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Depleted uranium casts a shadow over Peace in Iraq 19 apr 03
To overcome Iraqi forces, coalition troops fired thousands of shells tipped with DU. But we still don'tfully understand its long-term health effects
WRECKED tanks and vehicles litter the Iraqi countryside. Ruined buildings dominate towns and cities. Many were blown to pieces by shells tipped with depleted uranium, a material that the US and Britain say poses no long-term health or environmental risks. But many Iraqis, and a growing band of scientists, are not so sure. Last week, the UN Environment Programme (UNEP) announced it wanted to send a scientific team into Iraq as soon as possible to examine the effects of depleted uranium (DU). People's fears that DU leaves a deadly legacy must be addressed, says UNEP. Some scientists go further. Evidence is emerging that DU affects our bodies in ways we do not fully understand, they say, and the legacy could be real. DU is both radioactive and toxic. Past studies of DU in the environment have concluded that neither of these effects poses a significant risk. But some researchers are beginning to suspect that in combination, the two effects could do significant harm. Nobody has taken a hard look at the combined effect of both, says Alexandra Miller, a radiobiologist with the Armed Forces Radiobiology Research Institute in Bethesda, Maryland. "The bottom line is it might contribute to the risk." She is not alone. The idea that chemical and radiological damage are reinforcing each other is very plausibleandgainingmomentum, says Carmel Mothersill, head of the Radiation and Environmental Science Centre at the Dublin Institute of Technology in Ireland. "The regulators don't know how to handle it. So they sweep it under the carpet." A by-product of the uranium enrichment process, DU is chemically identical to natural uranium. But most of the 235 isotope has been extracted leaving mainly the non-fissionable 238 isotope. It is used to make the tips of armour-piercing shells because it is extremely dense: 1.7 times as dense as lead.
"In 1991, an estimated 350 tonnes of DU was fired at Iraqi tanks. That figure is likely to be matched in the current conflict"
Also, unlike other heavy metals that tend to flatten, or mushroom, upon impact, DU has the ability to "self-sharpen" as material spread out by the impact ignites and bums off as the munition pierces its target. During the Gulf war in 1991, the US and Britain fired an estimated 350 tonnes of DU at Iraqi tanks, a figure likely to be matched in the course of the current conflict. In the years since then, doctors in southern Iraq have reported a marked increase in cancers and birth defects, and suspicion has grown that they were caused by DU contamination from tank battles on farmland west of Basra. As the Pentagon and the Ministry of Defence point out, this claim has not been substantiated. Iraq did not allow the World Health Organization to carry out an independent assessment. Given its low radioactivity and our current understanding of radiobiology, DU cannot trigger such health effects, the British and American governments maintain. But what if they are wrong? Though DU is 40 per cent less radioactive than natural uranium, Miller believes that its radiological and toxic effects might combine in subtle, unforeseen ways, making it more carcinogenic than thought. it's a controversial theory, but one for which Miller has increasing evidence. Uranium is "genotoxic" ' It chemically alters DNA, switching on genes that would otherwise not be expressed. The fear is that the resulting abnormally high activity in cells could be a precursor to tumour growth. But while the chemical toxicity of DU is reasonably well established, Mothersill points out that the radiological effects of DU are less clear. To gauge the risk from low-dose radiation, researchers extrapolate from tests using higher doses. But the relationship between dose and effect is not linear: at low doses radiation kills relatively fewer cells. And though that sounds like good news, it could mean that low radiation is having subtle effects that go unnoticed because cells are not dying, says Mothersill. Miller has found one way this may happen. She has discovered the first direct evidence that radiation from DU damages chromosomes within cultured cells. The chromosomes break, and the fragments reform in a way that results in abnormal joins (Milita?y Medicine, vol 167, p 120). Both the breaks and the joins are commonly found in tumour cells. More crucially, she has recently found that DU radiation increases gene activity in cultured cells at doses of DU not known to cause chemical toxicity (Molecular and CellularBiochemistry, in press). The possible consequences are made all the more uncertain because no one knows if genes switched on by DU radiation enhance the damage caused by genes switched on by DU's toxic effects, or vice versa. "I think that we assumed that we knew everything that we needed to know about uranium," says Miller. "This is something we have to consider now when we think about risk estimates." Britain's Royal Society briefly referred to these synergistic effects in its report last year on the health effects of DU munitions. "There is a possibility of damage to DNA due to the chemical effects being enhanced by the effects of the alpha-particle irradiation." But it makes no recommendations for future research to evaluate the risks.
