when was the first forth road bridge built

The first crossing at what is now the site of the bridge was established in the 11thÂ century by Margaret, queen consort of King Malcolm III, who founded a ferry service to transport religious pilgrims from Edinburgh to Dunfermline Abbey and St Andrews.[4] Its creation gave rise to the port towns of Queensferry and North Queensferry, which remain to this day; and the service remained in uninterrupted use as a passenger ferry for over eight hundred years. There were proposals as early as the 1740s for a road crossing at the site, although their viability was only considered following the construction of the Forth Bridge in 1890.[5]

Forth Road Bridge

The Forth Road Bridge is a suspension bridge in east central Scotland. The bridge, opened in 1964, spans the Firth of Forth, connecting Edinburgh, at Queensferry, to Fife, at North Queensferry. It replaced a centuries-old ferry service to carry vehicular traffic, cyclists and pedestrians across the Forth; railway crossings are made by the adjacent Forth Bridge, opened in 1890.

The Scottish Parliament voted to scrap tolls on the bridge from February 2008. The bridge was nearing the end of its life in the 2010s, and a parallel replacement was built. On 5Â September 2017 the bridge carried its final private cars, as the vast majority of traffic was transferred to the new Queensferry Crossing. Following a few weeks closure for repairs, the new role of the Forth Road Bridge will be as a public transport corridor, open only to buses, taxis, cyclists and pedestrians. At its peak, the Forth Road Bridge carried 65,000 vehicles per day (vpd), which is now expected to drop to only a few hundred following the opening of the Queensferry Crossing.

The importance of the crossing to vehicular traffic was underpinned when the Great Britain road numbering scheme was drawn up in the 1920s. The planners wished the arterial A9 road to be routed across the Forth here, although the unwillingness to have a ferry crossing as part of this route led to the A90 number being assigned instead.[6]

There was a period of renewed lobbying for a road crossing in the 1920s and 1930s, at which time the only vehicle crossing was a single passenger and vehicle ferry. Sir William Denny championed the expansion of that service in the 1930s, providing and operating on behalf of the London and North Eastern Railway two additional ferries that aimed to supplement the services of the adjacent railway bridge. Their success allowed for the addition of two more craft in the 1940s and 1950s,[7] by which time the ferries were making 40,000 crossings annually, carrying 1.5 million passengers and 800,000 vehicles.

With the then newest and nearest bridge spanning the Forth (the Kincardine Bridge, built in 1936) still around 15 miles (24Â km) upstream, the upsurge in demand for a road crossing between Edinburgh and Fife[8] prompted the UK Government to establish the Forth Road Bridge Joint Board (FRBJB) by Act of Parliament in 1947 to oversee the implementation of a new bridge to replace the ferry service. The authorities on both sides investigated in 1955, and drew up an alternative scheme for a tunnel beneath the estuary. This was known as the Maunsell Scheme, and was projected to run somewhat closer to the rail bridge than the present road bridge. The scheme was abandoned as being too ambitious, and consideration reverted to a bridge concept.[9]

The final construction plan was accepted in February 1958 and work began in September of that year.[10] Mott, Hay and Anderson and Freeman Fox and Partners carried out the design work and a joint venture of Sir William Arrol & Co., Cleveland Bridge & Engineering Company and Dorman Long constructed the bridge at a cost of £11.5 million, while the total cost of the project including road connections and realignments was £19.5 million. The resident design engineer was John Alexander King Hamilton FRSE (1900–1982).[11]

It was the longest steel suspension bridge in Europe.[12] 210,000 tons of concrete were involved in its construction, with 9 miles (14 kilometres) of grade-separated dual-carriageway approach roads. Reed and Mallik (known for Reema construction of houses) of Salisbury, Wiltshire, built the approach viaducts.

Twenty-four individual bridges were built for the approach roads. The 4 1⁄2-mile (7.2 km) southern approach road of the A90 began at Cramond Bridge, over the River Almond on the western outskirts of Edinburgh, near Craigiehall. There were two-level interchanges built at Burnshot, Dolphington (B924) and the Echline junction (A904 and B800). At Dalmeny there was a bridge over the railway. The southern approach roads were built by A.M. Carmichael Ltd. The 4 mi (6 km) northern approach road had three two-level junctions at Ferry Toll[13] (for the B980), Admiralty (for Rosyth Dockyard via the A985, and Inverkeithing via the A921) and at Mastertown/Masterton (for what would be the fledgling M90 southern terminus). The Masterton junction was an octopus junction, a variation of a clover-leaf junction, having six bridges and a 600 ft viaduct. There were fifteen bridges built for this approach road. The northern approach road terminated as the A823(M) at a roundabout with the A823 south of Dunfermline, next to Rosyth railway station.[14] The northern approach roads were built by Whatlings Ltd of Glasgow, later bought by Alfred McAlpine.

Seven lives were lost during construction before the bridge was opened by Queen Elizabeth II and the Duke of Edinburgh on 4 September 1964.[15] The ferry service was discontinued as of that date.

The bridge's management was delegated to the FRBJB, and remained so until 2002 when its operation was transferred to a new body with a wider remit, the Forth Estuary Transport Authority.[16]

On 1 December 2010, the bridge was closed for the first time due to heavy snow. After several accidents meant snowploughs were unable to clear the carriageways, the bridge was closed in both directions at 6.40Â a.m. and remained closed for several hours.[17] As part of celebrations of the fiftieth anniversary of the bridge's operation, artist Kate Downie was commissioned to create a print of the bridge and hold an exhibition of works portraying it.[18]

On 1 June 2015, Amey took over the maintenance and operating of the bridge on behalf of Transport Scotland from the Forth Estuary Transport Authority and are now called the Forth Bridges Unit.

The bridge's central main span is 1,006 metres (3,301 ft) long, its two side spans are each 408 metres (1,339 ft) long, and the approach viaducts are 252 metres (827 ft) on the north side and 438 metres (1,437 ft) on the south side. At a total length of 2,512 metres (8,241 ft), it was the longest suspension bridge span outside the United States and the fourth-longest span in the world at the time of its construction. The bridge comprises 39,000 tonnes of steel and 115,000 cubic metres of concrete. The towers reach 156 metres (512 ft) above mean water level. Its width comprises a dual carriageway road with two lanes in each direction bounded by cycle/footpaths on each side. The main strung cables are 590 millimetres (23 in) in diameter, comprising 11,618 high tensile wires, each five millimetres in diameter, and each cable carries 13,800 tonnes of the bridge's load.[1][2]

The bridge forms a crucial part of the corridor between south-east and north-east Scotland, linking Edinburgh to Perth, Dundee and Aberdeen by the A90 road and its sister M90 motorway, which begins 1 2⁄3 miles (2.7 km) north of the bridge's northern terminus. The bridge carried around 2.5 million vehicles in its first year but the annual figure has risen steadily over time to around 21.4 million vehicles in 2008.[19] The bridge carried its 250-millionth vehicle in 2002.

It was awarded Historic Scotland's Category A listed structure status in 2001.

FETA began to be concerned over the structural wear of the bridge in the 21st century. The planned theoretical capacity for the bridge (30,000 vehicles per day in each direction) was routinely exceeded as traffic levels outstripped predictions. The Scottish Government stated in 2006 that 60,000 vehicles travelled on more than half the days in a year.[20] This raised concerns about the lifespan of the bridge, originally planned at 120 years.[20]

In 2003, an inspection programme was launched (costing £1.2 million) to assess the condition of the main suspension cables after corrosion was discovered in a number of older bridges in the United States of a similar design and size. The study was completed two years later and reported that the main cables had suffered an 8–10% loss of strength. Future projections highlighted the likelihood of this accelerating, with traffic restrictions to limit loading required in 2014 in the worst-case scenario, followed by full closure by 2020.[21]

An acoustic monitoring system was commissioned in August 2006, using listening devices to monitor any further strands snapping and pinpoint their location within the main cables. In January 2006, the Scottish Executive completed a third-party audit on the bridge which concluded that FETA had performed the initial internal inspection and cable strength calculation in accordance with accepted practice. The report suggested that traffic restrictions could be required by 2013.[22]

Several options were implemented to increase the bridge's lifespan. These included a dehumidification programme that slowed the rate of corrosion in the main cables by keeping air in the voids between the main cables' strands below 40% humidity. Engineering consultants Faber Maunsell began work on the project in 2006, which took two and a half years to complete at a cost of £7.8 million.[23] As part of the works, some of the corroded cable strands were spliced.[24]

The southbound carriageway of the bridge was closed on 1 December 2015 after steelwork defects had been discovered during routine inspections[25] and traffic was restricted 7.5 tonne or less (public service vehicles excepted).[26] On 23 December the Road Bridge reopened for all traffic except heavy goods vehicles (HGVs). On 4 February, it was announced this had been pushed back to March, due to further problems with the truss end link pins in the southern towers, which required additional remedial work.[27][28][29]

On 20 January Scottish Parliament began an inquiry led by the Infrastructure and Capital Investment Committee (ICI) to determine the circumstances that led to the discovery of a cracked truss in the bridge's undercarriage.[30] Evidence was heard from; Forth Estuary Transport Authority (Feta), Transport minister Derek Mackay, engineers and officials from Amey along with a number of other experts and key personnel.

