8.1 BIOAEROSOLS
In general, illnesses associated with indoor air exposure to bioaerosols include two major categories: infections (e.g., measles, influenza, legionnaires disease), and hypersensitivities (e.g., humidifier fever, hypersensitivity pneumonitis, asthma, and allergic rhinitis). Although infectious diseases can be transmitted via indoor air (Bloch et al. 1985; Robinson et al. 1983; Bitton, 1980; Benenson 1985; Richardson and Barkley 1984), indoor bioaerosol investigations are most often only appropriate for assessing microorganisms potentially responsible for hypersensitivity diseases. This is because the sampling methodology and sampling efficiency for infectious agents (e.g., viruses that are known to be infective via the airborne route such as rhinovirus, influenza virus, coxsackievirus, adenovirus, and measles virus) are usually inadequate. Consequently, outbreaks of hypersensitivity diseases, such as interstitial lung disease and febrile syndromes are among the best-documented indoor air-related diseases. Numerous case reports have described exposure to microbial allergens from a variety of sources including home humidifiers, HVAC systems, car air conditioners, saunas, carpet, cooling towers, bathroom fixtures, and cooling process sprays (Morey and Feeley 1988; Burge et al. 1987; U.S. National Institute of Occupational Safety and Health 1987). In addition to the pulmonary diseases, recurrent outbreaks of fever, leucocytosis, chills, muscle aches, and malaise are part of the hypersensitivity disease spectrum. Attack rates have varied from 1 percent to 70 percent (Kreiss and Hodgson 1983). Various bacteria, fungi, and protozoans have been implicated in outbreaks and case reports, including Micropolyspora faeni, Bacillus subtilis, Flavobacteria, thermophilic Actinomyces, Penicillium species, and Amoebae species. The most specific clinical test for hypersensitivity pneumonitis is bronchial challenge with either antigen or the implicated source media (e.g., water); however, this test is restricted to clinical facilities because of the severity of reactions which may be possible.
Other tests of clinical or scientific interest include erythrocyte sedimentation rate, HLA-haplotpy, atopic status, rheumatoid factor, bronchoaveolar lavage, gallium scan, lymphocyte blast transformation, antigen in lung tissue at biopsy, electron micrographic findings, and nasopharyngeal swabs. Convincing demonstration of the specific microbial etiology of hypersensitivities (and infections) requires culture of air and water samples taken from plausible sources, as well as clinical evidence (e.g., body fluid cultures, medical evaluations, serum antibody levels).
Other hypersensitivity disorders, such as asthma and allergic rhinitis, are less clearly documented in the medical literature to be associated with saprophytic bioaerosols in indoor environments. Symptoms may occur within an hour of exposure or may be delayed for up to 6 to 12 hours. A pattern of exacerbation of asthma or rhinitis in relation to occupancy in indoor environments will usually be present when the issue of bioaerosols is raised, since these conditions are common in the general population.
Aircraft cabins present unique indoor air conditions and few indoor environments can serve to adequately predict potential health risks aboard aircraft. Submarine and spacecraft indoor environments are comparable, with the exception of their complete air recirculation systems (no outdoor air is available). Studies which have measured submarine and spacecraft indoor bioaerosols (Brockett and Ferguson 1975; Brockett et al. 1978; Watkins 1970) suggest that these environments generally do not have unusually high microbe concentrations (i.e., below 20 Colony Forming Units (CFU) per m3 of air sampled). However, the potential risk of contracting a contagious disease on an aircraft is exemplified by a report of an influenza epidemic on a grounded aircraft. The aircraft was grounded for four hours in Alaska and 72 percent of the passengers became ill (National Research Council 1986). This incident emphasizes the importance of adequate ventilation both during flights and particularly while on the ground.
The following sections discuss potential types and sources of bioaersols in aircraft, environmental factors associated with their growth, amplification, survivability, and transport. In addition, the results of this investigation with respect to measured bioaerosol concentrations in aircraft cabin air are presented, including their health significance and general recommendations for minimizing the risk of indoor air-related diseases for airliner passengers and cabin crew members.
8.1.1 Types and sources of Potential Bioaerosols in Aircraft Associated with Human Health Effects
At cruising altitudes, outside air contains relatively few particle-associated microbiological organisms (National Research Council 1986b). However, outside air which enters the aircraft while on the ground carries a considerable spectrum of microorganisms including viruses, bacteria, actinomycetes, fungal spores and hyphae, animal and human dander, and arthropod-associated particles (Burge 1985).
As mentioned previously, many viral diseases can be transmitted by the aerosol route (e.g., influenza, measles, chicken pox, smallpox, colds, rabies, Venezuelan Equine Encephalitis, Newcastle disease , Infectious Mononucleosis, Yellow Fever, Rift Valley Fever, Foot and Mouth Disease, Swine Vesicular Disease, and Poliomyelitis). The primary source of indoor viral and bacterial aerosols are humans and animals (Spendlove and Fannin 1983). Airliner passengers can create these aerosols by processes such as coughing, sneezing, talking, and singing (Letts and Doermer 1983). A sneeze, for example, produces large droplets which upon desiccation remain airborne. These particle-associated microorganisms can remain infective for hours and even days depending upon the environmental conditions. Bacterial species are usually not found in infectious concentrations in the outdoor air, with the exception of several species (e.g., soil organisms such as Legionella). However, bacteria have been well recognized in indoor environments, particularly in hospitals (e.g., nosocomial infections), as the etiological agents responsible for infections of the human respiratory tract (e.g., group A Streptococcus). Human dispersion (via skin desquamation, talking, coughing, and sneezing) of both Streptococcus and Staphylococcus species (e.g., Staphylococcus aureus) have also been studied as nosocomial infection risks (Benenson, 1985).
