1. Thanks Rod.
    I’m going on memory from a book I read the month before entering grad school: Lawrence and Oppenheimer by Nuel Pharr Davis, fairly recent at the time. That I still remember the title and author these many years might testify to it’s impact. The Lawrence here is Ernst Lawrence, John’s more famous brother and inventor of the cyclotron. The reviews at the link are insightful, particularly though not exclusively to some insights regarding General Grove’s philosophy regarding security, and worth a glance.

  2. Great story Rod.

    Since you enjoy historical vignettes so much, here’s some more about John Lawrence and a few others, and the sad story of Phosphorus-32.

    The text below is from Marshall Brucer’s “A Chronology of Nuclear Medicine”, Heritage Publications, Inc., St. Louis, Missouri, 1990

    p. 222 (Chronology from 1926 to 1939 – Vignettes on a New Physics with Radioisotopes):

    (Radioiron Was One Result)

    Hevesy read Fermi’s method of producing radioisotopes in 1934. He found a Copenhagen hospital with a RaRn cow [radium producing radon], borrowed some radon, and made a neutron source. With almost a week’s exposure he made nanocuries of P-32, enough to become obsessed with the almost infinite applications of radioisotope technology in biochemistry. He had to have a much larger supply of P-32 and fortunately he found one.

    Microcuries to Millicuries of P-32

    Neils Bohr was due to have a 50th birthday in 1935. Somebody, probably Hevesy, dropped a hint to the Union Haute Miniere who ran the Belgian Congo uranium mine. They were appreciative and Bohr was presented with a gigantic 600 mg radium-beryllium neutron source, Hevesy had an immediate use for neutrons. He could now produce massive doses of P-32. (Microcuries were massive in 1936.) Within a year the cyclotron at Berkeley was producing millicuries. Hearing of Hevesy’s needs, Ernest Lawrence asked Martin Kamen to periodically send Hevesy a few millicuries of P-32. (All done through ordinary mail.)

    P-32 was an answer to a twenty year old dream. (Even more than the first experiments with heavy water.) Easy GM tube detection of P-32 beta rays was much more sensitive. P-32 allowed heretofore impossible tags of naturally occurring phosphorus compounds. With O. Chievitz, Hevesy announced the first biological use of P-32. [Nature136:754, 1935] They fed Na32PO4 to rats and studied its distribution after a few days.

    The First Use of P-32 in Humans

    Because it did no harm to the rats, in the article describing their technical procedures [KDS 13:9, 1937] they included a human patient. Given 0.5 mg Na32PO4 (a few microcuries) mixed in the regular hospital diet, the patient’s urine and feces were assayed for 6 days. 21.7% of the dose was eliminated via urine, and 15.5% in feces. This dose, or Joe Hamilton’s first dose of Na-24 to himself, was the first use of a man-made radioisotope in humans.

    A Label for Blood Volume Studies

    In their many investigations of labeled phosphorus compounds, Hevesy found a labile pool of phosphate in plasma, and a lesser non-labile pool in red cells. The relatively permanent red cell P-32 could be, he thought, a non-destructive label for blood volume studies.

    Hevesy soon learned that red cells could be labeled in vitro. Upon reinjection of the animal’s own, but now radioactive, RBC all foreign body problems were avoided. It might even be a human clinical technique. He investigated the sources of error. [KDS 14:5, 1939]

    Mixing time for RBC in the blood stream was about 2½ minutes, versus about 6 minutes for the currently used dye-in-plasma methods. Loss of P-32 from RBC (about 1.5% during the testing period) was small compared to the leakage of dye from plasma. Labeling of new cells in vivo from the leaked 32P was insignificant. Some 32P in plasma was adsorbed on red cells without true labeling, but this was considered insignificant. Hemolysis was not a problem. [L. Hahn 8 G. Hevesy, APS 1940] Many years later Hevesy considered P-32 blood volumes his most significant contribution to medicine. But it doesn’t match the importance of his first isotope experiment (1913). The P-32 RBC label was a flawed “loose” label.