"There is a danger that laboratory experiments not specifically looking for this erred could miss animportant source of damage"
The bystander effect
Miller points to another reason to be concerned about DU: the so-called "bystander effect". There is a growing consensus among scientists that radiation damages more than just the cells it directly hits. In tests using equipment that allows single cells to be irradiated by individual alpha particles, gene expression increases both in irradiated cells, and in neighbouring cells that have not been exposed. "At high doses, 'bystander'is not an issue because you are killing so many cells. But at low doses that's not really true," says Miller. There is a danger that experiments not specifically looking for this effect could miss an important source of damage. A body of research has also emerged over the past decade showing that the effects of radiation may not appear immediately. Damage to genes may be amplified as cells divide, so the full consequences may only appear many generations after the event that caused it. And while the chemical toxicity of DU itself is more clear-cut, the possibility remains
that there may still be some unforeseen synergistic effects at a genetic level. Other heavy metals, such as tungsten, nickel and cobalt are similarly genotoxic. When Miller and her team exposed human cells to a mixture of these metals, significantly more genes became activated than when the cells were exposed to the equivalent amount of each metal separately (Molecular and CellularBiochemistry, in press). Miller and Mothersill say that recommended safe radiation limits are often based on the idea that only irradiated cells will be affected, and ignore both the bystander effect and the possible amplification over the generations. "Nothing should be written in stone when it comes to risk assessment," agrees Michael Clark at Britain's National Radiological Protection Board. But even if there were a case for re-evaluating the dosimetry for low-dose radiation, he says we should be cautious of the significance of Miller's lab-based research. "An in vitro effect is not a health effect." Also, says Clark, everyone has traces of natural uranium in their bodies. "If there was some sort of subtle low-dose effect I think we would have seen it," he says. Because none has shown up in epidemiological studies, it seems unlikely there are any health effects associated with DU, which is less radioactive. But Miller is not convinced. While most people have small amounts of uranium in their bodies, she says no studies have been done to see whether this contributes to cases of cancer in society at large. The military tends to dismiss such hazards as being of only theoretical significance, at least when it comes to civilians. According to the Pentagon, the only risk of exposure is during combat, when DU shells hit hard targets and the metal ignites. This creates clouds of uranium oxide dust that can be breathed in. But heavy oxide particles quickly settle, it says, limiting the risk of exposure. "A small dust particle is still very heavy," says Michael Kilpatrick of the US Deployment Health Support Directorate. "It stays on the ground." That sounds reassuring until you read UNEP's latest report on DU left over from conflicts in former Yugoslavia in the mid-iggos. Last month, a team of experts collaborating with the International Atomic Energy Agency, WHO and NATO concluded that DU poses little risk in Bosnia although it can still be detected at many sites. just 11 tonnes was fired in that conflict. But evidence that DU may be moving through the ground and could contaminate local water supplies should be investigated further, UNEP says. And on rare occasions, wind or human activity may raise DU-laden dust that local people could inhale. The Royal Society admits that localised areas of DU contamination pose a risk, particularly to young children, and should be cleared up as a priority. They also recommend the environmental sampling of affected areas (see "Royal Society Reports on DU, 2002", below). Such evidence is partly why UNEP is keen to study DU flred during the present conflict in Iraq. Assessments in former Yugoslavia were made up to seven years after DU weapons were used, UNEP admits, and a more immediate study in Iraq would give us a much better understanding of how DU behaves in the environment. Any hazards such a study identifies could be dealt with immediately, says UNEP. And even now, an investigation in Iraq could reveal risks remaining from DU fired during the Gulf war in 1991.
Veterans show ill effects
Cracks are also appearing in the argument that DU munitions have not proven harmful even to troops. In the 1991 war, more than 100 coalition troops were exposed to DU after being accidentally fired on by their own forces. The majority inhaled uranium oxide, while the rest suffered shrapnel injuries. Some still have DU in their bodies. Britain and America point out that none has developed cancers or kidney problems, as might have been expected if DU posed a long-term danger. But researchers at the Bremen Institute for Prevention Research, Social Medicine and Epidemiology in Germany have found that all is not well with the veterans. Last month they published results from tests in which they took blood samples from 16 of the soldiers, and counted the number of chromosomes in which broken strands of DNA had been incorrectly repaired. In veterans, these abnormalities occurred at five times the rate as in a control group Of 4o healthy volunteers (Radiation Protection Dosimetry, vol 103, p 211). "Increased chromosomal aberrations are associated with an increased incidence of cancers," says team member Heike Schr6der. The damage occurred, they say, because the soldiers inhaled DU particles in battle. The NRPB is unconvinced. "It is possible that exposure to significant amounts of DU could cause excess chromosome aberrations, but this study has technical flaws," says Clark. "There are no proper controls to compare results with soldiers who were not exposed to DU. And some of the reported excess aberrations are well known to be linked to chemicals rather than radiation."
