Etomidate vaping and e-cigarette

 

Etomidate vaping and e-cigarette–related reports accounted for 21 articles* as of April 18, 2026, raising concerns among clinicians and public health scholars worldwide. [1]

* = Etomidate vaping 4 articles + Etomidate e-cigarette 17 articles.

Substance : Etomidate（依托咪酯） by（Vaping）  

Schedule: Etomidate was officially classified as a Category 2 (Class II)

narcotic in Taiwan on November 27, 2024. [2]

 

Common name:

Clinical primary use: A short-acting intravenous anesthetic, commonly used for emergency intubation or brief surgical procedures. 0.2-0.3 mg/kg IV infused over 30-60 seconds.

Street names: “Zombie vape,” “Sleep vape,” “Space Trip.” Space Oil太空油 [3]

 

Involving system:

Etomidate acts as a GABA receptor modulator. It induces rapid sedation and anesthesia by enhancing the effects of GABA (gamma-aminobutyric acid), the primary inhibitory neurotransmitter in the central nervous system. [4].

Route of Administration: Vaping (E-cigarette Inhalation)

Illicit Transformation:

Powdered Etomidate is dissolved into e-liquid carriers, typically consisting of propylene glycol (PG) or vegetable glycerin (VG).

Pharmacokinetic Characteristics:

When inhaled, the drug is absorbed through the pulmonary capillaries, causing blood concentrations to spike instantaneously. By bypassing the hepatic first-pass effect, the substance acts directly on the brain, leading to exceptionally high and uncontrollable levels of toxicity and addictive potential.

Presentation

Typical scenario: young adult, often recreational e‑cigarette user, may present with agitation, hallucinations, impaired judgment, or bizarre behavior shortly after vaping (onset ~15–20 minutes).

 

Neurological/psychiatric: drowsiness or confusion, myoclonus/twitching, tremor, involuntary movements, aggression, self‑harm, psychosis‑like symptoms. [5]

Adrenal/endocrine: hypotension, shock, fatigue, nausea, hypokalaemia, unexplained hypertension (from chronic ACTH drive), and signs of adrenal insufficiency (hyponatraemia, hyperpigmentation in chronic users).[6].

Chronic use: insomnia, weight loss, endocrine dysfunction, and possible irreversible brain damage or neuropsychiatric sequelae.

Neurological symptoms: Control myoclonus or seizures with benzodiazepines; avoid phenytoin or other agents that may worsen CNS depression.

Antidote

• No specific antidote for etomidate toxicity; treatment is supportive and steroid‑based for adrenal suppression.
• Stress‑dose glucocorticoids (e.g., hydrocortisone 100 mg IV every 8 hours in shock, then taper as adrenal function recovers) are recommended for patients with hypotension or biochemical evidence of adrenal insufficiency (low cortisol, low ACTH). [7].
• Mineralocorticoid replacement is usually not needed, as adrenal suppression is mainly glucocorticoid‑mediated. [7].

Airway, breathing, circulation:

Protect airway if agitated or obtunded; consider sedation with benzodiazepines for agitation or seizures, avoiding further NMDA/ET‑1 agonists.

Treat hypotension with IV fluids and vasopressors if needed, plus stress‑dose hydrocortisone for suspected adrenal insufficiency.  

Provide psychiatric support and observation for agitation, aggression, or self‑harm risk.

 

Disposition:

Acute intoxication:

Observe ≥12–24 hours in an acute care setting if there is significant agitation, altered mental status, or hemodynamic instability.

Admit to ICU for severe agitation, recurrent seizures, respiratory depression, or circulatory shock, especially with hypotension responding to steroids.

Adrenal insufficiency:

Continue stress‑dose hydrocortisone until clinical recovery and evidence of adrenal axis recovery; arrange outpatient endocrine follow‑up.

Chronic misuse / addiction:

Screen for other co‑ingested drugs (opioids, stimulants, benzodiazepines) and electrolytes, glucose, renal/liver function. Refer to addiction or substance‑use services and psychiatry for ongoing dependence and mental health issues.

Counsel patient on the high risk of fatal poisoning, adrenal failure, and irreversible brain damage with continued use.

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/?term=etomidate+e-cigarette&sort=date&size=200

[2]. https://www.taipeitimes.com/News/taiwan/archives/2025/08/05/2003841506

[3]. https://pubmed.ncbi.nlm.nih.gov/41626923/

[4]. https://pubmed.ncbi.nlm.nih.gov/34060021/

[5]. https://pubmed.ncbi.nlm.nih.gov/38652218/

[6]. https://onlinelibrary.wiley.com/doi/10.1111/add.70151?af=R

[7]. https://www.hkmj.org/abstracts/v31n3/229.htm

 

Edited by Yu-Jang Su   April 19, 2026

  

Lithium Poisoning

Substance

Lithium is a commonly prescribed medication for bipolar disorder with a narrow therapeutic index. Therapeutic range: 0.6–1.2 mmol/L [1] [2]

Toxicity does not strictly correlate with serum levels

Brain concentration is more clinically relevant, especially in chronic toxicity

 

Common name

Lithium carbonate（most common）Lithium citrate

Trade names: Eskalith, Lithobid, Lithonate, Priadel

 

Involving system, [3]

 (1) Acute toxicity

Large ingestion in a lithium-naïve patient. High serum level, low CNS penetration initially, predominantly gastrointestinal symptoms.

(2) Chronic toxicity (most dangerous)

Long-term use with impaired renal clearance, Prominent neurologic toxicity

 (3) Acute-on-chronic toxicity (most common)

Acute ingestion on top of chronic therapy

Mixed presentation (GI + neurologic)

 Clinical pearl:  Chronic toxicity is associated with the worst outcomes

 

Toxico-kinetics, Absorption, Immediate-release: peak at 1–2 hours [2]

Sustained-release: peak at 4–5 hours (may have delayed/multiple peaks) [4]

Distribution: No protein binding, distributed in total body water

Brain equilibrium is delayed up to 24 hours [5]

Elimination: 95% renal excretion, Clearance: 10–40 mL/min

Prolonged in the elderly or those with CKD.

Renal handling, Lithium behaves like sodium, 80% reabsorbed in the proximal tubule [6]

 

Predisposing Factors increasing lithium levels: Volume depletion (Major Trigger!), Hyponatremia, Thiazides, NSAIDs, ACE inhibitors / ARBs [3] [7]

 

Presentation  

(A) Gastrointestinal (acute): Nausea, vomiting, Diarrhea [7][8]

 (B) Neurologic (most important) Tremor (fine → coarse) Ataxia, Confusion/delirium,

Seizures, Coma [7]

 (C) Renal, Nephrogenic diabetes insipidus (NDI), the most common chronic adverse effect, occurs in up to 40% of patients [9].

 (D) Endocrine, Hypothyroidism, Hyperparathyroidism/hypercalcemia [8][9]

 (E) Cardiac, T wave flattening, usually nonspecific ECG changes. Serious arrhythmias are rare [10].

 (F) Severe complication,  SILENT syndrome (Syndrome of Irreversible Lithium-Effectuated Neurotoxicity) , Persistent neurologic deficits > 2 months after discontinuation, Predominantly cerebellar dysfunction [11].

Risk factors: Fever, Dehydration. Concomitant antipsychotic use

Serum lithium level does NOT equal severity

 

Antidote and Management

Step 1: ABC stabilization, Airway usually preserved

Monitor for aspiration (due to vomiting)

Step 2: Gastrointestinal decontamination, NO NEED for using Activated charcoal

Ineffective (lithium is a monovalent ion)

Gastric lavage, Limited role (rapid absorption)

May use Whole bowel irrigation (WBI) [10]

Indications:  Sustained-release ingestion

Significant toxicity, No contraindications (e.g., ileus)

Step 3: Fluid resuscitation, Use 0.9% normal saline, Rate: 1.5–2 × maintenance

Improves renal perfusion, reduces lithium reabsorption

Step 4: Hemodialysis, based on ExTRIP (2015) recommendations [12].

Strong indications (regardless of level): Decreased consciousness Seizures, Life-threatening arrhythmias.

Suggested indications: Lithium > 4.0 mmol/L and Lithium > 2.5 mmol/L with symptoms.

Renal failure, and Failure of levels to decline; be aware of the rebound phenomenon  [13].  

 

Post-dialysis lithium levels may rise due to redistribution from intracellular compartments. Requires: Serial monitoring

Possible repeat dialysis, Modality First-line: Intermittent hemodialysis (IHD), If unstable: CRRT.  [14].

Emergency Department Approach, Treat the patient, not the number.”

 

Disposition

Asymptomatic with level <1.5 mEq/L, observation

Mild poisoning（1.5–2.0mEq/L）treat and observation

Neurologic manifestation: hospitalize, levels >2.0 mmol/L [10]

moderate-severe neurotoxicity: ICU [10]

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/19523343/

[2]. https://tapna.org.au/wp-content/uploads/2021/08/LithiumSummary-1628470971.4004.pdf

[3]. https://pubmed.ncbi.nlm.nih.gov/40281030/

[4]. https://canadiem.org/wp-content/uploads/2018/03/CC-lithium.pdf

[5]. https://pubmed.ncbi.nlm.nih.gov/708996/

[6]. https://pubmed.ncbi.nlm.nih.gov/2128949/

[7]. https://www.healthdirect.gov.au/lithium

[8]. https://my.clevelandclinic.org/health/diseases/25207-lithium-toxicity

[9]. https://pmc.ncbi.nlm.nih.gov/articles/PMC5164879/

[10]. https://www.ncbi.nlm.nih.gov/books/NBK499992/

[11]. https://pmc.ncbi.nlm.nih.gov/articles/PMC11117426/

[12] https://pubmed.ncbi.nlm.nih.gov/25583292/

[13]. https://pubmed.ncbi.nlm.nih.gov/19393483/

[14]. https://pmc.ncbi.nlm.nih.gov/articles/PMC11039482/

 

Edited by Yu-Jang Su, Mar 19, 2026

Hazards and Health Impacts of (Bisphenol A and Bisphenol S)

 

Substance

Chemical names:

Bisphenol A (BPA)

Bisphenol S (BPS) [1]

Chemical class: Synthetic diphenylmethane derivatives

Common use: Production of polycarbonate plastics, epoxy resins, food container linings, thermal receipt paper

Note: BPS is widely used as a “BPA-free” substitute.

 

 

Common name

塑膠雌激素「塑膠中的內分泌干擾物」

 BPS:「BPA 替代品」「BPA-free 雙酚類」

 

Involving system

Endocrine System (Primary Target), Estrogen receptor (ERα, ERβ) activation; Thyroid hormone disruption  Altered androgen signaling, Hypothalamic–pituitary–gonadal axis interference, Clinical relevance: Endocrine-disrupting chemicals (EDCs) [2]

Reproductive System: Reduced sperm quality and motility, Ovarian dysfunction, Menstrual irregularities; Impaired fertility; Developmental effects in offspring [3]

Metabolic System, Insulin resistance, Pancreatic β-cell dysfunction, Obesity association, Type 2 diabetes risk [4]

Cardiovascular System; Hypertension association, Endothelial dysfunction, Atherosclerotic risk, Possible cardiac electrophysiologic effects (more experimental data for BPS) [5]

Nervous System, Neurodevelopmental effects in children, Behavioral changes, Possible cognitive impact. [6]

Immune System, Pro-inflammatory cytokine modulation. Immune dysregulation (experimental data) [7]

Hepatic System, Altered liver enzyme activity, Lipid metabolism disruption [8]

Renal System, Urinary excretion pathway, Possible association with chronic kidney disease (epidemiologic correlations) [9]

Sources and Exposure: Oral ingestion (migration from food containers), Dermal absorption (thermal receipt paper), Inhalation (industrial settings), Exposure Pattern

Primarily chronic low-dose environmental exposure, Detectable in urine in >90% of the general population in biomonitoring studies. [10]

High-Risk Groups: Pregnant women, Infants and children, Workers handling thermal paper, Individuals with metabolic syndrome [11].