Fungal spores, some of which are of pathogenic significance (e.g., soil-associated Coccidioides immitis in the southwestern United States), are present in the outside air, and passengers and cabin crew members boarded on an aircraft could be exposed when the aircraft is grounded and the doors are opened for unloading passengers, baggage, and other materials. Many fungi can grow and reproduce on man-made surfaces, given appropriate organic substrates and moisture conditions. When disturbed, they can produce dense aerosols that can accumulate within enclosed environments. A wide variety of fungi have been isolated from air and many fungal diseases (e.g., aspergillosis, coccidiomycosis, histoplasmosis, blastomycosis, and cryptococcoses) are known to be transmitted via the transport of spores or spore-bearing soil particles. Sufficient exposure to fungal aerosols can result in hypersensitivity diseases, such as hypersensitivity pneumonitis, allergic rhinitis, and allergic asthma in susceptible persons (Burge 1985).
Other sources of bioaerosols could include cargo compartments transporting animals. Animal dander, feces, urine, arthropods, contaminated baggage, and microorganisms transported in culture could all potentially contribute to aerosols within aircraft. Aerosol transport to passenger sections could occur depending upon the airflow patterns for a given aircraft.
8.1.2 Environmental Factors Associated with Bioaerosol Emission, Transportation and Fate
Assessment of the risks associated with respiratory infection and hypersensitivity diseases resulting from exposure to indoor air bioaerosols involves many complex and interrelated environmental, host-specific, and microbe-specific factors. Factors involved in the experimental evaluation of respiratory risk include:
- source strength
- concentration of viable units
- spray factor
- biological behaviour
- type of environmental release
- influence of air volume
- ventilation rate
- host-specific factors (e.g., immune status)
- microbe-specific factors (e.g. pathogenicity)
- relative humidity
- temperature
- organism half-life in air.
The source strength on an aircraft would include variables such as the number of people (load factor), the number of people with respiratory or skin infections, and the ability of microbes to bioamplify, which depends upon substrate availability, nutrients, water, temperature, and pH. The source strength is also influenced by the degree of sporulation and spore-celt availability. These depend on relative humidity, temperature, light, viability, and colony morphology (National Research Council 1986). Host-specific factors such as immunological status, existing antibody titers, pre-existing illness, vulnerability of specific cells in the nasal and respiratory tracts to colonization and infection, and exposure duration could be highly variable for people on a given flight. Further microbe-specific factors such as inhalation dose-response relationships, are unknown for most organisms. For example, the number of fungal spores required for a given species to induce hypersensitivity diseases remains largely unknown and most likely varies considerably with the susceptibility of the host (Platts-Mills et al. 1985; Burge 1985).
As mentioned previously, disease transmission through the air is known to occur both by droplets and droplet nuclei (Spendlove and Fannin 1983; National Research Council 1986). Methods of aerosolization include dispersal by coughing, sneezing, talking, air movement, water splashing, and turbulence. Talking can produce as many as 2,000 particles per explosive sound and a sneeze can produce approximately 2 million viable particles (Spendlove and Fannin 1983). Usually, these particles do not remain airborne for long periods, but are respirable and highly infective.
The persistence of viruses, bacteria, and fungi in the airborne state (and consequently the risk of health effects) depends on numerous environmental factors, the most important of which are relative humidity, desiccation, solar radiation, and temperature. The decline of microbes in the airborne state proceeds at two stages. First, there is a rapid die-off of the microbe following initial shock due to desiccation. This stage lasts seconds and it has been estimated that 0.5 log10 of microbes undergo inactivation (Bitton 1980). The second stage is slower and is influenced by the variables of relative humidity, temperature, and solar radiation.
Relative humidity appears to have an inverse relationship with the viability of some viruses (Loosli et al. 1943), whereas for some bacteria this relationship is reversed; the higher the humidity, the longer the survival of bacterial aerosols. It is generally recommended that the relative humidity in indoor spaces be maintained at levels less than 70 percent and less than 50 percent where cold surfaces are in contact with room air (Burge et al. 1987). In most aircraft, the relative humidity is low, which would greatly inhibit bacterial survival. However, viruses could plausibly remain viable for longer time periods. Extreme temperatures (hot or cold) are limiting factors for bioamplification of most bacteria and fungi (viruses are intracellular parasites and require host cells for replication). However, the temperature ranges (i.e., average of approximately 75 oF) found on aircraft are not likely to have substantial limiting effects because of the need to maintain comfort.
8.1.3 Bioaerosol Concentrations in Airliner Cabins: Empirical Data, Health Significance and Risk Characterization
Bacterial and fungal aerosol concentrations measured as part of this investigation were presented previously in Tables 4-24 and 4-25, respectively. These tables list the average Colony Forming Units per cubic meter (CFU/m3) of air sampled for total bacteria and fungi on smoking and nonsmoking flights. In addition, Table 4-24 lists the concentrations of Staphylococcus species on smoking and nonsmoking flights. Tables 4-26 and 4-27 list the frequency of detection for predominant bacterial and fungal species, respectively, for both smoking and nonsmoking flights.
Interpretation of the health significance of these data is most appropriately approached by initially determining if aircraft bioaerosol concentrations could reasonably be anticipated to pose risks to “healthy” passengers and cabin crew members. If this evaluation suggests that measured bioaerosol concentrations do not pose significant risks, quantitative investigation of microbe-and host-specific factors (e.g., infectious dose, pathogenicity, organism survivability, susceptible subpopulation distribution on aircraft, epidemiological circumstances) are not necessary and successful recommendations can likely be made in general terms with respect to environmental (e.g., ventilation rates, relative humidity, temperature) and operational factors (e.g., time spent on the ground without ventilation, air filtration methods) which are necessary to minimize the possibility for bioamplification and exposure to pathogenic microorganisms in aircraft.
