AME case reports · 2026
Alcohol consumption "fuels" dimethyl sulfate vapor poisoning: a case report of three patients.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Xiang Baoliang, Wu Ting, Zeng Liangbo, Guo Wanyi, Wu Xianfeng
Аннотация
BACKGROUND: Dimethyl sulfate (DMS), (CH3)2SO4, is a highly toxic industrial chemical. Upon contact with moist mucosa, it hydrolyzes into sulfuric acid and methanol, causing severe corrosive damage to the eyes and respiratory tract. While its acute toxicity is well known, factors that may modify the severity of poisoning remain unreported. In particular, the potential interaction between alcohol consumption and DMS toxicity has not been previously described.
CASE DESCRIPTION: We present three patients with acute DMS vapor poisoning following occupational exposure. Notably, two patients consumed approximately 100 mL of 53% vol liquor (baijiu) after exposure and experienced a marked exacerbation of ocular pain, photophobia, corneal epithelial defects, and respiratory symptoms. In contrast, the third patient, who did not drink alcohol, had initially similar or even more severe symptoms but showed a faster and more stable recovery without exacerbation. This clinical divergence strongly suggests that ethanol intake amplified the chemical injury, likely through proinflammatory and metabolic pathways.
CONCLUSIONS: Alcohol consumption may worsen DMS poisoning and delay recovery. Clinicians should advise patients with known or suspected DMS exposure to avoid alcohol. This recommendation should be integrated into discharge instructions and occupational safety protocols. Further studies are needed to clarify the underlying mechanisms and to confirm this clinically relevant interaction.
CASE DESCRIPTION: We present three patients with acute DMS vapor poisoning following occupational exposure. Notably, two patients consumed approximately 100 mL of 53% vol liquor (baijiu) after exposure and experienced a marked exacerbation of ocular pain, photophobia, corneal epithelial defects, and respiratory symptoms. In contrast, the third patient, who did not drink alcohol, had initially similar or even more severe symptoms but showed a faster and more stable recovery without exacerbation. This clinical divergence strongly suggests that ethanol intake amplified the chemical injury, likely through proinflammatory and metabolic pathways.
CONCLUSIONS: Alcohol consumption may worsen DMS poisoning and delay recovery. Clinicians should advise patients with known or suspected DMS exposure to avoid alcohol. This recommendation should be integrated into discharge instructions and occupational safety protocols. Further studies are needed to clarify the underlying mechanisms and to confirm this clinically relevant interaction.