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Outbreak of Severe Methemoglobinemia during Maritime Migration

Outbreak of Severe Methemoglobinemia during Maritime Migration Published September 9, 2026 N Engl J Med 2026;395:983-991 DOI: 10.1056/NEJMoa2606487 Abstract Background Migrants crossing the Central Mediterranean sea route travel in overcrowded vessels, where fuel may leak and contaminate seawater accumulating on the vessel floor, resulting in prolonged dermal exposure and fuel-related skin injuries. Since March 2024, clusters of cases of severe acquired methemoglobinemia with no apparent cause have been identified by clinicians in Lampedusa at disembarkation among migrants arriving in Italy. Methods We conducted a coordinated clinical and toxicologic investigation to characterize these cases and identify the underlying cause. Biologic samples were obtained from a subset of patients and analyzed for methemoglobin-inducing agents. A fuel sample from a vessel associated with one of the case clusters was also analyzed. Results Between March 2024 and December 2025, a total of 82 patients with severe acquired methemoglobinemia were identified, 90% of whom were male; the median age of the patients was 22.5 years (interquartile range, 19.5 to 28.0). The median methemoglobin level at presentation was 44.6% (interquartile range, 32.0 to 55.7), with 43% of the patients having a level of 50% or greater. Methylene blue therapy was used in 90% of the patients, often in repeated doses. Hemolytic anemia occurred as a delayed complication in 38 patients, frequently leading to blood transfusion. Two patients died. Toxicologic analysis identified N-methylaniline (a gasoline additive) or its metabolites in 37 of 39 tested patients (95%) and N-methylaniline at a concentration of 1.1% in the fuel sample from the vessel. Conclusions This investigation identified dermal absorption of the gasoline additive N-methylaniline from fuel-contaminated seawater as the likely cause of recurrent, life-threatening methemoglobinemia associated with maritime migration. These findings underscore the importance of methylene blue availability and frontline diagnostic capacity in settings where similar exposure conditions may occur. The Central Mediterranean sea route, connecting primarily Libya and Tunisia with southern Italy, is one of the major maritime migration routes to Europe and has been associated with the largest number of reported migrant deaths and disappearances worldwide.1 Migrants commonly spend many hours or even days in overcrowded, unseaworthy vessels, where fuel may leak and contaminate seawater accumulating on the floor of the boat, resulting in prolonged dermal contact. Acute conditions, including hydrocarbon inhalation and fuel burns, have been described in this setting.2-6 However, reports of severe acquired methemoglobinemia, an uncommon but potentially life-threatening condition,7 have been lacking in the context of maritime migration. Beginning in March 2024, clinicians in Lampedusa, Italy, a primary point of arrival along the Central Mediterranean route, identified clusters of migrants presenting at disembarkation with severe methemoglobinemia. The recurrence of these cases suggested a shared exposure in this context. We conducted a coordinated clinical and toxicologic investigation to characterize these cases and identify the underlying cause. Methods Case Identification Cases were first identified in March 2024 during routine clinical evaluation of migrants at disembarkation in the emergency health care facility in Lampedusa, Italy. Elevated methemoglobin levels were incidentally detected on arterial blood gas analysis with CO-oximetry (a multiwavelength test that measures abnormal types of hemoglobin in the blood, including carboxyhemoglobin and methemoglobin), prompting consultation with the Pavia Poison Control Center (PPCC), a national referral center for clinical toxicology. These early cases served as sentinel events, initiating a coordinated investigation through the PPCC. As additional cases were identified, a recurring clinical pattern was recognized, and targeted assessment was progressively incorporated into triage at disembarkation and subsequent evaluation. The cases included in this investigation were identified between March 2024 and December 2025 from toxicologic consultation requests to the PPCC. Requests originated primarily from clinicians at the emergency health care facility in Lampedusa and from referral hospitals in Sicily, with a small number from other points of arrival. Migrants who had an elevated methemoglobin level detected at the initial evaluation after disembarkation were included in the study. Cases were grouped according to the date of disembarkation to