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 Establishing Proof
 
 By David Brown
 
   
 
 Marc Maurer was born on June 3, 1951, in Des Moines, the second child of a traveling salesman and a housewife. He was two months premature. As is often the case with babies born very early, his lungs were underdeveloped. He spent two months in the hospital. During the first, supplemental oxygen was pumped into his incubator continuously.
 
 In the same city three months earlier, Patricia Schaaf was born. Her father was a plumber, her mother was a school cook. Their first child, Patricia was 3 pounds, 10 ounces at birth and two months premature. She, too, got oxygen for at least a month.
 
 Today, both Maurer and Schaaf are blind.
 
 Maurer is president of the National Federation of the Blind, and his wife -- the former Patricia Schaaf  --  is its director of community relations. They work in South Baltimore in a refurbished factory that is the headquarters of the 50,000-member advocacy organization. Marc Maurer, a lawyer by training, has a spacious corner office overlooking the Patapsco River, which he cannot see.
 
 The Maurers were part of an epidemic that began in the early 1940s and peaked in 1951, the year of their birth. They were blinded by high concentrations of oxygen, which was routinely given to premature infants in the United States during and after World War II. It took 15 years to discover the link between oxygen and blindness -- 15 years in which a mysterious disease haunted America's best hospitals.
 
  This tragic outbreak was not the first time a medical treatment thought to be beneficial was shown to cause harm. Nor would it be the last.
 
 In recent years, hormone replacement therapy taken by millions of women turned out to cause heart attacks, not prevent them. Vitamin A supplements don't lower the risk of lung cancer, as many smokers once thought; it may increase it. Antidepressants relieve depression in some teenagers but appear to drive a small number toward suicide, depression's tragic endpoint. Three years ago the pain reliever Vioxx was the 15th most commonly prescribed drug in the United States, with $1.8 billion in annual sales. Today, some experts believe it may have contributed to as many as 160,000 heart attacks and strokes since its arrival in 1999.
 
 The story of oxygen and blindness is a distant mirror of these therapeutic surprises. But it is much more as well.
 
 Of all the elements on the periodic table, oxygen is the one that seems most to symbolize life and health itself. Could extra oxygen be dangerous to tiny babies struggling to survive? It seemed inconceivable! 
 
 But it was true. Two doctors proved it more than a half-century ago in a clinical experiment run in the wards of a hospital in Washington. The medical world didn't believe them, at least not enough to change routine practice. So a second, bigger experiment was conducted at more than a dozen American hospitals. 
 
 Fifty years ago this summer, the preliminary results of that trial were published. They changed medical history. Almost overnight, physicians stopped automatically giving supplemental oxygen to preemies, ending the epidemic of retrolental fibroplasia (RLF), as the disease was called then. (It is now known as retinopathy of prematurity.) 
 
 But the study's results did something else equally important and historic. They convinced many American physicians of the usefulness of randomized controlled trials, which had been "invented" less than 10 years earlier in Britain. Not least, the study taught doctors they couldn't assume that what seemed like a good idea  --  extra oxygen  --  would necessarily lead to a good outcome. 
 
 "Doctors have to approach their patients, and what they think they know, with a certain amount of humility," said Steven Goodman, a physician at Johns Hopkins University's Bloomberg School of Public Health and editor of the journal Clinical Trials. "This is one of the trials that taught us humility."
 
 The events that culminated 50 years ago is also a story of self-reliance, doggedness and even heroism on the part of the blind survivors of RLF and the two doctors who first proved the disease's cause. Those doctors, as it happens, are still alive.
 
 Arnall Patz went on to become the chairman of ophthalmology at Johns Hopkins University School of Medicine  . Now 84 and officially retired, he lives in Baltimore and still works part of nearly every day on some medical project. Last spring, President Bush awarded him the Presidential Medal of Freedom for a lifetime of scientific discovery that began with the oxygen experiment at Gallinger Municipal Hospital, the predecessor of D.C. General. His long-ago collaborator in that work is Leroy E. Hoeck, a 93-year-old retired pediatrician living in Fort Washington.
 