    Fe-55 is a Much Better (Maybe?) Label

    George Whipple, dean of the medical school at the U of Rochester, was not satisfied with the sloppy hematology of a “loose” label. He had heard of a radio-iron in Berkeley. A part of hemoglobin, radio-iron would be the perfect red cell tag. Labeling could be done in vivo in donor animals – no problem to hematologists. Far more difficult was the problem of measuring the soft electron capture emission of Fe-55. For this problem he hired Paul Hahn who found a major error Whipple should have seen himself. [P. Hahn & G. Whipple, JEM,1940]

    p. 225:
    (One of Two Beginnings of Nuclear Medicine)

    In 1935 G. Hevesy, then in Copenhagen, began using P-32 that he made in microcurie quantity with Bohr’s giant neutron source. His studies in P32 metabolism naturally gravitated towards blood, the easiest precision sample he could get from living animals. His P-32 supply was inadequate for many projected studies. At a European physics conference E.O. Lawrence heard of his short supply and offered to send him a regular supply from the Berkeley cyclotron. By 1937 he began to get millicurie amounts (by ordinary mail) prepared by Martin Kamen at Berkeley.

    Millicuries of P-32 in the blood stream causes the same radiobiological effect discovered in 1903 by Gottwald Schwarz (an early Austrian radiologist). Schwarz noted that total body X-irradiation caused changes in counts of formed elements in blood. Since 1923 the Royal Society of Medicine required periodic blood counts of all X-Ray technicians, and this routine was followed (but without much enthusiasm) in California medical installations. But not at the Berkeley cyclotron, probably the most powerful radiation source in the world. All attention was on the “beam” and its target. Physicists didn’t think in terms of danger. The cyclotron was not even shielded until a mouse was killed in 1935.

    But John Lawrence knew in 1936 that P-32 injected into the blood stream would kill blood cells. Therefore, diseases characterized by too many blood cells, leukemias and all of the polycythemias, might get symptomatic relief by killing a few of the cells with P-32 radiation. P-32 followed the protraction theory of H. Coutard and A. Baclere by delivering a slow steady low dose over a period of many weeks. Lawrence characterized intravenous P-32 as total body irradiation.

    First Treatment of Leukemia With P-32

    A few trials of IV P-32 in normal and leukemic mice, and in various lymphomas in animals, convinced John Lawrence that the wide discrepancy between animal and man kept the encouraging results from proving anything. He would have to take the big step and try P-32 therapy in man. Fortunately he had a patient who could give true “informed consent.” An anemic 29-year-old graduate student at Berkeley had been diagnosed in the fall of 1938 as having chronic myelogenous leukemia. He had greatly enlarged spleen and liver and understood his prognosis and the lack of any definitive therapy.

    Lawrence explained the theory behind P-32 therapy to the student and how it had worked in mice. With the patient’s enthusiastic support he was given 2.98 millicuries on 28 Nov 1938. The leukocyte count came down steadily each day until 12 Dec 1938 when it began to slowly rise. On 14 Jan 1939 a second dose, 2.81 millicuries of P-32, was given. The count came down even farther but began to increase on 9 May. On 15 June 1939 a third dose, this time 4.85 millicuries was followed by a decrease to normal leukocyte count levels and it stayed down. By 1940 neither liver nor spleen was palpable. The patient, symptomatically and by physical examination, was normal.

    The second patient was a qualified success. By 1940 Lawrence was able to report five patients with chronic myelogenous or lymphatic leukemia treated with reasonable success, to a doubting audience of radiologists. He described the patient response as similar to that achieved by X-ray or radium. But animal studies of P-32 distribution showed that simple uniform whole body radiation was not given by P-32. The radiation was highly localized to marrow, spleen, and liver. [Rad 35: 51, 1940]