On the first day, Richard Hornby, of engineering consulting firm Arup, stated that the truss end in question had been inspected 23 times since 2001, and no fault had been found. It was revealed a pin had seized up, which caused the truss end to crack, and was only the quality of the steel which had stopped its cracking appearing earlier. Hornby also made clear that even if the seized pin had been picked up earlier, it was "virtually impossible" to lubricate the bearing.[31][32] Several witnesses defended a decision by previous operator Forth Estuary Transport Authority (Feta) not to proceed with a £15 million truss end link replacement project in 2010. This claim was disputed by Barry Colford, former chief engineer and bridgemaster at the Feta. Lesley Hinds, Feta’s former convener, pointed out that the bridge budget had been cut by 58% in 2011, while senior staff at Feta had "deep concerns" about the transfer of bridge management to a private company.[33][34]

A programme of work is scheduled to take place in 2018 to replace expansion joints in both towers along with replacing the truss end links. Plans to replace these joints were postponed by the bridge management following the Scottish Government's commitment to the construction of the Queensferry Crossing; the original work proposals would have involved round-the-clock contraflows during the installation of ramps and mini-bridges to carry traffic over the work area, and heavy lorries being diverted.[35]

On 11 February 2008 tolls were abolished on the bridge.[36]

Initially, it was suggested that tolling would cease once the original cost of construction plus accrued interest was repaid â€“ this was done in 1993 and it was planned that tolls would not be levied after May 1995. Instead legislation enabling the continued levying of tolls was renewed by Parliament (originally that of the UK but now the Scottish Parliament) in 1998, 2003 and 2006.[37]

Originally, a toll was paid for each direction of travel with sets of toll booths on both carriageways. In 1997, the northbound toll was doubled (from 40p to 80p) and the southbound toll abolished on the presumption that almost all traffic makes a return journey across the bridge, and that the removal of the southbound toll would result in a reduction of congestion without reducing revenue.

The Forth Estuary Transport Authority (FETA) justified the continued use of tolls by suggesting they were necessary to fund maintenance and improvement works. These included the construction of defences around the submerged piers forming the bases of the main towers in the event of collision in the Firth. The main towers were also strengthened with internal steel columns (the original tower structure was hollow) and had hydraulic rams jack up these sections to transfer a portion of the load to the new steelwork. Also, the vertical cables suspending the deck had their bolts replaced after a detected failure. A new paint system required development for the bridge (the original was phased out due to environmental concerns).[38]

In late 2005, FETA's committee approved a proposal for a revamp of the tolls. The minimum toll would be set to the existing £1 figure, but would increase dependent on the time of day, rising to a maximum of £4 for evening rush hour travel. All tolls would be halved for cars with more than one occupant, as an incentive to drivers to share cars and make fewer journeys. According to FETA's chairman Lawrence Marshall, the system would provide the most efficiency, claiming that 80% of peak-time journeys are made by single-occupant vehicles. The proposal, passed with the chairman's casting vote after the committee was deadlocked, was referred to the Scottish Executive in December 2005, and implementation planned for October 2007 subject to approval by transport minister Tavish Scott. Environmental groups welcomed the proposal, although local politicians condemned it as simply a means of raising capital. At the same time, a counter-argument was tabled by Fife councillors proposing the complete removal of tolls.[39]

The Scottish Parliament debated the proposals in January 2006, and the affair became a major political issue after Westminster MPs Gordon Brown and Alistair Darling (Chancellor of the Exchequer and Secretary of State for Scotland respectively) were seen to describe the variable tolling plan as "dead in the water".[40] Scottish First Minister Jack McConnell insisted his Labour Party colleagues were misquoted and refused to rule out the plan, receiving crticism from the opposition Scottish National Party.[41]

By late January 2006, campaigning was under way for the Dunfermline and West Fife by-election, 2006 scheduled to take place for the Westminster constituency in which the north end of the bridge is situated. The by-election, scheduled for 9 February, was contested by – in addition to the major political parties in Scotland – an Abolish Forth Bridge Tolls Party. It was won by Liberal Democrat candidate Willie Rennie, overturning a large Labour majority on a 16% swing. In the aftermath of the by-election defeat, media speculation suggested the Executive had turned against the proposals, and Tavish Scott eventually confirmed their rejection and the retention of the existing toll structure on 1 March 2006. FETA condemned the decision, while local opposition MSPs charged the minister that his tolling review short-changed Fifers as tolls were axed on the Erskine Bridge leaving tolls on only the Forth and Tay Road Bridge.[42]

Following the formation of an SNP minority government after the Scottish parliamentary election of May 2007, a new debate on the abolition of tolls was opened by Transport Minister Stewart Stevenson on 31 May 2007, where it was agreed by a large majority. Toll levies at that point totalled £16 million annually.[43]

The Abolition of Bridge Tolls (Scotland) Bill, required to revoke legislation mandating toll collection on the bridge, was introduced to the Scottish Parliament on 3 September 2007, passed on 20 December 2007, and received royal assent on 24 January 2008.[44] The tolls were removed on 11 February 2008 at 00:01Â GMT.[45] This immediately followed a major upgrade and reconfiguration of the tolls on the northbound carriageway (the toll on the southbound carriageway had been removed some years before, simplifying the arrangement as most journeys were, and remain, two-way).[46]

The strategic transport importance of the road bridge and the threat of closure by 2020 if major structural work were not undertaken led to fears of serious economic consequences.[47]

Increasing traffic levels across the Firth of Forth had also led to the construction of the Clackmannanshire Bridge[48] adjacent to the existing Kincardine Bridge. This bridge opened in November 2008.

Proposals for a second road crossing at Queensferry had been made in the 1990s, but were shelved, despite preliminary work on route selection. Following the discovery of potentially serious structural issues with the Forth Road Bridge in 2005 the proposals were revisited and plans advanced. The decision to proceed with a replacement bridge was taken at the end of 2007, and it was announced the following year that the existing bridge would be retained as a public transport link.

The Forth Crossing Act received Royal Assent in January 2011, and construction began in September 2011. The Queensferry Crossing is a cable-stayed bridge, with an overall length of 1.7 miles (2.7 km). Around 2.5 miles (4.0 km) of new connecting roads were built, including new and upgraded junctions at Ferrytoll in Fife, South Queensferry, and Junction 1a on the M9. The new bridge continues the M90 motorway, (extending its southern terminus) from Admiralty to the M9 junction 1a (re-numbering the M9 spur). The crossing opened on 30 August 2017.


what happens when you have to much oxygen

The result of breathing increased partial pressures of oxygen is hyperoxia, an excess of oxygen in body tissues. The body is affected in different ways depending on the type of exposure. Central nervous system toxicity is caused by short exposure to high partial pressures of oxygen at greater than atmospheric pressure. Pulmonary and ocular toxicity result from longer exposure to increased oxygen levels at normal pressure. Symptoms may include disorientation, breathing problems, and vision changes such as myopia. Prolonged exposure to above-normal oxygen partial pressures, or shorter exposures to very high partial pressures, can cause oxidative damage to cell membranes, collapse of the alveoli in the lungs, retinal detachment, and seizures. Oxygen toxicity is managed by reducing the exposure to increased oxygen levels. Studies show that, in the long term, a robust recovery from most types of oxygen toxicity is possible.

Oxygen toxicity

Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen (O
2) at increased partial pressures. It is also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning. Historically, the central nervous system condition was called the Paul Bert effect, and the pulmonary condition the Lorrain Smith effect, after the researchers who pioneered its discovery and description in the late 19th century. Severe cases can result in cell damage and death, with effects most often seen in the central nervous system, lungs and eyes. Oxygen toxicity is a concern for underwater divers, those on high concentrations of supplemental oxygen (particularly premature babies), and those undergoing hyperbaric oxygen therapy.

Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial pressures, including underwater diving using compressed breathing gases, hyperbaric medicine, neonatal care and human spaceflight. These protocols have resulted in the increasing rarity of seizures due to oxygen toxicity, with pulmonary and ocular damage being mainly confined to the problems of managing premature infants.

In recent years, oxygen has become available for recreational use in oxygen bars. The US Food and Drug Administration has warned those suffering from problems such as heart or lung disease not to use oxygen bars. Scuba divers use breathing gases containing up to 100% oxygen, and should have specific training in using such gases.

The effects of oxygen toxicity may be classified by the organs affected, producing three principal forms:[2][3][4]

Central nervous system oxygen toxicity can cause seizures, brief periods of rigidity followed by convulsions and unconsciousness, and is of concern to divers who encounter greater than atmospheric pressures. Pulmonary oxygen toxicity results in damage to the lungs, causing pain and difficulty in breathing. Oxidative damage to the eye may lead to myopia or partial detachment of the retina. Pulmonary and ocular damage are most likely to occur when supplemental oxygen is administered as part of a treatment, particularly to newborn infants, but are also a concern during hyperbaric oxygen therapy.

Oxidative damage may occur in any cell in the body but the effects on the three most susceptible organs will be the primary concern. It may also be implicated in damage to red blood cells (haemolysis),[5][6] the liver,[7] heart,[8] endocrine glands (adrenal glands, gonads, and thyroid),[9][10][11] or kidneys,[12] and general damage to cells.[2][13]

In unusual circumstances, effects on other tissues may be observed: it is suspected that during spaceflight, high oxygen concentrations may contribute to bone damage.[14] Hyperoxia can also indirectly cause carbon dioxide narcosis in patients with lung ailments such as chronic obstructive pulmonary disease or with central respiratory depression.[14] Hyperventilation of atmospheric air at atmospheric pressures does not cause oxygen toxicity, because sea-level air has a partial pressure of oxygen of 0.21 bar (21 kPa) whereas toxicity does not occur below 0.3 bar (30 kPa).[15]

Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness. This may be followed by a tonic–clonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state).[16][17] The onset of seizure depends upon the partial pressure of oxygen in the breathing gas and exposure duration. However, exposure time before onset is unpredictable, as tests have shown a wide variation, both amongst individuals, and in the same individual from day to day.[16][18][19] In addition, many external factors, such as underwater immersion, exposure to cold, and exercise will decrease the time to onset of central nervous system symptoms.[1] Decrease of tolerance is closely linked to retention of carbon dioxide.[20][21][22] Other factors, such as darkness and caffeine, increase tolerance in test animals, but these effects have not been proven in humans.[23][24]

Pulmonary toxicity symptoms result from an inflammation that starts in the airways leading to the lungs and then spreads into the lungs (tracheobronchial tree). The symptoms appear in the upper chest region (substernal and carinal regions).[25][26][27] This begins as a mild tickle on inhalation and progresses to frequent coughing.[25] If breathing increased partial pressures of oxygen continues, patients experience a mild burning on inhalation along with uncontrollable coughing and occasional shortness of breath (dyspnoea).[25] Physical findings related to pulmonary toxicity have included bubbling sounds heard through a stethoscope (bubbling rales), fever, and increased blood flow to the lining of the nose (hyperaemia of the nasal mucosa).[27] X-rays of the lungs show little change in the short term, but extended exposure leads to increasing diffuse shadowing throughout both lungs.[25] Pulmonary function measurements are reduced, as noted by a reduction in the amount of air that the lungs can hold (vital capacity) and changes in expiratory function and lung elasticity.[27][28] Tests in animals have indicated a variation in tolerance similar to that found in central nervous system toxicity, as well as significant variations between species. When the exposure to oxygen above 0.5 bar (50 kPa) is intermittent, it permits the lungs to recover and delays the onset of toxicity.[29]

In premature babies, signs of damage to the eye (retinopathy of prematurity, or ROP) are observed via an ophthalmoscope as a demarcation between the vascularised and non-vascularised regions of an infant's retina. The degree of this demarcation is used to designate four stages: (I) the demarcation is a line; (II) the demarcation becomes a ridge; (III) growth of new blood vessels occurs around the ridge; (IV) the retina begins to detach from the inner wall of the eye (choroid).[30]

Oxygen toxicity is caused by exposure to oxygen at partial pressures greater than those to which the body is normally exposed. This occurs in three principal settings: underwater diving, hyperbaric oxygen therapy, and the provision of supplemental oxygen, particularly to premature infants. In each case, the risk factors are markedly different.

Exposures, from minutes to a few hours, to partial pressures of oxygen above 1.6 bars (160 kPa)—about eight times normal atmospheric partial pressure—are usually associated with central nervous system oxygen toxicity and are most likely to occur among patients undergoing hyperbaric oxygen therapy and divers. Since sea level atmospheric pressure is about 1 bar (100 kPa), central nervous system toxicity can only occur under hyperbaric conditions, where ambient pressure is above normal.[31][32] Divers breathing air at depths beyond 60 m (200 ft) face an increasing risk of an oxygen toxicity "hit" (seizure). Divers breathing a gas mixture enriched with oxygen, such as nitrox, can similarly suffer a seizure at shallower depths, should they descend below the maximum operating depth allowed for the mixture.[33]

The lungs and the remainder of the respiratory tract are exposed to the highest concentration of oxygen in the human body and are therefore the first organs to show toxicity. Pulmonary toxicity occurs only with exposure to partial pressures of oxygen greater than 0.5 bar (50 kPa), corresponding to an oxygen fraction of 50% at normal atmospheric pressure. The earliest signs of pulmonary toxicity begin with evidence of tracheobronchitis, or inflammation of the upper airways, after an asymptomatic period between 4 and 22 hours at greater than 95% oxygen,[34] with some studies suggesting symptoms usually begin after approximately 14 hours at this level of oxygen.[35]

At partial pressures of oxygen of 2 to 3 bar (200 to 300 kPa)—100% oxygen at 2 to 3 times atmospheric pressure—these symptoms may begin as early as 3 hours after exposure to oxygen.[34] Experiments on rats breathing oxygen at pressures between 1 and 3 bars (100 and 300 kPa) suggest that pulmonary manifestations of oxygen toxicity may not be the same for normobaric conditions as they are for hyperbaric conditions.[36] Evidence of decline in lung function as measured by pulmonary function testing can occur as quickly as 24 hours of continuous exposure to 100% oxygen,[35] with evidence of diffuse alveolar damage and the onset of acute respiratory distress syndrome usually occurring after 48 hours on 100% oxygen.[34] Breathing 100% oxygen also eventually leads to collapse of the alveoli (atelectasis), while—at the same partial pressure of oxygen—the presence of significant partial pressures of inert gases, typically nitrogen, will prevent this effect.[37]

Preterm newborns are known to be at higher risk for bronchopulmonary dysplasia with extended exposure to high concentrations of oxygen.[38] Other groups at higher risk for oxygen toxicity are patients on mechanical ventilation with exposure to levels of oxygen greater than 50%, and patients exposed to chemicals that increase risk for oxygen toxicity such the chemotherapeutic agent bleomycin.[35] Therefore, current guidelines for patients on mechanical ventilation in intensive care recommends keeping oxygen concentration less than 60%.[34] Likewise, divers who undergo treatment of decompression sickness are at increased risk of oxygen toxicity as treatment entails exposure to long periods of oxygen breathing under hyperbaric conditions, in addition to any oxygen exposure during the dive.[31]

Prolonged exposure to high inspired fractions of oxygen causes damage to the retina.[39][40][41] Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions.[42][43] Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants.[42][44] In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications.[42]

Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures.[43][45][46] It also occurs frequently in those undergoing repeated hyperbaric oxygen therapy.[40][47] This is due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift.[47][48] It is usually reversible with time.[40][47]

The biochemical basis for the toxicity of oxygen is the partial reduction of oxygen by one or two electrons to form reactive oxygen species,[49] which are natural by-products of the normal metabolism of oxygen and have important roles in cell signalling.[50] One species produced by the body, the superoxide anion (O
2âˆ’),[51] is possibly involved in iron acquisition.[52] Higher than normal concentrations of oxygen lead to increased levels of reactive oxygen species.[53] Oxygen is necessary for cell metabolism, and the blood supplies it to all parts of the body. When oxygen is breathed at high partial pressures, a hyperoxic condition will rapidly spread, with the most vascularised tissues being most vulnerable. During times of environmental stress, levels of reactive oxygen species can increase dramatically, which can damage cell structures and produce oxidative stress.[19][54]