 The discovery they made in 1951 and 1952 didn't come in time for Marc or Patricia Maurer. Nor did it come in time for RLF's most famous victim, Stevie Wonder, born prematurely in Michigan in 1950 as Steveland Judkins. Nor for 10,000 other babies born here and around the world who became blind from oxygen. But it did come in time for numberless preemies born in the last 50 years who can still see.
 Survivors and Pioneers 
  Nobody knows the first infant to become blind from retrolental fibroplasia. But the first recorded in the annals of medicine is James Edgar Pew II.
 
 Pew and his twin sister, Margaretta, were born on July 13, 1940, at the Boston Lying-In Hospital. They were seven weeks premature. Margaretta died in six hours. Her brother held on, thanks to oxygen.
 
 "The child was examined at the age of ten minutes, at which time the respirations were gasping and irregular . . . the baby was immediately given oxygen. After about ten hours, his condition improved," the pediatrician in charge of the premature nursery, Stewart H. Clifford, wrote in the hospital chart, according to an account published in the Saturday Evening Post magazine in 1955.
 
 The boy's father, George L. Pew, was extremely wealthy, a direct descendant of Joseph N. Pew, the founder of Sun Oil Company. (Today, the family name is best known for the foundation four of Joseph Pew's children endowed, the $4.1 billion Pew Charitable Trusts). Jimmy Pew received the best medical care money could buy. He spent two months in the hospital and got supplemental oxygen almost continuously. 
 
 When the boy was 7 months old, his parents and some visiting relatives became alarmed when he failed to track the movement of a cigarette lighter his father held in front of his face. (This anecdote, and many details of the following narrative, come from the magazine account by Steven M. Spencer and from a 1980 book, "Retrolental Fibroplasia: A Modern Parable," written by a pediatrician and historian named William A. Silverman.) 
 
 Even though it was a Sunday, the Pews summoned Clifford to their Beacon Hill house. He examined the child and told the parents he suspected the boy was blind. Curiously, Clifford had just seen a similar case, the infant daughter of a rabbi. "I was shocked to find my second case within a week of my first," he later said.
 
 The Pews insisted an eye doctor be called. With some effort, Clifford reached Theodore L. Terry, a Harvard professor of ophthalmology. He came and thought the problem might be congenital cataracts. Within a few days, however, that diagnosis was abandoned. The cause of the Pew baby's blindness was something else -- and it also appeared to be something new. 
 
 Terry wrote the case up for a medical journal, making reference to the rabbi's daughter and three other blind infants he saw soon afterward at the Massachusetts Eye and Ear Infirmary. All five babies had been born prematurely. In the American Journal of Ophthalmology in February 1942, he made a prophetic observation: "[S]ome new factor has arisen in extreme prematurity to produce such a condition."
 
 He also personally notified about 50 specialists of his findings and asked them to look for cases. Soon, he had more, and with them a fuller picture of what was happening.
 
 By the time blindness could be diagnosed for certain in the babies, their eyes contained a distinctly abnormal membrane in front of the retina, the eye's back wall, where the visual receptors lie. Terry believed the condition developed after birth, but somehow involved embryonic tissue. He tried to reproduce it in laboratory animals, but was unable to. He died in 1948 with 117 cases, and no answer.
 
 Proof that retrolental fibroplasia was new, and that babies weren't born with it, came from a look-back at records at Johns Hopkins Hospital. A husband-and-wife research team, Ella and William Owens, found no cases from 1935 and 1944, but five in premature infants born after 1945. All had normal eyes at birth.
 
 But what was causing it?
 
 There were dozens of theories. They included high-protein diets, large doses of vitamins, blood transfusions, hormone therapy and antibiotics -- all treatments given with varying frequency to premature infants. Too much light was the other main candidate. Some of the theories were put to the test in small experiments. None panned out.
 