    A Real Hematologist Takes Over

    By January 1941 P-32 therapy of chronic leukemias was taken seriously by a real hematologist. (John Lawrence never claimed expertise in hematology.) Edwin Osgood at the U of Oregon started a series in 1941 that reached 300 patients by 1961. Two thirds were chronic lymphocytic, one third granulocytic leukemias. The treatments were not an overwhelming 100% success, but were far better than anything else ever tried.
    As Osgood’s series extended he noticed that the dosage pattern did not make sense. He inaugurated “titrated” (meaning divided according to need) regularly spaced dosage. The amount and rate of P-32 administered was determined by the patient’s response to his previous dose. This change was not a criticism of Lawrence’s methods, but realization that no one in.1938 had any idea of how much should be given or how often. Lawrence started beta therapy before any unit of beta dose existed. Not even extrapolation from X-ray therapy dose was possible until Leo Marinelli invented the “e.r.” (equivalent roentgen) in 1940. Osgood had the advantages of Lawrence’s experience, Marinelli’s dosimetry, plus his recognition as a clinical hematologist.

    P-32 is a Victim of Radiation Hysteria

    By the time (c1950) the new AEC had got around to making P-32 available to physicians, P-32 therapy of the chronic leukemias and of polycythemia was well accepted. Then in 1952 the Atom Bomb Casualty Commission (ABCC) described a leukemic death in 47 of 110,000 survivors. The next year L. Heilmeyer announced that he had a chemotherapy as good as P-32. In private the word was spread that chemo was better than radioactive therapy because you didn’t need a special license with examinations in physics. Also AEC licensers might be snooping in your medical records, thus violating the sacred patient-physician relationship.

    Radioactive fallout from A-bomb tests in Nevada was being reported in ever more hysterical terms by newspapers. Hysteria prompted Congress’s Joint Committee on Atomic Energy to hold full scale hearings in 1957. In a pious display of concern for the people’s health, radiation hysteria was pushed to full swing. Then headlines said 99 survivors of the atom bomb had died of leukemia (eventually it would be about 110 or 0.1%). A few of the patients who had been treated with P-32 died in acute remission; naturally, commented Lawrence, that’s how most patients not treated with P-32 die.

    The Success is “Limited” by Politics

    In 1958 Lawrence pointed out that 80%, of his P-.32 treated lymphoblastoma patients lived a normal life span. (Ann Int Med, 1958) Osgood felt he was seeing the same thing, and hired a biostatistician to review his series. He found that chronic leukemia patients treated with P-32 had a life expectancy equal to that of the US , population. (J Nuc Med 5:139, 1964)

    However the NIH, already dominated by fund raising cancer societies, was pushing a new marginally successful “chemotherapy.” It did not require special AEC license. During the 1950s the 0.01% of Hiroshima atom bomb survivors developed “leukemia” in the glare of world wide publicity. When added to P-32 licensure the black stain was enough to stigmatize Leukemia therapy with P-32. A couple of offshoots of Lawrence’s discovery survived. Their story concerns polcythemia, barely mentioned in Lawrence’s first written report. (Rad 35:51, 1940) Polycythemia vera is still (1988) treated with P-32. Thrombocythemia P-32 treatments were added in 1958. The popularity of P-32 increases as the radiophobia of the 1970s relaxes.

    p. 258 (Chronology from 1940 to 1953 – Vignettes on Manhattan District Days and Atomic Medicine):

    (P-32 “Cures” Leukemias & Polycythemias)

    This story was told to me over a long beer in Oklahoma City in 1952. Lowell and I were attending an “isotope” meeting, but had become fed up with sample counting trivia and had left to regain enthusiasm at the bar. Lowell was then in pediatrics because he was an expert on P-32 therapy of leukemias. Leukemia was largely geriatric and most of his patients were over 40, but there was no “senior citizen” money in those days. Most of his research funds came from childhood leukemia. In his basic science research he could get all the blood he needed from little people. Erf’s primary interest was “blood,” not “disease.”

