Early clinical and pathological findings in the bombing victims

On the day of the Nagasaki bombing, Dr. Tatsuichiro Akizuki was on duty at his hospital in the Urakami district, 1800 m from the hypocenter. The building was damaged and partly destroyed by fire, but all of the staff and the patients quickly escaped and initially survived.

The attack had occurred at 11 a.m.; shortly afterwards, the first victims from outside began to arrive, seeking help:

About ten minutes after the explosion, a big man, half-naked, holding his head between his hands, came into the yard towards me … ‘Got hurt, sir,’ he groaned; he shivered as if he were cold. ‘I’m hurt.’

I stared at him, at the strange-looking man. Then I saw it was Mr. Zenjiro Tsujiomoto, a market gardener and a friendly neighbor to me and the hospital. I wondered what had happened to the robust Zenjiro. ‘What’s the matter with you, Tsujimoto?’ I asked him, holding him in my arms.

‘In the pumpkin field over there—getting pumpkins for the patients—got hurt…’ he said, speaking brokenly and breathing feebly. It was all he could do to keep standing. Yet it didn’t occur to me that he had been seriously injured.

‘Come along now,’ I said, ‘You are perfectly all right. I assure you. Where’s your shirt? Lie down and rest somewhere where it’s cool. I’ll be with you in a moment.’

His head and his face were whitish; his hair was singed. It was because his eyelashes had been scorched away that he seemed so bleary-eyed. He was half-naked because his shirt had been burned from his back in a single flash. … 

Another person who looked just like him wandered into the yard. … ‘Help me,’ he said, groaning, half-naked, holding his head between his hands. He sat down, exhausted. ‘Water … Water …’ he whispered.

As time passed, more and more people in similar plight came up to the hospital—ten minutes, twenty minutes, an hour after the explosion. All were of the same appearance, sounded the same. ‘I’m hurt, hurt! I’m burning! Water!’ … Half-naked or stark naked, they walked with strange, slow steps, groaning from deep inside themselves … they looked whitish. … One victim who managed to reach the hospital asked ‘Is this a hospital?’ before suddenly collapsing on the ground. … 

‘Water, water’ they cried. They went instinctively down to the banks of the stream [below the hospital], because their bodies had been scorched and their throats were parched and inflamed; they were thirsty. I didn’t realize then that these were the symptoms of ‘flash burn.’

Thus far, Akizuki has described victims whom he had encountered within one hour or so of the attack. At this early stage, we can make the following observations:

• Akizuki does not immediately recognize his ‘strange-looking’ neighbor, which suggests that his features are already somewhat distorted. They will be much more so later in the day.
• He notices some signs of immediate burns—singed hair and eyelashes, as well as nudity (see Section 9.4).
• Akizuki does not describe any other outward signs of injury; instead, he reassures his suffering neighbor that he is alright.
• The victims speak hoarsely; their throats are ‘parched and inflamed,’ and they are thirsty; their breath is labored.
• The victims are pale and weak, and some collapse.
• The victims are holding their heads between their hands, suggesting that they have a severe headache.

While the above observations capture the early stage of the injuries, the victims’ aspect is strikingly transformed later on. Here is Akizuki’s description:

In the afternoon a change was noticeable in the appearance of the injured people who came up to the hospital. The crowd of ghosts which had looked whitish in the morning were now burned black. Their hair was burnt; their skin, which was charred and blackened, blistered and peeled. Such were those who now came toiling up to the hospital yard and fell there weakly.

These victims might have come from another district of the city, further away from the hospital but closer to the hypocenter, where they might have suffered more severe immediate burns. However, a similar change is also apparent in the victims who had arrived earlier. While on his way to help an injured colleague, he again encounters some of them:

When I reached the little river, I came across an astonishing scene. Half-naked or nearly naked people were crouching at the water’s edge. All looked alike, without distinction of sex or age; long hair was the only clue to the female sex. On one side their bodies had been grilled and were highly inflamed. The procession of white ghosts which had passed me some time before had gathered here on the bank of the stream, seeking water to relieve the terrible thirst and the scorching pain of their bodies. Crowds of these victims lined the stream.