 

 

Presentation

Acute High-Dose Exposure （Rare）: Mild gastrointestinal irritation, Nausea

Vomiting, Skin irritation, Eye irritation, No specific toxidrome identified

Chronic Low-Dose Exposure （Primary Clinical Concern）

Reproductive System, Reduced sperm quality, Decreased sperm motility, [12].

Menstrual irregularities, Possible infertility [3]

Developmental abnormalities in offspring

Metabolic System, Insulin resistance, Increased risk of obesity, Association with type 2 diabetes [4]

Cardiovascular System, Possible hypertension, Endothelial dysfunction [5]

Atherosclerotic risk correlation

Neurodevelopmental / Nervous System, Behavioral changes in children [6]

Attention and cognitive alterations (reported in epidemiologic studies)

Endocrine System: Hormonal imbalance, Thyroid function interference [2]

Oncologic Associations (Under Investigation), Possible association with breast cancer [13], Possible association with prostate cancer [14]

 

 

Antidote and Management

Routine clinical testing is not recommended

Acute Exposure: Supportive care

Gastrointestinal decontamination is generally not indicated; Trial: Removal of Bisphenol S (BPS) by Adsorption on Activated Carbons Commercialized in Brazil) [15]

Chronic Exposure Risk Reduction in Mandatory

Avoid heating food in plastic containers [16].

Reduce canned food consumption [17].

Limit handling of thermal receipts

Encourage use of glass or stainless steel food containers

No specific antidote exists.

 

Disposition

Acute exposures generally benign.

Long-term health implications remain an area of ongoing research

Vulnerable populations (pregnant women and children) warrant precautionary exposure reduction; Toxicity concern is primarily related to chronic endocrine disruption, not acute poisoning. Effects may occur at low environmental doses.

Regulatory policies vary internationally.

 

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/41621464/

[2]. https://pubmed.ncbi.nlm.nih.gov/22100034/

[3]. https://pubmed.ncbi.nlm.nih.gov/41169278/

[4]. https://pubmed.ncbi.nlm.nih.gov/38021644/

[5]. https://pubmed.ncbi.nlm.nih.gov/34240201/

[6]. https://pubmed.ncbi.nlm.nih.gov/37842186/

[7]. https://pubmed.ncbi.nlm.nih.gov/41465419/

[8]. https://pubmed.ncbi.nlm.nih.gov/31901629/

[9]. https://pubmed.ncbi.nlm.nih.gov/40586299/

[10]. https://pubmed.ncbi.nlm.nih.gov/40940416/

[11]. https://pubmed.ncbi.nlm.nih.gov/40222108/

[12]. https://pubmed.ncbi.nlm.nih.gov/37001656/

[13]. https://pubmed.ncbi.nlm.nih.gov/41201099/

[14]. https://pubmed.ncbi.nlm.nih.gov/38657712/

[15]. https://pubmed.ncbi.nlm.nih.gov/38929038/

[16]. https://pubmed.ncbi.nlm.nih.gov/41441248/

[17]. https://pubmed.ncbi.nlm.nih.gov/36871506/

 

Edited by Yu-Jang Su  Feb 23, 2025

全氟和多氟烷基物質, Polyfluoroalkyl Substances, PFAS

 

Substance

PFAS（Per- and Polyfluoroalkyl Substances）[1].

一大類人工合成含氟有機化合物，具高度化學穩定性與生物累積性

常見代表：PFOA（Perfluorooctanoic acid）,PFOS（Perfluorooctane sulfonate）[1]

 

Common Name（常見名稱）

 

全氟／多氟烷基物質

永久化學物（Forever chemicals）

防水、防油、防污塗層化學品 [2]

列管物質：台灣已將 PFOA、PFOS、LPOS、POSF、PFHxS 等列為毒性或關注化學物質，有條件開放用途，如半導體、特定紡織品、滅火器等。

廣泛存在：市面上仍有許多未列管的PFAS種類流通，用於食品包裝、紡織品、化妝品、工業用途等，因其防水、防油特性。

台灣市售的許多隱形眼鏡都可能含有PFAS（全氟/多氟烷基物質）這類有機氟化物，主要用於提升鏡片光滑度、防止蛋白附著; 雖然專家認為從眼球進入體內的機會不大且致癌性未定，台灣消費者不必過度恐慌，但應關注,並追蹤 國際研究及美國 FDA 等單位對安全性的認定

