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Aerotoxic Angels
| BALPA: Health effects of contaminants in cabin air
Friday, 08 April 2011 08:30
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Concerns have been raised by members about the possible effects on health of oil or hydraulic fluid smoke or fume contamination incidents in pressurised aircraft. Specific concerns have been raised with respect to organophosphate compounds (OPs) in the cabin air environment and the effects on health of long term low-level exposure. In the era of the first generation jets, cabin air was supplied by mechanically driven compressors as had been the case with piston airliners. From around 1963, pressurised air bled from the engine compressors has been used and this has continued into the present day. Compressing air takes power and to reduce this requirement in later aircraft up to 50% of cabin air will be filtered and recirculated. Future aircraft with composite structures and high electrical generation capability will avoid the danger to that structure of the leakage of hot bleed air by dispensing with a hot air bleed system. Instead they will use compressors driven electrically to separately pressurise outside air and mix with the recirculated mass flow. British Aerospace recognised from 1984 that oil contaminated bleed air from the engines could contaminate the air conditioning ducting. From the early 90s issues were reported with cabin air quality concerning the BAe 146 with three minor events resulting in complaints of irritation, nausea and headaches. In 1998 measurements were made in British Columbia of the components of cabin air, including Tri Cresyl Phosphate (TCP), an OP being measured. The study was unable to detect any TCP during in-flight measurements, and was in fact unable to detect any health effects associated with the oil odour. Another study of cabin air quality on Boeing aircraft by Harvard University in the USA, also failed to detect any TCP during in-flight measurements. In 1999 the Australian Parliament conducted a Senate Investigation into air safety and cabin air quality. This followed concerns raised by crew members working for Ansett Airlines who reported feeling unwell due to unpleasant odours of engine oil inside BAe 146 aircraft. The Senate report concluded that the BAe 146 had a record of unpleasant odours in the cabin as well as occasional incidents of fumes from lubricating oil. Over a longer period, airline employees had reported a variety of adverse health effects. In response to the enquiry, BAe introduced further maintenance checks and subsequently redesigned the original air circulation system in the BAe 146. A number of health compensation claims were also filed against Ansett but no damages were awarded. In the UK similar odour problems were reported with Boeing 757 aircraft. It was thought to be linked to overfilling with engine oil which could lead to contamination of the environmental conditioning system (ECS). Aircrew who report incidents experience a variety of symptoms, mainly acutely irritant in nature. Less frequently, some aircrew report longer-term symptoms. However, the epidemiological evidence is hampered by inconsistency in reporting and the numbers are small. The UK CAA Mandatory Occurrence Reporting (MOR) System in 2007 noted 116 fume event reports out of 1.3 million passenger and cargo flights. Of the 20,000 UK professional pilot population, the CAA Medical Department in 2008 was aware of 21 pilots reporting medical symptoms associated with exposure to cabin air fumes, of whom 10 are long term unfit.
ORGANOPHOSPHATES IN ENGINE OIL Mobil Jet Oil II is commonly used for jet engines. This contains synthetic hydrocarbons and additives, including the organophosphate TCP which acts as an anti wear additive alongside flame retardant properties. Engine lubricating oil contains around 3% TCP. The term organophosphate encompasses a variety of chemical compounds that have a similar structure. Small differences in this structure alter the chemical properties of the compound and will thus alter any associated health affects. Exposure to large doses of some organophosphates by skin contact, inhalation or by swallowing may cause adverse effects on the nervous system. However, not every organophosphate compound will cause these problems. The toxic effect of the ortho isomers of the three cresyl groups which make up TCP, is impairment of neuromuscular and peripheral nerve synapse function; it is thought to have no toxic effect on centrally mediated cognitive function. The para and meta isomers are not toxic to humans. Since the 1980s, less than 1% of the feed stock of TCP is formed of ortho isomers, which would permit a maximum level of 0.3% ortho TCP in the oil. There have been no independently peer-reviewed recorded cases of neurological harm in humans following dermal