It is acknowledged that “nonhealthy” individuals, such as immuno-compromised persons, may be at risk for infection or hypersensitivity diseases in densely populated, enclosed indoor spaces. Further, it is assumed that these individuals do not represent the “average” airliner passenger population and that reductions in their risk of acquiring bioaerosol-related diseases would require isolation from such environments. Thus, for “healthy” passengers and cabin crew members qualitative risk assessment methods can be used to determine the health significance of the data presented in Tables 4-24 and 4-25 and whether these data justify further analyses and research. These qualitative risk assessment methods include: 1) “rank order assessment” and 2) assessment of the relationship of bioaerosol concentrations to critical environmental factors (“environmental factors assessment”), including source strength as expressed by passenger load factor, air recirculation conditions, air exchange rate, type of aircraft, smoking versus nonsmoking flights, temperature, and relative humidity.
8.1.3.1 Rank Order Assessment
As applied in most indoor air evaluations for bioaerosols, the rank order assessment involves comparison of the prevalence of taxa measured in the indoor environment to the prevalence of taxa simultaneously measured outdoors (Burge et al. 1987). In general, indoor levels of microorganisms, particularly fungal spores, should be approximately less than one-third of outdoor levels (Burge et al. 1987). It is important to note that the outdoor air should be the most predominant source of the organisms being evaluated and, thus, should be qualitatively similar to the indoor air. Higher concentrations of a given taxa indoors versus outdoors suggests bioamplification and the potential for adverse health effects given that the taxa is pathogenic for humans and there are susceptible persons being exposed. These ranked populations can be compared qualitatively or quantitatively using Spearman Rank Order Correlation (Dixon and Massey 1969). This statistical procedure is used because bioaerosols rarely follow a normal distribution which precludes the use of parametric statistical methods.
TABLE 8-1. AIRBORNE CONCENTRATIONS OF VARIOUSBACTERIA AND FUNGI MEASURED IN 240 HOMES1
| Summer (CFU/m3) | Winter (CFU/m3) | |||
|---|---|---|---|---|
| Indoor | Outdoor | Indoor | Outdoor | |
| Bacillus | ||||
| Average | 1273 | 603 | 818 | 260 |
| Range | 0-6000 | 0-6200 | 33-3300 | 1716 |
| Micrococcus | ||||
| Average | 71 | 16 | 68 | 26 |
| Range | 0-633 | 0-333 | 0-383 | 0-583 |
| Staphylococcus | ||||
| Average | 143 | 28 | 250 | 18 |
| Range | 0-5466 | 0-466 | 0-1450 | 0-283 |
| Penicillium | ||||
| Average | 870 | 1166 | 80 | 26 |
| Range | 0-6200 | 0-8066 | 0-3033 | 0-350 |
| Aspergillus | ||||
| Average | 482 | 342 | 45 | 17 |
| Range | 0-3000 | 0-5400 | 0-450 | 0-267 |
| Other Fungi and Yeast (Mucor, Fusarium, Candida) | ||||
| Average | 135 | 101 | 90 | 23 |
| Range | 0-1350 | 0-733 | 0-1266 | 0-216 |
|
||||
Measured (average) bacteria concentrations (Table 4-24) were somewhat higher in the smoking (163 CFU/m3) than nonsmoking sections (131 CFU/m3) of monitored smoking flights, and the average level in the nonsmoking sections on these flights was identical to that on nonsmoking flights (131 CFU/m3). Measured (average) fungi levels (Table 4-25) were somewhat higher on nonsmoking flights (9.0 CFU/m3) than smoking flights (5.5 CfU/m3). It is important to note the standard deviations for these mean values and the general observation that microorganism concentrations were very low in all cases.
Since outdoor air at cruising altitudes is likely to have few biological particles of any kind, the rank order assessment comparison is best performed using data from other bioaerosol studies where no significant health risks were found to exist. Several studies offer such comparison to the ranked cabin air bioaerosol data presented previously in Tables 4-26 and 4-27. Table 8-1 presents “normal background” airborne concentrations of various microflora measured in 240 homes (Tyndall et al. 1987). Tables 8-2 (Solomon 1976) and 8-3 (Kozak and Gallup 1984; Kozak 1979) present similar data from a study of the prevalence of fungi encountered indoors. With respect to bacterial taxa prevalence in cabin air, Micrococcus, Staphylococcus, Anthrobactor, Corynebacterium, and Bacillus were the most frequently identified taxa. These taxa are commonly found in indoor environments, such as homes, as suggested in Table 8-1 and most importantly, the concentrations measured in the airliner cabins in this study (Table 4-24) were low and not indicative of indoor bioaerosol problems. The presence of Staphylococcus aureus is probably an indication of the density of human occupancy because this organism is normally shed by humans on skin scales. No conclusion on risk of infection due to this organism should or can be made because it is associated with infections only with immunocompromised individuals or persons in critical care facilities.
