Aluminium in Fisch und Fischereierzeugnissen

Recent reports associating aluminium with several skeletal (osteomalacia) and neurological disorders (encephalopathy and Alzheimer’s disease) in humans suggest that exposure to aluminium may pose a hazard to health. This requires the examination of aluminiumcontent in different foodstuffs. Therefore, an analytical method for the determination of aluminium in fish and fishery products, especially in fishery products packaged in aluminium cans, was developed using graphite furnace atomic absorption spectrometry. Fillets of lean and fatty fish showed aluminium levels lower than 1mg/kg wet weight, muscle of crustacean, molluscan and shellfish had apparently higher aluminium levels (up to 20 mg/kg wet weight). The aluminium content in some aluminum-canned herring was much higher than the content found in herring caught in the North Sea. These results indicate that aluminium is taken up by the herring fillets in aluminium cans, presumably through the slight and slow dissolution of aluminium from the can wall, due to some defects in the protective lacquer layer. A comparison of the aluminium levels measured in canned herring with the average aluminium-intake (normally between 3 and 5 mg/day) or with the provisional tolerable daily intake of 1mg/kg body weight per day (WHO 1989) indicated, that the aluminium content of the edible part of aquatic food does not play a significant role. High consumption of fish fillets does not pose any health risk.

Harmful algal blooms in coastal waters: options for prevention, control and mitigation

This report is the product of a panel of experts in the science of blooms of unicellular marine algae which can cause mass mortalities in a variety of marine organisms and cause illness and even death in humans who consume contaminated seafood. These phenomena are collectively termed harmful algal blooms or HABs for short. As a counterpart to recent assessments of the priorities for scientific research to understand the causes and behavior of HABs, this assessment addressed the management options for reducing their incidence and extent (prevention), actions that can quell or contain blooms (control), and steps to reduce the losses of resources or economic values and minimize human health risks (mitigation). This assessment is limited to an appraisal of scientific understanding, but also reflects consideration of information and perspectives provided by regional experts, agency managers and user constituencies during three regional meetings. The panel convened these meetings during the latter half of 1996 to solicit information and opinions from scientific experts, agency managers and user constituencies in Texas, Washington, and Florida. The panel's assessment limited its attention to those HABs that result in neurotoxic shellfish poisoning, paralytic shellfish poisoning, brown tides, amnesic shellfish poisoning, and aquaculture fish kills. This covers most, but certainly not all, HAB problems in the U.S.

Osmotic stress does not trigger brevetoxin production in the dinoflagellate Karenia brevis

With the global proliferation of toxic Harmful Algal Bloom (HAB) species, there is a need to identify the environmental and biological factors that regulate toxin production. One such species, Karenia brevis, forms nearly annual blooms that threaten coastal regions throughout the Gulf of Mexico. This dinoflagellate produces brevetoxins, potent neurotoxins that cause neurotoxic shellfish poisoning and respiratory illness in humans, as well as massive fish kills. A recent publication reported that a rapid decrease in salinity increased cellular toxin quotas in K. brevis and hypothesized that brevetoxins serve a role in osmoregulation. This finding implied that salinity shifts could significantly alter the toxic impacts of blooms. We repeated the original experiments separately in three different laboratories and found no evidence for increased brevetoxin production in response to low-salinity stress in any of the eight K. brevis strains we tested, including three used in the original study. Thus, we find no support for an osmoregulatory function of brevetoxins. The original publication also stated that there was no known cellular function for brevetoxins. However, there is increasing evidence that brevetoxins promote survival of the dinoflagellates by deterring grazing by zooplankton. Whether they have other as yet unidentified cellular functions is currently unknown.

An assessment of polybrominated diphenyl ethers (PBDEs) in sediments and bivalves of the U.S. coastal zone

NOAA’s Mussel Watch Program was designed to monitor the status and trends of chemical contamination of U.S. coastal waters, including the Great Lakes. The Program began in 1986 and is one of the longest running, continuous coastal monitoring programs that is national in scope. NOAA established Mussel Watch in response to a legislative mandate under Section 202 of Title II of the Marine Protection, Research and Sanctuaries Act (MPRSA) (33 USC 1442). In addition to monitoring contaminants throughout the Nation’s coastal shores, Mussel Watch stores samples in a specimen bank so that trends can be determined retrospectively for new and emerging contaminants of concern. In recent years, flame retardant chemicals, known as polybrominated diphenyl ethers (PBDEs), have generated international concern over their widespread distribution in the environment, their potential to bioaccumulate in humans and wildlife, and concern for suspected adverse human health effects. The Mussel Watch Program, with additional funding provided by NOAA’s Oceans and Human Health Initiative, conducted a study of PBDEs in bivalve tissues and sediments. This report, which represents the first national assessment of PBDEs in the U.S. coastal zone, shows that they are widely distributed. PBDE concentrations in both sediment and bivalve tissue correlate with human population density along the U.S. coastline. The national and watershed perspectives given in this report are intended to support research, local monitoring, resource management, and policy decisions concerning these contaminants.

Liver genomic responses to ciguatoxin: evidence for activation of Phase I and Phase II detoxification pathways following an acute hypothermic response in mice

Ciguatoxins (CTX) are polyether neurotoxins that target voltage-gated sodium channels and are responsible for ciguatera, the most common fish-borne food poisoning in humans. This study characterizes the global transcriptional response of mouse liver to a symptomatic dose (0.26 ng/g) of the highly potent Pacific ciguatoxin-1 (P-CTX-1). At 1 h post-exposure 2.4% of features on a 44K whole genome array were differentially expressed (p ≤ 0.0001), increasing to 5.2% at 4 h and decreasing to 1.4% by 24 h post-CTX exposure. Data were filtered (|fold change| ≥ 1.5 and p ≤ 0.0001 in at least one time point) and a trend set of 1550 genes were used for further analysis. Early gene expression was likely influenced prominently by an acute 4°C decline in core body temperature by 1 h, which resolved by 8 h following exposure. An initial downregulation of 32 different solute carriers, many involved in sodium transport, was observed. Differential gene expression in pathways involving eicosanoid biosynthesis and cholesterol homeostasis was also noted. Cytochrome P450s (Cyps) were of particular interest due to their role in xenobiotic metabolism. Twenty-seven genes, mostly members of Cyp2 and Cyp4 families, showed significant changes in expression. Many Cyps underwent an initial downregulation at 1 h but were quickly and strongly upregulated at 4 and 24 h post-exposure. In addition to Cyps, increases in several glutathione S-transferases were observed, an indication that both phase I and phase II metabolic reactions are involved in the hepatic response to CTX in mice.