Abstract
Coughing, sneezing, talking, bed-making, turning pages of books, etc. all generate microbial aerosols which are carried and dispersed by air movements. Inhalation of these particles may cause allergic responses but whether or not infectious disease ensues depends in part on the viability and infectivity of the inhaled microbes and their landing sites. Desiccation is experienced by all airborne microbes; gram-negative bacteria and lipid-containing viruses demonstrate phase changes in their outer phospholipid bilayer membranes owing to concomitant changes in water content and/or temperature. These changes most likely lead to cross-linking reactions of associated protein moieties principally at mid to high relative humidity (RH). For lipid-free viruses these reactions of their surface protein moieties occur most rapidly at low RH. Radiation, oxygen, ozone and its reaction products and various pollutants also decrease viability and infectivity through chemical, physical and biological modification to phospholipid, protein and nucleic acid moieties. The extent of damage and the degree of repair together with the efficacy of host defence mechanisms largely controls whether the causative microbes take hold and spread disease via the airborne route. At least indoors, where desiccation is the predominant stress, the general reversibility of membrane-phase changes by vapour-phase rehydration when coupled with efficacious microbial enzymatic repair mechanisms under genetic control, virtually ensures the spread of disease by the aerobiological pathway.
