Interestingly, the activation of human bitter taste receptors by α-thujone was recently proven by Behrens et al. and it was found that the receptor is sufficiently sensitive to serve as protection against the ingestion of toxic amounts of this substance [78]. However, it is questionable if these findings can be transferred to the ingestion of thujone in alcoholic beverages. Possible receptor interactions between thujone and ethanol as well as differences between sober and inebriated persons must be taken into account.

The sometimes observed porphyrinogenic effect of thujone and other terpenoids is explained with the pathway of metabolization by the hepatic cytochrome P-450 system [46.76.79]. Under the presumption of relatively high thujone concentrations of 260 mg/l, Bonkovsky et al. speculated that if there is an appreciable hepatic first-pass extraction and if the rate of hepatic metabolism is not unusually rapid, the concentrations in the livers of absinthe drinkers could have been in the 20–200 μM range. Such concentrations would be sufficient to produce porphyric crises in patients with underlying defects in hepatic heme synthesis. An additional effect of ethanol, perhaps acting synergistically, was also anticipated, since ethanol and other short-chain alcohols found in alcoholic beverages are porphyrogenic [46].

Intoxication due to wormwood or thujone rarely occurs, either due to a misconceived belief in folk remedies or simple ignorance [80]. In 1862, Smith described a case of ingestion of about 14 ml of oil of wormwood by a male adult. The patient was insensible, convulsed, the jaw clenched, and foaming at the mouth; tendency to vomit was also present [81]. To our knowledge, there is only one recent clinical case report by Weisbord et al. from the U.S. dealing with obvious acute thujone intoxication [82]. A 31-year-old male had ingested "herbal oil," which he had assumed to be the spirit absinthe and had purchased over the internet from a website that sold essential oils for aromatherapy. Several hours later, the patient became listless, suffered tonic-clonic seizures and finally developed rhabdomyolysis and then acute renal failure. It is tempting to speculate that these symptoms were caused by thujone, however other ingredients of the herbal oil cannot be excluded as the culprit.

Very few data published only in non peer-reviewed literature exist about the pharmacology of thujone. Max pointed out that the typical 2–4 mg of thujone, which were consumed per drink were far below the level at which acute pharmacological effects are observed [83]. This is confirmed by Hinkelbein, who states that by the consumption of absinthe, up to a blood alcohol concentration of 2.5 g/l, approximately 3.5 mg of thujone are ingested (0.005 mg/kg bodyweight) [84]. In this order of magnitude, it is highly improbable that central effects can be caused by thujone.

A pilot drinking study by Kröner et al. resulted in high blood alcohol concentration, but as expected no thujone was detected [85]. The probands examined did not show any central effect caused by the terpenoids besides the effect of the alcohol. Therefore, the adverse potency of absinthe can be neglected, if the EU limit is obeyed.

The German federal institute for risk assessment holds the view that, even if the legal limit of 35 mg/l is significantly exceeded, the consumer does not ingest health-threatening amounts of thujone. Because of the high alcoholic strength it is advised against a continuous and excessive consumption [86].