Although the Salton Sea was once a thriving destination for humans and wildlife, it has now degraded to the point of ecosystem collapse. Increases in local dust emissions have introduced aeolian (wind-blown) microorganisms that travel, along with contaminants and minerals, into the atmosphere, detrimentally impacting inhabitants of the region. Proliferation of certain microbial groups in regions of the Sea may have a disproportionate impact on local ecological systems. Yet, little is known about how the biogeochemical processes of this drying lakebed influence microbial community composition and dispersal. To elucidate how these microorganisms contribute, and adapt, to the Sea's volatile conditions, we synthesize research on three niche-specific microbiomes — exposed lakebed (playa), the Sea, and aeolian — and highlight modern molecular techniques, such as metagenomics, coupled with physical science methodologies, including transport modeling, to predict how the drying lakebed will affect microbial processes. We argue that an explicit consideration of microbial groups within this system is needed to provide vital information about the distribution and functional roles of ecologically pertinent microbial groups. Such knowledge could help inform regulatory measures aimed at restoring the health of the Sea's human and ecological systems.

Background: A high incidence of asthma is prevalent among residents near the Salton Sea, a large inland terminal lake in southern California. This arid region has high levels of ambient particulate matter (PM); yet while high PM levels are often associated with asthma in many environments, it is possible that the rapidly retreating lake may contribute components with a specific role in promoting asthma symptoms. Objectives: Our hypothesis is that asthma may be higher in residents closest to the Salton Sea due to chronic exposures to playa dust. Playa emissions may be concentrating dissolved material from the lake, with microbial components capable of inducing pulmonary innate immune responses. Such inflammatory responses may contribute to the development of asthma-like symptoms in residents. To test this hypothesis, we used a mouse model of aerosol exposures to assess the effects of playa dust. Methods: From dust collected around the Salton Sea region, aqueous extracts were used to generate aerosols, which were injected into an environmental chamber for mouse exposure studies. We compared the effects of exposure to Salton Sea aerosols, as well as to known immunostimulatory reference materials. Acute 48-hour and chronic 7-day exposures were compared, with lungs analyzed for inflammatory cell recruitment and gene expression. Results: Dust from sites nearest to the Salton Sea triggered lung neutrophil inflammation that was stronger at 48-hours but reduced at 7-days. This acute inflammatory profile and kinetics resembled the response to innate immune ligands LTA and LPS while distinct from the classic allergic response to Alternaria. Conclusion: Lung inflammatory responses to Salton Sea dusts are similar to acute innate immune responses, raising the possibility that microbial components are entrained in the dust, promoting inflammation. This effect highlights the health risks at drying terminal lakes from inflammatory components in dust emissions from exposed lakebed.