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The Airliner Cabin Environment and the Health of Passengers and Crew 5 Health Considerations Related to Chemical Contaminants and Physical Factors The 1986 National Research Council (NRC) report on commercial airliner cabin air quality notes that information regarding the environmental characteristics (e.g., relative humidity and air pressure) and contaminants identified in surveys of airline cabin air “suggests a diverse set of adverse health effects that could arise from exposure to the cabin environment—from acute effects…to long-term effects.” Any consideration of health effects in the context of airline cabin air must distinguish between effects of exposures that result from the ambient environment encountered during boarding, waiting at the gate with the aircraft door open, and normal operation of the aircraft and effects of exposures that result from incidents during flight. Examples of the two categories of exposures are listed in Table 5–1. The myriad health complaints registered by flight crews and passengers are broad and nonspecific, and that makes it difficult to define or discern a precise illness or syndrome. Among the many plausible explanations of the complaints are the flight environment (e.g., partial pressure of oxygen (PO2) and relative humidity), chemical or biological contaminants, psychological and physiological stressors, and exacerbation of pre-existing medical conditions. (Biological agents are discussed in Chapter 4).
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The Airliner Cabin Environment and the Health of Passengers and Crew TABLE 5–1 Exposure Sources Relevant to Aircraft Cabin Air Quality Exposures Related to Normal Operations of the Aircraft Exposures Related to Incidents Ozone Carbon dioxide Temperature Relative humidity Off-gassing from interior material and cleaning agents Bioeffluents Personal-care products Allergens Infectious or inflammatory agents Ambient airport air Cabin pressure/partial pressure of oxygen Pesticides Jet exhaust fumes (runway) Alcohol Carbon monoxide Smoke, fumes, mists, vapors from leaks of engine oils, hydraulic fluids, and deicing fluids and their combustion products FLIGHT ENVIRONMENT Cabin Pressure As discussed in Chapter 2, at cruise altitude, the aircraft cabin is typically pressurized to the equivalent of an altitude of 6,000–8,000 ft (1,829–2,438 m), with a corresponding barometric pressure of 609–564 mm Hg and an ambient PO2 of 128–118 mm Hg (see Table 5–2). As specified in the Federal Aviation Regulation (FAR) 25.841, aircraft “cabin pressure altitude” must not exceed 8,000 ft at the aircraft’s highest operating altitude (14 CFR 1986). The reduced pressure in the cabin environment results in several physiological changes in the passengers and crew. Specifically, the reduced ambient air pressure will cause the gas in body cavities (e.g., middle ear, sinuses, and gastrointestinal tract) to expand in volume by as much as 25%. In the lungs, the lower PO2 in ambient air will reduce the oxygen (O2) pressure in the alveoli from the normal value of 105 mm Hg. That decrease will lower systemic arterial PO2. In healthy people, the arterial PO2 is usually about 5–10 mm Hg lower than the alveolar PO2 (see Table 5–2). It is the arterial PO2 that determines the amount of O2 that is carried by the hemoglobin in the blood, expressed as the percent hemoglobin saturation.