‘Oh, how it hurts! I’m hurting—burning!’ said Mr. Tsujimoto, groaning. His face, which had been whitish, when I saw him earlier, was now darker, blackened; his lips were swollen. His wife sat not far away, her face and body also blackened, moaning insensibly.

It is clear that, in this group of patients at least, overt symptoms have become manifest with a delay of several hours. They are now obvious even in the wife of Mr. Tsujimoto, whom Akizuki had not even mentioned as being afflicted earlier on.125 Still later in the day, Akizuki describes both Mr. and Mrs. Tsujimoto as ‘cinder-burnt.’ While Mrs. Tsujiomoto will live for a few more days, her husband expires the same night:

At about midnight, Mr Tsujimoto’s condition suddenly worsened. … By degrees, Mr. Tsujimoto’s breathing became harsher. I couldn’t feel any pulse. … Suddenly Mr. Tsujimoto went into a violent fit of convulsions; his eyes bulged. ‘His last moment has come!’ said someone.

Labored breathing in the bombing victims is confirmed by another eyewitness from Nagasaki, Akira Nagasaka [156, p. 74]:

A woman, probably in her mid-thirties, was lying on the ground, her hair wild, her clothes in tatters, her face red with blood. She was putting all the strength that remained in her to raise her head and murmur, “Water, water.”

When I had gathered my wits about me, I scooped some dirty water out of a nearby ditch and gave it to her. She drank it as if it were the most delicious thing ever to pass her lips, but most of it merely trickled down her chin onto her breast. “More, please,” she begged, but she could do no more than gasp for breath when I brought it, having no strength left to drink.

The testimony from Hiroshima is, if anything, even more gruesome.126 Eyewitness Kosaku Okabe [156, p. 35] was not near the hypocenter for the bombing, but he came upon the scene in downtown Hiroshima several hours afterwards:

Wherever a puddle of water had collected from burst water pipes, people had gathered like ants around a honey pot. Many had died where they lay at the water’s edge, their strength gone. Others had clambered over the dead bodies to get at the water, only to die in the same way, their bodies piling one on top of another.

Okabe also describes the aspect of the victims:

Most people had been wearing light summer shirts that morning. But most of the dead were bare chested, and many were completely naked, perhaps because their clothes had been burned off them. The parts of the body that had been exposed to the flash had suffered great burns, and the skin was turning purple and trailing from the body in strips.

In every case, the eyeballs of the dead were either protruding from their sockets or hanging out completely. Blood had gushed from the mouth, ears, and nose. The tongue had swelled to the size of a golf ball and had pushed its way out of the mouth, gripped tightly by the teeth. The whole anatomy seemed to have been destroyed. Most bodies were bloated, and it was often impossible to tell whether they were male or female.

The grisly, apocalyptic picture painted by Okabe’s testimony might seem exaggerated, but each detail is confirmed by other eyewitnesses [14,156,180]. While the victims described by Okabe are already dead, another witness depicts the scene when some of them are still alive. Hachiya [62] relates the observations told him on August 6^th by one of his visitors, Mr. Hashimoto, who was already mentioned in the preceding chapter. Like Okabe, Hashimoto entered the inner city after the bombing:

When I reached the Misasa railway bridge … I encountered a dead man. I saw many others in the water tanks fighting for breath. The sight was horrible.

Mr. Hashimoto also describes the days following the bombing:

During those days, wherever you went, there were so many dead lying around it was impossible to walk without encountering them—swollen, discolored bodies with froth oozing from their noses and mouths.

Overall, the testimony given by several independent witnesses from the two cities is remarkably consistent. We therefore can’t dismiss it, but instead must try to understand what exactly could have caused such terrible injury and disfigurement.

