From Poppers to Peril: Recreational Nitrite-Induced Methemoglobinemia.

Inhaled amyl nitrites, once used to alleviate chest pain, are more commonly now being used for their euphoric effects. The recreational use of inhaled nitrites can lead to methemoglobinemia, a life-threatening condition that hinders the utilization of oxygen in the body. In 2021, 2.2 million people aged 12 or older used inhalants in the past year. Methemoglobinemia has favorable outcomes with treatment. We present the case of a 43-year-old man, with a medical history of type 2 diabetes mellitus and hypertension presenting with bluish discoloration of the fingers that progressed to his tongue and lips. He disclosed using a recreational inhalant called "Rush" before coming in. Vital signs showed low oxygen saturation on room air, and further investigation revealed elevated methemoglobin levels on the venous blood gas. Methylene blue was used for treatment, with complete resolution of the patient's symptoms and the only side effect of green urine. The patient was later discharged home in a stable condition. History taking is a crucial part of managing methemoglobinemia, as presentation to the clinical setting could vary. Our case presents the milder version of the disease with quick complete recovery after appropriate treatment. It demonstrates inhalant abuse in a less common age group. The case also demonstrates a common side effect of methylene blue that is often forgotten.

Inhalant abuse among street-involved children and adolescents in India: Case for epistemic recognition and reorientation.

Contextualizing the void of research on inhalant abuse among adolescents as epistemic neglect, in this study, we use mixed-methods action research to understand inhalant abuse in a specific context in the Global South. Focusing on a large metropolitan city in Western India, we surveyed 158 street-involved children and adolescents (110 boys and 48 girls, age range from 5 to 17 years) in a group setting along with follow-up group interviews. Despite finding a high prevalence rate of inhalant abuse, our work suggests an absence of supporting structures and emphasizes the need to revisit our understanding and interpretation of substance-using behavior of street-involved youth. Instead of explaining inhalant-abusing behavior as emerging from pathological deficiencies in individuals or households, we stress the need to critically examine the exploitative environment they are embedded in. In doing so, we join efforts to decolonize conventional ways of understanding "deviant" behavior.

Brain and body disconnect: A retrospective case series of subacute combined degeneration of the spinal cord from chronic nitrous oxide use in Perth, Western Australia.

BACKGROUND: Chronic nitrous oxide (N2O) use causes inactivation of vitamin B12, resulting in neurological and psychiatric symptoms. This case series presents all N2O-related presentations to the emergency department at Royal Perth Hospital between June 2019 and June 2021, alongside the costs of these admissions. CASE PRESENTATION: Twenty-two patients were identified; 68% (n = 15) were male. The median age was 22.4 years (interquartile range [IQR], 20-30). Median daily number of N2O bulbs inhaled was 150 (IQR, 64-300) with a median duration of use of 9 months (IQR, 3-12). Presentations included ataxia, paraesthesia and falls (n = 18), urinary retention (n = 3) and psychotic symptoms (n = 2). Fourteen patients had severe symptoms prompting a magnetic resonance imaging of brain and spine, confirming 12 cases of subacute combined degeneration of the spinal cord. All patients had IMI vitamin B12 therapy, while 14 had oral methionine therapy. The median length of admission was 4 days (IQR 1-23 days). The median cost of admission per day for patients where costs were accessible (n = 7) was $2061 (IQR, $1903-$2860). DISCUSSION AND CONCLUSIONS: A case series of symptomatic chronic N2O use with severe neurological sequelae and significant costs associated per admission. Triangulation of emergency department and Ecstasy and Related Drugs Reporting System data helped prompt a swift public health response, including mandatory warning labels, limits to transaction amounts and legislative changes to the Medicines and Poisons Act to make it illegal for sale if there is a suspicion that it will be abused.

A skeleton in a huff: insights in etiologies of osteosclerosis.

A 30-yr-old man developed right lower leg pain and a palpable solid mass. Radiographic imaging revealed a periosteal reaction with an exostotic mass arising from the right distal fibula. Generalized skeletal osteosclerosis with periosteal reaction was discovered on a radiographic skeletal survey. A biopsy of the right fibular mass revealed reactive woven bone. The patient was referred to a metabolic bone disease clinic, where laboratory values were consistent with secondary hyperparathyroidism and increased bone turnover. A DXA bone density scan revealed high bone density, with an L1-4 spine Z-score of +9.3, a left femoral neck Z-score of +8.5, and a total hip Z-score of +6.5. A dental exam revealed generalized gingival inflammation, teeth mobility, generalized horizontal alveolar bone loss and widening of the periodontal ligament space, increased bone density around the teeth, and thickening of the radicular lamina dura. An extensive evaluation was performed, with the result of a single test revealing the diagnosis. The differential diagnoses of osteosclerosis affecting the skeleton, teeth, and oral cavity are discussed.