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The Airliner Cabin Environment and the Health of Passengers and Crew TABLE 5–2 Barometric Pressure and PO2 Altitude, ft (m) above sea level Barometric Pressure, mm Hg (kPa) Ambient PO2, mm Hg (kPa) Alveolar PO2 (for healthy person at rest), mm Hg Arterial PO2 (for healthy person at rest), mm Hg 0 760 (101.3) 160 (21.3) 105 95–100 6,000 (1,828) 609 (81.2) 128 (17.1) 76 66–71 8,000 (2,438) 564 (75.2) 118 (15.7) 72 62–67 Source: Adapted from Slonim and Hamilton (1971). Table 5–3 shows the arterial O2 saturation at various altitudes without supplemental O2. At an altitude of 7,500 ft (2,287 m), the PO2 begins to approach the steep-slope portion of the O2-hemoglobin dissociation curve (Figure 5–1 ). Further small changes in PO2 in the cabin can lead to large changes in the O2 content of the blood. The relationship between arterial PO2 and hemoglobin saturation is an Sshaped curve. As shown in Figure 5–1, at an arterial PO2 greater than 60 mm Hg, hemoglobin is more than 90% saturated with O2. For healthy adults at sea level, hemoglobin is 95–97% saturated. Even at an altitude of 8,000 ft (2,439 m), the O2 saturation of hemoglobin remains at least 90% for healthy adults at rest because their arterial PO2 is above 60 mm Hg. Below arterial PO2 of 60 mm Hg, there is a steep decline in the curve, over which a slight change in arterial PO2 can lead to large changes in hemoglobin saturation. The significance of this curve with respect to the aircraft TABLE 5–3 Hypobaric Pressure and Arterial O2 Saturation Pressure Altitude, ft Atmospheric Pressure, mm Hg PO2, mm Hga Arterial O2 Saturation Without Supplemental O2, % 0 760 160 96 2,500 694 147 95 5,000 632 133 95 7,500 575 121 93 10,000 523 110 89 a21% of atmospheric pressure. Source: NRC (1986).
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The Airliner Cabin Environment and the Health of Passengers and Crew FIGURE 5–1 O2-hemoglobin dissociation curve shows relationship between PO2 in blood (X-axis) and amount of O2 held by blood hemoglobin (Y-axis). Important feature of curve is sharp drop in O2 content of hemoglobin when PO2 falls below 60 mm Hg. environment is that at cruise altitudes (reduced air pressure), alveolar and arterial PO2 are reduced. However, the hemoglobin saturation decreases only slightly unless arterial PO2 falls below 60 mm Hg. A drop in arterial PO2 from 100 to 60 mm Hg will result in only a 10% drop in hemoglobin saturation. In persons with chronic obstructive pulmonary disease (COPD) or asthma, there may be inadequate O2 exchange between the air in the lungs and the blood. In this case, even at sea level, arterial PO2 may be considerably lower than alveolar PO2 (i.e., some affected persons may have less than 90% hemoglobin saturation when at rest; many more will experience this effect on exertion). The situation is worsened at higher altitudes or with exercise; under these conditions, hemoglobin saturation will be substantially lower than in healthy persons at sea level or in sedentary persons, respectively. For these people, lowering alveolar PO2 by lowering ambient air pressure may also decrease the arterial PO2 and substantially lower the amount of O2 carried by the blood The 1986 NRC report on airliner cabin environment summarized the effects of altitude on PO2 and recommended that passengers with heart or lung disease be educated about the risks posed by flight. It also recommended that passengers with middle ear problems be told about the effects of cabin pressure in general. However, that committee had few direct data on the hemoglo-
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The Airliner Cabin Environment and the Health of Passengers and Crew bin saturation that might be expected in passengers and cabin crew under normal flight conditions of commercial aircraft. Some studies have since examined the effects of cabin pressurization on PO2 in humans. Real-time continuous monitoring of hemoglobin saturation in flight has indicated that considerable changes can occur in a given person and that there are considerable differences among people. The effects of hypoxia have been studied in a number of situations, including combat flights and passenger transport (Ernsting 1978). Studies conducted during the 1940s suggested that the maximal acceptable degree of hypoxia in passenger aircraft corresponded to a cabin altitude of 8,000 ft, but it was recommended that under routine operating conditions cabin pressure altitude should not exceed 5,000–6,000 ft. The altitude of 8,000 ft was a compromise between the aircraft design and operation requirements and the human performance impairments. Studies by McFarland and Evans (1939), McFarland (1946), and others (Ernsting et al. 1962; Denison et al. 1966; Ledwith 1970) showed that mild hypoxia, as is found in subjects at 8,000 ft, might impair the learning of new tasks and the performance of complex tasks. Most of the studies were conducted on young, healthy men, primarily in the military, who were engaged in vigilance tasks. McFarland and Evans (1939) found an increase in the absolute brightness threshold of the dark-adapted eye at hypoxia