The ubiquity of anthropogenic debris in hundreds of species of wildlife and the toxicity of chemicals associated with it has begun to raise concerns regarding the presence of anthropogenic debris in seafood. We assessed the presence of anthropogenic debris in fishes and shellfish on sale for human consumption. We sampled from markets in Makassar, Indonesia, and from California, USA. All fish and shellfish were identified to species where possible. Anthropogenic debris was extracted from the digestive tracts of fish and whole shellfish using a 10% KOH solution and quantified under a dissecting microscope. In Indonesia, anthropogenic debris was found in 28% of individual fish and in 55% of all species. Similarly, in the USA, anthropogenic debris was found in 25% of individual fish and in 67% of all species. Anthropogenic debris was also found in 33% of individual shellfish sampled. All of the anthropogenic debris recovered from fish in Indonesia was plastic, whereas anthropogenic debris recovered from fish in the USA was primarily fibers. Variations in debris types likely reflect different sources and waste management strategies between countries. We report some of the first findings of plastic debris in fishes directly sold for human consumption raising concerns regarding human health.
The chronic effects of dietary selenium (Se) exposure in juvenile Sacramento splittail (Pogonichthys macrolepidotus) were investigated in the laboratory. A total of 960 (40 fish per tank, 3 tanks per diet) 7-month-old juvenile splittail were fed one of eight Purified-Casein diets supplemented with selenized yeast for 9 months in a flow-through system. These diets contained the following: 0.4 (control), 0.7, 1.4, 2.7, 6.6, 12.6, 26.0, and 57.6 mg of Se kg(-1) dry weight. Survival, Se tissue concentration, growth, gross morphology, and liver histopathology were assessed at 5- and 9-month of exposure. Mortalities occurred only in the two highest Se treatments and were accounted for 8.3 and 18.3% at 5-month and 10.0 and 34.3% at 9-month, respectively. Liver and muscle Se concentration were significantly correlated with dietary Se concentration. Fish exposed to 0.4-12.6 mg of Se kg(-1) diets had reached equilibrium in liver Se concentration by 5 month. Splittail fed diets at concentrations > or =26.0 mg of Se kg(-1) had not reached equilibrium in liver, and muscle Se concentrations and grew significantly slower (p < 0.05) at 5- and 9-month exposure. Se-induced deformities were observed in fish fed > or =2.7 mg of Se kg(-1) diets at 5-month and in fish fed > or =0.7 mg of Se kg(-1) diets at 9-month. Fish fed 26.0 and 57.6 mg of Se kg(-1) diets had higher liver lesion scores at 5-month while fish fed 6.6 and 57.6 mg of Se kg(-1) diet had higher liver lesion scores at 9-month. Results indicate that survivals, growth, changes of tissue Se concentrations, and histopathology of juvenile splittail were dose-dependent, but their response thresholds to dietary Se concentrations differed and depended on treatment concentrations and duration of exposure. Chronic exposure to 6.6 mg of Se kg(-1) diet induced deleterious health effects that can potentially impact survival of juvenile splittail.
Sacramento splittail (Pogonichthys macrolepidotus) is a species of special concern in California, due to multiple anthropogenic stressors. To better understand the potential impact of contaminant exposure, adult splittail were captured from the Sacramento-San Joaquin River Delta (California, USA) and analyzed for histopathology and contaminant exposure. Organochlorine contaminants (PCBs, DDTs, dieldrin, chlordanes, and PBDEs) and trace metals (Ag, As, Cd, Co, Cr, Cu, Fe, Mn, Mo, Ni, Pb, Se, Sn, V, and Zn) were detected in the tissues of all fish. In many samples, human health screening values were exceeded for PCBs (83 of 90 samples), DDTs (32 samples), and dieldrin (37 samples). In contrast, thresholds for fish effects were rarely exceeded. Histopathological analysis indicated the presence of macrophage aggregates in gonads, kidneys, and liver and a high incidence of liver abnormalities. In the liver, observed effects were often moderate to severe for glycogen depletion (55 of 95 fish), lipidosis (hepatocellular vacuolation; 51 fish), and cytoplasmic inclusion bodies (33 fish). Correlations between histopathology and tissue contaminant concentrations were weak and inconsistent. Significant correlations were observed between histopathology indicators and reductions in fish size, body condition, lipid content, and liver weight. These results suggest that splittail histopathology varies as a function of health and nutritional status, rather than exposure to legacy organic and metal pollutants.
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