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Arsenic Poisoning: Signs, First Aid, and Consequences
Last updated: 27.10.2025
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Arsenic exists in inorganic (highly toxic) and organic (usually low-toxic) forms. Clinically, we most often encounter acute poisoning from inorganic arsenic (salts, oxide/trioxide As₂O₃) or chronic arsenic (drinking water, food, occupational exposure). A special case scenario involves arsine (AsH₃), a gas that causes massive hemolysis within minutes of inhalation; this is a different toxicological entity, but it falls under the umbrella of arsenic intoxications. [1]
Acute oral poisoning manifests itself violently: vomiting (often with blood), "rice-like" watery diarrhea, severe abdominal pain, rapid dehydration, hypotension, and arrhythmia; without treatment, shock and multiple organ failure are possible. With arsine, the first symptoms to dominate are dark urine, lower back pain, weakness, and shortness of breath—signs of hemolysis and acute renal failure. [2]
Chronic exposure manifests itself gradually: hyperpigmentation and hyperkeratosis of the skin, peripheral nerve damage (polyneuropathy), weakness, gastrointestinal complaints; in the long term, the risk of skin, bladder, and lung cancer increases. The key to recognition is a proper anamnesis (well/borehole water, rice, occupation) and properly performed laboratory tests. [3]
Proper first aid and early initiation of chelation therapy for severe acute poisoning significantly improve the prognosis; in severe cases, minutes and hours matter. In chronic cases, source elimination, control of drinking water, and dietary practices are essential. [4]
Epidemiology
According to the WHO, arsenic in drinking water remains a global problem: the recommended limit is 10 µg/L (10 ppb); however, achieving and controlling this level is difficult in some regions of the world, particularly in rural areas with private wells. Long-term exposure is associated with increased cancer risks and cardiovascular outcomes. [5]
In the US and EU, drinking water standards also set a limit of 10 µg/L; the FDA sets the same quality level for bottled water. Some states (such as New Jersey) use even stricter guidelines. This is important for families using well water without centralized monitoring. [6]
Chronic dietary exposure is most often discussed in relation to rice and rice products (which accumulate inorganic arsenic from soil and water). International bodies are developing/updating maximum levels for infant formula and rice; children and pregnant women are vulnerable. [7]
Industrial/laboratory incidents involving arsine are rare but potentially catastrophic (contact of the acid with arsenic-containing alloys, electrochemical processes). The gas is non-irritating—victims may not realize their exposure until hemolysis develops. [8]
Reasons
Acute oral poisoning is associated with the ingestion of inorganic compounds (e.g., arsenic trioxide As₂O₃), sometimes with errors in everyday life/industrial settings, and less commonly with intentional poisoning. Historically, As₂O₃ was used in some rodenticides and medicinal products; today, access is limited, but cases do occur. [9]
Chronic exposure - long-term consumption of water with excess arsenic levels (private wells, regions with geological background) or a diet high in arsenic-accumulating foods (rice/rice drinks). Occupational factors (metallurgy, semiconductors, wood processing with CCA in the past) also contribute. [10]
Arsine (AsH₃) is formed when acids come into contact with arsenic-containing metals/ores (galvanizing, etching). It is a powerful hemolytic: even brief inhalation can cause life-threatening hemolysis and acute renal failure. [11]
Media noise is created by the topic of organic forms of arsenic from seafood: they give a “false positive” increase in total arsenic in urine, but are clinically non-toxic - analysis of species forms (speciation) is important for interpretation. [12]
Risk factors
Water source: private wells/boreholes without regular testing; areas with known natural contamination. Dietary habits: predominantly rice-based foods without arsenic reduction measures (e.g., boiling in excess water and then flushing). [13]
Occupation: Semiconductor industry, metallurgy, glass/pesticide manufacturing, work where exposure to arsine is possible. Lack of safety training, gas analysis equipment, and personal protective equipment increase the risks. [14]
Individuals: Children, pregnant women, and patients with chronic liver/kidney disease are more vulnerable to the effects of chronic exposure. Concomitant nutritional deficiencies (micronutrient deficiencies) may increase toxicity. [15]
Social: use of uncertified alternative medications/supplements, homemade remedies, and folk remedies containing arsenic. Proper source control of food and medications reduces these risks. (Summarized from clinical sources.)
