firstCITIZEN

Disaster Hiroshima and Nagasaki

firstcitizen — Mon, 07 Apr 2008 10:47:37 +0000

The atomic bombings of Hiroshima and Nagasaki were nuclear attacks during World War II against the Empire of Japan by the United States at the order of U.S. President Harry S. Truman. After six months of intense firebombing of 67 other Japanese cities, the nuclear weapon “Little Boy” was dropped on the city of Hiroshima on Monday^, August 6, 1945, followed on August 9 by the detonation of the “Fat Man” nuclear bomb over Nagasaki. These are to date the only attacks with nuclear weapons in the history of warfare.

The bombs killed as many as 140,000 people in Hiroshima and 80,000 in Nagasaki by the end of 1945, roughly half on the days of the bombings. Since then, thousands more have died from injuries or illness attributed to exposure to radiation released by the bombs.In both cities, the overwhelming majority of the dead were civilians.

Six days after the detonation over Nagasaki, on August 15, Japan announced its surrender to the Allied Powers, signing the Instrument of Surrender on September 2, officially ending the Pacific War and therefore World War II. (Germany had signed its Instrument of Surrender on May 7, ending the war in Europe.) The bombings led, in part, to post-war Japan adopting Three Non-Nuclear Principles, forbidding that nation from nuclear armament.

The mushroom cloud over Hiroshima after the dropping of Little Boy

The Fat Man mushroom cloud resulting from the nuclear explosion over Nagasaki rises 18 km (11 mi, 60,000 ft) into the air from the hypocenter.

The Manhattan Project

Main article: Manhattan Project

The United States, with assistance from the United Kingdom and Canada,^[4] designed and built the first atomic bombs under what was called the Manhattan Project. The scientific research was directed by the American physicist, J. Robert Oppenheimer. The Hiroshima bomb, a gun-type bomb called “Little Boy”, was made with uranium-235, a rare isotope of uranium. The atomic bomb was first tested at Trinity Site, on July 16, 1945, near Alamogordo, New Mexico. The test weapon, “the gadget,” and the Nagasaki bomb, “Fat Man”, were both implosion-type devices made primarily of plutonium-239, a synthetic element.^[5]

Choice of targets

Map showing the locations of Hiroshima and Nagasaki, Japan where the two atomic weapons were employed

The Target Committee at Los Alamos on May 10–11, 1945, recommended Kyoto, Hiroshima, Yokohama, and the arsenal at Kokura as possible targets. The committee rejected the use of the weapon against a strictly military objective because of the chance of missing a small target not surrounded by a larger urban area. The psychological effects on Japan were of great importance to the committee members. They also agreed that the initial use of the weapon should be sufficiently spectacular for its importance to be internationally recognized. The committee felt Kyoto, as an intellectual center of Japan, had a population “better able to appreciate the significance of the weapon.” Hiroshima was chosen because of its large size, its being “an important army depot” and the potential that the bomb would cause greater destruction because the city was surrounded by hills which would have a “focusing effect”.^[6]

Secretary of War Henry L. Stimson struck Kyoto from the list because of its cultural significance, over the objections of General Leslie Groves, head of the Manhattan Project. According to Professor Edwin O. Reischauer, Stimson “had known and admired Kyoto ever since his honeymoon there several decades earlier.” On July 25 General Carl Spaatz was ordered to bomb one of the targets: Hiroshima, Kokura, Niigata, or Nagasaki as soon after August 3 as weather permitted and the remaining cities as additional weapons became available.^[7]

The Potsdam ultimatum

On July 26, Truman and other allied leaders issued The Potsdam Declaration outlining terms of surrender for Japan. It was presented as an ultimatum and stated that without a surrender, the Allies would attack Japan, resulting in “the inevitable and complete destruction of the Japanese armed forces and just as inevitably the utter devastation of the Japanese homeland” but the atomic bomb was not mentioned. On July 28, Japanese papers reported that the declaration had been rejected by the Japanese government. That afternoon, Prime Minister Kantaro Suzuki declared at a press conference that the Potsdam Declaration was no more than a rehash (yakinaoshi) of the Cairo Declaration and that the government intended to ignore it (mokusatsu).^[8] The statement was taken by both Japanese and foreign papers as a clear rejection of the declaration. Emperor Hirohito, who was waiting for a Soviet reply to noncommittal Japanese peace feelers (see July 17 Allied discussion of the Japanese offer), made no move to change the government position.^[9] On July 31, he made clear to Kido that the Imperial Regalia of Japan had to be defended at all costs.^[10]

In early July, on his way to Potsdam, Truman had re-examined the decision to use the bomb. In the end, Truman made the decision to drop the atomic bombs on Japan. His stated intention in ordering the bombings was to bring about a quick resolution of the war by inflicting destruction, and instilling fear of further destruction, that was sufficient to cause Japan to surrender.^[11]

Hiroshima

Hiroshima during World War II

At the time of its bombing, Hiroshima was a city of some industrial and military significance. A number of military camps were located nearby, including the headquarters of the Fifth Division and Field Marshal Shunroku Hata’s 2nd General Army Headquarters, which commanded the defense of all of southern Japan. Hiroshima was a minor supply and logistics base for the Japanese military. The city was a communications center, a storage point, and an assembly area for troops. It was one of several Japanese cities left deliberately untouched by American bombing, allowing a pristine environment to measure the damage caused by the atomic bomb. Another account stresses that after General Spaatz reported that Hiroshima was the only targeted city without prisoner of war (POW) camps, Washington decided to assign it highest priority^{[citation needed]}.