Before identifying the causes, we must take a step back and consider what the clinical signs observed in these victims tell us about the underlying pathophysiology.

10.1.3.2

Circulatory shock and capillary leak syndrome

The initial paleness reported by Akizuki in patients who arrived on foot at his clinic suggests beginning circulatory shock. At a more advanced stage of shock, paleness may give way to cyanosis; this is observed by Akizuki in some of the initially pale patients at a later time, and it is also described by Okabe in the victims that he encounters several hours after the Hiroshima bombing.

Shock may be accompanied by capillary leak syndrome, which causes intense thirst and, after intake of large volumes of water, extreme edema (Figure 10.1). All of these symptoms were described in the bombing victims.

A related observation is the acute headache, which is suggested by Akizuki’s description of patients holding their heads between their hands. Headaches are caused by vascular distension in the meninges; the simultaneous occurrence with shock suggest that the latter was likely caused in part by the loss of vascular tone.

Figure 10.1: Patient with capillary leak syndrome (deceased; [181]). Left: the face is cyanotic and extremely swollen. Right: swelling of a limb has led to fascial compartment syndrome, in which nerves and blood vessels are compressed by the edematous muscle tissue within a tightly confined space. Transient incision of the fascia (a sheet of firm connective tissue) that encloses the compartment was carried out to relieve the compression.

What could have caused these three effects? The easy part of the answer is that neither ‘flash burn’ nor ionizing radiation can account for this entire clinical picture. As discussed in Section 9.6, flash burns should have been visible in some form immediately, but Akizuki fails to notice them in several patients whom he encounters shortly after the bombing. Without very severe exterior burns, there simply is no mechanism by which a flash of light could produce acute respiratory distress.

As regards ionizing radiation, here is the case description of a patient who received approximately five times a lethal dose of it [150, p. 218]:

In a nuclear criticality accident at Los Alamos in 1958, one worker received a total body dose of mixed neutron and γ-radiation estimated to be between 39 and 49 Gy. Parts of his body may have received as much as 120 Gy. This person went into a state of shock immediately and was unconscious within a few minutes. After 8 hours, no lymphocytes were found in the circulating blood, and there was virtually a complete urinary shutdown despite the administration of large amounts of fluids. The patient died 35 hours after the accident.

This patient received a dose of radiation about as high as it could have been near the hypocenter in Hiroshima. He promptly developed cerebrovascular syndrome and also general circulatory shock, and he quickly died of it—without intensive care, he probably would have died on the same day, as did many of the victims in Hiroshima and Nagasaki. However, no mention is made of facial or general cyanosis, respiratory distress, peeling skin, or dangling eyes. Since he lost consciousness so quickly, he would not have had time enough to find a puddle and drink enough water to swell up to any great extent. Thus, apart from shock and rapid death, his clinical picture bears no resemblance to that described in the victims at Hiroshima and Nagasaki.

Animal experiments reported by Bloom et al. [26] showed the lungs to have relatively low susceptibility to radiation; lethal whole-body doses of X-rays or neutrons produced little or no evidence of lung tissue damage when compared to controls.128 The skin, too, showed very minor effects at such doses. While these findings do of course not rule out lung or skin damage with supra-lethal irradiation, they exclude preferential damage to these organs, which is evident in the Hiroshima and Nagasaki victims.

The more difficult and interesting part of the answer concerns how we actually can account for the clinical picture. Since we already have evidence that napalm and mustard gas were used, we will examine if they can explain it.

In summary, therefore, I propose that napalm and mustard gas, alone or in combination, can account for the full clinical picture observed in the early fatalities, while radiation cannot. Mustard gas was very likely the dominant cause in those victims who initially appeared to be free of burns, such as Mr. Tsujimoto, but napalm may well have contributed significantly in many other victims. The use of other poisons is possible but cannot be demonstrated based on the limited evidence available.

