Industrial Health · 2003 · 13 citations · 20 references
Life SciencesImmunologyToxicologyImmunopathologyInflammationInnate ImmunityInflammatory SignalingInhalation InjuryMacrophage BiologyPulmonary InflammationPulmonary ToxicityVolcanic AshAlveolar InflammationAlveolar Macrophage ResponseBiomarkers Of Inhalation InjuryPulmonary Macrophage ResponseReverse Transcription Polymerase Chain Reaction (Rt-pcr)Sulfur Dioxide ToxicityVolcanic Ash FallVolcanic Ash Plumes
Local residents exposed to heavy falls of ash discharged by Mt. Sakurajima, an active volcano, have been reported to develop acute and chronic inflammation of the respiratory tract. The present study aimed to determine the primary cause of this inflammation using an experimental model. Wistar rats were exposed for 5 days (4 h/d) to air containing 100 mg/m3 volcanic ash (mass median aerodynamic diameter, 4.3 microm; geometric standard deviation, 1.7) with or without 1.5 ppm sulfur dioxide (SO2). The lungs were then lavaged, and mRNA was extracted from alveolar macrophages and assessed by reverse transcription-polymerase chain reaction (RT-PCR). In the lavage fluid, no change in cellularity or increase in the content of tumor necrosis factor (TNF)-alpha was detected. However, at 1 h following exposure, 80% of macrophages were seen to have phagocytosed the volcanic ash. This percentage was unchanged at 24 h after exposure. Profilin mRNA content of the macrophages was elevated, and c-jun mRNA was expressed. Alveolar macrophages exposed to volcanic ash and SO2, therefore, are likely to have some inflammatory and fibrogenic potential.
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