Putting everything together—a two-stranded helix, paired nucleobases, and the phosphate backbones on the outside—the unmistakable conclusion was that the two strands of nucleobases were somehow physically joined with each other interiorly in a conformation that would allow their phosphate studded backbones to spiral around each other in an endlessly repeating pattern reminiscent of a barber pole. After several days of playing with the sheet-metal nucleotide models back at the Cavendish, they settled on the only possible structural conformation that accounted for all the data. They called their final DNA structure the “B-form” of a double helix, as opposed to an alternative “A-form” that they had first considered but ultimately abandoned. They rejected the A-form because the DNA needed to be dehydrated for it to occur, and this wasn’t consistent with the fact that the DNA in cells is surrounded by water molecules. The A-form was, therefore, unlikely to be the correct structure for DNA in its native state. But they also disliked the A-form because it wasn’t “pretty.”
Something beyond physical beauty, however, spoke to the validity of Watson’s and Crick’s DNA structure; this was its functional simplicity. As every geneticist well knew, genes are replicated during cellular reproduction. The relative complexity of proteins, the very feature that allegedly made them likely harbingers of complex genetic information, was also seen as an obstacle to their easy replication. In contrast, just as form is said to follow function, the nucleobase pairing that was critical to holding the two strands of Watson’s and Crick’s double helix together, also formed templates with all the information needed to replicate one strand etched within the other. In other words, the two strands were not identical to each other, but instead were complementary. Just as a handprint in the sand is complementary to the palm that produced it, one strand of the DNA was complementary to the other. And just as a palm reader uses the lines on a person’s palm to read his fortune, the lines in the palm print should be equally informative in revealing that fortune.
In short, Watson’s and Crick’s double helical structure accounted for all the data, was physically beautiful, and functionally simple. How could it not be true? Higher quality x-ray photographs subsequently generated by various laboratories showed that the Watson-Crick structural model of DNA was absolutely correct, and that it was, in fact, very pretty.
Watson and Crick had kept most of their DNA activity out of the view of Willie, who thought the two had been working on protein structures. The duo misled Willie partly because they feared that the more people who knew what they were doing, the more likely information would leak out to Pauling or other competitors. They also knew that Willie disapproved of the Cavendish scientists infringing upon the research territory of Wilkins’s group at Kings College. Nevertheless, Watson and Crick, unlike Pauling, did not have the clout to rush their discovery to press. They needed Willie to get the attention of the editors at Nature (one of the world’s premier scientific journals) in order to publish their paper before Pauling. By virtue of his lofty scientific reputation, Pauling would certainly enjoy expedited publishing once he had realized his earlier error about the phosphate charges and corrected his mistake.
Willie found Watson and Crick’s findings sound and agreed to write a cover letter highlighting the importance of the manuscript they were submitting to the editors of Nature. Actually, it was hardly a manuscript, as it was only one printed page in length and included no data. Nevertheless, that one simple page contained all the important information. Pauling would certainly read it and weep, having come so close himself. In what was likely one of the rare understatements of Watson’s scientific career, the paper coyly concludes, “It has not escaped our notice that the specific pairing [of nucleotides] we have postulated immediately suggests a possible copying mechanism for the genetic material.”40
Encouraged by Willie to write a popular book about finding the structure of DNA so that the public could share in the excitement of scientific discovery, Watson set to the task. But the product, slated to be published by Harvard University Press and entitled Lucky Jim, was panned by many, including both Crick and Wilkins. As Watson’s colaureates for the Nobel Prize, they found the book to be both inaccurate and offensive to just about everyone other than its author.41 Crick told Watson that the book showed “such a naïve and egotistical view of the subject as to be scarcely credible,” and that his “view of history is that found in the lower class of women’s magazines.”42 The book was particularly insulting to Rosiland Franklin, who had been treated shabbily by Watson while alive, and who had since died of cancer.43 Harvard cancelled the publication. In response to the firestorm, Watson softened the prose, and the book was ultimately published as The Double Helix by Athenaeum Press, with a foreword written by Willie. Indeed, Watson himself believed that the book would never have been published at all had Willie not endorsed it by providing a foreword.44 Many scientists were appalled that Willie would lend his prestige to the book. Even Pauling, who had always had a good professional relationship with Willie, couldn’t understand his tolerance of Watson’s malicious grandstanding. Willie’s wife, Alice, was livid that Watson had described her husband as a “curiosity out of the past” who was “completely in the dark about what the initials DNA stood for” and got “more pleasure … showing his ingenious motion-picture film of how soap bubbles bump each other.”45 She strongly argued against Willie providing a foreword for a book that showed him such disrespect. But Willie, accustomed to abuse from upstarts, took a philosophical stance. He said the book was just “a record of [Watson’s] impressions rather than historical facts,” and explained that “the issues were often more complex … than he [Watson] realized at the time.” To other scientists who felt that they had been wronged by Watson, he consoled, “One must remember that his book is not a history, but an autobiographical contribution to a history which will someday be written.”46