Probably all of us have been warned against looking at a solar eclipse with unprotected eyes. Doing so may cause circumscribed burns to the retina, which will leave behind a permanent defect in the field of vision (a scotoma). The same would be expected in people who happen to look at a nuclear flash, and indeed Rose et al. [194] have reported on six American soldiers who developed just such burns after looking at the fireballs of later nuclear tests, from distances of up to ten miles. The authors also explain why retinal burns may occur at such large distance from the detonations; the reason is illustrated in Figure 10.2. While the light intensity at the pupil decreases with the square of the distance, this effect is exactly compensated by the diminishing size of the retinal image. The brightness of the latter decreases only in proportion to the haziness of the air, which thus becomes the limiting factor.131

Figure 10.2: Effects of pupil diameter and of object distance on retinal images. A: All light that originates from the same point on the object and falls onto the aperture (pupil) is focused onto the same point on the retina; this creates an inverted image of the object. B: If the pupil narrows, the size of the retinal image remains unchanged, but its intensity is reduced. C: If, relative to A, the pupil diameter stays the same but the object distance increases, then the light that falls onto the pupil is ‘spread thin’, but this is exactly compensated by the reduced size of the image—the intensity of the retinal image stays the same.

The size of the pupil also limits the light intensity at the retina, of course; that is, after all, its purpose. Since the pupil is wider at night than during the day, it follows that retinal burns will occur at greater distances by night. Rose et al. [194] do not provide any details on the time of day or the magnitude of the detonations that occasioned their clinical cases, which means that we cannot directly apply their findings to the conditions at Hiroshima and Nagasaki.

The quantitative aspects of retinal burns are somewhat more explicitly addressed by Byrnes et al. [195]. These authors present studies on 700 rabbits, which were exposed to the flashes of nuclear detonations at night, at distances of up to 42 miles. At all distances, the retinas suffered discrete burns, which with increasing distance decreased in size and in the degree of tissue destruction. Within eight miles of the detonations, the authors describe a ‘volcano-like’ appearance of the lesions,132 with prominent edges and a deep central hole, the bottom of which they made out to be the sclera, that is, the eyeball’s sturdy outer layer of connective tissue. The rabbit eye lesions appear similar to those in Rose’s human patients (Figure 10.3).

Figure 10.3: Nuclear flash burns of the retina in a human and in a rabbit. A: retinal burn in a soldier exposed 2 miles from the detonation, photographed 6 weeks after the event [194]. B: Early stage of retinal lesion in rabbit. C: Histological section through rabbit retinal lesion. The band of gray tissue is the sclera; the dark layer comprises the choroid and the retina. The retina is bulged and ruptured. B and C from Byrnes et al. [195].

Byrnes et al. [195] do not state the magnitudes of the detonations that burned those rabbit retinas. They do, however, apply the findings from their rabbit studies to provide explicit estimates for the range at which a ‘typical’ 20 kt fission bomb—as described theoretically in Glasstone [90], and as purportedly used in Hiroshima and Nagasaki—should cause retinal burns in humans, by day or by night, and under various conditions of visibility. They conclude that the range would be up to 40 miles by night, and some 10-20% less by day. However, they do not spell out all of the assumptions that went into these estimates, and it is not clear to me why the difference in range between day and night would be so small. Their assumed decrease of the pupil aperture from 8 mm by night to 4 mm by day will reduce the energy reaching the retina by a factor of 4; according to my own calculations, this should reduce the range by day to approximately half that by night, giving a maximum range a bit below the atmospheric visibility. Of note, the largest distance among Rose’s case reports [194] is 10 miles.

