OOS 17-9 - Antibiotic resistance and antimicrobial chemicals in the built environment

Tuesday, August 8, 2017: 4:20 PM
Portland Blrm 258, Oregon Convention Center
Erica Hartmann1, Roxana Hickey2, Tiffany Hsu3, Jing Chen4, Clarisse M. Betancourt Román2, Adam J. Glawe1, Jeff Kline5, Kevin Van Den Wymelenberg5, G.Z. (Charlie) Brown5, Rolf U. Halden4, Curtis Huttenhower3 and Jessica L. Green2, (1)Civil and Environmental Engineering, Northwestern University, Evanston, IL, (2)Institute of Ecology and Evolution, University of Oregon, Eugene, OR, (3)Department of Biostatistics, Harvard T. H. Chan School of Public Health, Boston, MA, (4)Biodesign Center for Environmental Security, Arizona State University, Tempe, AZ, (5)Department of Architecture, University of Oregon, Eugene, OR

The built indoor environment is enriched for antibiotic-resistant pathogens compared to natural outdoor environments. In our quest to diminish the number of viable antibiotic-resistant pathogens indoors, with the ultimate goal of halting the spread of infectious disease, we have created an arsenal of synthetic antimicrobial chemicals such as triclosan, which we now embed in various products, from baby toys to building materials. These chemicals, along with built environment microbes, accumulate in indoor dust, providing a window into phenomena transpiring within buildings.

In this study, we assess whether dust samples with higher concentrations of antimicrobial chemicals are indeed associated with decreased microbial viability. We further evaluate whether antimicrobial chemical concentrations correlate with antibiotic resistance genes in the dust microbiome and phenotypes in cultivable isolates. To that end, we collected dust samples from athletic facilities. From these samples, we extracted DNA for shotgun sequencing and antimicrobial chemicals for quantification using liquid chromatography-tandem mass spectrometry. We further performed culture-based assessment of bacterial viability and antibiotic resistance.


In an initial study, we collected 42 samples from a single facility. These samples had a median triclosan concentration of 200 ng/g, which is slightly below median concentrations reported elsewhere. From these samples, we found a correlation between the concentration of triclosan and the abundance of three antibiotic resistance genes: erm(X), tet(K), and vga(A). However, we did not find an association between triclosan, or any of the antimicrobial chemicals we surveyed, and changes in the microbial community.

As a follow-up study, we have collected samples from 45 different facilities. The preliminary results of this study show a slightly higher but comparable median triclosan concentration. Preliminary results also indicate that higher concentrations of triclosan are associated with the detection of fewer cultivable isolates. The relationship between triclosan and antibiotic resistance genes, as well as antibiotic resistance phenotypes in cultivable isolates, is being assessed.

Due to the relationship between antimicrobial chemicals and the spread of antibiotic resistance in the built environment and in other settings, it would be wise to limit the use of these chemicals.