Toxic Cyanobacteria: Education, Lake Protection
Creators: name: Hardy, Joan
name: Jacoby, Jean
name: Boothe Luse, Clare
name: Crayton, Mike
Publisher: name: No Publisher Supplied
Year: 1997

description: Washington State Department of Health received a Centennial Clean Water Fund grant in 1994 from Washington State Department of Ecology to investigate cyanobacteria blooms in western Washington. Objectives of the grant, entitled "Toxic Cyanobacteria: Education/Lake Protection," were to: (1) educate the public about potential health concerns and train citizens to recognize and report algal blooms in lakes, (2) investigate potential inhibitors of cyanobacteria, and (3) observe blooms in two western Washington lakes. During this grant, Pacific Lutheran University (PLU) tested field samples for toxicity and conducted research on cyanobacteria inhibitors. Seattle University (SU) conducted limnological field work in Lake Steilacoom and American Lake, Pierce County. A review of scientific literature on toxic cyanobacteria included the following topics: toxin-producing cyanobacteria, cyanobacterial toxins (neurotoxins, hepatotoxins, other toxins, detection), occurrence of freshwater cyanobacterial toxicity, impacts on human health, impacts on aquatic life (zooplankton, fish), and conditions leading to toxic bloom formation (nutrients, light and temperature, toxin production and growth cycle, zooplankton, other factors). Also in the literature review was information on control of toxic cyanobacteria blooms (lake management, copper sulfate, calcium hydroxide, aluminum sulfate, other treatments, and drinking water treatment). Education of lake groups and citizens was conducted during the grant. A large part of educating the public and public agencies about toxic cyanobacteria blooms occurred through response to requests for information, primarily from government agencies but also from citizens and businesses associated with aquatic activities. The above interactions were summarized in the final report. In addition, a brochure on toxic cyanobacteria was produced and distributed, a training manual on identification of potentially toxic cyanobacteria was distributed, and public meetings and local workshops on toxic cyanobacterial blooms were conducted. Local health district personnel were trained at three regional workshops in western Washington. Four public workshops were held for various groups, such as Phantom Lake Association (King County), Kitsap County, Long Lake Steering Committee (Thurston County), and the 1996 joint annual meeting of the Western Plant Management Society and North American Lake Management Society. Presentations on cyanobacteria toxicity were given at other conferences and meetings throughout the grant period.A total of 115 lake samples were tested for toxicity during the 30-month grant. Samples were collected from 20 different lakes in eight western Washington counties: Pierce (5), King (6), Thurston (3), Kitsap (2), Snohomish (1), Skagit (1), Mason (1), and Clark (1). An additional four lakes outside western Washington were tested: Wenas Lake, Yakima County, East Lake, California, and Big Creek Reservoir and Devil's Lake, Oregon. A database summarizing lakes sampled and results of toxicity tests was completed for the final report. Toxic blooms were confirmed by mouse bioassay in five of the twenty-one Washington lakes sampled. Lake Steilacoom, Spanaway Lake, Waughop Lake (Pierce County), and Wenas Lake (Yakima County) contained toxic Microcystis aeruginosa, while American Lake (Pierce County) contained toxic Anabaena flos-aquae. Microcystin-LR was the variant that occurred regularly in the microcystin-containing blooms. No other toxin-producing cyanobacteria was detected during this study, although several genera known to produce toxins were found. Most cyanobacterial blooms occurred during the late summer and early fall, while a small number occurred during the winter months in water temperatures as low as 5-7°C. Of primary public health concern were toxic cyanobacterial blooms in lakes which are used as a source of drinking water. Lake Young, a drinking water reservoir in King County, was monitored for cyanobacteria on a regular basis during the grant. Summit Lake, Thurston County, a source of drinking water to nearby residents, had a cyanobacterial bloom that tested negative for toxicity in July 1995. Residents of Lake Wenas, Yakima County, became ill after their drinking water became toxic in September 1995; the bloom showed microcystin-LR and -RR. In Oregon, a toxic Microcystis bloom in Big Creek Reservoir, the drinking water supply for Newport, led to notification of residents