-red due to nitrous oxide formation (cf car
\nsmog). This reaction happens whenever air is heated.<\/p>\n
When the cloud cools to air temperature, the water vapour starts to
\ncondense. The cloud turns from red to white.<\/p>\n
In the final stages, the cloud can get about 100km across and 40km high,
\nfor a megaton class explosion.<\/p>\n
============================================================================<\/p>\n
\t\t\tElectromagnetic Pulse (EMP)<\/p>\n
A nuclear explosion gives off radiation at all wavelengths of light. Some
\nis in the radio\/radar portion of the spectrum – the EMP effect. The EMP
\neffect increases the higher you go into the atmosphere. High altitude
\nexplosions can knock out electronics by inducing a current surge in
\nclosed circuit metallic objects – computers, power lines, phone lines,
\nTVs, radios, etc. The damage range can be over 1000km.<\/p>\n
============================================================================<\/p>\n
Here are some good references on radiation damage. See also the main
\nReferences file.<\/p>\n
AUTHOR: Sumner, David, D. Phil
\nTITLE: Radiation risks : an evaluation \/ David Sumner, Tom Wheldon, Walter
\n Watson. — 3rd ed.
\nISBN\/ISSN: 187078104X
\nIMPRINT: Glasgow [Scotland], Tarragon Press, 1991
\nPHYS DESC: 236 p., ill., map, 21 cm.
\nADD AUTH1: Wheldon, Tom
\nADD AUTH2: Watson, Walter
\nNOTE 1: Includes index Bibliography: p. 227-229
\nSUBJECT 1: Radiation–Physiological effect
\nSUBJECT 2: Cells–Effect of radiation on
\n[Good introductory work.]<\/p>\n
CALL NO: Me f 616.989707 LOW
\nTITLE: Low-level radiation effects: a fact book: prepared by Subcommittee
\n on Risks of Low-Level Ionizing Radiation: A. Bertrand Brill … [et
\n al.]
\nISBN\/ISSN: 0932004148
\nIMPRINT: New York, NY: Society of Nuclear Medicine: c1982-
\nPHYS DESC: 1 v. (loose-leaf): ill: 30 cm.
\nADD AUTH1: Brill, A. Bertrand
\nADD AUTH2: Society of Nuclear Medicine. Subcommittee on Risks of Low-Level
\n Ionizing Radiation
\nNOTE 1: To be kept up to date by inserts
\nSUBJECT 1: Ionizing radiation–Physiological effect
\nSUBJECT 2: Ionizing radiation–Toxicology
\nSUBJECT 3: Radiation injuries
\nSUBJECT 4: Low-level radiation–Physiological effect<\/p>\n
CALL NO: Me 574.1915 BIOL
\nTITLE: Biological effects of low-level radiation : proceedings of an
\n international symposium on the effects of low-level radiation with
\n special regard to stochastic and non-stochastic effects \/ jointly
\n organized by the International Atomic Energy Agency and the World
\n Health Organisation, and held in Venice, Italy, 11-15 April 1983
\nISBN\/ISSN: 9200101836
\nIMPRINT: Vienna, International Atomic Energy Agency, 1983
\nPHYS DESC: 682 p., ill, 24 cm. (Proceedings series)
\nADD AUTH1: International Atomic Energy Agency
\nADD AUTH2: World Health Organization
\nSERIES 1: Proceedings series (International Atomic Energy Agency)
\nNOTE 1: English and French
\nSUBJECT 1: Radiation–Toxicology–Congresses
\nSUBJECT 2: Radiation–Physiological effect–Congresses<\/p>\n
CALL NO: DS 574.1915 KIEF
\nAUTHOR: Kiefer, J (Jurgen) , 1936- [Biologische Strahlenwirkung. English]
\nTITLE: Biological radiation effects \/ Jurgen Kiefer
\nISBN\/ISSN: 3540510893
\nIMPRINT: Berlin, New York, Springer-Verlag, c1990
\nPHYS DESC: xvii, 444 p., ill, 24 cm.
\nNOTE 1: Rev. translation of: Biologishce Strahlenwirkung Includes
\n bibliographical references (p. [415]-435) and indexes
\nSUBJECT 1: Radiobiology
\nSUBJECT 2: Radiation–Physiological effect
\nSUBJECT 4: Radiation protection<\/p>\n
To learn more about air explosions, see the Reference by Kinney and Graham,
\n“Explosive Shocks in Air”.<\/p>\n
The Red Phoenix, 1994.<\/p>\n