While all the reaction mechanisms of these species within the body are not yet fully understood,[55] one of the most reactive products of oxidative stress is the hydroxyl radical (Â·OH), which can initiate a damaging chain reaction of lipid peroxidation in the unsaturated lipids within cell membranes.[56] High concentrations of oxygen also increase the formation of other free radicals, such as nitric oxide, peroxynitrite, and trioxidane, which harm DNA and other biomolecules.[19][57] Although the body has many antioxidant systems such as glutathione that guard against oxidative stress, these systems are eventually overwhelmed at very high concentrations of free oxygen, and the rate of cell damage exceeds the capacity of the systems that prevent or repair it.[58][59][60] Cell damage and cell death then result.[61]

Diagnosis of central nervous system oxygen toxicity in divers prior to seizure is difficult as the symptoms of visual disturbance, ear problems, dizziness, confusion and nausea can be due to many factors common to the underwater environment such as narcosis, congestion and coldness. However, these symptoms may be helpful in diagnosing the first stages of oxygen toxicity in patients undergoing hyperbaric oxygen therapy. In either case, unless there is a prior history of epilepsy or tests indicate hypoglycaemia, a seizure occurring in the setting of breathing oxygen at partial pressures greater than 1.4 bar (140 kPa) suggests a diagnosis of oxygen toxicity.[62]

Diagnosis of bronchopulmonary dysplasia in newborn infants with breathing difficulties is difficult in the first few weeks. However, if the infant's breathing does not improve during this time, blood tests and x-rays may be used to confirm bronchopulmonary dysplasia. In addition, an echocardiogram can help to eliminate other possible causes such as congenital heart defects or pulmonary arterial hypertension.[63]

The diagnosis of retinopathy of prematurity in infants is typically suggested by the clinical setting. Prematurity, low birth weight and a history of oxygen exposure are the principal indicators, while no hereditary factors have been shown to yield a pattern.[64]

The prevention of oxygen toxicity depends entirely on the setting. Both underwater and in space, proper precautions can eliminate the most pernicious effects. Premature infants commonly require supplemental oxygen to treat complications of preterm birth. In this case prevention of bronchopulmonary dysplasia and retinopathy of prematurity must be carried out without compromising a supply of oxygen adequate to preserve the infant's life.

Oxygen toxicity is a catastrophic hazard in diving, because a seizure results in near certain death by drowning.[33] The seizure may occur suddenly and with no warning symptoms.[17] The effects are sudden convulsions and unconsciousness, during which victims can lose their regulator and drown.[65][66] One of the advantages of a full-face diving mask is prevention of regulator loss in the event of a seizure. As there is an increased risk of central nervous system oxygen toxicity on deep dives, long dives and dives where oxygen-rich breathing gases are used, divers are taught to calculate a maximum operating depth for oxygen-rich breathing gases, and cylinders containing such mixtures must be clearly marked with that depth.[22][67]

In some diver training courses for these types of diving, divers are taught to plan and monitor what is called the oxygen clock of their dives.[67] This is a notional alarm clock, which ticks more quickly at increased oxygen pressure and is set to activate at the maximum single exposure limit recommended in the National Oceanic and Atmospheric Administration Diving Manual.[22][67] For the following partial pressures of oxygen the limits are: 45 minutes at 1.6 bar (160 kPa), 120 minutes at 1.5 bar (150 kPa), 150 minutes at 1.4 bar (140 kPa), 180 minutes at 1.3 bar (130 kPa) and 210 minutes at 1.2 bar (120 kPa), but it is impossible to predict with any reliability whether or when toxicity symptoms will occur.[68][69] Many nitrox-capable dive computers calculate an oxygen loading and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the partial pressure of oxygen in the breathing gas or by reducing the time spent breathing gas of greater oxygen partial pressure. As the partial pressure of oxygen increases with the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas, or by shortening the duration of exposure to oxygen-rich gases.[70][71]

Diving below 56 m (184 ft) on air would expose a diver to increasing danger of oxygen toxicity as the partial pressure of oxygen exceeds 1.4 bar (140 kPa), so a gas mixture must be used which contains less than 21% oxygen (a hypoxic mixture). Increasing the proportion of nitrogen is not viable, since it would produce a strongly narcotic mixture. However, helium is not narcotic, and a usable mixture may be blended either by completely replacing nitrogen with helium (the resulting mix is called heliox), or by replacing part of the nitrogen with helium, producing a trimix.[72]

Pulmonary oxygen toxicity is an entirely avoidable event while diving. The limited duration and naturally intermittent nature of most diving makes this a relatively rare (and even then, reversible) complication for divers.[73] Established guidelines enable divers to calculate when they are at risk of pulmonary toxicity.[74][75][76]

The presence of a fever or a history of seizure is a relative contraindication to hyperbaric oxygen treatment.[77] The schedules used for treatment of decompression illness allow for periods of breathing air rather than 100% oxygen (oxygen breaks) to reduce the chance of seizure or lung damage. The U.S. Navy uses treatment tables based on periods alternating between 100% oxygen and air. For example, USN table 6 requires 75 minutes (three periods of 20 minutes oxygen/5 minutes air) at an ambient pressure of 2.8 standard atmospheres (280 kPa), equivalent to a depth of 18 metres (60 ft). This is followed by a slow reduction in pressure to 1.9 atm (190 kPa) over 30 minutes on oxygen. The patient then remains at that pressure for a further 150 minutes, consisting of two periods of 15 minutes air/60 minutes oxygen, before the pressure is reduced to atmospheric over 30 minutes on oxygen.[78]

Vitamin E and selenium were proposed and later rejected as a potential method of protection against pulmonary oxygen toxicity.[79][80][81] There is however some experimental evidence in rats that vitamin E and selenium aid in preventing in vivo lipid peroxidation and free radical damage, and therefore prevent retinal changes following repetitive hyperbaric oxygen exposures.[82]

Bronchopulmonary dysplasia is reversible in the early stages by use of break periods on lower pressures of oxygen, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. One or two days of exposure without oxygen breaks are needed to cause such damage.[14]

Retinopathy of prematurity is largely preventable by screening. Current guidelines require that all babies of less than 32 weeks gestational age or having a birth weight less than 1.5 kg (3.3 lb) should be screened for retinopathy of prematurity at least every two weeks.[83] The National Cooperative Study in 1954 showed a causal link between supplemental oxygen and retinopathy of prematurity, but subsequent curtailment of supplemental oxygen caused an increase in infant mortality. To balance the risks of hypoxia and retinopathy of prematurity, modern protocols now require monitoring of blood oxygen levels in premature infants receiving oxygen.[84]

In low-pressure environments oxygen toxicity may be avoided since the toxicity is caused by high partial pressure of oxygen, not merely by high oxygen fraction. This is illustrated by modern pure oxygen use in spacesuits, which must operate at low pressure (also historically, very high percentage oxygen and lower than normal atmospheric pressure was used in early spacecraft, for example, the Gemini and Apollo spacecraft).[85] In such applications as extra-vehicular activity, high-fraction oxygen is non-toxic, even at breathing mixture fractions approaching 100%, because the oxygen partial pressure is not allowed to chronically exceed 0.3 bar (4.4 psi).[85]

During hyperbaric oxygen therapy, the patient will usually breathe 100% oxygen from a mask while inside a hyperbaric chamber pressurised with air to about 2.8 bar (280 kPa). Seizures during the therapy are managed by removing the mask from the patient, thereby dropping the partial pressure of oxygen inspired below 0.6 bar (60 kPa).[17]

A seizure underwater requires that the diver be brought to the surface as soon as practicable. Although for many years the recommendation has been not to raise the diver during the seizure itself, owing to the danger of arterial gas embolism (AGE),[86] there is some evidence that the glottis does not fully obstruct the airway.[87] This has led to the current recommendation by the Diving Committee of the Undersea and Hyperbaric Medical Society that a diver should be raised during the seizure's clonic (convulsive) phase if the regulator is not in the diver's mouth – as the danger of drowning is then greater than that of AGE – but the ascent should be delayed until the end of the clonic phase otherwise.[88] Rescuers ensure that their own safety is not compromised during the convulsive phase. They then ensure that where the victim's air supply is established it is maintained, and carry out a controlled buoyant lift. Lifting an unconscious body is taught by most diver training agencies. Upon reaching the surface, emergency services are always contacted as there is a possibility of further complications requiring medical attention.[89] The U.S. Navy has procedures for completing the decompression stops where a recompression chamber is not immediately available.[90]