"An immediate study in Iraq would give us a much better understanding of how DU behaves in the environment"
Tough decision to make Deciding whether DU is to blame will be tough. Independent research may confirm that rates of cancer have increased in the Iraqi population. But the Iraqi government has used chemical weapons on its own people that can produce the same outcome, and it is impossible to know for sure who may have been exposed. Soldiers may similarly have been exposed to chemicals in iggi. The only way to resolve the issue is more research, says Dudley Goodhead, director of Britain's Medical Research Council's Radiation and Genome Stability Unit at Harwell, near Oxford."Ijtls something important that needs to be explained." Miller admits it is entirely possible that DU contamination is safe. But many of the scientific investigations into DU have only just begun, and their results will be long coming."None of this has been looked at or even thought about it until the last few years," she says. As the dust begins to settle in Iraq, it remains to be seen when the ravages of war will end. Additional reporting by Rob Edwards 0
Slow farewell twixt man and ape
HUMANS and chimpanzees did not gradually evolve into different species by living geographically apart, as textbooks suggest. Our isolation from chimps occurred within our own chromosomes, not across the plains of Africa, says a team who compared human and chimp DNA. The study gives rise to the theory that the chromosomes of our common ancestors became accidentally rearranged during reproduction, and this gradually led to genetic "no-go" zones between protohumans and proto-chimps. The two could still mate, and swap genes between compatible parts of their chromosomes, but any mutations within non-compatible regions that conferred an evolutionary advantage would have been retained for good by each lineage. "It became utterly impossible to swap genes between those zones, so they became areas where you had increasingly separated gene pools," says Arcadi Navarro of the Pompeu Fabra University in Barcelona, who co-analysed the DNA with Nick Barton of the University of Edinburgh. The implications are huge. First, it means the parting of the ways between human and chimp was much more gradual than previously believed. Instead of the sharp division brought about by geographic separation, common ancestors destined to become either chimps or humans were able to interbreed with each other until their chromosomes were no longer compatible. Secondly, and more controversially, it means that the common ancestors of both species gradually diverged from one another despite sharing the same habitat and territory. "It might explain discrepancies in anthropological data about the time and location of divergence," says Christophe Soligo of the human origins research group at the Natural History Museum in London. "It implies there was a longer period of hybridisation than thought."
Humans have lo chromosomes that have undergone different rearrangements to those of chimps In 9 of these there are pericentric inversions - essentially a swapping of two large pieces of the chromosome around the centromere. The loth was created by the fusion of two smaller chromosomes, which remain separate in chimps (see Graphic). Navarro and Barton compared DNA from 115 genes, half of which sit on regions of the chromosomes useful mutations can be retained and evolve, backing the hunch that this is the genetic engine driving development of separate species (Science, VOI 300, P 321). "They are probably the genes that made the two species incompatible, producing traits that eventually stopped them choosing each other as mates," says Navarro. Other researchers have tried unsuccessfully to implicate chromosomal isolation as the driving force for the development of different species. Their ideas foundered, says Navarro, because chromosomal rearrangements were thought to either be lethal to the recipient, or to render them infertile. However, experiments in fruit flies and sunflowers over the past decade have shown organisms can survive with rearranged chromosomes, which are then passed down the generations. The divergence eventually prevents the exchange of genes and they become separate species. "For the first time it provides a plausible explanation for how speciation might have taken place without geographical or ecological separation," says Soligo.
that are rearranged differently in humans and chimps, and half on "colinear" chromosomal regions common to the two species. Although gene mutations occur at the same rate in both ordinary and rearranged chromosomes, the researchers found that mutations accumulated twice as often in the rearranged segments. In essence, they are a refuge within which
Worms and Ageing
"AT ITS most extreme, we were accused of fraud," recalls biologist Tom Johnson. Fifteen years ago, he and colleague David Friedman, both then at the University of California, Irvine, announced a result that contradicted everything biologists thought they knew about ageing and lifespan. They showed that a change in a single gene was responsible for making nematode worms live up to 65 per cent longer than normal. The finding was greeted with intense scepticism. Critics were vehement: a creature's lifespan couldn't possibly be manipulated so easily because ageing was not controlled by genes. Rather, it was simply a product of random, uncontrolled degeneration. To suggest otherwise was to imply that evolutionary theorists were completely wrong in what they believed about ageing. But since then, critics have had to eat their words as a growing body of results threatens to demolish long-standing theories of how and why we age. Scientists have come to accept that simple organisms such as flies and worms possess a simple switch that dictates lifespan. Some are even convinced that this switch works through a handful of molecular signals that affect the rate of ageing. In January this year came an even more surprising result. French researchers revealed that mammals possess a similar switch. They unveiled a single-gene mutation that extends longevity in mice via a molecular pathway similar to the one in the worm. This surprise finding is being hailed as powerful evidence that all animals have a genetic switch that can alter normal lifespan. The idea that lifespan has an inbuilt, genetically controlled flexibility has sparked a spirited debate. Some researchers believe such results fit nicely with existing theories of how and why we age but others argue it will force a major rethink. "It's quite clear that this pathway is regulating the rate of ageing," says Cynthia Kenyon, a geneticist at the University of California, San Francisco, and one of the leaders in the study of the genetics of ageing. What's more, she adds, human intervention could alter this pathway.
