yummy bream

[breamzy malone 0]

hey therei just thought i would let you know how good bream tastei cooked up 2 from the port river last nightboth around 40cmjust gut em and scale then stuff em with chicken stuffinginto the oven andummmmm yummy breami was always told the big ones dont taste goodbut ive found the bigger the betterstuff lettin them gostuff em and cook em :icon_lol:

[Ranger 48]

I cant complain if anyone wants to take or eat Bream, so long as they're above the legal size limit of 28cm, and below the daily bag limit, but I'm wondering if this post is really fair dinkum, or if it was just put here to stir the pot, given these comments and all we know about the slow growth of Bream:

2 from the port river both around 40cmthe bigger the betterstuff lettin them go

Excerpt from fishingwa.com

They grow relatively quickly for their first few years (which is still slow by other fish standards) but then slow down in their latter years only growing about 1cm a year. A large bream of 35-40cm is about 15 years or more of age. They can take anything from 5 to 10 years to reach legal size and they can reach a maximum age of over 25 years. Seeing as they are so slow to grow, it makes good sense to take care of the larger breeding bream as they are vital to ensure future populations.

fishvictoria.com

DID YOU KNOW: It can take up to NINE YEARS* for black bream to reach the minimum legal size of 26cm, another very good reason to return all undersize or unwanted bream safely to the water. See more information on handling and releasing fish here . Bream may live as long as 20 years and approximate growth rates* are: 1 year - 9cm2 years - 14cm3 years - 18cm4 years - 21cm5 years - 22cm6 years - 23cm7 years - 24cm8 years - 25cm26cm - Minimum Legal Size (vic)9 years - 26cm10 years - 30.5cm12 years - 33cm16 years - 36.5cm20 years - 38.75cm *Data from studies carried out by the Central Ageing Facility at the Marine and Freshwater Resources Institute, Queenscliff.

So lemme see! That's approximately 40 years worth of fish growth eaten in one meal! The equivalent of eating around 30 legal sized KG Whiting! Yep, I sure hope you enjoyed ya meal, me, I'll have 2 KG's instead thanks!

[kayakfisher 0]

I got that feeling too... but I'd just like to say I have never had a bream that tastes anywhere near good out of the port river, or just about any estuary around S.A. If you are lucky enough to get one from the surf they are great eating. But that doesn't happen too often.

[Ranger 48]

I'd just like to say I have never had a bream that tastes anywhere near good out of the port river, or just about any estuary around S.A.

40 years of living in that polluted, toxic filth, I'm hardly surprised!Here's some of the groovy stuff those fish are now "likely" to contain, and the problems this stuff will cause, and remember, this stuff is CUMULATIVE! Once it's in your system it DOESN'T go away! You just injest more and more as time goes by, and this stuff doesn't make you sick, it's TERMINAL illnesses this stuff causes:

