Hiroshima
HIROSHIMA AND THE BOMB
The "Little Boy" atomic bomb exploded over Hiroshima at 8:15 a.m. on August 6th 1945 at an altitude of
580 meters above Shima Hospital, close to the A-bomb dome. The atomic bomb employed 235 Uranium and was
equivalent in power to 15 kilotons of TNT. The dissipation of energy is believed to have been in the ratio:
bomb blast (50%), thermal rays (35%) and radiation (15%).
The radiation can be divided into initial one, which was released in mid-air within one minute
of the explosion and accounted for 5% of the total energy, and residual radiation, which was released
later at ground level over a long period of time and accounted for 10%.
The initial radiation was composed primarily of gamma rays and neutrons. The residual radiation
is classified into 2 types: first, the nuclear fission products and the 235 Uranium that had not
undergone nuclear fission dispersed in mid-air and were converted into a radiation source consisting of
gamma rays, beta rays and alpha rays. Second, the neutrons that bombarded the ground caused nuclear
reactions which led to induced radioactivity.
Physical effects:
a)heat: on explosion, a fireball was created in mid-air. At the instant of detonation the temperature reached
several million degrees Centigrade, and at the surface of the fireball it was 7.000� C after 0,3 seconds; the
heat content was calculated to be 99.6 cal/cm2 in the vicinity of the ground below the point of detonation
(the hypocenter), and 1.8 cal/cm2 at a point 3.5 km away;
b)bomb blast: the explosion created an extremely high pressure at the point of detonation equal to several
hundred thousand atmospheres; the surrounding air expanded greatly to form the bomb blast, with a velocity
of 280 m/sec around the hypocenter, and 28 m/sec at a point 3.2 km away. The leading edge of the bomb
blast advanced as a shock wave, and had traveled 3,7 km from the hypocenter after 10 seconds, and covered
11 km after 30 seconds. The shock wave spread outwards; at the instant that the wind had abated, a
weaker blast blew inwards from the outside (due to the reduced air pressure at the hypocenter) and produced
a mushroom cloud;
c)radiation: the dose of initial radiation at a point on the ground 500 meters from the hypocenter was
estimated at 35 Gy of gamma rays and 6.04 Gy of neutrons; at 2 km, 0.07 Gy and 0 Gy.
Casualty estimates: the number of dead was 114,000. 95% of the fatalities ocurred among people exposed
within 2 km of the hypocenter. Almost all of the 30,000 severely injured were exposed at 1.0-2.5 km from the
hypocenter. 48,000 were believed to have received minor injuries, with the vast majority exposed at a
distance of 1.0-3.0 km.
Malignant tumors: there were significant increases in leukemia (1950), thyroid cancer (1955), breast
and lung cancer (1965) and multiple myelomas, gastric and colon cancer (1975).
Leukemia; the incidence:
a) rose in direct proportion to radiation dose;
b) increased with decreasing age at the time of bombing;
c) peaked at 7-8 years after exposure;
d) the incidence of chronic myelocytic leukemia was clearly greater in Hiroshima than in Nagasaki.
Solid cancers: the cancer risk increased with dose and with decreasing age at the time of bombing.
Unlike leukemia, the latency period increased with decreasing age at the time of bombing, with a marked radiation
effect evident when survivors reached the age level at which the cancers frequently occur.
Thyroid disorders:
a) benign nodules: data shows an increase with dose, with the rate clearly high
amongst individuals aged
20 or less at the time of bombing. There was an increase in mild ypothyroidism cases and lower
autoantibody positive rate.
Hyperparathyroidism: it was found to increase with dose, with the frequency increasing with decreasing
age at the time of bombing. Adenomas accounted for 80% of the disease.
Cataracts: its frequency and severity are radiation dose-dependent; symptoms developed from
several months to years after exposure, with severe cases occurring soon but mild cases not appearing until
after a latency period. The frequency of cataracts increases with proximity to the hypocenter, with the maximum
exposure distance at which atomic bomb cataracts are formed believed to be 1.6 to 1.8 km.
