West lakes, are caught fish safe to eat

[marko 0]

OK folks the big question is, is it likely to cause major harm to eat your catch from West Lakes? Just interested to know your opinions as I have eaten ST, Gar, Flounder, Mullet, and bream I have caught there (seems to have done me no harm apart from the second head I have sprouted and the fifth eye I now have!). Does anyone know if any serious research has been done on water quality there and any build up of toxins in fish at West Lakes and for that matter West Beach? Cheers guys any thoughts appreciated Marko.

[archerfish 685]

G'day markoWithout digging too deeply into this site, I suspect this topic may have already had a bit of a run previously.I am not aware of any research that has been done re toxins in fish in West Lakes (or any other bread & butter fisheries, if it comes to that). My question is: If an edible fish (of any description) migrates from a so-called "suspect" area to a "safe" area, how the hell would you tell?!It hasn't affected me so far so far so far so far so far so far...oh shit!!!Cheersarcherfish

[smokeykebab 175]

I don't eat the bream, flounder or mulloway or any fish I think is a permanent resident of the lake. mullet, salmon, garfish, tommys and whiting come in seasonally so I eat them.

[brenton 637]

I don't eat the bream' date=' flounder or mulloway or any fish I think is a permanent resident of the lake. mullet, salmon, garfish, tommys and whiting come in seasonally so I eat them.[/quote']Good advice i reckon Smokey. cheers brenton

[WilliamPerry 0]

Personally,I steer clear of them all :sick:

[marko 0]

Thanks Moggy, it would be interesting if Pirsa tagged some of the common species just to get some idea of their range and if they get into some of the more polluted areas,you never quite know round the Metro waters just when the fish have been and what they are ingesting...... Maybe that can be an excuse I can use on my missus to go further afield more often!

[brenton 637]

Heaps on the net about the cadmium in the W.Ls area and most of the parks surrounding the lake are having the grass removed and trees planted because of the fear of pollution leaching into the water with the runoff. cheers brenton

[marko 0]

Heaps on the net about the cadmium in the W.Ls area and most of the parks surrounding the lake are having the grass removed and trees planted because of the fear of pollution leaching into the water with the runoff. cheers brenton

Cheers Brenton, that really gets me thinking, hmmm don't they use cadmium in high powered batteries? Bugger if I'm out fishing at night strike hookers will be able to recognise me ( I will be the bloke who glows brightly in the dark). Thanks mate, onya Marko.

[Ranger 48]

This is taken from a report produced back in 2007, by Dr Lindsay Swinden PhD, the CEO of OMIC Australia, on sediments taken during the dredging of Port Philip Bay, Victoria.You might find it quite interesting!

