The device, about the size and shape of a large matchbox, accompanies participants everywhere and is equipped with a sub-micron filter that traps particulate matter in the device. The data — bacteria, viruses, chemicals, fungi and anything else sucked up by the device — is brought back to Snyder’s lab and extracted for DNA and RNA sequencing, as well as chemical profiling, to identify all the collected organisms and chemicals that the person is exposed to.

This idea — to siphon up bits of an individual’s exposome and systematically categorize what’s in it — is novel, Snyder said. And it required Jiang to stitch together an entirely new database.

“Scientists had assembled separate bacteria, viral or fungi databases, but to fully decode our environmental exposures, we built a pan-domain database to cover more than 40,000 species,” Jiang said. It includes information on bacteria, viruses, fungi, animals, plants and more, all organized in a single searchable database.

“We sequenced these samples in incredible detail,” said Snyder, who is also the Stanford W. Ascherman, MD, FACS, Professor in Genetics. “No one has ever done a study this deep before. We ended up with about 70 billion readouts.”

Parsing particulates

Between participants, Snyder and Jiang found that exposomes could be vastly different, even in a reasonably tight geographic region — in this case, the San Francisco Bay Area. Snyder cited an especially well-controlled portion of the study, in which four participants, including Snyder, were closely monitored over one month, as a case in point.

Each person lived in a distinct region of the San Francisco Bay Area: Palo Alto, Sunnyvale, Redwood City and San Francisco (though the person who lived in Redwood City commuted across the bay to his job). “It turns out, even at very close distances, we have very different exposure profiles or ‘signatures,’” Snyder said. These personal signatures are essentially traces of specific fungi, plants, chemicals and bacteria that are consistently seen on or around a single person, but that vary between people. Many environmental aspects contribute to this microscopic amalgam — pets, household chemicals, flowers in bloom and even rain.

“The bottom line is that we all have our own microbiome cloud that we’re schlepping around and spewing out,” Snyder said.

Specific and unique signatures were captured for every individual (although Snyder added that DEET, an insect repellant, along with several carcinogens were found in just about every chemical sample). For example, the resident from San Francisco showed high rates of “sludge bacteria,” or bacteria typically found in wastewater and sewage treatments. Snyder had consistently high fungal exposures at home due to what he suspects is the use of “green” paint. “The guy who painted my house was a really environmentally friendly, green person. And he avoided using paints with a substance called pyridine in it,” Snyder said. Pyridine, which used to be a popular additive to house paints, has an inverse relationship with fungus, meaning the less pyridine, the more fungus.

Snyder’s profile was the most diverse, as he took the device everywhere he went, both nationally and internationally, for two years, swapping out its filters for every new location. Outside his pet exposures (Snyder has a cat, a dog and a guinea pig), his signature also showed evidence of eucalyptus in the early spring months, providing some nuanced information about what might be causing his April allergies.

Connecting it to human health

Besides the four highly controlled participants, a dozen participants were added during different times of the year, helping Snyder capture exposures brought by weather, seasons and location.

“There are a lot of findings that haven’t been described before — all kinds of fungal, bacterial and plant seasonal patterns,” Snyder said. Although the devices picked up potential pathogenic viral and bacterial sequences, it can be tricky to distinguish a threatening pathogen to humans from one of its harmless close cousins, he said.

The bottom line is that we all have our own microbiome cloud that we’re schlepping around and spewing out.

As for the carcinogens, it’s also more complicated than simply detecting them in the device. “We’re measuring individual exposures, not absolute levels,” he said. “So at this point the data isn’t generalizable enough to make broad claims.”

But that’s not to say that one day it won’t be. Snyder said that this study is just scratching the surface of human exposome data and how it relates to health, and his team’s future goals center on better understanding the exposome as it relates to human health. “We want to measure more people in more diverse environments,” Snyder said. “We also want to simplify the technology, ideally to the point that everyone can be out there measuring their own personal exposures — perhaps something like an exposome-detecting smartwatch.”

The work is an example of Stanford Medicine’s focus on precision health, the goal of which is to anticipate and prevent disease in the healthy and precisely diagnose and treat disease in the ill.

The other Stanford author of the study is postdoctoral scholar Qing Liu, PhD.

Snyder is a member of Stanford Bio-X, the Stanford Cardiovascular Institute, the Stanford Children Health Research Institute, the Stanford Cancer Institute and the Stanford Neurosciences Institute.

The study was supported by funding from National Institutes of Health (grant U54DK102556) and a Stanford Spectrum population health pilot grant.

Stanford’s Department of Genetics also supported the work.