Pathogenesis
Inorganic forms of arsenic disrupt cellular respiration and the metabolism of thiol-containing enzymes (inhibition of pyruvate dehydrogenase, etc.), causing mitochondrial dysfunction, lactic acidosis, and tissue energy starvation. At very high doses, endothelial toxicity and capillary leakage—shock, arrhythmia—are also observed. [16]
Chronic exposure increases oxidative stress, disrupts DNA methylation and cellular signaling pathways, which are associated with carcinogenesis (skin, bladder, lungs). Dermatological changes (hyperpigmentation/hyperkeratosis) are markers of long-term exposure. [17]
Arsine triggers massive intravascular hemolysis: hemoglobinuria, hyperkalemia, acute renal failure due to tubular damage by pigments; without support, disseminated intravascular coagulation (DIC) and shock are possible. Chelators are less effective against arsine than aggressive hemodynamic and renal support. [18]
Organic forms from seafood (arsenobetaine) are rapidly excreted and clinically nontoxic - but distort total arsenic in urine, so abstinence from seafood for 48-72 hours before testing or speciation is required. [19]
Symptoms
Acute oral: sudden nausea, vomiting (sometimes with blood), "rice" watery diarrhea, abdominal pain, metallic/garlic taste, salivation; then - dehydration, hypotension, tachycardia, arrhythmia, seizures, possible paresthesia and weakness in the extremities. Blood/electrolytes are quickly "broken off". [20]
Arsine (inhalation): within minutes to hours - weakness, headache, lower back/abdominal pain, shortness of breath; dark "Coke-cola" urine (hemoglobinuria), jaundice; laboratory findings - hemolysis, hyperkalemia, rapid drop in hemoglobin, increase in creatinine. Symptoms often appear after leaving the workplace. [21]
Chronic exposure: mottled hyperpigmentation, teardrop-shaped skin, hyperkeratosis of the palms/feet, brittle nails, polyneuropathy (burning pain, numbness), gastrointestinal complaints, moderate anemic syndrome. Memory and concentration problems may also occur. [22]
In children and the elderly, dehydration occurs more rapidly; in pregnant women, it is important to exclude arsenic as a risk factor for adverse outcomes. In any unexplained diarrhea with collapse and metabolic acidosis after exposure to chemicals, arsenic should be included in the differential. [23]
Forms and stages
Acute non-organic (oral): hypervomitis/diarrhea → hemodynamic instability → cardiac damage (QT prolongation, arrhythmias), seizures, metabolic acidosis. The earlier rehydration and chelation are started, the higher the chances. [24]
Acute inhalation (arsine): latent period is short; the "window for intervention" is hours. Hemolysis and renal failure predominate. Intensive support and early involvement of nephrologists (dialysis/replacement therapy if necessary) are required. [25]
Chronic form: progressive dermal and neurological changes over months to years; often detected incidentally by elevated arsenic in urine during water source screening. Hair/nail testing (biomarkers of long-term exposure) can be used to confirm this, but interpretation by a specialist is required. [26]
Mixed scenarios: acute on top of chronic (worsening of symptoms with additional dose from water/food) – require both urgent care and identification/elimination of the source. (Summary of clinical reviews.)
Complications and consequences
Early complications include shock, arrhythmias, seizures, acute renal failure, disseminated intravascular coagulation (DIC), liver damage, and severe metabolic acidosis. Without treatment, mortality from massive acute doses is high. [27]
With arsine - severe hemolysis, hyperkalemia (arrhythmia), acute tubulopathy and anuria within 24-48 hours. Urgent correction of electrolytes and renal support are required. [28]
Long-term effects of chronic exposure include increased risks of skin, bladder, and lung cancer, as well as cardiovascular and endocrine disorders. Skin changes and peripheral neuropathy may partially persist even after removal of the source. [29]
Diagnostic errors (interpretation of total arsenic in urine in the context of recent seafood consumption) lead to false alarms and incorrect management; therefore, speciation or repeat testing after 48–72 hours without seafood consumption are important. [30]
Diagnostics
The gold standard for immediate exposure is a 24-hour urine arsenic test (preferably with a species-specific analysis that distinguishes inorganic from organic forms from seafood). The patient should abstain from seafood for 48-72 hours before collection. Blood arsenic testing is less informative. [31]
In acute poisoning: clinical and metabolic profile (electrolytes, lactate, creatinine/urea), ECG (QTc, arrhythmia), coagulogram, liver enzymes. In case of arsine - hemolysis (LDH↑, reticulocytes↑), free hemoglobin, bilirubin, potassium, urine analysis (hemoglobinuria). [32]
To confirm chronic exposure, arsenic levels in hair and nails (biomarkers for recent months) are measured, but interpretation is complex (external contamination, variability). The decision rests with the clinician/toxicologist. [33]
Instrumental testing, as indicated, includes ECG monitoring, ultrasound/CT scans for complications, and neurophysiology for polyneuropathy. A sanitary and epidemiological assessment of the source (water/food analysis) is important to prevent relapse. (Summarized according to ATSDR/WHO.)