AldrinAldrin is an organochlorine insecticide which is oxidized in the insect toform dieldrin, a neurotoxin. Aldrin was formerly used to kill soil insectssuch as termites and grasshoppers to protect crops such as corn andpotatoes. It has been classified as a persistent organic pollutant. Due tohealth concerns regarding dieldrin, it is no longer manufactured or used inthe United States. In addition, aldrin is itself a carcinogen and mutagen.AntimonyAntimony is a chemical element in the periodic table that has the symbolSb (Latin: stibium, meaning "mark") and atomic number 51. A metalloid,antimony has four allotropic forms. The stable form of antimony is a bluewhitemetalloid. Yellow and black antimony are unstable non-metals.Antimony is used in flame-proofing, paints, ceramics, enamels, a widevariety of alloys, electronics, and rubber.Antimony and many of its compounds are toxic. Clinically, antimonypoisoning is very similar to arsenic poisoning. In small doses, antimonycauses headache, dizziness, and depression. Larger doses cause violentand frequent vomiting, and will lead to death in a few days.A study found that antimony is leaching from PET bottles (reported forsome acidic fruit drinks), but at levels below drinking water guidelines.The guidelines are: WHO, 20 μg l–1 US EPA, Health Canada and the Ontario Ministry of Environment, 6μg l–1 German Federal Ministry of Environment, 5 μg l–1[12] Japan, 15 μg l–1[13]The acidic nature of the drink is sufficient to dissolve small amounts ofantimony oxide contained in the packaging of the drink; modernmanufacturing methods prevent this occurrence. However, researchersare concerned that antimony levels correspond to duration the bottle isleft to stand - the longer the water has been bottled, the higher theantimony leached.6ArsenicArsenic is very similar chemically to its predecessor, phosphorus. Similarto phosphorus, it forms colorless crystalline oxides As2O3 and As2O5 thatare hygroscopic and readily soluble in water to form acidic solutions.Arsenic (V) acid, like phosphoric acid, is a strong acid. Like phosphorus,arsenic forms an unstable, gaseous hydride: arsine (AsH3). The similarityis so great that arsenic will partly substitute for phosphorus inbiochemical reactions and is thus poisonous. However, in subtoxic doses,soluble arsenic compounds act as stimulants, and were once popular insmall doses as medicinals by people in the mid 18th century. Leadhydrogen arsenate has been used, well into the 20th century, as aninsecticide on fruit trees (sometimes resulting in brain damage to thoseworking the sprayers), and Scheele's Green (a copper arsenate) has evenbeen recorded in the 19th century as a coloring agent in sweets. In thelast half century, monosodium methyl arsenate (MSMA), a less toxicorganic form of arsenic, has replaced lead arsenate's role in agriculture.Copper acetoarsenite was used as a green pigment known under manydifferent names, including 'Paris Green' and 'Emerald Green'. It causednumerous arsenic poisonings. Arsenic poisoning kills by allosteric inhibitionof essential metabolic enzymes, leading to death from multi-system organfailure.The LD50 for pure arsenic is 763 mg/kg (by ingestion) and 13 mg/kg (byintraperitoneal injection). For a 70 kg (~155 lb) human, this works out toabout 53 grams (less than 2 ounces). However, compounds containingarsenic can be significantly more toxic. Chronic arsenic poisoning resultsfrom drinking water with high levels of arsenic over a long period of time.This may occur due to Arsenic contamination of groundwater.Effects include changes in skin colour, formation of hard patches on theskin, skin cancer, lung cancer, cancer of the kidney and bladder, and canlead to gangrene. The World Health Organization recommends a limit of0.01 mg/L of arsenic in drinking water; consumption of higher levels overlong periods of time can lead to arsenicosis. Non-carcinogenic chroniceffects include liver injury - jaundice and cirrhosis, peripheral vasculardisease involving blueness of the extremities, Raynaud's syndrome, andblackfoot disease (a type of gangrene), anemia, resulting from impairedheme biosynthesis, hyperkeratosis of the skin. There are also multiplelines of evidence for the carcinogenic effects of arsenic.7Arsenic has been known to cause many problems in third world countrieswhere ground water supplies have been contaminated by arsenic derivedfrom geologically recent fluvial deposits containing arseno-pyrites. This isa particular problem in Bangladesh where tube wells installed since the1970s have intercepted ground waters flowing in the fluvial deposits.Concentrations in these wells can exceed 1 part per thousand whereas theWHO maximum level is 10 parts per billion.It has also been confirmed that natural arsenic contamination of drinkingwater has also been a problem in wells in New Hampshire, USA. Chroniclow level arsenic poisoning, or arsenicosis, such as is seen in Bangladeshcan potentially result in the victim developing cancer.

That's only the a's I've covered. Want me to continue, coz I've got the rest of the alphabet here?