 There seemed to be nothing in common with all the cases except prematurity and, ironically, good medical care. RLF wasn't a disease of incompetence, poverty or inadequate technology. Quite the opposite. Throughout the 1940s, reports of the disease trickled, and then began to flow, from Canada, Western Europe and Australia -- all places with advanced medical care and high standards of living.
 
 Eventually oxygen made it onto the list of possible causes.
 
 The person who put it there appears to have been an English doctor named Mary Crosse. She noticed that RLF didn't occur in Birmingham until 1948, when the National Health Service was created. Then, for the first time, many hospitals could buy American incubators and bottles of oxygen.
 
 The use of oxygen to treat asphyxiation in a newborn was first tried in 1780. It was studied and recommended again in 1900. By the early 1940s, supplemental oxygen was standard treatment for premature infants in the best-equipped hospitals. What seems to have initiated the epidemic of RLF, however, was the development of incubators that could keep pumped-in oxygen from leaking out. Molded plastics developed during the war made postwar incubators increasingly airtight.
 
 Crosse's observation came to the attention of an Australian pediatrician named Kate Campbell, who worked in three hospitals in Melbourne. One had incubators that could give premature babies air with two or three times the amount of oxygen in atmospheric air. The second used a less efficient way of delivering the gas. The third required patients to pay for supplementary oxygen, so it was "used with more economy," she wrote.
 
 She looked at the records of her patients for the years 1948 through 1950 and saw a remarkable effect. At the hospital where oxygen was given most intensively, 19 percent of premature babies developed RLF. At the other two where it was used sparingly, the rate was only 7 percent. She speculated that the adjustment to the "oxygen-rich" world outside the womb was a stress that premature infants somehow couldn't adjust to.
 
 It was a hunch that in broadest interpretation would turn out to be correct.
 Side Effects 
 When Marc Maurer was 6 months old, his parents took him to Minneapolis for an eye operation. He had a second when he was 3. He had a third when he was 6. That's the one he remembers.
 
 People with RLF often develop glaucoma, a condition in which the internal pressure in the eyeball rises because of problems in the circulation of fluid. Maurer had glaucoma and the surgery was intended to relieve it. It did that -- and more.
 
 Until then, Maurer had a small bit of residual vision in his left eye. He could see large objects at a distance of 20 feet. After the surgery, that was gone. "I lost what I thought of as vision," he recalled recently, speaking in a flat, nearly emotionless voice. "It was very depressing for a kid like me."
 
 When he returned home from the hospital, he refused to do anything but sit inside on a couch for a week. His mother eventually took him outside and forced him to go down a slide in the yard. With great protest, he did. Then she made him do it again. He got mad and decided to run away. He refused to go back inside.
 
  It was a crucial lesson, he believes. "It got me out of the theory that blindness would stop me from doing stuff." Still, he adds, his voice heavy with memory, "I know the discouragement of becoming blind. I remember it still."
 
 Maurer attended a school for the blind in Iowa for the first five grades. He learned Braille (as did his mother), and became an avid reader. In the fifth grade, he returned home to the town of Boone (pop. 12,000) and attended parochial school. He says now that he found no insuperable obstacles to learning what he wanted to. 
 
 In high school, he took extra courses at a junior college. After graduating, he spent a year in a program for blind students in Iowa. There, he expressed interest in auto mechanics; the state Commission for the Blind provided the tools for him to overhaul a car engine. Ultimately he graduated from Notre Dame and got a law degree from the University of Indiana.
 
 Patricia Maurer's parents suspected she couldn't see when at 6 months she failed to start reaching for things. They took her to the Mayo Clinic in Rochester, Minn. and a doctor there diagnosed RLF. She also had a small amount of light perception in one eye.
 
