Antimatter

From Wikipedia, the free encyclopedia

In modern physics, antimatter is defined as a material composed of the antiparticle (or "partners") to the corresponding particles of ordinary matter.

In theory, a particle and its anti-particle have the same mass as one another, but opposite electric charge, and other differences in quantum numbers. For example, a proton has positive charge while an antiproton has negative charge. A collision between any particle and its anti-particle partner is known to lead to their mutual annihilation, giving rise to various proportions of intense photons (gamma rays), neutrinos, and sometimes less-massive particle–antiparticle pairs.

Annihilation usually results in a release of energy that becomes available for heat or work. The amount of the released energy is usually proportional to the total mass of the collided matter and antimatter, in accord with the mass–energy equivalence equation, E = mc².^[1]

Antimatter particles bind with one another to form antimatter, just as ordinary particles bind to form normal matter. For example, a positron (the antiparticle of the electron) and an antiproton (the antiparticle of the proton) can form an antihydrogen atom. Physical principles indicate that complex antimatter atomic nuclei are possible, as well as anti-atoms corresponding to the known chemical elements.

There is considerable speculation as to why the observable universe is composed almost entirely of ordinary matter, as opposed to an equal mixture of matter and antimatter. This asymmetry of matter and antimatter in the visible universe is one of the great unsolved problems in physics.^[2] The process by which this inequality between matter and antimatter particles developed is called baryogenesis.

Antimatter in the form of anti-atoms is one of the most difficult materials to produce. Individual antimatter particles, however, are commonly produced by particle accelerators and in some types of radioactive decay. The nuclei of antihelium have been artificially produced with difficulty. These are the most complex anti-nuclei so far observed.^[3]

Play media

There are some 500 terrestrial gamma-ray flashes daily. The red dots show those spotted by the Fermi Gamma-ray Space Telescope in 2010. The blue areas indicate where potential lighting can occur for terrestrial gamma-ray flashes.Play media

A video showing how scientists used the Fermi Gamma-ray Space Telescope's gamma-ray detector to uncover bursts of antimatter from thunderstorms

 

 

 

 

 

 

 

Formal definition

Formally, antimatter particles can be defined by their negative baryon number or lepton number, while "normal" (non-antimatter) matter particles have a positive baryon or lepton number.^[4][5] These two classes of particles are the antiparticle partners of one another.

History of the concept

The idea of negative matter appears in past theories of matter that have now been abandoned. Using the once popular vortex theory of gravity, the possibility of matter with negative gravity was discussed by William Hicks in the 1880s. Between the 1880s and the 1890s, Karl Pearson proposed the existence of "squirts"^[6] and sinks of the flow of aether. The squirts represented normal matter and the sinks represented negative matter. Pearson's theory required a fourth dimension for the aether to flow from and into.^[7]

The term antimatter was first used by Arthur Schuster in two rather whimsical letters to Nature in 1898,^[8] in which he coined the term. He hypothesized antiatoms, as well as whole antimatter solar systems, and discussed the possibility of matter and antimatter annihilating each other. Schuster's ideas were not a serious theoretical proposal, merely speculation, and like the previous ideas, differed from the modern concept of antimatter in that it possessed negative gravity.^[9]

The modern theory of antimatter began in 1928, with a paper^[10] by Paul Dirac. Dirac realised that his relativistic version of the Schrödinger wave equation for electrons predicted the possibility of antielectrons. These were discovered by Carl D. Anderson in 1932 and named positrons (a portmanteau of "positive electron"). Although Dirac did not himself use the term antimatter, its use follows on naturally enough from antielectrons, antiprotons, etc.^[11] A complete periodic table of antimatter was envisaged by Charles Janet in 1929.^[12]

The Feynman–Stueckelberg interpretation states that antimatter and antiparticles are regular particles traveling backward in time.^[13]

Notation

One way to denote an antiparticle is by adding a bar over the particle's symbol. For example, the proton and antiproton are denoted as
p
and
p
, respectively. The same rule applies if one were to address a particle by its constituent components. A proton is made up of
u

u

d
quarks, so an antiproton must therefore be formed from
u

u

d
antiquarks. Another convention is to distinguish particles by their electric charge. Thus, the electron and positron are denoted simply as
e− and
e+ respectively. However, to prevent confusion, the two conventions are never mixed.

Properties

There are compelling theoretical reasons to believe that, aside from the fact that antiparticles have different signs on all charges (such as electric charge and spin), matter and antimatter have exactly the same properties.^[14][15] This means a particle and its corresponding antiparticle must have identical masses and decay lifetimes (if unstable). It also implies that, for example, a star made up of antimatter (an "antistar") will shine just like an ordinary star.^[16] This idea was tested experimentally in 2016 by the ALPHA experiment, which measured the transition between the two lowest energy states of antihydrogen. The results, which are identical to that of hydrogen, confirmed the validity of quantum mechanics for antimatter.^[17][18]

Origin and asymmetry

Almost all matter observable from the Earth seems to be made of matter rather than antimatter. If antimatter-dominated regions of space existed, the gamma rays produced in annihilation reactions along the boundary between matter and antimatter regions would be detectable.^[19]
Antiparticles are created everywhere in the universe where high-energy particle collisions take place. High-energy cosmic rays impacting Earth's atmosphere (or any other matter in the Solar System) produce minute quantities of antiparticles in the resulting particle jets, which are immediately annihilated by contact with nearby matter. They may similarly be produced in regions like the center of the Milky Way and other galaxies, where very energetic celestial events occur (principally the interaction of relativistic jets with the interstellar medium). The presence of the resulting antimatter is detectable by the two gamma rays produced every time positrons annihilate with nearby matter. The frequency and wavelength of the gamma rays indicate that each carries 511 keV of energy (i.e., the rest mass of an electron multiplied by c²).