A 30-yr-old man developed, over a short period, pain in his lower right leg accompanied by a hard mass. He also reported weight loss and night sweats for the past 6 months. After evaluation by his primary physician, an X-ray was ordered that reported a bony mass arising from the right fibula bone. A biopsy was performed of the mass, but no evidence of cancer or any other specific abnormality was found. The patient was then referred to a bone disease specialty clinic. Laboratory tests revealed a large increase in how quickly the patient's skeleton was remodeling, affecting the balance of bone formation and removal involved in maintaining a healthy skeleton. A bone density scan reported that the patient had very dense bones. Other unusual changes were also discovered in a dental exam, suggesting bone thickening. After an extensive evaluation, a single blood test revealed the cause of the fibular bone mass and dense bones.

Analytical methods for detecting butane, propane, and their metabolites in biological samples: Implications for inhalant abuse detection.

Worldwide, various inhalants are widely abused for recreational purposes, with butane and propane emerging as among the most commonly misused volatile substances, posing a significant risk of sudden death. The rapid elimination and oxidation of these highly volatile compounds upon inhalation necessitate the identification of butane and propane along with their metabolites in biological samples. Hence, the primary objective of this study is twofold: firstly, to establish a method for analyzing butane, propane, and metabolites, and secondly, to demonstrate the detection window and exposure indicators associated with the inhalation of butane and propane. In pursuit of this objective, we developed analytical methods for the determination of isobutane, n-butane, propane, and their nine metabolites in both blood and urine. Headspace-gas chromatography-mass spectrometry (GC-MS) and solid-phase microextraction-GC-MS were employed for the analyses, demonstrating acceptable precision and accuracy. An animal study revealed that isobutane and n-butane were only detectable below the limit of quantification (LOQ) in rat blood 5 min after exposure. Meanwhile, the three major metabolites-2-methyl-2-propanol, 2-butanol, and 2-butanone-were observed 5 min after exposure but persisted in rat urine even 5 h post-exposure. Additionally, human urine samples identified other metabolites, including acetone, acetoin, and 2,3-butanediol isomers. The presence of specific metabolites corresponding to each inhalant confirmed the abuse of butane and propane. This comprehensive approach provides valuable insights into the detection and assessment of inhalation to these volatile substances.

The Need for Action: Addressing Inhalant Abuse and Whitener Addiction Among Adolescents.

Inhalant abuse and whitener addiction are serious problems among adolescents that have significant consequences for physical and mental health, as well as for families, communities, and society as a whole. This review article discusses the causes and health consequences of inhalant abuse and whitener addiction among adolescents, as well as the challenges in addressing the problem. The paper also outlines strategies for addressing inhalant abuse and whitener addiction, including education and awareness campaigns; early intervention and treatment; collaboration between schools, healthcare providers, and community organizations; and support for families affected by inhalant abuse and addiction. The paper concludes with a call to action for policymakers, healthcare providers, and community members to prioritize and address inhalant abuse and whitener addiction among adolescents. By working together, we can help to prevent substance abuse and promote the health and well-being of our youth.

Recognizing Ethyl Chloride Neurotoxicity: Inhalant Abuse Hidden in Plain Sight.

Ethyl chloride is a common topical anesthetic. However, when abused as an inhalant, effects can range from headaches and dizziness to debilitating neurotoxicity requiring intubation. While previous case reports describe the short-term reversible neurotoxicity of ethyl chloride, ours show chronic morbidity and mortality outcome. During the initial evaluation, it is essential to consider the rising trend of commercially available inhalants being used as recreational drugs. We present a case of a middle-aged man presenting with subacute neurotoxicity due to repeated abuse of ethyl chloride.

Skeletal Fluorosis in a Patient With Computer Cleaner Inhalant Abuse.

