14 research outputs found

    BMAA in potable waters: An international assessment of exposure levels

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    Comparative toxicity of the cyanobacterial toxin cylindrospermopsin between mice and cattle: Human implications

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    The cyanobacterial toxin cylindrospermopsin is produced by Cylindrospermopsis raciborskii and Aphanizomenon ovalisporum in many parts of the world. A human poisoning incident occurring at Palm Island, Queensland, Australia in 1979 was subsequently ascribed to cylindrospermopsin. The structure of cylindrospermopsin, a tricyclic guanidinium moiety bridged to hydroxymethyluracil, was deduced in 1992. A number of studies have investigated the acute toxicity of cylindrospermopsin in mice. It is primarily a hepatotoxin with a 24-hour acute intraperitoneal (IP) LD50 of 2 mg/kg, a 5-day acute i.p. LD50 of 0.2 mg/kg and a 5-day acute oral LD50 of approximately 6 mg/kg. A human health risk assessment using data from longer-term oral dosing studies suggests a guideline value for cylindrospermopsin in drinking water of approximately 10 ÎĽg/L.We have recently studied cattle poisonings by cylindrospermopsin and detected the toxin in a number of tissues after necropsy. Concentrations of 1 mg/L or above in drinking water (dose is approximately 50 ÎĽg/kg/day) were shown to result in cattle death after short-term exposure (less than 10 days). Oral dosing of mice at levels up to 5 mg/L with cylindrospermopsin in drinking water for 90 days did not produce any significant toxicity. Human health risk assessment based on cattle however, which are much more sensitive to cylindrospermopsin than rodents, would produce a guideline for human drinking water of approximately 0.05 ÎĽg/L. A consideration of reported human poisoning incidents that implicate cylindrospermopsin suggests that humans may also be more sensitive than rodents to this toxin

    Concurrent outbreaks of cholera and peripheral neuropathy associated with high mortality among persons internally displaced by a volcanic eruption

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    Background: In October 2004, Manam Island volcano in Papua New Guinea erupted, causing over 10 000 villagers to flee to internally displaced person (IDP) camps, including 550 from Dugulaba village. Following violence over land access in March 2010, the IDPs fled the camps, and four months later concurrent outbreaks of acute watery diarrhea and unusual neurological complaints were reported in this population. Materials and Methods: A retrospective case-control study was conducted to identify the risk factors for peripheral neuropathy. Rectal swabs were collected from cases of acute watery diarrhea. Hair and serum metals and metalloids were analyzed by Inductively Coupled Plasma-Mass Spectrometry (ICP-MS). Results: There were 17 deaths among the 550 village inhabitants during the outbreak period at a crude mortality rate 21-fold that of a humanitarian crisis. Vibrio cholerae O1 El Tor Ogawa was confirmed among the population. Access tocommunity-level rehydration was crucial to mortality. Peripheral neuropathy was diagnosed among cases with neurological symptoms. A balanced diet was significantly protective against neuropathy. A dose-response relationship was seen between peripheral neuropathy and a decreasing number of micronutrient- rich foods in the diet. Deficiencies in copper, iron, selenium and zinc were identified among the cases of peripheral neuropathy. Conclusions: Cholera likely caused the mostly preventable excess mortality. Peripheral neuropathy was not caused by cholera, but cholera may worsen existing nutritional deficiencies. The peripheral neuropathy was likely caused by complex micronutrient deficiencies linked to non-diversified diets that potentially increased the vulnerability of this population, however a new zinc-associated neuropathy could not be ruled out. Reoccurrence can be prevented by addressing the root cause of displacement and ensuring access to arable land and timely resettlement

    First report of a toxic Nodularia spumigena (Nostocales/ Cyanobacteria) bloom in sub-tropical Australia. I. Phycological and public health investigations

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    Cyanobacterial blooms represent one of the most conspicuous and widespread waterborne microbial hazards to human and ecosystem health. Investigation of a cyanobacterial bloom in a shallow brackish water recreational cable ski lake in south-eastern Queensland, Australia revealed the dominance of the toxigenic species Nodularia spumigena. The bloom spanned three months, during which time cell concentrations exceeded human guideline thresholds for recreational risk, and concentrations of the hepatotoxic cyanotoxin nodularin exceeded 200 mu g L-1. Cyanotoxin origin and identification was confirmed by amplification of the ndaF-specific PCR product and sequencing of the 16S rRNA gene. From the limited data available leading up to, and throughout the bloom, it was not possible to establish the set of causative factors responsible for its occurrence. However a combination of factors including salinity, hydraulic retention time and nutrient status associated with an extended period of drought are likely to have contributed. This was the first known occurrence of this species in bloom proportions from sub-tropical Australia and as such represents a hitherto uncharacterized risk to human and ecosystem health. It highlights the need for adaptive monitoring regimes to ensure a comprehensive understanding of the potentially toxic cyanobacteria likely to inhabit any given region. Such monitoring needs to recognize that cyanobacteria have a significant capacity for range expansion that has been facilitated by recent changes in global climate

    Serum analysis (µg/L) of peripheral neuropathy cases, Papua New Guinea, 2010.

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    *<p>normal range in whole blood.</p><p>UDL  =  under detection limit.</p><p>Below normal range in bold <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072566#pone.0072566-McQuilty1" target="_blank">[29]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0072566#pone.0072566-London1" target="_blank">[30]</a>.</p
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