Bromazolam
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Bromazolam is a synthetic depressant of the benzodiazepine class. It is the direct 8-bromo structural analog of alprazolam, differing by a single halogen substitution. Bromazolam is a positive allosteric modulator of GABA-A receptors, producing its effects by amplifying the brain's primary inhibitory signaling system.
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Synthesized in the 1970s at The Upjohn Company as part of a triazolo-benzodiazepine research series, bromazolam was never developed for clinical use and remained obscure for decades.[1] The compound resurfaced on novel psychoactive substance markets after its first detection in Sweden in 2016, spreading to at least 17 countries by October 2023.[2] It was placed in Schedule IV of the UN Convention on Psychotropic Substances in March 2024 and is now controlled in most major jurisdictions.[3]
Subjective effects include sedation, anxiety suppression, muscle relaxation, euphoria, and delusions of sobriety. The experience is defined by a warm, disinhibiting calm paired with a deceptive sense of lucidity — users consistently report feeling far less impaired than they objectively are, a quality that distinguishes bromazolam from more overtly sedating designer benzodiazepines.[4] Amnesia, cognitive impairment, and compulsive redosing driven by impaired self-assessment are characteristic unsought effects.
Bromazolam produces physical dependence with chronic use, and no preclinical toxicity data have been published.[4][2] The dominant risk is polysubstance overdose — fentanyl appears in 75–88% of postmortem bromazolam-positive cases, and synergistic respiratory depression drives nearly all recorded fatalities.[5] No controlled human studies exist; the current understanding rests on a single binding study, WHO critical reviews, postmortem case series, and community reports.
History[edit]
Discovery
Bromazolam was first synthesized in the 1970s by J. B. Hester Jr. and P. von Voigtlander at The Upjohn Company, designated XLI-268 within a systematic investigation of triazolo-benzodiazepine analogs.[1] Despite showing pharmacological activity consistent with the benzodiazepine class, it was never selected for clinical development, received no generic drug name, and was not submitted for marketing authorization in any country.[4][2]
Emergence as a novel psychoactive substance
After decades of obscurity, bromazolam resurfaced when Swedish authorities detected it in 2016.[4][2] US reports followed in 2019,[4] and by October 2023 the compound had been identified in 17 countries, with 118 government seizures logged between 2020 and August 2023.[2] It rapidly displaced other designer benzodiazepines in several regions — in San Francisco alone, 44 bromazolam-related fatalities were recorded in 2023,[6] while in Scotland it became the predominant novel benzodiazepine found in "street valium".[7]
Scheduling
The WHO Expert Committee on Drug Dependence critically reviewed bromazolam at its 45th meeting in 2022, recommending continued surveillance.[4] A second review at the 46th meeting in 2023 produced a recommendation for international scheduling.[2] Bromazolam was added to Schedule IV of the UN Convention on Psychotropic Substances in March 2024,[3] triggering national-level controls: the UK classified it as Class C in 2024,[8] and the US DEA issued an emergency Schedule I placement effective March 2026.[9]
The name "bromazolam" follows standard benzodiazepine nomenclature: "brom-" for bromine, "-azol-" for the triazole ring, and "-am" for the benzodiazepine core. It never received an international nonproprietary name, reflecting its abandonment before clinical development. In online communities, it circulates under no widely established street name — users typically refer to it simply as "bromazolam" or abbreviate it to "bromaz."
Chemistry[edit]
Structural class
Bromazolam belongs to the triazolobenzodiazepine subclass — the same structural family as alprazolam, triazolam, and flubromazolam. Triazolobenzodiazepines fuse a 1,2,4-triazole ring onto the standard 1,4-benzodiazepine scaffold, a modification that generally increases potency and metabolic stability compared to non-fused benzodiazepines.[10]
Bromazolam is the direct 8-bromo structural analog of alprazolam: bromine replaces the chlorine at position 8 of the benzodiazepine ring. It also differs from Flubromazolam by the absence of a fluorine atom on the pendant phenyl ring.[4][2]
Molecular identity
| Molecular formula | C₁₇H₁₃BrN₄ |
| Molecular weight | 353.22 g/mol |
The core structure comprises a seven-membered diazepine ring fused to a brominated benzene ring and to a 1,2,4-triazole ring. A phenyl group is attached at position 6, and a methyl group sits at position 1 of the triazole. The bromine at position 8 — larger and more polarizable than chlorine — is the single modification that separates bromazolam from alprazolam.[4][2][11]
Stereochemistry
Bromazolam contains no chirality centers and exists as a single achiral species.[4][2]
Physical properties
In pure form, bromazolam is a white crystalline solid with a melting point of 272.0–275 °C. Solubility is moderate in organic solvents (dimethylformamide, DMSO, ethanol) but poor in aqueous systems.[4][2]
On unregulated markets, bromazolam has appeared as orange or green tablets and yellow powder — coloration that reflects excipients or impurities, not the compound itself.[2] No published data address stability under environmental conditions or long-term storage.
Pharmacology[edit]
Mechanism of action
Bromazolam is a positive allosteric modulator of the GABA-A — the brain's primary inhibitory ion channel. Rather than activating the receptor directly, it binds at the benzodiazepine site located between the α and γ₂ subunits of the receptor complex. When GABA is already present, bromazolam increases the frequency of chloride channel opening, amplifying the brain's own inhibitory signals and producing generalized central nervous system depression.[4][2]
The only published binding study found that bromazolam binds strongly to GABA-A receptors containing α1, α2, and α5 subunits, with no detectable binding at α3, α4, or α6 subtypes.[12] The α2 subtype mediates anxiolytic and muscle-relaxant effects; the α5 subtype is involved in sedation and memory suppression. This binding profile is consistent with the compound's observed mix of anxiolysis, sedation, and amnesia.
Functional assays cited in the WHO ECDD 46th meeting review confirmed that bromazolam acts as a full agonist at the benzodiazepine site — meaning it produces a maximal response, not a partial one.[2] In rat drug discrimination studies, bromazolam fully substituted for midazolam and its effects were blocked by the benzodiazepine antagonist flumazenil, confirming that activity occurs through the benzodiazepine binding site.[2]
Pharmacokinetics
No formal pharmacokinetic study has been published for bromazolam in humans. Parameters including half-life, bioavailability, volume of distribution, and protein binding remain uncharacterized — a significant evidence gap for a compound now widely circulating in unregulated drug supplies.
Oral administration is the dominant documented route — via tablets, capsules, dissolved powder, and gummies. Intravenous use has been inferred from a single case but is considered uncommon.[4][2]
Metabolism proceeds primarily through CYP3A4-mediated hydroxylation (Phase I), producing 4-hydroxy bromazolam and α-hydroxy bromazolam as key metabolites, followed by glucuronidation (Phase II).[13] The dominant role of CYP3A4 means that drugs inhibiting this enzyme (certain antifungals, antibiotics, and antivirals) could raise bromazolam blood levels, while CYP3A4 inducers could lower them.
Community-reported duration of action is 5–8 hours, with after-effects lasting up to 12 hours.[4][2] Community estimates of elimination half-life range from 16 to 20 hours, but these values lack analytical confirmation.safety citation needed Standard immunoassay benzodiazepine screens may not detect bromazolam; laboratory confirmation requires mass spectrometry methods.[13]
Neuroscience[edit]
Where it acts
Bromazolam amplifies inhibitory signaling across the brain by enhancing GABA-A activity. Its strongest binding is at receptor subtypes concentrated in the amygdala (α2, mediating anxiety reduction) and hippocampus (α5, mediating sedation and memory suppression).[12] The result is a broad dampening of cortical arousal, reduced threat reactivity in the amygdala, and impaired memory encoding in hippocampal circuits — mapping directly onto the experienced effects of calm, fearlessness, and amnesia.
Bromazolam also indirectly affects the brain's reward system. Benzodiazepines suppress inhibitory interneurons in the ventral tegmental area, which releases dopamine-producing neurons from their normal restraint and increases dopamine signaling in reward circuits.[2]inferred This mechanism underlies the euphoria and reinforcing properties that drive repeated use.
Why it matters
Chronic benzodiazepine exposure triggers compensatory neuroadaptation: the brain reduces GABA-A receptor availability and increases excitatory glutamate signaling to counterbalance persistent inhibition.[14]inferred This creates a new baseline in which anxiety and arousal are elevated when the drug is absent — the core driver of both dose escalation and the withdrawal (rebound effect anxiety, insomnia, and in severe cases, seizures).
Whether bromazolam's unusual selectivity profile — strong binding at α2 and α5 subtypes with no α3 binding — produces a different pattern of neuroadaptation compared to non-selective benzodiazepines remains unknown.
Bromazolam's subtype selectivity raises questions that current data cannot answer. Does its preferential α2/α5 binding produce a distinct tolerance profile — faster tolerance to sedation than anxiolysis, for example — or does it follow the standard benzodiazepine pattern? And why do users report less amnesia than expected, given the compound's strong α5 binding[12][4]?
Subjective Effects[edit]
Bromazolam produces a classical benzodiazepine experience — sedation, anxiety dissolution, and muscular looseness — but with a euphoric warmth and a deceptive sense of functional clarity that set it apart from more bluntly sedating compounds in its class. At lower doses, the anxiolytic and sociability-enhancing dimensions dominate; higher doses collapse into heavy sedation and sleep. Set and setting shape the balance: stimulating social environments tend to surface the disinhibiting, talkative quality, while quiet settings accelerate the transition into hypnosis.
Relative to alprazolam, community reports describe bromazolam as similar in character but with a more euphoric tone and less pronounced amnesia at comparable subjective doses. Compared to flubromazolam, it is shorter-acting and less overwhelmingly sedating, with a more navigable anxiolytic window before incapacitation sets in.
Effect Grid
A common dose delivers the full classical benzodiazepine experience: clear anxiolysis, moderate sedation, muscle relaxation, and a characteristic euphoric warmth that distinguishes bromazolam from more purely sedating designer benzodiazepines. Amnesia may begin — gaps in recall for events during the experience — though community reports suggest this is less pronounced than with flubromazolam or clonazolam at equivalent subjective doses.
Delusions of sobriety are prominent at this level. Users consistently report feeling sober or only mildly affected while exhibiting obvious impairment to observers. Motor coordination is meaningfully degraded; speech may become slurred. Thought deceleration, information processing suppression, and decision impairment are evident.
At the upper end of this range, hypnotic effects may emerge in quiet settings. Emotional suppression and reduced motivation are common. Duration of commitment is approximately 5–8 hours with residual effects persisting beyond.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Depth perception distortion · Visual acuity suppression · Visual haze / noise · Sleep-transition hallucinations · Visual processing suppression
Visual processing suppression
Body high · Breathing alteration · Dizziness · Nystagmus (eye wobbles) · Dry mouth · Heart rate perception changes · Headache · Laughter fits · Nausea · Sexual arousal suppression · Restlessness · Vomiting
Dry mouth · Heart rate perception changes · Headache · Laughter fits · Nausea · Sexual arousal suppression · Restlessness · Vomiting
Cognitive euphoria · Cognitive fatigue · Focus suppression · Information processing suppression · Memory fragmentation · Thought deceleration · Confusion · Delusions of sobriety · Language suppression · Motivation suppression · Suggestibility enhancement · Thought disorganization · Humor enhancement · Amnesia · Delirium
Information processing suppression · Memory fragmentation · Thought deceleration · Confusion · Language suppression · Motivation suppression · Suggestibility enhancement · Thought disorganization · Humor enhancement · Amnesia · Delirium
Emotional lability · Empathy suppression · Dysphoria · Irritability · Anxiety
Anxiety
Sociability enhancement · Social disconnection · Compulsive behavior reduction · Sociability suppression · Social connection · Trust enhancement · Automaticity · Depersonalization · Derealization · Cognitive disconnection
Social connection · Trust enhancement · Automaticity · Depersonalization · Derealization · Cognitive disconnection
Timeline
First perceptible anxiolysis and body relaxation emerge. A subtle softening of tension signals absorption.
Sedation and muscle relaxation deepen progressively. Euphoric warmth begins to surface; disinhibition becomes noticeable.
Full anxiolysis, sedation, euphoria, and muscle relaxation. Amnesia risk is highest. Delusions of sobriety are most prominent — impairment exceeds self-assessment.
Sedation gradually recedes; residual anxiolysis persists. Motor impairment may outlast perceived effects. Cognitive fog lingers.