Skeletal fluorosis is a metabolic bone disease caused by excessive consumption of fluoride from fluoride-contaminated water or foods. Such a condition often takes place in developing countries without proper handling of drinking water or food. However, in recent years, multiple cases of skeletal fluorosis have been observed in the United States due to the increasing frequency of recreational substance abuse. In this case report, a 26-year-old male with a history of polysubstance use disorder presented to the emergency department after being assaulted by store employees when attempting to steal computer cleaner inhalants. On evaluation for acute traumatic injury, he was incidentally found to have diffuse sclerosis of all visualized bones on knee, femur, and hip X-rays. Labs were significant for elevated serum alkaline phosphatase levels, secondary hyperparathyroidism, and hypovitaminosis D. Given the patient's history of computer cleaner inhalant misuse and imaging findings, serum and urine fluoride levels were obtained and supported the diagnosis of skeletal fluorosis. Skeletal pain and diffuse sclerosis on imaging should prompt clinicians to include skeletal fluorosis in the differential diagnosis. Cessation of substance use is the primary treatment of fluorosis in the setting of computer cleaner inhalant abuse. However, clinical symptoms and laboratory and imaging abnormalities may take decades to resolve due to the prolonged half-life of fluoride in bone. Proper hydration is crucial, as nephrolithiasis and hypercalciuria have been described during the skeletal unloading of fluoride.

The Clinical Assessment and Treatment of Inhalant Abuse.

Although inhalant abuse is common, it is one of the most neglected and overlooked forms of substance abuse. Inhalants refer to a wide variety of substances including volatile solvents, aerosols, gases, and nitrites. The mechanism of action of inhalants has not been fully defined. Several molecular targets contribute to the pharmacology, including ion-channel proteins that control neuronal excitability. These agents interact with various receptors and can cause changes in cell-membrane fluidity and nerve-membrane ion channels. Three main pharmacologic categories of inhalants, namely, volatile solvents and anesthetic gases, nitrous oxide, and volatile alkyl nitrites, have distinct pharmacologies, mechanisms of action, and toxicities. Inhalants are linked to multisystem damage affecting the pulmonary, cardiac, dermatologic, renal, hematologic, gastrointestinal, hepatic, and neurologic systems. Chronic inhalant abuse can also cause psychiatric, cognitive, behavioral, and anatomical deficits in humans, leading to reduced productivity and quality of life. Inhalant abuse during pregnancy is associated with fetal abnormalities. Clinical assessment for inhalant abuse should be done systematically. After decontamination and stabilization of the patient, further history and physical examination is necessary to establish an appropriate diagnosis based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Laboratory testing for inhalant abuse is very limited, and imaging studies may be helpful in certain situations. The treatment of inhalant use disorder is similar to that of other substance abuse disorders and includes supportive care, pharmacotherapy, and behavioral therapy. Preventive measures are essential.

Skeletal Fluorosis: A Case of Inhalant Abuse Leading to a Diagnosis of Colon Cancer.

Skeletal fluorosis is a long-term bone disease that develops when prolonged fluoride toxicity leads to osteosclerosis and bone deformities that result in crippling pain and debility. The disease is endemic to many countries due to environmental or industrial exposures. However, rare cases in the United States have been reported from various causes including heavy toothpaste ingestion, excessive tea consumption, voriconazole use, and inhalant abuse. Here, we present a case of a 41-year-old man who presented for weight loss and severe joint pains due to bony sclerotic lesions found on X-rays. Social history revealed that he had been recreationally inhaling compressed air dusters used for cleaning electronics. Owing to concern for malignancy, he underwent an extensive work-up which led to a diagnosis of colon cancer, but positron emission tomography/computed tomography (PET/CT) and bone biopsy were unexpectedly negative for metastatic bone disease. Further characterization of his lesions by skeletal survey led to a diagnosis of skeletal fluorosis secondary to inhalant abuse. As in this patient, the disease can be difficult for clinicians to recognize as it can be mistaken for various boney diseases such as metastatic cancer. However, once there is clinical suspicion for skeletal fluorosis, various tests to help confirm the diagnosis can include serum and urine fluoride levels, skeletal survey, and bone ash fluoride concentration. Treatment of skeletal fluorosis primarily involves cessation of fluoride exposure, and recovery can take years. Ultimately, further study is required to develop recommendations and guidelines for diagnosis, management, and prognosis of the disease in the United States.

Acute exposure to abuse-like concentrations of toluene induces inflammation in mouse lungs and brain.

