Influenza A has a clear seasonal pattern in temperate regions, yet the underlying cause for it remains controversial despite nearly a century of investigation. The literature identifies numerous factors that may influence influenza's seasonality: environmental conditions such as temperature, humidity, and ultraviolet radiation; immune function; school schedules; and human mobility patterns and contact rates 
. Among these, the leading contenders are humidity and temperature 
, and in indoor environments, where people spend ~90% of their time, humidity is the more variable factor. Particularly in the developed world where heating, ventilation, and air conditioning systems (HVAC) are the norm, indoor temperature tends to fall in a narrower range, and thus its influence is limited. Recent studies using a guinea pig experimental model 
indicate that low relative humidity (RH) favors aerosol transmission of influenza A viruses (IAVs), in which they are transmitted by small respiratory droplets expelled from infected hosts. Nevertheless, the precise mechanisms by which humidity might influence influenza viability and transmissibility via the aerosol route have not been elucidated.
Humidity may affect airborne IAV transmission via two important variables. The first is droplet size. When released from the respiratory tract (assumed to have 100% RH), droplets experience rapid evaporation and shrinkage upon encountering the unsaturated ambient atmosphere. The ultimate size of a droplet depends on ambient humidity, and size determines aerodynamic behavior and whether the droplet will settle to the ground quickly or remain suspended in the air long enough to possibly cause a secondary infection. Previous studies on evaporation of respiratory droplets usually used water or simple saline solutions (e.g., NaCl) to simulate respiratory fluid 
. However, respiratory fluid is a complicated combination of water, salts, and various organic compounds 
that affect the thermodynamics of evaporation, compared to pure water or saline solutions. The equilibrium droplet size is affected by surface curvature and solute effects, the combination of which is described by Köhler theory 
. While the vapor pressure is enhanced over curved versus flat surfaces, it is reduced by the presence of solutes. These competing effects are magnified at smaller droplet diameters and determine the equilibrium size at a particular RH.
The second variable that is sensitive to humidity is IAV viability 
. Hemmes et al. 
linked influenza's seasonality to the seasonal oscillation of RH indoors, based on their experiment on death-rate variation versus RH. Shaman and Kohn 
, on the other hand, concluded that absolute humidity (AH) rather than RH modulates influenza seasonality through constraint on viability, but whether AH or RH is controlling is under debate. For our purposes, differentiating between the two is not possible because this work focuses on a narrow range of typical indoor temperatures. Finally, it is possible that the two variables—final droplet size and viability—are linked, if evaporation and subsequent concentration of solutes in respiratory droplets affects IAV viability in aerosols.
Elucidating the causes of influenza's seasonality will require improved comprehension of transmission mechanisms, especially the aerosol route. To advance a mechanistic understanding of the role of humidity in aerosol transmission, we model the change in size of respiratory droplets and IAV inactivation at RHs ranging from 10% to 90%. Based on these results, we further model the dynamics of droplets emitted from a cough in an indoor environment and illustrate the evolution of infectious IAV concentrations and size distributions, considering removal by gravitational settling, ventilation, and viral inactivation. We are thus able to determine the magnitude by which humidity affects airborne concentrations of infectious IAVs.