1. Space Radiation Health Effects of Astronauts in Explorative Missions
Günther Reitz
Radiation Biology Department
Institute of Aerospace Medicine
German Aerospace Center (DLR)

2. ‘Fault tree’ of Fatal event
The most harmful environmental factors are
Cosmic ionizing radiation and secondary radiations produced by interaction of the cosmic primaries with atoms and molecules of the atmosphere or shielding material as well as the human body itself
Solar particle events that occur sporadically and may last over several days, which cause temporally substantial increases in the radiation dose
Reduced gravity of  g which is experienced by the crew after a trip in microgravity for nearly one year and a heavy g-load up to 6 g during landing 2

3. Fluxes of primary space radiation components
inner
Van Allen belt
protons

4. Effective Doses Low Earth Orbit Missions and Missions to the Moon

5. GCR exposure in interplanetary space
BON2011/BON2010≈ 1.35
BON2011/DLR
≈ 1.1
DLR
BON2010
BON2011

6. Worst$ case' SPE radiation exposures in Sv during different mission phases for critical tissues under different mass shielding

7. Limits for Astronauts in LEO (NASA as example)
Career non-cancer and Short term effects
Career cancer risk limits
Dose (Gy-Eq)
BFO
Eye
Skin
Career NA
4.0
Annual
0.5
2.0
3.0
30 days
0.25
1.0
1.5
Effective Dose (Sv)
Age
Male
Female 25
0.7
0.4 35 1
0.6 45
1.5
0.9 55 3
1.7
For reference: Limits for radiation workers on Earth:
20 mSv annual and 400 mSv career

8. How Astronauts are Affected by Cosmic Rays?

9. DNA is the MainTarget of Radiation Action
Energy deposition
DNA damage
Cell cycle arrest
Repair
Cellular Survival
Clonal Expansion
Transformation
Mis-repair
Mutations
Carcinogenesis
Cell death, e.g. by
Apoptosis
Misdifferentiation
Senescence
No repair
biological effects of radiation are a consequence of chemical reactions initiated by energy deposition in cells and tissues
these reactions modify the division processes by which cells reproduce as well as other cell functions required for healthy living organisms
cells repair themselves; when that repair is successful, the tissues and organisms return to their normal state, when repair is not successful, cells may die
tissue integrity and function may be impaired, as occurs in acute radiation effects
repair may be successful from the point of view of cell survival, but may contain latent errors that only manifest in subsequent generations of dividing cells
DNA lesions depend in type and quantity on the quality and dose of radiation
radiation-induced DNA damage affects cellular reproducibility and conservation of genetic stability
Resulting in cellular inactivation and mutation induction
cells have developed pathways to detect, signal and repair DNA damage
altered expression of regulatory proteins represent important early events in the process of oncogenic transformation
compensatory mechanisms exist, such as apoptosis, protein expression and processing, and signal transduction
modulation of gene expression is mediated by promoter specific interactions and regulatory elements like transcription factors
The cell-protective and cell-destructive responses to DNA damage are downstream of a common signal transduction network that has been studied intensively in recent years. While most protein components of this signaling network have been identified, the current knowledge does not explain when and why a damaged cell will choose to die.
In other words, we have not yet elucidated the rules that govern the cell death response to DNA damage.
Biological effects of radiation
Consequence of chemical reactions initiated by energy deposition in cells and tissues
Involve DNA damage recognition, repair, and induction of signalling cascades leading to cell cycle checkpoint activation, apoptosis, and stress related responses
Nuclear factor kB (NF-kB) is activated as a part of the DNA damage response and is thought to orchestrate a cell survival pathway
Is essential for maintenance of genome stability and avoiding the passage to neoplasia
Cellular Response to radiation is complex and relies on simultaneous activation of different networks.
It involves DNA damage recognition, repair, and induction of signalling cascades leading to cell cycle checkpoint activation, apoptosis, and stress related responses.
The fate of damaged cells depends on the balance between pro-and antiapoptotic signals.
In this decisive life or death choice, the transcription factor NF-kB has emerged as a prosurvival actor in most cell types.
As corollary, it appears to be associated with tumorigenic process and resistance to therapeutic strategies as it protects cancerous cells from death.
Nuclear factor kB (NF-kB) is activated as a part of the DNA damage response and is thought to orchestrate a cell survival pathway, which, together with the activation of cell cycle checkpoints and DNA repair, allows the cells in cases of limited damage to restore a normal life cycle unharmed. 9 9

