Alcohol consumption “fuels” dimethyl sulfate vapor poisoning: a case report of three patients

Introduction

Dimethyl sulfate (DMS), (CH₃)₂SO₄, is a colorless, volatile liquid widely used as an industrial chemical reagent. It is highly toxic, and its hydrolysis products can cause severe damage to the eyes and respiratory tract (1-4). Upon contact with moist mucosal tissues, DMS hydrolyzes to sulfuric acid, methanol, and formic acid. These hydrolysis products induce strong corrosive damage, chemical inflammation, and epithelial barrier destruction, leading to acute chemical eye injury, nasopharyngeal/oropharyngeal mucosal congestion and erosion, and chemical pneumonitis. Symptoms typically develop within hours of exposure (1). In severe cases, DMS exposure can also cause hepatic, renal, and central nervous system damage, with potential lethal risks (2). Given its inherent toxicity, strict occupational measures are mandatory to mitigate exposure risks. Notably, alcohol consumption has been widely confirmed to exert synergistic toxic effects with industrial solvents through metabolic interactions. Acute alcohol intake may compete with industrial solvents for shared metabolic enzymes (e.g., alcohol dehydrogenase), potentially leading to elevated concentrations of the parent compound or its toxic metabolites and enhanced toxicity (5).

Although the acute toxic effects of DMS are well-documented, factors that may modify the severity or clinical course of poisoning, such as co-exposure to other agents, remain poorly understood. In particular, a potential interaction between alcohol consumption and DMS toxicity has not been previously reported. We describe two patients who consumed alcohol after exposure experienced a marked exacerbation of ocular and respiratory symptoms, suggesting that alcohol may worsen the associated chemical injury. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0021/rc).

Case presentation

Case 1

A 61-year-old male with no significant past medical history presented to the emergency department on September 11 complaining of ocular pain, periorbital swelling, blurred vision, photophobia, lacrimation, throat burning, hoarseness, drooling, and dyspnea after consuming approximately 100 mL of 53% vol liquor (baijiu) at dinner. He subjectively denied fever, headache, cough, chest pain, or abdominal discomfort during the initial emergency department interview, with no contradictory objective clinical findings. Notably, earlier on September 7, he had been exposed to DMS vapour while repairing equipment in a chemical plant. This exposure initially caused photophobia, tearing, and blurred vision, leading to his first emergency department visit that evening. At that time, he reported no dyspnea, though a chest computed tomography (CT) showed mild bilateral pulmonary infiltrates. Ophthalmic examination revealed marked conjunctival injection, and he was managed with systemic intravenous corticosteroids in addition to conjunctival irrigation, topical levofloxacin, deproteinized calf blood extract eye gel, tropicamide, and pranoprofen eye drops, with significant improvement. He was discharged on the morning of September 10. However, on the evening of September 11, after consuming alcohol, he developed a more severe recurrence of similar symptoms. Upon readmission, examination indicated visual acuity of oculus dexter (OD) 0.4 and oculus sinister (OS) 0.4, intraocular pressure of OD 15.1 mmHg and OS 16.5 mmHg, pronounced eyelid swelling, conjunctival injection with chemosis, and large central corneal epithelial defects with positive fluorescein staining, though no retinal hemorrhages or exudates were observed. Ears, nose, and throat (ENT) laryngoscopy showed pharyngeal mucosal hyperemia suggestive of acute pharyngitis, while cardiopulmonary examination was unremarkable. Initial arterial blood gas showed pH 7.40, partial pressure of arterial oxygen (PaO₂) 40 mmHg, partial pressure of arterial carbon dioxide (PaCO₂) 67 mmHg, HCO₃⁻ 24.8 mmol/L. High-flow nasal therapy (HFNT) was initiated. Blood tests, including complete blood count (CBC), electrolytes, renal and liver function, were normal. A repeat chest CT revealed bilateral pulmonary infiltrates similar to the previous scan. HFNT was successfully discontinued after 2 days, with gradual improvement in ocular symptoms: visual acuity improved to OD 0.6 mmHg and OS 0.8 mmHg, and intraocular pressure decreased to OD 9.2 mmHg and OS 11.6 mmHg by discharge on day 7, although mild conjunctival injection persisted. The main clinical and imaging findings of this patient are presented in Figure 1.

Figure 1 Main clinical and imaging findings in dimethyl sulfate poisoning (Case 1). Right (OD) and left (OS) eyes at admission, showing significant eyelid swelling and conjunctival hyperemia. Notably, fluorescein staining revealed corneal epithelial defects. The same eyes at discharge, showing marked resolution of all acute signs. Admission nasopharyngoscopy revealing congestion of the pharyngeal mucosa and mild vocal cord congestion. Non-contrast chest CT scan on admission demonstrating minimal bilateral pulmonary infiltrates. CT, computed tomography; DMS, dimethyl sulfate; OD, oculus dexter; OS, oculus sinister.

