Impacts of antiseptic cetylpyridinium chloride on microbiome and its removal efficiency in aerobic activated sludge
This study evaluated short- and long-term exposure of activated sludge (AS) microbiome to cetylpyridinium chloride (CPC), a quaternary ammonium compound widely used as biocidal additive or cationic surfactant. Toxicity assay in batch mode showed that CPC (50 μg L−1) inhibited cell growth. However, i...
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Veröffentlicht in: | International biodeterioration & biodegradation 2019-02, Vol.137, p.23-29 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | This study evaluated short- and long-term exposure of activated sludge (AS) microbiome to cetylpyridinium chloride (CPC), a quaternary ammonium compound widely used as biocidal additive or cationic surfactant. Toxicity assay in batch mode showed that CPC (50 μg L−1) inhibited cell growth. However, in a continuous reactor, CPC concentration in the range of 50–500 μg L−1 did not result in any observable impact on the biological activities of the AS microbiome. Similarly, 16S rRNA gene-based community profiling revealed that CPC had no observable impact on microbial diversity. At the phylogenetic structure, Rhodobacter (15 ± 7% of the total) and Asticcacaulis (9 ± 3%) were the only two phyla with increasing population in the 500 μg L−1-exposed reactors. This was also supported by an observation of no major change in the community structure. The reactors could remove >60% of CPC at initial concentrations of 50–500 μg L−1, primarily by adsorption and biodegradation. The enrichment of Rhodobacter and Asticcacaulis genus might contribute to CPC biodegradation and emerge as a potential microbial niche for the removal of CPC.
•Activated sludge (AS) biological function was resilient to continuous CPC exposure.•Up to 500 μg L−1 CPC did not alter species richness and diversity.•Rhodobacter and Asticcacaulis potentially degrading CPC were selectively enriched.•The fate and effects of CPC in post-treatment processes of AS are recommended. |
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ISSN: | 0964-8305 1879-0208 |
DOI: | 10.1016/j.ibiod.2018.11.006 |