assess temporal clustering. Data Collection Clinical data were obtained from PPCC records, including data from Lampedusa, other disembarkation sites, and referral hospitals, with follow-up when available. Variables included demographic characteristics, date of disembarkation, clinical features at presentation, the methemoglobin level at presentation, treatments, complications, and outcomes. Clinical Management Clinical coordination among the PPCC, clinicians in Lampedusa, and referral hospitals was established to support case identification and management. The health care facility in Lampedusa faced considerable logistic and resource constraints, including limited laboratory capacity, lack of access to blood transfusion, and reliance on a single helicopter for transfer to referral hospitals in Sicily. Accordingly, a standardized management protocol that was based on methemoglobin levels, the presence of anemia, and clinical severity was implemented in Lampedusa to guide treatment and prioritize transfers (see the Supplementary Appendix, available with the full text of this article at NEJM.org). Methylene blue (a treatment for methemoglobinemia), which had been initially unavailable in Lampedusa, was subsequently stocked on site. Toxicologic Investigation The PPCC coordinated the obtaining of biologic samples from a subset of patients to identify potential causative agents. Samples were obtained at referral hospitals 6 to 48 hours after disembarkation. Timing and collection depended on logistic feasibility. Analyses included testing for inorganic methemoglobin-inducing agents (nitrite, nitrate, azide, and perchlorate, among others) and organic compounds, including anilines and related metabolites (e.g., N-methylaniline, aniline, N-methyl-p-aminophenol, and p-aminophenol), as well as nitroaromatic derivatives. Quantitative measurements were performed with the use of validated toxicologic methods, with targeted expansion of the analytic panel to include relevant compounds (see the Supplementary Appendix). Environmental investigations included air sampling from the hold of a vessel involved in a disembarkation event, with measurement of volatile organic compounds and combustion products under different engine conditions. A fuel sample from the same vessel was analyzed for anilines, nitroaromatic derivatives, and related compounds (see the Supplementary Appendix). Statistical Analysis Descriptive statistics were used in this study. Continuous variables are presented as medians with interquartile ranges or ranges, as appropriate, and categorical variables as counts and percentages. Results Clinical Findings A total of 82 patients with methemoglobinemia were identified, 74 (90%) of whom were male. The median age of the patients was 22.5 years (interquartile range, 19.5 to 28.0). The characteristics of the patients, including region of origin, are summarized in Table 1. Table 1 | Characteristic | Patients (N=82) | |---|---| | Male sex — no. (%)† | 74 (90) | | Age — yr‡ | | | Median (IQR) | 22.5 (19.5–28.0) | | Range | 15–47 | | Region of origin — no. (%) | | | South Asia | 27 (33) | | Sub-Saharan Africa | 15 (18) | | Middle East | 9 (11) | | North Africa | 8 (10) | | Unknown | 23 (28) | | Clinical presentation at first evaluation — no./total no. (%) | | | Dyspnea | 22/68 (32) | | Altered mental status | 19/68 (28) | | Evidence of fuel exposure — no. (%)§ | 51 (62) | | Methemoglobin level at first measurement¶ | | | Median (IQR) — % | 44.6 (32.0–55.7) | | Range — % | 3.6–68.0 | | ≥25% — no. (%) | 68 (83) | | ≥50% — no./total no. (%) | 34/79 (43) | | Treatment | | | Methylene blue | | | ≥1 Dose — no. (%) | 74 (90) | | Multiple doses — no./total no. (%) | 41/66 (62) | | Ascorbic acid — no. (%)‖ | 34 (41) | | N-acetylcysteine — no. (%)‖ | 39 (48) | | Blood transfusion among patients with hemolytic anemia — no./total no. (%)** | 26/26 (100) | | Laboratory findings — no./total no. (%)†† | | | Hemolytic anemia‡‡ | 38/51 (75) | | G6PD deficiency§§ | 16/44 (36) | | Complications and outcomes†† | | | Splenic rupture — no./total no. (%) | 4/30 (13) | | Death — no. (%) | 2 (2) | * G6PD denotes glucose-6-phosphate dehydrogenase, and IQR interquartile range. † Data on sex were obtained from clinical records. For comparison, according to data from the United Nations High Commissioner for Refugees, sea arrivals to Italy via the Central Mediterranean sea route during the study period comprised approximately 75% adult men, 5% adult women, and 20% children (sex unspecified).8,9 ‡ Data on age were available for 78 patients. § Evidence of fuel exposure included cutaneous burns and a strong gasoline odor. ¶ Methemoglobin values represent the first available measurement. In 3 patients, values that had been reported as