equivalent to 7,400 ft but concluded that the change was so small that it was of no practical significance. Ernsting (1978) noted that a “reduction of the cabin altitude from 8,000 to 6,000 ft is associated with a lower incidence of otiotic barotrauma and disturbances in passengers with cardiorespiratory disease.” Studies on performance deficit under hypoxic conditions—86% arterial oxyhemoglobin equivalent to 8,900 ft—showed no effect on performance, including night vision; the threshold for effects appeared to be 82% oxyhemoglobin (9,750 ft) (Fowler et al. 1987). Cottrell et al. (1995) used continuously reading pulse oximeters to measure O2 saturation in 38 pilots on 21 flights of about 4 h each. Pressure altitudes in the aircraft cockpits during the cruise portion of the flight were 6,000–9,000 ft (average, 7,610 ft). Maximal and minimal O2 saturations were 95–99% (mean, 97%±1.1%) and 80–93% (mean, 88.6%±2.9%), respectively. Of the 38 subjects, 20 (53%) developed an O2 saturation of less than 90% at some time during the flight (duration of time below 90% not given). Baseline O2 saturation was 95–99%; at 6,000–7,000 ft, saturation was 87–92%; and at 8,000 ft or more, it was 80–91%. No symptoms were reported, and no attempt was made to measure performance decrement. There was no correlation between the minimal oxyhemoglobin saturation and age, height, weight, length of flight,
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The Airliner Cabin Environment and the Health of Passengers and Crew maximal saturation, smoking history, peak cabin altitude, or whether the flight was during the day or night. In a study of the effects of hypoxia on healthy infants, 34 babies (1–6 mo old; average 3.1 mo) were exposed to 15% O2 in nitrogen for a mean duration of 6.3 h±2.9 h (Parkins et al. 1998). During exposure, there was a significant increase in the infants’ heart rate and time spent in periodic apnea and a decrease in the amount of time spent in regular breathing; respiratory rates did not change significantly. Baseline O2 saturation decreased from a median of 97.6% (range, 94–100%) in ambient air to 92.8% (range, 84.7–100%) in 15% O2. Four of the infants had to be removed from the hypoxic conditions early because their O2 saturation fell below 80% for more than 1 min. The authors suggest that exposure to reduced PO2, like that encountered on high-altitude flights can result in hypoxia in some infants. A newborn infant’s red blood cells contain up to 77% fetal hemoglobin (Delivoria-Papadopoulos and Wagerle 1990). At 6 mo, the red cells still contain up to 4.7% fetal hemoglobin. Fetal hemoglobin binds O2 with greater affinity than does adult hemoglobin (see Figure 5–2). That results in greater saturation for any given partial pressure, but it also means that at any given partial pressure fetal hemoglobin holds O2 more than adult hemoglobin. The net effect is that less O2 is available for tissue metabolic needs. Thus, infants who experience substantial falls in arterial O2 saturation may be at greater risk for tissue hypoxia than adults at the same O2 saturation. With decreasing cabin pressure, air in the middle ear and sinuses expands and escapes via nostrils and ostia to the outside via the nasopharynx. On descent, increasing ambient pressure requires gas to re-enter the middle ear and sinuses through the same pathways. Both movements can happen only if air can move freely in either direction. If there is blockage due, for example, to an upper respiratory infection, allergy, or tumor, the free flow of air may be impeded, and earache, a feeling of sinus fullness, or dizziness can ensue, particularly on descent. In severe cases, the pressure differential can cause extreme pain, bleeding, or rupture of a tympanic membrane. Likewise, gas in the respiratory tract and gastrointestinal tract expands and contracts with decreasing and increasing cabin pressure. Although gas readily escapes from those parts of the body, minor stomach cramping or bloating might still occur. At cabin altitudes during cruise, all crew and passengers are in a decreased-O2 environment. It is clear that under ordinary conditions of commercial flight, PO2 can be reduced substantially during rest or in situations of minimal exertion. As stated above, this relatively small decrement usually causes
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The Airliner Cabin Environment and the Health of Passengers and Crew FIGURE 5–2 Oxyhemoglobin equilibrium curves of blood from infants and adults. Source: Adapted from Delivoria-Papadopoulos and Wagerle (1990). no symptoms in healthy people because hemoglobin remains well saturated with O2 at altitude. Nevertheless, some people might be sensitive to a lowering of PO2 and experience various symptoms, including headache, dizziness, fatigue, numbness, and tingling (Sheffield and Heimbach 1996). The array of possible symptoms varies from person to person or even in the same person on different days. The PO2 values are such that substantial reductions in arterial O2 content occur and could pose a definite health risk for persons with underlying pulmonary or cardiac disease or untreated or partially treated anemia.