[Ranger 48]

BariumBarium is a chemical element. It has the symbol Ba, and atomic number56. Barium is a soft silvery metallic alkaline earth metal. It is never foundin nature in its pure form due to its reactivity with air. Its oxide ishistorically known as baryta but it reacts with water and carbon dioxideand is not found as a mineral.Barium compounds are extremely poisonous. At low doses, barium acts asa muscle stimulant, while higher doses affect the nervous system, causingcardiac irregularities, tremors, weakness, anxiety, dyspnea and paralysis.This may be due to its ability to block potassium ion channels which arecritical to the proper function of the nervous system. Unlike other heavymetals, barium does not bioaccumulate. However, inhaled barium dust canaccumulate in the lungs, a benign condition called baritosis.BerylliumBeryllium is the chemical element that has the symbol Be and atomicnumber 4. A bivalent element, elemental beryllium is a steel grey, strong,light-weight yet brittle, alkaline earth metal. It is primarily used as ahardening agent in alloys (most notably beryllium copper). Beryllium andits salts are toxic substances and potentially carcinogenic. Chronicberylliosis is a pulmonary and systemic granulomatous disease caused byexposure to beryllium. Acute beryllium disease in the form of chemicalpneumonitis was first reported in Europe in 1933 and in the UnitedStates in 1943. Cases of chronic berylliosis were first described in 1946among workers in plants manufacturing fluorescent lamps inMassachusetts. Chronic berylliosis resembles sarcoidosis in manyrespects, and the differential diagnosis is often difficult.8Some people (1-15%) become sensitive to beryllium. These individuals maydevelop an inflammatory reaction that principally targets the respiratorysystem and skin. This condition is called chronic beryllium disease (CBD),and can occur within a few months or many years after exposure tohigher than normal levels of beryllium (greater than 0.02 μg/m³). Thisdisease causes fatigue, weakness, night sweats and can cause difficulty inbreathing and a persistent dry cough. It can result in anorexia, weightloss, and may also lead to right-side heart enlargement and heart diseasein advanced cases. Some people who are sensitized to beryllium may nothave any symptomsThere are no studies on the health effects of children exposed toberyllium, although individual cases of CBD have been reported in childrenof beryllium workers from the 1940s. It is likely that the health effectsseen in children exposed to beryllium will be similar to the effects seen inadults. It is unknown whether children differ from adults in theirsusceptibility to beryllium. It is unclear whether beryllium is teratogenic.Compliance with the current U.S. Occupational Safety and HealthAdministration (OSHA) permissible exposure limit for beryllium of 2μg/m³ has been determined to be inadequate to protect workers fromdeveloping beryllium sensitization and CBD. The American Conference ofGovernmental Industrial Hygienists (ACGIH), which is an independentorganization of experts in the field of occupational health, has proposed athreshold limit value (TLV) of 0.05 μg/m³ in a 2006 Notice of IntendedChange (NIC). This TLV is 40 times lower than the current OHSApermissible exposure limit, reflecting the ACGIH analysis of bestavailable peer-reviewed research data concerning how little airborneberyllium is required to cause sensitization and CBD.

[Ranger 48]

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.

[Ranger 48]

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.12

[Ranger 48]

This 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.

[Ranger 48]

