Unraveling the Mystery of Diethylene Glycol Poisoning
Imagine a substance so sweet and harmless-looking that it could be mistaken for a common pharmaceutical ingredient, yet so toxic that a single teaspoon could be fatal.
This is the paradox of diethylene glycol (DEG), a chemical that has been responsible for numerous mass poisoning tragedies across the globe for nearly a century. From contaminated medications to tainted consumer products, DEG continues to pose a significant public health risk, particularly in regions with lax regulatory oversight.
Its sweet taste, colorless appearance, and viscous texture make it a perfect—and deadly—stand-in for safer solvents like glycerin or propylene glycol. This article explores the sinister nature of DEG poisoning through the lens of two documented cases, unraveling the science behind its toxicity and the ongoing efforts to prevent further tragedies.
Makes it easily mistaken for safe pharmaceutical ingredients
Mass poisonings across multiple continents over decades
Primary target organ is the kidneys, leading to acute failure
Despite hemodialysis and aggressive supportive care, the patient died seven days after presentation 1 .
12 of 15 poisoned patients (80%) died within seven days 3 .
| Aspect | Case 1 (Printer Ink) | Case 2 (Contaminated Medication) |
|---|---|---|
| Route of Exposure | Oral ingestion | Intravenous administration |
| DEG Concentration | 50% in printer ink | 30% in medication |
| Primary Symptoms | GI distress, renal failure, metabolic acidosis, cranial nerve paralysis | Acute renal failure, oliguria/anuria |
| Time Course | Death within 7 days | Renal failure 2-12 days post-exposure |
| Mortality | 1 death (100% of case) | 12 deaths (80% of poisoned patients) |
| Treatment | Hemodialysis, supportive care | Supportive care |
Diethylene glycol poisoning typically manifests in three distinct phases, though symptoms may overlap in some cases 1 2 .
Onset is rapid after ingestion but can be delayed by co-ingestants like food or ethanol 1 .
Delayed 1-2 weeks after initial exposure. Correlates with degree of nephrotoxicity 1 . Recovery is variable.
Ingestion or administration of DEG-contaminated substance
Nausea, vomiting, abdominal pain, possible inebriated appearance
Acute kidney injury, metabolic acidosis, potential hepatotoxicity
Neurological manifestations including cranial nerve palsies, peripheral neuropathies
Recovery with potential permanent damage, or death typically within 1-2 weeks
DEG is rapidly absorbed through oral ingestion, with dermal absorption also possible through broken or damaged skin 1 . Once in the body, it undergoes metabolism primarily in the liver through the same NAD-dependent pathway as ethanol and other toxic alcohols 1 .
Contrary to initial assumptions, DEG is not broken down into significant amounts of ethylene glycol in humans 1 2 . Instead, alcohol dehydrogenase (ADH) oxidizes DEG to 2-hydroxyethoxyacetaldehyde, which aldehyde dehydrogenase then further metabolizes to 2-hydroxyethoxyacetic acid (HEAA) and diglycolic acid (DGA) 1 2 .
These metabolites, particularly DGA, are now recognized as the primary culprits behind DEG's devastating effects on the kidneys.
Research has revealed that DGA is transported to proximal tubular cells in the kidneys, where it inhibits succinate dehydrogenase, a key enzyme in the citric acid cycle 2 . This inhibition blocks adenosine triphosphate (ATP) production, essentially starving cells of energy and leading to cell death.
| Compound | Formation Pathway | Toxic Mechanism | Primary Effects |
|---|---|---|---|
| Diethylene Glycol (Parent Compound) | Direct exposure | Precursor to toxic metabolites | Initial GI symptoms, osmolar gap |
| 2-Hydroxyethoxyacetaldehyde | Metabolism by alcohol dehydrogenase | Intermediate metabolite | Contributes to metabolic acidosis |
| HEAA | Metabolism by aldehyde dehydrogenase | Weak acid, contributes to acidosis | Metabolic acidosis, organ dysfunction |
| Diglycolic Acid (DGA) | From HEAA | Inhibits succinate dehydrogenase | Nephrotoxicity, acute renal failure |
Marked vacuolization and edema of epithelial cells obstruct the tubular lumen, reducing urine flow and resulting in anuria and uremia 2 .