CadmiumCadmium is a chemical element in the periodic table that has the symbolCd and atomic number 48. A relatively rare, soft, bluish-white, transitionmetal, cadmium is known to cause cancer and occurs with zinc ores.Cadmium is used largely in batteries and pigments, for example in plasticproducts. Cadmium is an occupational hazard associated with industrialprocesses such as metal plating and the production of nickel-cadmiumbatteries, pigments, plastics and other synthetics. The primary route ofexposure in industrial settings is inhalation. Inhalation of cadmiumcontainingfumes can result initially in metal fume fever but may progressto chemical pneumonitis, pulmonary oedema, and death.9Cadmium is also a potential environmental hazard. Human exposures toenvironmental cadmium are primarily the result of the burning of fossilfuels and municipal wastes. However, there have been notable instancesof toxicity as the result of long-term exposure to cadmium incontaminated food and water. In the decades following World War II,Japanese mining operations contaminated the Jinzu River with cadmiumand traces of other toxic metals. Consequently, cadmium accumulated inthe rice crops growing along the riverbanks downstream of the mines. Thelocal agricultural communities consuming the contaminated rice developedItai-itai disease and renal abnormalities, including proteinuria andglucosuria.Cadmium has been reported by many workers to be harmful to all livingsystems with no known biological requirement. Although work by VonZglinicki et al (1992) has postulated that very low levels of cadmium maystimulate DNA synthesis and cell growth. A relationship between thechemistry and the toxicity of cadmium was shown by Bienvenu et. al.,(1963) when he determined the dose of various soluble metal compoundsgiven to mice that resulted in the death of 50 % of the animals within 30days (LD50). He noted regularities between the relative toxicity and theposition of the element in the periodic table.The strongest trend appears to be the general decrease in the LD50 inthe order : M+ ions of group Ia, M2+ ions of group IIa, M3+ ions of groupIIIa, M2+ ions of the first transition series and then M+, M2+ and M3+ ionsof the post transition element groups Ib - IIIb. A second trend appearsin the M2+ transition metal cations, this is a decrease in the LD50 withincreasing atomic number. The greater toxicity of the heavy metals isalso apparent within groups IIb and IIIb. The graph highlights cadmium,a divalent, post transition metal, as one of the most toxic elements with aLD50 of 0.000033 g-moles/kg. Only indium (as In3+) and mercury (as Hg2+)were found to be more toxic .All heavy metals can form a wide variety of coordination compounds andions that bind to various polydentate organic ligands. The binding of suchmetal ions appears to link enzymes to substrates and may be partlyresponsible for the power of enzymes to catalyse biochemical reactions.The most important donor atoms that link metal ions to biologicalmolecules are oxygen (O), nitrogen (N) and sulphur (S). This can be shownas a series of bidentate ligands which are attached to the metal ion bytwo donor atoms to form a chelate complex : oxalate (OO), glycine (ON),ethylene diamine (NN), mercaptyl acetate (SO) and mercaptyl amine (SN).10It can be shown that cadmium should not displace any of the metalsshown from an oxygen donating ligand but will displace Mn2+ and Fe2+ fromnitrogen donors. Cadmium is bound to sulfur more strongly than all themetals shown except Cu2+ and Hg2+. The very extended capability ofcadmium to bind to nucleophillic sites of macromolocules (proteins, DNAand RNA) accounts for the multiplicity of toxic effects observed in vitroand in vivo. These chemical reactions and the relatively strong bonding ofcadmium to sulphur donating enzymes may partly explain the effect ofsmall amounts of cadmium on living systems.Long-term exposure to cadmium results in an irreversible tubularnephropathy that may develop into renal insufficiency. The cadmiummetallothioneincomplex is taken up almost quantitatively from theglomerular filtrate by epithelial cells of the proximal tubule and rapidlydegraded by lysosomes. Although biosynthesis of metallothionein, inresponse to cadmium ions liberated by proteolysis, also occurs in thesecells. It has been reported by a number of authors that part of thecadmium ions escapes this cytosolic binding system and reaches othersubcellular targets (such as the mitochondria and the nucleus). As aresult, the reabsorption of low molecular weight proteins (including β2-microglobulin), ions (calcium and phosphate) and small solutes (glucose andaminoacids) is irreversibly impaired.The relationship between the critical concentration of cadmium in renalcortex and the early signs of tubular dysfunction in humans has been thesubject of numerous studies in both groups of exposed workers andpopulations living in polluted areas. A limit of urinary cadmium excretionof approximately 4 g/g of creatinine has been derived from surveysconducted in the Ishikawa prefecture of Japan (Itai-Itai disease).Beyond this level the excretion of ß2-metallothionein-cadmium complexbecomes pathologicalBelgian studies have found evidence that the threshold of urinarycadmium for increased excretion of low molecular weight proteins,aminoacids and calcium is approximately 2 g/g. This is reached in 10 % ofsubjects in the general population and increases to 16 % of the populationover the age of 60 . The retrospective study of the causes of mortality,from 1969 to 1976, indicates a very significant increase in mortality fromnephrosis and nephritis in women over 60 and living in the Liegeconurbation. This area has been markedly polluted by cadmium emissionsfrom zinc smelters.11Although the Itai-Itai syndrome, in which