Case 2

A 39-year-old male colleague of the first case, who presented with eye pain, photophobia, tearing, and rhinorrhea for 3 hours. One day prior, he experienced mild eye discomfort and a foreign body sensation after exposure to DMS vapour at work. He initially paid little attention to it. His symptoms worsened dramatically the following afternoon after he consumed approximately 100 mL of 53% vol liquor (baijiu) with Case 1. He reported no chest tightness or shortness of breath. He received treatment identical to Case 1, with the exception of HFNT. By day 9, his symptoms had gradually improved, and his intraocular pressure decreased to 19.6 mmHg OD (from 29.1 mmHg) and 18.2 mmHg OS (from 18.0 mmHg) at discharge.

Case 3

The third case, a 60-year-old male who had worked with the second case on the same day, similarly developed ocular foreign body sensation and discomfort. His symptoms intensified the following day, prompting a visit to a local hospital where he received intravenous therapy. However, his condition showed no significant improvement. He subsequently presented to our facility at the same time as the first and second cases. Despite reporting more severe ocular, nasal, and pharyngeal symptoms than the second case, he had not consumed any alcohol. His treatment regimen was identical to that of the first case, excluding HFNT. By the time of discharge on day 7, his symptoms had gradually resolved, with intraocular pressures decreasing to 19.2 mmHg OD (from 20.2 mmHg) and 16.6 mmHg OS (from 22.2 mmHg).

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patients for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Herein, we report a cluster of DMS vapour poisoning cases in which symptoms were exacerbated by alcohol intake. To our knowledge, no similar cases have been reported in the literature.

DMS poisoning typically results from accidental occupational exposure or inadequate personal protective measures, and its toxic effects are mediated by the hydrolysis products that induce corrosive tissue damage and chemical inflammation, as described in the Introduction. The clinical manifestations of DMS poisoning in our three patients (e.g., ocular injury, pharyngeal mucosal hyperemia, pulmonary infiltrates) are consistent with the classic acute toxic phenotypes reported in previous studies (1,2,4). However, their subsequent clinical courses diverged significantly. The first case, who had been discharged after initial improvement, experienced a dramatic symptom rebound shortly after alcohol consumption and required readmission. The second case also showed acute deterioration following alcohol intake. In contrast, the third case, despite similar exposure and initial severity, did not consume alcohol and exhibited a more stable recovery without symptom exacerbation. This stark contrast suggests that alcohol consumption may exacerbate DMS-induced tissue damage. This hypothesis is supported by the clear temporal relationship observed between alcohol intake and clinical deterioration in Cases 1 and 2, although we acknowledge the absence of specific biomarkers to confirm this interaction.

Our observation aligns with the broader context of chemical-ethanol interactions noted in occupational medicine. Toffoletto et al. categorized clinical pictures of alcohol intolerance after toxic exposure, including the “antabuse syndrome” (disulfiram-like reaction) and the “degreaser’s flush syndrome” (6). While the classic disulfiram-like reaction involves inhibition of acetaldehyde dehydrogenase, our cases differ in primary symptoms and suspected mechanism.

Building on recent advances in understanding acute alcohol toxicity, we propose a refined mechanism that aligns with the temporal relationship observed in our patients. The exacerbations observed shortly after alcohol intake in Cases 1 and 2 suggest an underlying biological mechanism. Acute alcohol consumption induces a rapid pro-inflammatory state. Hillmer et al. showed that alcohol (targeting 120 mg/dL) significantly elevates interleukin (IL)-8 (7), a chemokine that not only directs neutrophil migration but also activates their effector functions, including granule exocytosis and respiratory burst (8). Similarly, Sturm et al. demonstrated that binge drinking (targeting 100 mg/dL) induces innate immune activation, including increased IL-6, Toll-like receptor 4 (TLR4) upregulation, and pro-inflammatory gene expression [C-X-C motif chemokine ligand 10 (CXCL10), myeloperoxidase (MPO)] (9), which could home to and amplify pre-existing tissue damage. Furthermore, alcohol disrupts cellular metabolism. Irwin et al. showed that acute alcohol causes nicotinamide adenine dinucleotide (oxidized) (NAD⁺⁾ depletion and an increased nicotinamide adenine dinucleotide (reduced) (NADH)/NAD⁺ ratio (10). NAD⁺ is critical for cellular repair and antioxidant enzyme function, and NAD⁺ depletion fuels inflammation by licensing key inflammatory pathways, such as nuclear factor kappa-B (NF-κB) and the NOD-like receptor family pyrin domain containing protein 3 (NLRP3) inflammasome (11). Consequently, its depletion could impair the recovery of already damaged corneal and respiratory epithelial cells.

The quantity of alcohol consumed by our patients (100 mL of 53% liquor) is physiologically relevant. This dose would yield an estimated peak blood alcohol concentration (BAC) of approximately 100 mg/dL in a 60 kg individual, a level comparable to or exceeding those used in the studies cited above (7,9). Therefore, the dose consumed was sufficient to trigger the systemic inflammatory and metabolic alterations documented in the literature.