Keloids: atomic bomb burns extended over large areas of the body surface, with high mortality
rates due to second or third degree burns. Even if recovery occurred, the scars were far greater in size than
in usual burn cases, and instead of being restricted to one site, scars formed over various parts of the body.
After an apparent recovery, the scars swelled in 1946 to 1947 and became keloids.
I)Initial period scars: they occurred in 60-70% of burn cases, a rate much higher than in normal cases;
47% were 1.0 - 1.3 km from the hypocenter; 68% 1.4-2.0 km, and 50% 2.1-2.5 km. Although scars can appear
anywhere on the body, the sites were restricted due to clothing cover. The scars sometimes display severe
pain and itchiness.
In cases undergoing early resection, there was an extremely high rate of recurrence (80%).
II) Non-active phase scars: they can be observed after 10 years or more. Post-operative recurrence
following surgical resection were low (under 5%).
Frequency of mental retardation: about 1.100 people are thought to have been prenatally exposed
within 2 km of the hypocenter. A relationship between atomic bomb radiation and both mental retardation and
microcephaly has been apparent since the mid 1950�s.
It was dose-dependent for survivors prenatally exposed at a gestacional age of either 8-15 or 16-25
weeks, with the tendency marked in the former group.
Cancer risk in prenatally exposed survivors: the mortality rates up to 1984 for maternal uterine
dose of > 0,60 Gy were high for infants and those aged 15-39. There was an increased cancer incidence.
No difference was found with respect to trimester of pregnancy. The risk is the same when exposed under 10
years of age.
Peripheral blood lymphocytes: even apparently healthy survivors exhibit chromosomal aberrations
in peripheral blood lymphocytes, and show significant correlation with dose.
30-45 years after exposure, 90% of the chromosomal abnormalities were stable aberrations; in heavily
exposed translocations were predominant.
Chromosomal aberrations were detected in the T- and B-lymphocytes of peripheral blood, myeloid cells
and dermal fibroblasts. The sites of chromosomal breaks vary with individuals and the cells concerned.
T-lymphocytes in older survivors exhibit decreased function and reduced cell counts. There was decreased
immunocompetence among heavily exposed survivors with respect to influenza viruses, the hepatitis B virus,
and the Epstein-Barr virus; also, increase in positive rates of serum rheumatoid factor, serum IgM and IgA
in females.
Myeloid cells: a strong correlation exists between aberration frequency and distance from the
hypocenter, and hence with radiation dose. Virtyally all chromosomal aberrations are of stable type,
with translocations predominant, followed by inversions.
Chromosomal aberrations in the bone marrow act as an indicator for the development of various
hematopoietic diseases, as leukemia.
Somatic cell mutations: even now a significant relationship with dose can be observed between the
frequency of mutant erythrocyte glycophorin A genes and the doses estimated by DS86 dosimetry.
No correlation exists between dose and the mutant frequencies of T-lymphocyte hypoxanthine guanine
phosphoribosyl transferase or T-lymphocyte T-cell receptor genes.
The T cells which cause the HPRT and TCR mutations are virtually all eliminated within a relatively
short period after exposure, whereas long-term persistence is seen in the case of GPA mutants, which is
believed due to generation of somatic cell mutations in erythrocyte progenitors whitin the bone marrow.
But the GPA technique is only applicable to individuals with MN blood type (50% of the human
population).
Genetic studies: no significant effects due to atomic bomb radiation in any of the categories: sex
ratio, stillbirths, neonatal deaths, and infant mortality rates for ages up to 9 months, and congenital
malformations in stillborn babies or within the first 9 months of life.
Chromosomes: no radiation effect was observed in either numerical abnormalities (XYY, XXY, XXX and
mosaicism) or in structural rearrangements (e.g. inversion of the Y chromosomes). No increase in Down�s
syndrome was observed in the children of survivors.
Growth: reduced heights and body weights were observed among individuals heavily exposed as
infants and among prenatally exposed survivors. The reasons? Radiation effects on bone formation, or
changes in systemic hormonal environment?