renal insufficiency isassociated with osteoprosis and osteomalacia, has been studied for morethan twenty years, the precise pathogenic mechanism of this disease hasnot been fully established. It is not known whether bone demineralisationis secondary to nephrotoxic damage or results from a direct effect onbone tissue. Studies conducted in Japan strongly suggest thatosteopathies and mortality, at least in women, are closely related to thekidney damage characterised by the urinary excretion of ß2-metallothionein-cadmium complex.Three hypotheses have been formulated for osteotoxicity and partiallyconfirmed by experiments on animals, tissue and cells in culture. The firstinvolves an inhibition of the formation of the dihydroxylated metaboliteof vitamin D3 leading to a reduction in the incorporation of cadmium in thebone and ultimately to osteomalacia. The production of this activemetabolite of vitamin D3 is dependant on cyclic AMP, adenylate cyclase,parathyroid hormone and cytochrome(s) P-450, all of which are factorsadversely affected by exposure to cadmium. The second hypothesisimplies that cadmium counteracts the absorption of calcium in the smallintestine, decreasing the bioavailability of this element and producing adecalcification of bone that is the primary characteristic of osteoporosis.The third proposes a disturbance of collagen in bone by inhibition oflysyl-oxidase.Nutritional deficiencies (calcium and vitamin D), multiparity and hormonalfactors are key factors in the development of cadmium-induced bonepathology. It has been reported that cadmium causes bone lesions inrodents when associated with a hypocalcic diet but this is at a lessermagnitude than that found in Itai-Itai patients. In Japanese women withrenal dysfunction that was associated with bone damage or not, theisozyme of alkaline phosphatase originating from bone tissue was elevatedby cadmium exposure. This indicates a direct effect of cadmium on bonemineralisation.Many studies, mostly carried out more than 15 years ago, havedemonstrated that chronic oral administration of low levels of cadmium torats, via food or drinking water, causes a rise of arterial pressure. Thesestudies indicate that the pressor effect of cadmium can only be observedin the presence of a range of experimental conditions (strain, compositionof the diet, exposure time, etc). None of these studies have shown themechanism(s) of the hypertensive effect of cadmium.12This is not surprising as blood pressure is regulated by many systems thatmay be mutually compensating. The pressor effect of cadmium may beregarded as a direct effect on vasculature, a functional damage to thekidneys and an altered liberation of neuromediators. Some surveys, onsmall groups of human with low-level environmental exposure, have founda positive association between the accumulation of cadmium and anincrease in blood pressure. Other surveys have failed to confirm it oreven have revealed negative correlations between the two variables.None of the studies conducted in several cadmium-polluted districts inJapan, the United Kingdom, Belgium or in the United States have shownevidence of a positive relationship between blood pressure, theprevalence of cardiovascular diseases and urinary cadmium. Also, thesignificant increase in mortality in Japanese suffering from tubularproteinuria is not associated with a greater prevalence of hypertensionand cardiovascular disease.In rodents, acute intratesticlar administration has long been shown toproduce vascular lesions and interstitial oedema provoking a reduction inthe production of androgens and a failure of spermiation. However, theeffect of low-level expose on male reproductive organs is less obvious.Data relating to man is very limited and indicates that moderate longtermexposure has little effect on male sterility. Pre- and post-natalexposure of female rats to cadmium produced a reduction of oestrogenproduction and development of the utero-ovarian function. This functionis also affected in adult females, particularly with regard to theimplantation and growth of the embryo.Exposure to cadmium during successive pregnancies increases the amountof metal stored in the kidneys of mice and it has been suggested that inmammals, including man, maternal exposure produces a placentalaccumulation of the metal with a subsequent loss of zinc. He suggestedthat the decrease in placental Zn/Cd ratio observed in mothers thatsmoke tobacco, may be associated with a reduced foetal growth andconsequently a decreased birth weight.Cadmium appears to be both a direct and indirect mutagenic agent in bothbacteria and mammalian cells. The most frequent chromosomicaberrations in eucaryote cells are ruptures and lacunae (gaps) rather thanexchanges. Aneuploidy and blockade of meiotic division have also beenfound in yeasts and oocytes, demonstrating that cadmium acts as a13cytoskeletal poison. Studies of lymphocyte chromosomes from humansubjects exposed to cadmium in the workplace or suffering from Itai-Itaihave produced conflicting results.Epidemiological data on groups of exposed workers in the USA and Europehas been collected from the beginning of 1960 and updated periodically.This shows a very clear relationship between long-term exposure tocadmium oxide dust and fumes and the prevalence of cancers of therespiratory tract and a weaker relationship to prostate cancers. Cadmiumhas been placed in group I of the IARC classification of carcinogens. Noclear relationship between the prevalence of internal cancers and thedietary intake of cadmium has been shown in countries such as Japan andBelgium where environmental contamination is high. Limited data fromCanada and the USA suggest that there may be a positive link betweenthe overall level of environmental pollution by cadmium and prostratecancer.