being “>30%” (above the upper reportable limit for the blood gas analyzer with CO-oximetry) were not included in the calculation of the median and interquartile range, so those data are based on 79 patients. In 3 other patients, measurements were obtained after the initial treatment. ‖ Adjunctive therapies were reported when documented during consultation with the Pavia Poison Control Center. ** Blood transfusion was administered to all 26 patients with hemolytic anemia for whom transfusion data were available. †† The duration of follow-up varied across patients. Laboratory findings, complications, and outcomes occurring after the available observation period may not have been captured. ‡‡ Anemia was defined according to World Health Organization hemoglobin cutoff values.10 Hemolytic anemia was classified as a clinical diagnosis documented in the medical record and supported by compatible clinical or laboratory findings of hemolysis. §§ G6PD test results may be falsely normal during acute hemolysis and leukocytosis; therefore, nondeficient results should be interpreted with caution. Among the 16 patients with G6PD deficiency, hemolytic anemia was documented in 13, was not documented in 2, and could not be assessed in 1. Among these patients, 14 received methylene blue; hemolytic anemia was documented after the administration of methylene blue in 12 patients, was not documented in 1, and could not be assessed in 1. Eighty patients were initially evaluated in Lampedusa and two patients at other points of arrival. Cases showed temporal clustering, including multiple cases within a single day and periods with increased case counts. The largest cluster occurred over a period of 4 consecutive days (October 19–22, 2025), with 21, 10, 3, and 7 cases reported on each of those days (Figure 1A). Figure 1 The methemoglobin level at presentation ranged from 3.6 to 68.0%, with a median level of 44.6% (interquartile range, 32.0 to 55.7). A total of 68 patients (83%) had a level of 25% or greater, and 34 of 79 patients (43%) with quantitatively reported values had a level of 50% or greater. In 3 patients, levels were reported only as exceeding a threshold of 30%. Among patients with available data, the most common symptoms at presentation were dyspnea and altered mental status. Evidence of fuel exposure, including cutaneous burns, a strong gasoline odor, or both, was documented in 51 of 82 patients (62%) (Figure 1B, Figure 1C, and Figure 1D). A total of 74 of 82 patients (90%) received intravenous methylene blue (at a dose of 1 to 3 mg per kilogram of body weight). Among 66 patients with documented infusion counts, 41 (62%) received multiple doses (maximum, five doses). After implementation of the clinical management protocol, methylene blue became available for on-site administration in Lampedusa. Of the 80 patients treated in Lampedusa, 63 (79%) received the initial dose on-site before transfer. During the largest cluster of cases, in October 2025, additional supplies of methylene blue were mobilized from the Italian National Antidote Stockpile, which has a stock typically reserved for nonconventional emergencies, to ensure timely treatment. During hospitalization, clinical data were variably available, and denominators differed across clinical variables (Table 1). Hemolytic anemia was a common delayed complication, documented in 38 patients and frequently severe enough to lead to blood transfusion. Hemolytic anemia was typically absent at the initial evaluation and became apparent during subsequent clinical follow-up, most commonly 2 to 4 days after disembarkation, although later onset, up to day 7, was also observed. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was identified in 16 of 44 tested patients; among these, 13 had evidence of hemolytic anemia. Splenic rupture occurred in 4 patients, all of whom underwent splenectomy. Hemolytic anemia had been documented before the diagnosis of splenic rupture in all 4 patients. Adjunctive therapies, including ascorbic acid and N-acetylcysteine, were administered in selected cases. Two patients died within 24 hours after disembarkation. Their first documented methemoglobin levels were 64.1% and 40.0%; the patient with the higher level was found in cardiac arrest during rescue operations and died within 12 hours. Toxicologic and Environmental Findings Quantitative toxicologic analyses were performed in 39 patients (48%) across multiple disembarkation events. N-methylaniline or related compounds were detected in available urine or blood samples from 37 of the 39 patients (95%) (Table 2). Among 37 patients with urine samples, 36 (97%) tested positive for N-methylaniline, aniline, or related metabolites. The principal metabolite of N-methylaniline, N-methyl-p-aminophenol, was