The occurrence of symptoms of bronchopulmonary dysplasia or acute respiratory distress syndrome is treated by lowering the fraction of oxygen administered, along with a reduction in the periods of exposure and an increase in the break periods where normal air is supplied. Where supplemental oxygen is required for treatment of another disease (particularly in infants), a ventilator may be needed to ensure that the lung tissue remains inflated. Reductions in pressure and exposure will be made progressively, and medications such as bronchodilators and pulmonary surfactants may be used.[91]

Retinopathy of prematurity may regress spontaneously, but should the disease progress beyond a threshold (defined as five contiguous or eight cumulative hours of stage 3 retinopathy of prematurity), both cryosurgery and laser surgery have been shown to reduce the risk of blindness as an outcome. Where the disease has progressed further, techniques such as scleral buckling and vitrectomy surgery may assist in re-attaching the retina.[92]

Although the convulsions caused by central nervous system oxygen toxicity may lead to incidental injury to the victim, it remained uncertain for many years whether damage to the nervous system following the seizure could occur and several studies searched for evidence of such damage. An overview of these studies by Bitterman in 2004 concluded that following removal of breathing gas containing high fractions of oxygen, no long-term neurological damage from the seizure remains.[19][93]

The majority of infants who have survived following an incidence of bronchopulmonary dysplasia will eventually recover near-normal lung function, since lungs continue to grow during the first 5â€“7 years and the damage caused by bronchopulmonary dysplasia is to some extent reversible (even in adults). However, they are likely to be more susceptible to respiratory infections for the rest of their lives and the severity of later infections is often greater than that in their peers.[94][95]

Retinopathy of prematurity (ROP) in infants frequently regresses without intervention and eyesight may be normal in later years. Where the disease has progressed to the stages requiring surgery, the outcomes are generally good for the treatment of stage 3 ROP, but are much worse for the later stages. Although surgery is usually successful in restoring the anatomy of the eye, damage to the nervous system by the progression of the disease leads to comparatively poorer results in restoring vision. The presence of other complicating diseases also reduces the likelihood of a favourable outcome.[96]

The incidence of central nervous system toxicity among divers has decreased since the Second World War, as protocols have developed to limit exposure and partial pressure of oxygen inspired. In 1947, Donald recommended limiting the depth allowed for breathing pure oxygen to 7.6 m (25 ft), which equates to an oxygen partial pressure of 1.8 bar (180 kPa).[98] Over time this limit has been reduced, until today a limit of 1.4 bar (140 kPa) during a recreational dive and 1.6 bar (160 kPa) during shallow decompression stops is generally recommended.[99] Oxygen toxicity has now become a rare occurrence other than when caused by equipment malfunction and human error. Historically, the U.S. Navy has refined its Navy Diving Manual Tables to reduce oxygen toxicity incidents. Between 1995 and 1999, reports showed 405 surface-supported dives using the helium–oxygen tables; of these, oxygen toxicity symptoms were observed on 6 dives (1.5%). As a result, the U.S. Navy in 2000 modified the schedules and conducted field tests of 150 dives, none of which produced symptoms of oxygen toxicity. Revised tables were published in 2001.[100]

The variability in tolerance and other variable factors such as workload have resulted in the U.S. Navy abandoning screening for oxygen tolerance. Of the 6,250 oxygen-tolerance tests performed between 1976 and 1997, only 6 episodes of oxygen toxicity were observed (0.1%).[101][102]

Central nervous system oxygen toxicity among patients undergoing hyperbaric oxygen therapy is rare, and is influenced by a number of a factors: individual sensitivity and treatment protocol; and probably therapy indication and equipment used. A study by Welslau in 1996 reported 16 incidents out of a population of 107,264 patients (0.015%), while Hampson and Atik in 2003 found a rate of 0.03%.[103][104] Yildiz, Ay and Qyrdedi, in a summary of 36,500 patient treatments between 1996 and 2003, reported only 3 oxygen toxicity incidents, giving a rate of 0.008%.[103] A later review of over 80,000 patient treatments revealed an even lower rate: 0.0024%. The reduction in incidence may be partly due to use of a mask (rather than a hood) to deliver oxygen.[105]

Bronchopulmonary dysplasia is among the most common complications of prematurely born infants and its incidence has grown as the survival of extremely premature infants has increased. Nevertheless, the severity has decreased as better management of supplemental oxygen has resulted in the disease now being related mainly to factors other than hyperoxia.[38]

In 1997 a summary of studies of neonatal intensive care units in industrialised countries showed that up to 60% of low birth weight babies developed retinopathy of prematurity, which rose to 72% in extremely low birth weight babies, defined as less than 1 kg (2.2 lb) at birth. However, severe outcomes are much less frequent: for very low birth weight babies—those less than 1.5 kg (3.3 lb) at birth—the incidence of blindness was found to be no more than 8%.[97]

Central nervous system toxicity was first described by Paul Bert in 1878.[106][107] He showed that oxygen was toxic to insects, arachnids, myriapods, molluscs, earthworms, fungi, germinating seeds, birds, and other animals. Central nervous system toxicity may be referred to as the "Paul Bert effect".[14]

Pulmonary oxygen toxicity was first described by J. Lorrain Smith in 1899 when he noted central nervous system toxicity and discovered in experiments in mice and birds that 0.43 bar (43 kPa) had no effect but 0.75 bar (75 kPa) of oxygen was a pulmonary irritant.[29] Pulmonary toxicity may be referred to as the "Lorrain Smith effect".[14] The first recorded human exposure was undertaken in 1910 by Bornstein when two men breathed oxygen at 2.8 bar (280 kPa) for 30 minutes while he went on to 48 minutes with no symptoms. In 1912, Bornstein developed cramps in his hands and legs while breathing oxygen at 2.8 bar (280 kPa) for 51 minutes.[3] Smith then went on to show that intermittent exposure to a breathing gas with less oxygen permitted the lungs to recover and delayed the onset of pulmonary toxicity.[29]

Albert R. Behnke et al. in 1935 were the first to observe visual field contraction (tunnel vision) on dives between 1.0 bar (100 kPa) and 4.1 bar (410 kPa).[108][109] During World War II, Donald and Yarbrough et al. performed over 2,000 experiments on oxygen toxicity to support the initial use of closed circuit oxygen rebreathers.[39][110] Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. They called having an oxygen toxicity attack "getting a Pete".[111][112]

In the decade following World War II, Lambertsen et al. made further discoveries on the effects of breathing oxygen under pressure and methods of prevention.[113][114] Their work on intermittent exposures for extension of oxygen tolerance and on a model for prediction of pulmonary oxygen toxicity based on pulmonary function are key documents in the development of standard operating procedures when breathing increased pressures of oxygen.[115] Lambertsen's work showing the effect of carbon dioxide in decreasing time to onset of central nervous system symptoms has influenced work from current exposure guidelines to future breathing apparatus design.[21][22][116]

Retinopathy of prematurity was not observed before World War II, but with the availability of supplemental oxygen in the decade following, it rapidly became one of the principal causes of infant blindness in developed countries. By 1960 the use of oxygen had become identified as a risk factor and its administration restricted. The resulting fall in retinopathy of prematurity was accompanied by a rise in infant mortality and hypoxia-related complications. Since then, more sophisticated monitoring and diagnosis have established protocols for oxygen use which aim to balance between hypoxic conditions and problems of retinopathy of prematurity.[97]

Bronchopulmonary dysplasia was first described by Northway in 1967, who outlined the conditions that would lead to the diagnosis.[117] This was later expanded by Bancalari and in 1988 by Shennan, who suggested the need for supplemental oxygen at 36Â weeks could predict long-term outcomes.[118] Nevertheless, Palta et al. in 1998 concluded that radiographic evidence was the most accurate predictor of long-term effects.[119]

Bitterman et al. in 1986 and 1995 showed that darkness and caffeine would delay the onset of changes to brain electrical activity in rats.[23][24] In the years since, research on central nervous system toxicity has centred on methods of prevention and safe extension of tolerance.[120] Sensitivity to central nervous system oxygen toxicity has been shown to be affected by factors such as circadian rhythm, drugs, age, and gender.[121][122][123][124] In 1988, Hamilton et al. wrote procedures for the National Oceanic and Atmospheric Administration to establish oxygen exposure limits for habitat operations.[74][75][76] Even today, models for the prediction of pulmonary oxygen toxicity do not explain all the results of exposure to high partial pressures of oxygen.[125]

