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The Airliner Cabin Environment: Air Quality and Safety (1986)

Chapter: 5 Cabin Air Pollutants: Sources and Exposures

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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Page 139
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Page 141
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
Page 142
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
Page 143
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
Page 144
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
Page 145
Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
×
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Suggested Citation:"5 Cabin Air Pollutants: Sources and Exposures." National Research Council. 1986. The Airliner Cabin Environment: Air Quality and Safety. Washington, DC: The National Academies Press. doi: 10.17226/913.
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Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

5 CABIN AIR POLLUTANTS: SOURCES AND EXPOSURES Little is known about the environment in the passenger cabins of commercial aircraft under routine flight conditions, and what is known is limited in scope. Relationships among source strengths of pollutants, physical factors (such as ventilation rates and operating modes), occupancy loads, and activities (such as eating and smoking) have not been systematically studied. Lacking a repository of the existing information, the Committee searched the published literature to obtain relevant material on pollutants known to be potentially hazardous or to cause acute irritation and on physical factors that affect comfort. On the basis of the results of the searches, this chapter discusses ozone, cosmic radiation, ground fumes, tobacco smoke and carbon monoxide, biologic aerosols, relative humidity, cabin pressure, carbon dioxide, volatile organic chemicals, and pesticides. OZONE OZONE IN COMMERCIAL AIRCRAFT CABINS Ozone is present in the atmosphere as a consequence of the photochemical conversion of oxygen by solar ultraviolet radiation. A marked and progressive increase in ozone concentration occurs between the tropopause and the stratosphere--i.e., it occurs within the flight altitude of commercial aircraft. The mean ambient ozone concentration increases with increasing latitude, is maximal during spring, and often varies with weather systems to result in high ozone plumes descending down to lower altitudes. 113

114 In the early 1960s, R. I. Brabets et al.24 established that Jet aircraft operating in the stratosphere encountered ozone and that it was only partially removed from the internal environment of the aircraft by the compression-ventilation system. In response to these findings, the Global Atmospheric Sampling Program (GASP), started by the National Aeronautics and Space Administration in 1977, measured ozone concentrations in the cabins of two commercially operated aircraft. In 1980, Nastrom et al.107 reported that over 5,600 observations were made in this project in a B-747-100 and a B-747-SP. The ozone concentrations measured in the outside air and in the cabin of an unmodified B-747-SP are shown in Figure 5-1. boon 800 ~2 C 600 of o z CD <( 400 200 o 0' ° e',' 0 '0 0 o 200 400 ATMOSPHERIC OZONE, ppb / O 0: ~007 ~ O o O 0 OOo8 ~ ooze ~ 0 a ~0 Q)~e 6E o or 1 1 1 1 1 1 600 800 1,000 o FIGURE 5-1 Correlation (slope, 0.82) of cabin with atmospheric ozone mixing ratios. Data were obtained during April, May, and June 1977 before changes were made in B-747-SP air circulation system. Squares show data taken in April. Reprinted from Perkins et al.ll 4

115 Crew members' and passengers' complaints of physical discomfort on high-altitude flights led the Federal Aviation Administration (FAA) to begin to collect information on possible causes.159 In 1977, the agency took five steps to investigate further whether ozone was the pollutant responsible for the complaints: · It published an advisory circular that defined ozone irritation, discussed its cause and symptoms, and described means of dealing with it.l59 · It initiated a research project in the Civil Aeromedical Institute to study the health effects of exposure to ozone in the aviation environment. · It issued Advance Notice of Proposed Rulemaking No. 77-22 to seek information concerning ozone. i57 . It initiated a project to measure the constituents of the upper atmosphere. · It initiated a study of available data on ozone concentrations at flight altitudes to provide an estimate of average atmospheric ozone at flight altitudes. On the basis of these efforts, FAA established a standard for cabin ozone concentration. 31 The Code of Federal Regulations of January 1, 1985, stated the following: "The airplane cabin ozone concentration during flight must be shown not to exceed 0.25 ppm, sea level equivalent, at any time above flight level 320 [32,000 ft at standard atmosphere]; or 0.10 ppmv during any 3-hour interval above flight level 270 [27,000 ft at standard atmosphere]." HEALTH EFFECTS OF OZONE UNDER HIGH-ALTITUDE CONDITIONS The following text discusses several experimental studies involving humans. See Chapter 6 for discussion of findings on human exposure and resulting effects during flight. Toxic effects of ozone on the respiratory system have been investigated in numerous human studies involving controlled exposures to ozone at concentrations observed in community air., 56 The characteristic odor

116 of ozone can be detected by some people exposed to it at concentrations as low as 0.001 ppm.~43 This may be important because of perception of exposure. The threshold varies among individuals, but most people can detect ozone at 0.02 ppm. Controlled human studies have reported respiratory symptoms and significant decrements in pulmonary function associated with ozone exposure. The severity of reported symptoms generally parallels the observed impairment in pulmonary function. Symptoms include cough, upper airway irritation, tickle in the throat, chest discomfort, substantial pain or soreness, difficulty or pain in taking a deep breath, shortness of breath, wheezing, headache, fatigue, nasal congestion, and eye irritation. Cough is the symptom most strongly correlated with the decrement in pulmonary function. These symptoms and the alteration in pulmonary function usually disappear soon after the termination of the exposure. Some subjects have reported persistence of changes in excess of 24 h, but most disappear within 2-4 h. If exposure is repeated within 24-48 h, pulmonary function decrements are markedly greater. 6 5 Studies in environmental chambers using at-rest (i.e., no-exercise) exposures to ozone have shown that ambient ozone at 0.5 ppm or more induces significant decrements in pulmonary function. 66 Impairment in pulmonary function occurs at much lower ambient concentrations of ozone if subjects are exercising. Subjects engaged in light exercise (ventilation, approximately 20-25 L/min) had significant pulmonary function decrements when ozone was present at 0.37 ppm. In persons exercising moderately to heavily (26-40 L/min), pulmonary decrements have been observed during exposures at 0~14-0-18 ppm. 5 0 ~ ~ ~ 7 Lategola and associates attempted more quantitative evaluation of problems associated with ozone exposures of flight attendants and passengers. Lategola et al. 85 exposed 55 young subjects (29 men and 26 women) to ambient air and to an ozone environment in an altitude chamber maintained at 1,829 m (6,000 ft). Subjects served as their own controls in each experiment. Two major experiments were conducted on 27 subjects (15 men and 12 women) and 28 subjects (14 men and 14 women).

117 In the first experiment, ozone concentrations* were O and 315 ~g/m3 (0.0 and 0.2 ppm), exposure time was 4 h (with four 10-min exercise periods, the first three at lower levels of activity and the fourth at a higher level), and pulmonary function and subjective evaluations were noted before and after exposure. Pulmonary function and subjective responses were recorded near sea level before and 10 min after the altitude exposures. Other studies--on vision, hand steadiness, and memory--were conducted during the high-altitude exposures. Men exercised at ventilation of 20 L/min in the first three exercise periods and 30 L/min in the last period, Just before descent; women exercised at 13 and 17 L/min, respectively. No alterations in measured pulmonary functions were found; although slight discomfort was reported, it was not significantly related to ozone exposure. In the second experiment, the ozone concentration was 475 ~g/m3 (0.3 ppm), and only three exercise periods were used. Men exercised at 24.9 L/min in the first two periods and 38.6 L/min in the last, and women at 16.4 and 20.9 L/min, respectively. Significantly greater symptom scores were found after the last exercise period and after termination of the experiment. In this experiment, differences between the no-ozone and ozone responses in all spirometry measures-- forced vital capacity (FVC), forced expiratory volume (FEV1), and forced expiratory flow (FEF25_75% and FEF75_95~0~--in each sex group were statistically significant (n < 0.05~. The two lung-volume measures manifested smaller changes than did flow-rate measures. Symptom scores were greater in men than in women during the last exercise (treadmill) period, but the difference was not statistically significant. The results indicate increased symptoms and pulmonary function decrements among normal subjects at 0.3 ppm, but not at 0.2 ppm with light exercise. * Note that, as ambient pressure decreases at high altitude, ozone concentration remains the same when expressed in parts per million, but decreases in proportion to increasing altitude when expressed in micrograms per cubic meter. Therefore, knowledge of atmospheric pressure and temperature is generally needed for correct conversion of ppm readings to ~g/m3 concentrations.

118 Lategola et al.86 also studied 40 middle-aged men-- 20 smokers and 20 nonsmokers--exposed in an altitude chamber (1,829 m) while resting for 3 h in environments containing ozone at O or 475 ~g/m3 (0.0 or O.3 ppm). Eye discomfort was the most frequently reported symptom; headache and nose and throat irritation were also reported. All subjects combined manifested small but statistically significant decrements in FVC, FEV1, and FEF7s_95%, primarily owing to changes in the nonsmoking group. Smokers reported fewer or less severe symptoms, in confirmation of observations reported by others. The study tended to confirm small but significant respiratory effects at 0.3 ppm among nonsmoking normal adults under high-altitude conditions. The ozone concentrations used in the Lategola et al. studier were, however, generally lower than those reported to occur in some aircraft at high altitudes. Determination of the effects of known aircraft cabin ozone concentrations on passengers and flight attendants will require additional information from studies conducted on board, as well as immediately after flights, with continuous measurements of the cabin environment. GROUPS AT INCREASED RISK OF HEALTH EFFECTS Epidemiologic investigations of high-risk groups have played a predominant role in the development of the current ambient air quality standard for ozone. As far back as 1961, Schoettlin and Landau1 3 5 studied 137 asthmatics in the Los Angeles basin during a 3-mo period when high oxidant concentrations due to smog were anticipated. They found a statistically significant increase in the number of mild attacks when peak oxidant concentrations exceeded 0.25 ppm. A further assessment by Heuss et al.59 associated these asthmatic attacks with hourly average concentrations as low as O.lS ppm. They concluded that, when the ozone concentration is 0.15 ppm, there is a loo chance of a 5% increase in asthmatic attacks. Barth et al. 2 ~ extrapolated these data and concluded that there "is a likelihood of an increased asthmatic attack incidence for very sensitive patients at levels well below 0.15 ppm rather than Just a chance of a small increase in attacks at the 0.15 ppm level."

119 RECOMMENDATIONS Chapter 3 pointed out that the federal regulations concerning aircraft cabin ozone concentrations may be complied with either through the use of air treatment equipment (usually a catalytic converter) or through the choice of routes and altitudes that avoid areas of high ozone concentration. Ozone concentrations in aircraft depend also on latitude, not only on altitude. In 1978-1979, FAA monitored ozone on flights (mostly at 30,000-40,000 ft) and found that lie were in violation of FAA's ozone concentration limits. i23 Because catalytic converters are subject to contamination and loss of efficiency, it is suggested that FAA establish policies for periodic removal and testing, so that the effective life of these units can be established. A program of monitoring is needed, to establish compliance with the existing standard and to determine whether the catalytic converters are operating normally and effectively. These data should be maintained in such a manner that they can be used for reference on Passenger and crew exposures to ozone and to document the concentrations of ozone. COSMIC RADIATION We are exposed to ionizing radiation from several sources. Some is natural, such as cosmic radiation and terrestrial radiation, and some is from man-made sources, such as medical x rays, radioisotope drugs, nuclear fallout, nuclear power-plant emission, uranium and phosphate mine tailings, and nuclear waste materials. The question before the Committee is whether the incremental exposure of passengers and crew of commercial subsonic aircraft results in an unacceptable risk. CHARACTERISTICS OF COSMIC RADIATION Cosmic radiation is both solar and galactic in origin. Galactic radiation is composed of protons (87%), alpha particles (11%), a few nuclei with atomic number of 3 or more (approximately 1%), and electrons at energies up to 102° eV (approximately 1%~. The normative range of energies is 108-1011 eV. The sun generates a continuous flux of lower-energy (approximately 103 eV)

12G charged particles, and occasional solar magnetic disturbances generate large quantities of particles with energies up to several billion electron volts; the typical range is 1-100 MeV. The integrated flux of solar particles with energies of 20 MeV or more to the top of the earth's atmosphere varies with the 11-yr solar cycle between 105 and 101° particles/cm2 per year. The integrated flux of galactic particles is more constant, at about 108 particles/cm2 per year. These primary solar and galactic particles are almost completely attenuated as they penetrate the atmosphere down to an altitude of about 20 km (65,600 it). However, as they pass through an increasingly dense atmosphere, they undergo nuclear interactions. Hence, at the altitude of 20 km only 50X of the original protons, 25% of the original alpha particles, and 3% of the heavier nuclei are left. But there is a buildup of secondary particles--neutrons, protons, and piano. Further plan decay produces electrons, photons, and muons. As a result, there is a cosmic-radiation maximum at 20 km. A net attenuation in particle flux density occurs at lower altitudes, reducing both the number and the energy of secondary particles produced. At altitudes below 6 km (19,700 it), muons and associated decay electrons are the dominant components of the cosmic-ray particle flux. Figure 5-2 illustrates the components of cosmic-radiation dose equivalent rates as a function of altitude. Secondary particles react with tissue through several mechanisms, including ionization (stripping of electrons) and direct inelastic and elastic collisions with nuclei. Both protons and gamma rays can interact with electrons and cause ionization of molecular structures in tissue. The heavier neutrons can have elastic collisions with lighter elements in tissue. Because of the abundance of the hydrogen nucleus in tissue, it is the most likely target nucleus for elastic scattering. Some of the energy is lost as gamma photons in inelastic collisions with heavier target nuclei. In both types of collisions, the now-energized target nucleus penetrates tissue as an ionizing particles Like directly ionizing proton particles, these recoil protons are massive, compared with electrons, and dissipate energy over a relatively short path. Thus, the biologic effectiveness of radiation depends on the characteristics of the radiation, and not only on its energy. Because

121 103: 1 o2 1 _ LLl' 1 0 a: a: LL in o m 10° cr o cn 10 10-2 Total ~ Electrons it/ // 0 5 1Q 15 20 Protons Neutrons \ Muons ~ Pions 1 1 1 1 1 25 30 ALTITUDE, km FIGURE 5-2 Absorbed dose rates at depth of 5 cm in 30-cm-thick slab of tissue from various components of cosmic radiation at solar minimum and at geomagnetic latitude of 55 degrees N. Reprinted with permission from National Council on Radiation Protection and Measurements.l09 muons and associated fast electrons are essentially unattenuated by the body, the dose equivalent rate, in millirems per hour, as a function of altitude is determined essentially by the flux of protons and fast neutrons. The flux rates for fast neutrons at various altitudes are shown in Figure 5-3. The dose equivalent rate of cosmic radiation in millirems per hour as a function of altitude is illustrated in Figure 5-4. The equivalent dose _ _ temporally (with time of maximal solar activity) and

122 1.2: 1.0 0.8 Cat C, - O 0.6 A_ c, v, ~ 0.4 J 0.2 o / I , I ~ I , I l I ~Thousands of Feet 0 20 40 60 80 100 ~1 0 5 1 0 1 5 20 25 30 ALTITUDE Ki iometers FIGURE 5-3 Altitude profile of atmospheric neutron flux. Adapted from Schaefer.1 31 with latitude. The spatial and temporal variations have been determined from several direct-measurement programs conducted during the late 1960s and early 1970s. At altitudes typical of subsonic commercial aircraft, 9-12 km (29,500-39,400 ft), the cosmic-ray dose equivalent rate is approximately 100 times the rate at sea level. The newer, higher-performance aircraft are certified to 46,000 ft (14 km). The cosmic-ray dose equivalent rate at 14 km is nearly twice the rate at 10 km (32,800 it). Variation in solar activity and the interaction of charged particles in the earth's magnetic field result in higher cosmic-radiation flux at higher latitudes and during solar flares. Figure 5-5 illustrates the profiles of dose equivalent rates by altitude, latitude, and solar-flare activity.