A postwar “Little Boy” casing mockup

The center of the city contained several reinforced concrete buildings and lighter structures. Outside the center, the area was congested by a dense collection of small wooden workshops set among Japanese houses. A few larger industrial plants lay near the outskirts of the city. The houses were of wooden construction with tile roofs, and many of the industrial buildings also were of wood frame construction. The city as a whole was highly susceptible to fire damage.

In front of the harbor of the city, on the island of Okunoshima, was a toxic gas factory linked to Unit 731.^[12] Different types of chemical weapons were produced there during the first part of the Shōwa era like mustard gas, yperite, lewisite and cyanide.^[13] Those gasses were used during World War II against Chinese soldiers and civilians and on the human experimentations of Shiro Ishii’s staff. ^[14]

The population of Hiroshima had reached a peak of over 381,000 earlier in the war, but prior to the atomic bombing the population had steadily decreased because of a systematic evacuation ordered by the Japanese government. At the time of the attack the population was approximately 255,000. This figure is based on the registered population used by the Japanese in computing ration quantities, and the estimates of additional workers and troops who were brought into the city may be inaccurate.

Seizo Yamada’s ground level photo taken from approximately 7 km northeast of Hiroshima.

The bombing

For the composition of the USAAF mission see 509th Composite Group.

Hiroshima was the primary target of the first nuclear bombing mission on August 6, with Kokura and Nagasaki being alternative targets. August 6 was chosen because there had previously been cloud cover over the target. The 393d Bombardment Squadron B-29 Enola Gay, piloted and commanded by 509th Composite Group commander Colonel Paul Tibbets, was launched from North Field airbase on Tinian in the West Pacific, about six hours flight time from Japan. The Enola Gay (named after Colonel Tibbets’ mother) was accompanied by two other B29s, The Great Artiste which carried instrumentation, commanded by Major Charles W. Sweeney, and a then-nameless aircraft later called Necessary Evil (the photography aircraft) commanded by Captain George Marquardt.^[15]

After leaving Tinian the aircraft made their way separately to Iwo Jima where they rendezvoused at 2440 m (8000 ft) and set course for Japan. The aircraft arrived over the target in clear visibility at 9855 m (32,000 ft). On the journey, Navy Captain William Parsons had armed the bomb, which had been left unarmed to minimize the risks during takeoff. His assistant, 2nd Lt. Morris Jeppson, removed the safety devices 30 minutes before reaching the target area.^[15]

Hiroshima, in the aftermath of the bombing

The release at 08:15 (Hiroshima time) was uneventful, and the gravity bomb known as “Little Boy“, a gun-type fission weapon with 60 kg (130 pounds) of uranium-235, took 57 seconds to fall from the aircraft to the predetermined detonation height about 600 meters (1,900 ft) above the city. It created a blast equivalent to about 13 kilotons of TNT. (The U-235 weapon was considered very inefficient, with only 1.38% of its material fissioning.)^[16] The radius of total destruction was about 1.6 km (1 mile), with resulting fires across 11.4 km² (4.4 square miles).^[17] Infrastructure damage was estimated at 90 percent of Hiroshima’s buildings being either damaged or completely destroyed.

About an hour before the bombing, Japanese early warning radar detected the approach of some American aircraft headed for the southern part of Japan. An alert was given and radio broadcasting stopped in many cities, among them Hiroshima. At nearly 08:00, the radar operator in Hiroshima determined that the number of planes coming in was very small—probably not more than three—and the air raid alert was lifted. To conserve fuel and aircraft, the Japanese had decided not to intercept small formations. The normal radio broadcast warning was given to the people that it might be advisable to go to air-raid shelters if B-29s were actually sighted, but no raid was expected beyond some sort of reconnaissance.

Announcement of the bombing in audio

Truman announcing the bombing of Hiroshima

President Truman announces the bombing of Hiroshima.

Problems listening to the file? See media help.

Japanese realization of the bombing

The energy released by the bomb was powerful enough to burn through clothing. The dark portions of the garments this victim wore at the time of the blast were emblazoned on to the flesh as scars, while skin underneath the lighter parts (which absorb less energy) was not damaged as badly.

The Tokyo control operator of the Japanese Broadcasting Corporation noticed that the Hiroshima station had gone off the air. He tried to re-establish his program by using another telephone line, but it too had failed.^[18] About twenty minutes later the Tokyo railroad telegraph center realized that the main line telegraph had stopped working just north of Hiroshima. From some small railway stops within 16 kilometers (10 mi) of the city came unofficial and confused reports of a terrible explosion in Hiroshima. All these reports were transmitted to the headquarters of the Japanese General Staff.

