RESUMO
The Pine River downstream of the Velsicol Superfund site has been contaminated with various hydrophobic organic pollutants for more than 50 years. Remediation and sediment dredging near the site began in spring of 1999, and was completed in 2006. In 2011, the Michigan Department of Environmental Quality completed a baseline assessment report long-term monitoring plan for the Pine River. However, there has been limited assessment of the benthic community since this evaluation. The objective of this research was to evaluate the risk of Pine River sediment to aquatic macroinvertebrates downstream from the Superfund site after decades of degradation and dredging using the Triad approach. Three sites were selected downstream from the Superfund site, and an upstream reference site was used. At each site, macroinvertebrates surveys were conducted and sediments were collected for chemical analysis of DDT (1,1,1-trichloro-2,2-bis (4-chlorophenyl) ethane) and its degradation products and for laboratory toxicity testing for mortality and sublethal effects using Hyalella azteca and Chironomus dilutus. Sediment concentrations of DDT, DDD, and DDE were below levels expected to cause toxicity, and there was no observed toxicity in laboratory tests. Additionally, there were no statistically significant differences in richness, richness of Ephemeroptera, Plecoptera, and Trichoptera (EPT) species, total EPT abundance, percent EPT, or percent dominant taxa between the reference site and the downstream sites. There was an observed decrease in abundance of macroinvertebrate taxa at all downstream sites and a shift in macroinvertebrate structure when comparing the reference with most impaired sites. Although the sites downstream of the Superfund site remain different than the upstream control, there are improvements in species composition and abundance. However, more research is needed to evaluate the potential effects on ecosystem function.
Assuntos
DDT/análise , Diclorodifenil Dicloroetileno/análise , Diclorodifenildicloroetano/análise , Monitoramento Ambiental/métodos , Sedimentos Geológicos/química , Locais de Resíduos Perigosos , Poluentes Químicos da Água/análise , Anfípodes/efeitos dos fármacos , Animais , Chironomidae/efeitos dos fármacos , DDT/metabolismo , Ecossistema , Michigan , Rios/química , Testes de ToxicidadeRESUMO
The cyanobacterium, Microcystis aeruginosa, can produce the hepatotoxin microcystin. When toxic M. aeruginosa overwinters in the sediments of lakes, it may be ingested by aquatic insects and bioaccumulate in nymphs of Hexagenia mayflies. When volant Hexagenia emerge from lakes to reproduce, they provide an abundant, albeit temporary, food source for many terrestrial organisms including bats. Little brown bats, Myotis lucifugus, feed opportunistically on aquatic insects including Hexagenia. To determine if microcystin moves from aquatic to terrestrial ecosystems via trophic transfer, we combined a dietary analysis with the quantification of microcystin in bat livers and feces. In June 2014, coincident with the local Hexagenia emergence, bat feces were collected from underneath a maternity roost near Little Traverse Lake (Leelanau County, Michigan, USA). Insects in the diet were identified via molecular analyses of fecal pellets from the roost and from individual bats. Livers and feces were collected from 19 female M. lucifugus, and the concentrations of microcystin in these liver tissues and feces were measured using an enzyme-linked immunosorbent assay (ELISA) and liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). We show that the majority of the bats' diets consisted of aquatic insects and that microcystin was detected in high concentrations (up to 129.9 µg/kg dw) in the bat feces by ELISA. Histopathological examination of three bat livers with the highest concentrations of microcystin showed no evidence of phycotoxicosis, indicating that M. lucifugus may not be immediately affected by the ingestion of microcystin. Future work could examine whether bats suffer delayed physiological effects from ingestion of microcystin.