The history of DEG poisoning spans nearly a century, with remarkably similar patterns repeating across different continents and decades.
| Year | Country | Contaminated Product | Reported Deaths |
|---|---|---|---|
| 1937 | United States | Sulfanilamide elixir | >100 |
| 1990-1992 | Bangladesh | Paracetamol syrup | 236+ children |
| 1995 | Haiti | Paracetamol syrup | 88 children |
| 1998 | India | Cough syrup | 36 children |
| 2006 | Panama | Cough syrup | Hundreds |
| 2008-2009 | Nigeria | "My Pikin" teething medication | 54 children |
| 2023 | Various | Multiple syrups | Ongoing investigations |
The first recorded mass poisoning occurred in the United States in 1937 when DEG was used as a solvent in an antibiotic elixir of sulfanilamide 1 5 .
Deaths were reported shortly after distribution, ultimately claiming over 100 lives—a third of them children 1 .
This catastrophe directly led to the passage of the 1938 Federal Food, Drug, and Cosmetic Act, which required manufacturers to demonstrate product safety prior to marketing 1 5 .
Tragically, DEG poisoning incidents continue to occur. Since September 2022, the World Health Organization has reported seven consecutive contamination episodes across at least nine countries 4 .
A concerning commonality is that at least 14 of the involved products were fixed-dose combinations marketed for symptomatic treatment of common cold or flu, many lacking sufficient evidence for efficacy and safety 4 .
Deaths in 1937 US incident
Child deaths in Bangladesh (1990-1992)
Mortality rate in Case 2 (China 2006)
Recent contamination episodes since 2022
Diagnosing DEG poisoning presents significant challenges. Measurement of serum DEG concentration is the most accurate method, but this test is often unavailable at most hospitals and can take weeks to return results from reference laboratories 1 .
Therefore, diagnosis is primarily clinical, based on patient history, physical examination, and basic laboratory tests 1 .
Current treatment approaches focus on three main areas:
Airway management, fluid/electrolyte balance, acid-base correction
Prevents formation of toxic metabolites (Fomepizole or ethanol)
Removes DEG and metabolites, corrects acid-base disturbances
The repeated pattern of DEG mass poisonings has revealed consistent vulnerabilities in pharmaceutical manufacturing and quality control.
| Tool/Method | Function | Importance |
|---|---|---|
| Gas Chromatography (GC) | Precise detection and quantification of DEG/EG impurities | Gold standard method for accurate measurement |
| Thin-Layer Chromatography (TLC) | Rapid screening for gross DEG contamination | Low-cost ($1/test) method accessible in resource-limited settings |
| Supplier Qualification | Verifying reliability of raw material suppliers | Prevents economically motivated adulteration at source |
| 100% Container Testing | Identity testing of every container of high-risk ingredients | Prevents isolated contamination events |
| Refractometry | Screening purity of glycerol and similar solvents | Cheap technology for initial screening |
Diethylene glycol poisoning represents a frustrating convergence of chemical similarity, economic incentive, and regulatory failure.
From the 1937 sulfanilamide tragedy that sparked modern pharmaceutical regulation in the United States to recent incidents, the pattern has repeated with devastating consequences. The cases presented here—one involving intentional printer ink ingestion and another featuring contaminated medication administered to vulnerable patients—illustrate the diverse pathways through which DEG exposure can occur.
While treatment protocols have advanced with the use of fomepizole and hemodialysis, prevention remains the most effective strategy. Implementation of rigorous quality control measures, thorough supply chain oversight, and simple, inexpensive screening tests could prevent most, if not all, future DEG poisoning events.
As global pharmaceutical supply chains continue to expand and complexify, maintaining vigilance against this preventable threat becomes increasingly critical. The sweet-tasting solvent that has claimed hundreds of lives over nearly a century serves as a sobering reminder that technological progress must be matched by unwavering commitment to quality and safety in medical products.