To gain a firmer footing, we can estimate the heat dose to the retina at Hiroshima and Nagasaki from the thermal radiation which purportedly prevailed on the outside (see Figure 9.1A), the geometrical constraints of ocular vision (see Figure 10.2), and the transmittance of the translucent parts of the eyeball. Following Byrnes et al. [195], the latter will be taken to be 0.4. We will assume a pupil diameter of 2 mm, which corresponds to full adaptation to bright sunlight—the bombings occurred on bright, sunny summer mornings—and a distance from the pupil to the retina of 24 mm.

According to Glasstone [90], the fireball has two distinct stages of high luminosity. The ‘early fireball’ exists at 1 ms after the detonation. It lasts only a very short time, during which a comparatively small cumulative amount of radiation is released; however, its small diameter of only 27 m means that this amount will be focused onto a small retinal image, where the intensity may still reach harmful levels. The late fireball is larger (200-300 m across) and also much longer-lived—up to 3 seconds, but most of the energy is released within the first second. It thus reaches a higher energy density across a larger retinal image. We will consider both stages of the fireball in our calculation.

Figure 10.4: Thermal energy density (A) and diameter (B) of retinal images of the Hiroshima and Nagasaki nuclear bombs. ‘Early’ and ‘late’ in A refer to the stage of the fireball. See text for details.

The results are depicted in Figure 10.4. For interpreting them, with need to know the thermal energy which, if transferred to the retina as a very brief flash, will produce a retinal burn. Byrnes et al. [195] estimate this value to be cal/cm² 0.1, and they also state that in a separate series of experiments, which is not described in detail in the cited study (and which I have not found published elsewhere), burns were indeed induced with an only slightly higher energy (cal/cm² 0.14). All data points in Figure 10.4A exceed that threshold.

What are the roles of early and late fireball, respectively, in the generation of retinal burns? On the short time scale of the early fireball (1 ms), no protective lid reflex will be triggered, so that anyone with the flash in their field of vision will receive at least this dose of energy in full. On the other hand, the longer duration of the late fireball means that some of the energy may be shut out by lid reflexes. The question therefore arises to what extent the late fireball contributes to the formation of retinal burns. The sizes of the burns observed by Rose et al. [194], when compared to the predicted ones in Figure 10.4B, suggest that the late fireball does contribute significantly; but since those authors do not tell us how similar those nuclear detonations were in size to the ‘typical’ 20 kt bomb—if they were larger, then maybe so were the early fireballs—we cannot be quite sure. In any event, even in the most stringent scenario—pupils adapted to a bright sky before the flash, and considering the early fireball only—the retinal doses of thermal radiation still exceed the burn threshold. Overall, therefore, both theoretical considerations and previous evidence [194,195] indicate that retinal burns should have been very common in both Hiroshima and Nagasaki.

The ophthalmologist John Flick arrived in Japan in early September and spent several weeks examining a large number of patients in both Hiroshima and Nagasaki. His report [193] is the most comprehensive and detailed of its kind. He writes:

At the end of the second day I had examined approximately 300 patients. I had found the usual traumatic lesions one sees in wartime but none of the corneal or lenticular syndromes I had expected to find. There were few ophthalmias among the sick and those found were of the nonspecific kind due to infection. Knowing the high degree of radioresistance of the tissues of the posterior segment I had paid little attention to ophthalmoscopic studies.133

The posterior segment of the eyeball includes the retina, and its examination uses an ophthalmoscope. Thus, Flick’s remark suggests that he was initially focused on the effects of ionizing radiation more than on those of the flash of light.134 Nevertheless, a short while later, he does make a thorough study of the retinal symptoms in survivors. This is prompted by his observation of retinal bleeding in two patients with hematopoetic syndrome (see Section 8.2.1):

On the third day I was examining two moribund Japanese soldiers with bloody diarrhea, bleeding from the gums, covered from head to foot with petechiae. Their white [blood cell] counts were 2,000 and 900. I examined their eyegrounds. Both had extensive hemorrhagic and exudative lesions of the retina. It seemed entirely consistent with the rest of the picture … these characteristic fundus [retinal] lesions were one of the most reliable criteria of radiation sickness.