Military bases repeatedly tried to call the Army Control Station in Hiroshima. The complete silence from that city puzzled the men at headquarters; they knew that no large enemy raid had occurred and that no sizable store of explosives was in Hiroshima at that time. A young officer of the Japanese General Staff was instructed to fly immediately to Hiroshima, to land, survey the damage, and return to Tokyo with reliable information for the staff. It was generally felt at headquarters that nothing serious had taken place and that it was all a rumor.

The staff officer went to the airport and took off for the southwest. After flying for about three hours, while still nearly 100 miles (160 km) from Hiroshima, he and his pilot saw a great cloud of smoke from the bomb. In the bright afternoon, the remains of Hiroshima were burning. Their plane soon reached the city, around which they circled in disbelief. A great scar on the land still burning and covered by a heavy cloud of smoke was all that was left. They landed south of the city, and the staff officer, after reporting to Tokyo, immediately began to organize relief measures.

Tokyo’s first knowledge of what had really caused the disaster came from the White House public announcement in Washington, D.C., sixteen hours after the nuclear attack on Hiroshima.^[19]

By August 8, 1945, newspapers in the US were reporting that broadcasts from Radio Tokyo had described the destruction observed in Hiroshima. “Practically all living things, human and animal, were literally seared to death,” Japanese radio announcers said in a broadcast captured by Allied sources.^[20]

Post-attack casualties

According to most estimates, the immediate effects of the blast of the bombing of Hiroshima killed approximately 70,000 people. Estimates of total deaths by the end of 1945 from burns, radiation and related disease, the effects of which were aggravated by lack of medical resources, range from 90,000 to 140,000.^[21] ^[2] Some estimates state up to 200,000 had died by 1950, due to cancer and other long-term effects.^[1] ^[22] ^[23] From 1950 to 1990, roughly 9% of the cancer and leukemia deaths among bomb survivors was due to radiation from the bombs. ^[24] At least eleven known prisoners of war died from the bombing.^[25]

Survival of some structures

Nakajima area around ground zero. There remains modern “Rest House” (right) and a few structures.

Some of the reinforced concrete buildings in Hiroshima were very strongly constructed because of the earthquake danger in Japan, and their framework did not collapse even though they were fairly close to the center of damage in the city. Eizo Nomura (野村英三, Nomura Eizō^?) was the known closest survivor, who was in a basement of modern “Rest House” only 100 m from ground-zero at the time of the attack.^[26] Akiko Takakura (高蔵信子, Takakura Akiko^?) was among the closest survivors to the hypocenter of the blast. She had been in the strongly built Bank of Hiroshima only 300 m from ground-zero at the time of the attack.^[27] Since the bomb detonated in the air, the blast was more downward than sideways, which was largely responsible for the survival of the Prefectural Industrial Promotional Hall, now commonly known as the Genbaku, or A-bomb Dome designed and built by the Czech architect Jan Letzel, which was only 150 meters (490 ft) from ground zero (the hypocenter). The ruin was named Hiroshima Peace Memorial and made a UNESCO World Heritage site in 1996 over the objections of the U.S. and China.^[28]

Events of August 7-9

After the Hiroshima bombing, President Truman announced, “If they do not not accept our terms, they may expect a rain of ruin from the air the likes of which has never been seen on this earth.” On August 8, 1945, leaflets were dropped and warnings were given to Japan by Radio Saipan. (The area of Nagasaki did not receive warning leaflets until August 10, though the leaflet campaign covering the whole country was over a month into its operations.)^[29]^[30]

The Japanese government still did not react to the Potsdam Declaration. Emperor Hirohito, the government and the War council were considering four conditions for surrender: the preservation of the kokutai (Imperial institution and national polity), assumption by the Imperial Headquarters of responsibility for disarmament and demobilization, no occupation, and delegation to the Japanese government of the punishment of war criminals.

The Soviet Foreign Minister Molotov informed Tokyo of the Soviet Union’s unilateral abrogation of the Soviet-Japanese Neutrality Pact on April 5. At two minutes past midnight on August 9, Tokyo time, Soviet infantry, armor, and air forces launched an invasion of Manchuria. Four hours later, word reached Tokyo that the Soviet Union had declared war on Japan. The senior leadership of the Japanese Army began preparations to impose martial law on the nation, with the support of Minister of War Korechika Anami, in order to stop anyone attempting to make peace.

Responsibility for the timing of the second bombing was delegated to Colonel Tibbets as commander of the 509th Composite Group on Tinian. Scheduled for August 11 against Kokura, the raid was moved forward to avoid a five day period of bad weather forecast to begin on August 10.^[31] Three bomb pre-assemblies had been transported to Tinian, labeled F-31, F-32, and F-33 on their exteriors. On August 8 a dress rehearsal was conducted off Tinian by Maj. Charles Sweeney using Bockscar as the drop airplane. Assembly F-33 was expended testing the components and F-31 was designated for the mission August 9.^[32]

Nagasaki

Nagasaki during World War II

Urakami Tenshudo (Catholic Church in Nagasaki) in January 1946, destroyed by the atomic bomb, the dome of the church having toppled off.

