[2] Exposure to ATR via ingestion or physical contact is toxic and can be fatal for both humans and animals, especially by kidney and liver failure.

[3] ATR acts as an effective ADP/ATP translocase inhibitor which eventually halts ADP and ATP exchange and the cell dies due to lack of energy.

Historically, atractyloside poisoning has been challenging to verify and quantify toxicologically, though recent literature has described such methods within acceptable standards of forensic science.

[6][2] After high-profile accidental poisonings—children in Italy and Algeria ate parts of the plant in 1955 and 1975, respectively—renewed interest in atractyloside resulted in future research.

[7] Historically, the ATR plant sources have been used for numerous reasons: whether for its therapeutic properties, magico-religious purposes, or its toxicity.

While its therapeutic uses may be due to the coincidental presence of other compounds, some uses of ATR-containing plants include treating sinusitis, headaches, syphilitic ulcers, and whitening teeth among other applications.

Particularly, the Atractylis gummifera is easily confused with wild artichoke and other vegetables, and its sweet-tasting roots facilitate its consumption.

[3] Ingestion of A. gummifera, C. laureola, Xanthium, or their extracts, may result in symptoms of gastrointestinal pain, nausea, diarrhea, and vomiting.

[13] The detection of herbal toxins has generally caused a diagnostic problem due to wide variety of plants and limited standard screening.

[4] The development of the below procedure relied on findings from unsuccessful methods of identification, primarily traced to the following literature in which the specificity and sensitivity was improved over time.

Due to the limited research on the subject of ATR identification, this literature represents the primary sources to review: The procedure by Carlier et al. uses high-performance liquid chromatography coupled with high-resolution tandem mass spectrometry (HPLC-HRMS/MS).

This lethal dose of ATR takes approximately 150–180 minutes after injection until acute tubular necrosis occurred.