In his paper, Flick individually summarizes and also tabulates several dozen of his cases. Of the retinal lesions he describes, he attributes not a single one to ‘flash burn’, nor do any of the lesions shown as illustrations exhibit the striking volcano crater aspect evident in Figure 10.3.

The dearth of clinical cases of retinal flash burn in Hiroshima and Nagasaki is acknowledged by Rose et al. [194], and Byrnes et al. [195]. Both papers do, however, cite one report which purportedly describes one actual case. From Rose et al.:

The literature reveals no report of such a burn except for a single case of bilateral central scotoma incurred in the Hiroshima atomic explosion.

The clinical picture described in the reference given by Rose and by Byrnes, however—Oyama and Sasaki [197]—is not at all characteristic.135 Thus, the medical literature documents not a single case of retinal flash burns in Hiroshima or Nagasaki.

Flick shows some histopathological pictures of retinas from deceased patients, which exhibit the sequelae of hemorrhages but again have no similarity with flash burn lesions [193]. Likewise, Liebow, who surveys the autopsy materials he had commandeered from Japanese pathologists while serving on the Joint Commission, mentions hemorrhage as the only type of retinal lesion [42].

Schlaegel has reported a study on autopsy materials from a series of patients at Nagasaki who had died from ‘radiation sickness’ approximately four weeks after the bombings [198]. He finds a variety of lesions, mostly to the anterior eye (see Section 10.3); however, he does not describe or discuss any cases of retinal flash burn. The same is true of another, shorter report by Wilder [199]. Overall, I have found not a single study that provided any evidence of retinal burns in autopsy materials from Hiroshima or Nagasaki.

In contrast to the medical literature, both Akizuki and Hachiya suggest that some sort of retinal burns indeed occurred. In early September, Akizuki is visited in his hospital by an American military physician, who proceeds to examine the eyes of his patients [167, p. 131]:

He seemed to be an eye specialist, for he began eventually to examine the patients eyes with an ophthalmoscope … The American remarked: “Most of them have had the optic nerves of their retinas damaged by the A-bomb’s flash, and their eyesight has been impaired. They may even lose it altogether.”

Similarly, in his diary entry from August 23^rd, Hachiya recounts a conversation with his hospital’s ophthalmologist, Dr. Koyama:

I asked Dr. Koyama what his findings had been in patients with eye injuries. “Those who were watching the plane had their eye grounds burned,” he replied. “The flash of light apparently went through the pupils and left them with a blind area in the central portion of their visual fields. Most of the eye-ground burns are third degree, so cure is impossible.”

On the next day, Hachiya muses about his own condition:

I recalled Dr. Koyama’s account of patients who had been blinded by looking directly at the pika. Their blindness was understandable because their eye nerves had been scorched. My exposure was indirect. I had seen only the flash, but the heat rays had not reached me so the “mirrors” in my eyes were not injured.

Hachiya’s distinction between exposure to the flash and the thermal rays is fictitious, however—‘thermal rays’ may comprise both visible light (‘the flash’) and infrared light, but with a nuclear fireball visible light should account for the greater share. Moreover, both visible and infrared light travel in a straight line; one cannot suffer one but be spared the other.

It is noteworthy that Oyama and Sasaki published their short abstract [197] while employed in the same hospital as Hachiya and Koyama. Presumably, the authors would have had access to the patients examined by Koyama, or at least to their files. In this hospital, a significant number of autopsies were carried out in the weeks after the bombing by Hiroshima medical school pathologist Dr. Tamagawa. His autopsy samples were later appropriated by Liebow, who makes no mention of retinal burns (see Section 10.2.4).