ChlordaneChlordane is a manufactured chemical that was used as a pesticide in theUnited States from 1948 to 1988. It does not occur naturally in theenvironment. It was sold by Chevron as a white powdery dust. Whenmixed with water it becomes a colourless to amber thick liquid. Until1983, chlordane was used as a pesticide on crops like corn and citrus andon home lawns and gardens. Chevron specifically marketed it as an ant andtermite killer.Because of concern about damage to the environment and harm to humanhealth, the Environmental Protection Agency (EPA) banned all uses ofchlordane in 1983 except to control termites. In 1988, the EPA banned alluses of chlordane. The EPA recommends that a child should not drinkwater with more than 60 parts of chlordane per billion parts of drinkingwater (60 ppb) for longer than 1 day. EPA has set a limit in drinking waterof 2 ppb.Chlordane sticks strongly to soil particles at the surface and is not likelyto enter groundwater and so as a result it can stay in the soil for over 20years and breaks down very slowly. Chlordane does not dissolve easily inwater. It affects animal species because it builds up in the tissues offish, birds, and mammals.Chlordane affects the nervous system, the digestive system, and the liverin people and animals. Headaches, irritability, confusion, weakness, vision14problems, vomiting, stomach cramps, diarrhea, and jaundice have occurredin people who breathed air containing high concentrations of chlordane oraccidentally swallowed small amounts of chlordane. Large amounts ofchlordane taken by mouth can cause convulsions and death in people.According to the ATSDR, a man who had long-term skin contact with soilcontaining high levels of chlordane had convulsions. Japanese workers whoused chlordane over a long period of time had minor changes in liverfunction. Animals given high levels of chlordane by mouth for shortperiods died or had convulsions. Long-term exposure caused harmfuleffects in the liver of test animals. It is not known if chlordane affectsthe ability of people to have children or whether it causes birth defects.Animals exposed before birth or while nursing developed behaviouraleffects later.

[Ranger 48]

ChromiumTrivalent chromium (Cr(III), or Cr3+) is required in trace amounts forsugar metabolism in humans (Glucose Tolerance Factor) and its deficiencymay cause a disease called chromium deficiency. In contrast, hexavalentchromium is very toxic and mutagenic when inhaled. Cr(VI) has not beenestablished as a carcinogen when not inhaled but in solution it is wellestablished as a cause of allergic contact dermatitis (ACD). Recently itwas shown, that the popular dietary supplement chromium picolinatecomplex generates chromosome damage in hamster cells. In the UnitedStates, the dietary guidelines for daily chromium uptake were loweredfrom 50-200 μg for an adult to 35 μg (adult male) and to 25 μg (adultfemale).[1]Chromium metal and chromium (III) compounds are not usually consideredhealth hazards, but hexavalent chromium (chromium VI) compounds canbe toxic if orally ingested or inhaled. The lethal dose of poisonouschromium (VI) compounds is about one half teaspoon of material. Mostchromium (VI) compounds are irritating to eyes, skin and mucousmembranes. Chronic exposure to chromium (VI) compounds can causepermanent eye injury, unless properly treated. Chromium(VI) is anestablished human carcinogen. World Health Organization recommendedmaximum allowable concentration in drinking water for chromium (VI) is0.05 milligrams per liter. Hexavalent chromium is also one of thesubstances whose use is restricted by the European Restriction ofHazardous Substances Directive. Hexavalent chromium in contact withskin acts as both sensitizer and irritant. After entering the organism, itgets reduced to trivalent chromium, which then binds to proteins and15creates haptens which trigger immune system reaction. Once developed,chrome sensitivity becomes fairly persistent; in such cases, even contactwith chromate-dyed textiles or wearing of chromate-tanned leathershoes can cause or exacerbate contact dermatitis.In an organism, hexavalent chromium undergoes reduction, first tometastable pentavalent chromium, then to trivalent chromium.Pentavalent chromium is a known carcinogen. If the material gets lodgedin tissues (lungs are especially vulnerable here, followed by fine capillariesin kidneys and intestines), its long-term action may lead to cancerousgrowth. In some parts of Russia, pentavalent chromium was reported asone of the factors of incidence of premature senility. The OSHA PEL forairborne exposures to hexavalent chromium is 5 μg/m3 (0.005 mg/m3).Researchers have recently reported discovering that vitamin C reactsinside human lung cells with chromium 6, causing massive DNA damage.Low doses of chromium 6, combined with vitamin C, produce up to 15times as many chromosomal breaks and up to 10 times more mutations,compared with cells lacking vitamin C. Outside cells, vitamin C actuallyprotects against the cellular damage caused by hexavalent chromium.As chromium compounds were used in dyes and paints and the tanning ofleather, these compounds are often found in soil and groundwater atabandoned industrial site, now needing environmental cleanup andremediation per the treatment of brownfield land. Primer paint containinghexavalent chromium is still widely used for aerospace and automobilerefinishing applications.

