Case of poisoning from red whelk.
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In this review the several data concerning phytotoxins as natural harmful substances of plants and phycotoxins--toxicants of algae were described. For example plants are source of pyrrolizidine alkaloids, glycoalkaloids, glucosinolates as well as glycosides, saponine and psolarens. Possible adverse effects of phytoestrogens as endocrine disruptors versus beneficial influence these substances on human organism were mentioned. About lectins as possible factors of some diseases was reported, as well as some proteins as allergens of soy and peanuts was mentioned. Accumulated by shellfish and fish the most important phycotoxins such as saxitoxin, okadaic acid, brevetoxins and ciguatoxins were described. Phycotoxins produced several poisoning symptoms. Microcystins and nodularin--cyanobacterial phycotoxins of freshwater, was mentioned. In conclusion, the need of limitation of permissible levels of some plant toxicants, development of analytical methods as well as knowledge of influence of some technological processes on toxic plant substances was highlighted. The importance of balanced diet as a tool of defense against plant toxicants was concluded.
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1. A crude preparation of toxin was extracted from a sample of mussels Mytilus edulis, part of a batch responsible for many cases of paralytic shellfish poisoning.2. The crude extract was partially purified by absorption on sodium Amberlite ion-exchange resin. Two toxins were recovered by elution from the Amberlite, and purified further by gel filtration.3. One toxin closely resembled saxitoxin in its behaviour on Amberlite and in its biological effects.4. The other toxin behaved quite differently on the Amberlite. Its molecule was small, comparable in size with saxitoxin. It was not tetrodotoxin. Its biological effects were similar, but not identical, to those of saxitoxin: it paralysed muscular contraction and inhibited conduction along nerves; it caused death of experimental animals by producing a peripheral paralysis of respiration; it did not depolarize the membrane of frog skeletal muscle fibres, but acted by preventing a stimulus from initiating a conducted action potential.5. The biological effects of the second toxin suggest that, like saxitoxin and tetrodotoxin, it is an inhibitor of inward sodium ion movement through electrically excitable membranes.
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The content of domoic acid in water and in the body of some aquatic animals was detected by HPLC in order to find out the pollutant condition. The result showed that HPLC analysis was a simple and effective method for determining domoic acid in water and aquatic animals. Domoic acid has been found in some marine shellfish and not in seawater or freshwater. It is necessary to strengthen monitoring the contamination of domoic acid to prevent the toxin poisoning.
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This report covers part of the assessment of a site in northern France polluted by industrial metal emissions. Our objectives were to assess the cadmium burden in children aged 8 to 11 years and look for factors that affected it. A cross-sectional population-based study took place in 1996-1997 and included 400 children (200 in the metal-polluted area). The geometric mean of the blood cadmium (CdB) levels of children living on the polluted site was 0.51 microg/L (95% CI=[0.49-0.53]); that of the nonexposed children was 0.47 microg/L (95% CI=[0.45-0.49]) (P<0.01). The geometric mean of the urinary cadmium (CdU) levels of children living on the polluted site was 1.16 microg/g creatinine (95% CI=[1.01-1.34]); that of the nonexposed children was 0.99 microg/g creatinine (95% CI=[0.86-1.14]) (P=0.10). Mean CdB was higher among children within 4 km of a zinc smelter and consuming > or =500 ml of tap water daily (x1.34; 95% CI=[1.14-1.51]) compared with children living more than 4 km away and consuming <500 ml of tap water daily. Independently of this association, consumption of fish and shellfish (> or =once a week vs. or =once daily vs. <once daily) was associated with higher mean CdB levels, respectively: x 1.14; 95% CI=[1.07-1.21] and x 1.25; 95% CI=[1.04-1.50]. Neither sex nor age was associated with CdB. Mean CdU was associated with paternal occupational cadmium exposure.
Shellfish have the capacity to accumulate chemical contaminants found in their biotope and therefore present a potential risk for consumers. This study was conducted to assess the chemical risks associated with consumption of shellfish harvested on the north shore of the St. Lawrence River's lower estuary. A survey was carried out on 162 recreational harvesters, and shellfish were sampled for chemical contaminant analysis. We quantified 10 metals, 22 polycyclic aromatic hydrocarbons (PAHs), 14 polychlorinated biphenyls (PCBs), and 10 chlorinated pesticides. We subsequently evaluated cancer and noncancer risks for four consumption scenarios based on our survey results and published results. Soft-shell clams (Mya arenaria) were by far the most consumed shellfish species. Of the 56 selected contaminants, 36 were detected in the 23 homogenates of soft-shell clam meat. None of the contaminants found in the soft-shell clams were associated with intakes that exceed the main exposure limit recommendations proposed to prevent noncancer effects. However, several limits must be considered before drawing conclusions about the relative safety of shellfish consumption regarding this end point. Furthermore, inorganic arsenic and PCBs were present in sufficient concentrations to lead to cancer risks exceeding the level often considered acceptable for environmental exposure (1 x 10 (-4) to 1 x 10(-6)) in each of the four scenarios, even for the lowest observed scenario of 15 meals of soft-shell clams per year.
In almost a quarter of outbreaks of gastroenteritis reported to the Public Health Laboratory service by medical officers of environmental health and environmental health officers as possible foodborne infection in 1980 food poisoning organisms were not isolated. In a third of this group the incubation period was longer than the usual range for bacterial food poisoning organisms, and possibly some of the outbreaks were viral in origin. Viruses were detected by electron microsocpy in 88% of faecal specimens from similar outbreaks associated with shellfish but in only 23% of specimens from outbreaks associated with other foods. Recommendations are made for future investigation of such outbreaks including the collection of epidemiological data and specimens for virological study.