detected in samples from all 36 of these patients, with a median urinary concentration of 137,328 μg per gram of creatinine (interquartile range, 68,930 to 528,596; maximum observed value, 1,052,534). Among 38 patients with blood samples, 14 (37%) tested positive for N-methylaniline or aniline. The 2 patients who died had among the highest blood concentrations of N-methylaniline (4800 μg per liter and 2540 μg per liter). No alternative methemoglobin-inducing agents were identified (see the Supplementary Appendix). Table 2 | Analyte and Matrix | Detected in Patient | Median Concentration (IQR) or Range† | |---|---|---| | no./total no. (%) | || | N-methylaniline | || | Urine | 26/37 (70) | 5008 (2033–10,500) | | Blood | 14/38 (37) | 504 (285–2025) | | N-methyl-p-aminophenol | || | Urine | 36/37 (97) | 137,328 (68,930–528,596) | | Blood | 1/38 (3) | 9500 | | Aniline | || | Urine | 17/37 (46) | 1475 (370–2339) | | Blood | 3/38 (8) | 740–2979 | | p-Aminophenol | || | Urine | 18/37 (49) | 6699 (3775–10,181) | | Blood | 0/38 | — | * N-methylaniline is primarily metabolized to N-methyl-p-aminophenol, with a minor pathway leading to aniline and subsequently to p-aminophenol.11 Biologic samples were obtained at varying time points after arrival, generally between 6 hours and 48 hours after disembarkation. Of the 39 patients evaluated, 36 had both urine and blood samples available; 1 had a urine sample only, and 2 had blood samples only. † Data are presented as medians with IQRs, as a range (when the number of patients is small), or as an exact value (for one patient), as appropriate. Urinary concentrations are expressed as micrograms per gram of creatinine, and blood concentrations as micrograms per liter. Environmental air sampling in the hold of a vessel that was involved in one disembarkation event identified elevated concentrations of gasoline-related volatile organic compounds under both engine-on and engine-off conditions. Fuel analysis showed an N-methylaniline concentration of 1.1%, with an aniline concentration of less than 0.05% (see the Supplementary Appendix). Discussion This investigation identified N-methylaniline exposure as the likely cause of severe methemoglobinemia in migrants rescued along the Central Mediterranean sea route. The repeated occurrence of severe methemoglobinemia at initial evaluation after disembarkation, with temporal clustering and the involvement of migrants from diverse geographic origins, suggested a shared exposure during maritime transit. No apparent cause of methemoglobinemia emerged from the initial clinical evaluation. Fuel exposure was the only consistent finding; however, gasoline is not known to cause methemoglobinemia, a factor that prompted further investigation. Quantitative toxicologic analyses identified N-methylaniline in biologic samples, with a metabolite profile consistent with its expected biotransformation.11 Experimental studies indicate that N-methylaniline undergoes oxidative metabolism by means of aromatic hydroxylation to N-methyl-p-aminophenol and by means of N-demethylation to aniline, with subsequent transformation to p-aminophenol.11 N-methyl-p-aminophenol, its principal metabolite, was detected in nearly all urine samples — a result supporting a shared exposure. Urinary concentrations of N-methyl-p-aminophenol reached approximately 106 μg per gram of creatinine, far exceeding levels reported in biomonitoring studies of related aromatic amines and their metabolites in both the general population and occupational settings12,13 — a finding indicating substantial exposure to N-methylaniline. Blood measurements confirmed systemic absorption, with N-methylaniline concentrations up to 4800 μg per liter. In a reported case, a methemoglobin level of 35% was associated with a blood aniline concentration of 130 μg per liter14; levels in our study were markedly higher. The distinct analytic patterns that we observed in blood and urine samples probably reflect the expected metabolism and elimination of N-methylaniline, as well as the timing of biologic sampling. Because specimens were obtained 6 to 48 hours after the end of prolonged exposure during maritime transit, decreasing blood concentrations of N-methylaniline together with continued urinary excretion of its metabolites would be expected. Although aromatic amines are established causes of methemoglobinemia,14-16 acute poisoning is now uncommon, and fuel exposure suggested an unexpected source in aniline-based fuel additives. Such compounds have been used to increase the octane rating of gasoline,17 and although restricted because of toxicity concerns, N-methylaniline has been detected in adulterated gasoline.18 Analysis of a fuel sample from a vessel involved in a