123 loo - CJ 6 it J > UJ lo 1 co o ~_~ 0 4 8 12 16 ALTITUDE, km 20 24 FIGURE 5-4 Total cosmic-ray dose equivalent rate at 5-cm depth in 30-cm slab of tissue at gammam = 55 degrees N (- ~ and 43 degrees N (-----) at solar minimum (upper curve) and solar maximum (lower curve). Quality factors for neutrons as function of energy are included in calculations. Reprinted with permission from National Council on Radiation Protection and Measurements.109 EXPOSURE OF PASSENGERS AND CREW From Figure 5-5, it is relatively easy to estimate the dose equivalent exposure for a particular flight or for an individual. A 5-h trans-Atlantic flight at midlatitude and an altitude of 12 km (39,400 ft) might result in an equivalent whole-body dose of 2.5 mrems. If the same flight goes over the pole during a time of more intense solar activity, the dose equivalent might be 10 mrems. In general, the hourly dose rate at a jet cruising altitude is approximately 100 times the ground- level rate. A person who lived near sea level would have to spend about 200-600 h/yr at cruising altitude to double his or her exposure to cosmic radiation.

- E E UJ CC 124 1.6r 1.4¢ 1.24 l.or lo LL > - UJ LL o 0.8 n 0.( n' 40 60 80 LATITUDE '1~111 ' O ! it| ~ 13 10 _, FIGURE 5-5 Best values for maximal and minimal galactic dose equivalent rate as function of latitude and altitude. Reprinted with permission from Bail. Wallace and Sondhausl65 calculated the cosmic- radiation exposure to passengers and crew in subsonic commercial travel. The database was for the year 1974 and was limited to domestic and overseas flights longer than 322 km (200 miles). The calculations were made for U.S. residents on the basis of some simplifying assumptions. A complex model was developed according to aircraft type, flight crew and passenger capacities, climb rates, cruise speeds, and flight paths. Matrices were developed for neutron and secondary charged- particle densities according to latitude, altitude, and solar conditions. The Aircraft Radiation Exposure (ACRE) model calculated a flight-dose profile and an accumulated total dose for each one-way flight of each type of aircraft. ACRE generated 1,895 calculated doses. On the basis of the passenger miles flown on each flight segment and the percent and frequency of flying by the American public, the cumulative and average doses to the crew, flying population, and total U.S. population were

125 calculated. The summary table from the ACRE paper is reproduced as Table 5-1. The paper reported good agreement between a series of in-flight measurements and calculations. It stated:~65 The ACRE average estimate resulting from the detailed air travel data is 160 mrem/year/crew member. This dose is less than the radiation guide limit of 170 mrem/year average additional dose above background recommended for the general public, and it is well below the 500 mrem/year maximum for any individual member of the general public. For occupational exposure of radiation workers, the corresponding limit is 5000 mrem/year. The values for dose equivalent from commercial flying derived here are 0.47 mrem/person/year when averaged over the total U.S. population and 2.8 mrem/person/year for that segment of the total adult U.S. population that traveled by airline at least once during the year. These compare well with the values of 0.48 mrem/person/year and 3.8 mrem/person/year previously reported [by Schaefer in 19721303. Because substantial changes have occurred in the commercial airline industry over the last decade, it is appropriate to re-evaluate the results cited above, which were based, in part, on Civil Aviation Board (CAB) data from the late 1960s and early 1970s. At that time, about 21-25% of the U.S. population surveyed had flown at least once during a 12-mo period. Other CAB surveys estimated that 66% of passengers traveled less than 1,600 km (1,000 miles), and 89.4% less than 3,200 km (2,000 miles). Since the time of the ACRE calculations and the CAB surveys, several changes have occurred in the U.S. commercial air travel industry. Passenger miles grew rather slowly more than 7%/yr between in the early 1980s, but grew at 1983 and 1985. Projected annual growth is 5% into the mid-1990s. In 1984, there were over 343 million domestic passenger enplanements; Figure 1-1 shows that that is expected to reach 500 million by 1995. Commuter-carrier revenue passenger miles, 3.4 billion in 1984, have been increasing rapidly since deregulation and are expected to triple by 1996.758

126 TABLE 5-1 Radiation Doses and Air Travel Statistics Based On Program ACREa With loop Occupancy With 60% (where applicable) Occupancy Flights per year Flights per day Average number of seats per flight Seats per day Seats per year Flight crew members per yearb Cabin crew members per yearb Seat-kilometers per year Flight crew-kilometers per year Cabin crew-kilometers per year Seat time, hJyr Plight crew time, h/yr Cabin crew time, h/yr Total seat dose, man-mrems/yr Total flight crew dose, man-mrems/yr Total cabin crew dose man-mrems/yr Average flight altitude, km Average flight distance,C Em Average flight time, h Average dose rate, mrems/h Average dose per flight, mrems Average dose per adult passenger,d mrems/yr Average dose rawer f 11~,' Ares ~ 0 member, mrems/yr Average dose per cabin crew member, mrems/yr Average dose to total U.S. populatlon,e mrems/person per year 2,991,000 8,194 156 1,281,000 468,000,000 16,803 22,996 581,000,000,000 9,372,000,000 13,000,000,000 736,000,000 12,100,000 16,600,000 164, 300,000 2,650,000 3,690,000 9.47 1,084 1.41 0.20 0.28 2.82 158 160 769,000 281,000,000 349,000,000,000 442,000,000 98,580,000 0.47 a Reprinted with permission from Wallace and Sondhaus.165 b Assuming a limit of 720 h per [till-time equivalent crew member at altitude per year, this number of crew members would be required. "Flight crew" refers to flight-deck crew, and "cabin crew" refers to flight attendants. Crew members flying 480 h/yr--instead of 720--would reduce their doses by a factor of 2/3. c According to F,M estimates, the average flight distance is 1,364 km and the median is 933 km. Average dose to those who flew in the 12 mo of 1973. Of the total adult population of 140 x 106, those who flew in the previous 12 ma were 35 x 106, who shared the 98.6 x 106 man-reins. The total yearly dose = (98.6 + 2.65 + 3.69) x 106 = 104.9 x 106 to passengers, flight deck crew, and cabin crew. This number divided by the total 225 x 106 U.S. population gives 0.47 mrem/yr.

127 Aircraft flights are increasing more slowly than passenger miles because of the trend to the use of larger two-engine jet aircraft in service (see Figure 1-3) and the gradual increase in passenger load factors for domestic flights. The international passenger load factor is expected to remain roughly stable over the next 10 yr (see Figure 1-2~. The FAA Aviation Forecasts (1985-1996) indicate a strong recovery in the domestic aviation industry in 1984 and 1985, after a 4-yr period of operating losses. Furthermore, the composition of the aircraft fleet has changed. Planes are being certified to fly up to 14 km (46,000 ft), where the radiation dose rate is about twice that at 10 km (32,800 ft). The jet aircraft fleet will increase primarily with two-engine wide- and narrow-body planes. This will reduce the number of cockpit flight crew members. The implication of these changes for the expected radiation dose to the crew will depend on changes in work practices. If increased flights and passenger trips result in increased employment by the airlines, the total radiation dose to the crew will increase, even if the dose to the average crew member does not. Bram1itt25 pointed out that the calculations of Wallace and Sondhaus probably underestimated crew radiation dose. Cockpit crew are allowed (by FAA regulations) to fly up to 100 h/mo. 48 FAA does not restrict flight attendant flight time. Some airlines are offering incentives to increase the monthly flight hours of attendants. Changes in flight altitudes, increases in passenger miles, increases in high-latitude flights, and increases in attendant flight time are expected to increase population and crew radiation exposure. Bramlitt25 2 6 argued that these changes render the Wallace and Sondhaus calculations of cosmic radiation exposure of 160 mremsfyr for flight and cabin crew members inappropriate for 1986. Crew and passengers flying more hours at higher latitudes and altitudes can receive substantially more radiation than 160 and 3 mrems/yr, respectively. By 1995, commercial flying might be expected to increase the integrated cosmic-radiation exposure to 1 mrem/person per year when averaged over

128 the total Ue S. population. The average exposure of the traveling segment of the U.S. population should stay at about 3 mrems/person per year, unless there is a shift to longer and more frequent flights per person. RADIATION EXPOSURE IN AIRCRAFT AND FROM OTHER NATURAL SOURCES Natural background constitutes the greatest source of ionizing radiation. The exposure is not uniform; such factors as altitude, geologic features, and living structures result in variations. The U.S. population is receiving genetically significant dose-equivalent radiation from natural background that ranges from 40 to 180 mrems/yr (see Figure S-6~. Oakley, i2 calculated the population exposure to cosmic and natural terrestrial radiation for the U.S. population on the basis of 1960 census data. He took into account the geographic distribution of population and the altitude, and he extrapolated the effects of terrestrial radiation from the Atomic Energy Commission-sponsored Aerial Radiological Measurement Surveys conducted from 1958 to 1963. Averaged across the U.S. population, a person receives 44 mrems/yr from cosmic radiation and 40 mrems/yr from terrestrial radiation. 20 to to - z o ~ 10 o cow 15 l ol l L I I I I I ~ n I 40 60 80 1 00 1 20 1 40 1 60 1 80 0 20 DOSE EQUIVALENT, mrems/yr FIGURE S-6 Population distribution vs. dose equivalent from terrestrial and cosmic radiation. Reprinted from Oakley. 112

129 In the mid-1970s, it was generally recognized that terrestrial radiation might be underestimated.378 Although structural features, such as homes and other buildings, offer some shielding from cosmic radiation (5-20%), structures can increase exposure to natural radiation by leading to accumulation of radon and its decay products indoors. Single-family residences might have a concentration of radon and radon decay products 10 times that outdoors, or even more. To calculate radiation doses due to flying, one can assume rates of 0.3-0.4 mrem/h at 36,000 ft (11 km) and O.6-0.8 mrem/h at 45,000 ft (13.7 km). Thus, a passenger or crew member would have to be at these altitudes for only about 100-300 h to receive a dose of ionizing radiation equivalent to that from natural background in a year at sea level. GROUPS AT INCREASED RI SK OF HEALTH EFFECTS There are approximately 100,000 commercial-aviation crew members in the United States. In addition, about 28% of the U.S. population flies at least once a year. For the vast majority of airline passengers, the additional equivalent radiation dose from flying is less than 3 mrems/yr. A crew member routinely flying 70-83 h/mo can receive a substantial additional dose. Depending on altitude and latitude of routes flown, a crew member might receive up to 1,000 mrems/yr from flying. Both the National Council on Radiation Protection and Measurements and the International Commission on Radiological Protection recommend that exposure of the fetus during the entire gestation period from occupational exposures of the expectant mother not exceed 0.5 rem. 68 Boa Stewart and co-workers, 144 - ~ 46 MacMahon, 95 and MacMahon and Hutchison9 6 have determined that fetuses are at high risk. Thev ~ - - ~ showed that all types of childhood cancer and leukemia are doubled by even extremely small doses of radiation. More specifically, Stewart and Knealel 44 indicated that 1.5 reds from x rays taken in the latter half of pregnancy doubled the frequency of leukemia in children. However, if x rays were taken

130 during the first trimester of pregnancy, only 0.3 red was needed to double the incidence of cancer in the first 10 yr of life. Pregnant flight attendants might receive radiation exposure in excess of 500 mrems over the duration of their pregnancy if they fly full-time (70-85 h/mo) on high-altitude flights. Airlines should investigate the policy options for informing female flight attendants about the possible risk involved in flying during pregnancy. In light of the Pregnancy Discrimination Act of 1978,11 6 the issues of employees' rights, the rights of fetuses, and airline-industry liability must be addressed in a comprehensive formulation of public and private policy on this matter. Now that the issue of increased radiation exposure among airline employees has been raised by Bramlitt and in this report, FAA and the Environmental Protection Agency, responsible for radiation-protection guidance for occupational exposure, should investigate the in-flight cosmic-radiation exposures of crew members. Of particular concern are increased exposures during solar flares. Bramlitt2 5 reported that 5 yr of continuous satellite monitoring by the National Oceanic and Atmospheric Administration had shown an average of seven enhanced solar flares per year; one per year is enough to increase the neutron flux on the ground. The time from detection to maximal activity is 19 h. At 40,000 ft (12.2 km), flares can increase the cosmic-radiation dose rate from 0.7 mrem/h to 200 mrems/h. Rare events can increase the rate to 2,000 mrems/h. GROUND FUMES While waiting for a plane to depart or arrive and while sitting in a taxiing plane, passengers can be exposed to substances emitted by aircraft engines and the engines of maintenance vehicles. There is relatively little information on actual exposures in aircraft during these periods, but some information on potential exposure to various substances can be obtained from a review of aircraft engine emission. Aircraft jet engines emit a variety of potentially toxic substances,92 93 \~8 \36 including carbon monoxide, oxides of nitrogen, hydrocarbons, aldehydes (especially

131 formaldehyde), particles, and polynuclear aromatic compounds. The rate of emission varies with the operation of the aircraft. When idling, engines are less efficient and might emit higher concentrations of some pollutants (e.g., carbon monoxide and hydrocarbons, but not oxides of nitrogen). Aircraft idling and taxiing are major sources of airport air pollution, 92 and idling time is often limited to meet local air pollution criteria. A study in 1970 evaluated aircraft engine emission as a source of air pollution at Los Angeles International Airport chiefly by monitoring carbon monoxide and particle concentrations in and around the airport. 92 It also included monitoring for carbon monoxide in aircraft on the runway or at the gate. This study demonstrated that carbon monoxide concentrations in the cabin paralleled those outside the aircraft. Cabin concentrations were highest (approximately 10-15 ppm) when the airplane was at the gate loading passengers; that reflected the higher concentrations of carbon monoxide (and particles) in that area of the airport. In general, the study found the highest concentrations of particles and carbon monoxide in or around the airport to be near the passenger terminals, where air and ground traffic was greatest. - Although ground fumes from jet engine exhaust contain substances that can cause respiratory irritation and other health effects, there is little available information from monitoring that indicates the exposure of cabin occupants to these substances. ENVIRONMENTAL TOBACCO SMOKE The air contaminant in an aircraft cabin that is most apparent to the passengers and crew is cigarette smoke. Cigarette-smoking contributes to environmental tobacco smoke (ETS) in four ways: it contributes smoke from the smoldering ends of cigarettes (sidestream smoke), smoke that escapes during puff-drawing from the burning cone, vapor that escapes through the paper of the cigarette, and smoke exhaled by smokers. Secondary reactions in these diluted smokes alter their physical and chemical characteristics. ETS is a complex mixture of gases and particles.: 6 ~

132 The proportion of passengers who are current cigarette smokers can be estimated from statistics that describe the passenger population (Chapter 1) and the distribution of smokers in the general American population. Some 54% of passengers are male and 46% female;51 37% of American males and 29X of females currently smoke.151 Therefore, the proportion of passengers who currently smoke is (0.37~0.54) ~ (0.29~0.46) = 32.3X. This agrees with the observation that somewhat less than one-third of passengers request seats in the smoking section. In 1970 and 1971, before establishing smoking restrictions on aircraft, FAA and the U.S. Public Health Service conducted a questionnaire survey of 20 military flights and 14 domestic civilian flights in conjunction with ambient air assessments (described in come detail later in this report. In that study, 31% of the domestic passengers smoked on the flights (an average of 2 cigarettes each), and 52% of the military passengers smoked on the flights (an average of 8 cigarettes each). In 1961, Halfpenny and Starrett58 found that smokers average 1.25 cigarettes/in on 2-h flights and that 51% of passengers smoke on aircraft. Both these studies were conducted before the smoking restrictions on aircraft. The current estimates of smoking rates are 2.1 and 2.2 cigarettes/in. 3 2 ~ 4 ~ The above numbers are estimated averages, and the actual smoking rates on aircraft are highly variable, as illustrated in Figure 5-7. Some aspects of cigarette-smoking on airplanes are peculiar to that situation. In public places generally, it might be expected to find one person in nine smoking at any given time. However, on aircraft, smokers are seated together, and smoking might be heaviest after the "no smoking" light is turned off and after a meal is consumed. This pattern of smoking results in higher transient concentrations of cigarette smoke than occur in other public places where smoking is permitted. High transient concentrations occur not only in the smoking section, but also in other parts of the cabin.