The main bone of contention is that if genes do control the rate of ageing, they must have somehow evolved for this purpose by natural selection. And for decades, evolutionary biologists were convinced that genes specifically for ageing couldn't have evolved, because the process starts after an organism has successfully reproduced and should therefore lie beyond the reach of natural selection. Leonard Hayflick, a gerontologist at the University of California, San Francisco - famous for his discovery that human cells cannot divide indefinitely - is firmly in this camp. Last year, he released a letter signed by 51 scientists warning the public against the notion of an ageing program that could be manipulated. "Ageing is not, as some might think, a genetically programmed process, playing itself out on a rigidly predetermined schedule," wrote Hayflick and his co-authors. "The way evolution works makes it impossible for us to possess genes that are speciflcauy designed to cause physiological decline with age, or to control how long we live.' The idea that ageing and death are evolved traits was first mooted after Darwin outlined his theory of evolution in 1859. Alfred Russel Wallace, who came up with the idea of natural selection at around the same time, suggested that individuals are programmed to die so as not to compete with their offspring, an argument expanded by influential German biologist August Weismann. But students of evolution later concluded this made little sense. For one thing, animals consistently live much longer in captivity. How could they have evolved a genetic program that never gets used in the wild? Secondly, if a death program did exist, selection would likely favour individuals who acquired genetic mutations that allowed them to escape that program, live longer and so have the chance of producing more offspring. By the time of his death in 1914, Weismann had largely changed his mind. In the 1920S, programmed ageing was dismissed as a "perverse extension of the theory of natural selection". Current explanations for why ageing occurs first emerged in the late 1940s when Peter Medawar began formulating his "mutation accumulation" theory. According to Medawar, genes that have a negative impact on health only late in life will tend to accumulate in the genome due to the absence of selective pressure to remove them. Take Huntington's disease, for example. This genetic disorder is deadly, but since its effects usually only begin to occur when carriers are in their 30s or 40s, the gene has already been passed on to the next generation. In 1957 noted American evolutionary biologist George Williams added a twist to this theory. According to Williams, ageing results from natural selection favouring mutations that bestow advantage to an individual early in life - regardless of the negative effects these same genes may have after reproduction is over. For example, Williams suggested that selection would favour a gene that helped calcify bones to make them stronger early in life, even if it meant calcification in arteries later on in life.
Balancing act In the late 1970s, gerontologist Tom Kirkwood, now at the University of Newcastle upon Tyne, built on Williams's notion that ageing is the result of a trade-off. According to Kirkwood, an organism has only a limited budget of energy to divide between reproduction and maintaining its own tissues. The result is a trade-off, with the organism diverting energy to reproduction and neglecting maintenance, resulting in ageing. The extent and pattem of this energy diversion will be dictated by a species'ecological circumstances. Mice, for example, live in harsh conditions and are the favourite meal of many a predator. Their need to invest in early and frequent reproduction helps explain their short lifespan. By the ig8os, as the revolution in molecular biology was helping researchers unravel the genetic pathways underlying complex processes such as embryonic development and growth, gerontologists were being told not to bother. Johnson's discovery that a single gene named age-1 altered the longevity of worms was not only doubted, it was downright ignored. But then, in 1993, Kenyon described a second longevity gene in worms, daf-2. This finding turned heads, partly because daf-2 had an even more dramatic impact on lifespan than age-1 - mutant worms lived on average twice as long as normal - and partly because the gene was known to be involved in sending worms into a weird physiological state called a dauer larva. Prior to adulthood, juvenile worms can enter this state in response to starvation. They stop growing and developing, and store extra fat and seal themselves up at both ends. This delay in their development can extend their normal two-week lifespan by months. Kenyon found that by altering the expression of daf-2 just a little, worms lived longer without becoming dauers. This raised the possibility that the extended lifespan was independent of the other changes associated with the dauer state. This finding took on greater significance in 1997 when scientists at Harvard Medical School in Boston cloned daf-2 and discovered that it codes for a worm version of the human insulin receptor, a molecule used for transporting insulin into cells that is key to regulating energy metabolism. For longevity researchers, this was an intriguing development. Since the 193os researchers have known that lab animals will live much longer when their calorie intake is restricted - 50 per cent longer in the case of rats. The same has been seen in species ranging from yeast to dogs. The parallels between long-lived daf-2 worm mutants and calorie- restricted animals suggested that Kenyon had found part of a molecular pathway that affects lifespan in most, if not all, animals. These discoveries in worms were followed by others showing that alterations to genes with similar functions in yeast and fruit flies also extended lifespan. January's big news, from a research team led by Yves Le Bouc at the Institute of Health and Medical Research in Paris, came from experiments on mice in which another insulin-related signalling pathway had been disabled. In this instance it was the insulin-like growth factor-1 (IGF-1) pathway, which regulates many functions including energy metabolism. In the mouse experiments, knocking out the pathwayextended average longevity bY 33 per cent in females and 16 per cent in males. It looked as though insulin-related pathways were involved in ageing in a mammals, too. "This finding is the most definitive evidence yet that this really is an evolutionarily conserved pathway," says Johnson.