Bear in mind, Cadmium is merely one single pollutant we find in the local area. I can produce reams of this stuff on many other pollutants in our environment!Wanna talk about aldrin, antimony, arsenic, barium, beryllium, chlordane, chromium, DDT, dieldrin, dioxins, endosulphan, and the list goes on and on.Us humans are very good at destroying our own environment, wheras most other animals dont actually sh*t in their own nests!Enjoy ya dinner!

[marko 0]

Thanks Ranger certainly makes some scary bed time reading. Guess I might think twice about chewing on a West Lakes fish in future. The new thread I put up about: "fish shaped coffins" might become a reality if I am not careful! Cheers mate think I will aim for waters further a field. That's what happens when you are an ignorant Pom like me, we fish the Thames river (major U.K. river) which is recycled 7 times before it hits the sea, imagine what nasties are in those Pommy fish! Thanks again, Marko.

[Ranger 48]

Marko, I think we all need to get this into some sort of perspective.All around the world, wherever there are built up populations (cities), industry, or even farming, there will also be a subsequent build up of pollutants. Down through the years we've also used some pretty nasty stuff, and even though these days some of the more nasties have been banned for use, it still lays buried in the soil and buried in the silt beneath our waterways.It's very simple for anyone to take a sample and identify what is actually down there, ie: if an element is present or not, but it's much more difficult to quantify how much of any given substance lies beneath the soil or water.The only real way to get a true guage, is to dig it all up, and test it all, which of course is an impossibility.So at the end of the day, yes there are pollutants in our environment, but none of us know how much, how safe the fish is to eat, the water is to drink, or the soil to plant.I think it's important that we are all AWARE of pollutants, but our decisions on what to eat, drink and breathe, are individual decisions we all must make for ourself.Me personally, I don't eat any of the slow growing or resident species in our local waterways.You may make an entirely different decision.At the end of the day, some pollutant may cause me to die from cancer, or I could get cancer from the years of cigarette smoking behind me. Then again, I could get hit by a bus tomorrow, because buses can be dangerous too. I could fall of a cliff in a drunken stupor, crash my car, get blown up in a terrorist bombing, nuked in the next global conflict, do a Steve Irwin with a stingray, be beaten to death by an angered wife, or meet any number of ways to imminent demise.I just try to be aware of dangers, weigh up risks, and live my life accordingly.

[WilliamPerry 0]

be beaten to death by an angered wife

I don't think that you would be the Lone Ranger there mate (pun intended),but they do get angry at times,but I don't know why?????Forgotten anniversary / birthday,late,fishing again, pi$$ed again,watching footy / cricket / Com Games on TV.....what's their problem;)

[silaflex 103]

Probably no worse than eating the good old Mekong Catfish :sick: aka supposedly a lot of the imported fleshy fish sold in supermarkets and fish shops under many different names.

[Ranger 48]

Probably no worse than eating the good old Mekong Catfish :sick: aka supposedly a lot of the imported fleshy fish sold in supermarkets and fish shops under many different names.

Pacific Dory, Catfish, etc.Now that names have been standardised it's only known as Basa, and country of origin must now also be stated.

[spog777 1]

Its ok to eat the WL fish - just not to swallow them after chewing Actually i dont eat WL of Port River species-you can easily tell the difference-PR species glow. The chances of the fish being affected by chemicals, toxic sea weeds etc isnt worth the risk-i just catch, photo and release