 

Involving System（影響系統）

 

Multisystem, predominantly chronic effects

Liver: Elevated liver enzymes and hepatic steatosis [1]

Endocrine/Metabolic: Thyroid dysfunction and dyslipidemia [3] [4]

Immune system: Reduced vaccine antibody responses and immunosuppression [5]

Reproductive and developmental: Infertility, low birth weight, and developmental delay

                      increased FSH and decreased AMH, estradiol, and progesterone. [6]

Kidneys: Increased risk of chronic kidney disease [7].

Cardiovascular: Hypercholesterolemia and increased risk of atherosclerosis [4]

 

 

Presentation（臨床表現）

 

Acute exposure:

Mostly no obvious acute symptoms

Chronic exposure (common):

Asymptomatic with laboratory abnormalities:

ALT / AST ↑ [1]

Long-term epidemiological associations:

Metabolic syndrome [8]

Chronic kidney disease (CKD)[8]

Impaired immune function [5]

 

Antidote（解毒劑）

 

No specific antidote

Management principles:

Cessation of exposure (most important)

Supportive care

Investigational strategies (non-standard treatments):

Cholestyramine / bile acid sequestrants: may enhance elimination via interruption of Cholestyramine treatment led to a 23.1-fold increase in serum-adjusted fecal PFOS excretion. [9], 1 week 1 pack qd-bid ac

Over a 12-week period, colesevelam intervention reduced serum PFOS levels by an average of 38%, significantly outperforming the 2% decline observed in the control group [9]

Hemodialysis: does not work (largely ineffective for PFAS due to high protein binding)

 

Disposition（處置與去向）

                  Emergency department:

o    Asymptomatic or mildly symptomatic → outpatient follow-up

o    Routine hospitalization or gastric lavage is not required

Outpatient care / follow-up:

o    For individuals with occupational or environmental exposure:

§  Regular monitoring of:

§  Liver function

§  Lipid profile

§  Thyroid function

§  Renal function

o    Notify environmental or occupational medicine authorities (e.g., in cases of clustered exposure)

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/41543329/

[2]. https://pubmed.ncbi.nlm.nih.gov/41181096/

[3]. https://pubmed.ncbi.nlm.nih.gov/41391234/

[4]. https://pubmed.ncbi.nlm.nih.gov/41428216/

[5]. https://pubmed.ncbi.nlm.nih.gov/41456666/

[6]. https://pubmed.ncbi.nlm.nih.gov/41465861/

[7]. https://pubmed.ncbi.nlm.nih.gov/41440749/

[8]. https://pubmed.ncbi.nlm.nih.gov/40609416/

[9]. https://pubmed.ncbi.nlm.nih.gov/40974835/

Edited by Yu-Jang Su   Jan 17, 2026  

 

Acetone poisoning

 

Substance

 

去光水的主要成分是揮發性有機溶劑，最常見的丙酮(Acetone) 和 甲苯(Toluene)，用於溶解指甲油中的高分子聚合物。 市面上也有較溫和的無丙酮去光水，可能含有乙醇(Ethanol)、醋酸乙酯(Ethyl Acetate)、異丙醇(Isopropyl Alcohol) , 醋酸丁酯 (Butyl acetate)或是添加大豆油酸甲酯等滋潤成分。 選擇時應注意標示，避免含有禁用的甲醇，並在通風處使用。 常用成分

丙酮(Acetone): 最常見的溶劑，溶解力強，但也容易使指甲乾燥、脆弱。

甲苯(Toluene): 也是常用成分，具有揮發性，但對健康影響較大。

醋酸乙酯(Ethyl Acetate): 另一種常見的有機溶劑。

異丙醇(Isopropyl Alcohol): 常用於無丙酮配方中。

 

Common name

去光水、卸甲液、洗甲水、除甲水。

英文名：Nail Polish Remover。[1] CH3COCH3 [2]

 

 

Involving systems

Acetone:  metabolism of acetone is independent of the route of absorption and occurs primarily in the liver [1] excreted through the lung and a little through the urine irrespective of the route of exposure, and elimination is usually completed within 48-72 hours after exposure.