Observations by the European Space Agency's INTEGRAL satellite may explain the origin of a giant antimatter cloud surrounding the galactic center. The observations show that the cloud is asymmetrical and matches the pattern of X-ray binaries (binary star systems containing black holes or neutron stars), mostly on one side of the galactic center. While the mechanism is not fully understood, it is likely to involve the production of electron–positron pairs, as ordinary matter gains kinetic energy while falling into a stellar remnant.^[20][21]

Antimatter may exist in relatively large amounts in far-away galaxies due to cosmic inflation in the primordial time of the universe. Antimatter galaxies, if they exist, are expected to have the same chemistry and absorption and emission spectra as normal-matter galaxies, and their astronomical objects would be observationally identical, making them difficult to distinguish.^[22] NASA is trying to determine if such galaxies exist by looking for X-ray and gamma-ray signatures of annihilation events in colliding superclusters.^[23]

Natural production

Positrons are produced naturally in β⁺ decays of naturally occurring radioactive isotopes (for example, potassium-40) and in interactions of gamma quanta (emitted by radioactive nuclei) with matter. Antineutrinos are another kind of antiparticle created by natural radioactivity (β⁻ decay). Many different kinds of antiparticles are also produced by (and contained in) cosmic rays. In January 2011, research by the American Astronomical Society discovered antimatter (positrons) originating above thunderstorm clouds; positrons are produced in gamma-ray flashes created by electrons accelerated by strong electric fields in the clouds.^[24][25] Antiprotons have also been found to exist in the Van Allen Belts around the Earth by the PAMELA module.^[26][27]

Antiparticles are also produced in any environment with a sufficiently high temperature (mean particle energy greater than the pair production threshold). It is hypothesized that during the period of baryogenesis, when the universe was extremely hot and dense, matter and antimatter were continually produced and annihilated. The presence of remaining matter, and absence of detectable remaining antimatter,^[28] is called baryon asymmetry. The exact mechanism which produced this asymmetry during baryogenesis remains an unsolved problem. One of the necessary conditions for this asymmetry is the violation of CP symmetry, which has been experimentally observed in the weak interaction.

Recent observations indicate black holes and neutron stars produce vast amounts of positron-electron plasma via the jets.^[29][30][31]

Observation in cosmic rays

Satellite experiments have found evidence of positrons and a few antiprotons in primary cosmic rays, amounting to less than 1% of the particles in primary cosmic rays. This antimatter cannot all have been created in the Big Bang, but is instead attributed to have been produced by cyclic processes at high energies. For instance, electron-positron pairs may be formed in pulsars, as a magnetized neutron star rotation cycle shears electron-positron pairs from the star surface. Therein the antimatter forms a wind which crashes upon the ejecta of the progenitor supernovae. This weathering takes place as "the cold, magnetized relativistic wind launched by the star hits the non-relativistically expanding ejecta, a shock wave system forms in the impact: the outer one propagates in the ejecta, while a reverse shock propagates back towards the star."^[32] The former ejection of matter in the outer shock wave and the latter production of antimatter in the reverse shock wave are steps in a space weather cycle.
Preliminary results from the presently operating Alpha Magnetic Spectrometer (AMS-02) on board the International Space Station show that positrons in the cosmic rays arrive with no directionality, and with energies that range from 10 GeV to 250 GeV. In September, 2014, new results with almost twice as much data were presented in a talk at CERN and published in Physical Review Letters.^[33][34] A new measurement of positron fraction up to 500 GeV was reported, showing that positron fraction peaks at a maximum of about 16% of total electron+positron events, around an energy of 275 ± 32 GeV. At higher energies, up to 500 GeV, the ratio of positrons to electrons begins to fall again. The absolute flux of positrons also begins to fall before 500 GeV, but peaks at energies far higher than electron energies, which peak about 10 GeV.^[35] These results on interpretation have been suggested to be due to positron production in annihilation events of massive dark matter particles.^[36]

Cosmic ray antiprotons also have a much higher energy than their normal-matter counterparts (protons). They arrive at Earth with a characteristic energy maximum of 2 GeV, indicating their production in a fundamentally different process from cosmic ray protons, which on average have only one-sixth of the energy.^[37]

There is no evidence of complex antimatter atomic nuclei, such as antihelium nuclei (i.e., anti-alpha particles), in cosmic rays. These are actively being searched for, because the detection of natural antihelium implies the existence of large antimatter structures such as an antistar. A prototype of the AMS-02 designated AMS-01, was flown into space aboard the Space Shuttle Discovery on STS-91 in June 1998. By not detecting any antihelium at all, the AMS-01 established an upper limit of 1.1×10⁻⁶ for the antihelium to helium flux ratio.^[38]

Artificial production

Positrons

Positrons were reported^[39] in November 2008 to have been generated by Lawrence Livermore National Laboratory in larger numbers than by any previous synthetic process. A laser drove electrons through a gold target's nuclei, which caused the incoming electrons to emit energy quanta that decayed into both matter and antimatter. Positrons were detected at a higher rate and in greater density than ever previously detected in a laboratory. Previous experiments made smaller quantities of positrons using lasers and paper-thin targets; however, new simulations showed that short, ultra-intense lasers and millimeter-thick gold are a far more effective source.^[40]

Antiprotons, antineutrons, and antinuclei

The existence of the antiproton was experimentally confirmed in 1955 by University of California, Berkeley physicists Emilio Segrè and Owen Chamberlain, for which they were awarded the 1959 Nobel Prize in Physics.^[41] An antiproton consists of two up antiquarks and one down antiquark (
u

u

d
). The properties of the antiproton that have been measured all match the corresponding properties of the proton, with the exception of the antiproton having opposite electric charge and magnetic moment from the proton. Shortly afterwards, in 1956, the antineutron was discovered in proton–proton collisions at the Bevatron (Lawrence Berkeley National Laboratory) by Bruce Cork and colleagues.^[42]

In addition to antibaryons, anti-nuclei consisting of multiple bound antiprotons and antineutrons have been created. These are typically produced at energies far too high to form antimatter atoms (with bound positrons in place of electrons). In 1965, a group of researchers led by Antonino Zichichi reported production of nuclei of antideuterium at the Proton Synchrotron at CERN.^[43] At roughly the same time, observations of antideuterium nuclei were reported by a group of American physicists at the Alternating Gradient Synchrotron at Brookhaven National Laboratory.^[44]