Recreational scuba divers commonly breathe nitrox containing up to 40% oxygen, while technical divers use pure oxygen or nitrox containing up to 80% oxygen. Divers who breathe oxygen fractions greater than of air (21%) need to be trained in the dangers of oxygen toxicity and how to prevent them.[67] In order to buy nitrox, a diver has to show evidence of such qualification.[126]

Since the late 1990s the recreational use of oxygen has been promoted by oxygen bars, where customers breathe oxygen through a nasal cannula. Claims have been made that this reduces stress, increases energy, and lessens the effects of hangovers and headaches, despite the lack of any scientific evidence to support them.[127] There are also devices on sale that offer "oxygen massage" and "oxygen detoxification" with claims of removing body toxins and reducing body fat.[128] The American Lung Association has stated "there is no evidence that oxygen at the low flow levels used in bars can be dangerous to a normal person's health", but the U.S. Center for Drug Evaluation and Research cautions that people with heart or lung disease need their supplementary oxygen carefully regulated and should not use oxygen bars.[127]

Victorian society had a fascination for the rapidly expanding field of science. In "Dr. Ox's Experiment", a short story written by Jules Verne in 1872, the eponymous doctor uses electrolysis of water to separate oxygen and hydrogen. He then pumps the pure oxygen throughout the town of Quiquendone, causing the normally tranquil inhabitants and their animals to become aggressive and plants to grow rapidly. An explosion of the hydrogen and oxygen in Dr Ox's factory brings his experiment to an end. Verne summarised his story by explaining that the effects of oxygen described in the tale were his own invention.[129] There is also a brief episode of oxygen intoxication in his "From the Earth to the Moon".[130]


what happened to mac in one flew over the cuckoo's nest

In the novel's climax, McMurphy sneaks two prostitutes into the ward to take Billy's virginity, while he and the others throw a party. Ratched catches them and threatens to tell Billy's mother—the only woman he fears more than her—which terrifies him so much that he commits suicide by slitting his throat. Enraged, McMurphy attacks Ratched and nearly strangles her, but is knocked unconscious by one of her associates. For this, Ratched has McMurphy lobotomized, which is to be seen as a kind of castration: "If she [Ratched] can’t cut below the belt she’ll do it above the eyes".[2] Chief Bromden smothers McMurphy in an act of euthanasia, and then breaks a window to flee from the asylum, fulfilling McMurphy's wish for him to be free.

Randle McMurphy

Randle Patrick "Mac" McMurphy known as R.P. McMurphy, is the protagonist of Ken Kesey's novel One Flew Over the Cuckoo's Nest (1962). He appears in the stage and film adaptations of the novel as well. Jack Nicholson portrayed Randle Patrick McMurphy in the film adaption, earning him an Academy Award for Best Actor. He was nominated on the "Heroes" list of AFI's 100 Years... 100 Heroes and Villains, but did not make the final list.[citation needed] He was ranked by film magazine Empire as the 61st Greatest Movie Character of All Time.[1]

Randle Patrick McMurphy (April 22, 1925-December 11, 1963) is an Irish-American brawler found guilty of battery, gambling and statutory rape. He is a Korean War veteran who was a POW during the war and was awarded the Distinguished Service Cross for leading a breakout from a Chinese camp, but was dishonorably discharged for insubordination. He is sentenced to a fairly short prison term and decides to have himself declared insane in order to be transferred to a mental institution, where he expects to serve the rest of his time in comparative comfort and luxury.

McMurphy's ward in the mental institution is run by the tyrannical Nurse Ratched, who has cowed the patients into submission. McMurphy makes it his mission to flout Ratched's regime of rules and punishment and to liberate the other patients from her grip.

During his short stay at the hospital, McMurphy forms deep friendships with two of his fellow patients: Billy Bibbit, a stuttering manchild whom Ratched has dominated into a suicidal mess; and Chief Bromden, a selectively mute Native American. In the former, McMurphy sees a younger brother figure whom he wants to teach to have fun, while the latter is his only real confidant.

McMurphy becomes ensnared in a number of power-games with Nurse Ratched. He ends up as the clear winner, reminding the other patients how to enjoy life and stand up for themselves, and persuading them to act out against Ratched's bullying. Ratched unsuccessfully tries to break his spirit through repeated shock therapy treatments.

Richard Gray, author of A History of American Literature, said that McMurphy is an "authentic American rebel", an urban cowboy, plain-speaking, hard-living, a gambler and a risk-taker," and "the hero" of the story.[3] Glen O. Gabbard and Krin Gabbard, authors of Psychiatry and the Cinema, write that McMurphy "becomes a Christ figure for whom shock therapy is the crown of thorns and lobotomy the cross".[4]

McMurphyâ€™s domination of Ratched is described as a heroic sacrifice, for the redemption and freedom of the men of the ward.[5] When Ratched returns to the ward following the attack, she is bruised and fearful, and no longer has the same measure of control over her patients due to McMurphy exposing her vulnerabilities.[6]

McMurphy has been played on stage by Jérôme Pradon, Kirk Douglas, Leonard Nimoy, Aleksandr Abdulov, Gary Sinise, Christian Slater, Shane Ritchie, Roman Wilhelmi, (Polish adaptation), Bernard Tapie (French adaptation), Ibrahim Amr, (Egyptian adaptation), Jiří Hrdina, (Czech adaptation), and most recently by Uri Meir.


what is the name of the phoenix airport

Phoenix Sky Harbor International Airport (IATA: PHX, ICAO: KPHX, FAA LID: PHX) is a civil-military public airport 3 miles (2.6 nmi; 4.8 km) southeast of downtown Phoenix, in Maricopa County, Arizona, United States.[1] It is Arizona's largest and busiest airport, and among the largest commercial airports in the United States.

In 2017, PHX served 43,921,670 passengers, making it the forty-first busiest airport in the world.[3] It handles more than 1,200 aircraft operations a day, 120,000 passengers and more than 800 tons of cargo. Federal Aviation Administration (FAA) records show that the airport had 21,185,440 commercial passenger boardings (enplanements) in calendar year 2017 and 20,896,265 in 2016.

The airport serves as the sixth-largest hub for American Airlines with over 300 daily departures to 91 destinations in 4 countries.[4] American carries nearly 46% of all PHX passengers as of December 2017 (more than 20 million passengers) and employs nearly 9,500 people, making it the airport's largest carrier.[4][5] The airport also serves as one of the largest operating bases for Southwest Airlines with 188 daily departures to 53 cities across the United States.

Sky Harbor Airport's unique name was conceived by J. Parker Van Zandt, the owner of Scenic Airways, in 1928. However, the reasoning for the name is apparently unknown. Scenic Airways collapsed in 1929 after the infamous Black Friday stock market crash.[6][7]
Sky Harbor was the fourth airport built in Phoenix.[7] This fourth airport was built with one runway in 1928. Acme Investment Company owned the airport until 1935 after the collapse of Scenic Airways. During this time, American Airlines began the airport's first scheduled passenger and air mail service in 1930. The city of Phoenix purchased the airport from Acme for $100,000 in 1935, and TWA began service to San Francisco in 1938.[8]

After the war the airport began work on a new passenger terminal, as well as a new parallel runway and a diagonal runway.[9] On the February 1953 C&GS diagram runways 8L and 8R are each 6,000 feet (1,800 m) long and runway 3 is 5,500 feet (1,700 m).

The $835,000 Terminal 1 (originally called the "West Wing") which also had the first control tower, opened in October 1952.[9] It was torn down in 1991 and replaced by a cell phone waiting lot, with Terminal 1's parking lot now being the West Economy lot.

The April 1957 OAG shows 42 scheduled airline departures a day: 16 American, 11 TWA, 10 Bonanza and 5 Frontier. American began a nonstop DC-7 to New York (Idlewild) in summer 1959.

The airport's master plan was redesigned in 1959 to eliminate the cross runway to make room for new terminals.[9] American and TWA began jet service to Phoenix in 1960 and 1961 respectively, and Terminal 2 (originally called the "East Wing") still in use today, opened in 1962.[10] Terminal 3 opened in October 1979,[9] when the "East" and "West" names were dropped, since they were no longer the only two terminals.

