Week 8 part 2 Flashcards
What is the risk of Neonatal deaths in humans compared to normal incidence?
200-500 deaths per million exposed to 10mSv
compared to 2500 per million (unexposed)
What is the probability of severe mental retardation, compared to normal incidence of mental retardation?
40% (or 4 hundred thousand) incidence at 1 Gy per million exposed
compared to 5000 per million exposed
Is mental Retardation a deterministic effect? If so , why?
Yes, because there is likely threshold of 0.2 Gy
What is the observed shift in IQ (due to pregnancy radiation)?
30 per Gy (during the sensitive period
What is the Largest study regarding in utero irradiation and childhood cancer?
The Oxford Study
What is the Oxford Study?
Considered approx 8,000 cases of malignant childhood death (looked into radiological history of mother during pregnancy)
+ compared it to data for children who died <10 years from a malignant disease
What did the Oxford Study find?
Obsetric Radiography resulted means increased risk of malignancy in childhood
Besides the oxford study, where do we get in-utero related childhood cancer data?
Limited data from A-bomb survivors (1620 prenatally exposed)
Are the findings of the oxford study backed up by A-bomb survivors?
Yes
The risk estimate for the prenatally exposed (due to a-bomb) was?
200-250 deaths (before age 10) from cancer, per million exposed in utero
-1/2 of these were leukemia
Being exposed in what trimester, has the greatest risk?
the first trimester
What is the natural incidence of fatal childhood cancer?
1 in 2000
What is a limitation of collected data regarding, in utero radiation?
We don’t have the full picture of true cancer as the total risk period is 20 years
Which type of cancer’s risk of incidence of doubled due to in utero radiation?
Leukaema
Is an adult, child, or embryo most sensitive to cancer induction?
Embryo
Once a pregnancy is known by a radiation worker, and reported to management, what happens next?
The total dose of the worker becomes the same as the public
Go to slide 24 on week 8 and memorise table
do it
Where do we get our data for genetic effects?
virtually NO human, mostly animals
Does radiation produce the same type of mutations as those observed in natural incidence?
Yes
Data of A-bomb survivors failed to show any statistically significant increase in what?
- Congenital abnormalities
-cancer
-chromosome aberrations
-mutational blood protein changes
BUT… we don’t have enough human data to be “statistically significant”
What are the reasons for low human data on genetic effects of IR?
- Long life cycle
- studies require large population > 1 million
- too few offspring in families
- large incidence of natural genetic damage
Is there ample evidence of IR causing heritable mutations in plants and animals?
yes there is, therefore we must assume the same for humans
A recent study of Hiroshima survivors and their offspring concluded what?
All indiactors of data, concluded that genetic damage my result from exposure to IR
Indicators of A-bomb survivors included?
- untoward pregnancy outcome
- death of a live born child < 17 years
- sex chromosome aneuploidy
What did early results of IR exposure (on insects) indicate?
1) there is no threshold
2) the dose/effect relationship is proportional
3) there is no effect of fractionation
THIS INDICATES THERE IS NO REPAIR
What is the summary of information gained from the MEGAMOUSE EXPERIMENT? (name 4)
1) different gene loci have different rates of induction and mutation
2) mutation frequency is dose-rate and sex dependent
3) time between irradiation and conception is important
4) magnitude of the effect depends on stage of sex cell
Out of the 7 loci studied what was the variation factor of genes?
35- different gene loci have different rates of induction + mutation
At high dose rates >1 Gy/min, do the spermatogonia and oocytes have a similar sensitivity?
Yes
What happens as the dose rate decreases to <10^-2?
Both male and female sensitivity decrease BUT the oocytes decreases far more than sperm
At low dose rates, is the mutation frequency in oocytes distinguishable from natural incidence? (compared to IR)
No, even for several Gy
On average are male cells more sensitive than females to IR?
Males are more sensitive and carry genetic burden at low dose rates
How can you reduce the effect of IR?
Delaying time between conception after IR exposure (due to repair)
6 months assumed to provide safety margin
The latter stages of male and female sex cells are more sensitive by approx how many times compared to early stages?
latter stage are 5 times more senitive
How are risk estimates of genetic damage expressed in relative terms?
- The doubling dose
(radiation dose doubles at random rate) - or in absolute terms
(no. mutations per million per 10mSv)
What is the doubling dose risk for low dose rate exposure? (in humans)
1 Gy
What is the absolute risk for low dose rate in whole population?
100 mutations/ million births/10mSv of parental exposure
What is the absolute risk for low dose rate in working population?
60/million/10mSv
In males and females, what dose causes temporary sterility?
0.2 Gy females
150 mGy males
In males and females what dose causes permanent sterility? (sundry effects
4 Gy females
6 Gy Males
In females what dose may delay menstruation? (sundry effects)
0.1 Gy
What dose causes cataract formation? is there a threshold? and what is the latent period? (sundry effects)
1-2 Gy
>10 Gy get 100% induction
-latent period of 6 months to 30 years
What dose causes skin damage? Explain the two waves of effects?
(sundry effects)
3-10 Gy
mild erythema subsides followed by a second wave
*>10 gy
second wave maybe followed by desquamation
dose causing epilation? (sundry effects)
3-4 Gy