Mild residual sedation and anxiolysis. Sleep architecture may be altered. Cognitive fog can persist for hours.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Life-threateningfatal risk
- Tolerance buildup
- moderate
- Tolerance reset
- 21 days
- Physical
- High
- Psychological
- High
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- benzodiazepines · alcohol · barbiturates
Toxicity
No preclinical toxicity data have been published for bromazolam. No LD₅₀, therapeutic index, or organ-specific toxicity data exist.[4][2]safety citation needed No fatalities have been attributed to bromazolam in isolation. In the largest postmortem case series (96 cases, England and Wales), multiple co-intoxicants were present in the vast majority of deaths.[16]
Acute toxicity
Clinical case reports describe loss of consciousness and minimal responsiveness following bromazolam intake.[13] A cluster of three patients in Chicago who consumed counterfeit alprazolam tablets presented with seizures, fever, and heart injury — a severe presentation atypical for benzodiazepines and currently unexplained.[15]
Synergistic respiratory depression from benzodiazepine–opioid co-exposure is the dominant mechanism in most fatal cases involving bromazolam.[5] Fentanyl was co-detected in 75% of US postmortem bromazolam-positive cases[4] and 88% of Canadian cases.[2]
Adulterant risk
Bromazolam frequently appears in counterfeit Alprazolam and diazepam tablets and as an unintended adulterant in opioid and stimulant supplies.[15][17][18] Dosing variability is extreme: Scottish prison samples ranged from 0.34 to 2.33 mg per tablet.[19] Standard immunoassay drug screens may not detect bromazolam; laboratory mass spectrometry confirmation is required.[13]
Impaired driving
Bromazolam has been detected in samples from impaired drivers in the United States at an average blood concentration of 61 ng/mL.[4]
Psychological Risks
Delusions-of-sobriety are the signature psychological risk. Users believe they are less impaired than they are, leading to dangerous redosing, driving while impaired, and risky behavior.[4]
Amnesia occurs at active doses, consistent with bromazolam's strong binding at α5-containing GABA-A receptors.[12] Community reports suggest amnesia may be less pronounced than with some other designer benzodiazepines, though this comparison is anecdotal.[4]
Cognitive-impairment and Decision impairment — slowed reaction time, poor judgment, and reduced executive function — are expected at all active doses.inferred No data exist on bromazolam-induced psychosis in isolation, though withdrawal-associated psychosis and hallucinations have been reported after chronic use in combination with phenibut.[4]
Tolerance & Dependence
No formal tolerance or dependence studies exist for bromazolam. By benzodiazepine class inference, chronic use produces tolerance through GABA-A receptor downregulation and compensatory excitatory upregulation.[14]inferred Tolerance to sedation typically develops faster than tolerance to anxiolysis.
Physical dependence develops with regular use. Published case evidence documents clinically significant withdrawal:
- A case of bromazolam and Phenibut co-dependence required hospitalization for medically supervised withdrawal.[20]
- A seizure followed abrupt cessation of multiple substances including bromazolam, managed with symptom-based diazepam stabilization.[21]
- Online reports describe withdrawal-associated psychosis and hallucinations following chronic combined bromazolam and phenibut use.[4][2]
No validated bromazolam-to-diazepam dose equivalency has been published. This gap directly complicates clinical withdrawal management.[21][20]
Full cross-tolerance is expected with other benzodiazepines, alcohol, barbiturates, and Z-drugs (zopiclone, zolpidem).inferred
Drug Interactions
Opioids: The most dangerous interaction. Synergistic respiratory depression from benzodiazepine–opioid co-exposure is the dominant mechanism in most bromazolam-associated fatalities.[5] Fentanyl is co-detected in 75–88% of postmortem cases.[4][2] Naloxone reverses the opioid component but does not reverse bromazolam's effects.[5]
Alcohol: Additive-to-synergistic respiratory and CNS depression.[14]
Gabapentinoids (pregabalin, gabapentin): Additive CNS depression. Gabapentinoids were frequently co-detected in UK fatalities involving bromazolam.[16]
CYP3A4 inhibitors (azole antifungals, macrolide antibiotics, ritonavir, grapefruit juice): Expected to raise bromazolam blood levels and prolong effects, as CYP3A4 is the dominant metabolic pathway.[13]
CYP3A4 inducers (rifampin, carbamazepine, St. John's wort): Expected to lower bromazolam levels, potentially precipitating withdrawal in dependent users.[13]
Kratom (Mitragyna speciosa): mitragynine inhibits enzymes involved in benzodiazepine metabolism, potentially prolonging bromazolam exposure.[21]
Phenibut: Co-dependence has been documented. Both compounds are GABAergic, and combined withdrawal has been associated with psychosis.[20][4]
Stimulants (methamphetamine, cocaine): Frequently co-detected in fatalities. Stimulants mask perceived sedation but do not protect against respiratory depression, increasing overdose risk.[17][22]
Flumazenil: The benzodiazepine antagonist reverses bromazolam's effects (confirmed in animal studies[2]), but clinical use requires caution in polydrug contexts and in dependent patients, where it may precipitate withdrawal seizures.