The city of Nagasaki had been one of the largest sea ports in southern Japan and was of great wartime importance because of its wide-ranging industrial activity, including the production of ordnance, ships, military equipment, and other war materials.

In contrast to many modern aspects of Hiroshima, the bulk of the residences were of old-fashioned Japanese construction, consisting of wood or wood-frame buildings, with wood walls (with or without plaster), and tile roofs. Many of the smaller industries and business establishments were also housed in buildings of wood or other materials not designed to withstand explosions. Nagasaki had been permitted to grow for many years without conforming to any definite city zoning plan; residences were erected adjacent to factory buildings and to each other almost as closely as possible throughout the entire industrial valley.

Nagasaki had never been subjected to large-scale bombing prior to the explosion of a nuclear weapon there. On August 1, 1945, however, a number of conventional high-explosive bombs were dropped on the city. A few hit in the shipyards and dock areas in the southwest portion of the city, several hit the Mitsubishi Steel and Arms Works and six bombs landed at the Nagasaki Medical School and Hospital, with three direct hits on buildings there. While the damage from these bombs was relatively small, it created considerable concern in Nagasaki and many people—principally school children—were evacuated to rural areas for safety, thus reducing the population in the city at the time of the nuclear attack.

To the north of Nagasaki there was a camp holding British Commonwealth prisoners of war, some of whom were working in the coal mines and only found out about the bombing when they came to the surface. At least eight known POWs died from the bombing.^[33]

The bombing

A post-war “Fat Man” model

For the composition of the USAAF mission see 509th Composite Group.

On the morning of August 9, 1945, the U.S. B-29 Superfortress Bockscar, flown by the crew of 393rd Squadron commander Major Charles W. Sweeney, carried the nuclear bomb code-named “Fat Man“, with Kokura as the primary target and Nagasaki the secondary target. The mission plan for the second attack was nearly identical to that of the Hiroshima mission, with two B-29’s flying an hour ahead as weather scouts and two additional B-29’s in Sweeney’s flight for instrumentation and photographic support of the mission. Sweeney took off with his weapon already armed but with the electrical safety plugs still engaged.^[34]

Illustration of the implosion concept employed in “Fat Man”.

Observers aboard the weather planes reported both targets clear. When Sweeney’s aircraft arrived at the assembly point for his flight off the coast of Japan, the third plane, Big Stink, flown by the group’s Operations Officer, Lt. Col. James I. Hopkins, Jr. failed to make the rendezvous. Bockscar and the instrumentation plane circled for forty minutes without locating Hopkins. Already thirty minutes behind schedule, Sweeney decided to fly on without Hopkins.^[34]

Nagasaki before and after bombing

By the time they reached Kokura a half hour later, a 7/10 cloud cover had obscured the city, prohibiting the visual attack required by orders. After three runs over the city, and with fuel running low because a transfer pump on a reserve tank had failed before take-off, they headed for their secondary target, Nagasaki.^[34] Fuel consumption calculations made en route indicated that Bockscar had insufficient fuel to reach Iwo Jima and they would be forced to divert to Okinawa. After initially deciding that if Nagasaki were obscured on their arrival they would carry the bomb to Okinawa and dispose of it in the ocean if necessary, the weaponeer Navy Commander Frederick Ashworth decided that a radar approach would be used if the target was obscured.^[35]

At about 07:50 Japanese time, an air raid alert was sounded in Nagasaki, but the “all clear” signal was given at 08:30. When only two B-29 Superfortresses were sighted at 10:53, the Japanese apparently assumed that the planes were only on reconnaissance and no further alarm was given.

A few minutes later, at 11:00, The Great Artiste, the support B-29 flown by Captain Frederick C. Bock dropped instruments attached to three parachutes. These instruments also contained an unsigned letter to Professor Ryokichi Sagane, a nuclear physicist at the University of Tokyo who studied with three of the scientists responsible for the atomic bomb at the University of California, Berkeley, urging him to tell the public about the danger involved with these weapons of mass destruction. The messages were found by military authorities but not turned over to Sagane until a month later.^[36] In 1949 one of the authors of the letter, Luis Alvarez, met with Sagane and signed the document.^[37]

A Japanese report on the bombing characterized Nagasaki as “like a graveyard with not a tombstone standing”.