Antihydrogen atoms

In 1995, CERN announced that it had successfully brought into existence nine hot antihydrogen atoms by implementing the SLAC/Fermilab concept during the PS210 experiment. The experiment was performed using the Low Energy Antiproton Ring (LEAR), and was led by Walter Oelert and Mario Macri.^[45] Fermilab soon confirmed the CERN findings by producing approximately 100 antihydrogen atoms at their facilities. The antihydrogen atoms created during PS210 and subsequent experiments (at both CERN and Fermilab) were extremely energetic and were not well suited to study. To resolve this hurdle, and to gain a better understanding of antihydrogen, two collaborations were formed in the late 1990s, namely, ATHENA and ATRAP.
In 1999, CERN activated the Antiproton Decelerator, a device capable of decelerating antiprotons from 3500 MeV to 5.3 MeV — still too "hot" to produce study-effective antihydrogen, but a huge leap forward. In late 2002 the ATHENA project announced that they had created the world's first "cold" antihydrogen.^[46] The ATRAP project released similar results very shortly thereafter.^[47] The antiprotons used in these experiments were cooled by decelerating them with the Antiproton Decelerator, passing them through a thin sheet of foil, and finally capturing them in a Penning–Malmberg trap.^[48] The overall cooling process is workable, but highly inefficient; approximately 25 million antiprotons leave the Antiproton Decelerator and roughly 25,000 make it to the Penning–Malmberg trap, which is about 1/1000 or 0.1% of the original amount.

The antiprotons are still hot when initially trapped. To cool them further, they are mixed into an electron plasma. The electrons in this plasma cool via cyclotron radiation, and then sympathetically cool the antiprotons via Coulomb collisions. Eventually, the electrons are removed by the application of short-duration electric fields, leaving the antiprotons with energies less than 100 meV.^[49] While the antiprotons are being cooled in the first trap, a small cloud of positrons is captured from radioactive sodium in a Surko-style positron accumulator.^[50] This cloud is then recaptured in a second trap near the antiprotons. Manipulations of the trap electrodes then tip the antiprotons into the positron plasma, where some combine with antiprotons to form antihydrogen. This neutral antihydrogen is unaffected by the electric and magnetic fields used to trap the charged positrons and antiprotons, and within a few microseconds the antihydrogen hits the trap walls, where it annihilates. Some hundreds of millions of antihydrogen atoms have been made in this fashion.

In 2005, ATHENA disbanded and some of the former members (along with others) formed the ALPHA Collaboration, which is also based at CERN. The primary goal of these collaborations is the creation of less energetic ("cold") antihydrogen, better suited to study.^{[citation needed]}

In 2016 a new antiproton decelerator and cooler called ELENA (E Low ENergy Antiproton decelerator) was built. It takes the antiprotons from the antiproton decelerator and cools them to 90 keV which is "cold" enough to study. More than a hundred antiprotons can be captured per second, a huge improvement, but it would still take several thousand years to make a nanogram of antimatter.

Most of the sought-after high-precision tests of the properties of antihydrogen could only be performed if the antihydrogen were trapped, that is, held in place for a relatively long time. While antihydrogen atoms are electrically neutral, the spins of their component particles produce a magnetic moment. These magnetic moments can interact with an inhomogeneous magnetic field; some of the antihydrogen atoms can be attracted to a magnetic minimum. Such a minimum can be created by a combination of mirror and multipole fields.^[51] Antihydrogen can be trapped in such a magnetic minimum (minimum-B) trap; in November 2010, the ALPHA collaboration announced that they had so trapped 38 antihydrogen atoms for about a sixth of a second.^[52][53] This was the first time that neutral antimatter had been trapped.

On 26 April 2011, ALPHA announced that they had trapped 309 antihydrogen atoms, some for as long as 1,000 seconds (about 17 minutes). This was longer than neutral antimatter had ever been trapped before.^[54] ALPHA has used these trapped atoms to initiate research into the spectral properties of the antihydrogen.^[55]

The biggest limiting factor in the large-scale production of antimatter is the availability of antiprotons. Recent data released by CERN states that, when fully operational, their facilities are capable of producing ten million antiprotons per minute.^[56] Assuming a 100% conversion of antiprotons to antihydrogen, it would take 100 billion years to produce 1 gram or 1 mole of antihydrogen (approximately 6.02×10²³ atoms of anti-hydrogen).

Antihelium

Antihelium-3 nuclei (3He
) were first observed in the 1970s in proton–nucleus collision experiments at the Institute for High Energy Physics by Y. Prockoshkin's group (Protvino near Moscow, USSR)^[57] and later created in nucleus–nucleus collision experiments.^[58] Nucleus–nucleus collisions produce antinuclei through the coalescense of antiprotons and antineutrons created in these reactions. In 2011, the STAR detector reported the observation of artificially created antihelium-4 nuclei (anti-alpha particles) (4He
) from such collisions.^[59]

Preservation

Antimatter cannot be stored in a container made of ordinary matter because antimatter reacts with any matter it touches, annihilating itself and an equal amount of the container. Antimatter in the form of charged particles can be contained by a combination of electric and magnetic fields, in a device called a Penning trap. This device cannot, however, contain antimatter that consists of uncharged particles, for which atomic traps are used. In particular, such a trap may use the dipole moment (electric or magnetic) of the trapped particles. At high vacuum, the matter or antimatter particles can be trapped and cooled with slightly off-resonant laser radiation using a magneto-optical trap or magnetic trap. Small particles can also be suspended with optical tweezers, using a highly focused laser beam.^[60]

In 2011, CERN scientists were able to preserve antihydrogen for approximately 17 minutes.^[61]