133 40 1 35 _~4 ~. ~5 - A o u" - - - z o 1 1 Al 1 . At_ . L 5:30 p.m. 7:30 p.m. EASTERN DAYLIGHTTIME 9:30 p.m Figure 5-7 Top, NO2 concentration vs. time during flight from Boston to Denver. Bottom, number of cigarettes smokers on same flight. NO2 measured approximately once a minute; smokers (passengers with lighted cigarettes) counted approximately 15 s after NO2 measurement. Data from D. H. Stedman (personal communication, 1985~. AIRCRAFT VENTILATION AND SMOKE CONCENTRATIONS Table 5-2 is a partial list of compounds in cigarette smoke. Many of these are more heavily concentrated in the sidestream. The sidestream- mainstream ratios presented in the table were measured under standardized laboratory conditions. In the cabin

134 air, the relationship among the constituents in ETS varies with the brand of cigarette, smoking behavior, and environmental conditions (e.g., humidity and air mixing). Many of the chemical components of ETS are known to be toxic (e.g., acrolein and carbon monoxide) or carcinogenic (e.g., N-nitrosodiethylamine and benzo~aipyrene) in humans or animals. As discussed in Chapter 7, measurements of carbon monoxide, nitrogen oxides, respirable suspended particles (RSP), and light-scattering are all used as surrogates to detect ETS. ~ components are proportional to the measured gas phase and particle phase of ETS. It is reasonable to assume that the harmful If cigarette-smoking on aircraft were at a constant rate, a steady-state concentration of smoke would be achieved after 5-10 min under typical ventilation rates-- about twice the typical air exchange time (see Chapter 2~. On aircraft without recirculated air, the steady- state density will be approximately proportional to the product of the rate of smoke production and inversely proportional to the flow of outside air. Other factors also affect ETS concentrations, such as deposition on surfaces, especially fabrics. Under normal conditions, the rate of chemical and physical removal in the cabin is much less than the rate of removal by ventilation. The ETS concentration can be decreased by decreasing the source (i.e., the number of cigarettes smoked) or by increasing the rate of flow of outside air (i.e., decreasing the air-exchange time). Decreasing the size of the smoking section might increase the concentration of ETS in that section, if the same number of smokers are concentrated in fewer seats. The above relationships neglect the recirculation patterns common on modern aircraft. In most aircraft, there is no physical barrier between the smoking . . . ~ and nonsmoking sections. Consequently, there will be some mixing between sections. In some wide-body jets, air is recirculated to the zone from which it is taken. In this design, if a zone is designated smoking or nonsmoking, recirculation should not affect mixing in other areas of the aircraft. Recirculation patterns in which air is mixed throughout the whole aircraft distribute gaseous smoke products and submicrometer particles throughout

135 the aircraft. The filter systems described in Chapter 2 should be adequate to remove micrometer-sized particles and a portion of the submicrometer smoke particles. However, ETS vapors would not be removed. Furthermore, if the optional charcoal absorption beds are installed and maintained, gaseous contamination will be substantially reduced. However, efficiency of charcoal absorption varies with compounds, water vapor, flow rate, and time. These complexities could be taken into account in the model described in Appendix A. TABLE 5-2 Distribution of Compounds in Nonfilter-Cigarette Undiluted Mainstream and Diluted Sidestream Smokea Total Emission in Sidestream-to Mainstream Smoke, Mainstream Total Compound p~/cizarette Emission Ratio Vapor Chase . Carbon monoxide 10,000-23,000 2.~:1-4.7:1 Carbon dioxide 20,000-40,000 8:1-11:1 Carbonyl sulfide 18-42 0.03:1-0.13:1 Benzene 12-48 10:1 Toluene 160 6:1 Formaldehyde 70-100 0.1:1-50:1 Acrolein 60-100 8:1-15:1 Acetone 100-250 2:1-5:1 Pyridine 16-40 6.5:1-20:1 3-Methylpyridine 12-36 3:1-13:1 3-Vinylpyridine 11-30 20:1-40:1 Hydrogen cyanide 400-500 0.1:1-0.25:1 Hydrazine 0.032 3:1 Ammonia 50-130 40:1-170:1 Methylamine 11.5-28.7 4.2:1-6.4:1 Dimethylamine 7.8-10 3.7:1-5.1:1 Nitrogen oxide 100-600 4:1-10:1 N-Nitrosodimethyl- 0.01-0.04 20:1-100:1 amine N-Nitrosopyrrolidine 0.006-0.03 6:1-30:1 Formic acid 210-490 1.4:1-1.6:1 Acetic acid 330-810 1.9:1-3.6:1

136 TABLE 5-2 (continued) Total Emission in Sidestream-to Mainstream Smoke, Mainstream Total Compound ~g/cizarette Emission Ratio Particulate chase: Particulate matter 15,000-40,000 1.3:1-1.9:1 Hico tine 1,000-2,500 2.6:1-3.3:1 Anatabine 2-20 <0.1:1-0.5:1 Phenol 60-140 1.6:1-3.0:1 Catechol 100-360 0.6:1-0.9:1 Hydroquinone 110-300 0.7:1-0.9:1 Aniline 0.36 30:1 2-Toluidine 0.16 19:1 2-Naphthylamine 0.0017 30:1 4-Aminobiphenyl 0.0046 31:1 Benz~ajanthracene 0.02-0.07 2:1-4:1 Benzo~a~pyrene 0.02-0.04 2.5:1-3.5:1 Cholesterol 22 0.9:1 y-Butyrolactone 10-22 3.6:1-5.0:1 Quinoline 0.5-2 8:1-11:1 Harman 1.7-3.1 0.7:1-1.7:1 N'-Nitrosonornicotine 0.2-3 0.5:1-3:1 NNKb 0.1-1 1:1-4:1 N-Nitrosodiethanolamine 0.02-0.07 1.2:1 Cadmium 0.1 7.2:1 Nickel 0.02-0.08 13:1-30:1 Zinc 0.06 6.7:1 Polonium-210 0.04-0.1 psi 1.0:1-4.0:1 Benzoic acid 14-28 0.67:1-0.95:1 Lactic acid 63-174 0.5:1-0.7:1 Glycolin acid 37-126 0.6:1-0.95:1 Succinic acid 110-140 0.43:1-0.62:1 a Total emissions are given for fresh, undiluted mainstream smoke generated by a smoking machine under conditions of 1 puff/min of 2-s duration and 35-ml volume, i.e. 10 puffs/cigarette. Sidestre~m values are given for smoke collected with an airflow of 25 ml/s, which is passed over the burning cone. Compiled by D. Hoffmann (personal communication, 1986) from Elliott and Rowe, 45 Hoffmann et al., 64 Klus and Kuhn, 78 Sakuma et al.,124 - \26 and Schmeltz et al. \34 b 4-(N-Methyl-N-nitrosamino)-1-~3-pyridyl)-1-butanone.

137 CONCENTRATIONS OF ETS CONSTITUENTS MEASURED ON AIRCRAFT Aircraft air quality has not been a subject of systematic investigation by independent researchers. Various airlines have conducted their own studies of airborne contaminants. Several airlines--such as Air France,, 64 United Airlines, 8 and Lufthansa German Airlines94--have conducted tests, and some Committee members have conducted a few "measurements of opportunity." That is, the measurements have not been conducted under experimental situations or have not been conducted systematically for a variety of aircraft. As discussed in Chapter 7, isolated measurements are likely to be highly variable, even if made with accurate instruments. The distribution of smoke in the aircraft cabin is not uniform, but rather exhibits spatial and temporal variability. The concentration measured in any area would depend on location of the sampler in relation to the smoke source and the ventilation in that area. In 1970 and 1971, in one of the earliest studies, FAA and the U.S. Public Health Services 60 measured carbon monoxide, aromatic hydrocarbons, aldehydes, ketones, and total particulate mass on 20 military flights and 14 domestic civilian flights. These studies were done before smokers were segregated in the aircraft cabin, so their relevance to present conditions is not clear. Data from more recent studies are listed in Table 5-3. Lufthansa9 4 provided material that contained useful information about relative humidity; however, because the instruments used for measuring contaminants had limits of detection above the expected values, these data are not included in the table. Members of the Committee have used portable instruments to measure ETS concentrations on commercial flights. These measurements were not accompanied by detailed documentation of ventilation or numbers of people smoking. They are included here only to illustrate further the concentrations that could be encountered on aircraft. A hand-held nephelometer (see DC-10 flight data from Spengler in Figure 5-3) and piezoelectric balance (see B-747 flight data) were used to measure mass concentration of suspended particulate

138 TABLE 5-3 Examples of Measurements of Pollutants on Airliners Constituent Source of Measurement Aircraft Heasured D. H. Stedman (personal communication, 1985) FAA and USPHSi60 B-727-200 NOR 0-40 ppb Several, CO 1970-1971 RSP Concentration Max., 5 ppm Agog., 140 ~g/m3; peak, 1,200 ~g/m3 United Airlines8 B-747 CO Max., 3 PPm3 RSP 60-320 ~g/m DC-10 CO Max., 5 ppm3 RSP 19-400 ~g/m DC-8-61 CO Max., 5 ppm3 RSP 70-260 ~g/m B-727 CO Max., 5 ppm3 RSP 40-140 ~g/m B-737 CO Max., 5 ppm RSP 80-200 ~g/m3 Air Prancel64 B-747 CO Max., 5 ppm J. Spengler (personal B-747 RSP 10-50 ~g/m3 communication, 1986) nonsmoking RSP 50-500 ~g/m3 in smoking section;3 peak, 1,000 ~g/m DC-lOa RSP 10-40 ~g/m3 in nonsmoking aft cabin with no cigarette odor 100~20 ~g/m3 in nonsmoking forward cabin with cigarette odor RSP a Load factor, 40-60X. 300~200 ~g/m3 in smoking section; peak, 750 ~g/m 550-1,200 ppm

139 matter. The nephelometer responds optimally to particles in the submicrometer range. The RSP concentrations were about 10-50 ~g/m3 in the two-thirds-filled nonsmoking section of a wide-body airliner, about 100 ~g/m3 at the front of the smoking section, and over 500 ~g/m3 in the rear of the smoking section near the lavatories Occasional readings exceeded 1,000 ~g/m3. Similar concentrations were recorded on a DC-10 over six segments of a round-trip flight between Boston and Anchorage. Load factors were between 40 and 60~o. STANDARDS FOR OTHER ENVIRONMENTS There are no federal standards for ETS in any environment, although smoking has been prohibited in many public buildings by municipal and state ordinances. The occupational and ambient standards for carbon monoxide and particulate matter that are often applied to ETS do not take into account the other toxic materials present in ETS, which contains measurable concentrations of several known carcinogens and cocarcinogens. The national ambient air quality standards for carbon monoxide and total suspended particles (TSP) are shown in Table I-1 (in the introduction). An additional indoor air standard for particle density in office buildings is the Japanese standard of 150 ~g/m5.9 For carbon monoxide, the EPA and ASHRAE standards of total l-h concentration of 35 ppm and 8-h concentration of 9 ppm appear unlikely to be violated in typical airliner cabins. However, the TSP standard is a particle-mass standard designed mainly for protection from pollutants like fly-ash, and not designed to take into account the toxicity or size distribution of ETS. The TSP standards (150-260 ~g/m3 for 24 h) also do not take account of particle size. That is, the TSP standard deals with only total mass, which usually is dominated by larger particles of a size that ordinarily cannot enter the lungs during breathing. However. rescirable Darticles have little mass. A standard that would be specific to RSP is likely to be considerably lower than a comparable TSP standard, because RSP contributes little to the TSP mass. Because aircraft cabin RSP concentrations of 250 ~g/m3 are not unusual, it is apparent that a majority of the air quality measurements given in Table 5-3 would violate the Japanese standard for particle density and,

140 in many cases, the less stringent EPA 24-h standard for TSP. Ventilation standards for smoking areas in other public places are designed to produce acceptable air in which there are no known contaminants at harmful concentrations and with which a substantial majority (80%) of the occupants do not express dissatisfaction. These standards led to the ASHRAE suggestion of ventilation at 20-50 cfm/person for a variety of settings where smoking is allowed. 4 The maximal flow ventilation distribution in 1985, shown in Figure 2-6, indicates that about 80% of the flights had airflow of less than 40 cfm/passenger. By the above guidelines, it is apparent that aircraft ventilation would not meet the criterion of acceptability to at least 80X of nonsmokers if the nonsmokers were forced to work in, traverse, or wait in an active smoking section. EXPOSURE TO ETS ON AIRLINERS According to a National Research Council report (see National Research Council, Committee on Indoor Pollutants,~° p. 8), "public policy should clearly articulate that involuntary exposure to tobacco smoke has adverse health effects and ought to be minimized or avoided where possible." Several different groups of people are characterized by different kinds of exposure to ETS. On commercial aircraft, the people with the greatest exposure are the cabin crew, who are exposed to ETS regularly. In some aircraft, the galley is in the smoking section, so cabin crew are exposed to ETS at the same concentrations and for the same durations as passengers in the smoking section. Thus, cabin crew, including pregnant flight attendants, are likely to be exposed to ETS at high concentrations. Although policies vary among airlines, some attendants are permitted to fly (with their doctors' permission) up to the twenty-eighth week of pregnancy. Passengers will not be exposed daily. However, nonsmoking passengers in the smoking section, such as spouses and children, will be exposed to the ETS. Passengers in the few nonsmoking rows adjacent to the

141 smoking section are likely to be exposed to the next highest transient concentrations, because of air motion and ETS diffusion from the smoking section. In aircraft without air recirculation, passengers well into the nonsmoking sections, flight crew members, and cabin crew members whose duties do not take them into the smoking sections are relatively unexposed. The nature of exposure to ETS and its composition is complicated by the fact that all aircraft now in production have some form of recirculation system. The complexity arises because of differences in ventilation equipment between aircraft and differences in operating procedures that change the proportion of outside to recirculated air. In addition, there is usually a filter that removes some particulate matter; however, the passage of gases through the filter is usually unimpeded. Thus, the composition of ETS after it passes through filters has not been characterized for the full range of filters that might be found on an airplane. Cain et al. 3 3 demonstrated in chamber studies that nonsmokers report dissatisfaction with and irritation by cigarette-generated smoke, even when the smoke is filtered with an electrostatic precipitator. This was true when smoke concentrations were low, as determined by measurement of surrogate carbon monoxide concentrations at 5 ppm and even as low as 1 ppm. Filtration of 80~o of particles with Cambridge filters, which are currently in use on aircraft that have recirculation systems, has reduced irritation substantially i68 (see Chapter 2~. HEALTH EFFECTS IN AIRPLANES The irritant properties of cigarette smoke have given rise to complaints about the Mali tv of al rarefy environments. , _ _ ~ ~ Irritation affects general health and we' tare and thus affects performance of the crew. Records of passenger or flight attendant complaints compiled by the Association of Flight Attendants listed "smoky" as a complaint in 73 of 297 air quality complaints; the cause was listed in only 113 of the 297 cases. In a 1980 questionnaire study of 1,961 Scandinavian Airlines System (SAS) cabin attendants, only 4% were not at all bothered by smoky air, whereas 69~ were "bothered to a great extent." The data are shown in Table 5-4.

142 TABLE 5-4 Results of 1980 Questionnaire Survey of SAS Cabin Attendantsa Attendants Bothered by Factors Listed Below, 70 Not at All Subject of Complaint Noise 13 Cold 29 Cabin temperature variation 32 Heat 43 Variation in cabin pressure 36 Drafts 27 Static electricity 44 Dry air 10 Turbulence 22 Dust 62 Smoky air Odors Pungent smells 26 59 a Data from Ostberg and Mills-Orring. 113 To a Certain Extent 53 56 55 49 51 47 45 31 60 31 26 61 34 To a Great Extent 34 15 13 8 13 26 11 59 17 7 69 13 7 In one study of six nonsmoking flight attendants, increases in blood nicotine and urinary cotinine (a nicotine metabolite) were observed after flights of 8 h.49 However, Duncan and Greaney44 found no increase in carbon monoxide in exhaled breath of 16 flight attendants after 10 h of flying (Los Angeles to Honolulu and back). HEALTH EFFECTS IN OTHER ENVIRONMENTS Given the limited number of studies of exposure to ETS in aircraft, evidence of adverse health effects necessarily is inferred from studies in other environments. These include studies of chronic exposure, relevant to the cabin crew, and studies of acute effects of exposure, relevant to the passengers.