    Lowell Erf’s Formal Introduction to P-32

    Fourteen years earlier, in 1938, Erf had been assigned to an internship under an unknown Dr. John Lawrence at UC – Berkeley. The new 36 inch cyclotron was producing radioisotopes faster than anybody could write papers to announce them. Hematology was also a newly recognized field. Lowell went into Hematology because patients were rarely emergencies. Hematology was quiet and clean. The only dirt would be an occasional spot of blood on his uniform.

    Lowell reported to the Crocker Lab, expecting to examine patients. He was dressed in white coat and pants and had the required stethoscope hanging around his neck. In addition to the excitement of his first day as an intern – stories at medical school told of non-stop 25 hour days with hundreds of patients waiting in line – he learned that his service had one patient. But, he was told he had the honor of being the first man in history to use a new medicine; it was called phosphorus. New interns were chosen for their strong legs and would he please climb the hill to the cyclotron lab to pick up the phosphorus.

    Now Lowell had heard of phosphorus even before medical school in Boston: firecrackers, matches, sodas, that sort of stuff. But who could account for the lack of learning among Californians? He climbed the hill to what he expected to be a sparkling clean pharmacy called cyclo-something. He was directed to an old wooden building that was undoubtedly the oldest on campus. Upon entering, he was appalled by the machine shop, or was it a foundry – had anyone ever swept, let alone scrubbed, the floor?

    The first to greet Erf was a small mongrel dog with an obvious, but clinically undiagnosed, diabetes insipidus. With no chairs in evidence, Lowell sat down on a small lead pot and played with the dog. “Nice doggie,” said Lowell patting the dog on the head. The dog answered on the pot after the manner of his kind.

    Suddenly the hum of the cyclotron died down. The sterile smell of ozone plus a touch of insolvency tainted the air, and Paul Aebersold’s voice screamed out from behind a mountain of 5-gal water cans used for shielding,

    “Keep that fool dog away from the pot you’re sitting on!”
    “That’s the medicine for your patient.”

    Thus, Lowell Erf MD was introduced to the high-tech of “radioisotope medicine.”

    Polycythemia Vera: An Afterthought in Rx

    G. Hevesy’s 1935 phosphorus metabolism studies required more P-32 than the nanocuries he could make on Bohr’s neutron howitzer. E.O. Lawrence furnished him with millicurie runs from the cyclotron, and got first hand reports of P-32 tracer biochemistry in return. This led Gilbert Lewis, Dean of Chemistry at Berkeley, to set up the first school of radiochemistry in conjunction with the Rad Lab at Berkeley. Martin Kamen, and then Waldo Cohn, made tremendous (for then) amounts of P-32 for the whole range of tracer chemistry.

    John Lawrence was most interested in the therapeutic possibilities of the cyclotron and the isotopes that poured out of it. In his first paper describing the therapy of chronic leukemias with P-32 he mentioned polycythemia vera therapy almost as an afterthought. It would be reported separately because this job had been assigned to Lowell Erf. (AnlM, 15:487, 1941)

    Erf explained that the P-32 did not destroy red blood cells, rather it depressed hematopoiesis in bone marrow. Because of a red cell’s 120 day life span, immediate relief of symptoms was not expected. Phlebotomies for immediate relief always preceded an oral dose of 3 to 4 millicuries (150 MBq). Red cell counts done frequently were expected to show a slow fall in cells in about six weeks, to a maximum effect in about three months. The RBC count may continue to fall for up to 7 months, but more often resumes a slow climb back to polycythemic levels. A second dose, usually after about 4 to 6 months, was usually required.

