Pathways and contributions of sulfate reducing-bacteria to arsenic cycling in landfills

Abstract

Sulfate-reducing bacteria (SRB) are generally found in sanitary landfills and play a role in sulfur (S) and metal/metalloid geochemical cycling. In this study, we investigated the influence of SRB on arsenic (As) metabolic pathways in refuse-derived cultures. The results indicated that SRB promote As(III) methylation and are beneficial for controlling As levels. Heterotrophic and autotrophic SRB showed significant differences during As cycling. In heterotrophic SRB cultures, the As methylation rate increased with As(III) concentration in the medium and reached a peak (85.1%) in cultures containing 25mgL−1 As(III). Moreover, 4.0%–12.6% of SO42− was reduced to S2−, which then reacted with As(III) to form realgar (AsS). In contrast, autotrophic SRB oxidized As(III) to less toxic As(V) under anaerobic conditions. Heterotrophic arsM-harboring SRB, such as Desulfosporosinus, Desulfocurvibacter, and Desulfotomaculum, express As-related genes and are considered key genera for As methylation in landfills. Thiobacillus are the main autotrophic SRB in landfills and can derive energy by oxidizing sulfur compounds and metal(loid)s. These results suggest that different types of SRB drive As methylation, redox reaction, and mineral formation in landfills. These study findings have implications for the management of As pollutants in landfills and other contaminated environments. Environmental ImplicationsSulfate-reducing bacteria (SRB) are widely pervasive in sanitary landfills since a mass of sulfate is produced during refuse biodegradation. The sulfite reductase b-subunit (dsrB) genes are positively correlated with arsM gene, a functional gene for arsenic methylation pathway. Thus, the links between SRB (including heterotrophic and autotrophic) and As biotransformation have been explored systematically in landfills. Results implicate differences of heterotrophic and autotrophic SRB on As cycling and managing As pollution in landfills.