Differential diagnosis
Acute: dysentery/cholera-like gastrointestinal infections, other toxicants (mercury, organophosphorus), iron poisoning, cyanides (lactic acidosis), severe foodborne toxic infections. ECG, biochemistry, and chemical exposure history help to quickly narrow the range. [34]
Hemolysis/dark urine: hydrogen arsenide (arsine), hemolytic anemias (autoimmune, G6PD deficiency), poisonous mushrooms/favism, copper. Exposure history (acids + metals, galvanics), gas analysis, and hemolysis profile are key. [35]
Chronic neuropathy: diabetic, alcoholic, B₁₂-deficiency, lead/mercury. Dermatological markers (hyperpigmentation/hyperkeratosis) and arsenic in urine/keratin clarify the diagnosis. [36]
Falsely high total arsenic in urine: seafood 48 hours before analysis (organic forms). Solution: speciation or repeat 24-hour collection after a "moratorium" on seafood. [37]
Treatment
First aid. Immediately cease exposure, assess the ABCs (airway-breathing-circulation), begin aggressive rehydration and electrolyte replacement. In case of early oral ingestion, activate charcoal (if there is no vomiting/risk of aspiration and within the "therapeutic window"); if large quantities of As₂O₃ are ingested, intermittent bowel irrigation may be necessary at the discretion of a toxicologist. Gastric lavage at home is prohibited. [38]
Chelators (antidotes).
- Dimercaprol (BAL, British anti-Lewisite) is the classic drug of choice for severe acute arsenic poisoning (IM, regimens with 3-5 mg/kg every 4-6 hours with gradually increasing intervals). Start as early as possible, as effectiveness decreases over time. Pain at the injection site, hypertension, and vomiting may occur. [39]
- DMSA (succimer) is an oral chelator; it is widely used for lead, and off-label for arsenic. Traditional regimens are 10 mg/kg 3 times a day for 5 days, then 10 mg/kg 2 times a day for 14 days (adapted individually); some sources mention fixed doses for arsenic in adults. Liver/blood function should be monitored. [40]
- DMPS is a water-soluble analogue for parenteral/oral administration (not registered in the USA, used in a number of countries); can be used as a bridge to DMSA. [41]
When to chelate. In severe clinical cases and probable exposure, do not wait for laboratory confirmation – begin chelation immediately after stabilization, submitting test results simultaneously. The best effect is achieved within the first few hours. Moderate/chronic cases require an individual risk/benefit assessment and, as a rule, source elimination and maintenance therapy. [42]
Arsine. The main treatment is intensive support: oxygen, correction of hyperkalemia, red blood cell transfusions in severe anemia, and early initiation of dialysis in cases of progressive renal failure. Chelators have limited proven benefit in arsine; if concomitant absorption of inorganic arsenic is present, a toxicologist may consider them on a case-by-case basis. [43]
Table 1. Quick reference: acute vs. chronic vs. arsine
| Parameter | Acute oral (As₂O₃, etc.) | Chronic exposure | Arsine (AsH₃, inhalation) |
|---|---|---|---|
| Debut | Watch | Months-years | Minutes-hours |
| Dominates | Vomiting, rice-like diarrhea, shock | Skin, neuropathy | Hemolysis, Hemoglobinuria, acute renal failure |
| Key test | 24-hour urine arsenic (speciation) | Urine + hair/nails | Hemolysis, K⁺, creatinine |
| Antidote | BAL/DMSA/DMPS | Depending on the situation (less often) | Support (dialysis), chelators are questionable |
Table 2. Diagnostic algorithm for suspected arsenic
| Step | What to do | For what |
|---|---|---|
| 1 | History (water, food, profession, seafood for 48-72 hours) | Clarify the source and eliminate false positives |
| 2 | 24-hour urine arsenic ± speciation | Confirming the exposure now |
| 3 | General/biochemistry, lactate, coagulogram, ECG | Assess severity/risks |
| 4 | Hair/nails (in chronic cases) | Long exposure marker |
| 5 | Environmental testing of water/food | Prevention of relapse |
Table 3. Chelators for arsenic (diagrams and notes)
| Preparation | How is it prescribed? | Notes |
|---|---|---|
| Dimercaprol (BAL) | 3-5 mg/kg IM every 4-6 hours with subsequent prolongation of intervals | Start in severe acute; it is better to start earlier. Side effects: pain, hypertension. [44] |
| DMSA (succimer) | 10 mg/kg 3 times a day for 5 days → 10 mg/kg 2 times a day for 14 days (adapt) | Off-label for arsenic; monitor liver enzymes/blood. [45] |
| DMPS | 3-5 mg/kg intramuscularly orally at intervals of 4-12 hours (then less frequently) | Not approved in the US; alternative in some countries.[46] |
| Arsine | - | Chelators of limited benefit; emphasis on support/dialysis. [47] |
Table 4. Standards and guidelines