and to further tests for microcystins in tapwater throughout the bloom. Three reports of illness after swimming in a cyanobacterial bloom were documented. Numerous youths became ill after swimming in a Gloeotrichia bloom in Mason Lake, Mason County, during Labor Day weekend 1995. Reports of human illness, dead trout, and a dead kingfisher were received after a bloom in Goss Lake, Island County. Fort Lewis Fish and Wildlife reported a bloom, a fish kill, and a sick child at Little American Lake, Pierce County, 1995. In each of the above cases, the cyanobacterial bloom had dissipated or decayed before samples were taken for toxicity tests. Several other reports of fish kills associated with blooms were received during the grant. In efforts to isolate cyanobacteria inhibitors, PLU isolated a water-soluble material from the green seaweeds Ulva and Monostroma. The isolate exhibited killing activity (cell lysis) against a toxic strain of Anabaenaflos-aquae. Real-time videomicroscopy showed that the substance caused cell wall perforation, followed by outward extrusion of the cell contents, and death within 1-2 hours. Bioactivity-directed fractionation was used to partially purify the lytic agent from both seaweeds. The agent appeared to be a small glycoprotein (MW=1,000-4,000) and was stable for several months at room temperature. SU investigated two lakes with histories of toxic blooms, American Lake and Steilacoom Lake (Pierce County) in order to: (1) identify and evaluate possible relationships between environmental factors and development of toxic blooms, (2) determine the relationship between the presence and abundance of potentially toxic species and toxin production, and (3) incorporate information gained into approaches for managing toxic cyanobacterial blooms. The two lakes were monitored during 1994 and 1995 for toxicity and for physical, chemical, and biological indicators.No samples collected in American Lake during winter 1994-1995 elicited a toxic response in mouse bioassays, although low levels of microcystin were detected in selected samples by ELISA. One sample collected near Veterans Hospital along the northern shoreline was identified as toxic in February 1996. Since this sample was the only toxic sample observed, it was not possible to identify relationships between toxicity and environmental conditions in American Lake. A prolonged toxic bloom of Microcystis aeruginosa occurred in Steilacoom Lake during summer 1994. Total microcystin concentrations at the deep-water station ranged from 209 to 1286 ug/g bloom material. During most of summer 1995, cyanobacteria were not abundant and samples tested for toxicity did not give a toxic response. Only one sample in October 1995 was toxic by mouse bioassay.In Lake Steilacoom, cyanobacterial blooms were associated with decreased water column light intensity and transparency as measured by Secchi depth, and stable water column conditions as estimated by relative thermal resistance to mixing (RTRM). Although cause and effect relationships cannot be discerned from field observations, there was a significant linear relationship between increasing percent cyanobacteria and decreasing Secchi depth measurements (r = 0.69, p &lt; 0.001), a negative exponential relationship between the concentration of cyanobacteria and Secchi depth (r = 0.82, p &lt; 0.0001), and a negative exponential relationship between Microcystis concentration and Secchi depth (r = 0.76, p &lt; 0.0005). RTRM was significantly higher during summer 1994 (p &lt; 0.05), indicating more stable conditions due to a greater density gradient and more resistance to mixing. Stable and turbid conditions during summer 1994 possibly gave buoyancy-regulating cyanobacteria like Microcystis an advantage at obtaining optimum light conditions for photosynthesis. The same type of cyanobacterial bloom did not occur in summer 1995, possibly due to greater water column transparency and lower stability.Increased water column transparency can be partially explained by trophic level interactions between planktivorous fish, zooplankton, and phytoplankton. Zooplankton abundance dramatically increased between 1994 and 1995 (means of 18.4 and 62.9/L, respectively) concurrent with a large decrease in the number of young hatchery fish planted in the lake and upstream creeks. The number of fingerlings and fry planted in Steilacoom Lake and upstream creeks in 1995 (201,150) was approximately half of the number planted in 1994 (395,050). Phytoplankton losses due to zooplankton grazing were estimated to be greater during 1995 than 1994, with losses due to grazing potentially contributing approximately 80 percent of the total loss. The large zooplankton population in 1995 exerted a large grazing pressure on phytoplankton and kept the phytoplankton biomass low through September. With a less stable water column and high transparency due to zooplankton grazing, low light conditions (which would have. favored cyanobacteria) did not develop until October 1995. Other factors were associated with cyanobacterial dominance in 1994. Mean surface water temperature in 1994 was higher than in 1995 (22.6°C and 20.6°C, respectively). Temperature exceeded 20°C in both years, but temperature in 1994 was greater than 22°C more often than in 1995.Mean surface pH was significantly higher in Lake Steilacoom during the toxic bloom in 1994 (p &lt; 0.05), with pH values consistently close to 10 from mid-July through September. Greater phytoplankton growth earlier in the summer increased pH levels earlier in 1994. Cyanobacteria increase pH during photosynthesis and, in turn, are favored by the high pH conditions that they create. Also, the large biomass of macrophytes present during summer 1994 (both submerged and floating) removed C02 from solution and contributed to the raised pH. Macrophytes were scarce the second summer. Mean summer total phosphorus (TP) concentrations were also different between the years (p &lt; 0.05), with a significant positive relationship between cyanobacteria concentration and surface TP concentration (r = 0.66, p &lt; 0.0005). Additionally, mean summer total nitrogen (TN) was significantly higher during the toxic bloom in 1994 than in 1995 (p &lt; 0.05). Low No3-N concentrations in Lake Steilacoom in 1994 may partly explain the success of Microcystis that year; the only peak in cyanobacteria biovolumn that occurred during 1995 was after No3-N concentrations dropped below 20 ug/L. Microcystin concentration in Lake Steilacoom was not related to Microcystis in the water column. Different limnological conditions probably affect growth of Microcystis and microcystin production. Microcystin concentration increased with increasing soluble reactive phosphorus (SRP) between 1 and 10 ug/L; toxin production by Microcystis may have been limited by SRP. Management approaches to prevent occurrences of a toxic bloom are the same as those that would be used to address any nuisance phytoplankton blooms. The most important factor to be managed is nutrient loading to the lake. Management methods include dredging, dilution, treatment or diversion of point sources, and watershed best management practices. Sources of P and N should be identified, and if TP inputs to the lake can be decreased, cyanobacterial blooms will be less likely.Factors that may reduce phytoplankton in Lake Steilacoom are increased dilution and flushing of the lake and a large zooplankton population. Increased flushing rate decreases inflow nutrient concentrations if the inflow concentration is less than the lake concentration. Increased flushing may also increase the phytoplanktonloss rate. Zooplankton populations can be significantly affected by planktivorous fish grazing; increased planktivorous fish mortality may protect zooplankton which then graze phytoplankton. Treatment with algicides such as copper sulfate effectively removes phytoplankton cells from the water column. However, treatment by chemicals causes phytoplankton cells to lyse and release all intracellular compounds, including the toxin. It would be unwise to cause toxin release without concern and caution for public health; toxins may remain in the water for up to 40 days. Avoiding cell lysis and toxin release is imperative when treating drinking water reservoirs that have cyanobacterial blooms. Alternative chemical treatment methods would be alum, lime, or another chemical coagulant.Lakes with toxic bloom potential should be monitored for the presence of large blooms of cyanobacteria or scums on the surface, especially along the shoreline. Lake residents should be educated to watch for scum formation and alert their public health agency when a large bloom is occurring so that the bloom can be tested for toxicity; toxicity analysis should be conducted using a quantitative technique such as HPLC or ELISA. If a surface scum is observed, lake residents should restrict domestic animal and human use of waters. Lakes or reservoirs serving as drinking water sources should be periodically monitored for cyanobacteria presence and abundance, and, if a potential toxin-producing species is found, a concentrated sample should be analyzed for toxicity. Toxin-producing cyanobacteria may pose a danger to human health due to the potential tumor-promoting characteristics of their toxins.