Toluene is an aromatic hydrocarbon commonly abused by young adolescents for its central nervous system depressant effects. Although toluene's pharmacological effects at high concentrations are relatively well-known, few studies have assessed toluene's effects on lung and brain tissues. The present study characterized the pathological effects of acute inhaled toluene exposure in the lungs and brains of male Swiss-Webster mice (N = 68). Using a static vapor exposure chamber, mice (PND 28) received a single 30-min toluene administration (0, 1000, 2000, or 4000 ppm). Lung and brain tissues were extracted 24-h post-exposure. Histology results revealed significant changes in the morphology of lung tissue (e.g., irregular cellular architecture) with the 2000- and 4000-ppm exposures expressing greater signs of pathology than control 0-ppm exposure. Markers of immune system activity (F4/80 and Ly-6G) and cellular proliferation (Ki-67) in the lung revealed no significant differences. Additionally, brain tissues were analyzed for changes of astrogliosis (glial fibrillary acidic protein [GFAP]) and oxidative stress (glutathione peroxidase [GPx]). GFAP showed increased astrogliosis in the striatum with 2000-ppm toluene showing significantly higher expression than control (p < 0.05) and a marginal effect in the hippocampus. No other markers showed significant changes. The increased signs of inflammation and cellular damage suggest that exposure to a single high concentration of toluene, typical of abuse, is capable of producing pathology in both lung and brain tissue.

Just 'nanging' around - harmful nitrous oxide use: a retrospective case series and review of Internet searches, social media posts and the coroner's database.

BACKGROUND: The chronic recreational inhalation of nitrous oxide (N2 O) 'nanging', can have adverse neurological and psychiatric effects. AIM: To evaluate cases of chronic N2 O use presenting to two hospitals, as well as to evaluate nationally N2 O deaths reported to the coroner and trends in Internet searches and social media posts related to N2 O. METHODS: Retrospective review of two toxicology units, from July 2017 to October 2020, of patients presenting with chronic N2 O use and neurological and/or psychiatric symptoms. We evaluated 10 years (2010-2019) of Internet search and social media trends involving N2 O and the National Coronial Information System (NCIS) database for deaths across Australia. RESULTS: Twenty-two patients were identified: median age 22 years, half female, 17 Asian background and 15 students. Presentations included decreased mobility or unsteady gait (n = 15) and psychiatric symptoms (n = 5). The median reported bulb use/day was 300 (interquartile range (IQR): 200-370), for a median of 6 months (IQR: 3-24). On magnetic resonance imaging, 10/18 had subacute combined degeneration of the spinal cord and 7/7 sensorimotor neuropathy on nerve conduction studies. All received high-dose intramuscular vitamin B12 and 11 methionine. Despite prolonged rehabilitation, nine required walking aids on discharge. Since 2017, social media posts and Internet searches for N2 O increased rapidly, the latter mostly directed at obtaining N2 O canisters. From the NCIS, 36 deaths were identified, 12 unintentional (recreational drug use), 20 intentional self-harm and 4 traumatic. CONCLUSION: We report a case series of symptomatic chronic N2 O use, many with ongoing neurological sequelae. Furthermore, a sharp increase in Internet searches to obtain N2 O cannisters was noted. Education of high-risk student groups on the long-term sequelae is important.

Chronic thinner inhalation alters olfactory behaviors in adult mice.

Volatile solvents exposure can result in various behavioral impairments that have been partly associated to altered adult hippocampal neurogenesis. Despite recent evidence supporting this association, few studies have been devoted to examine the impact on olfactory functioning and olfactory bulb (OB) neurogenesis, although olfactory system is directly in contact with volatile molecules. Thus, this study was designed to evaluate in adult mice the potential modifications of the olfactory functioning after acute (1 day), subchronic (6 weeks) and chronic (12 weeks) exposure to thinner vapor at both behavioral and cellular levels. Firstly, behavioral evaluations showed that chronic thinner exposure impacts on odor detection ability of treated mice but does not affect mice ability to efficiently discriminate between two different odors. Moreover, chronic thinner exposure produces impairment in the olfactory-mediated associative memory. Secondly, analysis of the effects of thinner exposure in the subventricular zone (SVZ) of the lateral ventricle and in the OB revealed that thinner treatments do not induce apoptosis nor glial activation. Thirdly, immunohistochemical quantification of different markers of adult olfactory neurogenesis showed that inhalant treatments do not change the number of proliferating progenitors in the SVZ and the rostral migratory stream (RMS), as well as the number of newborn cells reaching and integrating in the OB circuitry. Altogether, our data highlight that the impaired olfactory performances in chronically-exposed mice are not associated to an alteration of adult neurogenesis in the SVZ-OB system.

