Apollo Lunar Astronauts Show Higher Cardiovascular Disease Mortality: Possible Deep Space Radiation Effects on the Vascular Endothelium

Abstract

As multiple spacefaring nations contemplate extended manned missions to Mars and the Moon, health risks could be elevated as travel goes beyond the Earth's protective magnetosphere into the more intense deep space radiation environment. The primary purpose of this study was to determine whether mortality rates due to cardiovascular disease (CVD), cancer, accidents and all other causes of death differ in (1) astronauts who never flew orbital missions in space, (2) astronauts who flew only in low Earth orbit (LEO), and (3) Apollo lunar astronauts, the only humans to have traveled beyond Earth's magnetosphere. Results show there were no differences in CVD mortality rate between non-flight (9%) and LEO (11%) astronauts. However, the CVD mortality rate among Apollo lunar astronauts (43%) was 4-5 times higher than in non-flight and LEO astronauts. To test a possible mechanistic basis for these findings, a secondary purpose was to determine the long-term effects of simulated weightlessness and space-relevant total-body irradiation on vascular responsiveness in mice. The results demonstrate that space-relevant irradiation induces a sustained vascular endothelial cell dysfunction. Such impairment is known to lead to occlusive artery disease, and may be an important risk factor for CVD among astronauts exposed to deep space radiation.

Figure 1. The proportional mortality rate due to cardiovascular disease in the United States among individuals age 55–64 years, non-flight astronauts, astronauts that flew only low Earth orbit missions, all flight astronauts, and Apollo astronauts that flew missions to the Moon.

*Significantly different from the US population 55–64 years of age at the time of death, P ≤ 0.05. ^†Significantly different from the non-flight astronaut group, P ≤ 0.05. ^‡Significantly different from the low Earth orbit astronaut group, P ≤ 0.1.

Figure 2. Effects of hindlimb unloading (HU) and total body irradiated (TBI), individually and combined (TBI+HU) on ACh-mediated vasodilator responses in gastrocnemius muscle feed arteries.

Values are mean ± SE. n = the number of animals studied. *Denotes significant dose by group interaction between groups, P ≤ 0.05; TBI and TBI+HU group responses are different from that of control (Con).

Figure 3

Effects of HU, TBI, and TBI+HU on ACh-mediated vasodilator responses in the presence of (A) the NOS inhibitor L-NAME, and (B) L-NAME and the COX inhibitor indomethacin (Indo), in gastrocnemius muscle feed arteries. Values are mean ± SE. n = the number of animals studied. ACh-mediated vasodilator responses are not different among groups.

Figure 4. Effects of HU, TBI, and TBI+HU on Dea-NONOate-induced vasodilator responses in gastrocnemius muscle feed arteries.

Values are mean ± SE. n = the number of animals studied. Vasodilator responses are not different among groups.

Figure 5

Effects of HU, TBI and TBI+HU on xanthine oxidase (XO) protein levels in (A) gastrocnemius muscle feed arteries and (B) coronary arteries. Values are mean ± SE. *Denotes significant difference from Con group.