Hexahydrocannabinol and Hexahydrocannabiphorol Poisonings: Data From the Czech Toxicology Information Centre and Effects of Legislative Changes

ABSTRACT

Hexahydrocannabinol, a hydrogenated derivative of cannabinol, first came to the Czech Toxicological Information Centre (TIC) following reports of poisonings in May 2022. We conducted a retrospective observational study examining self‐reported cases of hexahydrocannabinol and hexahydrocannabiphorol exposure reported to the TIC from May 17, 2022, to April 30, 2024. Of 236 cases reported, 40 (17%) were excluded. The median age of patients was 18 years (range 1.5–73), with a male predominance of 55.8%. Notably, 39 children under 15 years constituted 19% of the cases. The primary exposure routes were ingestion (196 cases; 67.5%) and inhalation via smoking or vaping (62 cases; 31.5%). The clinical manifestations included neurological (74%), cardiovascular (43.1%), gastrointestinal (42.6%), psychiatric (21%), ocular (24.9%), and metabolic symptoms (14.7%). Physician intervention was required in 172 cases (87.8%). Severity assessment revealed mild symptoms in 119 patients (60.4%), moderate in 66 (33.5%), and severe in 12 (6.1%). Outcomes were favorable with recovery in 98% of cases; no fatalities were reported. Hexahydrocannabinol and hexahydrocannabiphorol exposures primarily resulted in neurological, cardiovascular, gastrointestinal effects, and other symptoms, with several cases being serious. Legislative changes impacting these poisonings require further evaluation.

Development in the number of HHC and HHC‐P intoxications before and after the government ban on sales.

Abbreviations

CB

cannabinoid receptor

CBD

cannabidiol

EUDA

European Union Drug Agency

HHC

hexahydrocannabinol

HHC‐O

hexahydrocannabinol‐O‐acetate

HHC‐P

hexahydrocannabiphorol

THC

tetrahydrocannabinol

THCP

tetrahydrocannabiphorol

TIC

Toxicological Information Centre

1. Introduction

The endocannabinoid system is essential for maintaining homeostasis, especially within the nervous system. Endocannabinoids, produced mainly by central nervous system (CNS) neurons, act on two types of receptors: cannabinoid receptor 1 (CB1), primarily found in the CNS and the main target of Δ9‐tetrahydrocannabinol (THC); and cannabinoid receptor 2 (CB2), which is largely present in the immune system and to a lesser extent in neurons and glial cells [1].

Natural cannabis contains compounds such as Δ9‐tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol. THC, known for its psychoactive effects, is classified under Schedule I of the 1961 United Nations Convention on Narcotic Drugs [2]. CBD lacks psychoactive properties and functions through different mechanisms [3]. In the Czech Republic, products derived from technical hemp with less than 1% THC are legally salable [4]. However, THC itself faces restrictions on sale and consumption. Notably, Cannabis sativa is used medicinally, particularly in pharmacy‐prepared extemporaneous products.

Hexahydrocannabinol (HHC), a hydrogenated derivative of cannabinol first identified in 1940, gained attention after its recent emergence in consumer products. The EUDA (European Union Drug Agency) noted its use in the United States in 2021 and in Europe by May 2022, following the Danish police seizure of a sleep aid product “CBN night” [5]. Although HHC naturally occurs in trace amounts in Cannabis sativa , its commercial presence requires hemisynthesis, typically from cannabidiol or through the reduction of THC or Δ8‐tetrahydrocannabinol. HHC exists in various diastereomeric forms, including (9R)‐hexahydrocannabinol and (9S)‐hexahydrocannabinol, with studies suggesting that the (9R) form has a higher affinity for endocannabinoid receptors, influencing the effectiveness of hemp‐derived products [6, 7]. Despite its complex synthesis, HHC is available in forms like “flowers,” resin, vaping liquid, e‐liquid, drops, “energy drinks” (Figure 1), and edibles such as gummy bears, jellies, brownies, and cookies, often marketed as a CBD alternative.

