Hall Book Ch 11 (Heritable Effects of Radiation)

Question 1

In the male, doses as low as ( ) Gy result in oligospermia (diminished sperm count) after a latent period of about 6 weeks.

Doses greater than ( ) Gy result in azoospermia (absence of living spermatozoa) and therefore temporary sterility.

Recovery time depends on ( ).

Answer 1

0.15, 0.5, dose

Question 2

Permanent sterility in the male requires a single dose in excess of ( ) Gy.

In the male, ( ) doses cause more gonadal damage than a ( ) dose.

Permanent sterility can result from a dose of ( ) Gy in a fractionated
regime over 2 to 4 weeks.

Answer 2

6, fractionated, single

2.5 to 3

Question 3

In the female, radiation is highly effective in inducing permanent ovarian
failure, with a marked ( ) dependence on the ( ) required.

The dose required for permanent sterility in the female varies from (    ) Gy
prepubertal to (   ) Gy premenopausal.

Answer 3

age, dose, 12 Gy, 2 Gy

Question 4

The induction of sterility in males does not produce significant changes in hormone balance, libido, or physical capability, but in the female, it leads to pronounced ( ).

Answer 4

hormonal changes comparable to natural menopause

Question 5

Exposure of a population can cause adverse health effects in the descendants because of mutations induced in germ cells. These used to be called “genetic” effects but are now more often called “heritable” effects.

Heritable diseases are classified into three principal categories: mendelian,
chromosomal, and multifactorial.
Radiation does not produce new, unique mutations but increases the incidence
of the same mutations that occur spontaneously.
Information on the heritable effects of radiation comes almost entirely from
animal experiments.
The earlier mutation experiments were carried out with the fruit fly, D.
melanogaster.
Relative mutation rates have been measured in the megamouse project by
observing seven specific locus mutations. This leads to an estimate of the
“doubling dose.”
The doubling dose is the dose required to double the spontaneous mutation
incidence; put another way, it is the dose required to produce an incidence of
mutations equal to the spontaneous rate. Based on the mouse data, the
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doubling dose for low dose-rate exposure in the human is estimated to be 1
Gy.
Not more than 1% to 6% of spontaneous mutations in humans may be ascribed
to background radiation.
To estimate the risk of radiation-induced heritable diseases in the human, two
quantities are required: (1) the baseline mutation rate for a human, which is
estimated to be 738,000 per million, and (2) the doubling dose from the
mouse data, which is about 1 Gy.
Two correction factors are needed: (1) to allow that not all mutations lead to a
disease—this is MC, which varies for different classes of heritable diseases,
and (2) to allow for the fact that the seven specific locus mutations used in
the mouse experiments are not representative of inducible heritable diseases
in the human because they are all nonessential for the survival of the animal
or cell.
The ICRP estimates that the heritable risk of radiation is about 0.2% per sievert
for the general population and about 0.1% per sievert for a working
population.
In terms of detriment, expressed in years of life lost or impaired, congenital
anomalies (i.e., resulting from effects on the developing embryo and fetus)
are much more important than heritable disorders.
First-generation children of the atomic bomb survivors have been studied for a
variety of end points, including several common polygenic multifactorial
diseases, but there is no evidence that the incidence of any of them is
associated with paternal or maternal radiation dose.
Since the 1950s, concern for the heritable effects of radiation has declined
continuously and has been replaced by carcinogenesis as the principal effect
of low doses of radiation.
Epigenetics refers to changes in gene expression that take place without a
change in the DNA sequence. The most studied mechanisms include DNA
methylation and changes in chromatin packaging by posttranslational histone
modification.
There is evidence from animal studies that prenatal and early postnatal
environmental factors, including exposure to radiation, can alter epigenetic
programming with subsequent changes in the risk of developing disease in
later life.