"The long-lived mice provide the most definitive evidence yet thatthesegenes have been conserved throughout evolution"
Assuming that this system exists in most animals, how might it work? How could just a few genes affect the duration of life? The mutant animals created by researchers such as Kenyon seem to be more resistant to cellular damage, and accumulated damage is believed to be the main cause of ageing. Numerous studies show that virtually every one of these long-lived animals is better at avoiding the kind of cellular damage normally caused by exposure to chemicals, extreme temperature and UV radiation. Could these signalling pathways damp down the activity of cellular repair machinery, and so promote ageing? Evidence to support this idea comes from the finding that worms with a mutant daf-2 gene lose their life-extension if they also lack parts of their damage repair machinery. Cells have a range of proteins and molecules that protect them from damage - such as the antioxidant enzyme superoxide dismutase They also come equipped with repair mechanisms to undo damage after the fact (New Scientist, 15 March, P 40). WOrms without daf-2 will lose their extra longevity if they are also missing daf-16, a gene needed for the production of two key enzymes that prevent cell damage - cytosolic catalase and manganese superoxide dismutase. But how does the dof-2 pathway actually work? At the moment it's not clear, but there are some clues. From investigations done in Kenyon's lab and elsewhere it appears, in worms at least, to involve neurons releasing insulin-like hormones. These trigger the release of a second hormone that travels to cells throughout the body. No one knows what this hormone does, but researchers speculate that it somehow acts as a general inhibitor of the damage limitation and repair systems.
Slowly does lt
For Kenyon, this all adds up to one thing: animals lacking genes such as daf-2 live longer because they age more slowly. But Hayflick and others disagree. They say there is at least one other feasible explanation. What if longevity is being increased because such gene mutations make individuals more resistant to one particular cause of death - say heart disease?
To address this question, researchers are now attempting to deftne and measure ageing in worms at the cellular level, so they can see if the process is actually slower in long-lived mutants. In one recent set of experiments, Delia Garigan, working with Kenyon, identified several age-related changes in worm cells. These included a gradual blurring of the boundary ofthe cell nucleus and a change in the texture of cytoplasm from smooth to curdled. Garigan also noted a correlation between these changes and the loss of mobility that also strikes aged worms. Next, Garigan looked at cells from daf-2 mutant worms and saw a delay in the signs of ageing. Nuclear boundaries for instance, remained visible for approximately 2o days, whereas in normal worms they disappeared after only five days.
The researchers who accept that a single genetic pathway can affect ageing, are now arguing over whether such a process evolved specifically to cause ageing. Those who think it did not argue that the ageing pathway is compatible with existing evolutionary theories that see ageing as the price paid for successful reproduction. According to this idea, animals faced with food shortages undergo changes that include storing more fat, delayed reproduction and a ramping up of the mechanisms that maintain, repair and protect cells from molecular damage. Proponents of this view see delayed reproduction as the primary effect of the survival mechanism, and added longevity as a secondary effect. Evidence for this view comes from experiments showing that when large numbers of flies are selectively bred to lay eggs when young, their lifespans shorten over the generations, while those bred to lay eggs when they are older live longer. What's more, the price of the trade-off is evident in the extreme side-effects experienced by most long-lived mutant organisms. These range from complete or partial disruption in fertility, to dwarfism. "I really don't believe there is a set of genes that are designed to make you age," says Monica Driscoll, a geneticist at Rutgers University in Piscataway, New jersey. "There are certain genes that contribute to how you age. But the idea of a program analogous to what you have for development is probably not right.' But another recent set of experiments from Kenyon's lab seems to support the idea that this genetic pathway evolved, at least partly, to promote ageing. Andrew Dillin turned down daf-2 activity in normal worms until they reached young adulthood, when he returned it to normal.
"I'm startingto like the idea that it s ops animals from competing with their young'
He discovered that these animals experienced the same reduced fertility as in daf-2 mutants, but failed to live longer. But when he disrupted dof-2 after the normal worms reached adulthood, the animals lived as long as daf-2 mutants but without the accompanying reduction in fertility. This suggests that the daf-2 signalling pathway's control over longevity is separate from its effect on reproduction. Kenyon thinks this points to a separate genetically determined ageing program. Perhaps Wallace was right after all. "Why does daf-2 remain active during adulthood, if the only apparent effect of its action is to speed up ageing?" says Kenyon. "I'm starting to like the idea that it prevents animals from competing with their young.' There is also growing doubt over whether a trade-off is always a necessary condition of added longevity. The long-lived IGF-I n-dce seemed normal in almost every way: normal body temperature, normal circadian rhythms, normal metabolism, normal litter sizes, normal number of pregnancies, normal onset of infertility. The only difference was a slight reduction in size. In females, this size reduction was eight per cent, not a bad swap for a lifespan extended by a third.
While this debate remains up in the air, there are researchers from both sides who are now prepared to say it's wrong to view ageing as a process that can't be altered. The powerful effects that genes appear to have on the body's ability to withstand the ravages of time, whether or not they actually evolved for that purpose, suggest that a fountain of youth may be out there after all. The trick is to find it.