FIGURE 1.

Text found on products from the sellers: “WARNING: This is a collector's item, intended for horticultural, industrial and collector purposes. Definitely not intended for direct consumption or burning!” (downloaded from: https://www.kazdejdenkybl.cz/daily‐lean‐extra‐strong/).

The toxicological profile of HHC, especially its psychoactive properties, is not well established. Molecular dynamic simulations reveal that both HHC and THC exhibit strong affinities for CB1 and CB2 receptors [8]. Nikas et al. have explored how HHC interacts with these receptors [9]. Additionally, in vitro studies indicate that the isomers 9a‐hexahydrocannabinol and 9b‐hexahydrocannabinol stimulate human CB1 and CB2 receptors [10], while in vivo experiments in various animals have shown psychoactive effects similar to THC [11, 12]. Hexahydrocannabiphorol (HHC‐P), a semisynthetic cannabinoid, is legal and purportedly more potent than THC, though its exact affinity for CB1 is not yet determined. The purpose of our study is to present a case series of poisonings associated with HHC and HHC‐P reported to the Czech Toxicology information centre (TIC).

2. Methods

The Czech Toxicology Information Centre (TIC), serving over 10.5 million residents, is the nation's sole consultation body for toxicological incidents. In 2023, the center handled over 27 000 consultations. Consultations are conducted via telephone by medically trained staff, including doctors and pharmacists. The TIC maintains an electronic records database for storing queries and a regularly updated substance database. For this retrospective observational study, we focused on cases of poisoning involving hexahydrocannabinol (HHC) and hexahydrocannabiphorol (HHC‐P) reported between May 17, 2022, and April 30, 2024. Data analysis involved extracting and examining anonymous case details from the TIC's electronic records and associated hospital discharge reports. Searches for HHC and its derivatives were performed by a single TIC staff member, without secondary review. The study parameters included the location of the call, exposure circumstances, patient demographics (age and sex), clinical manifestations (reported symptoms and observed signs), timing (onset and duration of symptoms), product details (form, purchase location), exposure route, quantity involved, and treatment. Each case was assessed using the Poisoning Severity Score (PSS) [13], and treatment outcomes were determined from medical discharge reports. Cases involving uncertain products or combined poisonings were systematically excluded to maintain data integrity. Laboratory analyses (selected among others: serum potassium, blood glucose, general toxicological urine screening) were conducted during the patients' hospitalization period. Due to the fully anonymized nature of the data used in this study, it was conducted without the need for ethics committee approval.

3. Results

In our analysis, we identified 236 cases of poisonings related to HHC and HHC‐P (Figure 2). Following the exclusion of 40 cases (16.9%) for various reasons—22 due to combined poisoning, 7 from uncertain product identification, 8 missing symptom‐related information, 1 involving a dog, and 2 for other unspecified reasons (the callers wanted to know whether HHC passes into breast milk and the other, positivity in the caller's urine without further details)—a total of 196 cases were considered for further evaluation. This included 185 cases associated with HHC and 11 cases linked to HHC‐P poisoning. These findings are illustrated in a detailed flowchart (Figure 3).

FIGURE 2.

Geographical distribution of HHC and HHCP poisoning cases in the Czech Republic (May 2022–April 2024) (total number of cases per region).

FIGURE 3.

Flowchart of the study from recruitment to enrolment.

We observed a rising trend in the incidence of reported cases, reaching a peak in February 2024. After the prohibition of HHC, there was a noticeable decline in HHC‐related cases and a marginal increase in cases involving HHC‐P (Figure 4). The basic demographic data of the cases, the route of administration that led to exposure and subsequent intoxication, and the forms of HHC/‐P that were recorded are presented in Table 1.

FIGURE 4.

Monthly incidence of HHC and HHCP poisoning consultations reported to the Czech TIC (May 2022–April 2024).