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The Airliner Cabin Environment and the Health of Passengers and Crew Relative Humidity As noted in Chapters 1 and 2, the relative humidity in most aircraft cabins is low, typically from 10 to 20% (see Table 1–2) with an average of 15–19%, depending on the aircraft (Nagda et al. 2000). Although, low relative humidity is not an air contaminant, it can affect passenger and crew comfort and health (Rayman 1997). Low relative humidity may cause drying of the skin, mucous membranes, and conjunctivae in the latter case adding a risk for conjunctivitis with its symptoms of tearing and pain, especially in those wearing contact lenses (Eng 1979). Studies have indicated that passengers and cabin crews find the air in the aircraft cabin to be too dry and to lead to such symptoms as dry, itchy, or irritated eyes; dry or stuffy noses; and skin dryness or irritation (Lee et al. 2000). Stuffy, dry nose was the primary complaint in another study of 3,630 passengers in all cabin classes on standard and wide-body aircraft. Although symptoms could not be correlated with aircraft type (comfort rating, 5.34 of 7 for first-class versus 4.46 for coach and no difference in passenger comfort ratings for relative humidity between standard-body and wide-body aircraft), they did reflect flight length: longer flights resulted in more symptoms (Rankin et al. 2000). Low relative humidity has also been associated with fatigue, headaches, and nosebleeds (Space et al. 2000). Low humidity can have a greater effect on passengers who have respiratory infections, asthma, or tracheotomy (Rayman 1997). It has been found that in dry environments, mucus can concentrate; this can reduce ciliary clearance and phagocytic activities in the respiratory tract (Berglund 1998). In a study of the effects of low humidity on the human eye, Laviana et al. (1988, as cited in Nagda and Hodgson 2001) found that at a relative humidity of either 10% or 30%, eye pain (described as scratchiness, pain, or burning) increased over time up to the fourth hour of exposure (total exposure duration of 10 h) for both a naked eye and an eye covered with a soft contact lens. However, there was no difference in the severity of responses at either 10% or 30% relative humidity and the humidity level did not significantly affect acuity, refractive error or cornea curvature in either eye. In aircraft cabins, symptoms of low humidity, such as eye and nasal irritation, seem to occur within 2 h after exposure begins (Eng 1979); skin symptoms may require at least 4 h to occur (Carleton and Welch 1971, as cited in Nagda and Hodgson 2001). Furthermore, all symptoms increase in severity with time, and an adaptive response to low-humidity environments is not evident (Nagda and Hodgson 2001). At reduced barometric pressures (259–700 mm Hg), symptoms associ-
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The Airliner Cabin Environment and the Health of Passengers and Crew ated with low humidity develop more quickly and are more severe (Carleton and Welch 1971, as cited in Nagda and Hodgson 2001). In a review of the studies that examined potential health effects of exposure to low relative humidity, Nagda and Hodgson (2001) indicated that the study subjects in general were relatively young and that an older study population might have been more likely to perceive changes in relative humidity and also might be more susceptible to health effects of such exposures. They concluded that a modest increase in the relative humidity in an aircraft cabin (e.g., from the current average of 14–19% to about 22–24%) might have beneficial effects similar to those seen in building studies in which a 10% increase in humidity alleviated many of the symptoms of “sick-building syndrome.” Such humidities are below the values that may affect the safety of an aircraft—that is, that might cause condensation in and corrosion of the aircraft shell—or that would result in increased microbial growth. Although cabin relative humidity is well below the preferred values of 30– 60% suggested in American Society of Heating, Refrigerating and Air-Conditioning Engineers Standard 62–1999, it is questionable whether low humidity has substantial short- or long-term health effects. One investigator reported that in a room with 0% humidity, the degree of dehydration in undressed subjects was insignificant over a period of 7 h (Nicholson 1996). It might be expected that the adverse effects of low relative humidity experienced by crew and passengers will be temporary and will be alleviated when they leave the aircraft. The time required for rehydration will depend on individual physiology and the ambient environment. Humidity influences the perception of air quality. In one study, as relative humidity increased from 24% to 79%, the air was considered to be less fresh (Berglund 1998). Acceptability of air-quality decreases with increasing temperature and relative humidity (Fang et al. 1998a,b). CHEMICAL CONTAMINANTS OF CONCERN During flight, passengers and crew can be exposed to a variety of air contaminants. Some of them are naturally occurring chemicals, such as ozone (O3), which is found in greater concentrations in the upper troposphere and lower stratosphere; others result from incidents that suggest equipment failure; and still others result from preventive measures, such as the use of pesticides. The toxicity of these contaminants is discussed below.
