

Ben Harder
Particles that radiate from decaying radon atoms can ravage the living cells they strike and increase the likelihood that those cells will later become cancerous. Researchers have now directly demonstrated that neighboring cells not suffering direct hits can be harmed, too. They've also taken a step toward showing how this type of radiation, called alpha particles, indirectly hurts those bystanders.

Alpha particles struck the nuclei (blue) of some cells while missing other cells (red). Abnormalities (arrows) in unirradiated cells indicate that the DNA of these bystanders suffered indirect damage.
C. Geard/Columbia University
Radon derives from the decay of uranium and seeps naturally into the air from the ground. It's the primary environmental source of alpha particles, which contribute to cancer risk by causing aberrations in DNA. Alpha particles from inhaled radon are second only to smoking as a cause of lung cancer (SN: 3/7/98, p. 159).
Because a person's exposure to alpha particles typically is low, researchers have had to estimate public health threats from radon by extrapolating from the effects of higher doses of alpha radiation. Such data comes primarily from studies of survivors of the atomic bombs that destroyed Hiroshima and Nagasaki in Japan. The customary extrapolation, called the linear no-threshold model, assumes that cancer risk is proportional to the dose of radiation even at low doses.
According to a team of scientists led by Tom K. Hei of Columbia University, that model underestimates the risks from low-dose radiation. In the Dec. 4 Proceedings of the National Academy of Sciences, the researchers demonstrate more clearly than before that alpha particles striking and damaging the nuclei of a small fraction of the cells in a population can do enough indirect damage to nearby cells to increase cancer risk almost as much as if all the cells had been hit.
The researchers used a precision microbeam device to fire alpha particles into nuclei of human-hamster hybrid cells in petri dishes.
When the researchers irradiated all the nuclei with exactly one alpha particle each, 98 mutations of a certain gene occurred per 100,000 surviving cells. Zapping only 5 percent of the nuclei produced 57 such mutations per 100,000 cells, rather than the 5 mutations that a linear model predicts. Irradiating 20 percent of the nuclei produced more than 80 mutations, almost as many as resulted from 100 percent irradiation. Those data "suggest the need to reconsider the validity of the linear extrapolation," the researchers say.
Cell-to-cell communication channels called gap junctions appear to play a role in causing mutations in bystander cells. When the researchers bathed cells in a chemical that inhibits gap-junction communication and then irradiated the nuclei, they found fewer mutations among bystanders. Almost no bystanders were damaged in another experiment in which the cells lacked gap junctions.
"It's unequivocal that there's a bystander effect," says Eric J. Hall, the director of radiation research at Columbia, who wasn't an author on the paper. "The beauty of the microbeam technique is that you know which cells have been hit" and can observe mutations in nontargeted cells, he says. Previous studies using other techniques have found a bystander effect, but this is the first to directly demonstrate mutations, which are a cancer risk.
Philippe Duport, a radiation researcher at the University of Ottawa in Ontario, calls the study "very well designed and conducted," but sees "reasons to doubt" that risks are disproportionately high at low doses.
Radiation's effects in cell cultures don't necessarily reflect what happens in "a whole organism, with its full range of defense-repair mechanisms," says Duport. Processes such as DNA repair and cell death triggered by radiation damage could cancel the effect on bystander cells observed in the lab, he suggests.
Furthermore, while a bystander effect can contribute to cancer, other cell-to-cell interactions in living tissues "may mitigate against increased risk," says Barry D. Michael, a radiation biophysicist at the Gray Cancer Institute in Northwood, England. One of these interactions halts cell division and hence cancer. "The jury is still out on whether [cell-to-cell] effects lead to a greater or lower risk," Michael says.
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The work in this article does show nonlinearity of cell damage from alpha radiation in the dose range studied, but the lowest dose studied (5 percent of all cell nuclei hit) is probably several orders of magnitude above the mean lethal dose for any organism. The researchers need to look at linearity through the dose range where real organisms sustain survivable damage.
Charles Klabunde
Oak Ridge, TN
Over the course of a lifetime, many people receive alpha particle hits to a proportion of their cells similar to that in the study. Although many of these particles would miss nuclei, evidence suggests that they cause damage greater than that predicted by the linear model.—B. Harder
This article was biased toward the linear, no-threshold theory on radiation health effects. Especially troubling was the comment that radon is the second leading cause of lung cancer. Studies of homes in China, Japan, and the United States having radon levels up to five times the average indicate that the people in those homes have lower cancer death rates, if they are non-smokers.
Martin Healey
Cobb, WI
Zhou, H., T.K. Hei, et al. 2001. Radiation risk to low fluences of α particles may be greater than we thought. Proceedings of the National Academy of Sciences 98(Dec. 4):14410–14415. Abstract available at http://dx.doi.org/10.1073/pnas.251524798.
Helmuth, L. 1999. More than one way to mutate a cell's DNA. Science News 155(May 1):278.
Raloff, J. 1998. Radon—lung cancer risk high for smokers. Science News 153(March 7):159.
Philippe Duport
International Center for Low Dose Radiation Research
Institute of the Environment
University of Ottawa
555 King Edward Avenue
Ottawa, ON K1N 6N5
Canada
Eric J. Hall
Center for Radiological Research
Columbia University
630 West 168th Street
New York, NY 10032-3702
Barry D. Michael
Gray Cancer Institute
Mount Vernon Hospital
Northwood, Middlesex HA6 2JR
United Kingdom
From Science News, Volume 160, No. 23, December 8, 2001, p. 356.