Integrating these findings, we propose a hypothesis whereby initial DMS exposure creates vulnerable tissue, and subsequent alcohol intake at a physiologically active dose triggers systemic inflammation and metabolic stress, which together amplify local injury and delay repair. This mechanism explains the dramatic exacerbation in Cases 1 and 2 compared to the stable recovery of the non-drinking Case 3. Future studies measuring inflammatory biomarkers (e.g., IL-6, IL-8) and redox status in similar poisoning cases could test this hypothesis directly and provide more definitive evidence.

Additionally, we consider concomitant methanol poisoning from impure alcohol to be improbable in this cluster, as none of the patients exhibited characteristic signs of methanol toxicity, such as central nervous system depression, visual disturbances, optic neuropathy, or high-anion-gap metabolic acidosis (12). Additionally, while not the primary mechanism herein, the potential for alcohol to alter the metabolic fate of DMS or its hydrolysis products cannot be entirely ruled out and warrants investigation.

The management of our cases underscores the importance of supportive care, including decontamination, topical therapies, and systemic corticosteroids for controlling inflammation, as demonstrated by the eventual improvement in all patients. However, our key new finding is the need for a crucial preventive measure, and we recommend that explicit warnings against alcohol consumption must be given to all patients following known or suspected DMS exposure. This advice should be integrated into standard discharge instructions and occupational health safety protocols for handling DMS and potentially other irritating industrial chemicals.

Our study has the primary limitations inherent to its observational nature. The lack of quantitative measurements of DMS or its metabolites, as well as biomarkers of inflammation, prevented us from confirming the exact biological mechanism. Nevertheless, the strong clinical narrative and the clear link between alcohol consumption and symptom worsening provide a solid foundation for a testable hypothesis.

Conclusions

We identify alcohol consumption as a potential precipitant for clinical worsening in DMS poisoning. This interaction likely involves the amplification of the inflammatory response and impairment of tissue repair. Therefore, we recommend that informing patients and workers of this danger should be a primary preventive strategy, while further studies are conducted to clarify the underlying mechanisms.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0021/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0021/prf

Funding: This work was supported by the Anshun Science and Technology Project in Guizhou Province of China (No. KeShe 2024-69).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0021/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patients for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Wang Y, Xia J, Wang QW. Clinical report on 62 cases of acute dimethyl sulfate intoxication. Am J Ind Med 1988;13:455-62. [Crossref] [PubMed]
2. Ip M, Wong KL, Wong KF, et al. Lung injury in dimethyl sulfate poisoning. J Occup Med 1989;31:141-3.
3. Zhang J, Zhou X, Ma J, et al. Dimethyl sulfate poisoning in China: a fatal case and a 45-year retrospective study. Forensic Sci Med Pathol 2024;20:1404-11. [Crossref] [PubMed]
4. Mizuta S, Miyakoshi T, Matsui K, et al. Three Cases of Chemical Burns Caused Due to Dimethyl Sulfate Poisoning. Cureus 2024;16:e57060. [Crossref] [PubMed]
5. Hills BW, Venable HL. The interaction of ethyl alcohol and industrial chemicals. Am J Ind Med 1982;3:321-33. [Crossref] [PubMed]
6. Toffoletto F, Crippa M, Torri D. Interactions between alcohol and work exposure to chemical substances. Med Lav 2007;98:513-20.
7. Hillmer AT, Nadim H, Devine L, et al. Acute alcohol consumption alters the peripheral cytokines IL-8 and TNF-α. Alcohol 2020;85:95-9. [Crossref] [PubMed]
8. Matsushima K, Shichino S, Ueha S. Thirty-five years since the discovery of chemotactic cytokines, interleukin-8 and MCAF: A historical overview. Proc Jpn Acad Ser B Phys Biol Sci 2023;99:213-26. [Crossref] [PubMed]
9. Sturm R, Haag F, Rinderknecht H, et al. Granulocyte function in response to acute alcohol consumption: temporal shifts from proinflammatory activation to antiinflammatory modulation in healthy volunteers. J Leukoc Biol 2025;117:qiaf081. [Crossref] [PubMed]
10. Irwin C, van Reenen M, Mason S, et al. The 1H-NMR-based metabolite profile of acute alcohol consumption: A metabolomics intervention study. PLoS One 2018;13:e0196850. [Crossref] [PubMed]
11. Mann R, Stavrou V, Dimeloe S. NAD + metabolism and function in innate and adaptive immune cells. J Inflamm (Lond) 2025;22:30. [Crossref] [PubMed]
12. Nekoukar Z, Zakariaei Z, Taghizadeh F, et al. Methanol poisoning as a new world challenge: A review. Ann Med Surg (Lond) 2021;66:102445. [Crossref] [PubMed]