Bonanza Airlines moved its headquarters from Las Vegas to Phoenix in 1966. Bonanza merged with two other airlines to form Air West, which became Hughes Airwest after Howard Hughes bought it in 1970.[11]

After airline deregulation in 1978 former Hughes Airwest executive Ed Beauvais formed a plan for a new airline based in Phoenix. He founded America West Airlines in 1981, which began service from Phoenix in 1983 and doubled in size during its first year. By the end of the decade America West had a nationwide network and was lobbying for transpacific service.[11]

In the meantime Southwest Airlines arrived at Phoenix in January 1982 with thirteen daily flights to twelve cities; by 1986 it had 64 daily flights from Phoenix and had a crew base there. Southwest opened a maintenance facility at PHX in 1992 which was its largest.[12]

In October 1989 ground was broken for Terminal 4, the largest terminal.[13] It opened on November 2, 1990[14] with four concourses: N2 and N3 on the north side and S3 and S4 on the south side. In 1994 the N4 International Concourse was opened, adding 10 gates and a sterile walkway to the S4 concourse. In 1997 construction began on the 14-gate N1 concourse for America West Airlines. It was completed in June 1998 at a cost of $50 million,[15] completing the expansion of the north side of the terminal. On the south side of the terminal, construction began in 2002 on the eight-gate S2 concourse for Southwest Airlines. This project was completed in 2004 and has a different architectural design from the other six concourses. The eighth and final concourse for Terminal 4 will be built when needed. Terminal 4 is named after former Arizona Senator and 1964 Presidential candidate Barry M. Goldwater. After Goldwater's death in 1998, the mayor of Phoenix proposed renaming the airport in Goldwater's memory but was deluged with public support for the familiar "Sky Harbor" name.[16]

America West filed for Chapter 11 bankruptcy protection in 1991 and sold its larger aircraft and Japanese route authority, but continued growing its domestic operations from Terminal 4 in cooperation with Continental Airlines. Although AWA enjoyed further growth at Phoenix during the 1990s the aftermath of the September 11, 2001 attacks strained its financial position. AWA ended its relationship with Continental and merged with US Airways in 2005. US Airways moved its headquarters to the AWA campus in Tempe and retained many AWA managers to run the merged company.[11]

In 2007 the Transportation Security Administration introduced the first of its backscatter X-ray machines at PHX.[17]

Sky Harbor's private airplane area is also one of eight service centers for the Medevac airline Air Evac.[18]

Since 1951 through the end of 2017, nearly 1.2 billion passengers (domestic and international, enplaned and deplaned) have transited through PHX, an annual average of 17.6 million passengers. In the same time frame there has been over 27 million aircraft movements (commercial, military, general aviation) at PHX, an annual average of 400 thousand movements. PHX has grown over the years into a major US hub, and ranks in the top 40 airports worldwide and in the top dozen US airports in passenger volume.

PHX covers 3,400 acres (1,400 ha) at an elevation of 1,135 ft (346 m). The airport has three parallel concrete/grooved runways:[1]

All three runways allow aircraft with a Maximum takeoff weight of 900,000+ lbs.[1]

The airport's current 326 ft (99 m) tall air traffic control tower began operations on January 14, 2007. The tower stands just east of the Terminal 3 parking garage, and also houses the Phoenix TRACON. This is Sky Harbor's fourth control tower and is among the tallest control towers in North America.[citation needed]

The airport has 116 aircraft gates in three Terminals (2, 3, 4). Free ad-supported wireless internet access provided by Boingo Wireless is available in all terminals, with premium paid internet access with higher speeds and no advertisements also available to travelers.

The airport administration states that the designation Terminal 1 has been "retired", and that it did not wish to renumber the other terminals since passengers were already familiar with the numbers in place.

Terminal 2 has 17 gates (numbered consecutively 1â€“15 and two additional lettered gates C & D) and three parking slots. It was designed by the Phoenix architectural firms of Weaver & Drover and Lescher & Mahoney and opened in 1962.[19] Currently, the terminal is used primarily by United Airlines and Alaska Airlines. Terminal 2 also includes a mural by French-American artist Paul Coze in the main lobby area. In November 2006, a Military and Veterans Hospitality Room, sponsored by the Phoenix Military and Veterans Commission, was opened in Terminal 2. It has since relocated to Terminal 4 as the new USO. This terminal has undergone two renovation projects. The first was completed in 1988.[20] The second project, which cost $24 million and was designed by DWL Architects + Planners, Inc., was completed in 2007.[19][21]

Terminal 2 is expected to close after the completion of the Terminal 3 South Concourse expansion.[22] The Terminal 3 South Concourse expansion will add nine additional gates to the concourse, fully replacing Terminal 2.

Airlines currently using Terminal 2:

The 880,000-square-foot (82,000 m2), $35 million Terminal 3, designed by DWL Architects + Planners, Inc., broke ground in January 1977 and opened in October 1979 and has 23 gates, separated into two concourses by a central building outside of security.[10][19] The south concourse houses gates 1–14 (Gate 3 is missing) and the north concourse houses gates 15–26 (Gates 21 and 22 are missing). The terminal was remodeled in 1997.[24] Its only lounge – Delta's Crown Room Club – was closed on April 30, 2008 but will re-open in November 2018

A future three-part construction and renovation project is underway and will combine Terminal 2 and Terminal 3, and update the facilities. Part One has created a consolidated security checkpoint, new airline ticket counters, a Museum Gallery and a West Arrival Plaza (outdoor area with Animal Relief area). Part Two will be a brand new South Concourse as a 15 gate, linear concourse. Part Three entails renovating the North Concourse.  Both the South and North Concourses will feature new food and beverage outlets, new retail shops, and other customer service amenities.  A new Delta Lounge is slated to open in the South Concourse. After the Terminal Modernization Project is complete in 2020, Terminal 2 will be closed and its operations will move to Terminal 3.

Airlines currently using Terminal 3:

Terminal 4, also designed by DWL Architects + Planners, Inc., opened in 1990 and has 86 gates, divided into seven satellite concourses connected behind security.[19]

Airlines currently using Terminal 4:

British Airways provides nonstop service to Londonâ€“Heathrow, as well as the only passenger flights on a Boeing 747 to the airport. Condor Airlines began service to Frankfurt, Germany, from Phoenix Sky Harbor on May 18, 2018. American Airlines will begin seasonal nonstop service to London-Heathrow, using a Boeing 777-200ER beginning in March of 2019. Lufthansa had operated another transatlantic flight to Frankfurt Airport many years ago, and America West once operated trans-Pacific Boeing 747 flights to Hawaii and Japan, but these services have since ended.[25] However, several airlines offer non-stop service outside the Continental United States to Hawaii and Costa Rica, as well as cities in Mexico and Canada. Service is also provided to parts of Alaska.

While Phoenix is one of the busiest airports in the world, the lack of international destinations has initiated the Air Service Development Marketing Program. The Aviation Department offers an international air service development program to encourage new air service between PHX and qualified, unserved, international destinations. Airlines that launch new service to qualifying, unserved international markets during the program period will be eligible for marketing reimbursements and landing fee waivers. The proposed program is open to all airlines. To qualify for the funds the airline must maintain at least three new, weekly round-trips for one consecutive year. Up to $1 million will be awarded, depending on the frequency and destination. As well as intercontinental routes, they will fund airlines who increase or create new flights to North American destinations such as Mexico City, Toronto, and Boston, among others.[26]

The strategy began to pay off when, on June 22, 2017, Condor announced it would begin flying a Phoenix-Frankfurt route during 2018, marking the return of a German airline to Sky Harbor.[27]

PHX has an average of 1,183 aircraft operations per day.[59]

There are 69 aircraft based at PHX.[59]

Travelers can access East Economy Parking from the PHX Sky Train at Terminal 4.[70]  Shuttle bus service connecting the terminals and the economy parking lots was discontinued when the Terminal 3 extension of the PHX Sky Train opened, however, the airport continues to provide shuttle bus service between the terminals and the rental car center with separate routes serving each terminal.

