So-called superspreading events and even “superspreader” individuals have defined the COVID-19 pandemic from the beginning. Individuals characterized as superspreaders have a higher propensity of transmitting the infection to others, even if they are asymptomatic themselves.
But what makes a person a superspreader? Researchers at Tulane University, Harvard University, MIT and Massachusetts General Hospital recently identified three factors that correlate to increased spread of COVID-19—obesity, age and date of infection.
SARS-CoV-2 transmits through the air via large droplets exhaled when someone coughs or sneezes, as well as small droplets people generate when they naturally breathe. However, the researchers discovered that the exhaled aerosol particles vary greatly between individuals.
Using data from 194 healthy people as well as non-human primates with COVID-19, the researchers characterized subjects as low spreaders—those who exhale less than 156 particles per liter of air—or high spreaders—those who exhale greater than 150 particles/L.
Next, the researchers looked at how a person’s age, sex and body mass index (BMI) affect the number of exhaled aerosol particles. While there was no correlation with sex, both age and BMI were factors—specifically BMI-years, which researchers generated by multiplying age x BMI.
According to the study results, published in PNAS, 50% of individuals with less than 650 BMI-years exhaled “significantly less aerosol” than the half of the group with more than 650 BMI-years. Essentially, the elderly, the obese and the obese elderly are at a heightened risk of transmission. Conversely, study participants younger than 26 and those under 22 BMI were all found to be low spreaders.
Within the high-producing group (> 156 particles/L), 18% of individuals accounted for 80% of the exhaled particles. The distribution follows the 20/80 rule seen in other infectious disease epidemics, meaning 20% of infected individuals are responsible for 80% of transmissions.
“We've seen a similar increase in droplets during the acute infection stage with other infectious diseases like tuberculosis," said Chad Roy, corresponding author and director of infectious disease aerobiology at the Tulane National Primate Research Center. "It seems likely that viral and bacterial infections of the airway can weaken airway mucus, which promotes the movement of infectious particles into this environment."
The scientists examined the effect of lung infection on transmission in both non-human primate subjects and human subjects. In the primates, the number of exhaled breath particles began to increase starting 3 days after COVID-19 infection, and continued to rise through day 7, when the number started to drop until almost baseline levels by day 14. Meanwhile, an extraordinarily high number of exhaled particles were observed in an infected human subject on days 8 and 9 post-symptoms, before falling sharply on days 10 and 11.
Notably, as infection with COVID-19 progressed, viral particles got smaller, reaching the size of a single micron at the peak of infection. These tiny particles, the study authors day, are more likely to be expelled as people breathe, talk or cough. They can also stay afloat much longer, travel farther in the air and penetrate deeper into the lungs when inhaled.
While the world heads toward mass vaccination, the study authors suggest examining the behavior of exhaled aerosols as an alternative way to management COVID-19.
“It may be advisable for the scientific community to additionally focus on management of COVID-19 through the restoration of airway lining mucus barrier function, and, notably, in the reduction of the propensity of airway lining mucus to disintegrate under the force of natural breathing, which it is otherwise disinclined to do in the airways of the young and uninfected,” they conclude.