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The Airliner Cabin Environment and the Health of Passengers and Crew Ozone Although ground-level O3 is a major contributor to photochemical air pollution in urban air, the presence of O3 in the upper troposphere and lower stratosphere provides a necessary health benefit to humans by screening out harmful ultraviolet radiation. As discussed in Chapter 3, many commercial flight paths are at altitudes where O3 concentration might be greater than those typically found at ground level. O3 in the cabin is required not to exceed 0.25 ppm (250 ppb) during a flight (FAR 25.8321). Mean O3 measured on aircraft has ranged from 22 ppb (Nagda et al. 1989) to 200 ppb (Waters 2001). The health effects of ground-level O3 have been well studied (EPA 2001). Those effects are relevant to travelers who might be exposed to increased O3 during high-altitude flights if the aircraft is not equipped with an O3 converter or the equipment is not operating properly. The ground-level national ambient air-quality standard for O3, established by the Environmental Protection Agency (EPA) in 1997, is 0.12 ppm by volume for a 1-h exposure and 0.08 ppm by volume for 8-h exposures (EPA 1997). O3 can cause acute respiratory problems, aggravate asthma, and impair the body’s immune system making people more susceptible to respiratory illnesses, including bronchitis and pneumonia (EPA 1996). Exposures to O3 as low as approximately 0.08–0.10 ppm for about 6 h have resulted in impairments of the immune system (EPA 1996). Inflammatory responses occurred within 1 h after a 1-h exposure to O3 at 0.3 ppm or more. Exposures for up to 7 h to O3 as low as 0.08 ppm caused small decrements in lung function and increases in respiratory symptoms (EPA 1996). Those effects are exacerbated by exercise. In a study of healthy adults exposed during exercise to ambient O3 at 21–124 ppb, there was a statistically significant decrement in lung function (Spektor et al. 1988a). Similar lung function decrements were seen in healthy children (at a summer camp) exposed to O3 at the ambient air standard of 120 ppb, where average forced vital capacity (FEV), forced expiratory volume in the first second (FEV1), peak expiratory flow rate (PEFR), and forced expiratory flow (FEF25–75) decrements were 4.9%, 7.7%, 17%, and 11%, respectively (Spektor et al. 1988b). 1 FAR Section 25.832 Cabin ozone concentration: “(a) The airplane cabin ozone concentration during flight must be shown not to exceed: (1) 0.25 parts per million by volume, sea level equivalent, at any time above flight level 320, and (2) 0.1 parts per million by volume, sea level equivalent, time-weighted average during any 3-hour interval above flight level 270.”