10. Radiation Effects

11. Early morbidity/mortality for worst case SPE behind 10 gm/cm2 in interplanetary space

12. How Real are Radiation Risks for Astronauts from SPEs ?
Radiation dose to astronauts from solar events during the Apollo era missions
The August 1972 event, just between Apollo 16 and 17 missions) reached doses up to 30 Gy (LD50/30 = 3.5 Gy, 50 % lethality within 30 days) 12

13. Uncertainties in Radiation Risk Projection Risk Projections
10%
Maximum Acceptable Risk
Mars ▲ 1% ▲
ISS Mission
SPE??
Lunar
0.1% ▲
95% Confidence Interval
“95% Confidence Interval”
Shuttle Mission ▲
0.01%
Individual’s Fatal Risk
Point Estimate

14. Major sources of uncertainty of risk estimation from space radiation field

15. Radiation Risk in a 550 day mission to Mars
Cucinotta (Space Radiation Risk Calculation)
45 Year old male, US Population, 20g/cm^2 shielding
Aug 72 Solar Particle event, 340 mSv
REID 0.98 % (0,23;2.59)
550 day Mission to Mars GCR ,550 mSv)
REID % (0.33;5.01)
ICRP
550 day mission
Excess Risk/Sv 4x 10^-2 results in 3.6%

16. Significance of Shielding Material for GCR (20g/cm^2 shielding, 40-yr males)

17. Light Light Flash Observations

18. Observation of Cataracts
RBE ~ 200 !!
F. A. Cucinotta et al., 2001

19. Countermeasures against radiation effects
develop proper risk criterion for exploratory LONG term missions
integrate radiation risk assessment into total risk analysis
reduce uncertainties for exposure estimates
reduce uncertainties for dose effect relations (late & early)
Improve
advance
risk assessment
optimise shielding design, include storm shelters (material & thickness )
optimise mission design
duration
timeline relative to solar activity cycle
guarantied shelter accessibility
advance forecasting capabilities for solar particle events
monitor and document exposure history and health status
Minimise
radiation
exposure
select genetically resistant individuals
modify dose response curve of ‘normal’ crew members
attenuate early effects by prior and post medication
mitigate late effects by prophylactic nutrition
Maximise
radiation
resistance

20. Radiation Assessment Detector (Cruise Measurements)
SPE Exposures
mSv
23-29 Jan
March 19.5
17-18 May
GCR Exposure/day
1.8

21. Conclusions GCR Risks SPE Risks
Stochastic effects such as cancer induction and mortality or late deterministic effects, such as cataracts or damage to the central nervous systems are of concern
Doses present no acute health effects in deep space missions
There are no data for human exposures to these radiation to estimate risks of astronauts
Usual methods of estimating risk by calculating dose equivalent or equivalent dose are questionable to be appropriate for these particles
Upper 95% C.I. for excess cancer risks from GCR for an mission to Mars may exceed current limits defined for Low Earth Orbits
During interplanetary cruise shielding is limited and will therefore not significantly reduce GCR risks
SPE Risks
Risks are manageable by shielding measures
Shielding should limit excessive exposure to prevent acute effects
Hydrocarbon shields offer a reduction of a factor of two compared to Aluminium
Exploration vehicles shielding should focus on SPE instead on GCR

22. SPARES

23. Solar corona and sudden release of a huge clouds of particles

24. Excess Relative Risk as a function of rate of exposure
Gregoire O. et.al., Radiat. Biol., 2006

25. Excess Relative Risk as function of dose rate

26. Fatal Cancer Risks near Solar Minimum (20 g/cm^2 shielding)
Slide Courtesy of F. A. Cucinotta

27. Fatal Cancer Risk Near Solar Maximum (PHI=1100MV including 1972 SEP)
Slide Courtesy F. A. Cucinotta