    Reaction to P-32 Therapies

    With the initial declassification of MED reports (Manhattan Engineering District Declassified Documents), D. Anthony revealed that the LD50 of IV P-32 for man (derived from animal data) was in the range of 270 mCi (10 GBq). Even with a tremendous error for translation from animal to man, this data made P-32 a very safe drug. By 1955 J. Harman said P-32 was the treatment of choice in England (BRIT MED J, 1955). After over 15 years followup J. Lawrence said his patients were living a normal life span. In 1958 J. Fountain began treating thrombocythemia patients with equal success. (BRIT MED J, 1958)

    The occasional death from leukemia of an atom bomb survivor became, in 1960 newspapers, a 100% certainty of radiation leukemia after even minimal exposure to radiation. (Actually, 40 years later it turned out to be an 0.2% chance of leukemia and only in those surviving >200 R exposure.) A number of patients given P-32 were reported, in great flares of publicity, to have died of acute leukemia. In 1959 J. Lawrence pointed out that a flare-up of acute leukemia was the expected cause-of-death in polycythemia. The high incidence in patients not treated with P-32, and so few in patients treated, suggested that P-32 prevented the acute leukemia death. Then in 1960, E. Lesli, working from a long series of patients, gave statistical proof that P-32 prolonged the life span of polycythemia patients. (CR, 1960)

    Radiophobia and the Decline of P-32

    During the 1970s P-32 gradually lost its popularity for reasons easily understood. Every hematologist needed only one license to do chemotherapy; however, in order to use P-32 on even an occasional polycythemia patient he had to have an MD plus a second “license to use radioisotopes.” A recent (1983) issue of Current Therapy points out that the choice therapy must be given by a physician with a special license. Along with each radioisotope license came inspection by arrogant, often insulting, inspectors and increased insurance rates.

    In 1984 the Sixth International Colloquium on Radioimmunoassay at Lyons, France, reported that chemotherapy has its own morbidity; it is dreaded by many patients, and subtracts rather than adds to the life span. The major fault of radioactivity as choice therapy, they said, was government bureaucracy.

    Much the same story of avoiding the stifling AEC licensure occurred after J. Fountain announced “cures” of thrombocythemia. (BRIT MED J, 1958) The licensure criteria forbids use in normal patients, but the recommendation is for dosage even before the patient becomes symptomatic. Chemotherapy was slightly successful in treating the chronic leukemias, but nobody has yet repeated Osgood’s feeling that his P-32 patients were actually living longer, and healthier, lives than the controls in his series.

    In a 15 April 1986 NY Times story on the results of the billions of’ $$$ wasted in the War-on-Cancer, the GAO (General Accounting Office) found no improvement in 20 years, but much exaggeration, in the treatment of chronic leukemias. However, the patient’s discomfort from chemotherapy cannot match his doctor’s discomfort with the Nuclear Regulatory Commission.

    A Remnant of the P-32 Success Story

    Lowell Erf’s first patient, as an intern on John Lawrence’s service in Berkeley, was one of the first to receive therapeutic P-32. After the secrecy of all things nuclear subsided around 1950, P-32 became the world wide therapy of choice for polycythemias. After 50 years it remains so except in the USA, where an insane regulatory mania and newspaper radiophobia has minimized its use.

    1. @Jaro

      That’s probably the longest comment I’ve ever allowed to be posted on Atomic Insights, but it includes useful information. It even included a mention of the suffocated rat — though it called the dead animal a mouse and did not share the true story that the rat was suffocated, not killed by a radiation dose. Thank you.

      During my two decades of involvement with people seeking to move beyond the “no safe dose” assumption [stubborn, financially motivated assertion?] most nuclear energy professionals assumed that nuclear medicine was ignored by the antinuclear movement. They would point to doses associated with imaging and scanning and assure themselves that it was proof of the “illogic” of people who were afraid of radiation.

      Your chronology — along with efforts like “Imgage Gently” to spread concern about CT scans and minimize their use — is another bit of evidence showing that there is irrationality in the use of radiation in medicine. I fear that similar financial motives are involved. Big Pharma does not give chemotherapy drugs away. Even though doctors tend to be service oriented people, there are plenty of people in the profession who entered it because of the high salaries they could earn and because of family pressures to get lucrative jobs.

      There is even an overlap in the funding sources used to spread fear of radiation in order to suppress it as a competitor; the Rockefeller Foundation has been a huge source of money for scientific medicine for nearly 100 years.