TABLE 1.

Demographic data, route of administration, and exposure form of HHC/‐P (N = 196).

Age, median (years), (IQR)	18 (1.5–73)
Male/Female	109 (55.6%)/84 (42.8%)
Unreported sex	3 (1.5%)
Children 15 ≤ years	39 (19%)
Preschool‐aged children 6 ≤ years	12 (6.1%)
Psychiatric medical history	14 (7.1%)
Route of administration
Oral ingestion	132 (67.5%)
Inhalation	62 (31.5%)
Unknown	2 (1%)
Forms of HHC reported, known in 177 cases (90%)
Gummi bears, jellies, or bonbons	67 cases (37.6%)
Cigarettes, joints, or vaporizer	62 cases (35%)
Cookies	33 cases (18.6%)
Liquid drops	7 cases (4%)
Drinks	5 cases (2.8%)
Chewing gums	2 cases (1.1%)
Oral spray	1 case (0.5%)
Unknown	20 cases (10%)

The time to hospital admission after exposure showed substantial variability, ranging from less than an hour to up to 3 days. To focus on more immediate cases, we excluded those where admission exceeded 8 h (33 cases), those with unknown admission times (33 cases), and instances of repeated use (2 cases). This left 128 cases for analysis, representing 79.5% of the original 161 cases. The mean time to hospital admission within this group was 137 min (SD ±86 min), with a median of 120 min (range 59–360 min). These statistics indicate that approximately 80% of patients were admitted within 2–3 h following the onset of symptoms. Information about the source of the product was available for 36 patients: six purchased their products online, seven from brick‐and‐mortar stores, five from public vending machines, twelve received them from friends, two obtained them at parties, and four cases involved HHC products received as Christmas gifts.

The dose of HHC consumed was reported in 60 cases (30.5%), with an average consumption of 245 mg and a median of 77.5 mg (range 20–3000 mg). This translates to approximately 3.5 mg/kg or 1.11 mg/kg for a 70‐kg adult, respectively.

Additionally, in 15 cases (7.6%), doses were estimated based on product labels provided by patients, with a mean dose of 146 mg (or 2.1 mg/kg for a 70‐kg adult) and a median of 100 mg (or 1.4 mg/kg for a 70‐kg adult), ranging from 30 to 500 mg.

According to the PSS, the distribution of poisoning severity was as follows: minor (PSS 1) in 118 patients (60.2%), moderate (PSS 2) in 66 patients (33.5%), and severe (PSS 3) in 12 patients (6.1%). All evaluated patients exhibited symptoms, but there were no fatalities among the 103 patients (52.3%) whose outcomes were known.

Due to data limitations, the duration of symptoms was indeterminate. The predominant symptoms observed were neurological, followed by cardiovascular, gastrointestinal, metabolic, respiratory, ophthalmological, and dermatological. A detailed breakdown of these symptoms is provided in Table 2.

TABLE 2.

Clinical features observed in HHC and HHCP poisoning cases (N = 196).