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The Airliner Cabin Environment and the Health of Passengers and Crew Asthmatics, particularly children, show an increase in respiratory symptoms and decrements in peak expiratory flow rate with increasing O3 (EPA 1996). Studies on children with moderate-to-severe asthma found that increasing O3 from 84 to 160 ppb for 1 h resulted in increased medication use and an increase in the number of chest symptoms (Thurston et al. 1997). The long-term sequelae of inhalation exposure are unknown, but continued exposure O3 at low concentrations could result in chronic effects in humans (EPA 1996). The committee was able to identify only one study that examined the possible effects of O3 on flight attendants (Tashkin et al. 1983). The authors attempted to determine, on the basis of symptoms reported on a questionnaire distributed to flight attendants on high-altitude flights of Boeing 747SP aircraft, whether the symptoms were consistent with possible exposure to increased O3. Although the authors concluded that the reported symptoms were consistent with exposure to toxic concentrations of O3 (0.4–1.09 ppm, measured onboard other 747SP aircraft), no O3 measurements were made on flights where the questionnaire was used. There were substantial limitations in the study, as discussed in Chapter 6. Engine Oils and Hydraulic Fluids Engine lubricating oils and hydraulic fluids are complex mixtures of primarily organic compounds (see Table 3–12 for major components). Among the major additives to the petroleum base of these mixtures are organophosphate compounds, of which those organophosphates, of greatest toxicological concern are tricresyl phosphate (TCP) derivatives and the generation of trimethylolpropane (TMPP). Other organophosphates that can be present in the oils and fluids are tributyl phosphate, dibutyl phenyl phosphate, and triphenyl phosphate. The general toxicity of these agents is discussed below. Engine lubricating oils and hydraulic fluids have been reported to enter the passenger cabin of aircraft through the environmental control system (ECS) as discussed in Chapter 3. The fluids (and their possible pyrolysis products) can result in mists, fumes, vapors, and smoke in the cabin. The major pyrolysis products of jet engine oils and hydraulic fluids, at less than very high temperatures, will probably be volatile organic compounds (VOCs) and carbon monoxide (CO). Although there is considerable toxicological information on the major constituents of engine oils and hydraulic fluids, there are few data on the toxicity of the formulated oils and fluids themselves. Only a couple of studies were found in the published literature, and they are discussed below.
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The Airliner Cabin Environment and the Health of Passengers and Crew FIGURE 5–3 PO2 in six healthy subjects and nine subjects with chronic air-flow limitation (CAL; FEV1/FVC≤70%) during hypobaric high-attitude simulation. Data at 8,000 ft are at rest and after 2 min of “light exercise” (approximate work rate, 200 kJ/min) to approximate a short walk on aircraft. Source: Naughton et al. 1995. Redrawn from the American Journal of Respiratory and Critical Care Medicine; copyright 1995, American Thoracic Society. People with medical conditions that may require treatment during travel (e.g., COPD, asthma, and autoimmune diseases) should carry letters describing their condition and treatment. Various types of medical alert tags and bracelets are available and should be worn to inform emergency-care providers of appropriate treatments or precautions for various medical conditions and how to reach travelers’ health-care providers. Populations that may be particularly sensitive to CO poisoning are anemic persons who have low hemoglobin concentrations, children who have higher metabolic rates that would exacerbate the adverse effects of CO, persons with a history of coronary heart disease or respiratory disease, and the elderly. Smokers typically have increased COHb and may have an adaptive response to elevated COHb (EPA 2000). People with coronary arterial disease and reproducible exercise-induced angina have decreased exercise tolerance at COHb concentrations of 3–6% (EPA 2000). Pregnant women may be at particular risk. The fetus may be very susceptible to the effects of CO be