disembarkation event showed the presence of N-methylaniline, with only trace amounts of aniline, a finding that supported its role as the primary source of exposure. In overcrowded migrant vessels, fuel may leak and accumulate in seawater on the floor of the boat, leading to prolonged dermal contact with fuel-contaminated seawater during maritime transit. Because N-methylaniline is readily absorbed through the skin,16 this exposure scenario is likely to explain the high systemic levels we observed, which are unlikely to occur in other settings. Methemoglobin at presentation indicated severe, potentially life-threatening poisoning, with more than 40% of the patients having levels of 50% or greater and receiving urgent treatment with methylene blue. Outcomes in persons with severe methemoglobinemia are influenced by age, overall clinical condition, and underlying cardiovascular or hematologic disease — factors that increase susceptibility to tissue hypoxia.7 The predominantly young age of the patients in this study may therefore have contributed to survival despite the severity of poisoning. In this emergency context, G6PD status was not available at the time of treatment; although methylene blue may precipitate hemolysis in G6PD deficiency,19,20 its use remains indicated in severe methemoglobinemia. Hemolytic anemia was frequently observed as a delayed complication and was often treated with transfusion; this finding indicates the importance of monitoring beyond the acute phase. The onset of hemolytic anemia, typically 2 to 4 days after presentation, is consistent with previous reports of aromatic amine poisoning.21-23 Aromatic amines are recognized causes of hemolysis even in the absence of G6PD deficiency,23 and reduced antioxidant capacity in G6PD deficiency may increase susceptibility to their hemolytic effects, with methylene blue treatment representing a possible additional contributing factor. However, the available data do not permit the relative contributions of toxic exposure, genetic susceptibility, and antidotal treatment to be distinguished. These observations highlight the potential value of rapid point-of-care G6PD testing in prehospital and maritime reception settings, particularly for clinically stable patients with less-severe methemoglobinemia, in whom alternative treatments such as ascorbic acid may be considered. Migration along the Central Mediterranean route is shaped by conflict, persecution, socioeconomic vulnerability, and unsafe transit through North Africa.1 Reliance on irregular maritime crossings may force travel under hazardous conditions, creating circumstances in which unusual and unexpected toxicologic risks may arise. The reasons for the apparent recent emergence of N-methylaniline–related methemoglobinemia in this setting remain uncertain. Possible explanations include changes in fuel composition or regional fuel-adulteration practices, although data on the occurrence and geographic distribution of such practices are limited. Although fuel-related illness, including chemical burns4 and fatal hydrocarbon intoxication,5,6 has previously been described in migrants crossing the Central Mediterranean sea route, reports of methemoglobinemia had not been apparent in this setting. Recognition of methemoglobinemia in this context is challenging. Cutaneous cyanosis may be less readily appreciated in patients with darker skin pigmentation,24 blood gas analysis with CO-oximetry may be unavailable or difficult to obtain in prehospital or resource-limited settings, and conventional pulse oximetry is unreliable in methemoglobinemia.25 In the absence of systematic toxicologic surveillance in this setting, smaller clusters or isolated cases may therefore have gone unrecognized. This study has limitations. Data collection evolved during the investigation, and the emergency context and coordination across multiple sites limited completeness and follow-up. Case identification was not uniform over time, and increased clinical awareness probably led to more frequent detection as time progressed. Nevertheless, centralized coordination through the PPCC facilitated recognition of recurring clinical and exposure patterns across sites that might otherwise have gone undetected. Toxicologic analyses were performed in a subset of patients, reflecting sample availability and expanding analytic capacity. These findings identify a cause of severe, recurrent methemoglobinemia in migrants along the Central Mediterranean sea route, which was attributable to dermal absorption of N-methylaniline from fuel-contaminated seawater during maritime transit. The resulting severe methemoglobinemia is frequently life-threatening, and prompt recognition and treatment with methylene blue are critical, even in resource-limited reception settings where this antidote may not be routinely available. Ensuring the availability of methylene blue and frontline diagnostic capacity, including pulse CO-oximetry and rapid point-of-care G6PD testing, is essential to improve outcomes in prehospital and maritime rescue settings where similar exposure conditions may occur. Notes Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Supplementary Material References 1. McAuliffe M, Oucho LA, eds. World migration report 2024. Geneva: International Organization for Migration, 2024 (https://mena.iom.int/sites/g/files/tmzbdl686/files/documents/2024-05/pub2023-047-l-world-migration-report-2024_1.pdf). 