Garry Hamifton is a freelance science writer living in Seattle, Washington
Asteroids - are we doing Enough?
We are monitoring the skies for asteroids on a collision course with Earth,and the public isbeginning to realise the devastation an impacy could cause. But is this enough?In thefollowing pages we look at the latest predictions of what mighthappen if disaster strucl(, and what could be done to avert an impact if we saw it coming. Butfirst,ErikAsphaug, an expertin modellingplanetary collisions,tal(esa critical look at theprecautionsalready in place, andconcludes that it'stime to stop playing around.
SOMETIME in the next lo,ooo years an enormous rock will crash into an ocean, and loo-metre waves will radiate out to flood coastal cities and distant lowlands. The human toll could be tens of millions of lives, and the economic loss could be measured in trillions of dollars. I am talking about the impending collapse of Cumbre Vieja, the unstable southem flank of the island of La Palma, part of the Canaries in the western Atlantic. The geological record shows that collapses of this magnitude occur about every 2o,ooo years, whereas asteroids or comets large enough to produce comparable waves strike Earth only a fifth as often. Indeed, the impact of a near-Earth object, or NEO - an asteroid or comet whose orbit comes close to Earth - represents just one of several low-probability, high-consequence calamities that can befall humankind. Topping the list may be warfare, plague and ecological collapse triggered by human disregard. So why, if these other threats are greater, should we care about hazardous NEOS? Beyond their broad and novel appeal to space buffs and doomsayers alike, there are rational motives for designing strategies to deal with hazardous comets and asteroids. Quite unlike any other natural disaster, the NEO risk can be reduced almost to zero through achievable, feasible means. Indeed, the most dangerous NEOs could even benefit mankind. If we could move them to safe nearby orbits, they would be readily accessible outposts for human exploration and exploitation, science fiction made real. We cannot do much about volcanoes or earthquakes other than identify active regions and tell people not to build there. But cataclysmic asteroids are predictable: given sufficient lead time and a precisely determined trajectory, a tiny diversion applied decades in advance can change the future. Isaac Newton, inventor of the clockwork heavens, knew of gravitational perturbation, and argued that God had to occasionally nudge the orbits of comets to prevent them from eventually colliding with Earth. Perhaps it is our role to keep the wayward comets and asteroids on track. Today, of the $4 million spent annually on investigating NEOS, almost all goes towards detection and orbit prediction. The process of asteroid detection has far outpaced the scientific understanding of what asteroids are, and what we can do about them. This is partly because no govemment agency deals with hazardous NEOs in any direct way, other than counting them and cataloguing their orbits. It is easy to list the national and worldwide agencies that deal with volcanic eruptions, earthquakes, tsunamis, disease, famine and warfare. Indeed, many agencies exist solely to deal with a particular hazard. But while many (including Hollywood) assume that NASA is in charge of NEO defence, NASA has no such mandate. Neither does the US Air Force or any other agency. NEOs fall into the cracks: they are a hazard without a home. NASA and space agencies in Europe and japan do, however, play a leading role in ftindamental exploration of asteroids and comets. We now know that they are surprisingly complex entities. Indeed, we have figured out that we wouldn't know how to divert one even if some agency were in cha@ge. Until recently, the favoured NEO diversion scenario was a blast from a nuclear explosion (see page 38). But new data have shown that many asteroids are not solid rocks but loosely connected multi-component objects - rubble piles, in fact. This makes them very hard to disrupt or move predictably by impulsive force. By doing no more than detecting asteroids, or treating them as geophysical curiosities, we are generating increasing concem without following through with a plan. Because of uncertainties in measuring their orbits, asteroids that have a finite initial chance of hitting Earth sometime down the road are frequently discovered. Collision is almost always ruled out by follow-up observations, but not before we read in the moming paper that we all are doomed. The painful irony is that these detection programmes should be making the public feel tangibly safer. Thanks to ceaseless efforts at a handful of small observatories, half of the kilometre-sized NEOs have been logged, and none is on a collision course with Earth: we can feel twice as safe as we did. With sufficient effort in the form of larger telescopes, and significant funds for observations and follow-up research, we could soon have nearly all the hazardous rocks in the heavens tracked in a celestial version of air traffic control. Most likely (a thousand to one) this survey, when completed, would signal the all-clear for any object larger than 300 metres across headed for a collision within a century. But if we are gravely unlucky and we find something large is headed our way, we would want to do better than finding the biggest rocket available and strapping on the biggest nuclear warhead it could carry. This may not work, and it's a scenario appropriate only to an unprepared civilisation scrambling for a last- minute solution. The purpose of a detection effort is hopefully to signal the all-clear, and failing that, to buy us the long lead time required to engineer a reliable and cost-effective deflection strategy. It must be accompanied by a growing understanding of how to apply a small diversion to an asteroid. It is not going to be easy, unless you compare it with other space-related endeavours such as visiting the Moon. The basic research requires ambitious spacecraft missions to determine detailed geological characteristics for a wide range of comets and asteroids. This will not come cheap, unless you measure it in military metrics. For the cost of a single B2 bomber, we could launch a major NEO geophysical reconnaissance mission (at about $300 minion per mission) every five years for the next 30 years. This would take us from this place of ignorance to one where clear decisions can be made - and where a future human presence in near-Earth space is all but certain. We cannot afford spacecraft exploration ff it means diminished asteroid surveillance. But we are clearly at the stage where surveillance alone will not do. With surveillance comes the public expectation that we have a plan for Teaming more about hazardous NEOS, including how to divert one. But we are scrambling for a plan, for funding, and for an agency to take on this difficult charge.
