While air travel contributes to the spread of influenza epidemics, the magnitude of impact is not clear compared to other factorsa crucial issue when considering a flight ban in the context of pandemic planning. Recent modeling efforts simulating the spread of pandemic influenza have concluded that such an intervention would matter little relative to other interventions . But this assessment has now been challenged by an observational study of influenza in the winter following the post-9/11/2001 depression in air traffic. Brownstein and colleagues'' study published in the September issue of PLoS Medicine correlates variations in air traffic volume with patterns of timing and spread in influenza epidemics, based on United States mortality data from nine epidemic seasons between 1996 and 2005. While we find the study interesting, we have identified several important caveats and question the robustness of the conclusions.
The core of this study''s results lies in the observation that the 20012002 influenza epidemic immediately following 9/11 was late in the season and peaked in March (week of year 11), whereas the eight surrounding epidemics peaked between the end of December and the end of February (week of year 52 to 9). The authors attribute this delay to the 27 decline in air traffic that followed 9/11.
Given the complexities of influenza virus subtype cycling and antigenic drift ,, it is essential to consider longer-term disease data spanning much more than nine years to interpret the lateness of the 20012002 epidemic. Using US national vital statistics data covering 30 winters from 1972 to 2002 , we identified four epidemics peaking in the month of March (13), including the 20012002 epidemic following 9/11, but also two epidemics in the 1970s and the more recent 19911992 epidemic (A). Furthermore, the average timing of influenza epidemics has not changed between 1972 and 2002despite a concurrent and steady increase in air traffic volume by over 300 (A) . Indeed, during the earlier part of the last century when air traffic was minimal, influenza epidemics rapidly circulated around the world. Moreover, real-time influenza virus surveillance data from the US Centers for Disease Control and Prevention show that last winter''s (20052006) epidemic was even more delayed than the epidemic following 9/11, despite a 20 increase in air passenger traffic compared to the situation before 9/11 . Clearly, late-season influenza epidemics have occurred and are still occurring even in the absence of restrictions on air travel. Hence a longer time perspective, with observations from both prior and more recent data, challenges this study''s conclusions.
In addition to comparing the timing of influenza epidemics across different seasons, Brownstein et al. analyzed the rate of disease spread among US administrative regions for their nine seasons of interest (19962005). In our previous work, we estimated the rate of influenza spread among all US states for 30 consecutive seasons (19722002) . Our analysis shows that the epidemic following 9/11 spread at a rate comparable to other epidemics (B), even after adjusting for the subtype of circulating viruses . To increase our understanding of the spread of influenza, it is essential to quantify the relative importance of different modes of transportation. As an example, our recent study considered multiple modes of transportation (including air travel) and identified travel to and from work as a key determinant of the regional spread of epidemics .
In conclusion, Brownstein and colleagues'' analysis of the natural experiment of the post-9/11 season is innovative and ingeniousbut in and of itself could not demonstrate a robust association or a causal link between the decrease in air traffic and delayed timing of influenza epidemics. Even if there in fact had been a delay as hypothesized, the study lacked power to address the hypothesis, because this single natural experiment wa