or inhalation exposure to TCP. The substance is harmful if swallowed in large enough quantity, but no harmful effects have been reported from this particular mixture being absorbed through the skin or from contaminated air. The majority of cases of tricresyl phosphate poisoning have been associated with the swallowing of contaminated food or drink, not with occupational exposure. The most frequent occupational exposures occur during manufacture, packaging, shipping and storage, not at the point of product use, and reports of occupational intoxication are rare. British Airways commissioned a study by an independent specialist on indoor air quality, BRE, the former Building Research Establishment, to investigate cabin air in 2001. The BRE specialists found that the concentrations of all oil compounds detected on the B757 in routine operation were each less than 100 parts per billion, which is well below the toxicological threshold for humans. These tests were performed in the normal situation with no fumes present. However specific fume events do occur and campaigners believe that these lead to health problems for aircraft occupants. They are also concerned that crew health is being affected by long term exposure to very small amounts of contaminants which may be present in bleed air as a result of leaking engine oil seals, in the absence of specific fume events. In 2004 the UK government Aviation Health Working Group commissioned a study into cabin air quality carried out by BRE. The study analysed a wide range of air quality parameters during different phases of flight aboard BAe 146 and older Boeing aircraft, including tests for oil vapours. The project supplemented an earlier 2001-2003 EU-funded research project, CabinAir, which monitored air quality on 50 European airline flights. Both surveys concluded that no air pollutant exceeded recommended health limits; hardly any trace of oil vapour was detected. A similar finding was reached by another EU-funded project, Health Effects in Aircraft Cabin Environment (HEACE), which examined all aspects of the aircraft cabin working environment during 2001-2005. However, neither of these EU studies specifically targeted the presence of TCP or contaminants which present themselves during a fume event. In 2005 BALPA organised a two day conference on contaminated air production at Imperial College London which included presentations from many of the leading campaigners. The conference called upon the government to take action on the grounds of health and safety. Because of continuing concerns of possible effects on aircrew health of cabin air contamination, the UK Department for Transport (DfT) commissioned the Committee on Toxicity of Chemicals in Food Consumer Products and the Environment (COT) to undertake an independent scientific review of data submitted by BALPA. This was completed in 2007 and the findings of the COT are as follows.
Following the COT review, the DfT commissioned further in-flight studies which began during 2008. HUMAN TOXICOLOGY Virtually every chemical, including water, can produce an adverse effect on the human body in sufficient amount. Toxic agents can be classified by the potency or relative dose required to elicit a specific adverse effect, which creates a spectrum of poisons with potencies differing by many orders of magnitude. First a toxic substance must be absorbed into the body usually by inhalation. Next it must be distributed throughout the body based on its solubility in fat or as a result of specific binding sites. Ultimately a toxic substance will be eliminated either via the kidneys in urine or via the liver in bile. Other chemicals, particularly those which have been inhaled can be excreted as vapour through the lungs. Individuals can vary in their response to toxic insult because of age, health status, previous exposure or genetic differences. It has long been recognised that some individuals are more susceptible to adverse effects when exposed to certain chemicals; the genetic basis for differences in susceptibility is being increasingly understood. In addition, it can be difficult to disentangle the physical, psychological and emotional components of well-being, and there is no doubt that different people may respond in different ways on different occasions. The human senses, particularly the sense of smell, are generally very effective in detecting potentially hazardous substances at a level well below that which causes harm (the major exception is carbon monoxide, which is odourless and colourless). The fact that a potentially hazardous substance can be smelt does not necessarily imply that it is of sufficient concentration to cause harm. For most volatile organic compounds, the concentration level for detection by a normal healthy human is around 1,000 times less than the concentration level which is likely to harm health.
