Infectious diseases have been major drivers of evolution and of human evolution in particular. The vast majority of infections are acquired from the environment or transmitted from humans or other animals. Therefore, factors that affect the physical environment, how we build in it, and how we share it with other humans are critical determinants of the infections to which we are exposed and how we perpetuate the exposures. Seasonal variation—a complex summing of multiple influences ranging from sunlight to moisture to wind speed and varying by region—has also been recognized as a critical influence on infectious-disease epidemiology dating back to Hippocrates (Naumova, 2006). Thus, climate change in general and indoor-air exposure in particular are major elements in the spread or interruption of infectious diseases in humans. Despite the extensive knowledge base on the effects of climate change on environmental growth of microorganisms and their vectors and hence infections, however, data on the effects of climate change on indoor air and infectious diseases are incomplete.
This section briefly reviews some of the most pertinent model systems that highlight elements of the knowledge in direct effects of climate on infectious disease. It explores them by category of infection, inasmuch as each kingdom (for example, bacteria, fungi, and viruses) has distinct features and is involved in different processes and exposures. One critical factor is that air and moisture, and therefore water, are inextricably linked. Most microorganisms are exquisitely sensitive to moisture, either requiring it or avoiding it. Therefore, the study of indoor air is closely linked to the state of indoor water, its aerosols, and the magnitude of humidity. Furthermore, pipes and other water-delivery systems are prone to development of biofilms, thin, removal-resistant layers of metabolically inaccessible bacteria that are constantly available for release into water and indoor air through taps, showers, humidifiers, and the like.
Experience dating back thousands of years has taught that infectious diseases can be affected by seasonal changes; this suggests that environment plays a critical role in the modulation of disease load, spread, and susceptibility. Obvious and recurring examples are provided by the respiratory viruses, most notably influenza viruses, respiratory syncytial virus (RSV), and the rhinoviruses. Mechanisms of spread are varied and include aerosol, fomite,1 and direct contact. Direct contact, such as hand-to-hand transfer, is the most easily modified and is a major contributor to the spread of respira-
1 Fomites are inanimate objects or substances—a door knob, for example—that function to transfer infectious organisms from one individual to another.