143 The possible health effects of ETS on nonsmokers cannot simply be extrapolated from the health experience of active smokers, for the following reasons. First, smokers and nonsmokers differ in exposure and deposition of smoke particles in the lung. 60 Particles in mainstream smoke (which the smoker takes in from the cigarette) become much larger than those in sidestream smoke, because they are more highly concentrated and agglomerate in the respiratory tract. Because of lung aerodynamics, larger particles (~1 ~m) tend to be deposited in the bronchus, whereas smaller particles (<1 ~m) can be carried deeper into the lung and deposited in the smaller tubules and alveolar sacs. 6 9 The extent to which ETS particles are hydroscopic and increase in size will affect the deposition pattern. However, 89% of the inhaled sidestream smoke particles are exhaled. 6 ~ The membranes of various regions of the lung differ substantially, e.g., in thickness and presence of cilia. Second, the deposition of smoke particles in the lung is also affected by the breathing patterns of the individual; some smokers inhale smoke more deeply than nonsmokers. The 1982 EPA report on particles and sulfur oxidesl 5 4 discusses deposition of particles for nose breathing, compared with mouth breathing. The deposition curve peak shifts downward from 3.5- to about 2.5-~m diameters. The peak is much less pronounced (about 25%, compared with 50% for mouth breathing), with a nearly constant pulmonary deposition of about 20% for all sizes between O.1 and 4 ~m. In a 1985 Gallup poll, 3 over 85% of nonsmokers and 60X of smokers felt that smoking should be restricted in the workplace and that, in the presence of nonsmokers, smokers should curtail their smoking. Speerl 40 interviewed nonallergic people regarding their subjective reactions to cigarette smoke. They reported eye ~, neaaacnes, nasal symptoms, and coughing. Unacceptable odor is often the first complaint of people exposed to ETS. Nonsmokers are more likely to find ETS odor unacceptable than smokers. 32 Cain et al. 32 systematically varied environmental conditions--including temperature, humidity, and ventilation rates--to determine the intensity of ETS-associated odor for visitors to and occupants of an experimental chamber. They found that odor sensitivity to ETS increased as relative humidity was increased from 50% to 75%. Tobacco smoke odor does not decay rapidly. 3 6 ~ __3 ~ ~ ~ ~ __ ~ _ ~

144 The odor characteristics of ETS in the airliner cabin need to be studied, to determine how low humidity and other environmental conditions affect discomfort of these types. Cain et al. 32 determined that, with as few as lox of the occupants in a space smoking at any time, a ventilation rate of 5.3 cfm/occupant was required to make the air acceptable to at least 80% of the occupants, especially nonsmokers, who are more sensitive to the odor than smokers.32 Kerka and Humphreys77 demonstrated that, although perceived tobacco smoke odor in reduced over time owing to olfactory adaptation while the person stays in the chamber, the degree of sensory irritation increases. Both odor and irritation are perceived to be more intense at lower humidities (30% vs. 65%) (Figure 5-8~. The Committee could find no information on studies done at relative humidities below 10X, which are typical of aircraft. The eye is the most readily affected site of irritation. Weber and colleagues have studied the effects of ETS on the eyes extensively. \68-~72 There are no data on the combined effects of ETS, low humidity, and photochemical oxidants (including ozone, formaldehyde, and acrolein) on the eye; contact-lens wearers in particular should be studied in this environment. 3: 1 TIC 4=~ Odor 30% RH \\ ~,.itat~°~ 1 - - 3 4 5 6 TIME, min Figure 5-8 Relationship of relative humidity to odor and irritation during continuous short-term exposure to cigarette smoke generated in a chamber Ventilation, 14 cfm/cigarette; ambient temperature, 25°C. Adapted from Kerka and Humphreys. 7 7 .

145 Other health effects of ETS have been studied in chronically-exposed nonsmokers compared with unexposed nonsmokers. Chronic exposure studies are more relevant to flight attendants who are chronically exposed occupationally than to passengers who are not otherwise chronically exposed. Extrapolation from these studies to the experience of persons in an aircraft cabin is not straightforward, but the studier do indicate the range of possible health effects to consider. There have been several studies of lung cancer risk in nonsmoking spouses of smokers. In 1981, studies in Japan62 63 and Greecel50 showed that women with smoking husbands had a statistically significantly higher risk of lung cancer than other women and that the risk increased with the number of cigarettes that their husbands smoked. Since then, several investigators have examined this association with case-control and prospective studies. 35 4} 52 55 62 63 76 80 82 ~27-i29 i50 i77 Because of sample sizes, most of the observed differences are not statistically significant. However, of the 15 studies that separated nonsmokers from smokers, most found an increase in risk associated with chronic exposure to ETS. A positive association of lung cancer with ETS exposure is biologically plausible (ETS does contain toxic and carcinogenic chemicals), and results are consistent between ~~ - ~ and cultural settings. . studies and across study designs Therefore, the Committee concludes that there is a positive association between lung cancer and chronic exposure to ETS. Exposure values in these studies were developed from questionnaire data that indicated that the nonsmoking subjects were chronically and regularly exposed to ETS at home. The Committee on Passive Smoking of the National Research Council is currently reviewing the available published literature on the health risks associated with ETS exposure and will prepare a report. To evaluate the relevance of occupational exposures to ETS for the cabin crew in aircraft, we assumed that a flight attendant worked 800 h/yr in the smoking section of an airplane, where the average concentration of total particles might be 250 ~g/m3. Assuming a breathing rate consistent with modest exercise--i.e., 15 L/mine-under these circumstances the integrated exposure to ETS would be 1.8 x 105 ~g/yr. Spengler et al., 42 reported that a home with a 1-pack/d smoker is likely to have

146 particle concentrations at least 20 ~g/m3 higher than a home without smokers. But if a nonsmoker lives with a 1.5-pack/d smoker, sharing approximately 70X of his or her time at home and breathing at a resting rate of 10 L/min, the nonsmoker would have an integrated exposure of 1.1 x 105 ~g/yr. Thus, it is likely that a flight attendant working full-time is receiving an integrated exposure to ETS approximately equal to that associated with living with a 1.0-pack/d smoker. Most studies of the effects of ETS on the lung of adults have investigated pulmonary function changes that might indicate early disease. Many studies of chronic exposure of children indicate that the prevalences of respiratory symptoms and illness are increased and pulmonary function can be decreased.16, However, there have been relatively few studies in adults. White and Phoebe 7 4 reported that nonsmoking healthy adults exposed to tobacco smoke at work had lower forced expiratory flow rates than nonsmokers not so exposed. However, these results have been questioned by several investigators.! 16 67 87 Kentner et al., 76 in another study of the effect of smoking in the work environment, found no significant change in the results of any pulmonary function test among working adults. There have been a number of studier of changes in pulmonary function of adults in relation to exposure to smoke in the home environment. Comstock et al. 3 9 and Brunekreef et al. 2 9 detected decreases in pulmonary function, although the decreases were insignificant. Kauffmann et al., 74 75 in two studies, detected significant decreases in standardized forced expiratory volume, especially in women over age 40. Thus, it is difficult to draw any firm conclusion on the use of forced expiratory rates in determining health effects of ETS. It in unclear whether the investigators were treating the observed changes in pulmonary function as representative of a health effect of long or short exposure to ETS and whether the changes were symptomatic of pulmonary disease. There were no assessments of ambient conditions or biochemical measures of components of tobacco smoke in most studies. Therefore, it is difficult to extrapolate the results of these studies to potential health effects in passengers and crew members in airliner cabins. Some chemicals in tobacco smoke, however, are known to cause mucociliary stasis, toxicity to alveolar macrophages, increased permeability of the mucosal barrier, and changes in immunoglobulins. 3 ~ 4 7

147 There are few data on the potential effects of ETS on cardiovascular disease. Investigations have centered on carbon monoxide and nicotine, because of their known effects on the oxygen-carrying capacity of blood and on the sympathoadrenal system. }62 A recent comprehensive review of laboratory and clinical data on animals and humans with respect to nicotine and carbon monoxide uptake in passive smoking and its potential effect on the cardiovascular systems 3 3 concluded that passive smoking should have no cardiovascular effects in humans. However, the reports of cardiovascular complications in previously normal people exposed to ETS raise the possibility of deleterious effects associated with exposure . 5 3 5 5 6 2 6 3 In summary, the cabin crew are chronically exposed to substantial ETS concentrations. The total exposures might approach those experienced by spouses of smokers. Therefore, the health effects assessed in spouses of smokers could be relevant for the cabin crew. The cabin crew and asymptomatic passengers are subject to acute health effects of Exposure to ETS. Furthermore, given the low relative humidity and other environmental conditions of the cabin, such as high ozone concentration, the irritation and discomfort effects are likely to be important for occupants of the smoking and nearby sections and to others who need to move through the smoking section. GROUPS AT INCREASED RISK Other persons who might have a different risk of exposure to ETS on aircraft are passengers with pulmonary or cardiovascular diseases. Dahms et al. 42 found that asthmatic patients had a significant linear decrease in pulmonary function after exposure to ETS, with reductions in forced expiratory volume, forced expiratory flow, and forced vital capacity. The etiology of these changes has not been defined clearly, although some suggest that the smoke might increase airway resistance in patients with bronchial asthma, whose pulmonary function was already lower than that of normal subjects. Wiedemann et al. i76 also studied asthmatics. However, his patients were not on medication and had normal or nearly normal lung function. After their exposure to ETS, they found a significant decrease

148 in airway reactivity, as assessed by a methylcholine challenge test. Shephard et al.,1 3 7 however, found decreases in pulmonary function among medicated asthmatic patients when they were exposed to ETS, but the changes were not significant. It has been suggested but never proved, that patients with angina are at increased risk of recurrence in the presence of ETS. Aronow et al. 14 reported an exposure-related subjective outcome, angina, in persons with severely compromised cardiovascular systems-- patients who had previously suffered from angina pectoris. Similar findings of early-onset angina were observed when patients were exposed to carbon monoxide at concentrations characteristic of those noted during the ETS exposure experiments.~° \2 is The validity of these findings has been questioned, i55 and the studies are currently being repeated by both the National Institute of Environmental Health Studies and the Health Effects Institute. Other groups that might be at increased risk due to exposure to ETS are people with various chronic pulmonary diseases, including chronic obstructive pulmonary disease, emphysema, alpha-l-antitrypsin deficiency, and cystic fibrosis. However, the effects of ETS on these people have not been studied. PREVENTION OF EXPOSURE TO ETS Occupational exposure of flight attendants to ETS could be limited by configuring aircraft without any work stations (galleys) in the smoking section. Exposure of nonsmoking passengers would be lessened if access to lavatories did not require passage through the smoking section. Total isolation of smokers and their air is possible, but would be a mayor engineering task whose cost would presumably be borne by the flying public through higher ticket costs. Light-weight, high-performance, economical filter systems that effectively remove gases and particles from ETS could eliminate many of the problems of and objections to onboard smoking. Such systems that are compatible with requirements for installation on airplanes have not yet been developed.

149 The ultimate prevention of exposure will be achieved only when there is no smoking on aircraft. However, it has been argued that the acute withdrawal from compounds in tobacco smoke would be accompanied by symptoms that are both physical and psychologic in origin and that heavy smokers might find it difficult to endure the stress of long airplane flights without smoking. Murray and Lawrencel06 have described the state of knowledge regarding withdrawal symptoms. The weight of evidence does not support the view that unpleasant physical and psychologic effects necessarily follow abstinence from smoking. Weight gain, craving for cigarettes, etc., are highly idiosyncratic and do not occur with high frequency in smokers who are temporarily required to cease smoking. Those who sutt~er a doctor the use the discomfort. ~O withdrawal symptoms should discuss with of nicotine substitutes to alleviate The Civil Aeronautics Board (CAB) suggested in 1981, and later withdrew, a ban on smoking on flights lasting less than 2 h.i53 The ban was withdrawn because it would be particularly troublesome on multisegment flights where smoking would be permitted at some times, and then prohibited during other parts of the trip. In addition, such a ban would require arbitrary line drawing. It might create a perverse incentive for some carriers to rearrange their schedules to evade it. We conclude on balance that the limited benefits are outweighed by the difficulties associated with the proposal. In the judgment of the Committee, the potential health effects of passive smoking are of more concern than effects of withdrawal, and more people are at risk. We believe that CABts suggested 2-h limit did not provide adequate protection to passengers on longer flights. Therefore, the ban on smoking should be extended to all domestic flights. Limiting the ban on smoking to domestic flights would allow smokers the option of taking planes with stopovers that would enable them to smoke in smoking areas of the airport. The use of nicotine substitutes could discourage surreptitious smoking, as could strict enforcement of no-smoking rules with the threat of fines. The hazard of in-flight fires resulting from surreptitious smoking in lavatories can be reduced through the use of nonremovable smoke detectors. ~ .

150 After a period of adjustment and with strict enforcement, prohibiting smoking should reduce onboard fire risk, cleaning costs, and costs of replacing and repairing damaged materials. Removing tobacco smoke from the aircraft environment would reduce cabin ventilation requirements, and that would result in additional fuel savings while reducing irritation and health risk. SUMMARY - The concentration of ETS is directly proportional to the strength of the source (number of active smokers) and inversely proportional to the flow of outside air in a smok ng area. Recirculation in various configurations complicates the distribution, but does not fundamentally change the relationship between smoke generation and the steady state of the total mass of contaminants in the cabin. Currently available filters on airplanes only remove particles. Some particles and tars are removed through settling and adsorption onto cabin surfaces. Carbon monoxide and respirable particulate matter are measured as surrogates for ETS, which is a complex mixture of many components. Peak concentrations of carbon monoxide and RSP of about 5 ppm and 500 ~g/m3, respectively, are to be expected and have been measured. However, the data supporting these values are sparse. and most have not been subjected to peer review. _ ~ ~ The measured values do not violate U.S. ambient or workplace carbon monoxide standards, but do violate a Japanese standard for indoor air quality. Cigarette smoke contains known human and animal carcinogens that would be strictly regulated if the source were something other than tobacco. Ventilation standards that have been set to avoid irritation by ETS in buildings are not met by standard aircraft practices. The most regularly exposed nonsmoking populations are cabin crew members whose duties require them to spend long periods in the smoking section and passengers who are seated in or near the smoking section. Health-effects data from other environments do not permit us to present reliable quantitative risk estimates related to the health impact of present concentrations of

151 ETS on exposed nonsmokers in an aircraft environment. One report that presented a risk-assessment calculation for ETS suggested that a reduction by more than a factor of 10 in present aircraft concentrations would be necessary to bring the risk calculated in that report into the range permitted for regulated toxic environmental contaminants. This degree of change, which might be technologically possible, is likely to be economically unrealistic if smoking were permitted in aircraft. Patients with severe asthma or angina are at higher risk from exposure to ETS than other exposed people, because of the increased likelihood of acute symptoms. The Committee considered several ways of reducing ETS in aircraft. Solutions requiring structural or engineering changes--such as increasing ventilation, moving lavatories and galleys, and separating smoking compartments by physical barriers--are not likely to be economically feasible. Increasing ventilation for the smoking zone to be in compliance with ASHRAE guidelines is not technically feasible on existing aircraft. The amount of air that can be extracted from the engines is limited and might not support the high ventilation rates; in addition, the high rates would require ECU redesign, increased distribution ducting, outlet redesign, and control modification. A return to the random distribution of smokers throughout the cabin would decrease the peak concentrations of contaminants, but the Committee feels that this probably would be unacceptable to a majority of the traveling public. The Committee recommends a ban on smoking on all domestic commercial flights, for four major reasons: to lessen irritation and discomfort to passengers and crew to reduce potential health hazards to cabin crew associated with ETS, to eliminate the possibility of fires caused by cigarettes (see Chapter 1), and to bring cabin air quality into line with established standards for other closed environments (see discussion on ventilation in Chapter 2 and on specific pollutants in Chapter 5~. The ban might have the added benefit of reducing airline maintenance costs for removal of tobacco tars. We note that some habitual smokers might experience nicotine deprivation on flights longer than 3 h. However, in the judgment of the Committee, the J

