Use of plants for toxicity assessment of estuarine ecosystems.

Estuarine ecosystems are being rapidly degraded by environmental toxicants from municipal and industrial wastes, agricultural runoff, recreational boating, shipping, and coastal development, ranking them as the most anthropogenically degraded habitat types on earth. Toxicity tests are used to establish links between adverse ecological effects and the toxicity of environmental chemicals. However, most toxicity tests used for regulating the release of chemicals into the environment have used animals as test species, with the erroneous assumption that toxicant levels protective of fish or invertebrates are also protective of plants. Most plant toxicity tests have used terrestrial crop plants, whereas the few aquatic test species used have been primarily freshwater algae. Even though estuarine and marine vascular plants are highly vulnerable to environmental chemicals, phytotoxicity studies using native coastal plants have been limited, and no such studies are required for testing by regulating agencies. The relevance of toxicity tests of estuarine sediments and of wastes entering the estuary should depend on the use of estuarine and marine plant species. This review summarizes toxicity testing of marine plants used in biomonitoring, phytotoxicity, biotransformations of toxicants, bioaccumulation, and phytoremediation. Challenges to marine plant testing are discussed and include developing standard test protocols, identifying species with minimal salinity and toxicant interaction, defining and choosing a suitable sediment for sediment-bound toxicant testing, selecting endpoints with low variability, producing viable seeds, and culturing test plants. Progress in acquiring a suitable database is being made, but at a rate that is inadequate to create the sound, scientific foundation needed for safeguarding our estuarine ecosystems in the near future.

Life-cycle toxicity of bis(tributyltin) oxide to the sheepshead minnow (Cyprinodon variegatus).

The effects of tributyltin (TBT) to the life cycle of the estuarine fish Cyprinodon variegatus were examined in a 180-day flow-through exposure. The study was initiated with embryos less than 24 h postfertilization and monitored through hatch, maturation, growth, and reproduction under continuous exposure to mean measured TBT concentrations of 5.4, 3.2, 1.3, 0.66, and 0.41 microg TBT/L. Progeny isolated at the onset of reproduction by the parental generation (F0) were monitored for survival as embryos, survival as fry/juveniles, and growth 30 days postisolation. TBT, at a concentration of 5.4 microg/L, significantly reduced embryo survival of the F0 generation sheepshead minnows. By day 145 of the exposure, significant effects to the survival of this generation increased and included all test concentrations >/=0.66 microg/L. Survival of 0.66 microg/L was reduced 59% relative to control survival by termination of the F0 generation. Growth of F0 generation organisms as measured by standard length was significantly reduced only on day 90 at 3.2 microg/L, however no significant reductions of wet or dry weight related to treatment concentration were detected. Due to complete mortality of organisms exposed to 5.4 microg/L by study day 7, effects to fecundity and progeny were monitored at measured concentrations of 3.2, 1.3, 0.66, and 0.41 microg TBT/L. Fecundity, as measured by the production of viable eggs produced per female per day, was unaffected by any of the test treatments. All F1 generation embryos isolated from treatment chambers into 3.2 microg/L died. Survival, standard length, wet and dry weight of the F1 generation at the remaining treatment concentrations were unaffected. The results of this study indicate that exposure to TBT reduced survival of the F0 generation sheepshead minnow and establishes the lowest observed effect concentration (LOEC) as 0.66 microg TBT/L, and the no observed effect concentration (NOEC) as 0.41 microg TBT/L for this species.http://link.springer-ny. com/link/service/journals/00244/bibs/37n2p258.html

Stability of a commercially prepared fish oil (omega-3 fatty acid) laboratory rodent diet.