Symptoms a	Number of cases (%)
Neurological	145 (74)
Somnolence	74
Tremor	38
Vertigo	33
Slowed psychomotor speed	18
Confusion	12
Slurred speech	10
Muscle twitching	9
Hallucination	9
Paresthesia (tingling)	6
Disorientation	4
Headache	4
Sopor	3
Seizures	2
Dystonia	2
Transient aphasia	1
Coma	1
Hyperreflexia	1
Decortication posture	1
Psychiatric	41 (21)
Anxiety	20
Restlessness	10
Agitation (negative state)	4
Excitation (energetic)	3
Euphoria	3
Laugh	2
Paranoia	1
Depression mood	1
Psychosis	1
Gastrointestinal	84 (42.6)
Vomiting (including repeated, 2–10 vomits)	56 (24)
Nausea	38
Stomachache	3
Increased appetite	2
Cardiovascular	85 (43.1)
Tachycardia (generally reported)	48
including tachycardia in adults above 140 beats/min	8
Including tachycardia in children above 160 beats/min	1
Palpitation	24
Hypertension	11
Chest pain	9
Hypotension	7
Precollapse state	3
Collapse	2
Prolonged PQ interval	2
Prolonged QT interval	1
Bradycardia	2
Metabolic	29 (14.7)
Hyperglycemia above 7.80 mmol/L	25
Hypokalemia ≤ 3.40 mmol/L	8
Increased lactate (median 4 mmol/L, range 2.10–4.60)	5
Respiratory alkalosis	2
Acidosis	1
Respiratory	6 (3.0)
Hyperventilation	3
Hyposaturation	3
Tachypnea	1
Ophthalmological	49 (24.9)
Mydriasis	36
Conjunctival hyperemia	13
Blurred vision	2
Photophobia	2
Dermatological and mucocutaneous	22 (11.2)
Pale skin	10
Dry mouth	10
Sweating	5
Other	11 (5.6)
Weakness	11

^a Patients may have more symptoms.

Tachycardia was generally reported by physicians in 48 cases. Electrocardiography was performed in 62 cases. Among these, the average heart rate for six individuals over 14 years old was 148 ± 23 beats per minute. In children, recorded rates included 161 beats per minute for a 6‐year‐old boy and 156 beats per minute for a 2.5‐year‐old girl.

Out of the 196 patients studied, 172 (87.8%) were admitted to the hospital. Twenty patients (10.2%) did not require hospitalization, while the hospitalization status of 4 patients (2.0%) could not be confirmed. The time to hospital admission postexposure was recorded in 163 cases (Table 3). The median time was 101 min (range 59–380 min., IQR: 121 min).

TABLE 3.

Time from exposure to consultation for HHC and HHCP poisoning cases (N = 196).

Time, hours	Number of cases (%)
Up to 1 h	40 (20.4)
1–2 h	18 (9.2)
2–3 h	37 (18.9)
3–4 h	12 (6.1)
1–4 h	6 (3.1)
4–8 h	17 (8.7)
8–24 h	24 (12.2)
24 h up to 72 h	7 (3.6)
Repeated exposure	2 (1.0)
Unknown	33 (16.8)

Discharge reports were obtained for 101 of the 172 admitted patients (from which 37 patients were admitted to ICU), accounting for 58.7% of those cases. Of those with a known outcome, 99 patients recovered without any sequelae, typically within 48 h after exposure and following medical intervention (Table 4). Two patients required transfer to another hospital for further treatment.

TABLE 4.

Length of hospital stay for HHC and HHCP poisoning cases (N = 172).

Length	Number of cases (%)
Outpatient	31 (18)
Up to 24 h	46 (27.2)
Up to 48 h	15 (8.5)
Up to 72 h	6 (3.3)
7 days (Case No. 5 in Table 1)	1 (0.6)
Transferred to higher‐level hospital	1 (0.6)
Unknown	72 (41.9)

The length of hospital stay (LHS) was documented for all 172 admitted patients and detailed in Table 4.

Of the 172 patients admitted to the hospital, 97 (56.4%) received no treatment or their treatment was not documented. The remaining 75 patients (43.6%) required medical interventions, as detailed in Table 5. The most severe symptoms, corresponding to a PSS of 3, are outlined in Table 6.

TABLE 5.

Treatment administered to patients with HHC and HHCP poisoning (N = 172).