Cost

Scientists claim that antimatter is the costliest material to make.^[62] In 2006, Gerald Smith estimated $250 million could produce 10 milligrams of positrons^[63] (equivalent to $25 billion per gram); in 1999, NASA gave a figure of $62.5 trillion per gram of antihydrogen.^[62] This is because production is difficult (only very few antiprotons are produced in reactions in particle accelerators), and because there is higher demand for other uses of particle accelerators. According to CERN, it has cost a few hundred million Swiss francs to produce about 1 billionth of a gram (the amount used so far for particle/antiparticle collisions).^[64] In comparison, to produce the first atomic weapon, the cost of the Manhattan Project was estimated at $23 billion with inflation during 2007.^[65]
Several studies funded by the NASA Institute for Advanced Concepts are exploring whether it might be possible to use magnetic scoops to collect the antimatter that occurs naturally in the Van Allen belt of the Earth, and ultimately, the belts of gas giants, like Jupiter, hopefully at a lower cost per gram.^[66]

Uses

Medical

Matter–antimatter reactions have practical applications in medical imaging, such as positron emission tomography (PET). In positive beta decay, a nuclide loses surplus positive charge by emitting a positron (in the same event, a proton becomes a neutron, and a neutrino is also emitted). Nuclides with surplus positive charge are easily made in a cyclotron and are widely generated for medical use. Antiprotons have also been shown within laboratory experiments to have the potential to treat certain cancers, in a similar method currently used for ion (proton) therapy.^[67]

Fuel

Isolated and stored anti-matter could be used as a fuel for interplanetary or interstellar travel^[68] as part of an antimatter catalyzed nuclear pulse propulsion or other antimatter rocketry, such as the redshift rocket. Since the energy density of antimatter is higher than that of conventional fuels, an antimatter-fueled spacecraft would have a higher thrust-to-weight ratio than a conventional spacecraft.

If matter–antimatter collisions resulted only in photon emission, the entire rest mass of the particles would be converted to kinetic energy. The energy per unit mass (9×10¹⁶ J/kg) is about 10 orders of magnitude greater than chemical energies,^[69] and about 3 orders of magnitude greater than the nuclear potential energy that can be liberated, today, using nuclear fission (about 200 MeV per fission reaction^[70] or 8×10¹³ J/kg), and about 2 orders of magnitude greater than the best possible results expected from fusion (about 6.3×10¹⁴ J/kg for the proton–proton chain). The reaction of 1 kg of antimatter with 1 kg of matter would produce 1.8×10¹⁷ J (180 petajoules) of energy (by the mass–energy equivalence formula, E = mc²), or the rough equivalent of 43 megatons of TNT – slightly less than the yield of the 27,000 kg Tsar Bomba, the largest thermonuclear weapon ever detonated.

Not all of that energy can be utilized by any realistic propulsion technology because of the nature of the annihilation products. While electron–positron reactions result in gamma ray photons, these are difficult to direct and use for thrust. In reactions between protons and antiprotons, their energy is converted largely into relativistic neutral and charged pions. The neutral pions decay almost immediately (with a lifetime of 85 attoseconds) into high-energy photons, but the charged pions decay more slowly (with a lifetime of 26 nanoseconds) and can be deflected magnetically to produce thrust.

Charged pions ultimately decay into a combination of neutrinos (carrying about 22% of the energy of the charged pions) and unstable charged muons (carrying about 78% of the charged pion energy), with the muons then decaying into a combination of electrons, positrons and neutrinos (cf. muon decay; the neutrinos from this decay carry about 2/3 of the energy of the muons, meaning that from the original charged pions, the total fraction of their energy converted to neutrinos by one route or another would be about 0.22 + (2/3)⋅0.78 = 0.74).^[71]

Weapons

Antimatter has been considered as a trigger mechanism for nuclear weapons.^[72] A major obstacle is the difficulty of producing antimatter in large enough quantities, and there is no evidence that it will ever be feasible.^[73] However, the U.S. Air Force funded studies of the physics of antimatter in the Cold War, and began considering its possible use in weapons, not just as a trigger, but as the explosive itself.^[74]

Coverage of Extreme Events in the IPCC AR5

Posted by Roger Pielke, Jr. at 10/03/2013 03:40:00 PM

 I had been scheduled to testify before the House Science Committee next week in a hearing on extreme events, but the gong show in Washington has put that off.

In the process of updating Senate testimony given back in July (here in PDF) I did compile some key statements from the IPCC AR5 WGI Chapter 2 on extremes.

Here are a few:

• “Overall, the most robust global changes in climate extremes are seen in measures of daily temperature, including to some extent, heat waves. Precipitation extremes also appear to be increasing, but there is large spatial variability"
• "There is limited evidence of changes in extremes associated with other climate variables since the mid-20th century”
• “Current datasets indicate no significant observed trends in global tropical cyclone frequency over the past century … No robust trends in annual numbers of tropical storms, hurricanes and major hurricanes counts have been identified over the past 100 years in the North Atlantic basin”
• “In summary, there continues to be a lack of evidence and thus low confidence regarding the sign of trend in the magnitude and/or frequency of floods on a global scale”
• “In summary, there is low confidence in observed trends in small-scale severe weather phenomena such as hail and thunderstorms because of historical data inhomogeneities and inadequacies in monitoring systems”
• “In summary, the current assessment concludes that there is not enough evidence at present to suggest more than low confidence in a global-scale observed trend in drought or dryness (lack of rainfall) since the middle of the 20th century due to lack of direct observations, geographical inconsistencies in the trends, and dependencies of inferred trends on the index choice. Based on updated studies, AR4 conclusions regarding global increasing trends in drought since the 1970s were probably overstated. However, it is likely that the frequency and intensity of drought has increased in the Mediterranean and West Africa and decreased in central North America and north-west Australia since 1950” 
• “In summary, confidence in large scale changes in the intensity of extreme extratropical cyclones since 1900 is low”

There is really not much more to be said here -- the data says what it says, and what it says is so unavoidably obvious that the IPCC has recognized it in its consensus. 

Of course, I have no doubts that claims will still be made associating floods, drought, hurricanes and tornadoes with human-caused climate change -- Zombie science -- but I am declaring victory in this debate. Climate campaigners would do their movement a favor by getting themselves on the right side of the evidence.

1918 flu pandemic

From Wikipedia, the free encyclopedia

 

Soldiers from Fort Riley, Kansas, ill with Spanish influenza at a hospital ward at Camp Funston.

