Ciguatoxins Poisoning

 

Substance Ciguatoxins (CTXs)

雪卡毒素，又名雪卡魚毒素或西加魚毒素。

 

Common names

Ciguatera toxins in 熱帶與亞熱帶的珊瑚礁魚類

Ciguatera fish toxins: resistant to cooking, freezing, drying, and gastric acid.

Ciguatoxins are potent marine neurotoxins produced by benthic dinoflagellates of the genera Gambierdiscus and Fukuyoa, which inhabit coral reef ecosystems in tropical and subtropical oceans. [1, 2]

Herbivorous reef fish ingest these microalgae, allowing the toxins to bioaccumulate and become progressively concentrated through the marine food chain. [1] Consequently, large predatory reef fish contain the highest toxin concentrations and are responsible for most cases of human poisoning.

 

Geographic Distribution

Ciguatera fish poisoning (CFP) is endemic in tropical and subtropical coral reef regions between approximately 35°N and 35°S, particularly in the Pacific Ocean, Caribbean Sea, and Indian Ocean. Increasing sea surface temperatures and coral reef disturbances associated with climate change have expanded the distribution of toxin-producing dinoflagellates, leading to a gradual increase in CFP cases in previously unaffected regions.

 

Common Toxic Fish

Frequently implicated species include:

Barracuda (Sphyraena spp.)梭魚 [3].

Grouper (Epinephelus spp.)石斑魚 [4].

Coral trout (Plectropomus spp.)豹紋鰓棘鱸/珊瑚鱒 [5].

Snapper (Lutjanus spp.)笛鯛 [3].

Amberjack (Seriola spp.)琥珀魚/鰤魚 [6].

Moray eel (Gymnothorax spp.)裸胸鱔/海鰻 [7].

The liver, roe, intestines, and head generally contain higher toxin concentrations than skeletal muscle.

 

Involving System

 

Toxicity and mechanism

Ciguatoxins are lipid-soluble, heat-stable polyether compounds that activate voltage-gated sodium channels, causing persistent membrane depolarization and neuronal hyperexcitability.  [8]

Several congeners have been identified, including Pacific (P-CTX), Caribbean (C-CTX), and Indian Ocean (I-CTX) ciguatoxins, with Pacific ciguatoxins (太平洋雪卡毒素) generally exhibiting the greatest potency. [9].

 

Gastrointestinal: Nausea; Vomiting, Abdominal cramps, Diarrhea [3, 10].

Neurological: Circumoral and distal paresthesia, Temperature sensation reversal (cold allodynia or cold–hot reversal), [10]

 

 

Presentation

Clinical Manifestations, Onset

Symptoms usually develop within 1–24 hours after ingestion of contaminated fish.

Musculoskeletal: Pruritus, Myalgia, Arthralgia, Weakness [10].

Dizziness, ataxia [10].

 

Neurological symptoms may persist for weeks to months and occasionally for years. [11].

Cold temperature reversal is a characteristic clinical feature.

Cardiovascular: Bradycardia, hypotension, cardiac conduction abnormalities (occasionally) [12].

Severe poisoning may require intensive supportive care.

 

Diagnosis is primarily clinical and relies on:

Recent consumption of tropical or subtropical reef fish [1]

Characteristic neurological findings, particularly cold temperature reversal

Compatible gastrointestinal and cardiovascular manifestations

 

Routine laboratory investigations are generally nonspecific. Specialized toxin detection using liquid chromatography–mass spectrometry (LC–MS/MS) is available only in selected reference laboratories. [13].

 

Antidote and Treatment

There is no specific antidote. Treatment is primarily supportive, with no established antidote.

Management consists of:

Airway, breathing, and circulation stabilization

Intravenous fluid replacement

Antiemetics and analgesics

Atropine for symptomatic bradycardia, [14].

Vasopressors for refractory hypotension

 

Intravenous mannitol has been reported to improve neurological symptoms when administered within 24–48 hours after exposure; however, clinical evidence remains inconsistent, and its routine use is controversial. Persistent neuropathic symptoms may be managed with gabapentin, pregabalin, or amitriptyline on an individual basis.

 

Disposition

Avoid consuming large predatory coral reef fish from endemic regions.

Do not consume fish liver, roe, intestines, or head.

　

Travelers to endemic tropical regions should be informed of the potential risk of ciguatera fish poisoning.

　

Ciguatoxins are heat-stable, lipid-soluble marine neurotoxins.

Poisoning results from eating contaminated coral reef fish rather than shellfish. [1]

Prevention through avoidance of high-risk reef fish remains the most effective strategy.