TABLE 8-2. PREVALENCE PARAMETERS FOR FUNGI ENCOUNTERED INDOORS IN WINTER1| Recovered in Homes | Mean Indoor Levels Where Recovered | |||
|---|---|---|---|---|
| No. | % | Xmean | Type Range | |
| Penicillium | 138 | 92.0 | 71.3 | 1-2,260 |
| Cladosporium | 122 | 81.2 | 3.7 | 1-43 |
| Rhodotorula | 114 | 75.9 | 173.0 | 1-8,412 |
| Nonpigmented yeasts 62 | 70.7 | 39.1 | 2-1,485 | |
| Aspergillus | 47 | 31.3 | 24.4 | 1-946 |
| Alternaria | 37 | 24.6 | 1.1 | 1-6 |
| Geotrichum | 28 | 18.6 | 110.7 | 1-2,614 |
| Aureobasidium | 26 | 17.3 | 4.2 | 1-36 |
| Cephalosporium | 17 | 11.3 | 189.1 | 2-3,760 |
| Sporobolomyces | 14 | 9.3 | 576.2 | 9-8,113 |
| Candida | 14 | 9.3 | 1.7 | 1-7 |
| Eppicoccum | 14 | 9.3 | 1.6 | 1-10 |
| "Paecilomyces - like" | 10 | 6.7 | 3,817.2 | 6-18,436 |
| Verticillium | 10 | 6.7 | 313.9 | 1-2,064 |
| Sporothrix | 9 | 6.0 | 307.6 | 4-886 |
| Sphaeropsidales | 8 | 5.3 | 2.7 | 1-6 |
| Fusarium | 8 | 5.3 | 197.4 | 3-624 |
| Trichosporon | 4 | 2.7 | 88.2 | 2-341 |
| Scopulariopsis | 3 | 2.0 | 104.6 | 1-310 |
| Bullera | 2 | 1.3 | 289.5 | 13-566 |
| Miscellaneous identified | 42 | 28.0 | 3.3 | 1-21 |
| Unidentified sporulating | 5 | 3.3 | 3.0 | 1-6 |
| Unidentified nonsporulating | 21 | 14.0 | 5.7 | 1-28 |
|
||||
| Mold Genera | Percent of Homes in which Genera solated | Range of Spores/m3 | Mean of Spores/m3 |
|---|---|---|---|
| Cladosporium | 100 | 12-4673 | 437.7 |
| Penicillium species | 91·2 | 0-4737 | 168.9 |
| Nonsporulating mycellia | 89.7 | 0-494 | 44.3 |
| Alternaria | 87·0 | 0-282 | 30.7 |
| Streptomyces | 58.8 | 0-212 | 28.1 |
| Epicoccum | 52.9 | 0-153 | 9.6 |
| Aspergillum species | 48.5 | 0-306 | 15.0 |
| Aureobasidium | 44.1 | 0.294 | 8.0 |
| Drechslera (Helminthosporium) | 38.2 | 0-94 | 6.9 |
| Cephalosporium | 36.7 | 0-59 | 5.3 |
| Acrenomium | 35.3 | 0-188 | 3.6 |
| Fusarium | 25.0 | 0-47 | 4.5 |
| Botrytis | 23.5 | 0-54 | 2.9 |
| Aspergillus niger | 19.1 | 0-59 | 2.9 |
| Rhizopus | 13.2 | 0-29 | 1.4 |
| Rhodotorula | 11.8 | 0-29 | 1.5 |
| Beauveria | 10.3 | 0-12 | 0.7 |
| Chaetomium | 8.8 | 0-47 | 1.2 |
| Unknown | 8.8 | 0-34 | 1.2 |
| Scopulariopsis | 8.8 | 0-25 | 0.9 |
| Mucor | 7.4 | 0-14 | 1.4 |
| Curvularia | 7·4 | 0-12 | 1.1 |
| Rhinocladiella | 4.4 | 0-12 | 0.5 |
| Verticillium | 4.4 | 0-12 | 0.4 |
| Plenozythia | 4.4 | 0-6 | 0.3 |
| Pithomyces | 2·9 | 0-25 | 0.4 |
| Zygosporium | 2·9 | 0-18 | 0.4 |
| Paecilomyces | 2·9 | 0-12 | 0.3 |
| Stachybotrys | 2·9 | 0-12 | 0.3 |
| Aspergillis fumigatus | 2·9 | 0-5 | 0.2 |
|
|||
With respect to the ranked order of fungi measured in cabin air (Table 4-25), Cladosporium, Alternaria, Aspergillus, Penicillium, and Epicoccum were the revalent taxa. As shown in Tables 8-2 and 8-3, fungal prevalence indoors during the winter is very similar to that found in airliner cabin air. Further, the fungal concentrations found in cabin air (Table 4-25) are low and not indicative of an indoor bioaerosol problem.
8.1.3.2 Environmental Factors Assessment
Tables 5-13 and 5-14 describe the relationship of bacterial and fungal measurements, respectively, to selected aircraft factors (i.e., type of aircraft, air recirculation, air exchange rate, and passenger loading factor) for smoking flights. The type of aircraft (wide or narrow body) did not appear to have a dramatic effect on average bacterial or fungal air concentrations (CFU/m3). The presence of air recirculation appeared to slightly increase bacterial and fungal concentrations. However, this effect was not significant. Increased air exchange rate appeared to lower the average bacterial concentrations, with little effect apparent for average fungal concentrations. The passenger load factor appeared to increase average bacterial and fungal concentrations when comparing <50 percent loading to >90 percent loading. Finally, the temperatures in the cabins of monitored aircraft averaged 75 oF for both smoking and nonsmoking flights and the relative humidity levels were quite low, averaging below 25 percent on both smoking and nonsmoking flights. The measured humidity levels were somewhat lower on smoking than nonsmoking flights.