At 11:01, a last minute break in the clouds over Nagasaki allowed Bockscar’s bombardier, Captain Kermit Beahan, to visually sight the target as ordered. The “Fat Man” weapon, containing a core of ~6.4 kg (14.1 lbs.) of plutonium-239, was dropped over the city’s industrial valley. Forty-three seconds later it exploded 469 meters (1,540 ft) above the ground exactly halfway between the Mitsubishi Steel and Arms Works in the south and the Mitsubishi-Urakami Ordnance Works (Torpedo Works) in the north. This was nearly 3 kilometers (2 mi) northwest of the planned hypocenter; the blast was confined to the Urakami Valley and a major portion of the city was protected by the intervening hills.^[38] The resulting explosion had a blast yield equivalent to 21 kilotons of TNT. The explosion generated heat estimated at 3900 degrees Celsius (7000 degrees Fahrenheit) and winds that were estimated at 1005 km/h (624 mph).

Casualty estimates for immediate deaths range from 40,000 to 75,000.^[39] ^[40] ^[41] Total deaths by the end of 1945 may have reached 80,000.^[2] The radius of total destruction was about 1.6 km (1 mile), followed by fires across the northern portion of the city to 3.2 km (2 miles) south of the bomb.^[42] ^[43]

An unknown number of survivors from the Hiroshima bombing had made their way to Nagasaki, where they were bombed again.^[44]^[45]

Plans for more atomic attacks on Japan

The United States expected to have another atomic bomb ready for use in the third week of August, with three more in September and a further three in October.^[46] On August 10, Major General Leslie Groves, military director of the Manhattan Project, sent a memorandum to General of the Army George Marshall, Chief of Staff of the United States Army, in which he wrote that “the next bomb . . should be ready for delivery on the first suitable weather after 17 or 18 August.” On the same day, Marshall endorsed the memo with the comment, “It is not to be released over Japan without express authority from the President.”^[46] There was already discussion in the War Department about conserving the bombs in production until Operation Downfall, the projected invasion of Japan, had begun. “The problem now [August 13th] is whether or not, assuming the Japanese do not capitulate, to continue dropping them every time one is made and shipped out there or whether to hold them . . . and then pour them all on in a reasonably short time. Not all in one day, but over a short period. And that also takes into consideration the target that we are after. In other words, should we not concentrate on targets that will be of the greatest assistance to an invasion rather than industry, morale, psychology, and the like? Nearer the tactical use rather than other use.”^[46]

The surrender of Japan and subsequent occupation

Main articles: Surrender of Japan and Occupation of Japan

Up to August 9, the war council was still insisting on its four conditions for surrender. On that day Hirohito ordered Kido to “quickly control the situation” “because Soviet Union has declared war against us”. He then held an Imperial conference during which he authorized minister Togo to notify the Allies that Japan would accept their terms on one condition, that the declaration “does not compromise any demand which prejudices the prerogatives of His Majesty as a Sovereign ruler”.^[47]

On August 12, the Emperor informed the imperial family of his decision to surrender. One of his uncles, Prince Asaka, then asked whether the war would be continued if the kokutai could not be preserved. Hirohito simply replied “of course”.^[48] As the Allied terms seemed to leave intact the principle of the preservation of the Throne, Hirohito recorded on August 14 his capitulation announcement which was broadcast to the Japanese nation the next day despite a short rebellion by militarists opposed to the surrender.

In his declaration, Hirohito referred to the atomic bombings :

“

Moreover, the enemy now possesses a new and terrible weapon with the power to destroy many innocent lives and do incalculable damage. Should we continue to fight, not only would it result in an ultimate collapse and obliteration of the Japanese nation, but also it would lead to the total extinction of human civilization.Such being the case, how are We to save the millions of Our subjects, or to atone Ourselves before the hallowed spirits of Our Imperial Ancestors? This is the reason why We have ordered the acceptance of the provisions of the Joint Declaration of the Powers.

”

In his “Rescript to the soldiers and sailors” delivered on 17 August, he stressed the impact of the Soviet invasion and his decision to surrender, omitting any mention of the bombs.

During the year after the bombing, approximately 40,000 U.S. occupation troops were in Hiroshima. Nagasaki was occupied by 27,000 troops.

Atomic Bomb Casualty Commission

In the spring of 1948, the Atomic Bomb Casualty Commission (ABCC) was established in accordance with a presidential directive from Harry S. Truman to the National Academy of Sciences-National Research Council to conduct investigations of the late effects of radiation among the survivors in Hiroshima and Nagasaki. Among the casualties were found many unintended victims including:

Allied POWs.
Korean and Chinese labourers.
Students from Malaya on scholarships.
Some 3,200 Japanese American citizens.^[49]

One of the early studies conducted by the ABCC was on the outcome of pregnancies occurring in Hiroshima and Nagasaki, and in a control city, Kure located 18 miles (29 km) south from Hiroshima, to discern the conditions and outcomes related to radiation exposure. Some would say ABCC was not in a position to offer medical treatment to the survivors except in a research capacity. One author has claimed that the ABCC refused to provide medical treatment to the survivors for better research results.^[50] In 1975, the Radiation Effects Research Foundation was created to assume the responsibilities of ABCC.

The Hibakusha

Monument at ground zero in Nagasaki.