152 potential health effects of passive smoking are of more concern than the discomfort of withdrawal, and more people are at risk. BIOLOGIC AEROSOLS TYPES OF BIOLOGIC POLLUTANTS POSSIBLE IN AIRCRAFT Most biologically derived particles that are known to become airborne could be present in aircraft cabin air. These include viruses, bacteria, actinomycetes, fungal spores and hyphae, arthropod fragments and droppings, and animal and human dander.30 Viruses that are known to be infective through the airborne route include rhinoviruses, influenza viruses, coxsackievirus, adenovirus, and measles virus. Disease transmission through the air is known to occur both by droplets and by droplet nuclei, which can be transported over relatively long distances .7 9 A wide variety of bacteria have been isolated from air. Those which have caused disease through airborne carriage include streptococci, mycobacteria, staphylococci, legionellae, pseudomonads, and klebsiellae. 79 Actinomycetes (so-called filamentous bacteria) that cause invasive disease are rarely isolated from air, but thermophilic (heat-loving) actinomycetes that have been implicated in hypersensitivity pneumonitis always produce disease through the airborne route. These include one or more species in the following groups: ThermoactinomYces, Thermomonospora, Saccharomonospora, and MicropolYSpora. 20 Most fungi produce spores and often hyphal fragments or single vegetative cells that can become airborne. Many of these fungi can grow and reproduce on surfaces within man-made structures and, when disturbed9 produce dense biologic aerosols that accumulate within an enclosed space and cause hypersensitivity diseases--such as hypersensitivity pneumonitis, allergic rhinitis, and allergic asthma--and rarely invasive diseases in susceptible people. 30 Many infectious fungal diseases (including coccidioidomycosis, histoplasmosis, blastomycosis, and cryptococcosis) are also known to be

153 transmitted through air carriage of spores or spore- bearing soil particles. Various arthropod particles, including mites and cockroach droppings, have been recovered from air; these are known to be important allergens where they are abundant.73 Flean and mosquitoes become airborne through their own actions and can cause discomfort (bites), as well as transmit serious diseases.~39 \66 }75 Finally, animal dander and human dander accumulate in any occupied space, and both can be allergenic. SOURCES OF BIOLOGIC POLLUTANTS Potential sources of biologic aerosols in cabin air include outside air, the cargo compartment, passengers and crew, and structural contamination of the aircraft. At cruising altitudes, outside air contains very few biologic particles of any kind (a few dark fungal spores per cubic meter of alr). These are unlikely to constitute any risk to airline passengers. Outside air that comes in through doorways while a plane is on the ground carries a wide variety of fungal spores, including a few pathogens. In the Southwest, where Coccidioides immitis is endemic, soil particles bearing infective spores often enter enclosures, especially during dust storms. Passengers boarding in these areas would have been exposed in transit to the airport. Passengers and crew stopping over (and not leaving the plane) could receive cabin-associated exposure when doors are open to unload passengers, galley materials, and baggage. Similar situations can arise for other airborne pathogenic fungi. However, control of such exposure would be difficult, because doors must be opened eventually. Most fungi in outdoor air are routinely encountered by everyone and, although allergenic for many, do not constitute a special risk in aircraft cabins. Bacteria are usually not present in outdoor air in concentrations sufficient to cause disease. Exceptions are species of Le~ionella, soil organisms that multiply in cooling towers and related man-made environments. Infected cooling towers are potential sources of aerosol-borne infection. How far such aerosols can travel in outdoor air and remain infective is unknown.

154 Cargo compartments can contain animals (which have dander, feces, and urine), arthropods, microorganisms in culture, and contaminated baggage. Aerosols from all there sources could accumulate in a cargo compartment to a point that would be detrimental to human health. However, the potential for contamination of passenger compartments is less clear. Barriers to air circulation between passenger and cargo compartments can range from structural and excellent (Class D) to virtually nonexistent and dependent entirely on airflow patterns (Class B). The greatest danger from cargo sources would be associated with pathogenic microorganisms in cultures that are damaged during transit. The infective dose of some pathogens is a single call. Pathogens can be transported by mail and are allowed in passenger aircraft if properly packaged. These microorganisms should not be permitted in passenger aircraft, and any nonpathogenic microorganisms in culture should be packed so as to eliminate any possibility of escape. Primary sources of indoor bacterial and viral aerosols are humans and animals. \4} In addition to bacteria and viruses, clothen-borne fungi and actinomycetes can be carried by people and pets, as can mites. Bacteria are freely shed from human skin with minute skin scales. Clothing contains some of this contamination, and its abrasive action also detaches outer skin layers and increases shedding.141 Thus, bacteria from this source would be expected to increase during boarding and settling activities and during meal and beverage distribution and to decrease during inactive periods. Occupants can also spread bacteria and viruses by coughing, sneezing, talking, singing, etches Coughing and sneezing produce the biologically richest aerosols. A sneeze produces very large droplets (200 Em and larger). 14\ Immediately on release, respiratory droplets begin to dry. Many become droplet nuclei, which are very small, remain airborne for long periods, and (depending on the organisms and environmental conditions) can remain infective for hours or even days. There is no evidence that the HTLV-III virus, which is associated with acquired immune deficiency syndrome, is transmitted through the air or by casual human contact. Structural contamination--especially in heating, ventilation, and air-conditioning systems--is of

155 increasing concernel02 Fungi, actinomycetes, bacteria (including species of Le~ionella), and protozoans have been found to inhabit such systems in large buildings and have caused widespread disease outbreaks when introduced in aerosol form through the action of the systems themselves. In an aircraft, possible sites of such contamination are the ventilation systems (with their associated filters and water removers) and a wide variety of surfaces 9 including carpets, upholstered seats, and even metallic surfaces that are persistently or repeatedly wet. Fungi and actinomycetes, in particular, can withstand repeated wet-dry cycles and temperature extremes. FACTORS AFFECTING AIRBORNE CONCENTRATIONS OF_BIOLOGIC POLLUTANTS AND THEIR HEALTH EFFECTS Factors that can affect airborne concentrations of biologically derived particles include source strength, methods of aerosolization, viability, stability, and ventilation. Source-strength factors include the number of people and animals in the enclosed space, the number with respiratory or skin infections, and a wide variety of aspects of microbial growth, such as amount of total growth available (which depends on substrate availability, nutrients, water, temperature, and pH), degree of sporulation (which depends on light, temperature, and relative humidity), and spore-cell availability (which depends on viability and colony surface configuration). Methods of aerosolization include active spore discharge and passive dispersal--coughing, sneezing, talking, air movement, water splashing, and Jarring and turbulence. A sneeze produces approximately 2 million viable particles. i4} These do not remain airborne very long, but are highly infective and can be inhaled by people near the infected source. Talking can produce as many as 2,000 particles per explosive sound. Most important for dissemination of fungal aerosols are passive modes, such as air movement over contaminated surfaces. Other biogenic particles--such as skin bacteria, arthropod remains, and dander--are usually introduced into the air through jarring. This can

156 result from human activity (walking on contaminated surfaces, sitting on contaminated seats, or vacuum- cleaning or dusting surfaces) or from jarring of the entire structure (as might be possible in an airplane during turbulent weather). Such antigens as those from fungi, arthropods, and dander do not need to be living to cause hypersensitivity responses, but bacteria and viruses must be viable to be infective. Among many factors that influence the length of time that bacterial and viral aerosols remain viable are relative humidity, temperature, and time. \20 For viruses, relative humidity and viability are inversely proportional.91 ~ 05 For some bacteria, the situation is reversed: the higher the humidity, the longer the survival. Thus, although the low relative humidities present in most aircraft during flight can be deadly for some bacteria, such conditions probably augment the viability of most viruses. Temperature, which is limiting in extremely cold or extremely hot environments, is unlikely to be a strong factor in an aircraft, where temperature is usually maintained within a comfortable range for the passengers. All organisms die eventually, and each has its own life span. Under ideal conditions, this span can vary among microorganisms, from minutes to many years. Certainly, many microorganisms that cause human disease live long enough even in the stressful environment outside their human hosts to cause disease in enclosed situations. The ventilation characteristics that directly affect concentrations of biologic particles are the ones that affect concentrations of all interior particles: the quality and quantity of outside air and the quality of filtration in the recirculation systems. The outside air supplied to aircraft cabins during flight is essentially clean. Enough outside air needs to be supplied to dilute the inevitably produced bacterial aerosols to the point where the risk of infection is minimized. Filters currently used in aircraft ventilation systems probably remove only a ve On small fraction of the continually produced bioaerosols, although data are not available to assess this accurately.

157 AIRBORNE CONCENTRATIONS NECESSARY TO CAUSE HEALTH EFFECTS OR DISCOMFORT Dose-response relations for most organisms are unknown and differ widely from one organism to another. One infectious droplet is sufficient to cause tuberculosis infection, but thousands of droplets are probably necessary to transmit rhinoviruses. In fact, infective dose varies not only with the individual virus or bacterium, but also with such host susceptibility factors as vulnerability of specific cells in the respiratory tract, antibody concentrations, and the presence of predisposing conditions. 7 9 For example, a person who is in any way immunocompromised--through disease, chemotheraDv. or radiar;nn th~r~n=__] ~ h ~ of ~ x, susceptible to all forms of infection and should not frequent indoor spaces occupied by potentially infectious people. The numbers of spores or particles or concentrations of antigens required to induce hypersensitivity diseases remain completely unknown and most likely vary greatly with the susceptibility of exposed persons. 5 -rip ~ ~ _, ~ ~^~ ~ in'' ~ AVAILABLE DATA Available Predictive Data from er Sources No other environment closely approximates the unusual conditions present in aircraft cabins, but data from a few other sources can be used to predict potential problems aboard aircraft and to provide direction for the design of research. Submarine and spacecraft environments are most nearly like the commercial aircraft environment, except that all their air must be recirculated, because outside air is unavailable. In both, recirculation systems are designed with that in mind, and the quality of air filtration far exceeds that in commercial airliners. In submarines, as many as 30,000 bacteria/ft3 of air were isolated d,~rin~ .~Pw~" handling procedures.: 6 7 . However, concentrations generally remain below 20/ft3, comparable with those in surface ships. i03 Microbiologic measurements were made in the Apollo and Skylab missions.27 28 In neither case were concentrations above those expected in other types of interiors. In one Skylab mission, fungal spores were more numerous than expected (but still less numerous than

158 in ground-level outside air), because moldy garments were on board. These data are only marginally relevant to the aircraft environment, because there are major differences in ventilation, air filtration, and passenger load. Data from doctors' offices and schools clearly indicate that viruses can be circulated through ventilation systems, remain viable, and infect people who have had no physical contact with the source.22 '21 In aircraft cabins, this effect might be augmented by the low relative humidity, which would prolong the life of airborne viruses. It is also apparent from the literature on environmentally tight buildings that microbiologic contamination of heating and ventilation systems can be a serious problem.120 Although aircraft systems differ substantially from ground-based systems, they have a potential for surface contamination, because temperature differences can cause water to condense and provide suitable substrates for microbial growth. Available Data on Aircraft No well-designed research studies that document routine concentrations of microbiologic air contaminants in the aircraft cabin environment have been reported. Studies of other cabin air characteristics either ignore microbiologic contaminants or dismiss them with an unsupported statement that they were "not found." One study, by Air Canada, 37 was carefully designed to assess the risks to healthy passengers and crew associated with transporting passengers with contagious diseases. Bacterial endospores were sprayed from a position five rows from the rear of the aircraft (the position determined, by smoke tracer studies, least likely to cause cabin-wide contamination). During the pretakeoff phase, when the plane was on recirculated air, these spores, although most heavily concentrated near the release site, circulated throughout the cabin and into the cockpit. On takeoff, concentrations away from the source decreased rapidly, but they increased again during descent and landing. The authors stated that background concentrations were low because of the high rate of air exchange in the cabin, but did not present background data. They concluded that infectious passengers should be carried in the left rear of the aircraft (B-707) and that the engines should be started and forced ventilation

159 begun before such passengers board. Even under those circumstances, it is apparent that a strongly emitting source can contaminate the whole aircraft and that the risk is greatest on the ground and when recirculation is a component of the ventilation. The risk of contracting epidemic disease on a grounded aircraft is emphasized by ~ report of an epidemic of influenza directly traceable to a passenger aboard a plane grounded for 4 h in Alaska; 72% of the passengers became ill from the exposure. i04 The absence of other such reports in the literature does not lessen the danger implicit in conditions in a crowded airplane with little or no outside ventilation. This particular epidemic was unusual, in that most patients saw the same physician (in Kodiak), who was in a position to recognize the implications of the situation. If the flight had terminated in Washington, D.C., for example, no physician would have been in a position to recognize even that an epidemic had occurred. Because of the heavy potential risk of spread of infectious disease in aircraft on the ground with no outside ventilation, we recommend that no aircraft with passengers on board remain on the ground without operational forced ventilation for longer than 0.5 h. Open doors are not adequate ventilation sources in this situation. If forced ventilation cannot be initiated within 0.5 h, passengers should be returned to the terminal. This O.5-h time limit in based on practical consideration of the time required to return a full load of passengers to the terminal. In fact, microbial concentrations will begin to increase as soon as ventilation fails, and risks related to these exposures are unknown. There are at least four reports of malaria contracted by passengers on aircraft or by visitors to airports shortly after aircraft arrived from areas where malaria was endemic. These cases of malaria very likely resulted from aircraft carriage of malaria-carrying mosquitoes. 139 166 175 CONCLUSIONS AND RECOMMENDATIONS Microbial concentrations have not been measured in aircraft, and therefore accurate risk assessments cannot be made. The Committee feels that microbial aerosols

160 should be measured. A protocol for sampling microbial aerosols in commercial aircraft was developed at the University of Michigan for a pilot study (H. A. Burge, personal communication). This protocol should be tested and expanded into a substantial research effort. Despite the lack of data, the potential for microbial aerosols in aircraft exists, and concentrations can be predicted to be related to ventilation characteristics. Therefore- when ventilation systems are inoperative, passengers should leave the plane within 0.5 h. In addition, physicians should be reminded of the rules stating that infectious passengers must not travel on commercial airliners. It is recognized that many infectious conditions are transmissible long before symptoms appear, rendering this rule relatively valueless, except for severe contagious illnesses. If the risk of infection is to be minimized, the amount of outside air supplied to each passenger during flight should be maximized, because outside air at cruise altitude is essentially clean. The dangers of extensive use of unfiltered, untreated recirculated air should be carefully considered. Every feasible effort should be made to ensure that wet surfaces are prevented or scrupulously cleaned routinely, to prevent structural contamination. Finally, cargo compartments should be kept free of animal excrement, as well as arthropod pests, and pathogenic microorganisms should never be transported on passenger-carrying aircraft. ,, RELATIVE HUMIDITY Relative humidity is the ratio of the amount of water vapor in the air at a given temperature to the capacity of the air at that temperature. The term is generally used to mean the percentage of moisture present relative to the amount the air can hold at a given temperature and pressure. The term "vapor pressure" (expressed as millimeters of mercury) refers to the pressure exerted by the (water) vapor on the air mixture at a given temperature and pressure. "Water vapor content" or "water content" (expressed as weight per unit volume or weight of dry air) means the actual amount of water present in the air. All these terms are used in the literature related to relative humidity.

161 With ~ constant supply of moisture, relative humidity decreases as temperature increases. The outside air used to ventilate aircraft cabins during flight in very cold and contains very little moisture. On a typical temperate-zone day, ambient air temperature falls from +60°F to -60°F (+15.6°C to -51.1°C) linearly between sea level and 35,000 ft (10.7 km), and the water content falls from 10 g/kg to less than 0.15 g/kg of dry air. This small amount of moisture plus whatever is accumulated from human sweat, respiration, and cooking activities is all that is available during flight. AIRCRAFT VENTILATION AND RELATIVE HUMIDITY In most aircraft, fresh air is brought in from outside through the engines, cooled, and delivered directly to the cabin with no humidification. Available water from this source, then, remains at about 0.15 g/kg, and9 at 20-22°C (68-71.6°F); the relative humidity of the fresh air is less than 1%. The relation between relative humidity and amount of air supplied per passenger is shown in Figure 2-7. Moisture from the passengers themselves will cause relative humidity to increase, depending on the outside-air ventilation rate and the load factor, and it will decrease as rate of outside ventilation increases. MEASURED RELATIVE HUMIDITY IN AIRCRAFT Humidity measurements that have been made in aircraft cabins are summarized in Table 5-~. Because of the paucity of data and the failure to indicate outside-air ventilation rates, correlations among relative humidity, load factors, and duration of flight cannot be based on these data. The Lufthansa data94 (one flight on one aircraft) indicate a fall in relative humidity during flight from 25~o to 8.5%. At cabin temperatures of 20-23°C (68-73.4°F), these data suggest that actual water content falls from 4.3 to 1.8 g/m3 as a function of duration of flight. These values correspond to vapor pressures in the range of 2-6 mm Hg.