The results of this investigation suggest that airliner cabin air concentrations of bacteria and fungi, and the prevalence of their respective taxa, are not indicative of significant potential for illnesses (e.g., hypersensitivities) associated with some indoor environments. It is recognized that this conclusion is appropriate for “healthy” passengers and not necessarily for immunocompromised persons. Consistent with recommendations made by the National Research Council (1986), if the risk of illness, whether due to an infection or a hypersensitivity disease; is to be reduced, the amount of outside air supplied to each passenger should be maximized because of the low levels of contaminants associated with this air. Further, if ventilation systems are not operating, passengers should not stay aboard the plane for long time periods (i.e., greater than 30 minutes). Consistent with general indoor hygiene, efforts should be made to maintain dry surfaces to prevent structural contamination. Based on this investigation, temperature and relative humidity ranges present on monitored flights were consistent with acceptable levels for discouraging the survival and growth of microorganisms. Cargo compartments in aircraft should be kept free of animal excrement and arthropods. Pathogenic microorganisms should not be transported on aircraft carrying passengers (National Research Council, 1986).
This study does not address the role of viruses as infectious agents in the cabin air environment. The relative importance of viruses as sources of indoor-related illnesses (e.g., influenza) can be seasonally related (Joklik 1985). Additionally, in the case of influenza viruses, the periodicity of epidemics and pandemics is related to the genetic stability of the virus and the appearance of a new virus with altered surface antigens (Joklik 1985). The monitoring conducted for this investigation occurred during the spring/summer season and not the winter season, which is associated with an increase in virus-related illnesses (Joklik 1985). Monitoring of viruses in aircraft cabins was not undertaken because of contractual constraints. To meet the contract schedule, monitoring had to be conducted during April through June when seasonal prevalence of viruses would have been low. Thus no monitoring for viruses was conducted. Nonetheless, viruses are recognized as the predominant etiologic agent for respiratory infections, estimated to cause 50 to 60 percent of all community-acquired illnesses (Feeley 1985).
8.2 COSMIC RADIATION
8.2.1 Exposure to Cosmic Radiation
The major source of radiation exposure to humans is natural in origin. This includes external sources such as cosmic radiation and terrestrial radiation from radioactive substances in the ground and building materials, and internal sources such as naturally occurring radionuclides in the body inhaled or ingested from air and diet. Natural radiation exposes virtually the world population at a relatively constant rate throughout time and is virtually independent of human activity.
According to the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), the mean annual effective dose equivalent is estimated to be 2.4 millisieverts (mSv) per year or 240 millirem (mr) per year1 (UNSCEAR, 1988).
For airline passengers and cabin crew members, the major contributing factor to any increase in the overall radiation dose is cosmic radiation, high energy radiation that enters the atmosphere from cosmic space originating usually at either the sun or in deep space. Primary cosmic rays enter the atmosphere and interact with the nuclei of atoms present in the air, resulting in the formation of secondary cosmic rays such as neutrons, protons, pions, and kaons, and a variety of reaction products (cosmogonic nuclides) such as 3H, 7Be, 10Be, 14C, 22Na, and 24Na. The high-energy secondary cosmic rays thus formed react further with nuclei in the air to form additional secondary particles (electrons and muons).
In the lower atmosphere, dose rates from the ionizing component vary little with latitude but significantly with altitude, doubling approximately every 1,500 meters (4,875 feet). Measures of absorbed dose rates in air, derived from ionization chamber measurements on aircraft, yield dose rates of 30 nGy/hr (one Gray, Gy, is equal to 100 RAD) at sea level for any latitude and from there increase to about 4 uGy/hr at an altitude of 12 km (39,600 feet) closer to the poles. At sea level, the absorbed dose rate in outdoor air from the ionizing component of cosmic rays was reported to be 32 nGy/hr (UNSCEAR 1982). This value was taken to be numerically equivalent to the effective dose equivalent. The doses are somewhat lower indoors due to the shielding effect of building structures. A shielding factor of 0.8 has been used to yield an average indoor absorbed dose index rate (at sea level) of 26 nGy/hr (UNSCEAR 1988). Using a value of 1 for the quality factor and an indoor occupancy factor of 0.8, the annual effective dose equivalent is estimated to be about 240 uSv per year at sea level.
Variation of the neutron component with altitude and latitude is similar to that of the ionizing component. At sea level, the neutron flux rate is approximately 0.008 cm-2s-1. Using an estimate of 2.4 nSv/hr for the average dose equivalent rate, and neglecting the shielding effect of building structures, the annual effective dose equivalent for the neutron component is estimated to be about 20 uSv at sea level (UNSCEAR 1982).
When the data are transformed to a cumulative effective dose equivalent as a function of altitude, a per capita effective dose equivalent for the world population is found to be 355 uSv (not time dependent), with the ionizing component accounting for 300 uSv and the neutron component accounting for 55 uSv. This increased dose equivalent estimate is due to the range of altitudes and latitudes in which people live. It is important to note that the dose equivalent from the neutron component, which is small at sea level, increases more rapidly than the dose from the ionizing component and becomes more important at altitudes above 6 km (19,800 feet).
Elevated exposures result from prolonged presence at high altitudes. Populations living in such high altitude cites as Bogota, Lhasn, or Quito receive annual effective dose equivalents from cosmic radiation in excess of 1 mSv. It follows that commercial airliner passengers and cabin crew members will be exposed to higher dose rates than the general nonflying population. These dose rates will vary according to flight altitude, flight latitude, and the amount of solar activity.
With decreasing altitude from the top of the atmosphere, the dose equivalent rate from galactic radiation first increases, then decreases. The increase is a consequence of the multiplicity and characteristics of the secondary particles produced after collision of high energy cosmic particles with the atomic nuclei of gases in the atmosphere. Many of the impacting and generated particles maintain enough energy to form additional secondary particles. The altitude at which the dose equivalent rate is maximum depends on the geomagnetic latitude. With decreasing altitude below 21.2 km (70,000 feet) at all latitudes, continued energy degradation and cannibalization of particles results in a decreasing dose equivalent rate. In the contiguous United States, the dose equivalent rate at 12.1 km (40,000 feet) is about 40 percent of the rate at 21.2 km (70,000 feet) (Federal Aviation Administration 1989).