That's the a, b and c's of the sorta crap we've pumped into ourt waterways. Want the rest of the alphabet?

[Ranger 48]

Oh, and for anyone interested, that excerpt forms part of a report put forth in June 2007, by expert witness Dr Lindsay Swinden PhD, Laboratory Manager and CEO, OMIC Australia as part of the ongoing dredging debate.His credentials:Royal Australian Chemical InstitutePublic Analyst (Victorian Food Act 1984)Food Technology Association (Technical Committee)Approved Analyst (Japanese Ministry of Health and Welfare)Approved Analyst (Korean Food and Drug Administration)Auditor, National Association of Testing Authorities, Australia1997 Joint Citizen of the Year, Wyndham City CouncilPast Group Councillor, Cairnmiller InstituteDeputy Chairman, Western Region Environment Centre

[David Ciaravolo 34]

Some Good info there Ranger :)if people want they can keep 10 per day. BUT I WOULD NEVER KEEP a 40cm Fish from the Port for really good 2 reasons 1) It would be FULL OF Heavy Metals and other nasties, which unless ya planning on having a GOOD BLEED with be with ya FOR LIFE! (thus shortening it)2. Its a big breader for that system.I would not think twice about eating one this size from the Coorong; thats a different kettle of fish! and those fish taste way better.Like ranger said not too sure if the post is genuine, anyhow thats a pretty average recipe, I can think of atleas 10 better ways to enjoy a fresh bream!

[Ranger 48]

All that stuff I posted is pretty heavy reading, but it gives an idea of how we've done our best to destroy our waterways over the years.Coz there's so much to post, I'll just give ya a short list of other things you'll find down there without all the associated explanations, just so breamsy malone knows exactly what he IS eating:AldrinAntimonyArsenicBariumBerylliumCadmiumChlordaneChromiumDDTDieldrinDioxinsEndosulfanLeadMercuryp-CresolsPolychlorinated biphenylsPolycyclic aromatic hydrocarbonsSeleniumTributyl tinYep.......YUMMY BREAM!!!Methinks they're stuffed with a whole lot more than chicken stuffing, but hey, enjoy ya meal! ;)I had someone once try to argue that "you'd get sicker eating a meat pie than eating a fish". Obviously he had simply no idea what he was talking about, and didn't understand the difference between a bacterial infection causing vomiting, nausea and diarrhoea, which can usally be cleared up quickly with antibiotics, and the dangers and long term effects associated with consuming toxins and heavy metals!

[Ranger 48]

IF this post was put up just to stir the pot, I'd like to thank the poster for giving me the chance to put up all this material to support reasons why we SHOULDN'T catch and kill Bream, and I'll let you all make your own minds up on whether you'd like to eat them.IF this post was put up as a recipe, I'd have to say that

just gut em and scale then stuff em with chicken stuffinginto the oven

is a bit of a crap recipe, coz most of the recipes I've ever seen would have provided the ingredients for the stuffing, cooking time, oven temp, etc, etc. what about seasoning with salt pepper? Scoring the flesh? Covering the fish? Smearing with oil? Etc, etc, etc?

[brenton 637]

I personally wouldn,t eat a bream these days as i have an affinity for them and there are a lot of better eating fish.On the toxicity of fish from the port i reckon that if the above chemicals are in those fish then the health authorities should make it know to the general public.I do know 2 people who have developed an allegic reaction from eating one too many Snapper and can no longer eat them because of the effects.....tingling in the mouth and throat,headaches and nausea etc etc etc.I would also like to take this opportunity to warn people of eating shellfish from the St Kilda/Section bank area as the levels of Ecoli and heavy metal contamination has been documented in the area,which i wish i,d been aware of previous to me eating some and being sick as a dog for 6 weeks with nausea,chills ,sweats,headaches and chronic fatigue.....all classic symptoms of heavy metal poisoning ....so enjoy your bream but i don,t really want to add any more toxins to my system. cheers brenton

[YoBBo 0]

I think that breamzy malone has put his hooks out in this thread, and a couple have taken the bait very well.