162 TABLE 5-5 Relative Humidity Measured in Aircraft Cabins S tudY Relative Humidity, % Aircraft Range Min. Mean Max. Lufthansa9 4 B-747 8.5-25 13 Applegate ~B-747 6.0-40 9.1 16 DC-10 5.0-34 10.75 22.75 DC-8 6.0-25 10.5 15.0 B-727 6.0-16 8.75 12.5 B-737 17-31 22 25 Water Content, e/ka of drv air Balvanz B-727 1.5 et al.19 B-737 1.74 B-747 1.39 B-767 0.739 DC-9 2.8 DC-10 6.0 STANDARDS FOR OTHER ENVIRONMENTS ASHRAE Standard 55-1981, Thermal Environmental Conditions for Human OccunancY,s calls for vapor pressure to range from 5 to 14 mm Hg. The lower end of thin scale represents 20X relative humidity at an adjusted dry-bulb temperature of about 72°F (22.2°C). EFFECTS OF LOW RELATIVE HI~IlDITY ON PAS SENGERS AND CREW Documented direct effects of low relative humidity on passengers and crew are few. Corneal ulcerations have been reported in wearers of contact lenses after long flights, possibly owing to low oxygen partial pressure, as well as low relative humidity. Hydrophilic contact lenses tend to lose water, but not to the detriment of vision. 46 Removal of contact lenses and the wearing of contact lenses specially designed for use in dry air are successful remedial actions. 40 70 Eng et al.46 reported that a high percentage of flight

163 attendants complain of dry eyes; however, the value of this questionnaire study is limited because of possible selection bias and lack of controls (see Chapter 6~. Of 293 flights on which incidents regarding cabin air quality were reported (presented by the Association of Flight Attendants before a Senate subcommittee), only 27 flights (9%) included complaints of dry eyes, dry throat, dry nose, or dry air. On only three flights were there complaints of "dry air".15 Mendez Martin9 9 and Kohler81 showed that urinary calculosis was common among flight personnel, possibly because of low relative humidity, but the Committee found no corroboration of this finding (see Chapter 6~. REPORTED HEALTH EFFECTS OF LOW RELATIVE HUMIDITY IN OTHER ENVIRONMENTS Water loss from airways might be an important stimulus of exercise-induced asthma under dry conditions,7 s7 and a slight reduction in lung capacity has been noted in asthmatics at rest in dry environments. In addition, low relative humidity can increase bronchomotor effects of sulfur dioxide in mild asthmatics. At 0X relative humidity, sulfur dioxide at 0.1-0.25 ppm is sufficient to cause a 100% increase in specific airway resistance. This effect has not been studied in the normal population, and synergistic effects between low relative humidity and other pollutants have not been examined. However, low relative humidity itself probably does not cause bronchoconstriction in normal people. In fact, no significant changes in nasal mucus flow rates, nasal or tracheobronchial resistance, or comfort were found in a group of eight healthy men maintained at 9% relative humidity for 79 h. 6 Rappaport et al.~19 indicated that reduced relative humidity (15-40%) might be beneficial to pollen-asthma sufferers. Abrupt changes in relative humidity (more than 10%) can cause discomfort in some people, but re-equilibration tends to occur within about 15 min. Evidence on the common belief that low relative humidity increases the risk of respiratory infection is conflicting. The Jaeger steadiest with mice and chicks found some correlation between virus titers and low

164 humidity with high temperature, a combination not common in aircraft. Mucociliary clearance rates in chicks exposed to a range of temperatures and vapor pressures were increased at low vapor pressures; most of these experiments failed to duplicate aircraft cabin temperatures and humidity. Baetjer commented on possible effects of temperature and vapor pressure on the skin (including absorption of noxious chemicals), but presented no data to indicate that low vapor pressures diminish or amplify skin absorption. Melia et al.98 reported a positive correlation of respiratory infections with relative humidity, i.e., as humidity increased, respiratory infections increased; but the relative humidity was higher than that in aircraft. The one disease state in which high relative humidity has been thought to be at least palliative, croup, has been shown to be unaffected by even very high humidities. 2 3 It has been shown that people overwintering at the Antarctic station, where indoor relative humidities approach those in aircraft cabins, are not at increased risk of respiratory infections after their return to a more temperate environment.72 These data are only marginally relevant to cabin air quality, because there are major differences in conditions and patterns of exposure. Lidwell et al.89 demonstrated that increased incidence of respiratory infection in winter is related to temperature, not to relative humidity, and stated that this analysis "contradicts any arguments based on virus survival in relation to indoor humidity or on a postulated damaging effect, due to drying, on the mucous membranes, predisposing to the initiation of infection when the indoor humidity falls in cold weather." However, after a less extensive study, Gelperin54 reported that the rate of upper respiratory infection was 5-10% lower in humid barracks (relative humidity, 40%) than in unhumidified barracks (relative humidity, 20%~. He resorted an equivalent decrease in foot infections that is difficult to explain. Green et al.56 reported data from Saskatoon schools that indicated slightly lower absenteeism (4.6% vs. 5.1%) in schools with slightly higher relative humidity (overall relative humidity range, 18.4-38.6%~; the data show a marginal effect of relative humidity in a range not comparable with that found in aircraft cabins.

165 Low relative humidity has been shown to be a factor in dry, scaly skin rashes when specific irritants are also presently 3 and to contribute to winter drying and chapping of hands and face when accompanied by exposure to excess cold or water. Assuming that flight attendants wash their hands often, dry aircraft air could cause increased problems with rough dry hands, but would be unlikely to affect passengers, who are exposed relatively briefly. Indirect effects of relative humidity on passengers and crew are associated primarily with the viability of microorganisms. Humidification of schools has been considered important for many years as a means of decreasing virus survival, but decreased concentrations of viruses in humid school air have not been documented. It has been shown that concentrations of some bacteria can be directly related to relative humidity: as humidity decreases, bacterial concentrations decrease. As mentioned earlier, indoor fungal spore concentrations are also directly related to relative humidity. SUMMARY The health risks associated with clean, dry air appear quite low, especially for normal people, and probably do not justify the cost and potential microbiologic complications that would attend installation of active humidification systems in aircraft. PRESSURIZATION The Committee recognizes that pressurization of the cabin to an equivalent altitude of 5,000-8,000 ft is physiologically safe--no supplemental oxygen is needed to maintain sufficient arterial oxygen saturation. The percentage of oxygen remains virtually unchanged (21%) at all altitudes. But partial pressures of gases change, as shown in Table 5-6, where the partial pressure of oxygen is shown to decrease from 160 mm Hg at sea level to 110 mm Hg at 10,000 ft. The oxygen- hemoglobin dissociation figures, which indicate the amount of oxygen held by hemoglobin at various partial pressures of oxygen, clearly show that the dissociation

166 TABLE 5-6 Hypobaric Pressure and Arterial Oxygen Saturationa Oxygen Atmospheric Partial Pressure, Pressure,b mm He Pressure Altitude, ft mm He 0 760 160 96 2,500 694 147 95 5,000 632 133 95 7,500 575 121 93 10,000 523 110 89 a Data from Mohlerel°l b 20% of atmospheric pressure. Arterial Oxygen Saturation Without Supplemental Oxygen, X of oxygen from hemoglobin decreases with decreasing partial pressure of oxygen. There is a decrement in night vision at 4,000-6,000 ft. and a 7-10% decrement in maximal performance at altitudes between 7,000 and 10,000 ft. Cabin altitudes can legally reach 8,000 ft. but after failure of the pressurization system could reach as high as 15,000 ft. At these altitudes, people with advanced cardiopulmonary disease might be at some risk. The normal rates of change of cabin pressure (500 ft/min in increasing altitude and 300 ft/min in decreasing altitude) do not pose a problem for passengers in normal health. However, persons suffering from upper respiratory infections might experience pain of varied severity, temporary loss of hearing, and tinnitus due to inflammation of the nasopharyngeal orifice of the eustachian tube or due to swelling of mucous membranes in the sinus ostia. Cabin crew members should be advised as to the symptoms and procedures to alleviate them. The Committee sought evidence of operating practices in which an aircraft was pressurized at altitudes above 8,000 ft. but could not find any records that would confirm the existence of such a practice. Because operation of the pressure control system on modern jet aircraft is usually fully automatic, the likelihood of

167 excursions above 8,000 ft is small. In addition, regulations require that an audible or visible warning be given to the crew if the cabin altitude exceeds 10,000 ft. Nevertheless, the Committee believes that systematic measurement of cabin pressure on a representative sample of routine commercial flights would be advisable. The information gathered could be used to assess the adequacy of current requirements or establish a basis for regular monitoring, if necessary. The Committee recognizes that properly informing the public about health risks is complicated and difficult. Many physicians advise their patients about health risks of flying, but passengers do not always consult physicians about their travel plans, so this method is not as effective as it should be. Carefully worded messages could be made available to potential airline passengers with acute or chronic middle ear problems, heart problems, or lung disease. This could be accomplished through provision of the information at ticket counters or through travel agents and others who sell tickets. CARBON DIOXIDE Carbon dioxide is the product of normal human metabolism, which is the predominant source in aircraft cabins. The carbon dioxide concentration in the cabin depends on the ventilation rate, the number of people present, and their individual rates of carbon dioxide production, which vary with activity and (to a smaller degree) with diet and health. Federal Aviation Regulationsl 6 3 specify that "carbon dioxide in excess of 3 percent by volume (sea level equivalent) is considered hazardous in the case of crewmembers. Higher concentrations of carbon dioxide may be allowed in crew compartments if appropriate protective breathing equipment is available" (see Chapter 3~. In contrast, ASHRAE Standard 62-1981, Ventilation for Acceptable Air QualitY' 4 bases indoor ventilation requirements on a carbon dioxide production rate of 0.61 cubic foot per hour (cfh) per person and outside air containing 0.03% carbon dioxide. Ventiiation calculations are based on a limit of 0.5X carbon dioxide. However, as an additional safety factor

168 to cover individual activity levels and diet and health variations, a recommended limit of O.25% carbon dioxide is used, and that establishes a ventilation rate of 5 cfm/person. In comparison, the environmental exposure limit adopted in 1984-1985 by the American Conference of Governmental Industrial Hygienists (AGGIH) gives 5,000 ppm as the time-weighted average (TWA). 2 The TWA is the concentration, for a normal 8-h workday and a 40-h workweek, to which nearly all workers can be repeatedly exposed, day after day, without adverse effects. The Occupational Safety and Health Administration also lists the 5,000-ppm concentration as the TWA for workers.! 4 9 ACGIH has a short-term exposure limit (STEL) of 15,000 ppm, although it has issued a notice of intended change to 30,000 ppm. A STEL is defined as a 15-min TWA exposure that should not be exceeded at any time during a working day. Under normal conditions, carbon dioxide at 0.6% has little effect on lung function, increasing it only about 10X above normal. As carbon dioxide concentration increases, there is an increase in both the rate and the depth of breathing, which reaches twice normal at 3% carbon dioxide. At that concentration, there is some discomfort; as it increases, headache, malaise, and fatigue occur, and the air is reported as stale. At altitudes up to 8,000 ft. the reduced pressure has no significant effect on the symptoms or other response to increased carbon dioxide concentrations. In discussing federal regulations, Chapter 3 pointed out that the current FAR concerning acceptable cabin concentrations of carbon dioxide is several decades old. The Committee finds that there is a need to consider revision of this standard and recommends that FAA review it in the light of more recent scientific findings and in comparison with standards established for air quality in buildings occupied by the general public and with workplace exposure limits adopted by ACGIH. If any potential for hazardous concentrations is discovered, the analysis should be supported by appropriate testing. OTHER POTENTIAL EXPOSURES Aircraft occupants can be exposed to a number of pollutants from materials used to construct or maintain

169 the cabin. These include volatile organic chemicals emitted by materials used in furnishing the cabin, pesticides, and cleaning agents. Volatile organic chemicals in the aircraft cabin nave numerous potential sources: adhesives, lubricants, elastomers, sealing compounds, coatings, etc., used in the construction or maintenance of the cabin interior. Some of these products have been tested for offgassing of volatile chemicals as part of a government space study.~17 The offgassing chemicals include acetone, ethanol, benzene, toluene, and n-butanol. Many of them have serious toxicity (for example. benzene is a known human carcinogen). ~ _ However, exposure to them would be attecteo by the type and amount of the offgassing products used in the aircraft, the rate of offgassing under the conditions of use, the age of the products, and the ventilation rate in the aircraft. The Committee could find no monitoring data on the concentrations of volatile organic chemicals in aircraft cabins during operation. Insecticides can be used on aircraft to control pests of public-health or agricultural importance. The Centers for Disease Control (CDC) Division of Quarantine is authorized to require removal of insects from aircraft leaving foreign areas that are infected with insect-borne communicable disease, if the aircraft are suspected of harboring insects of public-health importance. 43 Insecticides used by the airlines must be approved by CDC. In 1979, it approved resmethrin (2% aerosol) and d-phenothrin (2% aerosol) for use in aircraft.lS: However, CDC does not now require the use of pesticides on aircraft (B. Coull, personal communication, 1986~. If an aircraft is suspected of harboring insects of particular agricultural importance (notably the Japanese beetle), the Department of Agriculture can require fumigation. 7\ d-Phenothrin is used in some aircraft traveling from regulated airports in the eastern United States to protected areas in the western United States, when inspectors deem it advisable. d-Phenothrin and resmethrin, like other pyrethroids, are neither skin irritants nor skin sensitizers. Inhalation toxicity and dermal toxicity are fairly low. Neither is teratogenic in rats, mice, or rabbits or mutagenic in various bacterial strains.~°° Both are

170 highly effective in killing some species of flies, mosquitoes, and other flying insects. 34 \32 In test of physical and insecticidal properties of (~-phenothrin, Lil~edahl et al.90 found that none of the cabin crew or scientists who were present experienced any odor or irritation during the use of the insecticide or from the residual deposit. Sullivan et al.,147 in worldwide aircraft trials, found resmethrin to be acceptable to 92X of the passengers questioned after the cabin was sprayed. Although no health problems among cabin occupants or crew have been reported as a result of the use of insecticides, there is always a potential for health problems due to their improper application. Disinfectants and cleaning chemicals used on aircraft can also be a source of exposure to occupants and might cause health problems in some people. For example, carpet shampoos have been linked to outbreaks of respiratory illness among people exposed soon after shampoo application. 83 \22 Although the Committee has no data or other documentation on health problems caused by these types of chemicals used on aircraft, it is reasonable to assume that they could occur on aircraft if appropriate precautions were not followed. REFERENCES 1. Adlkofer, F., G. Scherer, and H. Weimann. Small-airways dysfunction in passive smokers. N. Engl. J. Med. 303:392, 1980. (letter) 2. American Conference of Governmental Industrial Hygienists. Carbon dioxide, pp. 69-70. In Documentation of the Threshold Limit Values. 4th ed. Cincinnati, Ohio: American Conference of Governmental Industrial Hygienists, 1984. 3. American Lung Association. Americans Want Smoke-Free Air at Work. New York, N.Y.: American Lung Association, Dec. 5, 1985.

171 4. American Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc. ASHRAE Standard: Ventilation for Acceptable Air Quality. ASHRAM 62-1981. Atlanta, Gal: American Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc., 1981. 5. American Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc. Thermal Environmental Conditions for Human Occupancy. ANSI/ASHRAE 55-1981. Atlanta, Gal: American Society of Heating, Refrigerating and Air-Conditioning Engineers, Inc., 1981. 6. Andersen, I., G. R. Lundqvist, P. L. Jensen, and D. F. Proctor. Human response to 78-hour exposure to dry air. Arch. Environ. Health 29:319-324, 1974. 7. Anderson, S. D., R. E. Schoeffel, R. Follet, C. P. Perry, E. Daviskas, and M. Kendall. Sensitivity to heat and water loss at rest and during exercise in asthmatic patients. Eur. J. Respir. Dis. 63:459-471, 1982. 8. Applegate, W. C. Aircraft Cabin Air Quality Study. (unpublished document, United Airlines 1982) 9. Araki, Y., and K. Kasano. and dust collectors. Mitsubishi Denki Giho 48:470-477, 1974. (in Japanese) Building control law 10. Aronow, W. S. Aggravation of angina pectoris by two percent carboxyhemoglobin. Am. Heart J. 101:154-157, 1981. 11. Aronow, W. S. Effect of carbon monoxide on cardiovascular disease. Prev. Med. 8:271-278, 1979. 12. Aronow, W. S. Effect of passive smoking on angina pectoris. N. Engl. J. Med. 299:21-24, 1978.