The 1918 flu pandemic (January 1918 – December 1920) was an unusually deadly influenza pandemic, the first of the two pandemics Involving H1N1 influenza virus.^[1] It infected 500 million people around the world,^[2] including remote Pacific islands and the Arctic, and resulted in the deaths of 50 to 100 million (three to five percent of the world's population^[3]), making it one of the deadliest natural disasters in human history.^[4][5][6] Disease had already greatly limited life expectancy in the early 20th century. A considerable spike occurred at the time of the pandemic, specifically the year 1918. Life expectancy in the United States alone dropped by about 12 years.^{[7][8][9][10]}

Most influenza outbreaks disproportionately kill juvenile, elderly, or already weakened patients; in contrast, the 1918 pandemic predominantly killed previously healthy young adults.

There are several possible explanations for the high mortality rate of the 1918 influenza pandemic. Some research suggests that the specific variant of the virus had an unusually aggressive nature. One group of researchers recovered the original virus from the bodies of frozen victims, and found that transfection in animals caused a rapid progressive respiratory failure and death through a cytokine storm (overreaction of the body's immune system). It was then postulated that the strong immune reactions of young adults ravaged the body, whereas the weaker immune systems of children and middle-aged adults resulted in fewer deaths among those groups.^[11]

More recent investigations, mainly based on original medical reports from the period of the pandemic,^[12][13] found that the viral infection itself was not more aggressive than any previous influenza, but that the special circumstances (malnourishment, overcrowded medical camps and hospitals, poor hygiene) promoted bacterial superinfection that killed most of the victims typically after a somewhat prolonged death bed.^[14][15]

Historical and epidemiological data are inadequate to identify the pandemic's geographic origin.^[2] It was implicated in the outbreak of encephalitis lethargica in the 1920s.^[16]

To maintain morale, wartime censors minimized early reports of illness and mortality in Germany, the United Kingdom, France, and the United States.^[17][18] However, papers were free to report the epidemic's effects in neutral Spain (such as the grave illness of King Alfonso XIII).^[19] This reporting dichotomy created a false impression of Spain as especially hard hit,^[20] thereby giving rise to the pandemic's nickname, Spanish Flu.^[21] In Spain, a different nickname was adopted, the Naples Soldier (Soldado de Nápoles), which came from a musical operetta (zarzuela) titled La canción del olvido (The Song of Forgetting), which premiered in Madrid during the first epidemic wave. Federico Romero, one of the librettists, quipped that the play's most popular musical number, Naples Soldier, was as catchy as the flu.^[22]

History

Hypotheses about source

The site of the very first confirmed outbreak was at Camp Funston, Fort Riley, Kansas, then a military training facility preparing American troops for involvement in World War I. The first victim diagnosed with the new strain of flu on Monday, March 11, 1918, was mess cook Private Albert Gitchell.^[23][24] Historian Alfred W. Crosby recorded that the flu originated in Kansas,^[25] and popular writer John Barry echoed Crosby in describing Haskell County, Kansas, as the point of origin.^[26]

In contrast, investigative work in 1999 by a British team led by virologist John Oxford^[27] of St Bartholomew's Hospital and the Royal London Hospital identified the major troop staging and hospital camp in Étaples, France, as being the center of the 1918 flu pandemic. These researchers postulated that a significant precursor virus, harbored in birds, mutated to pigs that were kept near the front.^[28]

Earlier hypotheses of the epidemic's origin have varied. Some hypothesized the flu originated in East Asia.^[29][30] Dr. C. Hannoun, leading expert of the 1918 flu for the Institut Pasteur, asserted the former virus was likely to have come from China, mutating in the United States near Boston and spreading to Brest, France, Europe's battlefields, Europe, and the world using Allied soldiers and sailors as main spreaders.^[31] He considered several other hypotheses of origin, such as Spain, Kansas, and Brest, as being possible, but not likely.

Political scientist Andrew Price-Smith published data from the Austrian archives suggesting the influenza had earlier origins, beginning in Austria in the spring of 1917.^[32]

In 2014, historian Mark Humphries of Canada's Memorial University of Newfoundland stated that newly unearthed records confirmed that one of the side stories of the war, the mobilization of 96,000 Chinese laborers to work behind the British and French lines on World War I's western front, might have been the source of the pandemic. In the report, Humphries found archival evidence that a respiratory illness that struck northern China in November 1917 was identified a year later by Chinese health officials as identical to the Spanish flu.^[33][34] However, a report published in 2016 in the Journal of the Chinese Medical Association found no evidence that the 1918 virus was imported to Europe from Chinese and Southeast Asian soldiers and workers. In fact, it found evidence that the virus had been circulating in the European armies for months and potentially years before the 1918 pandemic.^[35]

Spread

When an infected person sneezes or coughs, more than half a million virus particles can be spread to those close by.^[36] The close quarters and massive troop movements of World War I hastened the pandemic, and probably both increased transmission and augmented mutation; the war may also have increased the lethality of the virus. Some speculate the soldiers' immune systems were weakened by malnourishment, as well as the stresses of combat and chemical attacks, increasing their susceptibility.^[37]

A large factor in the worldwide occurrence of this flu was increased travel. Modern transportation systems made it easier for soldiers, sailors, and civilian travelers to spread the disease.^[38]

In the United States, the disease was first observed in Haskell County, Kansas, in January 1918, prompting local doctor Loring Miner to warn the U.S. Public Health Service's academic journal. On 4 March 1918, company cook Albert Gitchell reported sick at Fort Riley, Kansas. By noon on 11 March 1918, over 100 soldiers were in the hospital.^[39] Within days, 522 men at the camp had reported sick.^[40] By 11 March 1918, the virus had reached Queens, New York.^[41] Failure to take preventative measures in March/April was later criticised.^[5]

In August 1918, a more virulent strain appeared simultaneously in Brest, France; in Freetown, Sierra Leone; and in the U.S. in Boston, Massachusetts. The Spanish flu also spread through Ireland, carried there by returning Irish soldiers. The Allies of World War I came to call it the Spanish flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November 1918. Spain was not involved in the war and had not imposed wartime censorship.^[42]

Mortality

Around the globe

The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics – deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line)^[43]