[Ranger 48]

I think that breamzy malone has put his hooks out in this thread, and a couple have taken the bait very well.

Not at all! Of course I believe that breamzy malone has put his hooks out. After all, 4 posts here, the first two about being chased off by West Lakes Council for fishing where he shouldn't be, and then being made aware of how old large Bream really are. The next post wanting to enter a 23' sharkcat with 400hp in our bream tournaments and wanting ME as his partner, and now this 4th telling us to kill the large bream!But I also believe a couple have then used that "bait" he set as a platform for their own concerns of promoting C&R on this species! That's something at least one angler here loves to talk about, and will use any chance available to rattle on about, so BM has actually done that angler a favour! ;)Anyways, BM's one hell of a fisherman to just nip down the port and pull in a coupla 40cm fish! Oughta write a book letting the rest of us know his secrets I recon! Maybe follow it up with a cookbook for old, dry and unpalatable fish! The Fisherman's Guide to Toxic Cuisine, Vomit and Explosive Diarrhoea or maybe Slow Death and Fishsticks-a Toxic Guide to Gastronomical Disaster And if he wants to waste his time registering, then coming here putting up these posts, who am I to complain? Brenton, we know those chemicals are down there! The problem is, no-one, not even the experts can quantify it and tell you how much of the stuff is in our waterways, hence no-one can tell what danger it actually poses. Some of this stuff has been banned for use in Australia for over 30 years now, but it's sitting at the bottom of our rivers, suspended in the silt, and as long as it's there, I aint gonna eat Bream, Mulloway or any other resident species! I'll take a few st's which only inhabit the area for very short times, and which have a fast growth rate, but that's it for me.The tingling, headaches nausea, etc are actually symptoms of another disease which affects fish at the top of the food chain, and is a common problem in our northern climes. The name escapes me at the moment (although I'm sure someone here will know) and it's caused by a dinoflagellate (microscopic organism) Gymnodinium catenatum which exudes a toxin, but is not caused by toxins we've dumped. It has however been introduced to Spencer Gulf, within the ballast water dumped by shipping.

Toxins produced by G. catenatum can cause Paralytic Shellfish Poisoning (PSP). The toxins are accumulated in shellfish (oysters, mussels and scallops) which then become toxic to humans and other organisms. In extreme cases, PSP causes muscular paralysis, respiratory difficulties, and can lead to death. G. catenatum also poses threats to wild and aquaculture shellfish industries, due to economic losses resulting from farm closures.

Here's something from CSIRO about it which you should find very interesting: http://www.marine.csiro.au/crimp/images/NIMPIS_PDF/6927.PDFIn regards to the shellfish and E.coli contamination, a warning was put out quite some time ago about a ban on taking shellfish north of outer harbour. A ban which has since been withdrawn. E. coli is an indicator organism (bacteria). It indicates faecal contamination. Strangely enough, no-one has been able to tell us how or why this contamination occured, but try joining the dots yourself! There's only one place I know of up that way which deals with faecal matter, but I'm sure SA Water will tell you the Bolivar sh*tworks are as safe as houses, and there's no way untreated water would ever escape into our gulf! Maybe seagull poo is responsible for that one!

[YoBBo 0]

I think that breamzy malone has put his hooks out in this thread, and a couple have taken the bait very well.

Not at all! I believe that breamzy malone has put his hooks out, but I also believe a couple have then used that bait as a platform for their own concerns of promoting C&R on this species!

I know m8 ;)That is why I think he has actually started a healthy and educational post here. OOPS BACKFIRE!