The geomagnetic field of the earth deflects many charged particles of solar and galactic origin that would otherwise enter the atmosphere. Shielding is most effective at the geomagnetic equator, where the geomagnetic lines of force are nearly perpendicular to the surface of the earth. At airliner cruise altitudes, the cosmic radiation dose equivalent rate over the geomagnetic poles is approximately twice that over the geomagnetic equator. Most high-altitude flights of U.S. commercial aircraft occur with scheduled flights between the United States and Europe or Asia (Federal Aviation Administration 1989).
The cycle of rise and decline in the intensity of the cosmic radiation incident on the atmosphere lasts approximately 11 years, with the intensity inversely related to solar activity. Charged particles are continuously ejected from the sun but are generally too low to contribute to the radiation level at airliner flight altitudes. On infrequent occasions, the energy levels and quantities of ejected solar particles are high enough to substantially increase the dose equivalent rate at typical cruise altitudes. During the period from 1956 to 1972, there were four solar particle events during which the dose equivalent rate on polar routes at 12.4 km (41,000 feet) probably exceeded 100 uSv/hr (Federal Aviation Administration 1989).
TABLE 8-4. DOSE EQUIVALENTS FROM GALACTIC COSMIC RADIATION RECEIVED ON AIRLINER FLIGHTS| Single Nonstop One-way Flight 0rigin – Destination | Highest Altitude KM (feet, thousands) | Air Time (in hrs) | Block Time1 (in hrs) | Dose2 (in micro- sieverts) |
|---|---|---|---|---|
| Houston - Austin | 6.1 (20) | 0.5 | 0.6 | 0.1 |
| Seattle - Portland | 6.4 (21) | 0.4 | 0.6 | 0.1 |
| Miami - Tampa | 7.3 (24) | 0.6 | 0.9 | 0.4 |
| St. Louis - Tulsa | 10.7 (35) | 0.9 | 1.1 | 2.0 |
| Tampa - St. Louis | 9.4 (31) | 2.0 | 2.2 | 5.4 |
| San Juan, PR - Miami | 10.7 (35) | 2.2 | 2.5 | 7.2 |
| New Orleans - San Antonio | 11.9 (39) | 1.2 | 1.4 | 4.3 |
| Denver - Minniapolis | 10.1 (33) | 1.2 | 1.5 | 4.7 |
| New York - San Juan, PR | 11.3 (37) | 3.0 | 3.5 | 13.0 |
| Los Angeles - Honolulu | 10.7 (35) | 5.2 | 5.6 | 22.0 |
| Chicago - New York | 11.3 (37) | 1.6 | 2.0 | 8.5 |
| Honolulu - Los Angeles | 12.2 (40) | 5.1 | 5.6 | 25.0 |
| Washington, DC - Los Angeles | 10.7 (35) | 4.7 | 5.0 | 24.0 |
| Tokyo, Japan - Los Angeles | 11.3 (37) | 8.8 | 9.2 | 46.0 |
| Los Angeles - Tokyo, Japan | 12.2 (40) | 11.7 | 12.0 | 62.0 |
| New York - Chicago | 11.9 (39) | 1.8 | 2.3 | 12.0 |
| Minniapolis - New York | 11.3 (37) | 1.8 | 2.1 | 11.0 |
| London - Dallas/Ft. Worth | 11.9 (39) | 9.7 | 10.1 | 53.0 |
| Dallas/Ft.Worth - London | 11.3 (37) | 8.5 | 8.8 | 49.0 |
| Seattle - Anchorage | 10.7 (35) | 3.4 | 3.7 | 21.0 |
| Lisbon - New York | 11.9(39) | 6.5 | 6.9 | 41.0 |
| Chicago - San Francisco | 11.9 (39) | 3.8 | 4.1 | 26.0 |
| Seattle - Washington, DC | 11.3 (37) | 4.1 | 4.4 | 29.0 |
| London - New York | 11.3 (37) | 6.8 | 7.3 | 9.0 |
| New York - Seattle | 11.9 (39) | 4.9 | 5.3 | 36.0 |
| San Francisco - Chicago | 12.5 (41) | 3.8 | 4.1 | 29.0 |
| Tokyo - New York | 12.5 (41) | 12.2 | 12.6 | 91.0 |
| London - Los Angeles | 11.9 (39) | 10.5 | 11.0 | 80.0 |
| Chicago - London | 11.3 (37) | 7.3 | 7.7 | |
| New York - Tokyo, Japan | 13.1 (43) | 13.0 | 13.4 | 93.0 |
| London - Chicago | 11.9 (39) | 7.8 | 8.3 | 62.0 |
| Athens, Greece - New York | 12.5 (41) | 9.4 | 9.7 | 93.0 |
|
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Dose equivalents for flights typical of continental U.S. latitudes and circumpolar transoceanic routes are presented in Table 8-4. Since total radiation dose is the simple sum of individual exposures, this table enables any individual to ascertain cumulative radiation dose by adding appropriate flights (as actually listed or as representatives of similar flights) according to their specific frequencies of occurrence. The summed value represents the relevant individual exposure in the determination of risk, as described in Section 8.2.3.
