ABSTRACT
In this study, the microbial community within compost, emitted into the airstream, downwind and upwind from a composting facility was characterized and compared through phospholipid fatty acid analysis and 16S rRNA gene analysis using denaturing gradient gel electrophoresis and bar-coded pyrosequencing techniques. All methods used suggested that green-waste composting had a significant impact upon bioaerosol community composition. Daily variations of the on-site airborne community showed how specific site parameters such as compost process activity and meteorological conditions affect bioaerosol communities, although more data are required to qualify and quantify the causes for these variations. A notable feature was the dominance of Pseudomonas in downwind samples, suggesting that this genus can disperse downwind in elevated abundances. Thirty-nine phylotypes were homologous to plant or human phylotypes containing pathogens and were found within compost, on-site and downwind microbial communities. Although the significance of this finding in terms of potential health impact was beyond the scope of this study, it clearly illustrated the potential of molecular techniques to improve our understanding of the impact that green-waste composting emissions may have on the human health.
Subject(s)
Aerosols/analysis , Air Microbiology , Refuse Disposal/methods , Bacteria/classification , Bacteria/genetics , Bacteria/growth & development , Biodiversity , Environmental Monitoring , Humans , Soil , Soil MicrobiologyABSTRACT
Because of the lack of effective methodology, the biological effects of environmental endotoxin have not been assessed. Here we have collected and measured airborne endotoxin at different locations around composting sites. Increased endotoxin concentrations were observed close to composting activities and also at nearby boundary areas. Analysis of proinflammatory effects of the environmental endotoxin on interleukin (IL)-8 and IL-6 release from human D562 pharyngeal epithelial and MM6 monocytic cell cultures showed an association between endotoxin level and cytokine induction. The cytokine-inducing effect of bioaerosol extracts was inhibited by polymyxin B, indicating that endotoxin was the cause of cytokine responses we found. The environmental endotoxin was also more active for stimulating cytokines in airway epithelial cells than commercially purified Escherichia coli endotoxin. Our results suggest that these in vitro inflammatory cell models may contribute to the assessment of health impacts of environmental endotoxin.