Erik Asphaug is associate professor of earth silences at the University of Califbmia, Santa Cruz
THANKS to Hollywood, we already know what to do if an asteroid big enough to wipe out life on Earth is spotted coming our way. Haul out our surplus nuclear weapons and get Bruce Winis on the phone.
But there's a catch. In the past year, asteroid researchers have been warning that it would be a big mistake to rely on nuclear bombs to save the planet. Nuking a killer asteroid as it approaches could be the worst thing our superhero could do, even compared with doing nothing. In February, asteroid researchers submitted a report to NASA headquarters in Washington DC calling for more research into deflection technologies that are a far cry from the "all guns blazing" approach. If they have their way, our toolbox for saving the planet will include ways of gently coaxing the killer into a safe orbit, either by slowing its irregular spin, by giving it a whitewash or even by parcelling it up in wrapping paper. At first glance, blowing a killer asteroid to smithereens seems like a good idea. Asteroids a kilometre across - the size that threaten the future of our civilisation - should be no match for a io-megaton nuclear bomb, among the largest in current arsenals. Push the red button with several months to spare and the debris should disperse in time. "You get one hell of a meteor display on the night that was previously going to be Armageddon," says Alan Harris, an asteroid researcher who retired last year from NASA's Jet Propulsion Laboratory in Pasadena, California. But as fans of the movie Armageddon know, simply firing a warhead at the asteroid and exploding it on the surface won't destroy it. Our heroes will need to land on the rock and bury the bomb at least ioo metres deep. This is bound to be a high-risk strategy, however, because getting the depth and digging technique right for an unknown material will be fraught with difficulty. Get it wrong and you risk creating a blast of chunky shrapnel that wfll spread more devastation across the planet than a localised collision. These concems have led researchers to consider using a nuke to deflect rather than destroy an asteroid. Deflection depends on transferring lots of sideways momentum, rather than explosive energy, to the asteroid. Detonating a bomb on the surface will only vaporise a small portion of the asteroid, but detonating a nuclear bomb well above the surface - about 200 metres for a i-kilometre asteroid - will vaporise a greater mass. As the mass is blown off the surface, the rest of the asteroid will gain an equal amount of momentum in the opposite direction. A bomb with a kick ofbetween loo kilotons and i megaton, detonated 200 metres above the surface of a solid asteroid a kilometre across, should vaporise the top 20 centimetres- This would be enough to give it a sideways shove that would change its velocity in this direction by about io centimetres per second. That would ensure a miss, given seven years'notice.
Unfortunately, this now also looks tricky. In 2002, a series of optical and radar images taken from Earth and from probes overthrew a key assumption underpinning these calculations. Instead of being solid rocks, most asteroids are porous piles of rubble barely hanging together in space. As many as one in six known asteroids is not even doing that. They are binaries - two rubble piles orbiting each other.
This disturbing discovery led Keith Holsapple of the University of Washington in Seattle to study the effect of nuclear nudges on porous rubble piles. "A very porous material is very effective at absorbing energy," Holsapple says. Push hard on a rock and it moves; push hard on a porous material and it crushes like polystyrene packing material. Holsapple cakulates that a megaton nuclear blast 200 metres away would push a 1-kilometre rubble- pile asteroid only a thousandth as effectively as it would a solid body. So to deflect a i-kilometre asteroid you'd need a 1-megaton blast up close, says Holsapple. To deflect a lo-kilometre asteroid like the one that saw off the dinosaurs, you'd need a 1-gigaton bomb - a hundred times more powerful than any ever tested. Holsapple's work has prompted a change in tactics. At NASA's Workshop on Asteroid Mitigation last September, no one was talking about nukes. Instead, the motto behind many of the ideas was "softly- softly". Several researchers proposed using engines that would thrust gently for a long time, rather than explosively. Former astronaut Rusty Schweickert talked about landing an ion rocket engine on the asteroid and using it to shunt the asteroid gradually to the side. Such engines use solar energy or a small nuclear reactor to heat propellant slowly and eject it continuously, producing a thrust so gentle that the object's delicate structure should not matter. Schweickert is chairman of the B612 Foundation (named after the home planet of the Little Prince in Antoine de Saint-Exup6ry's book of the same name). The private group, based in Houston, hopes to persuade a consortium of NASA and private funders to let them try changing the orbit of a loo-metre rubbly asteroid by 2015. As well as designing the propulsion system, the group is planning the delicate space operations needed to pick a landing site, dock there and begin to push the asteroid. "You don't have to use a lot of fuel, but you have to use a lot of brains," says Schweickert. Asteroids typically spin on their axis as well as orbiting the Sun. So to push an asteroid in one direction rather than simply increasing or decreasing its spin, an engine on the surface could fire only once per rotation. Instead Schweickert says the engine will land on the equator, line up with the asteroid's spin, then fire in the opposite direction. With an asteroid completing one rotation in a few hours, an ion engine should take several months to a year to stop it spinning. The engine can then swivel through go' and push the asteroid continuously in one particular direction. But the asteroid's rotation may not be known precisely, so researcher lay Melosh of the University of Arizona favours an altemative approach. He suggests using a "solar concentrator" - a giant parabolic mirror - to focus sunlight onto the asteroid's surface. As the asteroid spins, the light and heat should evaporate material from whatever part of the surface happens to fall in the focal spot. As long as the light is shone at a constant angle to the surface, the gradual momentum gain by evaporating material will move the asteroid gently in the opposite direction. To steady the mirror's position against the force of the solar wind, which would be significant on a large mirror, a low-thrust rocket engine - similar to those being developed by the B612 Foundation - would be needed. Jim Pawlowski, a specialist in asteroids and orbital debris who has just retired from NASA's Johnson Space Center in Houston, estimates that a 32-metre mirror would take lo years to deflect a typical i-kilometre near-Earth asteroid from its destructive course.
Ideally, researchers would prefer a scheme that, like a nuclear explosion, only required a one-off intervention, but that moved the asteroid very gently over a long time. One idea is to change how much light the asteroid reflects in order to change its orbit.
The orbits of asteroids aren't just determined by the gravitational forces in the Solar System; other effects also play a part. The @unlit side of a dark asteroid continuously absorbs light energy from the Sun. The momentum ofthe solar photons is transferred to the asteroid, altering its orbit continuously by an amount that
depends on how well it absorbs the light. There is also a second, less obvious phenomenon. As the asteroid rotates, the "Yarkovsky effect" comes into play. Several hours after having the Sun directly overhead, the surface re-emits absorbed energy in the infrared. The asteroid effectively donates some momentum to the infrared photons, and recoils, altering its orbit. This sets the stage for a big idea. Most asteroids are so dark they absorb all but a few per cent of the incident light, but if they were coated with something shiny or white, the light would bounce off instead. If the energy is not absorbed, it cannot be emitted later. So a whitewash would all but remove the Yarkovsky effect on the asteroid's orbit. In the absence of the effect, a typical killer near-Earth asteroid will be deflected by a few millimetres per second from the path it would have taken. Over a couple of centuries, that would be enough for it to miss the Earth. But how could we possibly hope to change an asteroid's surface properties? Compared to timing a nuke or training a solar concentrator, it is relatively easy, says Jon Giorgini of the jet Propulsion Laboratory. Splatting the surface with white paint could do it, but the quantity needed would be heavy and expensive to transport to the asteroid's orbit. More likely, reflective glass beads or a white powder, such as chalk dust, would be fired into the asteroid's gravitational field. Because the field is so irregular, the particles would bounce to ground over a variety of different trajectories, eventually covering the entire surface. But to make the covering really even, Giorgini favours a solar sail. If a giant piece of reflective material were unfolded in the path of the asteroid, it could be made to envelop it, covering the whole thing like a giant birthday present. "It's technology we could do now," says Giorgini, although it will take centuries to work. Not everyone is convinced by the potential for the Yarkovsky effect to save the planet. "Exactly how efficient it is remains to be learned," says Mike Belton, co-organiser of the NASA workshop and head of Belton Space Exploration Initiatives in Tucson, Arizona. Part of the problem is that the Yarkovsky effect is smaller than the uncertainties in many asteroid's orbits. This means that even if researchers think a rock is on course for us, they may not know whether changing the Yarkovsky effect on it would be enough. Even proponents of prospective schemes agree that developing them into a real toolbox of alternatives could take decades. And there's no time to lose. Although none of the currently known 48o or so near-Earth asteroids over 1 kilometre in size is classed as hazardous, imprecision in measuring their orbits makes it impossible to predict this more than a century into the future. One exception is asteroid 195oDA, which orbits unusually far from other perturbing objects and in such a way that the gravitational effect of the Earth on it varies in a simple, regular way, a phenomenon known as a resonance. If 195oDA is spinning in one particular direction - and we don't actually know how it is spinning - there is a i in 300 chance it will hit the Earth on 16 March 288o. If it spins the other way, the Yarkovsky effect on it will be different and it is sure to miss. As surveys continue, they are likely to tum up other relatively high-risk candidates for astronomers to keep an eye on. But if all goes according to plan, by the time we find our first killer asteroid we will be ready with a shiny coat to send it on its way. Saving humanity with baking foil may not seem as daring as blasting the asteroid to kingdom come, but if it works, not even Hollywood will complain.