Contraindications
No bromazolam-specific contraindication data have been published. The following are inferred from the benzodiazepine classinferred:
Absolute:
- Concurrent opioid use without medical supervision — synergistic respiratory depression is the primary cause of death in bromazolam-associated fatalities[5]
- Severe respiratory disease — GABA-A-mediated respiratory depression compounds pre-existing breathing impairment
- Known hypersensitivity to benzodiazepines
Relative:
- Liver disease — CYP3A4-dependent metabolism predicts impaired clearance[13]
- History of substance use disorder — full agonist activity and confirmed reinforcing properties indicate high abuse liability[2]
- Concurrent CYP3A4 inhibitors — predicted elevation of blood levels[13]
- Pregnancy — benzodiazepine-class risk to the developing fetus; no bromazolam-specific datasafety citation needed
- Myasthenia gravis — muscle relaxation may worsen neuromuscular weaknessinferred
- Elderly patients — increased sensitivity, fall risk, and likely reduced metabolic clearanceinferred
Harm Reduction[edit]
Forms & Identification
Bromazolam's primary identification challenge is that it most often appears in forms designed to look like something else. Counterfeit alprazolam and diazepam tablets are the most common vectors, and no visual inspection can distinguish these from pharmaceutical products. Color, imprint, and shape are unreliable — the only way to confirm what a tablet contains is analytical testing.
Standard immunoassay benzodiazepine urine screens frequently miss bromazolam.[13] This means a negative "benzo" test strip does not rule out bromazolam exposure. Where drug checking services with mass spectrometry are available, they are the most reliable option. Fentanyl test strips should be used on any unverified tablet or powder, given that 75–88% of postmortem bromazolam-positive cases also contained fentanyl.
Guidelines
- Test every dose. Use drug checking services where available. At minimum, use fentanyl test strips on any unverified product.
- Start extremely low. Illicit tablet content varies from 0.34 to 2.33 mg.[19] A single tablet is not a standardized dose. If using powder, a milligram-precision scale is essential.
- Pre-set a firm limit. Decide on a dose before onset and remove access to additional supply. Delusions of sobriety will make you feel ready for more when you are not.
- Do not combine with opioids, alcohol, or other depressants. Respiratory depression from combinations is the primary cause of death in bromazolam-related fatalities.
- Avoid driving and operating machinery. Bromazolam has been detected in impaired drivers at significant blood concentrations.[4] Impairment may outlast the subjective sense of effect.
- Tell someone what you have taken. If a medical emergency occurs, knowing the substance can save your life.
Set & Setting
Bromazolam's defining risk factor is delusions of sobriety — the persistent feeling of being "fine" while objectively impaired. This effect makes solo use and unsupervised environments particularly dangerous, as impaired self-monitoring leads to redosing, driving, and poor decisions without the user recognizing impairment.
A sober, trusted companion who can observe behavior and intervene if needed is the single most effective environmental safeguard. Vehicle keys, additional substances, and access to dangerous environments should be placed out of reach before onset.
Aftercare & integration. Bromazolam's amnestic effects mean that users may have limited or no memory of their behavior during intoxication. Checking in with people who were present, reviewing messages or activity, and honestly assessing any consequences is an important first step after use.
Allow at least 24 hours for full cognitive recovery before driving, making important decisions, or returning to work. Sleep architecture may be disrupted for one to two nights following use. Hydration, nutrition, and rest support recovery. If bromazolam was not taken intentionally (e.g., in counterfeit tablets), consider accessing drug checking services for remaining supply.