 She spent her entire career in public school. She didn't even learn Braille until she was 15, when she mastered it over the course of a summer with the help of a teacher. She took part in school activities in what seemed a normal way.
 
 "As a child you really don't understand why things happen the way they do," she recalled. Of her blindness, she says: "I got to the place where I thought it was the way it was supposed to be for me. I knew I didn't want to just sit around. I knew I wasn't going to give up."
 
 She met her future husband in the same training program where he rebuilt the car engine. She graduated from Drake University in Des Moines, where she studied special and elementary education. The couple married in 1973. They have two children, both sighted.
 
 Jimmy Pew remembers Theodore Terry, the doctor who made him the first recorded case of RLF, "as a very kind, gentle man." Terry operated on him twice for glaucoma. Pew can see shadows in both eyes, but has no useful vision.
 
 When Pew was about 7, his family moved to Maine. He lived in a large house outside Portland with his parents and an older brother, and eventually also with four cousins taken in after their parents were lost at sea. He learned Braille and as a child was a ham radio operator. He attended Brooks School, a boarding school north of Boston, where he was the only blind student. In his senior year, he got a guide dog, the first of six. He, too, is glad he was mainstreamed.
 
 "My parents wanted me to go to regular schools. I think it was a good decision."
 
 Pew also went to college, majoring in psychology at the University of Maine. He earned a doctorate from the University of Detroit and is now a clinical psychologist in San Francisco, where he moved in 1972.
 First Suspicions 
 Arnall Patz grew up in Elberton, Ga., the grandson of Lithuanian Jews who immigrated to Baltimore. His father was a peddler who eventually put down roots in a town on his southern route.
 
 One of seven children, Patz attended college and medical school at Emory University, both under accelerated, wartime schedules. He graduated from medical school in 1945, and after an internship at a hospital in Baltimore entered the Army. During a posting at Walter Reed Army Hospital, he decided he wanted to be an ophthalmologist. This was also the time he first heard about retrolental fibroplasias, a growing epidemic of unknown cause. When he was discharged in July 1948, he took an ophthalmology residency at Gallinger, the District's public hospital.
 
 It was an unlikely choice for an ambitious young doctor who'd already published a paper (on several cases of a rare allergic reaction he'd seen as an intern) in the New England Journal of Medicine. But Gallinger beckoned for one reason. In the unvarnished parlance of medical training, it had "good pathology" -- an abundant and varied harvest of disease.
 
  Working at the hospital when Patz arrived was a pediatrician, Leroy E. Hoeck. He was seven years older and in charge of the newborn nursery.
 
 Hoeck grew up in Iowa, graduated from medical school there and practicing briefly before being called into military service. After discharge in 1946, he took a short post-graduate course in pediatrics at George Washington University's medical school. He then entered a three-year training program at Gallinger.
 
 From a distance of more than 50 years, both men remember a signal moment that drew them irretrievably into the search for an answer to what caused RLF.
 
 Patz's came in the summer of 1948, right after his residency began, when he visited the newborn nursery to look for babies with RLF. "I noticed in the nursing notes for the first time a single entry about oxygen. The nurse had recorded that the baby [was] 'receiving oxygen at six liters flow' [per minute]. My interest in oxygen stemmed, really, from that one nursing note."
 
  Hoeck's also involved a single infant  --  the first baby born under 1,000 grams (2.2 pounds) in Gallinger's history to survive. He was a boy, 997 grams, and Hoeck was his doctor. The baby was "a save" in medical lingo, and Hoeck was proud of his work. 
 
 "The problem was that when I happened to see him in the outpatient clinic four months later, that particular baby -- " Hoeck stops, unable to go further. He is choked with emotion. After 10 seconds of silence, he resumes. " -- he was completely blind." He takes a breath. "And that was devastating. I just felt we had to find the cause."
 