Absorption and Distribution of Chemicals Foreign or exogenous chemicals (xenobiotics) must be absorbed from the surrounding environment and transported to their target site in the body for a toxic effect to occur. The chemical has to cross many cell membranes which form a lipoprotein barrier to the outside as well as maintaining the integrity of the cell. Most xenobiotics are transported by simple methods and not complex carrier-associated processes (there are exceptions such as paraquat transport into lung cells). Lipid solubility is one of the major factors determining the extent and rate of simple diffusion through a lipoprotein membrane. In the UK, the Health and Safety Executive (HSE) sets the exposure limits (OELs) for hazardous substances at work and these are published by the HSE in Document EH40 (www.hse.gov.uk). The European legal limits are known as Indicative Occupational Exposure Limit Values (IOELVs), and are broadly in line with the UK HSE occupational exposure standards. EFFECTS OF ALTITUDE Ascent to altitude is associated with a fall in air pressure paralleled by decreases in density and temperature. Thus at 18,000 feet in the Standard Atmosphere atmospheric pressure is half its value at sea level and the ambient temperature is about -20oC. Respiratory Physiology The relationship between the oxygen saturation of haemoglobin and oxygen tension is reflected in the shape of the oxyhaemoglobin dissociation curve. Inspection shows a plateau indicating that the oxygen saturation does not fall below 90% until the altitude exceeds about 10,000 feet (which equates to an alveolar oxygen tension of approximately 55 mm Hg). As altitude rises above 10,000 feet the percentage saturation of haemoglobin falls precipitously resulting in hypobaric hypoxia. Respiration increases under the hypoxic drive to help alleviate cerebral hypoxia but is ineffective, and the symptoms and signs of hyperventilation develop alongside those of hypoxia. Hyperventilation is a normal response to a fall in alveolar oxygen partial pressure to below 55 – 60 mm Hg and may be the dominant clinical feature. Symptoms both of hypoxia and hyperventilation can include light-headedness, feelings of unreality and anxiety, paraesthesiae, visual disturbances and palpitations. HYPERVENTILATION In the aviation environment it is generally recognised that hyperventilation is a common condition, often related to anxiety or emotional stress. Studies have shown that a large proportion of aircrew under training hyperventilate, as do experienced aircrew when confronted with an unusual event or in-flight emergency. A 2009 study raised concerns about the prevalence of unrecognised hyperventilation amongst airline pilots and the potential risk to flight safety (Karavidas KK, Lehrer PM. In-flight hyperventilation among airline pilots. Aviat, Space, Environ Med 2009; 80 (5): 495-6). Symptoms can include light-headedness, headache, feelings of unreality and anxiety, paraesthesiae, visual disturbances, palpitations, cognitive impairment, loss of concentration and, in extreme cases, muscular tetany and paralysis. The interaction of factors contributing to chronic hyperventilation remains uncertain. One possible scenario is that an acute episode of hyperventilation, such as might occur on exposure to fumes in flight, leads to symptoms which are misdiagnosed or incorrectly diagnosed. The symptoms can be alarming and as a consequence, the individual’s anxieties are increased which may lead to perpetuation of the problem. AEROTOXIC SYNDROME Individuals reporting that they suffer from aerotoxic syndrome describe a wide range of individual symptoms and signs, with insufficient consistency to fulfil the requirements for the definition of a medical syndrome. Many of the reported acute symptoms are normal symptoms frequently experienced. The Aerospace Medical Association reviewed the scientific evidence and concluded that there was insufficient consistency and objectivity to support the establishment of a clearly defined syndrome and the US National Academy of Sciences reached the same conclusion. Of the UK professional pilot population of approximately 20,000, in 2008 the CAA Medical Department was aware of 21 pilots reporting medical symptoms associated with the condition. Of these, 10 have been assessed as long-term unfit, 2 temporarily unfit, and 3 have allowed their medical certificates to expire. Symptoms reported by some crew members who have been exposed to fumes in the cabin are similar to those reported by individuals complaining of conditions such as sick building syndrome, chronic fatigue syndrome, Gulf War syndrome, Lyme disease and chronic stress. In all these conditions, there is lack of consistency in reported symptoms and signs and wide individual variability. CONCLUSION There has been an increase in reported incidents of in-flight smoke/fume events since 1999, with a small number of crew members reporting adverse health effects which they associate with the events. Sources of oil contamination of engine bleed air were identified in early versions of the BAe 146 and the Boeing 757 and engineering and operational modifications were implemented. A range of chronic health effects are reported by some crew members. The reported symptoms are wide-ranging with insufficient consistency to justify the establishment of a medical syndrome. Airborne research has been conducted into the constituents of cabin air without identifying a specific chemical trigger. It remains difficult to identify why some crew in a limited geographical area complain of a wide variety of symptoms which they attribute to contaminated air. Although the same equipment is flown all around the world and millions of passengers fly every day breathing the same air as the flight crew, these complaints come from only a few countries and never from passengers. According to recent figures from the Air Transport Users Council, out of a total of 29,000 written complaints since January 2001, 64 were categorised as medical and the main issues raised were pregnancy; ski injuries; allergies, typically from peanuts; and infectious diseases. Since it is only flight crew that report problems, there may indeed be an element of stress contributing to the issue. Pilots who have removed themselves from the environment do improve and become symptom free but with numbers so small, an assessment of long term health effects is very difficult. The main strategy remains research to identify the true constituents of contaminated bleed air and avoid the consideration of only one possible mechanism. |
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