Abstract
Fish consumption is a potential route of human exposure to the hepatotoxic microcystins, especially in lakes and reservoirs that routinely experience significant toxic Microcystis blooms. Understanding the rates of uptake and elimination for microcystins as well as the transfer efficiency into tissues of consumers are important for determining the potential for microcystins to be transferred up the food web and for predicting potential human health impacts. The main objective of this work was to conduct laboratory experiments to investigate the kinetics of toxin accumulation in fish tissue. An oral route of exposure was employed in this study, in which juvenile yellow perch (Perca flavescens) were given a single oral dose of 5 or 20 μg of microcystin-LR (MC-LR) via food and accumulation in the muscle, liver, and tank water were measured over 24 h. Peak concentrations of the water soluble fraction of microcystin were generally observed 8–10 h after dosing in the liver and after 12–16 h in the muscle, with a rapid decline in both tissues by 24 h. Up to 99% of the total recoverable (i.e., unbound) microcystin was measured in the tank water by 16 h after exposure. The relatively rapid uptake and elimination of the unbound fraction of microcystin in the liver and muscle of juvenile yellow perch within 24 h of exposure indicates that fish consumption may not be a major route of human exposure to microcystin, particularly in the Great Lakes.
Highlights
Cyanobacterial harmful algal blooms (HABs) are increasingly prevalent in the Great Lakes as well as smaller inland lakes and reservoirs throughout the world, fueled by eutrophication and perhaps increasing global temperatures [1,2]
Concentrations of microcystins ranged 1–30 μg g−1 in benthic macroinvertebrates in Michigan lakes with Microcystis, 0.017–1.19 μg g−1 in the muscle and liver of Lake Erie juvenile yellow perch and 0.2–1352 μg g−1 in zooplankton [17,28]
These are approximations and the exact concentration of microcystins in each component of the diet is not known, for chironomids which are a significant part of the diet at this life stage, daily exposure to microcystins for this size fish via an early summer diet during a toxic Microcystis bloom is estimated to be in the range of 1–25 μg for yellow perch
Summary
Cyanobacterial harmful algal blooms (HABs) are increasingly prevalent in the Great Lakes as well as smaller inland lakes and reservoirs throughout the world, fueled by eutrophication and perhaps increasing global temperatures [1,2]. Warm, nutrient enriched regions of the North American Great Lakes, such as the western basin of Lake Erie, Saginaw Bay (Lake Huron), and Green Bay (Lake Michigan), summer HAB blooms dominated by Microcystis are common and produce the hepatotoxic microcystins [4,5]. The most commonly occurring variant, as well as one of the most toxic, is microcystin-LR (MC-LR) and the World Health Organization has established a provisional guideline for MC-LR in finished drinking water of 1 μg L−1 [7]. Symptoms of acute microcystin exposure in humans has included gastroenteritis (vomiting, diarrhea, abdominal cramping) and blistering around the mouth and pneumonia during incidences of immersion [9,10,11]
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