[jewie 3]

you would think with all those toxins in the fish they would be dead?..surely it cant be that bad. i believe in keeping the breeders released but there is a bag of 10 fish a day as long as that is followed along with the size limit there shouldnt be much problem. maybe we should try get a minimum and maximum size limit if its going to have big effects on the future bream stocks???and as said before i think this post was to stir the pot.

[Ranger 48]

there is a bag of 10 fish a day as long as that is followed along with the size limit there shouldnt be much problem.

Agreed!

I cant complain if anyone wants to take or eat Bream, so long as they're above the legal size limit of 28cm, and below the daily bag limit

maybe we should try get a minimum and maximum size limit if its going to have big effects on the future bream stocks???

I know of those at the moment who've considered pushing for the bag limit to be reduced to 5 per day!

[pellipeeli11 0]

Hi rangerI'm wondering if your thinking of "Ciguateria"Its bad in larger fish species in warmer waters ,Its a cumulative toxin/ poison/ that gets higher in some pelagic fish as they get bigger from eating smaller fish which have small amounts of same ,it never disipates or leaves the fish so when the fish is caught,cooked and eaten it can and has killed people :'(

[Ranger 48]

Hi rangerI'm wondering if your thinking of "Ciguateria"Its bad in larger fish species in warmer waters ,Its a cumulative toxin/ poison/ that gets higher in some pelagic fish as they get bigger from eating smaller fish which have small amounts of same ,it never disipates or leaves the fish so when the fish is caught,cooked and eaten it can and has killed people :'(

Ciguatera is exactly the word I was looking for, thanks bloke! ;D

Large reef-feeding fish that inhabit warmer tropical waters are potential carriers of theCiguatera toxin.The Ciguatera toxin is produced by a tiny micro-organism which attaches itself to algaegrowing in reef areas. Small fish eat this and accumulates through the food chain andpasses to larger predatory species.Ciguatera is a serious food safety risk. The toxin is not destroyed or eliminated byprocessing, freezing or cooking.Ciguatera Fish Poisoning occurs when people consume fish carrying the Ciguateratoxin. Most cases of Ciguatera result from people eating large predatory reef fish caughtrecreationally.Symptoms of Ciguatera include tingling/numbness, rash, vomiting, hot and cold sensations,muscle weakness and in extreme cases may result in death (there has only been onerecorded Ciguatera related death in Australia which occurred in the late 1960’s in QLD).Symptoms present around 12-14 hours after consuming the affected fish. If you presentwith symptoms seek medical advice/treatment.To minimise the risk of Ciguatera Fish Poisoning;• Check with State/Territory Guides on fishing• Avoid fishing in known ciguatera areas• Concentrate on smaller, non-predatory species• Avoid larger fish of species known to be implicated in Ciguatera Fish Poisoning

[pescados 1]

I would not eat bream either but it just makes me wonder aboutother species in the river and back of the island and St Kilda as well as those species who might visit the river for a period of time and than return to the gulf and what about those species who spawn at the back of the island and live there for who knows how long and then move on ..................Going by Rangers posts and you want to stay healthy we might shortly see an abundance of fishing gear and boats up for sale

[Ranger 48]

it just makes me wonder aboutother species in the river and back of the island and St Kilda as well as those species who might visit the river for a period of time and than return to the gulf and what about those species who spawn at the back of the island and live there for who knows how long and then move on ..................

I've also read ther SARDI environmental impact study, performed prior to the dredging at outer harbour, so if ya like I ca also list the other species identified in that study which inhabit the area for ya too:SPAWNING AREA FORJumper Mullet Yellow-eye Mullet Garfish BreamYellowfin WhitingNURSERY AREA FORYellow-eye Mullet Garfish BreamMullowayKing George WhitingYellow Fin WhitingAustralian SalmonBlue Swimmer CrabWestern King PrawnFEEDING AREA FOR ADULTJumper Mullet Yellow-eye Mullet Garfish BreamYellow Fin WhitingSnapperBlue Swimmer Crab

Going by Rangers posts and you want to stay healthy we might shortly see an abundance of fishing gear and boats up for sale

Everything I have posted here I have the facts and cold hard data to back up. Not from any Tom, Dick or Harry with something to say either, but instead from a recognised leader in his field, and also from our gevernment's own research institute (arguably the best in the business). For anyone questioning it, I'm more than happy to share the sources, so ya can read it for yaself and make up ya own mind, rather than listen to what I say or take my word for it.