Central Nervous System (CNS): Primary target system. [3, 4]

Respiratory System: Mucous membrane irritation and potential respiratory depression.[3, 4]

Gastrointestinal (GI) System: Direct mucosal irritation. Vomiting, abdominal pain and gastrointestinal bleeding.[1]

Cardiovascular System: Potential for hypotension and tachycardia.[1]

Dermal/Ocular: Local irritant effects.[4]

 

 

Presentation

CNS Effects (Dose-dependent) [3]

• Feeling of inebriation or drunkenness.
• Headache, dizziness, and lethargy.
• Confusion, drowsiness, and ataxia (lack of coordination).
• Severe Cases: Stupor, coma, and respiratory arrest.

Respiratory Effects [3]

• Irritation of the nose, throat, and lungs. Bronchial edema [1]
• Coughing and dyspnea (shortness of breath).
• Hypoventilation (decreased respiratory rate).
• Risk of aspiration pneumonitis if vomiting occurs.

GI Effects [1]

• Nausea and vomiting.
• Abdominal pain.
• Sweet, fruity odor on the breath (characteristic of acetone).

Cardiovascular Effects

• Hypotension (low blood pressure).[1]
• Tachycardia (fast heart rate).[1]

Local Effects (Skin/Eyes)

• Ocular: Eye irritation, pain, redness, and tearing. Corneal injury [4]
• Dermal: Skin drying, cracking, and redness upon prolonged contact.

 

 

Antidote and Management

• Supportive Care is Paramount: Focus on Airway, Breathing, and Circulation (ABC). [1]
• Airway and Breathing: [1]
• Monitor oxygen saturation and respiratory function closely.
• Administer supplemental oxygen as needed.
• Intubation and mechanical ventilation may be required for severe respiratory depression or failure.
• Circulation:
• Establish intravenous access (IV access).[1]
• Administer IV fluids to manage hypotension.
• Monitor ECG.
• Decontamination (Ingestion):
• DO NOT induce vomiting (risk of aspiration).
• Gastric lavage is generally discouraged and rarely necessary, but may be considered for massive ingestion if performed early and with a protected airway.
• Activated charcoal is ineffective against acetone.
• Specific Monitoring:
• Monitor acetone and serum ketone levels.
• Monitor fluid and electrolyte status.
• No Specific Antidote Exists.

 

 

Disposition

• Mild to Moderate Exposure: Patients typically recover completely within hours to days, as acetone is relatively quickly metabolized and excreted.
• Severe Intoxication: Prognosis depends on the severity and duration of CNS and respiratory depression.
• Patients surviving the initial 48 hours generally have a favorable outcome.
• Death is rare but can occur due to profound respiratory failure or aspiration pneumonitis.

For blood acetone levels of 20-30 mg/dl (severe intoxication), symptoms such as somnolence (drowsiness), ataxia (lack of coordination), slurred speech, and potentially deep coma may occur. A blood level of 55 mg/dl or higher is often considered the fatal level, based on concentrations detected in documented fatal poisoning cases. [1]

LD50:  oral LD50 value of 3,687 mg/kg was found for male guinea pigs (Strieger and Carpenter 1961). [4]

• Discharge Criteria: Patients can typically be discharged once symptoms (especially CNS depression) have fully resolved and they are observed for a period of 4–6 hours post-exposure (depending on the dose and route). 

 

 

References

1.      https://pubmed.ncbi.nlm.nih.gov/34754632/,

2.      https://www.ncbi.nlm.nih.gov/books/NBK208291/

3.      https://pubmed.ncbi.nlm.nih.gov/3362729/

4.      https://www.ncbi.nlm.nih.gov/books/NBK590392/

 

Edited by Yu-Jang Su  Dec 9, 2025