Aerosolized aqueous dust extracts collected near a drying lake trigger acute neutrophilic pulmonary inflammation reminiscent of microbial innate immune ligands.

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, and exposed playa or lakebed, 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. 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-h 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-h 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.

Salton Sea aerosol exposure in mice induces a pulmonary response distinct from allergic inflammation.

In communities surrounding the Salton Sea, high rates of asthma are associated with high aerosol dust levels. However, the Salton Sea itself may play an additional role in pulmonary health. Therefore, to investigate a potential role of the Salton Sea on pulmonary health, we exposed mice to aerosolized Salton Sea water for 7 days and assessed tissue responses, including cellular infiltration and gene expression changes. For reference, mice were also exposed to aerosolized fungal allergen (Alternaria sp.) and Pacific Ocean aerosols. Exposure to aerosolized Alternaria sp. induced dramatic allergic inflammation, including neutrophil and eosinophil recruitment to the bronchoalveolar lavage fluid (BALF) and lung tissue. By contrast, Salton Sea "spray" induced only B cell recruitment to the lung tissue without increased inflammatory cell numbers in BALF. However, there were consistent gene expression changes suggestive of an inflammatory response. The response to the Salton Sea spray was notably distinct from the response to Pacific Ocean water, which induced some B cell recruitment but without an inflammatory gene expression profile. Our studies suggest that soluble components in Salton Sea water promote induction of a unique inflammation-associated response, though any relationship to asthma remains to be explored.