There is evidence that highly unsaturated omega-3 fatty acids present in fish oils can provide a cancer-protective effect; however, when added to laboratory rodent formulations, these fatty acids are subject to rapid and/or extensive oxidation and other chemical changes by exposure to air, light, or heat during processing of pellets or when stored for various lengths of time. An animal diet with 16% refined fish oil and 4% corn oil was commercially prepared with antioxidants (butylated hydroxytoluene and butylated hydroxyquinone in addition to alpha-tocopherol) present, and precautions were taken to prevent oxidation at all stages of production and handling. Fatty acid composition of dried powdered diet as well as freshly processed dried pellets was analyzed from four lots at the beginning and end of a 45-day feeding period. Additionally, fatty acid analyses were carried out on pellets dried by both vacuum and air techniques, and pellets were left exposed to air at room temperature for 96 hours. No statistical difference in overall fatty acid composition was observed among lots due to pelletization or drying procedures. Moreover, 4 days of exposure of pellets to air at ambient temperatures and 45 days of freezer storage had no significant effect on their fatty acid composition. It would appear that rodent diets containing omega-3 fatty acids can be reliably prepared commercially and safely substituted for diets prepared manually and in bulk on a weekly basis.

Carcinogenic effects of some polycyclic aromatic hydrocarbons on the Japanese medaka and guppy in waterborne exposures.

In this paper, we review studies on the carcinogenic effects of two polycyclic aromatic hydrocarbons (PAHs), benzo(a)pyrene (BaP) and 7,12-dimethylbenz(a)anthracene (DMBA), on the Japanese medaka (Oryzias latipes) and the guppy (Poecilia reticulata). Exposure media were prepared by adding PAHs to water, with and without dimethylformamide (DMF) as a carrier, and passing this solution through various sized filters. The low exposure medium was a 0.45 micron filtrate without DMF that contained less than 5 micrograms L-1 PAH. The intermediate medium was a DMF-mediated 0.45 micron filtrate which contained 30-50 micrograms L-1 of PAH. The high medium was a DMF-mediated glass-fibre filtrate which contained 150-250 micrograms L-1 of PAH. Young fish specimens (6-10 d old) were given a 6 h exposure once weekly for 2 to 4 wk. Both BaP and DMBA induced hepatic neoplasms in the two species, with the medaka being more sensitive than the guppy, and DMBA being a stronger carcinogen than BaP. Liver neoplasms almost exclusively developed after exposure to BaP and the neoplasms were limited to the high concentration exposure, whereas DMBA caused a substantial number of extrahepatic neoplasms as well as hepatic ones, especially in the medaka. Furthermore, all three concentrations of DMBA induced hepatic neoplasms in the medaka and all but the low concentration induced neoplasms in the guppy. These studies demonstrate the carcinogenic effects of two waterborne PAHs on two small fish species following brief exposures to very low concentrations, and support the contention that environmental PAHs can contribute to the occurrence of cancer in wild fishes.

Dose-related carcinogenic effects of water-borne benzo[a]pyrene on livers of two small fish species.

Benzo[a]pyrene (BaP) administered by water-borne exposures caused dose-related carcinogenic effects in livers of two small fish species, the Japanese medaka (Oryzias latipes) and the guppy (Poecilia reticulata). Medaka and guppies each were given two 6-h exposures. The first exposure was conducted on 6- to 10-day-old specimens. The second exposure was given 7 days later. The tests incorporated five treatment groups: (1) control, (2) carrier (dimethylformamide) control, (3) low BaP dose (not detectable--4 ppb), (4) intermediate BaP dose (about 8-47 ppb BaP), and (5) high BaP dose (200-270 ppb). Following the high-dose exposure, hepatocellular lesions classified as foci of cellular alteration (altered foci), adenomas, and hepatocellular carcinomas occurred in both species. In medaka, the lesions appeared to develop sequentially with the appearance of altered foci followed by adenomas and then hepatocellular carcinomas. Most lesions in guppies, however, were classified as altered foci although a few adenomas occurred in the early (24-week) sample and hepatocellular carcinomas occurred in the late (52-week) sample. When total lesions were combined, medaka had an 11% incidence at 24 weeks after the initial exposure and 36% incidence at 36 weeks. In guppies, 8% had liver lesions at 24 weeks, 19% at 36 weeks, and 20% at 52 weeks. A single extrahepatic neoplasm, a capillary hemangioma in a gill filament, occurred in a medaka from the 36-week high-dose sample. The results suggest that the medaka and guppy are capable of metabolizing water-borne BaP to carcinogenic metabolites which initiate hepatic tumor development.