Okadaic acid (OA) is a shellfish toxin produced by dinoflagellates, in mussels. It is a potent tumour promoter and represents a potential threat to human health even at low concentrations. OA targets mainly the gastrointestinal tract in acute poisoning, causing diarrhoea. Therefore the present investigations were designed to study the ability of okadaic acid to induce cytotoxicity and DNA lesions in a human colonic cell line (Caco-2). Incubation of Caco-2 cells with OA (3.75-60 ng/ml, i.e. 4.6 x 10(-3)-7.5 x 10(-2) microM) causes a significant reduction in cell viability. Moreover, okadaic acid inhibits protein and DNA synthesis with, respectively, IC50 of 16 and 6.5 ng/ml after 24 h incubation. It also provokes cell cycle arrest, characterised by an increase in the number of S phase cells, correlated with a significant decrease in G0/G1 phase cells at high concentration. One of the main results obtained in these investigations is the apoptosis induced by OA in Caco-2 cells of intestinal origin, shown by DNA laddering in agarose gel electrophoresis (250-1000 base pairs). OA also induces clastogenic effects evaluated by DNA fragmentation analysis using the method of Higuchi and Aggarwal (52% for 60 ng/ml) and comet assay (increase of the frequency of comets and their tails length). Therefore, the cell death induced by OA seems clearly to be concentration-dependent after 24 h of incubation. The cytotoxic properties of okadaic acid and its ability to damage DNA result in cell death, mainly by apoptosis. Since consumption of shellfish contaminated with acceptable okadaic acid concentrations exposes colonic cells to harmful concentrations of this toxin, the possibility that OA would display its toxic effects on intestinal cells in vivo should be evaluated in human primary intestinal cells and human intestinal slices for cytotoxic effects, DNA fragmentation and apoptosis.
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There is an enormous diversity and complexity of venoms and poisons in marine animals. Fatalities have occurred from envenoming by sea snakes, jellyfish, venomous fish such as stonefish, cone snails, and blue-ringed octopus. Deaths have also followed ingestion of toxins in shellfish, puffer fish (Fugu), and ciguatoxin-containing fish. However antivenoms are generally only available for envenoming by certain sea snakes, the major Australian box jellyfish (Chironex fleckeri) and stonefish. There have been difficulties in characterizing the toxins of C. fleckeri venom, and there are conflicting animals studies on the efficacy of C. fleckeri antivenom. The vast majority of C. fleckeri stings are not life-threatening, with painful skin welts the major finding. However fatalities that do occur usually do so within 5 to 20 minutes of the sting. This unprecedented rapid onset of cardiotoxicity in clinical envenoming suggests that antivenom may need to be given very early (within minutes) and possibly in large doses if a life is to be saved. Forty years of anecdotal experience supports the beneficial effect of stonefish antivenom in relieving the excruciating pain after stonefish spine penetration. It remains uncertain whether stonefish antivenom is efficacious in stings from spines of other venomous fish, and the recommendation of giving the antivenom intramuscularly needs reassessment.
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This paper examines the age-specific human health risks exposed to inorganic arsenic through arsenic-contaminated farmed fish/shrimp and groundwater consumptions in arseniasis-endemic areas of blackfoot disease (BFD)-endemic area and Lanyang Plain in Taiwan, based on an probabilistic integrated risk assessment framework. We employ an age-dependent predictive physiologically-based pharmacokinetic model to account for arsenic concentrations in target organs. We reconstruct age-specific dose-response profiles for arsenicosis and arsenic-induced cancers by best fitting a pharmacodynamics-based three-parameter Hill equation model to published epidemiological data from West Bengal and Taiwan. The predicted median arsenic concentrations in age group-specific skin, lung, and bladder ranged from 2.24-5.70, 3.76-9.46, and 5.11-20.71 micro g g(-1) in BFD-endemic area, whereas 4.98-12.04, 8.23-19.92, and 11.07-43.45 micro g g(-1) in Lanyang Plain, respectively. Risk analysis indicates that consumption of arsenic-contaminated farmed fish/shrimp and groundwater in arseniasis-endemic areas may increase threat to prevalence of arsenicosis for all age groups, whereas adults may undergo potential risks of arsenic-induced skin, lung and bladder cancers. We show that peoples in Lanyang Plain are more readily associated with higher morbidities for arsenicosis and skin cancer as well as fatalities for lung and bladder cancers than that of peoples in BFD-endemic area. Here we report the first case in which theoretical human health risks for consuming As-contaminated farmed fish/shrimp and groundwater in the arseniasis-endemic areas are alarming under a conservative condition based on a probabilistic risk assessment framework.
An enzyme immunoassay employing recombinant Norwalk virus capsid protein was evaluated for the measurement of IgA responses. Tests on 23 volunteers and patients known to have been infected with Norwalk virus (NV) showed that 19 developed significant IgA responses, 2 had unchanging levels of IgA and 2 failed to respond. There was no evidence of IgA responses to NV following infection with Hawaii or Snow Mountain-like viruses. Tests on sera from patients involved in outbreaks associated with eating contaminated shellfish suggest that some patients may have been infected with more than one strain of calicivirus. The use of the rNV EIA for measuring IgA and IgG responses in patients involved in a major outbreak of food poisoning affecting hospital staff indicated that the causative agent was probably NV.