It’s said that all publicity is good publicity. Perhaps this partly explains Willie’s tolerance of Watson’s unflattering book. Or maybe he was so delighted that the structure of DNA had finally been discovered that no book, even one burdened with gossip, could detract from his joy. Watson had his own explanation for Willie’s support of his book: “The solution to the structure [of DNA] was bringing genuine happiness to Bragg. That the results came out of the Cavendish [and not elsewhere] was certainly a factor. More important was the unexpected marvelous nature of the answer, and the fact that the x-ray method he had developed 40 years before was at the heart of a profound insight into the nature of life itself.”47
If publicity for the Cavendish was Willie’s objective, then he certainly got it. The book became a best seller and one of the most popular science books of all time. It has been in continuous publication since 1968, with multiple editions; the most recent edition was 2012, and there is even a BBC television dramatization of it.48
It is no small irony that the x-ray—that mysterious penetrating radiation that Roentgen had discovered so many years before and used to reveal the bone structure of his wife’s hand—was ultimately used as tool to reveal the structure of DNA, its own biological target. It is unclear whether we would even now know the structure of DNA had x-rays not first been discovered. Remarkably, in pursuing the goal of finding the chemical structure of genes, mankind has learned not just that DNA is the substance of genes, but also how radiation can produce cell death, mutations, and cancer—by damaging DNA. We’ve even learned how agents that damage DNA, such as radiation, can be exploited to cure cancer. It is an important scientific advancement, and it was achieved over a relatively short period of time. It is a truly remarkable story with many heroes, most of them unsung.
Willie died in 1971, at age 82. He had lived a long and highly productive life that contained its fair share of triumph as well as heartache. At 25 years of age he was, and remains, the youngest scientist to ever win a Nobel Prize. It was awarded for his discovery that x-rays can actually reflect off stacked atomic planes just as light reflects off stacked pan
es of glass, a phenomenon now known as Bragg reflection. However, it is likely that Willie’s proudest discovery was his first—his boyhood identification of a new species of cuttlefish, Sepia braggi, which he recognized solely by the unique structure of its internal bony skeleton. Paradoxically, Willie probably never saw a live specimen of the species he discovered, since that particular species of cuttlefish inhabits the ocean depths. Nonetheless, knowing his cuttlefish only by its internal structure was probably enough gratification for Willie.
In 2013, scientists at the University of California, Santa Barbara, discovered one of the tricks that cuttlefish, octopi, and other cephalopods use as a camouflage tool to reflect light and blend in with their surrounding environment.49 It seems they have cells in their skin that can fold their cellular membranes into pleats, forming stacked planes of membranes that the animal can adjust at will, to modify its body’s reflection of light. This newly discovered camouflage organelle has been termed a tunable Bragg reflector in acknowledgement of the man who originally discovered this reflection phenomenon; that is, William Lawrence Bragg.
CODA TO PART TWO
This brings us to the end of Part Two. In this part, we looked at the various health effects produced by radiation and learned the types of illness that radiation will produce is determined largely by two factors: (1) the dose level of the radiation; and (2) the exact type of tissue that is exposed. High doses (>1,000 mSv) produce cell death in exposed tissues, and the nature of the health consequence is determined by loss of the normal function of those cell types that are killed. Most of these various radiation illnesses are exceedingly rare, because, thankfully, few people ever experience doses this high.
At lower doses (<1,000 mSv), cell death ceases to be a problem and cellular mutations become the chief concern. Mutations are worrisome because they are the precursors to both cancer and inheritable mutations. In contrast to the rare radiation sicknesses, cancers and inheritable mutations have natural background levels within the population that are higher than most people realize. Radiation adds to these high background levels in relatively small increments that are directly proportional to dose. Radiation does not produce any new types of cancer or inheritable mutations that are unique to radiation.
Regardless of the specific health effect or dose level, the target for radiation’s health effects is always the same—cellular DNA. At high doses, the damage to DNA is so extensive that cells die. At low doses, the DNA damage is less and is mostly mended by cellular DNA repair systems. Nevertheless, there is a finite probability that some of the damage will scramble encoded genetic information, thus producing a mutation. We cannot completely prevent this. We can only lower the risk that it will happen.
Whether or not a low dose of radiation will produce any noticeable health effects largely comes down to luck of the draw. If you don’t want to draw a joker, then ask the dealer to draw you fewer cards. In the same way, if you don’t want a radiation-induced cancer, lower your radiation exposure as much as possible. Unfortunately, it’s not as simple as it sounds, because if you are too vigilant about keeping your exposure down, you will deprive yourself of some of the benefits of radiation technology. What’s a person to do? We’ll address that question next.
PART THREE
WEIGHING THE RISKS AND BENEFITS OF RADIATION
CHAPTER 12
SILENT SPRING: RADON IN HOMES
Probably one of today’s most serious public health issues.
—Vernon Houk, former assistant surgeon general of the US Public Health Service
Get your facts first, and then you can distort them as much as you please.