172 Aronow, W. S., J. Cassidy, J. S. Vangrow, H. March, J. C. Kern, J. R. Goldsmith, M. Khemka, J. Pagano, and M. VawterO Effect of cigarette smoking and breathing carbon monoxide on cardiovascular hemodynamics in anginal patients. Circulation 50:340-347, 1974. - 14. Aronow, W. S., and M. W. Isbell. Carbon monoxide effect on exercise-induced angina pectoris. Ann. Intern. Med. 79:392-395, 1973. IS. Association of Flight Attendants. Exhibit A (passenger comments and flight attendant symptoms, 01/77-01/82~. In U.S. Senate, Committee on Commerce, Science, and Transportation, Subcommittee on Aviation (97th Congress, 2nd Session). Airliner Cabin Safety and Health Standards: Hearing on S. 1770, May 20, 1982. Washington, D.C.: U.S. Government Printing Office, 1982 e 16. Aviado, D. M. Small-airways dysfunction in passive smokers. N. Engl. J. Med. 303:393, 1980. (letter) 17. Battier, A. M. Role of environmental temperature and humidity in susceptibility to disease. Arch. Environ. Health 16:565-570, 1968. 18. Baily, P. E. Neutron radiation dosimetry in high altitude flight personnele Aviat. Space Environ. Med. 53:808-817, 1982. 19. Balvanz, J., S. C. Bowman, A. Fobelets, T. Lee, K. Papamichael, and R. Yoder. Examination of the Cabin Environment of Commercial Aircraft. Ames, Iowa: Iowa State University, 1982. 20. Banaszak, E. F., J. Barboriak, J. Fink, G. Scanlon, D. Schlueter, A. Sosman, W. Thiede, and G. Unger. Epidemiologic studies relating thermophilic fungi and hypersensitivity lung syndromes. Am. Rev. Respir. Dis. 110:585-591, 1974.

173 Barth, D. S., J. C. Romanovsky, J. H. Knelson, A. P. Altshuller, and R. J. Horton. National air quality standards for automotive pollutants: A critical review. J. Air Pollut. Control Assoc. 21:544-548, 1971. 22. Bloch, A. B., W. A. Orenstein, W. M. Ewing, W. H. Spain, G. F. Mallison, K. L. Herrmann, and A. R. Hinman. Measles outbreak in a pediatric practice: Airborne transmission in an office setting. Pediatrics 75:676-683, 1985. 23. Bourchier, D., K. P. Dawson, and D. M. Fergusson. Humidification in viral croup: A controlled trial. Aust. Paediatr. J. 20:289-291, 1984. 24. Brabets, R. I., C. K. Hersh, and M. J. Klein. Ozone measurement survey in commercial jet aircraft. J. Aircraft 4:59-64, 1967. Bramlitt, E. T. Commercial aviation crewmember radiation doses. Health Phys. 49:945-948, 1985 . Bramlitt, E. T. Radiation safety requirements for crewmembers: Petition for rulemaking. Federal Register 49:31298, 1984. Brockett, R. M., and J. K. Ferguson. Microbiological sampling of the spacecraft atmosphere during a simulated Skylab mission. Aviat. Space Environ. Med. 46:30-32, 1975. 28. Brockett, R. M., J. K. Ferguson, and M. R. Henney. Prevalence of fungi during Skylab missions. Appl. Environ. Microbiol. 36:243-246, 1978. 29. Brunekreef, B., P. Fischer, B. Remijn, R. van der Lende, J. Schouten, and P. QuanJer. Indoor air pollution and its effect on pulmonary function of adult non-smoking women. III. Passive smoking and pulmonary function. Int. J. Epidemiol. 14:227-230, 1985.

174 30. Burge, H. A. Indoor sources for airborne microbes in indoor air and human health, pp. 139-148. In R. B. Gammage and S. V. Kaye, Eds. Indoor Air and Human Health. Chelsea, Mich.: Lewis Publishers, 1985. 31. Cabin ozone concentrations. Code of Federal Regulations, Title 14, Pt. 25.832. Washington, D.C.: U.S. Government Printing Office, 1985. 32. Cain, W. S., B. P. Leaderer, R. Isseroff, L. G. Berglund, R. J. Huey, E. D. Lipsitt, and D. Perlman. Ventilation requirements in buildings. I. Control of occupancy odor and tobacco smoke odor. Atmos. Environ. 17:1183-1197, 198 33. Cain, W. S., T. Tonun, L. C. See, and B. Leaderer. Environmental tobacco smoke: Sensory reactions of occupants. Atmos. Environ. 1986. (in press) 34. Cawley, B. M., W. N. Sullivan, M. S. Schechter, and J. U. McGuire. Desirability of three synthetic pyrethroid aerosols for aircraft disinfection. Bull. WHO 51:537-540, 1974. 35. Chan, W. C., and S. C. Fung. Lung cancer in non-smokers in Hong Kong, pp. 199-202. In E. Grundmann, J. Clemmesen, and C. S. Muir, Eds. Geographical Pathology in Cancer Epidemiology. Cancer Campaign. Vol. 6. Cancer Epidemiology. Stuttgart: Gustaav Fischer Verlag, 1982. 36. Clausen, G. H., P. O. Fanger, W. S. Cain, and B. P. Leaderer. Stability of tobacco smoke odor in enclosed spaces, pp. 437-441. In B. Berglund, T. Lindvall, and J. Sundell, Eds. Indoor Air: Sensory and Hyperreactivity Reactions to Sick Buildings. Vol. 3. Stockholm: Swedish Council for Building Research, 1984. Clayton, A. J., D. C. O'Connell, R. A. Gaunt, and R. E. Clarke. Study of the microbiological environment within long- and medium-range Canadian Forces aircraft. Aviat. Space Environ. Med. 47:471-472, 1976.

175 38. Cohen, D., S. F. Arai, and J. D. Brain. Smoking impairs long-term dust clearance from the lung. Science 204:514-517, 1979. Comstock, G. W., M. B. Meyer, K. J. Helsing, and M. S. Tockman. Respiratory effects on household exposures to tobacco smoke and gas cooking. Am. Rev. Respir. Dis. 124:143-148, 1981. 40. Corboy, J. M., and J. C. Tannehill. Effects of air travel on contact lens wearers. Am. J. Ophthalmol. 76:166-167, 1973. 41. Correa, P., L. W. Pickle, E. Fontham, Y. Lin, and W. Haenazel. Passive smoking and lung cancer Lancet 2:595-597, 1983. 42. Dahms, T. E., J. F. Bolin, and R. G. Slavin. Passive smoking: Effects on bronchial asthma. Chest 80:530-534, 1981. 43. Disinsection of aircraft. Code of Federal Regulations, Title 42, Pt. 71.44. Washington, D.C.: U.S. Government Printing Office, 1985. 44. Duncan, D. B., and P. P. Greaney. Passive smoking and uptake of carbon monoxide in flight attendants. JAMA 251:2658-2659, 1984. (letter) Elliott, L. P., and D. R. Rowe. Air quality during public gatherings. J. Air Pollut. Control Assoc. 25:635-636, 1975. 46. Eng, W. G., L. K. Harada, and L. S. Jagerman. The wearing of hydrophilic contact lenses aboard a commercial jet aircraft. I. Humidity effects on fit. Aviat. Space Environ. Med. 53:235-23B, 1982. 47. Ferin J., G. Urbankova, and A. Vlckova. Influence of tobacco smoke on the elimination of particles from the lungs. Nature 206:515-516, 1965. 48. Flight time limitations: All flight crewmembers. Code of Federal Regulations, Title 14, Pt. 121.471. Washington, D.C.: U.S. Government Printing Office, 1985.

176 49. Foliart, D., N. L. Benowitz, and C. E. Becker. Passive absorption of nicotine in airline flight attendants. New Eng1. J. Med. 308:1105, 1983. (letter) 50. Folinsbee, L. J., B. L. Drinkwater, J. F. Bedi, and S. M. Horvath. The influence of exercise on the pulmonary function changes due to exposure to low concentrations of ozone, pp. 125-145. In L. J. Folinabee, Ed. Environmental Stress: Individual Herman Adaptations. New York, N.Y.: Academic Press, 1978. 51. Gallup Organization, Inc. 1985 Air Travel Survey. Washington, D.C.: Air Transport Association of America, 1985. Garfinkel, L., O. Auerbach, and L. Joubert. Involuntary smoking and lung cancer: A case-control study. JNCI 75:463-469, 1985. Garland, C., E. Barrett-Connor, L. Suarez, M. H. Criqui, and D. L. Wingard. Effects of passive smoking on ischemic heart disease mortality of nonsmokers. Am. J. Epidemiol. 121:645-650, 1985. 54. Gelperin, A. Humidification and upper respiratory infection incidence. Heating/Piping/Air Conditioning 45~3~:77-78, 1973. Gillis, G. R., D. J. Hole, V. M. Hawthorne, and P. Boyle. The effect of environmental tobacco smoke in two urban communities in the west of Scotland. Eur. J. Respir. Dis. 65(Suppl. 133~:121-126, 1984. 56. Green, G. H., K. Sareen, and A. D. Osborne. The effect of ventilation and relative humidity upon airborne bacteria in schools. ASHRAE Trans. 91~2a):13-28, 1985. 57. Hahn, A., S. D. Anderson, A. R. Morton, J. L. Black, and K. D. Fitch. A reinterpretation of the effect of temperature and water content of the inspired air in exercise-induced asthma. Am. Rev. Respir. Dis. 130:575-579, 1984.

177 58. Halfpenny, P. F., and P. S. Starrett. Control of odor and irritation due to cigarette smoking aboard aircraft. ASHRAE J. 3~3~:39-44, 1961. 59. Heuss, J. M., G. J. Nebel, and J. M. Colucci. National air quality standards for automotive pollutants: A critical review. J. Air Pollut. Control Assoc. 21:535-544, 1971. 60. Biller, F. C. Deposition of sidestream cigarette smoke in the human respiratory tract. Prev. Med. 13:602-607, 1984. 61. Biller, F. C., K. T. McCusker, M. K. Mazumder, J D. Wilson, and R. C. Bone. Deposition of sidestream cigarette smoke in the human respiratory tract. Am. Rev. Respir. Dis. 124:406-408, 1982. . 62. Hirayama, T. Cancer mortality in nonsmoking women with smoking husbands based on a large-scale cohort study in Japan. Prev. Med. 13:680-690, 1984. 63. Hirayama, T. Non-smoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan. Br. Med. J. 282:183-185, 1981. 64. Hoffmann, D., N. J. Haley, K. D. Brunnemann, J. D. Adams, and E. L. Wynder. Cigarette Sidestream Smoke: Formation, Analysis and Model Studies on the Uptake by Nonsmokers. U.S. Japan Meeting, New Etiology of Lung Cancer, Honolulu, Hawail, March 21-23, 1983. 65. Horvath, S. M., J. A. Gliner, and L. J. Folinebee. Adaptation to ozone: Duration of effect. Am. Rev. Respir. Dis. 123:496-499, 1981. 66. Horvath, S. M., J. A. Gliner, and J. A. Matsen-Twisdale. Pulmonary function and maximum exercise responses following acute ozone exposure. Aviat. Space Environ. Med. 50:901-905, 1979.

178 Huber, G. L. Small-airways dysfunction in passive smokers. N. Engl. J. Med. 303:392-393, 1980. (letter) 68. International Commission on Radiological Protection. Statement from the 1983 Meeting of the International Commission on Radiological Protection. Ann. ICRP 14~1~:v-vii, 1984. 69. International Radiological Protection Commission, Task Group on Lung Dynamics. Deposition and retention models for internal dosimetry of the human respiratory tract. 12:173-207, 1966. 70. Jagerman, L. S. Health Physics Effects of air travel on contact-lens wearers. Am. J. Ophthalmol. 75:533, 1973. 71. Japanese beetle. Code of Federal Regulations, Title 7, Pt. 301.48. Washington, D.C.: U.S. Government Printing Office, 1985. 72. Jennings, L. C., and J. L. Faoagali. A study of the susceptibility of Antarctic winter--over personnel to viral respiratory illness on their return to New Zealand. N. Z. Antarctic Record 3~1~:29-30, 1980. 73. Kang, B., and J. L. Chang. Allergenic impact of inhaled arthropod material. Clin. Rev. Allergy 3:363-375, 1985. 74. Kauffmann, F., D. W. Dockery, F. E. Speizer, and B. G. Ferris, Jr. Respiratory symptoms and lung function in women with passive and active smoking. Am. Rev. Respir. Dis. 133:A157, 1986. 75. Kauffmann, F., J. F. Tessier, and P. Oriol. Adult passive smoking in the home environment: A risk factor for chronic airflow limitation. Am. J. Epidemiol. 117:269-280, 1983. 76. Kentner, M., G. Triebig, and D. Weltle. The influence of passive smoking on pulmonary function: A study of 1,351 office workers. Prev. Med. 13:656-669, 1984.

179 77. Kerka, W. F., and C. M. Humphreys. Temperature and humidity effect on odor perception. ASHRAE Trend. 62: 531-552, 1956. 78. Klus, H., and H. Kuhn. Distribution of various tobacco-smoke components among mainstream and sidestream smoke: A survey. Beitr. Tabakforech. 11:229-265, 1982. 79. Knight, V. Airborne transmission and pulmonary deposition of respiratory viruses, pp. 1-9. In V. Knight, Ed. Viral and Mycoplasmal Infections of the Respiratory Tract. Philadelphia, Pa.: Lea & Febiger, 1973. 80. Knoth, A., H. Bohn, and F. Schmidt. Passive smoking as cause of lung cancer in women non-smokers. Med. Klin. 78~2~:66-69, 1983. (in German) 81. Kohler, F. P. Asymptomatic upper urinary tract lithiasis in flying personnel. J. Urol. 86:370-372, 1961. 82. Koo, L. C., J. H-C. Ho, and D. Saw. Is passive smoking an added risk factor for lung cancer in Chinese women? J. Exp. Clin. Cancer Res. 3:277-283, 1984. 83. Kreiss, K., M. G. Gonzales, K. L. Conright, and A. R. Scheere. Respiratory irritation due to carpet shampoo: Two outbreaks. Environ. Int. 8:337-341, 1982. 84. Kulle, T. J., L. R. Sander, J. R. Hebel, and M. D. Chatham. Ozone response relationships in healthy nonsmokers. Am. Rev. Respir. Dis. 132:36-41, 1985 85. Lategola, M. T., C. E. Melton, and E. A. Higgins. Effects of ozone on symptoms and cardiopulmonary function in a flight attendant surrogate population. Aviat. Space Environ. Med. 51:237-246, 1980.

180 86. Lategola, M. T., C. E. Melton, and E. A. Higgins. Pulmonary and symptom threshold effects of ozone in airline passengers and cockpit crew surrogates. Aviat. Space Environ. Med. 51:878-884, 1980. 87. Lee, P. N. (letter) Passive smoking. Lanced 1: 791, 1982. 88. Letts, R. M., and E. Doermer. Conversation in the operating theater as a cause of airborne bacterial contamination. J. Bone Joint Surg. 65:357-362, 1983. 89. Lidwell, O. M., R. W. Morgan, and R. E. O. Williams. The epidemiology of the common cold. IV. The effect of weather. J. Hyg. Camb. 63: 427-439, 1965 . 90. LilJedahl, L. A., H. J. Retzer, W. N. Sullivan, M. S. Schechter, B. M. Cawley, N. O. Morgan, C. M. Amyx, B. A. Schiefer, E. J. Gerberg, and R. Pal. Aircraft disinfection: The physical and insecticidal characteristics of (+~-phenothrin applied by aerosol at "blocks away." Bull. WHO 54:391-396, 1976. 91. Loosli, C. G., H. M. Lemon, O. H. Robertson, and E. Appel. Experimental air-borne influenza infection. I. Influence of humidity on survival of virus in air. Proc. Sac. Exp. Biol. Med. 53:205-206, 1943. Los Angeles County Air Pollution Control District. Study of Jet Aircraft Emissions and Air Quality in the Vicinity of the Lon Angeles International Airport. APTD-0662. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, Air Pollution Control Office, 1971. (available from NTIS as PB-198699) 93. Lozano, E. R., W. W. Melvin, Jr., and S. Hochheiser. Air pollution emissions from jet engines. J. Air Pollut. Control Assoc. 18:392-394, 1968.