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The Airliner Cabin Environment and the Health of Passengers and Crew cause it readily crosses the placenta and might result in neurological damage to the infant (EPA 2000). Asthmatics may be especially sensitive to formaldehyde. Cabin crews as a cohort population are relatively healthy. Air-transport pilots are required by FAA to undergo a flight physical examination every 6 mo, and must be granted an exception for significant illness or some classes of medications. Air-transport pilots can no longer fly as pilots once they are 60 yr old. However, flight attendants are required to undergo only an entry physical examination. There is no requirement for periodic medical examinations as there is for pilots. There are no health requirements for passengers. CONCLUSIONS The flight environment, with its lowered barometric pressure, may result in passenger and crew discomfort and in susceptible people, in health effects. Infants may also be at greater risk for hypoxia under conditions of reduced PO2. Although low relative humidity in the aircraft cabin can result in temporary discomfort as a result of the drying of mucous membranes and eye, nose, and respiratory tract irritation, symptoms are expected to subside after exposure is discontinued. There is no information on the potential for long- or short-term adverse effects associated with exposure to low relative humidity. High-altitude flights might result in increased O3 levels in an aircraft. Elevated O3 concentrations have been associated with increased respiratory symptoms, such as coughing, wheezing, and asthma. Phosphate esters, formaldehyde, other aldehydes, and CO—found in engine oil, hydraulic fluids, and their pyrolysis products—may cause respiratory and neurological effects, particularly at high concentrations. However, more data are needed to establish an association between the presence and concentrations of cabin contaminants and potential health effects in passengers and crew. Although pyrethroid pesticides, used for disinsection on some aircraft, have very low toxicity in humans, they can cause adverse effects and are recognized as neurotoxins. In passengers and cabin crew who have pre-existing illness—such as anemia, asthma, COPD, and coronary arterial disease—the stresses of flight could exacerbate symptoms.
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The Airliner Cabin Environment and the Health of Passengers and Crew RECOMMENDATIONS Potential synergistic and interactive effects of exposure in the aircraft cabin to reduced barometric pressure, low humidity, O3, other chemical contaminants, and pesticides should be examined. If future research, such as that described in Chapter 8, indicates that some cabin air contaminants or other environmental characteristics, such as relative humidity, pose hazards to the health of passengers or crew, FAA should work with other organizations—such as the Occupational Safety and Health Administration, EPA, and ACGIH—to establish standards or guidelines to regulate them. REFERENCES ACGIH (American Conference of Governmental Industrial Hygienists). 1980. Documentation of the Threshold Limit Values, 4th Ed. Cincinnati, OH: ACGIH. ACGIH (American Conference of Governmental Industrial Hygienists). 2001. 2001 TLVs and BEIs: Threshold Limit Values for Chemical Substances and Physical Agents: Biological Exposure Indices. Cincinnati, OH: ACGIH. Aerospace Medical Association. 1997. Medical Guidelines for Airline Travel. Alexandria, VA: Aerospace Medical Association. Allred, E.N., E.R.Bleecker, B.R.Chaitman, T.E.Dahms, S.O.Gottlieb, J.D.Hackney, M. Pagano, R.H.Selvester, S.M.Walden, and J.Warren. 1991. Effects of carbon monoxide on myocardial ischemia. Environ. Health Perspect. 91:89–132. Ammann, H.M. 1999. Microbial volatile organic compounds. Pp. 26.1–26.17 in Bioaerosols: Assessment and Control, J.M.Macher, H.M.Ammann, H.A.Burge, D.K.Milton, and P.R.Morey, eds. Cincinnati, OH: American Conference of Government Industrial Hygienists. Apte, M.G., W.J.Fisk, and J.M.Daisey. 2000. Associations between indoor CO2 concentrations and sick building syndrome symptoms in U.S. office buildings: An analysis of the 1994–1996 BASE study data. Indoor Air 10(4):246–257. ATSDR (Agency for Toxic Substances and Disease Registry). 1997. Toxicological Profile for Ethylene Glycol and Propylene Glycol. U.S. Department of Health and Human Services, Public Health Service, Atlanta, GA. ATSDR (Agency for Toxic Substances and Disease Registry). 1999. Toxicological Profile for Formaldehyde. U.S. Department of Health and Human Services, Public Health Service, Atlanta, GA. Backman, H., and F.Haghighat. 2000. Air quality and ocular discomfort aboard commercial aircraft. Optometry 71(10):653–656. Ballarin, C., F.Sarto, L.Giacomelli, G.B.Bartolucci, and E.Clonfero. 1992. Micronucle-
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Representative terms from entire chapter: