Ammonia is a relatively toxic compound generated in water and sediments by heterotrophic bacteria and accumulates in sediments and pore water. Recent data suggest that unionid mussels are sensitive to un-ionized ammonia (NH3) relative to other organisms. Existing sediment exposure systems are not suitable for ammonia toxicity studies with juvenile unionids; thus, we modified a system to expose juveniles to ammonia that was continuously infused into sediments. This system maintained consistent concentrations of ammonia in pore water up to 10 d. Juvenile Lampsilis cardium mussels were exposed to NH3 in pore water in replicate 96-h and 10-d sediment toxicity tests. The 96-h median lethal concentrations (LC50s) were 127 and 165 microg NH3-N/L, and the 10-d LC50s were 93 and 140 microg NH3-N/L. The median effective concentrations (EC50s) (based on the proportion affected, including dead and inactive mussels) were 73 and 119 microg NH3-N/L in the 96-h tests and 71 and 99 microg NH3-N/L in the 10-d tests. Growth rate was substantially reduced at concentrations between 31 and 76 microg NH3-N/L. The lethality results (when expressed as total ammonia) are about one-half the acute national water quality criteria for total ammonia, suggesting that existing criteria may not protect juvenile unionids.
We examined the effects of atrazine (0-20 mg/L) on embryos, larvae, and adult anuran amphibian species in the laboratory. Atrazine treatments did not affect hatchability of embryos or 96-h posthatch mortality of larvae of Rana pipiens, Rana sylvatica, or Bufo americanus. Furthermore, atrazine had no effect on swimming speed (measured for R. pipiens only). However, there was a dose-dependent increase in deformed larvae of all three species with increasing atrazine concentration. In adult R. pipiens, atrazine increased buccal and thoracic ventilation, indicating respiratory distress. However, because atrazine had no affect on hemoglobin, this respiratory distress was probably not indicative of reduced oxygen-carrying capacity of the blood. Frogs exposed to the highest atrazine concentration stopped eating immediately after treatment began and did not eat during the 14-d experiment. However, no decreases in mass were measured even for frogs that were not eating, probably because of compensatory fluid gain from edema. Atrazine concentrations found to be deleterious to amphibian embryos and adults are considerably higher than concentrations currently found in surface waters in North America. Therefore, direct toxicity of atrazine is probably not a significant factor in recent amphibian declines.
Abstract-A recent ecological risk assessment of the herbicide atrazine found that the ecosystems at greatest risk within North America are the streams, rivers, and reservoirs of the midwestern corn-growing regions. Habitats adjacent to application areas could be exposed to high levels of atrazine during periods of amphibian activity such as breeding and migration. Because fertilizer application coincides both spatially and temporally with atrazine application in agricultural areas, we tested the effects of atrazine and nitrate on northern leopard frog (Rana pipiens) larvae in the laboratory. Larvae were exposed to atrazine (0, 20, and 200 g/ L) and nitrate (0, 5, and 30 mg NO 3 -N/L) from first-feeding stage through metamorphosis in a factorial design. Atrazine concentrations in metamorphosed juveniles were approximately six times the concentration in the water, indicating bioconcentration of atrazine by larvae. Atrazine, nitrate, and their interaction had no significant effect on development rate, percent metamorphosis, time to metamorphosis, percent survival, mass at metamorphosis, or hematocrit. However, nitrate slowed growth of larvae. Though this growth inhibition is statistically significant, it is probably not biologically important when compared with natural variation in the environment. Thus, concentrations of atrazine and nitrate commonly found in the environment do not appear to pose a significant threat to R. pipiens larvae through direct toxicity.
A ecent ecological rsk assessment of the herbicideatrazinefound that theecosystemsat greatest risk within North America are the streams, rivers, and reservoirs of the midwestern corn‐growing regions. Habitats adjacent to application areas could be exposed to high levels of atrazine during periods of amphibian activity such as breeding and migration. Because fertilizer application coincides both spatially and temporally with atrazine application in agricultural areas, we tested the effects of atrazine and nitrate on northern leopard frog (Rana pipiens) larvae in the laboratory. Larvae were exposed to atrazine (0, 20, and 200 μg/L) and nitrate (0, 5, and 30 mg NO3‐N/L) from first‐feeding stage through metamorphosis in a factorial design. Atrazine concentrations in metamorphosed juveniles were approximately six times the concentration in the water, indicating bioconcentration of atrazine by larvae. Atrazine, nitrate, and their interaction had no significant effect on development rate, percent metamorphosis, time to metamorphosis, percent survival, mass at metamorphosis, or hematocrit. However, nitrate slowed growth of larvae. Though this growth inhibition is statistically significant, it is probably not biologically important when compared with natural variation in the environment. Thus, concentrations of atrazine and nitrate commonly found in the environment do not appear to pose a significant threat to R. pipiens larvae through direct toxicity.
We conducted a series of in situ tests to evaluate the effects of pore-water ammonia on juvenile Lampsilis cardium in the St. Croix River (WI, USA). Threats to this river and its associated unionid fauna have accelerated in recent years because of its proximity to Minneapolis-St. Paul, Minnesota, USA. In 2000, caged juveniles were exposed to sediments and overlying water at 12 sites for 10 d. Survival and growth of juveniles was significantly different between sediment (mean, 47%) and water column (mean, 86%) exposures; however, these effects were unrelated to pore-water ammonia. During 2001, juveniles were exposed to sediments for 4, 10, and 28 d. Pore-water ammonia concentrations ranged from 0.3 to 62.0 microg NH3-N/L in sediments and from 0.5 to 140.8 microg NH3-N/L within exposure chambers. Survival (mean, 45, 28, and 41% at 4, 10, and 28 d, respectively) and growth (range, 3-45 microm/d) of juveniles were highly variable and generally unrelated to ammonia concentrations. Although laboratory studies have shown unionids to be quite sensitive to ammonia, further research is needed to identify the route(s) of ammonia exposure in unionids and to understand the factors that contribute to the spatial variability of ammonia in rivers.
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