—Mark Twain
POLYESTER
On December 2, 1984, Stanley J. Watras, an engineer working on construction of the new Limerick nuclear power plant near Pottstown, Pennsylvania, arrived at work. The plant, just seven miles from his home in Boyertown, was scheduled to begin generating power within three weeks, and the construction crew had just installed radiation detectors at the plant doors—a standard safeguard to ensure that nuclear workers don’t exit the plant with any radioactive contamination on their bodies. When Watras arrived that day, he set off the alarms on the detectors as he walked into the plant. Over the following two weeks he would set off the alarms every morning. Further investigation revealed that his clothes were contaminated with radioactivity that he had picked up at his home!1
When radiation safety personnel from the plant visited Watras’s home, they discovered what they didn’t think possible. There was more radon gas in the Wastras split-level house than was found in a typical uranium mine … about 20 times as much! Surprised, the radiation safety technicians checked the radon levels in the neighboring houses. “Our house,” Watras remarked in consternation, “had perhaps the highest contamination level in the world, but our next door neighbors had none.”2 How could this be?
The Watras house was located on the Reading Prong, a geological formation full of uranium deposits. It extends from the town of Reading, in southeastern Pennsylvania, through northern New Jersey, and up into southern New York. Radon, a radioactive gas produced through the uranium decay chain, leaks from the ground in this area and then mixes with aboveground air.
The fact that radon seeps from the ground over uranium-containing earth had been known since 1908, when geologist Carl Schiffner first mapped the geographic distribution of radon gas in the Saxon region of Germany (see chapter 5). This map subsequently led to the discovery that air in the Schneeberg mines contained high levels of radon. Nevertheless, geologists hadn’t previously appreciated how spotty radon leakage could be. Some ground locations can have virtually no leakage, while a spot a few hundred feet away could have huge amounts of radon streaming out. As it turns out, subterranean radon behaves like subterranean water. Just as underground water gathers in pockets and travels great distances along crevices in the bedrock, often to emerge in discrete locations on the ground surface in the form of a natural spring of water, radon travels along ground faults to emerge as a “spring” of gas. The Watras home was built right on top of a spring of radon gas.
FIGURE 12.1. STANLEY WATRAS’S RADIOACTIVE HOME. In 1984, Stanley Watras activated radiation detector alarms each morning when he entered his work facility at a Pennsylvania nuclear power plant. His radioactive contamination was ultimately traced to his home, which happened to have one the highest radon concentration levels ever recorded. This spurred the US Environmental Protection Agency to survey other homes, and led to the discovery that many homes in America had hazardous levels of this radioactive gas. (Source: Copyright Bettmann/Corbis/AP Images; image used with licensed permission from AP Images)
The Watras family discovered their radon exposure only because Stanley Watras happened to be monitored for radioactivity as a nuclear worker, and because he happened to be wearing clothing made from polyester. Polyester tends to produce static electricity, and that static electricity attracted radon-contaminated dust in the air of his home onto his clothes. The Watras family case was the first time people realized that natural radon levels in homes could be higher than in mines.3 How many other houses built on radon springs were out there and, more importantly, how much danger did they pose to their residents?
PROGNOSIS
The Watras family had moved into their house in January of that year, so they had been exposed to the radon for less than a full year. Nevertheless, doctors told them, based on US Environmental Protection Agency’s (EPA) risk estimates, their brief exposure to radon made them seven times more likely to die of lung cancer within 10 years compared to a person without radon exposure. Their children, Michael, 6, Christopher, 3, and Cynthia, 1, might not make it to adulthood.4
The family moved out of the house immediately and tried to resume their normal lives. As Stanley Watras explained at the time, “[If we] keep worrying about it, we might not live long enough to see whether the doctors were right, because depression and psychological pressure would be too much for us to survive.
”5
It had been firmly established since 1944 that breathing a lot of radon carries a substantial lung cancer risk. The risk of radon seems to be exclusively lung cancer. No other illness has been attributed to radon exposure, which makes sense given that only lung tissue receives a significant radiation dose when breathing this radioactive gas. No one seriously contests these basic facts. But after that, things get a little murky. Why? Because another major cause of lung cancer poses a much bigger threat than radon, and this of course is cigarette smoking. Cigarette smoke produces a statistical haze through which all radon data must be viewed.
Expert panels have evaluated mountains of data on miners in an attempt to precisely determine the amount of lung cancer risk that could be attributed specifically to radon exposure, rather than to smoking.6 In addition to the historical Schneeberg findings on miners that we’ve already discussed, scientists had multiple modern cohort studies from radon-containing mines in various European countries, as well as in China and North America, including the mines of the Colorado Plateau. (This Colorado mining area includes the Paradox Valley, where the Flannery brothers of Pittsburgh, and Kelly and Douglas of Baltimore, had mined their carnotite ore in order to purify radium; see chapter 6.) In addition, there were also case-control studies of lung cancer risk from radon in homes, but serious methodological issues surrounding their design rendered them unreliable and of limited value for quantifying cancer risk, so the mineworker cohort studies became the primary data resource for the risk assessment.7
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