    2. Jaro, your excerpt is from a 1990 publication.
      This from a 1994 publication
      The treatment of polycythemia vera with 32phosphorus (32P) raises two problems: 1) what is its therapeutic efficacity? 2) Does the use of 32P increase the risk of acute leukemia? The large series of treated patients have shown the remarkable efficacy of 32P. This is particularly evident when comparing the recent series of patients treated with 32P with those of Videbaek whose patients were treated by phlebotomies only. Patients are treated one time with 3.7 x 10(6) mBq (0.1 mCi) of 33P per kg of body weight. Granulocytes and platelets are rapidly affected, whereas red cells show a response 3 months later due to their longer survival. Remission lasts from a few months to three years. If the result is not satisfactory, another dose can be given 3 months after the first one. Resistance to 32P may arise but may be reversible after a course of chemotherapy. The clear therapeutic effect of 32P renders it especially valuable for patients with a high vascular risk. Some authors have claimed that polycythemia vera evolves towards acute leukemia, but Modan’s study has demonstrated that 32P is indeed responsible for the occurrence of acute leukemia; this has been largely confirmed by others. The dose to the bone marrow is not negligible and the leukemic incidence following the treatment is a factor which limits its indication. Trials were conducted to search for therapies with alkylating agents, such as Chlorambucil or Busulphan, which would be less leukemogenic. The Polycythemia Vera Study Group found that Chlorambucil was at least 2.3 fold more leukemogenic than 32P. The EORTC compared the leukemogenic effect of 32P with that of Busulphan.(ABSTRACT TRUNCATED AT 250 WORDS)

      So . . . 32P was then thought to bring on acute leukemia BUT it was still better than some chemo treatments.

      1. Thanks very much for the update.
        I wonder if that assessment still holds today, and if P32 is still used in some countries ?
        BTW, would you mind sharing the citation for that reference, please ?

      2. Wait. “Resistance to 32P may arise but may be reversible after a course of chemotherapy.
        What is that supposed to mean???

        1. I noticed that, too.
          Sounds as if some people’s systems develop a sort of “immunity” to the radiation, but that chemo can “undo ” the immunity.
          Very odd — and unlikely.

          1. Really. Where is a radiation oncologist when you need one? ‘Cept Polycythaemia Vera itself isn’t a cancer, though the condition sometimes does progress to leukemia, particularly after 32P therapy. From the progressive myeloproliferative neoplasm (MPN) research foundation’s page:
            “Nearly all PV patients have a mutation called “JAK2V617F” (found in the JAK2 gene) in their blood-forming cells. This mutation is one of the ways that JAK (Janus kinase) pathway signaling can become dysregulated and cause the body to produce too many blood cells.”
            and from Clinical and laboratory assessment and therapeutic problems in longstanding polycythaemia vera:
            “With the very long life expectancy of Polycythaemia V 0.5 MeVera late complications are often observed: progressive resistance to treatment, bad tolerance to maintenance by phlebotomy, progression towards myelofibrosis. Resistance to phosphorus 32 is reflected by a progressive reduction in the duration of remission and by a gradually decreasing remission rate. A complete resistance appears after a mean duration of disease of 7 years. In the maintenance treatment by hydroxyurea, there is a secondary resistance in one third of cases with a poor control of t 0.5 MeVhe excess platelets. Resistance to Pipobroman is less frequent (10%). The phosphorus resistance could be delayed by addition of maintenance treatment by Hydroxyurea. In the presenc 0.5 MeVe of resistance to 32 P, Hydroxyurea and Pipobroman often remain effective. In the case of resistance to Hydroxyurea or Pipobroman, we have several possibilities: inversion of chemotherapy, other chemotherapy as Busulfan, 32 phosphorus…”

            Here it would seem (to me) that some chemotherapies might hold greater efficacy than 32P when a chemical disruption or suppression specific to one or more metabolic pathways critical to blood cell production can be tolerated. Of course, just as 32P doesn’t discriminate between cells — it can only preferentially kill those cells that preferentially uptake whatever metabolite it labels — one usually can’t find a chemical agent that disrupts just one and only one pathway. Both radiation and chemo are toxic one way or another.