 

References

[1]. https://pubmed.ncbi.nlm.nih.gov/42301912/

[2]. https://pubmed.ncbi.nlm.nih.gov/40628156/

[3]. https://pubmed.ncbi.nlm.nih.gov/39997191/

[4]. https://pubmed.ncbi.nlm.nih.gov/41591150/

[5].  https://pubmed.ncbi.nlm.nih.gov/36977121/

[6]. https://pubmed.ncbi.nlm.nih.gov/37044166/

[7]. https://pubmed.ncbi.nlm.nih.gov/41295841/

[8]. https://pubmed.ncbi.nlm.nih.gov/29306662/

[9]. https://pubmed.ncbi.nlm.nih.gov/41802301/

[10]. https://pubmed.ncbi.nlm.nih.gov/22275728/   

[11]. https://pubmed.ncbi.nlm.nih.gov/27613284/

[12]. https://pubmed.ncbi.nlm.nih.gov/31151977/

[13]. https://pubmed.ncbi.nlm.nih.gov/40452308/   

[14]. https://pubmed.ncbi.nlm.nih.gov/25019942/

   

Edited by Yu-Jang Su, July 13, 2026

History, Aim and Scope

The Taiwan MacKay Memorial Hospital Emergency Department Poison Center (TWMMHEDPC) is a leading clinical toxicology and poisoning referral center in Taiwan. The center provides comprehensive consultation, diagnosis, and treatment for patients with acute poisoning and toxic exposures. Its major areas of expertise include severe poisoning management, extracorporeal toxin removal therapies, pesticide poisoning, venomous snakebites, Hymenoptera envenomation, carbon monoxide poisoning and hyperbaric oxygen therapy, emerging drugs of abuse, and toxicological emergencies. In addition to clinical services, TWMMHEDPC is actively engaged in medical education, toxicology research, and the development of evidence-based poisoning management strategies.

MacKay Memorial Hospital, founded in 1880, has played a pivotal role in the development of medical toxicology in Taiwan. Its major strengths include the management of critically ill poisoned patients, extracorporeal toxin removal therapies, treatment of pesticide poisoning, management of venomous snakebites, research on Hymenoptera venom envenomation, carbon monoxide poisoning and hyperbaric oxygen therapy, management of emerging drugs of abuse, as well as clinical toxicology research and education. The hospital has remained steadfast in its commitment to advancing the field of toxicology and improving patient care.

During the presidency of Dr. Wen-Han Chang, the Poison Center was established in July 2017. In December 2019, the Center's first director, Dr. Yu-Jang Su, launched the Poison Center website. Since its inception, the website has been updated monthly with the latest developments in toxicology and poisoning management, drawing extensively from the biomedical literature indexed in the National Library of Medicine's PubMed database. The platform was created to provide healthcare professionals, researchers, and the general public worldwide with convenient access to reliable toxicology information and reference materials.

Subsequently, the Division of  Toxicology within the Department of Emergency Medicine was formally established in July 2022. Upholding its original mission, the website continues to provide regular updates on advances in toxicology and poisoning medicine, while also compiling and showcasing scholarly publications produced by the Division of Medical Toxicology, Department of Emergency Medicine, MacKay Memorial Hospital, in international peer-reviewed journals for academic reference.

Edited by Yu-Jang Su, MD. June 20, 2026 

Arecoline / Areca Nut Toxicity

 

Arecoline / Areca Nut Toxicity

Substance

Arecoline is one of the main alkaloids in areca (betel) nut. It acts as a muscarinic receptor agonist and is associated with both acute toxicity and long-term health risks. [1]

 

Common Name

檳榔鹼, substance in betel nut 倒吊子: King of the betel nut [2][3].

The main toxic constituents include arecoline, arecaidine, and tannins. Arecoline and its nitrosamine derivatives have been linked to carcinogenicity, while chronic exposure to areca nut is associated with oral submucous fibrosis and oral cancer. [4].

 

Involving system

Arecoline and related alkaloids activate muscarinic receptors and may cause neurotoxicity [5], cardiotoxicity: pathologic heart hypertrophy [6], hepatotoxicity: fatty degeneration [7], and developmental toxicity. Oxidative stress, apoptosis, inflammation, and disrupted signaling pathways are considered important mechanisms.

Oral mucosal damage: [8].

 

Presentation/ Clinical Manifestations

Acute toxicity may present with salivation, nausea, vomiting, abdominal pain, sweating, dizziness, palpitations, tachycardia, hypotension, dyspnea, bronchoconstriction drowsiness, and in severe cases, coma. [9, 10].

OHCA [3].