The surviving victims of the bombings are called Hibakusha (被爆者, Hibakusha^?), a Japanese word that literally translates to “explosion-affected people”. The suffering of the bombing is the root of Japan’s postwar pacifism^{[citation needed]}, and the nation has sought the abolition of nuclear weapons from the world ever since. As of 31 March 2007, there were 251,834 hibakusha recognized by the Japanese government; most live in Japan.^[51] The government of Japan recognizes about 1% of these as having illnesses caused by radiation.^[52] The memorials in Hiroshima and Nagasaki contain lists of the names of the hibakusha who are known to have died since the bombings. Updated annually on the anniversaries of the bombings, as of August 2007 the memorials record the names of almost 400,000 hibakusha — 253,008^[53] in Hiroshima, and 143,124^[54] in Nagasaki. News accounts often use these figures as a source for the numbers of people who have died because of the bombings.^{[citation needed]}

Korean survivors

During the war Japan brought many Korean conscripts to both Hiroshima and Nagasaki to work as forced labor. According to recent estimates, about 20,000 Koreans were killed in Hiroshima and about 2,000 died in Nagasaki. It is estimated that one in seven of the Hiroshima victims was of Korean ancestry.^[55] For many years Koreans had a difficult time fighting for recognition as atomic bomb victims and were denied health benefits.^{[citation needed]} Though such issues have been addressed in recent years, issues regarding recognition linger.^{[citation needed]}

Debate over bombings

Main article: Debate over the atomic bombings of Hiroshima and Nagasaki

Those who argue in favor of the decision to drop the bombs generally assert that they caused the Japanese surrender. This prevented massive casualties on both sides in the Operation Downfall invasion of Japan and from an otherwise prolonged war.

Those who argue against the decision to drop the bombs characterize them as inherently immoral, war crimes or, crimes against humanity and/or state terrorism. They may also argue that they were militarily unnecessary.

Mutation

firstcitizen — Sun, 30 Mar 2008 07:32:36 +0000

Definition

A Mutation occurs when a DNA gene is damaged or changed in such a way as to alter the genetic message carried by that gene.A Mutagen is an agent of substance that can bring about a permanent alteration to the physical composition of a DNA gene such that the genetic message is changed.Once the gene has been damaged or changed the mRNA transcribed from that gene will now carry an altered message.

The polypeptide made by translating the altered mRNA will now contain a different sequence of amino acids. The function of the protein made by folding this polypeptide will probably be changed or lost. In this example, the enzyme that is catalyzing the production of flower color pigment has been altered in such a way it no longer catalyzes the production of the red pigment.

No product (red pigment) is produced by the altered protein.

In subtle or very obvious ways, the phenotype of the organism carrying the mutation will be changed. In this case the flower, without the pigment is no longer red.

In biology, mutations are changes to the nucleotide sequence of the genetic material of an organism. Mutations can be caused by copying errors in the genetic material during cell division, by exposure to ultraviolet or ionizing radiation, chemical mutagens, or viruses, or can occur deliberately under cellular control during processes such as hypermutation. In multicellular organisms, mutations can be subdivided into germ line mutations, which can be passed on to descendants, and somatic mutations, which are not transmitted to descendants in animals. Plants sometimes can transmit somatic mutations to their descendants asexually or sexually (in case when flower buds develop in somatically mutated part of plant). A new mutation that was not inherited from either parent is called a de novo mutation.Mutations create variations in the gene pool. Less favorable (or deleterious) mutations can be reduced in frequency in the gene pool by natural selection, while more favorable (beneficial or advantageous) mutations may accumulate and result in adaptive evolutionary changes. For example, a butterfly may produce offspring with new mutations. Many times those are have no effect; but one might change the color of one of the butterfly’s offspring, making it harder (or easier) for predators to see. If this color change is advantageous, the chance of this butterfly surviving and producing its own offspring are a little better, and over time the number of butterflies with this mutation may form a larger percentage of the population.Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no significant effect on an organism’s fitness. Also, DNA repair mechanisms are able to mend most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.

Classification

By effect on structure

Illustrations of five types of chromosomal mutations.The sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health depending on where they occur and whether they alter the function of essential proteins. Structurally, mutations can be classified as:

Small-scale mutations, such those as affecting a small gene in one or a few nucleotides, including:
- Point mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another^[1]. Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mis-pairing, or mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality). These changes are classified as transitions or transversions^[2]. An example of a transversion is adenine (A) being converted into a cytosine (C). There are also many other examples that can be found. Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for:
  - Silent mutations: which code for the same amino acid.
  - Missense mutations: which code for a different amino acid.
  - Nonsense mutations: which code for a stop and can truncate the protein.
- Insertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements (e.g. AT repeats). Insertions in the coding region of a gene may alter splicing of the mRNA (splice site mutation), or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reverted by excision of the transposable element.
- Deletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are generally irreversible: though exactly the same sequence might theoretically be restored by an insertion, transposable elements able to revert a very short deletion (say 1-2 bases) in any location are either highly unlikely to exist or do not exist at all. Note that a deletion is not the exact opposite of an insertion: the former is quite random while the latter consists of a specific sequence inserting at locations that are not entirely random or even quite narrowly defined.
Large-scale mutations in chromosomal structure, including:
- Amplifications (or gene duplications) leading to multiple copies of all chromosomal regions, increasing the dosage of the genes located within them.
- Deletions of large chromosomal regions, leading to loss of the genes within those regions.
- Mutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl). These include:
  - Chromosomal translocations: interchange of genetic parts from nonhomologous chromosomes.
  - Interstitial deletions: an intra-chromosomal deletion that removes a segment of DNA from a single chromosome, thereby apposing previously distant genes. For example, cells isolated from a human astrocytoma, a type of brain tumor, were found to have a chromosomal deletion removing sequences between the “fused in glioblastoma” (fig) gene and the receptor tyrosine kinase “ros”, producing a fusion protein (FIG-ROS). The abnormal FIG-ROS fusion protein has constitutively active kinase activity that causes oncogenic transformation (a transformation from normal cells to cancer cells).
  - Chromosomal inversions: reversing the orientation of a chromosomal segment.
- Loss of heterozygosity: loss of one allele, either by a deletion or recombination event, in an organism that previously had two different alleles.

By effect on function

Loss-of-function mutations are the result of gene product having less or no function. When the allele has a complete loss of function (null allele) it is often called an amorphic mutation. Phenotypes associated with such mutations are most often recessive. Exceptions are when the organism is haploid, or when the reduced dosage of a normal gene product is not enough for a normal phenotype (this is called haploinsufficiency).
Gain-of-function mutations change the gene product such that it gains a new and abnormal function. These mutations usually have dominant phenotypes. Often called a neo-morphic mutation.
Dominant negative mutations (also called anti-morphic mutations) have an altered gene product that acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular function (often inactive) and are characterised by a dominant or semi-dominant phenotype. In humans, Marfan syndrome is an example of a dominant negative mutation occurring in an autosomal dominant disease. In this condition, the defective glycoprotein product of the fibrillin gene (FBN1) antagonizes the product of the normal allele.
Lethal mutations are mutations that lead the death of the organisms which carry the mutations.

By aspect of phenotype affected

Morphological mutations usually affect the outward appearance of an individual. Mutations can change the height of a plant or change it from smooth to rough seeds.
Biochemical mutations result in lesions stopping the enzymatic pathway. Often, morphological mutants are the direct result of a mutation due to the enzymatic pathway.

By inheritance

The human genome contains two copies of each gene- a paternal and a maternal allele.

Wildtype or Homozygous non-mutated is when neither allele is mutated.
A Heterozygous mutation is when only one allele is mutated.
A Homozygous mutation is when both the paternal and maternal alleles have an identical mutation.
Compound heterozygous mutations or a Genetic compound is when the paternal and maternal alleles have two different mutations.

Special classes

Conditional mutation is a mutation that has wild-type (or less severe) phenotype under certain “permissive” environmental conditions and a mutant phenotype under certain “restrictive” conditions. For example, a temperature-sensitive mutation can cause cell death at high temperature (restrictive condition), but might have no deleterious consequences at a lower temperature (permissive condition).

Causes of mutation

Two classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens.Spontaneous mutations on the molecular level include:

Tautomerism - A base is changed by the repositioning of a hydrogen atom.
Depurination - Loss of a purine base (A or G).
Deamination - Changes a normal base to an atypical base; C → U, (which can be corrected by DNA repair mechanisms), or spontaneous deamination of 5-methycytosine (irreparable), or A → HX (hypoxanthine).
Transition - A purine changes to another purine, or a pyrimidine to a pyrimidine.
Transversion - A purine becomes a pyrimidine, or vice versa.

Benzopyrene, the major mutagen in tobacco smoke, in an adduct to DNA. Produced from PDB 1JDG.Induced mutations on the molecular level can be caused by:

Chemicals
- Nitrosoguanidine (NTG)
- Hydroxylamine NH₂OH
- Base analogs (e.g. BrdU)
- Simple chemicals (e.g. acids)
- Alkylating agents (e.g. N-ethyl-N-nitrosourea (ENU)) These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can only mutate the DNA when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions.
- Methylating agents (e.g. ethyl methanesulfonate (EMS))
- Polycyclic hydrocarbons (e.g. benzopyrenes found in internal combustion engine exhaust)
- DNA intercalating agents (e.g. ethidium bromide)
- DNA crosslinker (e.g. platinum)
- Oxidative damage caused by oxygen(O) radicals
Radiation
- Ultraviolet radiation (nonionizing radiation) excites electrons to a higher energy level. DNA molecules are good absorbers of ultraviolet light, especially that with wavelengths in the 260 to 280 nm range.^{[citation needed]} Two nucleotide bases in DNA - cytosine and thymine-are most vulnerable to excitation that can change base-pairing properties. UV light can induce adjacent thymine bases in a DNA strand to pair with each other, as a bulky dimer.
- Ionizing radiation

DNA has so-called hotspots, where mutations occur up to 100 times more frequently than the normal mutation rate. A hotspot can be at an unusual base, e.g., 5-methylcytosine.Mutation rates also vary across species. Evolutionary biologists have theorized that higher mutation rates are beneficial in some situations, because they allow organisms to evolve and therefore adapt more quickly to their environments. For example, repeated exposure of bacteria to antibiotics, and selection of resistant mutants, can result in the selection of bacteria that have a much higher mutation rate than the original population (mutator strains).