8. Health Effects from Exposure to Cosmic Radiation
There are two types of effects from exposure to radiation: nonstochastic and stochastic. Nonstochastic effects are those for which the probability and severity of the effect vary with dose and a threshold for the effect exists. Examples of nonstochastic effects include pancytopenia following irradiation of bone marrow, and pneumonitis and pulmonary fibrosis following irradiation of the lung. Stochastic effects are those for which the probability of the occurrence of effect, and not its severity, varies as a function of dose in the absence of a threshold. The major stochastic effects are heritable genetic effects and cancer.
Early to intermediate effects of exposure to radiation can be taken to include the somatic effects of exposure to irradiation, excluding carcinogenesis and shortening of life span which are late somatic effects. Genetic effects of irradiation include gene mutation and chromosome aberrations.
Tumors caused by radiation are indistinguishable from tumors caused by other sources (e.g., chemicals), and health effects other than cancer are also very similar to those occurring spontaneously or induced by exposure to other agents. The health effects of radiation are often augmented by other factors that tend to increase overall risk; these include tobacco smoking and dietary factors (UNSCEAR 1988).
8. Quantitative Estimation of Risk
Risk was determined for cancer, fetal retardation, and birth defects using an algebraic combination of the exposure assessment and dose-response risk coefficients. Radiation risk coefficients used in this investigation were based on UNSCEAR dose-response relationships and modeling protocols (UNSCEAR 1986; 1988). The Fourth Report of the Committee on Biologic Effects of Ionizing Radiation, National Research Council (BIER IV for cosmic radiation) was not complete at the time analyses were conducted.
TABLE 8-5. RISK COEFFICIENTS FOR A RANGE OF HEALTH EFFECTS ASSOCIATEDWITH EXPOSURE TO COSMIC RADIATION
| Health Effect | Risk Coefficient | Period of Vulnerability |
|---|---|---|
| Fetal structural abnormalities | 500/1million/mSv | Weeks 2-8 of pregnancy |
| Mental retardation in fetus | 800/1million/mSv | Weeks 8-15 of pregnancy |
| 100/1 million/mSv | Weeks 16-26 of pregnancy | |
| Childhood cancer | 20/1million/mSv | Full term of pregnancy |
| Adult cancer (leukemia and solid tumors) | 70/1million/mSv |
Risk coefficients for cosmic radiation exposure in utero leading to birth defects, mental retardation, and childhood cancer, as presented in Table 8-5, were derived from epidemiological studies of children exposed in utero during the bombing of Hiroshima and Nagasaki. The risk coefficient for childhood cancer was assumed to be constant during prenatal development, although there is evidence suggesting that risk is higher in the first trimester (UNSCEAR 1986).
Risk coefficients for adult cancer (solid tumors and leukemia) were derived from epidemiological studies of atom bomb survivors, patients with ankylosing spondylitis (spinal arthritis), and patients with cervical cancer. Estimates were computed using an assumed exposure of 1 Gy and linear dose-response relationship for solid tumors. Additive and multiplicative projection extrapolation models were used to determine risks. Minimum latency for leukemia was set at 2 years and for all other sites at 10 years. The plateau was 40 years for leukemia and lifetime for all other sites. Cancer mortalities in Japan and the United Kingdom were used as baseline mortality rates. The risk coefficients assumed a quality factor of 1. This value is the sum of the relative risk for leukemia and the relative risk for other malignancies (UNSCEAR 1988).
Dose-response plots presented in Figures 8-1, 8-2, and 8-3 for adult cancer, childhood cancer, and fetal retardation and birth defects, respectively, were constructed using the risk coefficients contained in Table 8-5. The procedure for determining risk can be illustrated using the same three example flying profiles presented in Section 7.0 of this report to illustrate cancer risks from exposure to ETS. The parameters of these examples are summarized in Table 7-7. For purposes of illustration, an additional assumption is made here that half of the total flying time indicated for the individuals in the three examples is between New York and Seattle (representing a constant latitude in the continental U.S.) and the other half is between New York and Tokyo (representing a circumpolar flight at high altitude). Additional flights, and their associated cumulative doses and cancer risks, are presented in Tables 8-6 and 8-7 for domestic and international flights, respectively. In each case, flights of varying duration, latitude, and direction were chosen as examples. It should be noted that the cancer risks or cosmic radiation and ETS are additive.
Example 1. The individual is a cabin crew member who flies 960 hours per year for 20 years. Assuming that 10 years are spent flying from New York to Seattle (dose equivalent of 36 uSv for 5.3 hours from Table 8-4), the dose Equivalent for this segment is 65 mSv. Assuming that the next 10 years are spent flying from New York to Tokyo (dose equivalent of 99 uSv for 13.4 hours from Table 8-4), the dose equivalent for this period is 71 mSv. The total dose equivalent for 20 years of flying is 136 mSv (65 + 71). Referring to Figure 8-1 for adult cancer risk, a lifetime exposure of 136 mSv in flight results in a lifetime
cancer risk of 952 cancer deaths per 100,000 or a risk of 1 in 105.
Example 2. This individual is a frequent flyer who logs 480 our year for 30 years. Assuming that the first 15 years are spent flying from New York to Seattle, the dose equivalent for this period is 49 mSv. Similarly, the dose equivalent for 15 years of flying from New York to Tokyo is 53 mSv. The combined dose equivalent for 30 years of flying is 102 mSv. From Figure 8-1, the risk is 714 cancer deaths per 100;000 or a risk of 1 in140.
Example 3. This individual flies 48 hours/year for 40 years. For the last 20 years, Flights between New York and Seattle result in a dose equivalent of 6.5 mSv. For the next 20 years, flights between New York and Tokyo result in a dose equivalent of7.1 mSv. With a lifetime dose of 13.6 mSv acquired in flight, the risk is 95 cancer deaths per 100,000 or a risk of 1 in 1,053.
