The Biological Effects of Radon and its Progeny
- In 1987, 150,000 of the 950,000 new cancer cases identified by the
American Cancer Society (ACS) were
lung cancer.
- From data compiled in 1988, 87% of all lung cancer patients die within
five years (136,000 out of 483,000 total deaths from cancer).
- The EPA estimates that 7,000 to
30,000 deaths per year are attributable to lung cancer caused by radon.
- The ACS estimates that 83% of annual lung cancer deaths are caused by
smoking, which leaves at most 23,000 deaths that may be
attributed to radon.
Radon and the Human Body
As 222Rn decays in the lungs, 218Po and 214Po either attach to the
bronchial wall, form a molecular aggregate with other airborne
particles, or exist in the air transiently as ions. Although only
soluble in fatty tissues, radon is usually inhaled and cleared back out
of the blood in a few minutes, however the decaying
progeny remain. How much radiation an individual may receive
depends on the dustiness of the
surrounding air, the time elapsed before attachment to the bronchiolar
epithelium, and lung morphology. The major radiation dose received by
persons affected by radon comes from 218Po and 214Po, which emit alpha particles as they decay. These
alpha particles move through the lining
membrane in the bronchial region and can cause cell abnormalities.
Exactly how alpha particles cause cancer is not known, however it is
possible that their large mass (relative to beta and
gamma particles) has sufficient energy to break a DNA chain that
a less massive particle may pass through. When cellular repair
systems are unable to repair the breaks in DNA
caused by alpha particles, permanent cell damage results.
The tissue lining the lung is known as the epithelium, and has a
basal layer approximately 7 microns thick and an outer layer covered by a
mucus layer of variable thickness (40-80 microns thick). A layer of
mucus 10-20 microns thick coats the outer epithelium, helping the cilia
move particulate matter out of the lungs and respiratory tract. In the
basal layer, cell division is common and therefore susceptible to damage
from radiation. The mucus layer and epithelium protect the basal layers
with their combined thickness of about 60 microns, however in some areas
the basal layer is only 20-30 microns from the surface.
| --Element-- | --Penetration Distance-- |
| 222Rn | 41 microns |
| 218Po | 48 microns |
| 214Po | 71 microns |
Source: Nazaroff and Nero, 1987
The primary effects of radiation:
- suppression of cell division, and
- the promotion of DNA mutations and/or
chromosomal abnormalities
There are two general stages in the establishment of a cancer:
- initiation: the alteration of the cell genome leading to loss
of control of cell division
- promotion: the process affecting
regulatory control or cells leading to cancer
Even at high doses of
radiation, we have no direct genetic evidence of effects on humans except
for reciprocal translocations detected in spermatocytes by cytology.
There are two methods used to estimate the changes in incidence of
disorders caused by gene mutations:- the continuous exposure method
- the single gene method.
According to the National Academy of Science:
- the estimated
mutation
risk is 0.02-0.004 muations per rem.
- the current incidence
of human genetic disorder is 107,000 cases per million liveborn
- the
increase per rem of parental exposure is 60-1,100 mutations per million
liveborn
- the effects
in a single generation after parental exposure of 1 rem before
conception to be 5-65 disorders per million liveborn offspring
- In what
are known as estimates of persistence, the NAS recommended five
generations for autosomal dominant diseases and ten generations for
irregularly inherited diseases, which agree with the estimates for
single-generation effects and the estimates for effects observed at
equilibrium after long-term exposure.
DNA,
deoxyribonucleic acid, is the genetic material which directs
the reproduction and maintenence of the cell. DNA is composed of
sequences of four types of nucleotides, adenine, guanine, cytosine, and
thymine, that are grouped in triplets known as codons. These codons
correspond with the production of amino acids which make up proteins that
carry out cellular processes. Little DNA codes for proteins--most of
it has an unknown function. A mutation is any change in the nucleotides of
the DNA sequence.
- chromosomal aberration: a change in the organization of a
chromosome(s).
- genome mutation: a chromosomal mutation involving a change in the number
of sets of chromosomes in the genome.
- gene mutation: an alteration of the DNA sequence of an individual gene.
- base-pair substitution mutation: the replacement of one base pair with
another.
- transition mutation: change in the chemical structure of the nucleotide
from a purine to pyrimidine or vice versa (ex. CG to TA).
- transversion mutation: the change of a purine-pyrimidine base pair to a
pyrimidine-purine base pair at the same site. (ex. GC to TA).
- missense mutation: a base pair change changing the amino acid coded for
by the codon.
- nonsense mutation: a base pair change changing the codon into a
chain-terminating codon such as UGA, UAA, or UAG.
- neutral mutation: base pair change in the gene that changes the
resulting amino acid without affecting the protein's function.
- frameshift mutation: the addition or deletion of a base pair shifting
the reading frame by one base, often creating a non-functional protein.
Expressions Describing Radiation Dosage
A larger class of mutations arises from the breakage of the chromosome
itself and the subsequent rearrangement of the fragments. There is a
curvilinear relationship of yield to dose for the data
for genetic damage, with the slope increasing with dose over the dose
range.
Generally, an expression of the form
y = aD + bD2 + C
describes the curve, where y is yield, D is dose, and C is estimated
zero-dose incidence. The coefficients a and b measure the admixture of
one- and two-track events. A modification of the theory would assign
these values to the physical nature of radiation absorption, with the
damage resulting from the interaction of lesions arising from either
single-track or two separate tracks.
The dose-effect relationship is given by
e = k(gD + D2)
where e is effect, g is the dose average of the specific energy deposited
in the target volume by single ionizing events, an k is a "sensitivity
coefficient." This relationship yields good values for the coefficients
when good data is used, and leads to precise estimation of the effects of
low doses and low dose rates. One element that must be taken into
account is the ability of the cell to repair itself, therefore time must
be introduced as a variable.
G = 2(v/T)2(T/v - 1 + e-T/v)
where G is a correction factor for yield of two-track events, v is the
average time between damage and repair, and T is treatment duration. A
more rigorous explanation may involve multiple cellular repair mechanisms
working together. Moreover, there may by more than one class of event
involved in a point mutation and further mutations may be introduced by
repair systems. Clearly, the age of the subject and the relative
efficiency of individual repair systems may change, making an exact
quantification impossible, however the best estimate of damage at very
low doses may be an linear extrapolation through the origin, i.e. zero
dose = zero yield.
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