The Effects of Sediment Toxicity on Florida Bay Turtle Grass: A Synthesis of Field Experiments (1990-2000).
Paul Carlson, Laura Yarbro, Brad Peterson, and Alice Ketron.
Florida Fish and Wildlife Conservation Commission, Florida Marine Research Institute, St. Petersburg, Fl USA.
Between 1990 and 2000, we performed eight field experiments which tested the impact of porewater sulfide and ammonia concentrations on seagrasses in Florida Bay. The experiments were directed primarily toward turtle grass (Thalassia testudinum) because it was the species most affected by widespread die-off between 1987 and 1991. However, early experiments also tested the impact of elevated sediment concentrations on shoal grass (Halodule wrightii) and manatee grass (Syringodium filiforme). The objectives of this paper are to describe the dose-response relationship of sulfide toxicity for Thalassia growing in situ , the disparity between field and laboratory sulfide toxicity experiments, and the role of sulfide toxicity in Florida Bay seagrass die-off.
In each experiment, polyethylene sleeves (30 cm d. x 36 cm h.) were used to isolate columns of sediment in seagrass beds. Sediment chemistry within sleeves was manipulated by adding amendments to porous polyethylene tubes inside the sleeves. Varying amounts of glucose were added in different experiments to stimulate sulfate reducing bacteria and to elevate sediment sulfide concentrations. Sodium molybdate was added to serve as a competitive inhibitor for bacterial sulfate reduction, and potassium nitrate served to stimulate denitrifying bacteria, respectively. Both treatments effectively lowered porewater sulfide concentrations. Ammonium chloride was added in some experiments to test the toxicity of ammonia to Thalassia. Combined treatments of glucose and ammonia were also used in some experiments. Experiments were carried out in all four seasons.
In all experiments, elevated sulfide concentrations caused significant declines in Thalassia shoot survival, belowground biomass, shoot leaf area, blade width, and blade length. The negative relationship between shoot survival and sulfide concentration was generally linear (Figure 1, below), but the slope and coherence of the relationship varied among experiments. However, our results indicate lowered Thalassia survival even at 2 mM sulfide concentrations. The disparity between field and laboratory sulfide toxicity experiments might result from unusually low belowground:aboveground tissue ratios in laboratory experiments. Excised shoots used for laboratory experiments also have a limited life span and are vulnerable to artifacts associated with wound response. These data suggest that laboratory studies of sulfide toxicity are flawed and drastically overestimate sulfide tolerance of Thalassia.
Sodium molybdate and potassium nitrate amendments lowered porewater sulfide concentrations significantly (Table 1). Shoot leaf area, blades per shoot, and mean blade length were higher in nitrate and molybdate treatments than in glucose addition treatments. These results indicate that, even at sublethal concentrations, sulfide inhibits the growth of Thalassia.
Table 1: Effects of Sediment Amendments on Porewater Sulfide Concentrations and Thalassia morphology- Fall 2000. Data in each column with the same letter subscript are not significantly different.
Porewater / Shoot / Blades / MeanTreatment / Sulfide / Leaf Area / per Shoot / Blade Length
Nitrate / 136 / d / 26.6 / a / 3.1 / a / 10.6 / ab
Molybdate / 1120 / d / 27.1 / a / 2.8 / ab / 11.3 / a
Outside control / 320 / d / 22.8 / ab / 2.6 / ab / 11.3 / a
Bucket control / 3300 / c / 20.1 / ab / 2.5 / ab / 9.3 / abc
Very low glucose / 6880 / a / 15.5 / b / 2.2 / b / 8.9 / bc
Low glucose / 6020 / ab / 16.8 / b / 2.3 / b / 8.8 / bc
High glucose / 5020 / b / 16.1 / b / 2.3 / b / 8.3 / c
The factor or factors responsible for the development of hypoxia, sulfide toxicity, and ensuing basin Thalassia mortality have not yet been identified. However, the recurrence of seagrass die-off at Barnes Key in 1999 casts doubt on the role of factors such as hyperthermia , hypersalinity, and lack of hurricanes suggested by Robblee et al. (1991) as possible causes of die-off episodes in 1988 through 1991. The new episode of die-off occurred under climatic conditions very different from the earlier event. The occurrence of die-off at Barnes Key, however, does support observations by Robblee et al. that anthropogenic factors probably did not contribute to seagrass mortality in Florida Bay because Barnes Key is far from mainland freshwater discharge points and well flushed by tides. Our experiments also indicate that ammonia and Labyrinthula are unlikely causes of primary die-off.
These results indicate that sulfide is a chronic stressor on Thalassia communities growing in carbonate sediments. It is also a by-product, and possibly a causal factor in basin seagrass mortality. As noted by Carlson et al. (1994), sulfide can be a primary cause of Thalassia die-off in one of two ways: 1) If physical or chemical factors change in a way that porewater sulfide concentrations increase suddenly, concentrations can exceed acute toxicity thresholds, or 2) Sulfide stress might also occur without changes in porewater sulfide concentrations if the oxygen balance of seagrasses is affected by decreased photosynthetic or oxygen transport capacity. In the absence of data or a mechanism to explain sudden increases in sediment porewater sulfide concentrations, we suggest that seagrass die-off events in Florida Bay have probably been initiated by the latter mechanism. Yarbro et al. (1989) proposed that chronic sulfide stress and shifts in the oxygen balance of Thalassia plants were involved in basin die-off, and more recent studies by Borum et al. (2001) support that hypothesis.
Paul Carlson, Florida Fish and Wildlife Conservation Commission, 100 Eighth Avenue SE, St. Petersburg, FL 33701. Phone: 727-896-8626, Fax: 727-823-0166, , Question 4.