[A case of subacute combined degeneration of spinal cord caused by inhaling laughing gas].

Laughing gas (Nitrogen monoxide) is currently abused due to its low price and easy availability. This article discussed the clinical manifestations of a patient with subacute combined degeneration of the spinal cord caused by inhalation of laughing gas. The patient developed numbness of extremities, unstable walking, and decreased serum vitamin B(12) level. MRI of the cervical spine showed abnormal signals in the lateral and posterior cords of the cervical spinal cord (C2-6) , neuroelectrophysiological examination showed peripheral nerve damage in the extremities. After treatment with vitamin B(12) supplementation, the patient's condition gradually improved. Clinicians diagnose subacute combined degeneration of the spinal cord, especially when the patient has no gastrointestinal disease, diet, malnutrition, etc., they need to carefully inquire about the history of nitrous oxide inhalation to avoid missed diagnosis.

Acute Inhalant-Induced Atrial Fibrillation With Severe Hypocalcemia: A Case Report and Review of the Pathophysiology.

The recreational use of inhalants is associated with various detrimental health effects ranging from inebriation to cardiac arrest. It also presents a challenging clinical problem as the diagnosis is made by the presentation and patient's history, which is often difficult to obtain in an intoxicated or obtunded individual. The incidence of inhalant use is relatively high. National surveys have reported that nearly 21.7 million Americans aged 12 and older have used inhaled substances at least once in their lives. There is no reversal agent or antidote for inhalants and supportive care is generally recommended. We present a case of a young patient presenting with acute inhalant toxicity accompanied by atrial fibrillation with a rapid ventricular response and severe hypocalcemia.

Analysis of some commonly found inhalants using gas chromatography-mass spectrometry (GC MS) - Effect of substrates on the identification of inhalants.

Inhalant abuse is a serious and ever-evolving problem for our society. Inhalants are abused more commonly by teenagers and adolescents. Inhalants such as glue, paint thinners, correction fluid, and nail paint remover are easily available in the market which makes them readily abused. Out of various methods of abuse, huffing (placing a piece of cloth soaked with inhalant is placed in the mouth), bagging (placing head in a polythene bag containing inhalant), and ballooning (balloons filled with inhalant are used for inhaling vapors through the mouth) are most common. Inhalant abuse results in multiple target organ dysfunction with neuritis and brain damage due to the dissolution of the myelin sheath. In acute poisoning cases, it might cause death due to asphyxia and sudden sniffing syndrome. In such cases, various articles containing traces of inhalants could be retrieved from the scene of incidence and to detect these traces become an important facet of the investigation. However, it might be difficult due to the rapid evaporation of inhalants and the formation of reaction product species. In the present study, an attempt has been made to study the effect of three substrates (balloon, cloth, polythene) on component profiles of four paint thinners and four nail paint removers. The study suggests that although some components are retained, there is the formation of a large number of reaction product species and these must be taken into consideration before furnishing the opinion. These reaction product species might also be inhalant specific which must be further explored.

Inhaled Solvent Abuse Mimicking Chronic Inflammatory Demyelinating Polyradiculoneuropathy.

Exposure to n-hexane or toluene-containing solvents such as glue or gasoline can produce clinical symptoms and neurophysiological findings that can mimic chronic inflammatory demyelinating polyneuropathy. The authors present a case of a boy with severe sensorimotor polyneuropathy with demyelinating features. Cerebrospinal fluid testing and magnetic resonance imaging spine did not show findings typical of chronic inflammatory demyelinating polyneuropathy. His lack of response to immunosuppressive therapy prompted a nerve biopsy which was instrumental in confirming a diagnosis of chronic organic solvent exposure, subsequently confirmed on history. This case highlights the importance of additional testing to ensure diagnostic certainty which allows appropriate treatment and/or disease management to be tailored appropriately including in this instance, the involvement of mental health counseling and avoidance of immunosuppressant medication.

Skeletal Fluorosis: An Unusual Manifestation of Computer Cleaner Inhalant Abuse.