Three pandemic waves: weekly combined influenza and pneumonia mortality, United Kingdom, 1918–1919^[44]

The global mortality rate from the 1918/1919 pandemic is not known, but an estimated 10% to 20% of those who were infected died. With about a third of the world population infected, this case-fatality ratio means 3% to 6% of the entire global population died.^[2] Influenza may have killed as many as 25 million people in its first 25 weeks. Older estimates say it killed 40–50 million people,^[4] while current estimates say 50–100 million people worldwide were killed.^[45]

This pandemic has been described as "the greatest medical holocaust in history" and may have killed more people than the Black Death.^[46] It is said that this flu killed more people in 24 weeks than AIDS killed in 24 years, and more in a year than the Black Death killed in a century.^[11]

The disease killed in every corner of the globe. As many as 17 million died in India, about 5% of the population.^[47] The death toll in India's British-ruled districts alone was 13.88 million.^[48]

In Japan, of the 23 million people who were affected, 390,000 died.^[49] In the Dutch East Indies (now Indonesia), 1.5 million were assumed to have died among 30 million inhabitants.^[50] In Tahiti 13% of the population died during only a month. Similarly, in Samoa 22% of the population of 38,000 died within two months.^[51]

In the U.S., about 28% of the population became infected, and 500,000 to 675,000 died.^[52] Native American tribes were particularly hard hit. In the Four Corners area alone, 3,293 deaths were registered among Native Americans.^[53] Entire village communities perished in Alaska.^[54] In Canada 50,000 died.^[55] In Brazil 300,000 died, including president Rodrigues Alves.^[56] In Britain, as many as 250,000 died; in France, more than 400,000.^[57] In West Africa an influenza epidemic killed at least 100,000 people in Ghana.^[58] Tafari Makonnen (the future Haile Selassie, Emperor of Ethiopia) was one of the first Ethiopians who contracted influenza but survived,^[59][60] although many of his family's subjects did not; estimates for the fatalities in the capital city, Addis Ababa, range from 5,000 to 10,000, or higher.^[61] In British Somaliland one official estimated that 7% of the native population died.^[62]

This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.^[4] Symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera, or typhoid. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred".^[45] The majority of deaths were from bacterial pneumonia,^[63][64] a common secondary infection associated with influenza, but the virus also killed people directly, by causing massive hemorrhages and edema in the lung.^[64]

The unusually severe disease killed up to 20% of those infected, as opposed to the usual flu epidemic mortality rate of 0.1%.^[2][45]

Patterns of fatality

An unusual feature of this pandemic was that it mostly killed young adults. In 1918–1919, 99% of pandemic influenza deaths in the US occurred in people under 65, and nearly half in young adults 20 to 40 years old. In 1920 the mortality rate among people under 65 had decreased six-fold to half the mortality rate of people over 65, but still 92% of deaths occurred in people under 65.^[65] This is noteworthy, since influenza is normally most deadly to weak individuals, such as infants (under age two), the very old (over age 70), and the immunocompromised. In 1918, older adults may have had partial protection caused by exposure to the 1889–1890 flu pandemic, known as the Russian flu.^[66] According to historian John M. Barry, the most vulnerable of all – "those most likely, of the most likely", to die – were pregnant women. He reported that in thirteen studies of hospitalized women in the pandemic, the death rate ranged from 23% to 71%.^[67] Of the pregnant women who survived childbirth, over one-quarter (26%) lost the child.^[68]

Another oddity was that the outbreak was widespread in the summer and autumn (in the Northern Hemisphere); influenza is usually worse in winter.^[69]

Modern analysis has shown the virus to be particularly deadly because it triggers a cytokine storm, which ravages the stronger immune system of young adults.^[26]

In fast-progressing cases, mortality was primarily from pneumonia, by virus-induced pulmonary consolidation. Slower-progressing cases featured secondary bacterial pneumonias, and there may have been neural involvement that led to mental disorders in some cases. Some deaths resulted from malnourishment.

A study – conducted by He et al. – used a mechanistic modelling approach to study the three waves of the 1918 influenza pandemic. They tried to study the factors that underlie variability in temporal patterns, and the patterns of mortality and morbidity. Their analysis suggests that temporal variations in transmission rate provide the best explanation and the variation in transmission required to generate these three waves is within biologically plausible values.^[70]

Another study by He et al. used a simple epidemic model, to incorporate three factors including: school opening and closing, temperature changes over the course of the outbreak, and human behavioral changes in response to the outbreak to infer the cause of the three waves of the 1918 influenza pandemic. Their modelling results showed that all three factors are important but human behavioral responses showed the largest effects.^[71]

Deadly second wave

American Expeditionary Force victims of the flu pandemic at U.S. Army Camp Hospital no. 45 in Aix-les-Bains, France, in 1918

The second wave of the 1918 pandemic was much deadlier than the first. The first wave had resembled typical flu epidemics; those most at risk were the sick and elderly, while younger, healthier people recovered easily. But in August, when the second wave began in France, Sierra Leone and the United States,^[72] the virus had mutated to a much deadlier form.

This increased severity has been attributed to the circumstances of the First World War.^[73] In civilian life, natural selection favours a mild strain. Those who get very ill stay home, and those mildly ill continue with their lives, preferentially spreading the mild strain. In the trenches, natural selection was reversed. Soldiers with a mild strain stayed where they were, while the severely ill were sent on crowded trains to crowded field hospitals, spreading the deadlier virus. The second wave began and the flu quickly spread around the world again. Consequently, during modern pandemics health officials pay attention when the virus reaches places with social upheaval (looking for deadlier strains of the virus).^[74]

The fact that most of those who recovered from first-wave infections were now immune showed that it must have been the same strain of flu. This was most dramatically illustrated in Copenhagen, which escaped with a combined mortality rate of just 0.29% (0.02% in the first wave and 0.27% in the second wave) because of exposure to the less-lethal first wave.^[75] On the rest of the population it was far more deadly now; the most vulnerable people were those like the soldiers in the trenches – young previously healthy adults.^[76]

Devastated communities

A chart of deaths in major cities, showing a peak in the autumn of 1918.