181 94. Lufthansa German Airlines. Report on Air Quality Study with Half Pack Operation: 747. (unpublished, 1982) 95. MacMahon, B. Prenatal x-ray exposure and childhood cancer. JNCI 28:1173-1191, 1962. 96. MacMahon, B., and G. B. Hutchison. Prenatal x-ray and childhood cancer: A review. Acta Un. Int. Caner. 20:1172-1174, 1964. 97. McDonnell, W. F., D. H. Horstman, M. J. Hazucha, E. Seal, Jr., E. D. Haak, S. A. Salaam, and D. E. House. Pulmonary effects of ozone exposure during exercise: Dose-response characteristics. J. Appl. Physiol. 54:1345-1352, 1983. 98. Melia, R. J. W., C. du V. Florey, R. W. Morris, B. D. Goldstein, H. H. John, D. Clark, I. B. Craighead, and J. C. Mackinlay. Childhood respiratory illness and the home environment. II. Association between respiratory illness and nitrogen dioxide, temperature and relative humidity. Int. J. Epidemiol. 11:164-169, 1982. 99. Mendez Martin, A. Urolithiasis among flight personnel. Med. Clin. (Barcelona):72:65-70, 1979. (in Spanish) 100. Miyamoto, J. Degradation, metabolism and toxicity of synthetic pyrethroids. Environ. Health Perspect. 14:15-28, 1976. 101. Mohler, S. R. Physiologically Tolerable Decompression Profiles for Supersonic Transport Type Certification. AM 70-12. Washington, D.C.: U.S. Federal Aviation Administration, Office of Aviation Medicine, 1970. 102. Morey, P. R., M. J. Hodgson, W. G. Sorenson, G. J. Kullman, W. W. Rhodes, and G. S. Visvesvara. Environmental studies in moldy office buildings: Biological agents, sources, and preventive measures. Ann. Am. Conf. Gov. Ind. Hyg. 10:21-35, 1984.

182 103. Morris, J. E. W. Microbiology of the submarine environment. Proc. R. Sac. Med. 65:799-800, 1972. 104. Moser, M. R., T. R. Bender, H. S. Margolis, G. R. Noble, A. P. Kendal, and D. G. Ritter. An outbreak of influenza aboard a commercial airliner. Am. J. Epidemiol. 110:1-6, 1979. 105. Muchmore, H. G., A. J. Parkison, J. E. Humphries, E. N. Scott, D. A. McIntosh, L. V. Scott, M. K. Cooney, and J. A. R. Miles. Persistent parainfluenza virus shedding during isolation at the South Pole. Nature 289:187-189, 1981. 106. Murray, A. L., and P. S. Lawrence. Sequelae to smoking cessation: A review. Clin. Psychol. Rev 4:143-157, 1984. . 107. Nastrom, G. D., J. D. Holdeman, and P. J. Perkins. Measurements of cabin and ambient ozone on B747 airplanes. J. Aircraft 17: 246-249, 1980 108. National Council on Radiation Protection and Measurements. A Review of NCRP Radiation Dose Limit for Embryo and Fetus in Occupationally-Exposed Women. NCRP Report 53. Washington, D.C.: National Council on Radiation Protection and Measurements, 1977. 109. National Council on Radiation Protection and Measurements. Natural Background Radiation in the United States. NCRP Report 45. Washington, D.C.: National Council on Radiation Protection and Measurements, 1975. 110. National Research Council, Committee on Indoor Pollutants. Indoor Pollutants. Washington, D.C.: National Academy Press, 1981. 111. Newman, W. H., and M. R. Viele. Engine Bleed Air Reduction in DC-10. NASA-CR-159846. Long Beach, Cal.: Douglas Aircraft Company, 1980.

183 112. Oakley, D. T. Natural Radiation Exposure in the United States. ORP/SID 72-1. Washington, D.C.: U.S. Environmental Protection Agency, Office of Radiation Programs, 1972. 113. Ostberg, O., and R. Mills-Orring. Cabin Attendants' Working Environment: A Quentionnaire Study. Technical Report 180:74 T. Lulea: University of Lulea, Department of Human Work Sciences, 1980. (in Swedish) 114. Perkins, P. J., J. D. Holdeman, and D. J. Gauntner. Aircraft cabin ozone measurements on B747-100 and B747-SP aircraft: Correlations with atmospheric ozone and ozone encounter statistics. NASA TM-79060. Cleveland, Ohio: NASA Lewis Research Center, 1978. 115. Platts-Milln, T. A., F. Rawle, and M. D. Chapman. Problems in allergen standardization. Clin. Rev. Allergy 3:271-290, 1985. 116. Pregnancy Discrimination Act of 1978: An Act to Amend Title VII of the Civil Rights Act of 1964 to Prohibit Sex Discrimination on the Basis of Pregnancy. PL 95-555. U.S. Statutes at Large 92:2076-2077, 1978. 117. Pustinger, J. V., Jr., and F. N. Hodgaon. Identification of Volatile Contaminants of Space Cabin Materials. AMRL-TR-67-58. Dayton, Ohio: Monsanto Research Corporation, 1967. (available from NTIS as N67-37S51) 118. Quigley, S. Jet engine emissions. Assoc. 65:258-262, 1972. J. Ir. Med. 119. Rappaport, B. Z., T. Nelson, and W. H. Welker. The effect of low relative humidity at constant temperature on pollen asthma. J. Allergy 6:111-122, 1935. 120. Riley, R. L. Indoor airborne infection. Environ. Int. 8:317-320, 1982.

184 121. Riley, R. L. Indoor spread of respiratory infection by recirculation of air. Bull. Physiopathol. Respir. 15:699-705 9 1979. 122. Robinson, P. A., R. V. Tauxe, W. G. Winkler, and M. E. Levy. Respiratory illness in conference participants following exposure to rug shampoo. Infection Control 4:158-160, 1983. 123. Rogers, J. W. Results of FAA Cabin Ozone Monitoring Program in Commercial Aircraft in 1978 and 1979. FAA-EE-80-10. Washington, D.C.: U. S. Federal Aviation Administration, Office of Environment and Energy, 1980. 124. Sakuma, H., M. Kus~ma, S. Munakata, T. Ohaumi, and S. Sugawara. The distribution of cigarette-smoke components between mainstream and sidestream smoke. 1. Acidic components. Beitr. Tabakforsch. 12:63-71, 1983. 125. Sakuma, H., M. Kusama, K. Yamaguchi, T. Matsuki, and S. Sugawara. The distribution of cigarette-smoke components between mainstream and sidestream smoke. 2. Bases. Beitr. Tabakforsch. 12:199-209, 1984. 126. Sakuma, H., M. Kusama, K. Yamaguchi, and S. Sugawara. The distribution of cigarette-smoke components between mainstream and nidestream smoke. 3. Middle and higher boiling components. Beitr. Tabakforsch. 12:2S1-258, 1984. 127. Sandler, D. P., R. B. Everson, and A. J. WilcOxe Passive smoking in adulthood and cancer risk. Am. J. Epidemiol. 121:37-48, 1985. 128. Sandler, D. P., R. B. Everson, A. J. Wilcox, and J. P. Browder. Cancer risk in adulthood from early life exposure to parents' smoking. Am. J. Public Health 75:487-492, 1985. 129. Sandler, D. P., A. J. Wilcox, and R. B. Everson. Cumulative effects of lifetime passive smoking on cancer risk. Lancet 1:312-315, 1985. (preliminary communication)

185 130. Schaefer, H. J. Comparative Evaluation of Exposure Distributions for Air Travelers and Radiation Workers. NAMRL-1159. Pensacola, Fla. Naval Aerospace Medical Research Laboratory, 1972. (available from NTIS as AD-743482) 131. Schaefer, H. J. Radiation exposure on high-altitude passenger flights. Adv. Biol. Med. Phys. 13:153-206, 1970. 132. Schechter, M. S., and W. N. Sullivan. Gas-propelled aerosols and micronized dusts for control of insects in aircraft. II. Pesticide formulations. J. Econ. Entomol. 65:1444-1447, 1972. 133. Schievelbein, H., and F. Richter. The influence of passive smoking on the cardiovascular system Prev. Med. 13:626-644, 1984. , - 134. Schmeltz, I., A. dePaolis, and D. Hoffmann. Chemical studies in tobacco smoke. 31. Phytosterols in tobacco: Quantitative analysis and fate in tobacco combustion. Beitr. Tabakforsch. 8:211-218, 1975. 135. Schoettlin, C. E., and E. Landau. Air pollution and asthmatic attacks in the Los Angeles area. Public Health Rep. 76:545-548, 1961. 136. Shabad, L. M., and G. A. Smirnov. Aircraft engines as a source of carcinogenic pollution of the environment [benzo~a~pyrene studies]. Atmos Environ. 6:153-164, 1972. 137. Shephard, R. J., R. Collins, and F. Silverman. "Passive" exposure of asthmatic subjects to cigarette smoke. Environ. Res. 20:392-402, 1979. 138. Sheppard, D., W. L. Eschenbacher, H. A. Boushey, and R. A. Bethel. Magnitude of the interaction between the bronchomotor effects of sulfur dioxide and those of dry (cold) air. Am. Rev. Respir. Dis. 130:52-55, 1984.

186 139. Smeaton, M. J., P. J. Slater, and P. Robnon. Malaria from a 'tcommutert' mosquito. Lancet 1:845-846, 1984. (letter) 140. Speer, F. Tobacco and the nonsmoker: A study of subjective symptoms. Arch. Environ. Health 16:443-446, 1968. 141. Spendlove, J. C., and K. F. Fannin. Source, significance, and control of indoor microbial aerosols: Human health aspects. Public Health Rep. 98:229-244, 1983. 142. Spengler, J. D., D. W. Dockery, W. A. Turner, J. M. Wolfson, and B. G. Ferris, Jr. Long-term measurements of respirable sulfates and particles inside and outside homes. Atmos. Environ. 15:23-30, 1981. 143. Stahl, W. H., Ed. Compilation of Odor and Taste Threshold Values Data. DS48. Philadelphia, Pa.: American Society for Testing and Materials, 1973. 144. Stewart, A., and G. W. Kneale. Age-distribution of cancers caused by obstetric x-rays and their relevance to cancer latent periods. Lancet 2:4-8, 1970. 145. Stewart, A., and G. W. Kneale. Changes in the cancer risk associated with obstetric radiography. Lancet 1:104-107, 1968. 146. Stewart, A., J. Webb, and D. Hewitt. A survey of childhood malignancies. Br. Med. J. 1:1495-1508, 1958. 147. Sullivan, W. N., R. Pal, J. W. Wright, J. C. Azurin, R. Okamoto, J. U. McGuire, and R. M. Waters. Worldwide studies on aircraft disinfection at "blocks away." Bull. WHO 46:485-491, 1972. 148. Thayer, W. W. Tobacco smoke dilution recommendations for comfortable ventilation. ASHRAE Trans. 88~2~:291-306, 1982.

187 149. Toxic and hazardous substances. Code of Federal Regulations, Title 29, Pt. 1910.1000. Washington, D.C.: U.S. Government Printing Office, 1985. 150. Trichopoulos, D., A. Kalandidi, L. Sparros, and B. MacMahon. Lung cancer and passive smoking. Int. J. Cancer 27:1-4, 1981. 151. U.S. Bureau of the Census. Statistical Abstract of the United States, 1985, 105th ed. Washington, D.C.: U.S. Government Printing Office, 1984. 152. U.S. Centers for Disease Control. Disinsection of aircraft. Federal Register 44~12 Oct.~:58912, 1979. 153. U.S. Civil Aeronautics Board. Part 252 - Smoking Aboard Aircraft: Final Rule. Amendment 1 to Part 252. Docket 29044. Washington, D.C.: U.S. Civil Aeronautics Board, 1983. 154. U.S. Environmental Protection Agency. Air Quality Criteria for Particulate Matter and Sulfur Oxides. EPA-600/8-82/029a. 3 vol. Washington, D.C.: U.S. Environmental Protection Agency, 1982. 155. U.S. Environmental Protection Agency. Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An Addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide. EPA-600/8-83/033F. Washington, D.C.: U.S. Environmental Protection Agency, 1984. 156. U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office. Air Quality Criteria for Ozone and Other Photochemical Oxidants: External Review Draft No. 2. Vol. V. EPA-600/8-84-020B~ Research Triangle Park, N.C.: U.S. Environmental Protection Agency, Environmental Criteria and Assessment Office, 1985. 157. U.S. Federal Aviation Administration. Aircraft cabin ozone contamination: Advance notice of proposed rulemaking. Federal Register 42~6 Oct.~: 54427-54428, 1977. .

188 158. U.S. Federal Aviation Administration. FAA Aviation Forecasts, Fiscal Years 1985-1996. FAA-APO-85-2. Washington, D.C.: U.S. Federal Aviation Administration, 1985. 159. U.S. Federal Aviation Administration. Ozone Irritation During High Altitude Flight. Advisory Circular 00-52. Washington, D.C.: U.S. Federal Aviation Administration, 1977. 160. U.S. Federal Aviation Administration and U.S. National Institute for Occupational Safety and Health. Health Aspects of Smoking in Transport Aircraft. Cincinnati, Ohio: National Institute for Occupational Safety and Health, 1971. (available from NTIS as AD736097) 161. U.S. Surgeon General. Chronic Obstructive Lung Disease. DHHS (PHS) 84-50205. Washington, D.C.: U.S. Government Printing Office, 1984. 162. U.S. Surgeon General. The Health Consequences of Smoking: Cardiovascular Disease. Washington, D.C.: U. S. Government Printing Office, 1983. 163. Ventilation. Code of Federal Regulations, Title 14, Pt. 25.831. Washington, D.C.: U.S. Government Printing Office, 1985. 164. Vieillefond, H., P. Fourn, and R. Auffret. Characteristics in the atmosphere of long-range transport aircraft cabins. Aviat. Space Environ. Med. 48:503-507, 1977. 165. Wallace, R. W., and C. A. Sondhaun. Cosmic radiation exposure in subsonic air transport. Aviat. Space Environ. Med. 49:610-623, 1978. 166. Warhurst, D. C., C. F. Curtis, and G. B. White. A commuter mosquito's second bite? Lancet 1:1303, 1984. (letter) 167. Watkins, H. M. S. Epidemiologic investigations in Polaris submarines, pp. 9-53. In I. H. Silver, Ed. Aerobiology: Proceedings of the Third International Symposium on Aerobiology, University of Sussex, England, Sept. 1969. New York, N.Y.: Academic Press, 1970.

189 168. Weber, R. Travel involving long-distance flights: health rinks. Med. Monataschr. Pharm. 7~5~:147-151, 1984. (in German) 169. Weber, A., and T. Fischer. Passive smoking at work. Int. Arch. Occup. Environ. Health 47:209-221, 1980. 170. Weber, A., T. Fischer, and E. GrandJean. Passive smoking in experimental and field conditions. Environ. Res. 20:205-216, 1979. 171. Weber, A., T. Fischer, and E. GrandJean. Passive smoking: Irritating effects of the total smoke and the gan phase. Int. Arch. Occup. Environ. Health 43:183-193, 1979.

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Each year Americans take more than 300 million plane trips staffed by a total of some 70,000 flight attendants. The health and safety of these individuals are the focus of this volume from the Committee on Airliner Cabin Air Quality. The book examines such topics as cabin air quality, the health effects of reduced pressure and cosmic radiation, emergency procedures, regulations established by U.S. and foreign agencies, records on airline maintenance and operation procedures, and medical statistics on air travel. Numerous recommendations are presented, including a ban on smoking on all domestic commercial flights to lessen discomfort to passengers and crew, to eliminate the possibility of fire caused by cigarettes, and to bring the cabin air quality into line with established standards for other closed environments.

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