Pulmonary Toxicity of Pyrotechnic, Smokescreen, and Explosive-Derived Particulate Matter
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Military personnel may be exposed to hazardous emissions from the use of pyrotechnics, smokescreens, propellants, and explosives containing potentially toxic solid, liquid, and gaseous components. The objective of our study was to study the relationship between the particulate matter (PM) composition of these emissions and their effects on respiratory function and pulmonary toxicity. PM10 samples were collected on Teflon filters from burning an illumination Flare (containing magnesium, sodium nitrate, phenolic resin, binder) and M18 smokescreen grenade (magnesium carbonate, potassium chlorate, sucrose, mixed colors), and from the detonation of plastic-bonded explosive (PBX: 95% 1,3,5,7-tetranitro-1,3,5,7-tetrazocane, 5% binder). Filters were extracted with a methanol/water mixture, dried, and resuspended in sterile saline for lung toxicity testing in female CD-1 mice via oropharyngeal aspiration (100 µg of PM per mouse). Control animals received saline vehicle (negative) or lipopolysaccharide (LPS; positive), and all mice were necropsied 4 or 24 h after exposure. Whole body plethysmography showed that in comparison with pre-exposure baselines, significant reductions in breathing frequency were detected in the Flare (-26%) and LPS (-45%) groups at the 4 h time point, while significant increases in enhanced pause (PenH), an indicator correlating with airflow obstruction, were observed in the PBX (2.0 × baseline) and LPS (3.3×) groups at 4 h and the PBX group at 24 h (2.6×) post-exposure. PBX significantly increased pro-inflammatory cytokines in the bronchoalveolar lavage (BAL) fluid at 4 h (MIP-2, IL-6) and 24 h (MIP-2, IL-6, and TNF-a) post-exposure. BAL neutrophils were significantly increased (46% of total BAL cells) by PBX 24 h post-exposure. PBX also significantly increased BAL markers of lung injury at 4 h (LDH) and 24 h (protein, albumin, NAG, LDH) post-exposure. LPS caused significant increases in all these BAL endpoints, while none were affected by exposure to saline, Flare, or M18 grenade. These data show that PM isolated from PBX detonation emissions caused significant impairment of respiratory function and increases in indices of acute pulmonary inflammation compared with M18 grenade or Flare smoke PM, or several ambient PM samples collected from different locations across the United States. The results may be used to help quantify risk following exposure to various military-type activities under training or active-duty scenarios. [This abstract does not represent EPA policy].