Even in areas where mortality was low, so many were incapacitated that much of everyday life was hampered. Some communities closed all stores or required customers to leave orders outside. There were reports that the health-care workers could not tend the sick nor the gravediggers bury the dead because they too were ill. Mass graves were dug by steam shovel and bodies buried without coffins in many places.^[77]

Several Pacific island territories were particularly hard-hit. The pandemic reached them from New Zealand, which was too slow to implement measures to prevent ships carrying the flu from leaving its ports. From New Zealand, the flu reached Tonga (killing 8% of the population), Nauru (16%) and Fiji (5%, 9,000 people).^[78]

Worst affected was German Samoa, today the independent state of Samoa, which had been occupied by New Zealand in 1914. A crippling 90% of the population was infected; 30% of adult men, 22% of adult women and 10% of children died. By contrast, the flu was kept away from American Samoa when Governor John Martin Poyer imposed a blockade.^[78] In New Zealand itself, 8,573 deaths were attributed to the 1918 pandemic influenza, resulting in a total population fatality rate of 0.74%.^[79] In Ireland, the Spanish Flu accounted for 10% of the total deaths in 1918 which can be seen as quite detrimental considering World War 1 was still occurring.

Less-affected areas

In Japan, 257,363 deaths were attributed to influenza by July 1919, giving an estimated 0.425% mortality rate, much lower than nearly all other Asian countries for which data are available. The Japanese government severely restricted maritime travel to and from the home islands when the pandemic struck.

In the Pacific, American Samoa^[80] and the French colony of New Caledonia^[81] also succeeded in preventing even a single death from influenza through effective quarantines. In Australia, nearly 12,000 perished.^[82]

By the end of the pandemic, the isolated island of Marajó, in Brazil's Amazon River Delta had not reported an outbreak.^[83]

Aspirin poisoning

In a 2009 paper published in the journal Clinical Infectious Diseases, Karen Starko proposed that aspirin poisoning had contributed substantially to the fatalities. She based this on the reported symptoms in those dying from the flu, as reported in the post mortem reports still available, and also the timing of the big "death spike" in October 1918 which happened right after the Surgeon General of the United States Army, and the Journal of the American Medical Association both recommended very large doses of 8.0–31.2 g of aspirin per day.^[84] Starko also suggests that the wave of aspirin poisonings was due to a "perfect storm" of events: Bayer's patent on aspirin expired, so that many companies rushed in to make a profit and greatly increased the supply; this coincided with the flu pandemic; and the symptoms of aspirin poisoning were not known at the time.^[84]

As an explanation for the universally high mortality rate, this hypothesis was questioned in a letter to the journal published in April 2010 by Andrew Noymer and Daisy Carreon of the University of California, Irvine, and Niall Johnson of the Australian Commission on Safety and Quality in Health Care. They questioned this universal applicability given the high mortality rate in countries such as India, where there was little or no access to aspirin at the time.^[85] They concluded that "the salicylate [aspirin] poisoning hypothesis [was] difficult to sustain as the primary explanation for the unusual virulence of the 1918–1919 influenza pandemic".^[85]

But they overlooked that inexpensive aspirin had become available in India and other places after October 1918, when the Bayer patent expired. In responding, Starko pointed to anecdotal evidence of aspirin over-prescription in India and argued that even if aspirin over-prescription had not contributed to the high Indian mortality rate, it could still have been a major factor for other high rates in areas where other exacerbating factors present in India played less of a role.^[86]

End of the pandemic

After the lethal second wave struck in late 1918, new cases dropped abruptly – almost to nothing after the peak in the second wave.^[11] In Philadelphia, for example, 4,597 people died in the week ending 16 October, but by 11 November, influenza had almost disappeared from the city. One explanation for the rapid decline of the lethality of the disease is that doctors simply got better at preventing and treating the pneumonia that developed after the victims had contracted the virus, although John Barry stated in his book that researchers have found no evidence to support this.^[26]

Another theory holds that the 1918 virus mutated extremely rapidly to a less lethal strain. This is a common occurrence with influenza viruses: there is a tendency for pathogenic viruses to become less lethal with time, as the hosts of more dangerous strains tend to die out^[26] (see also "Deadly Second Wave", above).

Legacy

American Red Cross nurses tend to flu patients in temporary wards set up inside Oakland Municipal Auditorium, 1918.

Academic Andrew Price-Smith has made the argument that the virus helped tip the balance of power in the later days of the war towards the Allied cause. He provides data that the viral waves hit the Central Powers before they hit the Allied powers, and that both morbidity and mortality in Germany and Austria were considerably higher than in Britain and France.^[32]

In the United States, Britain and other countries, despite the relatively high morbidity and mortality rates that resulted from the epidemic in 1918–1919, the Spanish flu began to fade from public awareness over the decades until the arrival of news about bird flu and other pandemics in the 1990s and 2000s.^[87] This has led some historians to label the Spanish flu a "forgotten pandemic".^[25]

Various theories of why the Spanish flu was "forgotten" include the rapid pace of the pandemic, which killed most of its victims in the United States, for example, within a period of less than nine months, resulting in limited media coverage. The general population was familiar with patterns of pandemic disease in the late 19th and early 20th centuries: typhoid, yellow fever, diphtheria, and cholera all occurred near the same time. These outbreaks probably lessened the significance of the influenza pandemic for the public.^[88] In some areas, the flu was not reported on, the only mention being that of advertisements for medicines claiming to cure it.^[89]

In addition, the outbreak coincided with the deaths and media focus on the First World War.^[90] Another explanation involves the age group affected by the disease. The majority of fatalities, from both the war and the epidemic, were among young adults. The deaths caused by the flu may have been overlooked due to the large numbers of deaths of young men in the war or as a result of injuries. When people read the obituaries, they saw the war or postwar deaths and the deaths from the influenza side by side. Particularly in Europe, where the war's toll was extremely high, the flu may not have had a great, separate, psychological impact, or may have seemed a mere extension of the war's tragedies.^[65]

The duration of the pandemic and the war could have also played a role. The disease would usually only affect a certain area for a month before leaving, while the war, which most had initially expected to end quickly, had lasted for four years by the time the pandemic struck. This left little time for the disease to have a significant impact on the economy.

