Microbes in the Air
In 2018, many of us were startled by the news that antibiotic-resistant bacteria and genes could spread over long distances through air. 5 Furthermore, the research showed that antibiotic-resistant genes could be passed laterally to other airborne bacteria, immediately conferring resistant to treatment.
We already knew that indiscriminate use of antibiotics had forced the emergence of treatment-resistant bacteria, such as MRSA. Furthermore, we could take some comfort in the logical conclusion that controlling the use of antibiotics would contain and eventually reverse the spread of resistance microbes. Unfortunately, the World Health Organism (WHO) now says otherwise, stating that reducing the use of antibiotics alone will not reverse the trend because of the magnitude of the pool of resistant bacteria and genes that will continue to spread through environmental vectors, such as the air. 6, 6a
So, how can we control the spread of treatment-resistant pathogens?
New findings map bacterial resistance in humans to external sources (waste-water treatment plants, hospitals, animal farms using antibiotics, etc.) from which airborne transmission has occurred. The emission source of resistant microbes can be far away, with ARB and ARG travelling great distances through the atmosphere on fine airborne particles. This pattern, distinct from the spread of resistance through survival pressure following ingestion of antibiotics, has established the key connection between airborne PM2.5 and treatment-resistant pathogens.
Airborne particulate matter not only carries ARB and ARG, but inhalation of PM2.5 also makes the human airway more susceptible to infection. After inhalation, ambient PM2.5 stimulates the transfer of ARGs between the donor bacteria and recipient airway cell through inflammatory changes, such as changes in membrane permeability and alterations in the expression of genes involved in the transfer process. In urban areas with high levels of PM2.5, counts of inhaled ARGs range from 103 to 104 copies/day/adult. 7
In addition to PM2.5, inhalation of oxidative gases, such as O3 and NO2, alter airway cell permeability and protective microbes, increasing the vulnerability of exposed people to respiratory infections from ARB. Ozone also degrades chromosomal polypeptides, releasing free ARG into respiratory secretions and exhaled droplets, so that humans themselves are a source of ARGs and ARB. 8
More research is needed to understand and quantify the role of airborne pollutants in the transmission of antibiotic resistance. Despite the unknowns; however, the critical nature of controlling antibiotic resistance is enough to elevate management of IAQ to the top of our priority list.
The role of the indoor environment in shaping health is finally coming into focus — partly thanks to the COVID-19 pandemic. We are now calling on you, the IAQ professional, because you hold the hope for a better future.