Most of us spend most of our time indoors amidst suspended biological particles — spores, pollen, bits of dead skin, bacteria, viruses, and so on. We care about these particles because they may have human health impacts (positive or negative), effects on building materials, and possible forensic uses.
Two sources known to be important for biological particles in indoor air are: outdoor air, blown in through ventilation systems and leaked in through windows and doors; and the living occupants of a room — potentially humans, mold, dust mites, insects, rodents, plants, etc.
Our recent study in Indoor Air adds to the understanding of indoor bioaerosols through high-resolution (every 5 min) sampling that offers a glimpse into the influence of short-duration human dynamics (such as students walking into and out of a class) over the course of many days, in a way that has not been done in earlier studies, which used either short-term or time-averaged (e.g. collecting particles over a period of hours or days) approaches.
A key novelty of the bioaerosol sensor we utilized — an ultraviolet aerodynamic particle sizer (UV-APS) — is that it sizes particles as it counts them. Since size is a key parameter influencing particle behavior indoors (as was recently summarized by Brent Stephens), these data were important input parameters for the material balance model we used to quantify occupant emission rates based on observed concentrations.
In our study classroom — which, importantly, was ‘healthy’ with no history of water damage, and was located in the interior of a building with a good ventilation filtration system — we found that baseline (i.e., outdoor origin) bioaerosol concentrations were low. Levels spiked during the high-activity transitions between classes, and remained higher than the baseline even during the quiet occupancy conditions of lecture classes. During occupied periods — which are the most relevant for health impacts — people were by far the dominant source of indoor bioaerosols, across all seasons.
Here’s some more detail on our methods and areas of uncertainty.
We measured fluorescent particles in the 1-15 micron size range in a university classroom continuously during four separate weeks over the course of a year. Autofluorescence at characteristic wavelengths was treated as an indicator of biological origin, so the targeted particles were called fluorescent biological aerosol particles, or FBAPs. Emissions of numbers of FBAPs by students (via the processes of shedding and resuspension) — both in absolute terms and normalized by the mass of carbon dioxide emitted by the students — peaked in the 3-4 micron size range.
Photo courtesy of TSI Incorporated. We treated particles exhibiting fluorescence at characteristic wavelengths as proxies for biological particles (including non-microbial components such as skin flakes), and quantified them with a UV-APS (TSI, Inc.; www.tsi.com).
A caveat: Our results are based on autofluorescence. Various bioaerosol metrics are known to be influenced by room occupancy in different ways — e.g., bacteria have been more strongly linked to humans, whereas indoor fungi have been tied more strongly to outdoor sources. Moreover, our findings rely on numbers of particles; outcomes based on composition may tell a different story.
Looking forward, a host of questions remain open: We saw that classroom air particulate matter had a distinct fluorescent signal compared to urban ambient air. Occupants were the dominant proximate cause of the observed FBAPs. But what was the ultimate source of the occupant-emitted fluorescent coarse particles: the human body, building materials, consumer products, or bioaerosols that originated outdoors and were tracked in by humans or the ventilation system? What part of the fluorescent signal represents non-biological interferents, and can signatures based on size/fluorescence-intensity differentiate them from true biological particles? How useful is fluorescence as a tool for understanding the activity of indoor airborne microbes?
Overall, there remains much to learn about indoor bioaerosols. Better characterization of sources and dynamic behaviors can contribute.
[Credit to Rachel Adams for her helpful feedback]
Bhangar et al, 2014, Indoor Air (accepted article) has been posted to the Mendeley collection of articles by Sloan Foundation Microbiology of the Built Environment Program Grantees at http://www.mendeley.com/groups/949191/microbenet-collection-of-sloan-grantee-publications/
As I sat in the third row of a concert featuring 4 mezzo sopranos and a soprano, I suddenly wondered whether the audience ends up sharing “gifts” from the singers exhalations over and above the sonic delights.
Could any/some/all of the particles you detected originate via exhalation?
Indeed, it is now well known that sneezing, coughing, talking, and even breathing can be a source of airborne particles. It is also now known that the lungs are not sterile and the mouth and throat are certainly well populated with microbes. So, it follows that some of the particles leaving the human respiratory tract carry microbes. Additional support for these ideas is found from evidence that some disease transmission occurs via airborne routes. You may be interested to read an interesting editorial on the general theme, written by Prof Yuguo Li (University of Hong Kong), under the title “The Secret Behind the Mask.” (Indoor Air 21, 89-91, 2011.) Yuguo contributed to our understanding of how SARS could be transmitted via airborne routes.
Beyond particles…..into their nature and potential health impacts…. Here is a loose quote from Ed Nardell (Associate Professor of Public Health at Harvard Medical School (http://www.hsph.harvard.edu/edward-nardell/) that I find relevant to the current discussion/subject…. He has granted me permission to use his words and ideas here….
“The bottom line is that the presence of organisms does not necessarily mean risk, and the ability to monitor does not mean it is helpful to do so. Of course the biggest source of microbes in buildings are people, mostly from our gut and skin. We don’t monitor either of those sources but could – why, because we don’t know what it means and what to do with the information.
“I even object to routine sputum cultures because they come through the mouth and may not represent what is in the lungs, for example. Organisms in sputum may be lung pathogens or colonizers of the mouth.
“With molecular tests the problem is greater since the presence of DNA doesn’t even mean viability. mRNA has more significance, but even viability does not mean virulence – even for compromised sources. A whole other story with allergens like mold.”
Nardell will one of more than two dozen participants in the Sloan Symposium at Indoor Air 2014 in Hong Kong, July 7-12. More information available at http://www.indoorair2014.org. And on the Sloan Symposium that is an important part of the conference, info at http://www.indoorair2014.org/index.php/sloan-symposium#sloan.
Correction sent by Ed Nardell: It should read ““With molecular tests the problem is greater since the presence of DNA doesn’t even mean viability. mRNA has more significance, but even viability does not mean virulence – even for compromised sources hosts.—With molecular tests the problem is greater since the presence of DNA doesn’t even mean viability. mRNA has more significance, but even viability does not mean virulence – even for compromised [
sources] hosts.Please excuse me for my inability to format the correction above. the last word, “hosts,” should not be struck out; the end of the sentence should read “…even for compromised hosts.”