Regarding global economic effects, many businesses in the entertainment and service industries suffered losses in revenue, while the health care industry reported profit gains.^[91]

Historian Nancy Bristow has argued that the pandemic, when combined with the increasing number of women attending college, contributed to the success of women in the field of nursing. This was due in part to the failure of medical doctors, who were predominantly men, to contain and prevent the illness. Nursing staff, who were predominantly women, felt more inclined to celebrate the success of their patient care and less inclined to identify the spread of the disease with their own work.^[92]

In Spain, sources from the period explicitly linked the Spanish flu to the cultural figure of Don Juan. The nickname for the flu, the "Naples Soldier", was adopted from Federico Romero and Guillermo Fernández Shaw's operetta, The Song of Forgetting (La canción del olvido), the protagonist of which is a stock Don Juan type. Davis has argued the Spanish flu–Don Juan connection served a cognitive function, allowing Spaniards to make sense of their epidemic experience by interpreting it through a familiar template, namely the Don Juan story.^[93]

Spanish flu research

An electron micrograph showing recreated 1918 influenza virions.

Centers for Disease Control and Prevention as Dr. Terrence Tumpey examines a reconstructed version of the 1918 flu.

The origin of the Spanish flu pandemic, and the relationship between the near-simultaneous outbreaks in humans and swine, have been controversial. One hypothesis is that the virus strain originated at Fort Riley, Kansas, in viruses in poultry and swine which the fort bred for food; the soldiers were then sent from Fort Riley around the world, where they spread the disease.^[94] Similarities between a reconstruction of the virus and avian viruses, combined with the human pandemic preceding the first reports of influenza in swine, led researchers to conclude the influenza virus jumped directly from birds to humans, and swine caught the disease from humans.^[95][96]

Others have disagreed,^[97] and more recent research has suggested the strain may have originated in a nonhuman, mammalian species.^[98] An estimated date for its appearance in mammalian hosts has been put at the period 1882–1913.^[99] This ancestor virus diverged about 1913–1915 into two clades (or biological groups), which gave rise to the classical swine and human H1N1 influenza lineages. The last common ancestor of human strains dates to between February 1917 and April 1918. Because pigs are more readily infected with avian influenza viruses than are humans, they were suggested as the original recipients of the virus, passing the virus to humans sometime between 1913 and 1918.

An effort to recreate the 1918 flu strain (a subtype of avian strain H1N1) was a collaboration among the Armed Forces Institute of Pathology, the USDA ARS Southeast Poultry Research Laboratory and Mount Sinai School of Medicine in New York City. The effort resulted in the announcement (on 5 October 2005) that the group had successfully determined the virus's genetic sequence, using historic tissue samples recovered by pathologist Johan Hultin from a female flu victim buried in the Alaskan permafrost and samples preserved from American soldiers.^[100]

On 18 January 2007, Kobasa et al. (2007) reported that monkeys (Macaca fascicularis) infected with the recreated flu strain exhibited classic symptoms of the 1918 pandemic, and died from a cytokine storm^[101]—an overreaction of the immune system. This may explain why the 1918 flu had its surprising effect on younger, healthier people, as a person with a stronger immune system would potentially have a stronger overreaction.^[102]

On 16 September 2008, the body of British politician and diplomat Sir Mark Sykes was exhumed to study the RNA of the flu virus in efforts to understand the genetic structure of modern H5N1 bird flu. Sykes had been buried in 1919 in a lead coffin which scientists hoped had helped preserve the virus.^[103] However, the coffin was found to be split because of the weight of soil over it, and the cadaver was badly decomposed. Nonetheless, samples of lung and brain tissue were taken through the split, with the coffin remaining in situ in the grave during this process.^[104]

In December 2008, research by Yoshihiro Kawaoka of the University of Wisconsin linked the presence of three specific genes (termed PA, PB1, and PB2) and a nucleoprotein derived from 1918 flu samples to the ability of the flu virus to invade the lungs and cause pneumonia. The combination triggered similar symptoms in animal testing.^[105]

In June 2010, a team at the Mount Sinai School of Medicine reported the 2009 flu pandemic vaccine provided some cross-protection against the 1918 flu pandemic strain.^[106]

One of the few things known for certain about the influenza in 1918 and for some years after was that it was, out of the laboratory, exclusively a disease of human beings.^[107]

In 2013, the AIR Worldwide Research and Modeling Group "characterized the historic 1918 pandemic and estimated the effects of a similar pandemic occurring today using the AIR Pandemic Flu Model". In the model, "a modern day "Spanish flu" event would result in additional life insurance losses of between USD 15.3–27.8 billion in the United States alone" with 188,000–337,000 deaths in the United States.^[108]

In popular culture

The 1995 film Outbreak,^[109] the 2011 film Contagion and the 2013 film World War Z make reference to the pandemic.^[110]

The television show Resurrection uses the pandemic, in the episode "Afflictions" that aired on November 2, 2014, as the explanation for why many of the Returned were getting sick and disappearing.

In season four of British drama Upstairs, Downstairs, Hazel Bellamy dies of Spanish flu in 1918, after her husband James Bellamy survives injuries in the "Great War" (World War I). Her funeral takes place on 11 November, the day the war ends.

In season two of British drama Downton Abbey, Lavinia Swire dies of the Spanish flu in April 1919, after her fiancé Matthew Crawley recovers from injuries and temporary paralysis from the Great War.

Twentieth-century fiction includes at least three novels with the flu pandemic as a major theme: Katherine Anne Porter's Pale Horse, Pale Rider, Thomas Mullen's The Last Town on Earth, and Thomas Wolfe's Look Homeward, Angel.

In the one-act play 1918 by Horton Foote (part of his Orphans' Home Cycle (1979)), the presence and threat of the flu (and the tragedy it ultimately causes) is a major element of the plot. The play was made into a film of the same title, released in 1985, which was subsequently edited for broadcast by PBS as the last part of the miniseries "The Story of A Marriage".