We observed a significant association between total hours of smoky cabin exposure and reported sinusitis and middle ear infections among never smoking FAs who worked in the airline industry when smoking was allowed on airplanes. Our findings also suggest an increase in the odds of the development of asthma among FAs with increased exposure to smoky airplane cabins.
Previous surveys of cabin crews have consistently shown high rates of upper airway symptoms but have been focused on short-term effects [3
]. SHS has been observed to be independently, positively associated with respiratory tract symptoms such as sneezing, sore throat, and cough [7
] as well as nasal rhinitis [8
]. The association of SHS exposure and sinusitis has not been extensively studied in adults and most of the evidence concerning the association of SHS with middle ear infections comes from the pediatric literature [1
]. However, a pathophysiologic basis for causality exists as SHS causes inflammation in the nasal mucosa, and non smokers may have a heightened sensitivity to SHS exposure [9
]. Unfortunately and expectedly, research on the adverse health consequences associated with SHS exposure has been hindered by tobacco industry tactics to undermine United States regulatory agencies [10
We observed a significant association between smoky cabin exposure and asthma in our cohort of FAs, consistent with previous literature. SHS exposure has been associated with asthma in adults, and available data suggest that workplace exposure may be more detrimental than domestic exposure [11
]. In a cross-sectional study of 2195 never smoking Italian women, SHS exposure from spouse and work was significantly and positively associated with an asthma diagnosis or symptoms (OR 1.50; 95% CI 1.09–2.08) [12
]. In a cross-sectional study of 4197 never smoking adults in Switzerland, SHS was significantly associated with physician-diagnosed asthma (OR 1.39; 95% CI: 1.04–1.86) [13
]. In a cross-sectional study of 6817 adult never smokers in Estonia, SHS exposure outside the home was associated with physician-diagnosed asthma (OR 1.79; 95% CI: 1.02–3.16), and SHS outside the home was strongly related to all respiratory symptoms in a dose-response manner [14
]. In a nested-case control study of adult-onset asthma, an increased odds for the development of asthma was associated with SHS (OR 2.4; 95%, CI 1.4–4.1) [15
]. In a more recent cross-sectional study of 73,605 adults in India, individuals exposed to SHS were more likely to have a diagnosis of asthma compared to non-exposed individuals (OR 1.22; 95% CI 1.08–1.38) [16
]. In a prospective study of 3914 adult non smokers, SHS was significantly associated with the development of asthma over a 10-year period [relative risk (RR) = 1.45; 95% CI: 1.21–1.75] [17
]. The extant literature and our study suggest a dose-response relationship between SHS exposure and adult-onset asthma.
The main strength of our study was that the survey was conducted in a large sample of FAs who were never smokers with a median of greater than 18,000 hours of SHS exposure in smoky cabins.
Our study has several limitations. First, the response rate to our survey was 14%. Because we did not have access to the mailing list, we did not have complete information regarding the accuracy of the address information and, therefore, could not determine the total population who received the survey. We were also unable to perform the standard survey methodology of second and third mailings followed up by telephone calls which would have increased our response rate. Nonetheless, our response rate was similar to the 17% response rate of the only other survey of FAs larger than ours (N = 3,412) [18
]. While our sample of flight attendants is the second largest reported to date, it is the largest that reports on a subset of never smokers. Given the low response rate and partial blinding to study hypotheses, we cannot rule-out a potential non response bias whereby symptomatic individuals may have been more likely to respond to the survey than asymptomatic individuals. This bias would result in overestimating the prevalence of disease in this cohort. However, under the assumption that this response bias was independent of SHS exposure, the findings from the analyses assessing the association between SHS exposure and disease would not be affected. Second, the potential for recall bias exists which is an inherent limitation of self-reported medical surveys. Third, the survey design did not allow us to associate the timing of the exposure to the timing of the diagnosis for the index disease. Finally, SHS exposure is but one factor that may have contributed to our findings. Airplane cabin supply air is known to be contaminated with smoke and fumes containing pyrolyzed engine oil and/or hydraulic fluid which has been documented to cause respiratory complaints [19
]. The air supply can also contain ozone gas in-flight and deicing fluid and/or exhaust fumes during ground operations [21
]. Since 47 countries require that cabins be sprayed either in-flight or prior to boarding, pesticide exposure is another possible exposure and has been associated with respiratory illness [24
]. FAs have also been identified as more likely to report infectious respiratory illnesses than the population of ground-based working women [26
]. Notably, the per person ventilation rate in the aircraft is typically lower than in comparable ground-based environments which elevates bioeffluent levels and contaminants from cabin cleaners/deodorizers/offgassing cabin materials [27
]. Finally, reduced barometric pressure in-flight and regular pressure changes may contribute to some respiratory conditions [28
]. However, a previous study of smoking and non smoking airline flights observed a marked reduction in respirable particles and fewer symptoms such as ocular complaints, headaches, and fatigue in non-smoking flights [4
]. This study would suggest that the elimination of SHS, with all other factors remaining the same, has a significant positive impact on the respiratory system.