Abstract
BACKGROUND: On 20 March 2010, the Icelandic volcano Eyjafjallajokull erupted for the first time in 190 years. Despite many epidemiological reports showing effects of volcanic ash on the respiratory system, there are limited data evaluating cellular mechanisms involved in the response to ash. Epidemiological studies have observed an increase in respiratory infections in subjects and populations exposed to volcanic eruptions.
METHODS: We physicochemically characterized volcanic ash, finding various sizes of particles, as well as the presence of several transition metals, including iron. We examined the effect of Eyjafjallajokull ash on primary rat alveolar epithelial cells and human airway epithelial cells (20-100 mu g/cm(2)), primary rat and human alveolar macrophages (5-20 mu g/cm(2)), and Pseudomonas aeruginosa (PAO1) growth (3 mu g/10(4) bacteria).
RESULTS: Volcanic ash had minimal effect on alveolar and airway epithelial cell integrity. In alveolar macrophages, volcanic ash disrupted pathogen-killing and inflammatory responses. In in vitro bacterial growth models, volcanic ash increased bacterial replication and decreased bacterial killing by anti-microbial peptides.
CONCLUSIONS: These results provide potential biological plausibility for epidemiological data that show an association between air pollution exposure and the development of respiratory infections. These data suggest that volcanic ash exposure, while not seriously compromising lung cell function, may be able to impair innate immunity responses in exposed individuals.