That neither clinical files nor autopsies from Koyama’s own hospital furnished more than Oyama and Sasaki’s single case, which morphed into a ‘retinal flash burn’ only in the skilled hands of later American authors, strongly suggests that Koyama’s diagnosis was premature.136 The cases he observed may have been similar to those which Flick attributed to thrombocytopenia rather than to flash burns, and which would indeed have healed in those patients who survived their ARS in the end. In my view, therefore, the anecdotal reports are lacking in substance and cannot stand up to the uniformly negative evidence from the proper medical literature; they are discussed here only for completeness’ sake.

As noted before in Section 10.1.4, the lungs have low radiosensitivity, and they should not have been significantly affected by radiation in any victims that survived the bombing for more than a day. Nevertheless, in the relatively limited number of autopsies that were performed on victims who died within the first one or two weeks, emphysema (distension of lung tissue) was commonly found: Table 8.25 in Ishikawa et al. [8] notes emphysema in 5 patients out of 12 who died between August 9^th and 15^th, and whose bodies were dissected by the Japanese pathologist Yamashina.

In their loot of Japanese autopsy materials, Liebow et al. [42] also observe emphysema, as well as atelectasis, which is the opposite of emphysema—namely, lung tissue that is devoid of air because it has been cut off from ventilation. They find both in the majority of the limited number of early fatalities they survey. On page 856, they note:

The foci of pulmonary emphysema and atelectasis without hemorrhage observed in some of the early casualties (Fig. 20) are difficult to interpret. These were found frequently at death in patients who had not been exposed to blast.

Figure 10.6: Lung emphysema (excessive inflation) and atelectasis (excessive deflation) in an early fatality from Hiroshima. Photograph from Liebow et al. [42], annotations by this author.

Liebow’s Figure 20 (referred to in the quote) is shown here as Figure 10.6. The deceased patient is a thirteen years old boy, who is said to have died on the third day; thus, the lesions are truly acute and indicate some sort of obstruction of bronchioles (small bronchi).138

The difficulty which Liebow and colleagues perceived with interpreting their findings is readily dispelled if we consider causes other than atomic bombs. The book “The residual effects of warfare gases” discusses the effects of mustard gas on the lungs and observes [139, p. 92]:

Emphysema was frequently found in combination with bronchitis. It usually appeared immediately after gassing and was compensatory in character, due to the extensive atelectasis found following gassing with mustard.

The atelectasis, in turn, is understood to arise from bronchial obstruction. Thus, what we have here is a milder expression of the pathological changes in the lung which we invoked in Section 10.1.4 to account for the clinical picture in immediate fatalities on the day of the bombing.

The largest group of patients whose autopsy materials were surveyed by Liebow et al. were those who had succumbed within weeks 3 to 6 after the bombing. In slightly more than half of these cases, the authors found a varied picture with edema, hemorrhage, necrosis, and infection. These processes were focused on the bronchioles (small bronchi) but tended to expand and become confluent (see Figure 10.7).

Figure 10.7: Focal necrosis, inflammation, and hemorrhage in the lungs of bombing victims. Photographs taken from Figures 17 (A) and 19 (B) in [42].

With respect to this group of patients, Liebow et al. don’t express any puzzlement as to the causation; presumably, they ascribe their findings to the bone marrow suppression, which would pave the way for infections and also for the hemorrhage. This is indeed most likely an important contributing factor, and it would be equally well explained by radiation and mustard gas. We may note that the lesions remain centered on the bronchi, which suggests primary damage to them; this would be expected with mustard gas, yet not impossible in its absence. The same combination of findings was reported in a series of autopsies of German mustard gas victims (from the final months of World War I) by Heitzmann [28]. In summing up his findings, Heitzmann describes the appearance of the lungs as bunt, that is, checkered, which seems an apt description of the lungs shown in Figure 10.7. On the other hand, high-dose irradiation alone did not cause any of these changes in animal lungs [26, p. 704 ff]. Overall, while Liebow’s findings suggest causation by mustard gas rather than by radiation, the time elapsed between trauma and death means that this evidence is more ambiguous than the atelectasis and emphysema at the very early stage.