As COVID-19 continues to infect people around the world and Monkey Pox has reemerged in continents previously unaffected, understanding and managing the conditions that precede the emergence of viral diseases in our population has become urgent.
Throughout history, both new and reemerging infectious diseases afflicting humans have been caused by pathogens that were passed from nonhuman animals. Genetically, viruses are extraordinarily agile — a trait that can result in jumping from nonhuman to human hosts when the challenges to infect the new species are surmountable. Viral species switching from nonhumans to humans occurs when the following triad of changes converge: The virus undergoes a genetic mutation leading to increased virulence in a previously inhospitable ecosystem, the environment presents an advantageous transmission route, and a human host with less effective immune protection is encountered.
This “perfect storm” occurred 12,000 years ago, when the neolithic revolution marked the beginning of our intrusive domestication of nature. As humans disrupted microbial (viral, bacterial, and fungal) ecosystems by clustering in villages, herding animals, and altering the soil with crop planting, evolutionarily nimble microbes responded with the emergence of zoonotic diseases, such as smallpox, malaria, measles, and the Black Death plague. From the perspective of viruses, a better name for this epoch might be, “The First Documented Microbial Rebellion!”
Humans love scapegoats. We tend to blame the microbes for outbreaks of disease. To truly control species-jumping viruses, however, we must take responsibility for our part in facilitating the formation of perfect storm conditions before the pandemics occurs.
This is where your expertise as a building professional is essential. The most immediate and powerful tool to control all three components currently driving harmful host-pathogen evolution is properly managed IAQ.
Let’s use COVID-19 as the case study to consider how IAQ impacts the host–virus relationship.
The SARS-CoV-2 virus gains entry to the human host through tissues in direct contact with the indoor environment, such as skin, or indirectly, through inhalation to the deeper regions of the respiratory tract. Components of IAQ have a direct and immediate effect on the degree of protection provided by skin and respiratory immune defenses and physiologic barriers. A healthy immune response to SARS-CoV-2 starts with the capture of viral particles by hydrated nasal and upper airway mucous, transfer by cilia away from vulnerable lung tissue, and subsequent inactivation of the virus by a cascade of immune cells with precisely timed actions. This sophisticated, protective response includes macrophages to clear particles; neutrophils to control inflammation; and dendritic cells to organize the secondary adaptive immune defense and activated lymphocytes when needed.
Poorly controlled IAQ can interfere with both immediate and long-term immune protection. For example, when indoor relative humidity (RH) is too low (less than 40%), inhaled air dries the mucous and inactivates the cilia, allowing inhaled viral aerosols to penetrate more deeply into the respiratory system. If indoor air also contains even low levels of pollutants, such as particles, ozone, or combustion byproducts, the respiratory tract becomes inflamed, fragile, and more vulnerable to infection. If an effective immune response does not stop initial penetration, the virus can gain further access to deeper tissues and damage the liver, heart, and other internal organs. On the other extreme are overcompensating and damaging immune reactions, called cytokine storms, which follow an abnormally delayed release of protective interferon. Low RH and inhaled particles or gases are associated with delayed interferon release and subsequent mismanaged steps of the immune response. In addition to maladaptive responses to respiratory infections, correlations between air pollution, asthma exacerbations, and chronic obstructive pulmonary disease (COPD) are further examples of excessive stimulation of pro-inflammatory immune responses.
Managing the Environment to Mitigate Pandemics
To combat the impact of the environment on pandemics, there are serious endeavors to stop climate change through regulating carbon emissions with net-zero goals in place.
We already know indoor pollution can be worse than outdoor pollution; the human immune system is impaired by poor IAQ; and indoor particles, VOCs, and other gases contribute to cardiovascular, respiratory, and inflammatory diseases.
While climate change needs to be controlled, these regulations may worsen IAQ if occupant health is not simultaneously protected. Sick building syndrome emerged following the Clean Air Act, which resulted in tighter buildings for energy conservation. Will efforts to attain net-zero buildings cause worsening IAQ, consequent impairment of occupant immunity, and more human vulnerability to species-jumping viruses?
When discussing environmental contributions to pandemics, the focus needs to extend beyond ambient conditions to the indoor environment. Respecting the powerful relationship between IAQ and human immune systems must become the central focus for best practice recommendations and building standards. If this relationship in a single–minded quest to reduce building energy consumption is overlooked, viral species jumps could exacerbate and worsen human health.