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Active volcanism and nontuberculous mycobacteria lung disease: confounders and connections

Jennifer R. Honda1 , Rachel N. Wilsey1, Kristin T. Dean1, Michael Teve1, Riley Johnson2, David E. Damby4, Stephen T. Nelson3 and Adrian J. Hornby1

  • Affiliations: 1 Department of Cellular and Molecular Biology, School of Medicine, University of Texas at Tyler Health Science Center, Tyler, Texas; 2 School of Medicine, University of Texas at Tyler; 3 University of Utah, Salt Lake City, Utah; 4 Cascades Volcano Observatory, California

  • Presentation type: Talk [Invited]

  • Presentation time: Monday 16:00 - 16:15, Room R290

  • Programme No: 6.6.2

  • Theme 6 > Session 6

Abstract

The microbial content of aerosolized volcanic ash and consequences to respiratory health have yet to be fully quantified. We were the first to report that freshly erupted ash from the 2018 Kīlauea eruption harbored pathogenic nontuberculous mycobacteria (NTM). NTM are opportunistic pathogens that cause pulmonary disease (PD) in people with pre-existing lung conditions (e.g. cystic fibrosis, bronchiectasis). NTMPD prevalence shows geographic disparities, suggesting potential links with aerosol inhalation and volcanic exposures. Narrowly, we hypothesize that volcanic ash inhalation promotes NTMPD via pro-inflammatory pathway stimulation, including the inflammasome in lung cells. Broadly, we suspect NTMPD prevalence correlates with global volcanism and volcanogenic element enrichments in water supplies. Data compilation shows countries with active volcanism are significantly more likely to show high NTMPD cases. Using our Kīlauea ash (KA) sample and KA-derived NTM, we discovered the ability of airway epithelial cells and lung airway organoids to control KA-derived NTM infection did not differ with KA exposure and KA did not cause cell cytotoxicity. Thus, mafic ash exposure alone is not the sole driver for NTMPD. It's possible that dust's surface functional groups influence NTM viability. Using allophane and gibbsite, NTM growth was respectively unaffected or significantly reduced. Other exposures may increase NTMPD risk. For example, mafic volcanic products are enriched in metals such as vanadium. Using ICP-MS, we correlated areas with higher tapwater vanadium to higher NTMPD prevalence in the NTMPD hotspot of Hawai'i. Future work includes targeting transcriptomic responses of NTM and KA-exposed lung cells to mineral dusts using nebulized exposures.