INTRODUCTION Sulfate contamination of the Everglades is a serious water quality issue facing restoration of this ecosystem. Sulfate concentrations in some marsh areas are more than 60 times background concentrations, and sulfate in excess of background levels covers an estimated 60% of the freshwater Everglades (Orem et al., 1997; Stober et al., 1996 and 2001; Orem et al., 2004). The excess sulfate enters the Everglades in the discharge of canal water from the Everglades Agricultural Area (EAA). Excess phosphorus also enters the ecosystem in EAA canal water discharge (Koch and Reddy, 1992; Craft and Richardson, 1993; DeBusk et al. 1994; Zielinski et al., 1999). Existing data suggest that sulfur in fertilizer and soil amendments used in the EAA (both new additions and legacy sulfur in the soil) is a major source of excess sulfate entering the ecosystem (Bates et al., 2001 and 2002). Other potential sources of sulfate (including groundwater), however, need further investigation. The report by Gilmour et al. (2007b) in the 2007 South Florida Environmental Report provides a complete examination of the current state of knowledge of the sulfur contamination issue in the Everglades. Sulfate discharged from canals or leaking through levees into the ecosystem spreads out over a large area since, unlike phosphorus, it is not removed to any great extent by plant uptake. Sulfate slowly diffuses into the anoxic soils (peats) underlying the Everglades and stimulates microbial sulfate reduction (MSR), producing toxic hydrogen sulfide as a byproduct (Goldhaber and Kaplan, 1974; Berner, 1980; Rheinheimer, 1994). Hydrogen sulfide at contaminated sites may build up in sediments to concentrations thousands of times background levels (Gilmour et al., 2007b). The excess sulfate and sulfide has numerous deleterious impacts on the Everglades. One of the more environmentally important impacts is the link between sulfate contamination and methylmercury (MeHg) production in the ecosystem (Gilmour et al., 1998; Benoit et al., 1998, 1999a, b; Axelrad et al., 2007; Gilmour et al., 2007a). MeHg, a bioaccumulative neurotoxin, is produced primarily by methylation of ambient inorganic mercury during MSR (Compeau and Bartha, 1985; Gilmour et al., 1992; Munthe et al., 1995; Branfireun et al., 1999). Contamination of fish with MeHg is the most significant environmental contaminant issue in the USA in terms of number of locations impacted (Krabbenhoft and Wiener, 1999; USEPA, 1998). Neurotoxic MeHg represents a serious threat to wildlife (Bouton et al., 1999; Frederick et al., 1999; Heath and Frederick, 2005), and is a human health issue, with human exposure through fish consumption (Gilbert and Grant-Webster, 1995; Schober et al., 2003). In addition to its neurotoxic effects, MeHg may also be an endocrine disruptor that affects successful reproduction in fish and fish-eating wildlife (Klaper et al., 2006). South Florida has among the highest levels of MeHg in fish in the USA (Lambou et al., 1991). Experimental chamber (mesocosm) studies conducted in the Everglades have shown that sulfate addition stimulates the production and bioaccumulation of MeHg (Gilmour et al., 2007b). Inorganic mercury enters the Everglades primarily in rainfall, and most of the inorganic mercury in the rainfall appears to originate from outside of the USA (Hanisch, 1998). The origin of most inorganic mercury from outside of the USA severely limits the ability of state and Federal officials to limit MeHg production and bioaccumulation in fish in the Everglades by controlling emissions of inorganic mercury from various anthropogenic sources (e.g. coal-fired power plants, medical waste incinerators, cement manufacture). Thus, controlling sulfate inputs to the Everglades may represent the most effective way of minimizing MeHg production and bioaccumulation here. In addition to impacts on MeHg production and bioaccumulation, sulfur contamination has also dramatically altered redox p