[breamzy malone 0]

:icon_lol:

[Ranger 48]

:icon_lol:

Good reply! Obviously you were only posting to be disruptive and create trouble here! ::)In which case I will be watching your future posts with great interest! :icon_evil:

[coight 0]

Breamsy ya clown : :-\

[pellipeeli11 0]

gidday coight,Im with you mate .YOU DON'T HAVE TO HAVE FEATHERS TO BE A BL**DY GOOSE Breamsy . :icon_e_ugeek: :icon_e_ugeek:

[breamzy malone 0]

relax you lotit turned out to be a great threadwith all that excellent information posted by rangerand got us all discusing the health of our river and its inhabitantsthere is no way i would kill a bream never mind eat one out of the river YUKbut this is happening every day there are plenty of peoplewho fish the river and put the bream in their bucketas they have every right to under our current bag limits10 bream per person1!30 boat limit!!!!no wonder we are all finding it harder to catch em on luresmaybe we should be pushing for changes in these limitsthe government is quick enough to hit the whiting and snapper limits

[brenton 637]

The people who fill their buckets with bream don,t really stick to the regs IMO Breamzy and they aren,t too fussy about the size limits either.But since they are never going to get caught why would they worry.They keep the lot and then straight home and whack them in the stir fry. cheers brenton

[benny 1]

Yeah, those bucket fillers are pretty common in the Port and these people refuse to listen and cant be educated, plus they take whatever they see. What would ya do with 20 undersize bream? They don't taste that good especially from the port or west lakes. I'm glad a lot of these people aren't regular or good fishermen and I like to set an example by catching legal bream under their noses and releasing them, but it probably wouldn't work as these scum fail to appreciate life in general and are ignorant to the fact that bream take years to grow.

[Steve-Bream-Fishing 4]

t turned out to be a great threadwith all that excellent information posted by rangerand got us all discusing the health of our river and its inhabitantsthere is no way i would kill a bream never mind eat one out of the river YUKbut this is happening every day there are plenty of peoplewho fish the river and put the bream in their bucketas they have every right to under our current bag limits10 bream per person1!30 boat limit!!!!no wonder we are all finding it harder to catch em on luresmaybe we should be pushing for changes in these limitsthe government is quick enough to hit the whiting and snapper limits

Well said Breamzy some of the bream I've seen from the port are black and smell bad, the river sure does need a clean up 'in many ways'

Yeah, those bucket fillers are pretty common in the Port and these people refuse to listen and cant be educated, plus they take whatever they see. What would ya do with 20 undersize bream? They don't taste that good especially from the port or west lakes. I'm glad a lot of these people aren't regular or good fishermen and I like to set an example by catching legal bream under their noses and releasing them, but it probably wouldn't work as these scum fail to appreciate life in general and are ignorant to the fact that bream take years to grow

And they just P... you off > have to keep my scissors handy in the port and when ya see 'em fishing just snip away ;D I'd get into to trouble if I posted what I really wanted to do >

[benny 1]

I cant blame ya for that cuz the let em eat away cus then they can die of heavy metal poisoning.... :icon_evil: :icon_evil: :icon_evil: ;D

[mark1396235444 0]

o dear what can we eat that is not contaminated in some form or way or evan drink for that matter

[David Ciaravolo 34]

I think regardless of people doing the wrong thing; Being ALLOWED to Keep 10 Bream Is too Many!