Therapy	Number of cases (%)
Fluid therapy (crystalloids)	65 (37.8)
Other symptomatic or patient's chronic medication	20 (11.6)
Glucose	14 (8.1)
Benzodiazepines	10 (5.8)
Antiemetics	9 (5.2)
Proton pump inhibitors	6 (3.5)
Potassium salt	4 (2.3)
Magnesium sulfate	4 (2.3)
Activated charcoal	4 (2.3)
Insulin	2 (1.2)
Antibiotics*	2 (1.2)
Antiepileptics*	1 (0.6)
Naloxone	1 (0.6)
Oxygen	1 (0.6)
Antivirals*	1 (0.6)
Norepinephrine*	1 (0.6)
Thiopental*	1 (0.6)
Glucose‐potassium‐insulin infusion*	1 (0.6)
No treatment or not documented	97 (56.4)

Note: Only one patient, a 6‐year‐old boy with PSS 3, received a combination of treatments listed above and marked in the table*.

TABLE 6.

Severe HHC and HHCP poisoning cases (PSS = 3) (note (after read–delete): Column “Analysis of the patient's blood or urine” was not be able to track the changes and should have been deleted).

Case	Year	Age	Gender	Route	Form	Dose	Commercial name	Symptoms	Management site	Length of hospitalization (days)
1	2023	16	M	Oral	Unknown	Unknown	Unknown	Nausea, vomiting, precollapse, somnolence	Hospital	1
2	2023	30	F	Inhalation	Vaporizer	More inhales	Unknown	Psychosis (wanted to jumped out of window with baby)	Hospital	Unknown
3	2023	16	M	Inhalation	Cigarette	Unknown	Canapuff Premium HHC Maui Wowie Vintage	Slowed PMS, tachypnea, mydriasis, SpO2 shortly below 80%, myoclonus á 5–10 min, prolonged QT 445 ms, (than QT 401), vomiting, intermittent bradycardia, alkalosis (improved)	Hospital	1
4	2023	17	M	Inhalation	Vaporizer	2 inhales	Unknown	Precollapse state, anxiety, tremors, palpitations	Hospital	Unknown
5	2023	6	M	Oral	Cookie	2 pcs	Unknown	Somnolent (even with suspicion of hallucination), wide‐eyed, shaky, GCS 12, mydriasis, decorticate posture, EEG—seizure‐free status epilepticus	Hospital	7
6	2023	13	M	Inhalation	Vaporizer	Unknown	Unknown	GCS 8–9, severe mydriasis, vomiting, hypokalemia (2,9 mmol/L), ABR with lactic acidosis (lactate 4.6)	Hospital	3
7	2023	25	M	Oral	Bonbons	5 pcs	Unknown	Hallucinations, slurred speech, uncoordinated movements of the trunk and head, slight somnolence, dry mucous membrane of the oral cavity, lactic acidosis (4.11 mmol/L), hypokalemia (3.15 mmol/L)	Hospital	1
8	2023	3	F	Oral	Bonbons	1 pc	Unknown	GCS 10, upper limbs flexes, mydriasis (5‐6 mm) pain reaction (crying), hypoventilation (20 breath/min)	Hospital	2
9	2023	18	M	Oral	Cookie	1 pc	Bercanna, Premium Cookie	GCS 11–12, mild leukocytosis, lactate 4, later a drop in GCS 10, hyposaturation 91%, hypotension	Hospital	more than 1 day (transferred to another hospital)
10	2024	15	F	Inhalation	Cigarette	Unknown	Unknown (HHC‐P)	GCS 8–9, CPR by parents (after 20 min GCS 15), mydriasis, whole body tremor, hyperreflexia, hyperglycemia (10.5 mmol/L)	Hospital	2
11	2024	17	F	Oral	Unknown	Unknown	Unknown	GCS 14, responds with slight latency, mild hypokalemia (3.34 mmol/L), hyperglycemia (8.84 mmol/L), metabolic acidosis (pH 7.252–7.396), mild upper extremity twitching	Hospital	2
12	2024	17	M	Inhalation	Vaporizer	Unknown	Unknown (HHC‐P)	Slurred speech, mydriasis, tremor, precollapse state	Hospital	1

Blood glucose levels were measured in 73 subjects. Excluding one subject with a level of 12.12 mmol/L due to diagnosed diabetes mellitus type 1, the average glucose level was 7.34 mmol/L. Twenty‐four subjects had levels above 7.8 mmol/L (median 8.86 mmol/L, range 8.0–11.8 mmol/L) and were considered symptomatic with metabolic symptoms.