Valley Metro bus route 13 serves all of the airport terminals as a link to the rest of the Valley Metro bus system. The Valley Metro Rail has a stop at the nearby 44th St/Washington light rail station. A moving sidewalk bridge over Washington Street allows light rail passengers to arrive at the nearby PHX Sky Train station and then onward to stations at the East Economy Parking Lot and Terminal 4. Valley Metro bus routes 1 and 44 serve the PHX Sky Train station at 44th Street & Washington with route 3 stopping at the street corner near light rail.[71]

A number of taxi, limousine, and shuttle companies provide service between each airport terminal, the Phoenix metropolitan area, and other communities throughout the state.[72]

The airport is also home to the 161st Air Refueling Wing (161 ARW), an Air Mobility Command (AMC)-gained unit of the Arizona Air National Guard. The military enclave is known as the Goldwater Air National Guard Base. One of two flying units in the Arizona ANG, the 161 ARW currently flies the KC-135R Stratotanker aircraft. In addition to its domestic role as a National Guard unit, answering to the Governor of Arizona, the 161 ARW also performs both a stateside and overseas role as a USAF organization, supporting air refueling and air mobility missions worldwide.[73]

Located on the south side of the airport, the current Sky Harbor ANGB is a comparatively new facility. As a result of growth and on-going expansion programs at PHX, a new ANG base was planned at the airport to replace a smaller, outmoded facility that stood in the way of airport construction. Plans were approved in 1995 and the new base was built during the latter part of that decade. The current Sky Harbor ANGB includes over 275,000 square feet (25,500Â m2) of facilities, pavement, and infrastructure and is one of the most modern facilities of its kind in the Air National Guard.[74]

Over 1000 Air National Guard personnel are assigned to the 161 ARW, consisting of a combination of full-time Active Guard and Reserve (AGR) and Air Reserve Technician (ART) personnel, as well as part-time "traditional" air national guardsmen.

The airport is part of the story in the movie Ground Control[75] but many scenes involving an airport were recorded at California airports instead.[76]

Arizona band Jimmy Eat World released a song titled "Goodbye Sky Harbor" on their 1999 album Clarity.[citation needed]


where is the new texas rangers stadium being built

Globe Life Field is a baseball park under construction in Arlington, Texas. It will serve as the home of the Texas Rangers of Major League Baseball.[8] Globe Life and Accident Insurance Company, a subsidiary of McKinney, Texas-based Torchmark Corporation, owns the naming rights for the facility through 2048.[9] The new ballpark is going to be constructed across the street just south of Globe Life Park.

Globe Life Field

On May 20, 2016, the Rangers announced that they would vacate Globe Life Park in Arlington. The new stadium will be constructed in a public/private partnership and have a retractable roof.[10] The ballpark was approved on the following Election Day.[11] HKS, Inc. was announced as the architect on January 5, 2017.[3]

The Rangers cited weather as the reason attendances at Globe Life Park are lower than in other baseball stadiums in major metropolitan areas, since it is prone to high temperatures and rain delays. Therefore, the Rangers are proposing their new ballpark be constructed with a roof. Unlike its predecessors, the new stadium's center-field will face northeast, instead of southeast.[12]

In 2008, the NFL's Dallas Cowboys managed to move to a retractable roof stadium due to the frequent hot weather in the Metroplex.  The venue opened in time for the 2009 season. [13]

The preliminary 3D renderings[14] and artwork of the new stadium show the design to be very similar to the looks and layout of Minute Maid Park, the Houston Astros' stadium. Final designs have not been unveiled as of August 2017. A new shopping mall, as well as a Loews Hotel, and a ballpark village are planned to go along with the new stadium. The Rangers have also planned to make Globe Life Park in Arlington part of the Texas Live! complex.  The plans to build the stadium have generated a mixed reaction. The new stadium will mean a more comfortable environment to watch baseball but will extend existing taxes used to pay for AT&T Stadium. According to The Dallas Morning News, "The deal calls for the city to issue $500 million in bonds to help pay for the stadium. A half-cent of sales tax, 2 percent hotel occupancy tax and 5 percent car rental tax would pay off those bonds over an estimated 30 years. Voters also approved a ticket tax of up to 10 percent and parking tax of up to $3 at the new stadium. That money would be used for some of the Rangers' portion of the debt, which was criticized by the opposition campaign."[15]


america's best dance crew season 4 winners

The fourth season of America's Best Dance Crew premiered on August 9, 2009.[1] All three regular judges, host Mario Lopez, and backstage correspondent Layla Kayleigh returned. This was the last season to feature Shane Sparks as a judge. In the live finale, which aired on September 27, 2009, We Are Heroes was declared the winner.

America's Best Dance Crew (season 4)

On August 2, 2009, as a prologue for the season, the show premiered a special episode hosted by Randy Jackson called "The Top 10 Performances of All Time", where Randy showed his favorite routines from the first three seasons.

Nine dance crews were selected to compete on America's Best Dance Crew. The contestants auditioned in four cities: New York City, Chicago, Orlando, and Los Angeles. Similar to the previous season, the crews were not officially divided by region; however, the regions were still listed on each crew's banner. This was also the first season to showcase crews from three regions, instead of the usual four. The group Vogue Evolution featured the "Wonder Woman of Vogue," Leiomy Maldonado.

The nine new crews chose songs that best showcased their talent in the season premiere.[2] After the bottom three was chosen by the judges, the crews had to face each other in a dance battle to "Boom Boom Pow" by The Black Eyed Peas.[3]

Beyoncé stopped by to hand out the challenges for the crews, who had to use her music videos and tour performances as inspiration for their routines.[4]

The crews had to incorporate martial arts moves into their routines. Quest Crew's Steve Terada appeared as a guest instructor.[6]

The six remaining crews were challenged to infuse the flavor of Bollywood culture into their routines.[8] In order to learn the complex Indian-themed dance style, the crews met with Bollywood choreographer Nakul Dev Mahajan.[9]

The five remaining crews put their own spins on popular dance crazes.[11] In addition to the challenge, the crews also had use the trampoline built into the stage sometime during their routines.

The final four crews paid tribute to memorable performances from the MTV Video Music Awards.[13] The crews performed together in an opening number to "Smooth Criminal" by Michael Jackson.[14]

The crews competed against each other in two challenges: the Decade of Dance Challenge, in which the crews danced to a mix of five songs from the past five decades, and the Last Chance Challenge.[16]

The remaining three crews had to master dance styles from the last five decades. One crew was eliminated halfway through the show.

The two finalists were given one last chance to perform before the lines opened for the final voting session of the season.

All nine crews returned for a group performance in the season finale. The judges each picked three crews that complemented each other and their dance styles. Then, the winner was crowned.[18]


who has the most wins in wwe history

Overall, there have been 50 different official champions, with John Cena having the most reigns at thirteen. Seven men in history have held the championship for a continuous reign of one year (365 days) or more: Bruno Sammartino, Pedro Morales, Bob Backlund, Hulk Hogan, Randy Savage, John Cena and CM Punk.[10]

List of WWE Champions

The WWE Championship is a professional wrestling world heavyweight championship in WWE, currently on the SmackDown brand. It is the first world title established in WWE, having been introduced in 1963 as the World Wide Wrestling Federation (WWWF) World Heavyweight Championship. The promotion was renamed World Wrestling Federation (WWF) in 1979 and ended its affiliation with the National Wrestling Alliance (NWA) in 1983, with the title also renamed to reflect the changes. In 2001, it was unified with the World Championship (formerly the WCW World Heavyweight Championship) following the WWF's buyout of World Championship Wrestling (WCW) and became the Undisputed WWF Championship.[1][2] In 2002, the WWF was renamed World Wrestling Entertainment (WWE) and split its roster into two brands, Raw and SmackDown.[3][4] The title, now renamed WWE Championship, was then designated to the SmackDown brand while WWE established an alternate world title known as the World Heavyweight Championship for the Raw brand. A third alternate world title, the ECW World Heavyweight Championship, was reactivated for the ECW brand in 2006. It was vacated and decommissioned when the ECW brand disbanded in 2010.[5]

When WWE Champion Randy Orton defeated World Heavyweight Champion John Cena at the TLC: Tables, Ladders & Chairs pay-per-view on December 15, 2013, the World Heavyweight Championship was unified with the WWE Championship, resulting in the retiring of the former[6] and the renaming of the latter to the WWE World Heavyweight Championship. On June 27, 2016, the name was shortened back to the WWE Championship[7] before assuming the WWE World Championship name on July 26, when the brand extension returned. It became designated to the SmackDown brand and WWE again established an alternate world title known as the WWE Universal Championship for the Raw brand. In December 2016, WWE again shortened the title's name back to WWE Championship.[8]

The championship is generally contested in professional wrestling matches, in which participants execute scripted finishes rather than contend in direct competition. Some reigns were held by champions using a ring name, while others use their real name. The first champion was Buddy Rogers, who won the championship in 1963. The champion with the single longest reign is Bruno Sammartino with a reign of 2,803 days, while the record for longest combined reign is also held by Sammartino at 4,040. The current champion is AJ Styles, who is in his second reign. He won the championship by defeating Jinder Mahal on SmackDown Live in Manchester, England on November 7, 2017.[9]

As of April 9, 2018.

As of April 9, 2018.