Risks for childhood cancer, fetal retardation, and birth defects can be determined in a similar fashion, using the risk coefficients in Table 8-5. For a single transcontinental flight such as Washington to Los Angeles, the dose equivalent is 24 uSv. The risks for any of the childhood health effects are very small (about 1 per 100,000) according to Figures 8-2 and 8-3. For even a high exposure flight such as New York to Tokyo with a dose equivalent of 99 uSv, the risks are still small (about 5 per 100,000).
8.3 OZONE
Ozone levels in airliner cabins were measured on domestic and international flights to determine compliance with current federal standards and to ascertain if observed concentrations pose a health hazard to cabin crew members and passengers.
8.3.1 The FAA Standard for Ozone in Airliner Cabins and its Basis
In 1980, the Federal Aviation Administration (FAA) promulgated an ozone standard for aircraft cabins that included transport category airplanes of commercial air carriers (Federal Register 1980). The standard was prompted by research of the FAA Civil Aeromedical Institute (Federal Aviation Administration 1979, 1980) that demonstrated no significant health effects attributable to ozone at a sea level equivalent of 0.2 ppm for 4 hours, but which did demonstrate respiratory effects in exercising individuals at a sea level equivalent of 0.3 ppm. This suggested a threshold for effect between 0.2 and 0.3 ppm. At a cabin pressure altitude of 1.8 km (6,000 ft), where there is less air for a given volume, 0.3 ppm equates to a sea level equivalent of 0.25 ppm. Accordingly, the FAA established an instantaneous standard of 0.25 ppm (sea level equivalent) and a time-weighted three-hour standard of 0.1 ppm (sea level equivalent).1
Other regulatory agencies have established similar standards. The Occupational Safety and Health Administration’s Threshold Limit Value (TLV)2 for the workplace environment is 0.1 ppm. The Environmental Protection Agency’s one-hour ambient air standard remains at 0.12 ppm, although recent research on humans under conditions of controlled exposure has suggested the possibility of respiratory effects (i.e., lung infectivity) at ozone levels as low as 0.08 ppm (see below). In addition, there is scientific and regulatory debate over the need for an 8-hour ambient air standard lower than 0.12 ppm. The FAA’s standard of 0.1 ppm appears to be in the protective range.
___________________________________________
1 While the actual time-weighted average was 0.08 ppm, the FAA wished to have its standard in harmony with OSHA’s standard of 0.1 ppm.
2 A TLV is the time-weighted average concentration for a normal 8-hour workday and a 40-hour workweek, to which workers may be exposed, day after day, without adverse health effect.
8.3.2 Health Effects of Ozone
Extensive investigations of ambient air ozone in humans and experimental animals have been described in several definitive scientific reviews (National Research Council 1977; U.S. Environmental Protection Agency 1986; Lippmann 1989). The health effects are briefly summarized below.
Ozone in the ambient air, in sufficiently high concentrations, irritates the upper respiratory tract, causes measurable degradation of pulmonary function, enhances lung infectivity, and causes alterations in blood biochemistry related to immune response. Most of the reported effects were observed after administration of doses considerably higher than those to which humans are routinely exposed. Under these conditions, morphological effects of ozone on the respiratory tract include damage to ciliated cells, proliferation of bronchiolar cells, cellular inflammation, and thickening of pulmonary arteriolar walls. Short-term exposure to ozone affects pulmonary function by increasing the breathing frequency, various physiological measures of breathing volume, airway resistance, and airway reactivity. Tidal volume, lung compliance, and diffusion capacity are decreased. Long-term exposure to ozone causes increased lung volume and airway resistance, and decreased lung compliance, respiratory flow, and lung function indicators (e.g., FEV1). Biochemically, ozone causes increases in metabolic enzymes in lung and blood, permeability changes in the lung, and increased oxygen consumption. Finally, ozone affects host defense mechanisms by delaying mucociliary clearance, accelerating alveolar clearance, inhibiting bacterial activity, altering lung macrophages causing a decrease in function, altering the number of defense cells, increasing susceptibility to bacterial infection, and altering immune activity.
Currently at issue is whether exposure to low levels of ozone manifests any of these effects. Recent work was conducted by Horstman et al. (1989), who exposed humans to 0.08 ppm in six 50-minute cycles during exercise representative of a day of moderate or heavy work. At this level, often found in ambient air, clinically meaningful alterations in lung function were observed. The Clean Air Scientific Advisory Board of the EPA is divided on the implications of these findings for regulation. Nevertheless, this and other recent research is lending to a reexamination of the bases for current regulatory standards and the durations of exposure prescribed in those standards. One of the more prominent issues is the need for an 8-hour ambient air standard for ozone. Such reconsideration are applicable to the airliner cabin environment, particularly for cabin crew members engaged in the equivalent of moderate exercise at altitude for extended periods of time.
8.3.3 Comparison of Ozone Levels Measured in Airliner Cabins with Existing Standards
A summary of ozone levels measured on all flights in this investigation was presented in Table 4-28. Average concentrations, obtained by integrated sampling, were 0.010 ppm on smoking flights and 0.022 ppm on nonsmoking flights; the maximum concentrations measured among all flights sampled was 0.078 ppm. Concentrations appeared to be uniformly distributed throughout the cabin, precluding the need to consider weighted exposures of cabin crew members and passengers by cabin section. All values were consistently below flight, occupational, and environmental standards established by the Federal government, as indicated in Section 8.3.2. This and current scientific knowledge lead to the conclusion that ozone does not pose a health hazard to cabin crew members or passengers.
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