Chronic chewing is strongly associated with oral submucous fibrosis and oral cancer, especially in Taiwan and South Asia. [11].

 

Toxic Dose: the precise toxic dose in humans remains undefined, animal studies suggest systemic toxicity at doses of approximately 50–100 mg/kg [10].

 

Antidote/ Management

Treatment is mainly supportive. If residual betel nut remains in the mouth, it should be removed immediately and the oral cavity cleaned. Vital signs and mental status should be monitored closely.

Atropine sulfate (0.5–1.0 mg IV) is titrated every 3–5 minutes until bradycardia resolves.

ACLS for a life-threatening arrhythmia [3].

Disposition 

Depends on patient's status of airway, oxygen demand and hemo-dynamic condition.

References

[1]. Wu L, Yao N, Jiang W, Wu P, Liu Y, Ma Y, Ren H, Jin X, Shi H, Zhou X, Feng L. Arecoline regulates glycolipid and endoplasmic reticulum metabolisms in adult grass carp (Ctenopharyngodon idella). Anim Nutr. 2025 Apr 5;21:447-461. https://pubmed.ncbi.nlm.nih.gov/40510831/

[2]. Huang CY, Chuang CH. A Common Fruit but Potentially Hidden Crisis: A Case Report of Betel Nut Intoxication. J Acute Med. 2023 Mar 1;13(1):41-43. https://pmc.ncbi.nlm.nih.gov/articles/PMC10116037/

[3]. Chou CJ, Su HM, Lee HH, Ko YC, Chen PH, Chen BH. Life-threatening cardiac toxicity after chewing inverted nut (pinang-wang). Ann Emerg Med. 2009 Nov;54(5):757-8. https://pubmed.ncbi.nlm.nih.gov/19853786/

[4]. Yu N, Cai W, Zhang C, Cai Q, Zhang Z, Hu Y, Sun Y, Yin K, Ren F, Chang K, Jin M, Li D, Zhang L, Wu H, Li M. The multistep progression of areca nut-induced oral cancer: a mechanistic roadmap from pathogenesis to precision therapy. Life Med. 2026 Mar 27;5(2):lnag011. https://pubmed.ncbi.nlm.nih.gov/42100377/

[5]. Shih YT, Chen PS, Wu CH, Tseng YT, Wu YC, Lo YC. Arecoline, a major alkaloid of the areca nut, causes neurotoxicity through enhancement of oxidative stress and suppression of the antioxidant protective system. Free Radic Biol Med. 2010 Nov 30;49(10):1471-9.https://pubmed.ncbi.nlm.nih.gov/20691257/

[6]. Ho TJ, Chi-Kang Tsai B, Kuo CH, Luk HN, Day CH, Jine-Yuan Hsieh D, Chen RJ, Kuo WW, Kumar VB, Yao CH, Huang CY. Arecoline induces cardiotoxicity by upregulating and activating cardiac hypertrophy-related pathways in Sprague-Dawley rats. Chem Biol Interact. 2022 Feb 25;354:109810. https://pubmed.ncbi.nlm.nih.gov/34999050/

[7]. Cao Z, Mai W, Gan L, Huang L. A metabolomics and proteomics-based study on the metabolic effects of arecoline on the liver. Toxicon. 2025 Jun;260:108338. doi: 10.1016/j.toxicon.2025.108338.  https://pubmed.ncbi.nlm.nih.gov/40216365/

[8]. Peng J, Chen L, Xie J, Wang X, Wang X, Chen C, Wang R, Xie X. EGR1 regulates PDE12 mediated mitochondrial dysfunction to induce oral mucosal epithelial barrier damage in oral submucous fibrosis. Eur J Pharmacol. 2026 May 10;1023:178865. https://pubmed.ncbi.nlm.nih.gov/42000021/

[9]. Chu NS. Effects of Betel chewing on the central and autonomic nervous systems. J Biomed Sci. 2001 May-Jun;8(3):229-36. https://pubmed.ncbi.nlm.nih.gov/11385294/

[10]. Chen X, He Y, Deng Y. Chemical Composition, Pharmacological, and Toxicological Effects of Betel Nut. Evid Based Complement Alternat Med. 2021 Aug 18;2021:1808081. https://pmc.ncbi.nlm.nih.gov/articles/PMC8387188/?utm_source=chatgpt.com

[11]. Ranganathan K, Kavitha L. Clinical aspects of oral cancer and potentially malignant disorders in South and Southeast Asia. Oral Dis. 2025 May;31(5):1406-1419.  https://pubmed.ncbi.nlm.nih.gov/38817004/

 

 Edited by Yu-Jang Su M.D.     May 16, 2026.            

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