2. Cañardo G, Gálvez J, Jiménez J, Serre N, Molina I, Bocanegra C. Health status of rescued people by the NGO Open Arms in response to the refugee crisis in the Mediterranean Sea. Confl Health 2020;14:21-21. 3. van Boetzelaer E, Fotso A, Angelova I, et al. Health conditions of migrants, refugees and asylum seekers on search and rescue vessels on the central Mediterranean Sea, 2016-2019: a retrospective analysis. BMJ Open 2022;12(1):e053661-e053661. 4. Milia WR, Gervasi E, Alessandro G, Rizzo M, Pirrello R. Burn injuries among migrants crossing the Mediterranean Sea: a 10-year experience from a single center. J Burn Care Res 2026;47:363-369. 5. Pulin G, Pititto F, Bellacicco R, et al. It’s not always the sea’s fault: hydrocarbon poisoning killed two migrants in the central Mediterranean. Clin Ter 2025;176:266-270. 6. Marrone M, Paladini E, Pititto F, Pulin G, Vinci F, Marzullo A. Histopathological analysis of fuel burns in deceased migrants. J Travel Med 2025;32(1):taae104-taae104. 7. Coleman MD, Coleman NA. Drug-induced methaemoglobinaemia. Treatment issues. Drug Saf 1996;14:394-405. 8. Italy sea arrivals dashboard December 2024. Geneva: United Nations High Commissioner for Refugees, April 11, 2025 (https://data.unhcr.org/en/documents/details/115663). 9. Italy sea arrivals overview 2025. Geneva: United Nations High Commissioner for Refugees, March 9, 2026 (https://data.unhcr.org/en/documents/details/121482). 10. Guideline on haemoglobin cutoffs to define anaemia in individuals and populations. Geneva: World Health Organization, 2024. 11. Scheper T, Appel KE, Schunack W, Somogyi A, Hildebrandt AG. Metabolic denitrosation of N-nitroso-N-methylaniline: detection of amine-metabolites. Chem Biol Interact 1991;77:81-96. 12. Chinthakindi S, Kannan K. Variability in urinary concentrations of primary aromatic amines. Sci Total Environ 2022;831:154768-154768. 13. Rahimpoor R, Murtada K, Firoozichahak A, et al. Urinary bio-monitoring of aromatic amine derivatives by new needle trap device packed with the multi-component adsorbent. Sci Rep 2023;13:4243-4243. 14. Iwersen-Bergmann S, Schmoldt A. Acute intoxication with aniline: detection of acetaminophen as aniline metabolite. Int J Legal Med 2000;113:171-174. 15. Pizon AF, Schwartz AR, Shum LM, et al. Toxicology laboratory analysis and human exposure to p-chloroaniline. Clin Toxicol (Phila) 2009;47:132-136. 16. Lečbychová K, Káňová M, Dzurňáková P, Blahutová Š, Romanová T, Buršík D. Aniline-induced refractory methemoglobinemia in polytrauma: successful management with erythrocytapheresis. Int J Emerg Med 2025;18:232-232. 17. Lin M, Zhang X, Wen M, et al. Effects of unconventional additives in gasoline on the performance of a vehicle. Energies 2022;15:1605-1605. 18. Lima Logrado LP. Identification of N-methylaniline in automotive gasoline by GC-MS, MS/MS, and ATR-FTIR: a report of fuel adulteration. J Forensic Sci 2026;71:1488-1495. 19. Tatarinova O, Lund K, Bain BJ. Beware of methylene blue in possible G6PD deficiency. Am J Hematol 2024;99:2016-2017. 20. Rosen PJ, Johnson C, McGehee WG, Beutler E. Failure of methylene blue treatment in toxic methemoglobinemia. Association with glucose-6-phosphate dehydrogenase deficiency. Ann Intern Med 1971;75:83-86. 21. Taguchi K, Nishii K, Hata S, Kuyama S, Tanaka S. A case of aniline poisoning manifesting as cyanosis with unknown cause. Acta Med Okayama 2025;79:209-212. 22. Kearney TE, Manoguerra AS, Dunford JV Jr. Chemically induced methemoglobinemia from aniline poisoning. West J Med 1984;140:282-286. 23. Harvey JW, Keitt AS. Studies of the efficacy and potential hazards of methylene blue therapy in aniline-induced methaemoglobinaemia. Br J Haematol 1983;54:29-41. 24. Pusey-Reid E, Quinn L, Samost ME, Reidy PA. Skin assessment in patients with dark skin tone. Am J Nurs 2023;123:36-43. 25. Barker SJ, Tremper KK, Hyatt J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1989;70:112-117. Information & Authors Information Published In Copyright Copyright © 2026 Massachusetts Medical Society. 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