            But this 32P resistance is particularly interesting. Not all blood-cell producing cells in the bone marrow are as susceptible to 32P poisoning as others. Knock out the most susceptible, and only the strong survive.

            Evolution in action.

            Or so it would seem. But a 0.5 MeV beta is itself rather non-discriminatory. Why the development of 32P resistance? Why are some cells less susceptible? Is it development of radiation resistance per se, or do the affected cells have a different metabolism either less dependent on phosphorus itself, or less dependent on whatever particular therapeutic carrier compounds it is bound to? Or does the body just find a way to more efficiently regenerate blood-cell generators after successive radiation treatments repeatedly kill them off?

            Another Atomic Rat-hole. Still, inquiring minds want to know…

  3. I am reminded that “Image Gently” & other such campaigns, with the stated objective of reducing patient radiation exposure, have always appeared to me to be a back-door way of reducing practitioner exposure.
    Why? Well, because radiologists & radiographers are among the very few occupations with any important history of radiation injury ; and because medical professionals in general tend to disregard warnings about risks to themselves, but will take very seriously warnings about risks to patients. Never forget that Marie Curie overexposed herself until her hands blistered, taking X-rays of wounded French servicemen during the World War.

    1. I wouldn’t speculate. The operator station at all X-radiation facilities I’ve visited is always well removed from the beam and well shielded. I personally think “Image Gently” is just as it appears: a well intended if perhaps somewhat misguided attempt to do the very best by the patients.

      Ultrasound and MRI are preferred. They’re also different. I recall the early days of the field when the latter was termed Nuclear Magnetic Resonance Imaging — because that’s what it is and its roots are in NMR spectroscopy.

      The “N” was dropped because… the “N” word, you know?

      For patient acceptance. There are things NMRI can do that nothing else can, but with the patient immobile for a lengthy period in a very expensive and intimidating instrument. No point in having them needlessly dwell on “nuclear” during the experience, or refuse the tool in the first place.

      But I am always amazed at the difference. Step into virtually any chiropractors office and fist thing after signing up and eyeballing your natural posture, they do a set of full-trunk and neck x-rays, frequently using older surplus hospital equipment. Takes five minutes, the time required to get you located and the tech back and forth behind the switch station.

      And here x-ray gives exactly the information the chiropractor needs.

      It usually gave exactly the information Marie Curie needed as a field nurse as well, when she needed it. And she was acutely aware of the risks. But Marie Sklodowska Curie was an exceptional case.

      Highly exceptional.

  4. “It was found that neutrons were very dangerous so nobody ever got close to this beam after this. It was a beautiful beam to see sort of like the rainbow. You see the beam coming out of the cyclotron and it s very tempting to get in and look at it. ”

    I don’t know much about cyclotrons but I’d never considered that you can “see” them running. No surprise that the people in the lab would go take a look; the dead rat story (to scare off the sightseeing) makes sense.

  5. What’s sad is, scientists should KNOW BETTER than to draw grand sweeping conclusions from a sample size of. . . one. Really.

    If any scientists warns you about dangers from something, because ONE rat died that was near a radiation source, every other scientist should have been like, “Have you even *tried* to reproduce it? No? Get stuffed.”

    1. @Jeff S

      Your comment is well taken except for the historical reality that the physicists and chemists at Berkeley’s cyclotron were young, few in number and inexperienced. John Lawrence was a medical doctor in mid career and he was Ernest Lawrence’s brother. It’s not surprising that his word wasn’t questioned by grad students.

      There had also been a number of national scare stories about radiation hazards published already in relation to the radium dial watch painters and Eben Byers overdosing on Radithor.

      There wasn’t yet any real evidence that radiation DIDN’T cause long term damage so there was no reason to reject Lawrence’s direction. It’s intriguing to me that Lawrence, a man who was clearly interested in finding beneficial uses for radiation and radioactive materials, didn’t realize that he was teaching people to be afraid.

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