 Hoeck began to research the possibilities, which in early 1949 still comprised a long list. He spent days in the library of the Army Medical Museum, on the mall where the Hirshhorn Museum now stands, reading articles. Eventually, he found an article from the "Staff Meetings of the Mayo Clinic" of 1940 by three doctors, one an Army captain. They had examined the effects of varying concentrations of oxygen (as might be encountered by bomber pilots) on blood vessels in the eye. They reported that after 30 minutes of breathing pure oxygen, a person's retinal arteries narrowed markedly -- an observation not previously made "to our knowledge," they wrote. 
 
 With the nudge from that article, Hoeck realized that in addition to prematurity, the one thing all the babies with RLF had in common was exposure to supplemental oxygen. Of course, they shared that with lots of babies whose sight was unimpaired, too.
 
 Hoeck shared his suspicions with Patz, who was coming to have his own. Patz noticed that the retinal blood vessels in a premature baby on oxygen were narrowed and constricted, like the adults in the Mayo Clinic study. If the exposure to the high concentrations of oxygen was brief, the vessels returned to normal in 30 minutes or so. But in the babies who'd been in oxygen for days, the constriction seemed to persist indefinitely.
 
 Patz also looked back into Gallinger's nursery records. Even though they usually didn't record the exact oxygen flow rate, it was pretty clear that nearly all the babies who went on to develop RLF had had prolonged exposure to high concentrations of the gas. In fact, over three years it was 18 out of 21.
 
 "I said, 'Roy, the only thing we can do is a carefully controlled prospective study to test the oxygen,' " Patz recalled.
 
 (The fact that Patz understood the concept of a controlled trial -- and Hoeck apparently did, too -- is amazing in itself. The first such study, an English trial that proved the antibiotic streptomycin could cure tuberculosis, had only been published in October 1948.)
 
 Patz got a $4,000 grant from the newly created National Institutes of Health (NIH) after his initial application was rejected as unscientific and unethical. He reassured the reviewers that every premature baby who needed extra oxygen to stay pink and healthy would get it. But all the premature babies wouldn't get it automatically.
 The Trial 
 On Jan. 1, 1951, they started their experiment. Babies weighing under 3.5 pounds were alternately assigned, based on time of birth, to get either 80 percent oxygen for at least 28 days or 40 percent oxygen "only for specific clinical indications." Parents were told about the study after their child was assigned. But they weren't asked whether they wanted their child included, and they signed nothing. This lack of "informed consent" in the modern sense was standard for the time.
 
  "We weren't doing those babies any harm," Hoeck recalled thinking. "In fact, we were doing what we thought was beneficial in every way."
 
 There was a group worried about harm, though. It was the nurses. 
 
 Part of the mythology of this trial is that nurses would go around at night turning up the oxygen taps to the low-oxygen babies in a guerrilla operation to save the infants' lives. That story heightens the drama, but Patz today says it's mostly wrong.
 
 One or two night nurses did crank up the oxygen to all the incubators when they came on shift, but that occurred during a dry run for the experiment. Patz says he explained the protocol and asked them to stop, which they did.
 
 In May 1953, he and Hoeck stopped enrolling babies. This was what they found: 12 out of 60 premature babies assigned to standard care were blind from RLF. In the curtailed-oxygen group, one out of 60 was. There were also a lot of near-misses. In the high-oxygen group, 21 babies developed early RLF, which eventually regressed to normal. In the low-oxygen group, nine babies showed those changes.
 
 The young doctors published their first-year results in September 1952 (a year after Kate Campbell's report from Australia), and the final results two years later. By that time, Patz had successfully reproduced the disease in newborn mice, rats, kittens and puppies. However, even before the study was finished, the American Academy of Ophthalmology and Otolaryngology (AAOO) -- the professional organization of eye, ear, nose and throat doctors -- was making plans to do its own trial of oxygen use.
 
 As is usually the case in medicine, a single well-conducted trial wasn't enough to convince doctors to change their practice. The Gallinger study had the additional drawback of being relatively small (and therefore of greater uncertainty) and the product of two unknown researchers.
 