Recovery & Support
Benzodiazepine dependence — including dependence on designer benzodiazepines like bromazolam — requires medical supervision to discontinue safely. Abrupt cessation after regular use can cause seizures, which are potentially life-threatening.[21]
No standardized taper protocol exists for bromazolam because no validated dose equivalency to diazepam has been published.[21][20] Clinicians managing bromazolam withdrawal have used symptom-guided diazepam stabilization. If you are using bromazolam regularly and want to stop, consult a physician experienced in benzodiazepine withdrawal before making changes.
Support resources include the SAMHSA National Helpline (1-800-662-4357), local addiction medicine services, and online communities focused on benzodiazepine tapering and recovery.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Breathing slows to fewer than 10 breaths per minute, becomes shallow, or stops
- Skin or lips turn blue or grey
- The person cannot be woken or does not respond to a firm sternum rub
- Seizures occur (unusual for benzodiazepines alone — may indicate extremely high dose or co-intoxication)
- High body temperature or rigid muscles
Immediate steps:
- 1. Call emergency services immediately.
- 2. If opioid co-exposure is suspected or unknown, administer naloxone if available. Naloxone will not reverse benzodiazepine effects but will address the opioid component.
- 3. Place the person in the recovery position (on their side, mouth angled downward) to prevent choking.
- 4. Monitor breathing continuously until help arrives.
- 5. Do NOT induce vomiting. Do NOT leave the person alone.
What to tell the dispatcher: State the substance (bromazolam or "a designer benzodiazepine"), estimated amount if known, time of ingestion, and current symptoms. Mention any other substances involved. Good Samaritan laws in many jurisdictions protect callers from prosecution for drug-related offenses when seeking emergency help.
Reversal agents: Flumazenil can reverse benzodiazepine effects but carries significant risks in dependent users (may trigger withdrawal seizures) and in polysubstance situations. Its use is a clinical decision, not a field intervention.
Legal Status[edit]
Bromazolam was added to Schedule IV of the United Nations Convention on Psychotropic Substances in March 2024, following review by the WHO Expert Committee on Drug Dependence.[3][2] International scheduling triggered national-level controls across UN member states. Before this, bromazolam existed in a regulatory grey area in many jurisdictions — not specifically named in controlled substance schedules but potentially subject to structural analog or novel psychoactive substance legislation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| International (UN) | Schedule IV, Convention on Psychotropic Substances | Added March 2024 following WHO ECDD 46th meeting recommendation[3] |
| United States | Schedule I (temporary emergency) | DEA emergency placement published December 15, 2025; effective March 18, 2026. Prior to federal scheduling, the Federal Analogue Act could potentially apply as a structural analog of Alprazolam (Schedule IV)[9] |
| United Kingdom | Class C, Misuse of Drugs Act 1971 | Controlled under SI 2024/248 (England, Wales, and Scotland)[8] |
| Canada | Schedule IV, Controlled Drugs and Substances Act | Controlled prior to 2022[4] |
| European Union | Subject to Council Decision 2024/832 | Implementing UN Schedule IV placement across EU member states[3] |
| Germany | Controlled under NpSG | New Psychoactive Substances Act[4] |
| Finland | Narcotics Act | Listed by Finnish Medicines Agency (February 2022); subsequently scheduled[2] |
| Australia | Subject to import controls | Victoria Department of Health alert issued 2022. Detected in Australian postmortem cases.[23][24] Specific Poisons Standard entry not confirmedcitation needed |
Analog act considerations
As the 8-bromo analog of alprazolam (a Schedule IV controlled substance in the US and internationally), bromazolam falls within the structural definition of a controlled substance analog under the US Federal Analogue Act (21 USC §802(32)). The compound's placement in Schedule I in March 2026 renders this argument moot under US federal law, though analog provisions may remain relevant in jurisdictions without specific bromazolam scheduling.
references
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- [2]
- [3]
- [4]
- [5]
- [6] ^Rodda LN (2024) The surge of bromazolam-related fatalities replacing other novel designer benzodiazepines-related fatalities in San Francisco — Addiction doi:10.1111/add.16520