Symptoms of anatoxin-a toxicity include loss of coordination, muscular fasciculations, convulsions and death by respiratory paralysis.

Due to its high toxicity and potential presence in drinking water, anatoxin-a poses a threat to animals, including humans.

Gorham in the early 1960s, after several herds of cattle died as a result of drinking water from Saskatchewan Lake in Ontario, Canada, which contained toxic algal blooms.

[5] These expansive cyanobacterial harmful algal blooms, known as cyanoHABs, increase the amount of cyanotoxins in the surrounding water, threatening the health of both aquatic and terrestrial organisms.

Many cases of anatoxin-a related animal deaths have occurred due to ingestion of detached benthic cyanobacterial mats that have washed ashore.

From these experiments, they calculated that the oral minimum lethal dose (MLD) (of the algae, not the anatoxin molecule), for calves is roughly 420 mg/kg body weight.

They found that anatoxin-a kills mice 2–5 minutes after intraperitoneal injection preceded by twitching, muscle spasms, paralysis and respiratory arrest, hence the name Very Fast Death Factor.

[1] Laboratory studies using mice showed that characteristic effects of acute anatoxin-a poisoning via intraperitoneal injection include muscle fasciculations, tremors, staggering, gasping, respiratory paralysis, and death within minutes.

[11] There have been cases of non-lethal poisoning in humans who have ingested water from streams and lakes that contain various genera of cyanobacteria that are capable of producing anatoxin-a.

[15] One study found that anatoxin-a is capable of binding to acetylcholine receptors and inducing toxic effects with concentrations in the nano-molar (nM) range if ingested.

Recreational exposure to river, stream, and lake waters contaminated with algal blooms has been known to cause skin irritation and rashes.

In hippocampal and brain stem neurons, a 5 to 10 times greater concentration of anatoxin-a was necessary to activate nAchRs than what was required in the PNS.

[20] In normal circumstances, acetylcholine binds to nAchRs in the post-synaptic neuronal membrane, causing a conformational change in the extracellular domain of the receptor which in turn opens the channel pore.

[20] Injections of mice, rats, birds, dogs, and calves with lethal doses of anatoxin-a have demonstrated that death is preceded by a sequence of muscle fasciculations, decreased movement, collapse, exaggerated abdominal breathing, cyanosis and convulsions.

Domestic dog deaths due to the cyanotoxin, as determined by analysis of stomach contents, have been observed at the lower North Island in New Zealand in 2005,[22] in eastern France in 2003,[23] in California of the United States in 2002 and 2006,[24] in Scotland in 1992, in Ireland in 1997 and 2005,[2] in Germany in 2017[25] and 2020.

Numerous cattle fatalities arising from the consumption of water contaminated with cyanobacteria that produce anatoxin-a have been reported in the United States, Canada, and Finland between 1980 and the present.

The toxin is introduced into the birds via water contaminated with cyanobacterial mat communities that arise from the hot springs in the lake bed.

Cocaine is first converted into the endo isomer of a cyclopropane, which is then photolytically cleaved to obtain an alpha, beta unsaturated ketone.

Instead, a racemic mixture of 3-tropinone is used with a chiral lithium amide base and additional ring expansion reactions in order to produce a ketone intermediate.

The major differences in each pathway relate to the precursors used to produce the imium ion and the total yield of anatoxin-a at the end of the process.

[28] Anatoxin-a is unstable in water and other natural conditions, and in the presence of UV light undergoes photodegradation, being converted to the less toxic products dihydroanatoxin-a and epoxyanatoxin-a.

The photodegradation of anatoxin-a is dependent on pH and sunlight intensity but independent of oxygen, indicating that the degradation by light is not achieved through the process of photo-oxidation.

A study done by Kiviranta and colleagues in 1991 showed that the bacterial genus Pseudomonas was capable of degrading anatoxin-a at a rate of 2–10 μg/ml per day.

[15] The threat posed by anatoxin-a and other cyanotoxins is increasing as both fertilizer runoff, leading to eutrophication in lakes and rivers, and higher global temperatures contribute to a greater frequency and prevalence of cyanobacterial blooms.

[31][32] Anatoxin-a is not regulated under the Safe Drinking Water Act, but states are allowed to create their own standards for contaminants that are unregulated.

Anatoxin-a's presence on the CCL means that it may need to be regulated by the EPA in the future, pending further information on its health effects in humans.