 The AAOO proposed a trial in 18 hospitals east of the Mississippi River. It would enroll enough babies to answer the question beyond any doubt -- provided people could agree how to run it. Some doctors felt that because the chief problem of premature babies was respiratory distress, limiting oxygen to them was likely to cause brain damage or death. Others felt that giving supplemental oxygen indiscriminately would cause avoidable cases of blindness. Few people were in the middle -- and certainly not Arnall Patz and Leroy Hoeck. Neither Johns Hopkins Hospital, where by then Patz had an affiliation, nor Gallinger participated in the study.
 
 "I couldn't take part in it," Hoeck said. "I didn't have to be convinced any more."
 
  At a meeting in the mansion house of NIH's new campus in Bethesda, about 45 scientists met to draw up plans. They wrangled through an entire night, at one point placing a transatlantic telephone call to Austin Bradford Hill, the British biostatistician who had designed the streptomycin-for-TB study. He suggested a Solomonic compromise.
 
 The trial would basically be two studies run sequentially. For three months, premature infants would be randomly assigned to routine high oxygen, or oxygen only if they needed it, in a 1:2 ratio. That would answer the question whether oxygen caused RLF. Then -- assuming the study wasn't stopped because of higher mortality in the curtailed-oxygen group  --  all babies born in the following nine months would get oxygen only for clinical need. That would provide an estimate of the incidence of RLF under oxygen-sparing conditions -- a statistic nobody actually knew.
 
 Cobbled together with a speed inconceivable today, the 18-hospital study commenced on July 1, 1953. It was run out of a central office at the Kresge Eye Institute in Detroit by a biochemist named V. Everett Kinsey, who'd been interested in RLF since working with Theodore Terry in Boston a decade earlier. The study used random numbers, not every-other-baby assignment as in Washington, to determine which infants would get what treatments. Western Union provided a teletype machine for free, and seven days a week telegrams came and went from the 18 hospitals.
 
 "This was at the height of the McCarthy era," recalled William A. Silverman, who was in charge of enrolling preemies into the trial at Columbia's Babies Hospital in New York. "Some people from the FBI came up to see me to find out what kind of subversive activity was going on with all these suspicious telegrams." (Silverman died last December.)
 
 The trial closed on June 30, 1954. Before the summer was over, Kinsey and his collaborators had answers, which they presented to a meeting of eye doctors in New York that fall. 
 
 RLF severe enough to cause blindness occurred in 17 percent of the babies getting routine high oxygen, but in only 5 percent of the curtailed-oxygen group. The death rate in the two groups was similar -- 22 versus 25 percent. Oxygen -- and nothing else -- was responsible for the epidemic of blindness in premature infants. Doctors could safely turn it down.
 
 In fact, not to do so would soon be unforgivable.
 Change in the Air 
 The preliminary trial results, published in August 1955, and the final 62-page report of "The Cooperative Study of Retrolental Fibroplasia and the Use of Oxygen," which appeared in October 1956, might have been the end of the story. But it wasn't quite.
 
 The rate of RLF started dropping in 1952. By 1956 it was roughly at the level of 1946, the early period of the epidemic. In 1960, however, two physicians at Johns Hopkins Hospital wondered if this remarkable decline might have come at an unnoticed price.
 
 They reviewed autopsies of babies who had died in the premature nursery, looking especially for deaths from respiratory complications. They discovered that the percentage of babies dying in the first six days of life rose from 8 to 13 between 1948 and 1958. The fraction of autopsies that found lung immaturity as the cause increased by the same proportion during that time. In 1962, an English physician reported a related and similarly unsettling trend. The longer a premature infant with breathing problems got oxygen, the higher its risk of blindness -- but the lower its risk of brain damage and paralysis.
 
 Again, the culprit appeared to be oxygen. Only this time it was too little, not too much. Limiting supplementary oxygen to premature babies had a cost: death or brain damage, at least in some of them.
 