Potassium levels were measured in 47 subjects, averaging 3.93 mmol/L (range 2.60–6.47 mmol/L). Eight subjects had levels below 3.40 mmol/L (median 3.30 mmol/L, range 2.60–3.40 mmol/L), and were classified as symptomatic according to the PSS.

Urinalysis was performed in 50 cases (general toxicology screening) but without relevant results. Only one case involved a targeted serum analysis for HHC using Liquid Chromatography—High Resolution Mass Spectrometry to identify HHC metabolites.

4. Discussion

This study analyzed 236 self‐reported cases of exposure to HHC, primarily through ingestion. A notable increase in incidents was observed toward the end of the study period, culminating shortly before regulatory changes. On March 1, 2024, the Czech government banned the sale of HHC, THCP (tetrahydrocannabiphorol), and HHC‐O (Hexahydrocannabinol‐O‐acetate). This legislative action prompted a stockpiling phenomenon, as consumers hurried to purchase these substances before the enforcement of the law. Following the ban, there was a slight rise in incidents involving HHC‐P, which was not included in the prohibition (as shown in Figure 2).

No fatalities were reported among the patients with known outcomes. The toxic effects were evident in those exposed via oral ingestion and inhalation. The identification of specific products involved was complicated by their wide availability and affordability, with prices ranging from 6 to 20 euros. HHC products are easily accessible online and through vending machines located in public areas such as shopping centers, making them readily available to underage individuals. Additionally, these products are often sold alongside cannabidiol in retail stores, where they might be promoted by sellers despite limited information on potential adverse effects. The appealing packaging and the association with cannabidiol likely contributed to the increased use of HHC.

HHC is often advertised for its purported benefits, such as relaxation, anxiety relief, improved sleep, and general well‐being. Despite these claims, warnings on these products are typically minimal, generally noting only “Not intended for direct consumption” or designated as “A collector's item” or “Product for research and scientific purposes”. Although marketed as a less potent alternative to THC, the adverse effects observed—primarily neurological, cardiovascular, and gastrointestinal—mirror those commonly associated with cannabis use [14].

Despite these findings, there are currently no human comparative studies on receptor activation by HHC/‐P; highlighting a significant gap in the understanding of its pharmacological impact.

Our study found significant similarities between the clinical effects of HHC and THC. Neurological symptoms were observed in 74% of our cases, including convulsions in 2 cases (1%). This compares to a report by Noble et al. [15], which documented neurological effects in 80% of cases and convulsions in 3.6% following cannabis exposure. Cardiovascular symptoms were also common in our study, with sinus tachycardia occurring in 24.5% of cases and palpitations in 12%, aligning with severities documented for cannabis in other research [16, 17]. Tachycardia was determined based on an initial medical examination including pulse and/or electrocardiography. As “tachycardic” patient was determined by the examining physician during hospital admission.

Comparing our findings with a similar case series from French poison centers, which included 37 cases, we observed some variations in symptom prevalence—neurological symptoms in 85% (vs. 74% in our study), cardiovascular symptoms in 61% (vs. 43%), gastrointestinal symptoms in 33% (vs. 41%) and ophthalmological symptoms in 21% (vs. 24%) [18]. Due to the small sample size, establishing a clear dose‐effect relationship was challenging. Symptoms were reported even after minimal exposures, such as a single inhalation or one gummy bear, though precise doses in these instances were unclear.