| Wednesday | Threshold/norm | Comments |
|---|---|---|
| Drinking water (WHO, US/EPA, FDA for bottled) | 10 µg/L (ppb) | Recommended/mandatory limit; lower is better. [48] |
| Exposure biomarker | 24-hour urine arsenic (with speciation) | Avoid seafood 48-72 hours before collection.[49] |
| Food (rice/baby food) | Regulated by international/national authorities | Stay tuned for updates to recommendations. [50] |
Table 5. Red flags of emergency conditions
| Situation | What is dangerous? | Actions |
|---|---|---|
| Vomiting blood + "rice" diarrhea, collapse | Shock, arrhythmia | Infusions, electrolytes, ECG, BAL/DMSA as indicated |
| Dark urine, lower back pain, jaundice | Arsine - hemolysis/AKI | Oxygen, K⁺ correction, blood transfusion, dialysis |
| QTc↑, arrhythmia | Risk of sudden death | Monitoring, electrolytes, antiarrhythmic tactics |
| Neurological deficit | Toxic neuropathy | Neurologist, rehabilitation |
Table 6. Differential diagnosis of "arsenic-like" pictures
| Painting | What else is similar? | How to distinguish |
|---|---|---|
| Cholera-like diarrhea | Norovirus/cholera/toxins | Contact with chemicals, lactate↑, arsenic in urine |
| Hemolysis + acute renal failure | Hemolytic anemia, copper, favism | History (acid + metal → arsine), gas analysis of the site |
| Chronic neuropathy | Diabetes, alcohol, B₁₂ deficiency | Skin (pigmentation/keratosis), urine/hair/nails |
| "High arsenic in urine" | Seafood | Speciation or repeat after 48-72 hours without them [51] |
Table 7. Prevention: home, nutrition, work
| Level | Measure |
|---|---|
| House/water | Analysis of well/borehole water annually; if exceeded, filtration/alternative source |
| Nutrition | Rinse rice, cook in excess water and then drain; vary grains, monitor baby foods |
| Job | Gas analysis for arsine, separate storage of acids and arsenic-containing materials, personal protective equipment and training |
| Medical | Screening of risk groups, information about speciation and diet before urine analysis [52] |
Prevention
At home and in the home: If you use a private well, test your water for arsenic at least once a year and after significant hydrological events. If the level is exceeded, temporarily switch to bottled water or connect certified arsenic removal systems. In the kitchen, rinse rice and cook it in a large volume of water, then drain it; vary the grains in children's diets. [53]
At work: Avoid contact of acids with arsenic-containing metals (risk of arsine formation); provide gas analysis and emergency protocols, train personnel to recognize early signs of hemolysis (dark urine, weakness). If there is any suspicion of arsenic ingestion, prompt medical examination and documentation of exposure. [54]
Forecast
With early recognition and timely treatment (infusions, electrolyte correction, BAL/DMSA/DMPS chelators as indicated), acute oral poisoning may resolve favorably; delayed treatment leads to shock, arrhythmias, and multiple organ failure. Chronic exposure after source elimination often results in regression of some symptoms, but skin changes and neuropathy may persist. [55]
Arsin remains the most insidious scenario: the outcome is determined by the rate of intensive support (correction of hyperkalemia, blood transfusions, early dialysis). Even with visible "improvement," observation is required, as hemolysis and acute renal failure can increase in the first 24 hours. [56]
FAQ
- What are the first signs of acute arsenic poisoning?
Sudden vomiting, watery (sometimes "rice") diarrhea, severe abdominal pain, rapid dehydration, weakness, dizziness. This is an indication for emergency care. [57]
- Which analysis is the "most correct"?
For current exposure, 24-hour urine arsenic (speciation if possible). It is important not to eat seafood 48-72 hours before collection, otherwise total arsenic may be falsely high. [58]
- Is arsenic treated with an “antidote”?
Yes, for severe acute poisoning, chelators are used: dimercaprol (BAL), succimer (DMSA), and sometimes DMPS. Their effectiveness is higher if started within the first few hours. The decision is made by a toxicologist. [59]
- How does arsine differ from “regular” arsenic?
Arsine is a gas that causes immediate hemolysis and kidney failure; there is no specific "antidote", the main measures are oxygen, electrolyte correction, transfusions and dialysis. [60]
- Is it true that rice is dangerous because of arsenic?
Rice can accumulate inorganic arsenic, but the risks vary by region and technology. Reduce them by rinsing the grain, cooking it in excess water, and diversifying your diet. Water and nutrition standards are based on 10 μg/L for water; separate levels apply for rice. [61]
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