  Why hadn't this been recognized in either the Washington study or the 18-hospital study?
 
 Patz and Hoeck, surprisingly, didn't record the number of deaths in their study, although they wrote that there wasn't a significant difference between the high- and low-oxygen groups. In the 18-hospital study, however, the reason there appeared to be no mortality cost is now clear  --  it's because the babies weren't enrolled in the trial until they were 48 hours old. Before then, they could get supplemental oxygen.
 
  Those first two days of life were when the tiny infants, clinging to life, were most likely to die. Oxygen kept some of them alive. When the oxygen was then turned down, they not only lived, they escaped blindness. If the study had denied them oxygen in those first two days, a significant number would never have made it to the point where blindness was the worst outcome. They would have already died  --  which was the fate of some of the preemies cared for in the post-study years.
 
 Recognition of this led to a half-swing back of the pendulum by the early 1960s. Oxygen use was liberalized, especially in the first days of life.
 
 Fifty years after the dangers of oxygen were discovered, the safe maximum -- if there is one -- still isn't known. As increasingly premature babies can be saved, the prevalence of oxygen-induced blindness and damaged vision has ceased falling. The condition is not nearly as common as it was in the 1950s. But it's still here.
 Results 
 Over the years, a lot was learned about the mechanism of RLF.
 
 It's now clear that with prolonged exposure to supplemental oxygen, the arteries in the eye not only constrict, they become completely obliterated. That leads to a second growth of vessels, possibly because of a sensation of oxygen deficiency in the eye. This new crop of vessels grows wildly. It can destabilize the whole retina, which in severe cases peels back and rolls up into a useless mass behind the lens -- "retrolentally." Much of this knowledge came from the laboratories of Arnall Patz, his collaborators and students over the last half-century.
 
 Patz became chairman of the Wilmer Eye Institute, Johns Hopkins's renowned department of ophthalmology. Long before then, though, his RLF work was recognized with the Lasker Award, which are sometimes called "America's Nobels." He shared his in 1956 with Everett Kinsey, who ran the big RLF trial, and Jonas Salk, whose successful testing of a polio vaccine was the other big medical news of 1955. Helen Keller, the most famous blind person in the world, presented the award.
 
 Leroy Hoeck stayed at the renamed D.C. General Hospital until 1957. He then entered private practice in the Maryland suburbs of Washington until retiring in 1987. He was asked recently if he remembered the name of the 997-gram baby whose blindness still makes him choke back tears.
 
 "Do I know his name?" he answers with incredulity in his voice. "I know it like my own." But he won't say what it is. Perhaps the man is still alive. Perhaps he is still in Washington.
 
 Jimmy Pew, the index case of the RLF epidemic, has spent much of his career in clinical psychology treating the victims of another epidemic -- AIDS. As a gay man living in San Francisco since 1972, he witnessed that disease come out of nowhere. He blames no one for his blindness  , nor does he find it ironic that the best medical care in America took away his vision. "It was just something that happened," he says.
 
 This, too, is the view of Marc and Patricia Maurer.
 
 "I'm one of the luckiest people I know," asserts Marc Maurer. Lucky because he's been able to help a large number of blind people like himself find independence and happiness.
 
 "Now, certain things have changed because of blindness," he says. "There are some things that are different for us than they are for others. Have I ever seen the face of my own children? No. But it hasn't prevented me from working with them and loving them."
 
 He continues, in a heavy cadence.
 
 "Some people say to me, 'Aren't you sorry?' No, I'm not sorry. What the doctors did was give me what they knew to keep my alive. And I am grateful to them for that."
 
 Earlier in the conversation, the couple had been told of Hoeck's memory of the baby unwittingly blinded by his treatment. It was emotional even in the retelling.
 
 Patricia Maurer follows up what her husband has just said with this: "Maybe you can give that message to the good doctor who was so upset."• 
 
   

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