These comparisons suggest broad consistency across studies, though with notable differences in the specific prevalence of symptoms. The benchmark blood glucose level of 7.8 mmol/L is recognized in the literature as the postprandial norm for individuals aged 0–50 years [19]. In emergency settings, blood glucose levels can be highly variable, influenced by factors such as prehospital treatments, infusion administration, the body's endogenous stress response, and whether measurements are postprandial or fasting. While some of these factors are difficult to ascertain, a baseline value of 7.8 mmol/L is considered optimal for our analysis. The reason for monitoring selected biochemical markers such as serum glucose and serum potassium level is information from the Toxinz database, where under the keyword Delta‐9‐Tetrahydrocannabinol, in the Severity of Poisoning (Cannabinoid Receptor Agonist Toxicity) section, “Elevated blood glucose” is mentioned, thus verifying whether the monitored cannabinoids also do this. Serum potassium level was monitored during research process due to suspicion that it may affect potassium level (mild hypokalemia) that were seen in few patients.

Table 6 outlines the documented and reported symptoms among the subjects, categorized using the PSS score. In our methodology, the presence of one symptom from a PSS category was sufficient to classify a subject within this category. For subjects exhibiting multiple symptoms, the most severe symptom determined their inclusion in the respective PSS category. This approach ensures that the categorization reflects the most significant clinical impact on the subject.

Among our patients, 11 exhibited intoxication symptoms from HHC‐P. The clinical course and symptoms in these cases mirrored those observed in HHC poisonings, indicating similar toxicodynamic profiles for these substances. This parallel suggests that both HHC and HHC‐P share comparable pharmacological and toxicological characteristics.

5. Study Limitations

Our study encountered several limitations due to its retrospective design and the variability in data collection methodologies. Data was gathered through nonstandardized queries conducted by poison center experienced staff during medical phone interviews and from hospital discharge report transcripts. Consequently, this data may not fully capture all instances of HHC exposure in the Czech Republic during the study period. It is also noted that many hospitals reported a higher incidence of HHC intoxication cases than those consulted with the Czech Toxicology Information Centre (TIC), suggesting that our findings may not be universally applicable to other regions. A significant limitation was the infrequent analysis of patients' blood and urine. This lack of consistent biological verification means that we cannot conclusively affirm that the intoxications were solely due to HHC. The potential presence of other unreported substances, which were not analyzed, could have contributed to the clinical signs observed, adding another layer of complexity to the interpretation of our results. Information on whether it was HHC is only available through patients or treating doctors. However, in some cases, the original packaging of the products was also available, where it was stated that it was HHC and the amount in milligrams was stated. At this time, there was a boom in consumption and experimentation with this substance, so it can very likely be expected that all intoxications were associated with HHC.

6. Conclusion

HHC products are especially popular with young people under the age of 30. Data from the Toxicological Information Centre indicate the need to regulate the trade in these products, especially a strict ban on consumption by children and adolescents.

This study analyzed 196 cases of patients who reported using HHC, with the predominant clinical manifestations being neurological, cardiovascular, gastrointestinal, psychiatric, ocular, and metabolic. Following significant regulatory changes on March 1, 2024, HHC products were classified as illegal substances in the Czech Republic.

This study, as part of the solution to these cases after exposure to HHC/‐P, therefore provides valuable material for studying the occurrence of various poisonings in the Czech Republic thanks to the Toxicological Information Centre, the only one of its kind with nationwide coverage.

Author Contributions

Michal Čečrle: conceptualization, data curation, formal analysis, methodology, project administration, visualization, writing – original draft. Milada Běhounková: data curation, writing – review and editing. Kateřina Kotíková: data curation, supervision, writing – review and editing. Sergej Zacharov: conceptualization, methodology, supervision, writing – original draft, writing – review and editing.

Conflicts of Interest

The authors declare no conflicts of interest.

Čečrle M., Běhounková M., Kotíková K., and Zacharov S., “Hexahydrocannabinol and Hexahydrocannabiphorol Poisonings: Data From the Czech Toxicology Information Centre and Effects of Legislative Changes,” Pharmacology Research & Perspectives (2025): e70162, 10.1002/prp2.70162.

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.