Nomenclature

Nomenclature of mutations specify the type of mutation and base or amino acid changes.

Amino acid substitution - (e.g. D111E) The first letter is the one letter code of the wildtype amino acid, the number is the position of the amino acid from the N terminus and the second letter is the one letter code of the amino acid present in the mutation. If the second letter is ‘X’, any amino acid may replace the wildtype.
Amino acid deletion - (e.g. ΔF50 The Greek symbol Δ or ‘delta‘ indicates a deletion. The letter refers to the amino acid present in the wildtype and the number is the position from the N terminus of the amino acid were it to be present as in the wildtype.

Types of mutations

Adaptive mutation

Main article: Adaptive mutationIn mainstream biological thought it is held that while mutagenesis is non-random in many ways, the utility of a genetic mutation to the organism in which it occurs does not affect the rate at which it occurs. However experimental evidence exists that in some instances the rate of specific mutations arising is greater when they are advantageous to the organism than when they are not.

Back mutation

Back mutation is a change in a nucleotide pair of a point-mutated DNA sequence that restores the original sequence and hence the original phenotype.

Frameshift mutation

Main article: Frameshift mutationA frameshift mutation is a mutation caused by indels, ie. inserts or deletes a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can disrupt the reading frame, or the grouping of the codons, resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.

Missense mutation

Main article: Missense mutationMissense mutations or nonsynonymous mutations are types of point mutations where a single nucleotide is changed to cause substitution of a different amino acid. This in turn can render the resulting protein nonfunctional. Such mutations are responsible for diseases such as Epidermolysis bullosa, sickle-cell disease, and SOD1 mediated ALS(Boillée 2006, p. 39).

Neutral mutation

Main article: Neutral mutationA neutral mutation is a mutation that occurs in an amino acid codon (presumably within an mRNA molecule) which results in the use of a different, but chemically similar, amino acid. This is similar to a silent mutation, where a codon mutation may encode the same amino acid (see Wobble Hypothesis); for example, a change from AUU to AUC will still encode leucine, so no discernable change occurs (a silent mutation).

Nonsense mutation

Main article: Nonsense mutationA nonsense mutation is a frameshift mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional protein product.

Point mutation

Main article: Point mutationA point mutation, or substitution, is a type of mutation that causes the replacement of a single base nucleotide with another nucleotide. Often the term point mutation also includes insertions or deletions of a single base pair (which have more of an adverse effect on the synthesized protein due to nucleotides still being read in triplets, but in different frames- a mutation called a frameshift mutation).

Silent mutation

Main article: Silent mutationSilent mutations are DNA mutations that do not result in a change to the amino acid sequence of a protein. They may occur in a non-coding region (outside of a gene or within an intron), or they may occur within an exon in a manner that does not alter the final amino acid sequence. The phrase silent mutation is often used interchangeably with the phrase synonymous mutation; however, synonymous mutations are a subcategory of the former, occurring only within exons.

Harmful mutations

Changes in DNA caused by mutation can cause errors in protein sequence, creating partially or completely non-functional proteins. To function correctly, each cell depends on thousands of proteins to function in the right places at the right times. When a mutation alters a protein that plays a critical role in the body, a medical condition can result. A condition caused by mutations in one or more genes is called a genetic disorder. However, only a small percentage of mutations cause genetic disorders; most have no impact on health. For example, some mutations alter a gene’s DNA base sequence but don’t change the function of the protein made by the gene. Studies in the fly Drosophila melanogaster suggest that if a mutation does change a protein, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.

If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This is the case in hereditary diseases. On the other hand, a mutation can occur in a somatic cell of an organism. Such mutations will be present in all descendants of this cell, and certain mutations can cause the cell to become malignant, and thus cause cancer..Often, gene mutations that could cause a genetic disorder are repaired by the DNA repair system of the cell. Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because DNA can be damaged or mutated in many ways, the process of DNA repair is an important way in which the body protects itself from disease.

Beneficial mutations

A very small percentage of all mutations actually have a positive effect. These mutations lead to new versions of proteins that help an organism and its future generations better adapt to changes in their environment. For example, a specific 32 base pair deletion in human CCR5 (CCR5-Δ32) confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes.The CCR5 mutation is more common in those of European descent. One theory for the etiology of the relatively high frequency of CCR5-Δ32 in the European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People who had this mutation were able to survive infection; thus, its frequency in the population increased.It could also explain why this mutation is not found in Africa where the bubonic plague never reached. Newer theory says the selective pressure on the CCR5 Delta 32 mutation has been caused by smallpox instead of the bubonic plague.