Skeletal fluorosis is a metabolic bone disease caused by accumulation of fluoride and is generally associated with chronic exposure to fluoride-contaminated groundwater, a phenomenon endemic to developing countries. Whereas elevated water fluoride concentrations do not constitute a public health issue in the United States, emergence of skeletal fluorosis as a sequela of chronic recreational exposures has been described. In this case report, our 33-year-old male patient with a history of major depressive disorder and substance abuse was hospitalized for hyperkalemia and acute kidney injury discovered on routine bloodwork due to concomitant nonsteroidal anti-inflammatory drugs (NSAID) and antihypertensive use. Upon hospital admission, he was found to be anemic with a significantly elevated alkaline phosphatase. Given a history of low back pain in the setting of these laboratory abnormalities, lower spine and pelvic imaging revealed diffusely increased bone density and sclerosis. Hematologic evaluation ensued to include a peripheral smear and bone marrow biopsy. Given the patient's history of computer cleaner inhalant abuse, serum and urinary fluoride levels were obtained. Serum fluoride returned within normal limits though urinary fluoride was increased. Bone marrow histopathology revealed prominent diffuse sclerosis which in conjunction with urinary fluoride levels and computer cleaner inhalant abuse history supported the diagnosis of skeletal fluorosis. Skeletal fluorosis in the United States is rare and presents with non-specific findings requiring a high index of suspicion based on a detailed patient history for expedient diagnosis.

Air Duster Inhalant Abuse Causing Non-ST Elevation Myocardial Infarction.

Inhalant abuse, also known as huffing, is common among teenagers and adolescents in the United States and worldwide. Inhaled aerosols are dangerous due to both the presence of volatile hydrocarbons causing direct organ damage and the risk of the compressed air causing physical trauma (e.g. expansion, barotrauma) or skin trauma from chemical or temperature burn. Here, we present the case of a 35-year-old man who was inhaling multiple canisters of Dust-Off (Falcon Safety Products Inc., Branchburg, NJ) keyboard air duster daily for approximately one month. He presented with intermittent burning chest pains, and was found to have elevated troponin (peak 17 ng/mL, normal range 0-0.5 ng/mL) without ST-segment elevations, concerning for non-ST elevation myocardial infarction (NSTEMI) as well as elevated aminotransferases and elevated serum creatinine. He was treated conservatively with supportive measures, with successful resolution of his laboratory abnormalities as well as his chest pain. Clinicians should be aware of the possible medical complications of inhalant abuse, and the expected clinical course. In this case, we aim to demonstrate the acute onset and self-resolution of significant cardiomyocyte damage in a young male patient abusing duster.

Outcomes After Recurrent Intentional Methanol Exposures Not Treated With Alcohol Dehydrogenase Inhibitors Or Hemodialysis.

BACKGROUND: Relying on a treatment threshold for methanol poisoning of 20 mg/dL (6.2 mmol/L) as a stand-alone criterion may lead to unnecessary and invasive treatment because it is likely too conservative, especially for patients with repeated, intentional methanol exposures. OBJECTIVE: We investigated how often patients with recurrent intentional methanol exposures above this threshold developed biochemical or overt clinical toxicity despite not being treated with either an alcohol dehydrogenase inhibitor (ADHi) or hemodialysis. METHODS: We identified patients with ≥3 methanol-related emergency visits from 2002 to 2015 and selected every visit in which neither ADHi nor hemodialysis were administered despite serum methanol >20 mg/dL but neither metabolic acidosis nor end organ toxicity at presentation. The primary outcome was the incidence of visual deterioration or death. RESULTS: Four patients accounted for the 17 visits that met inclusion criteria. All exposures were intentional substance misuse, and 7 of 17 were via inhalation (i.e., huffing). Initial methanol concentrations ranged from 22 mg/dL to 35 mg/dL (7-11 mmol/L). Four of these 17 visits had undetectable initial ethanol concentrations at presentation, including 1 with an initial methanol concentration of 35 mg/dL. No patients developed visual deterioration, and all were known to have survived the exposure. CONCLUSION: Following recurrent, intentional methanol exposure, isolated serum methanol concentrations as high as 35 mg/dL (11 mmol/L) appear to be well-tolerated without treatment in the absence of metabolic acidosis or end-organ toxicity. To better define the methanol treatment threshold, prospective studies are warranted in which patients are followed closely while fomepizole is withheld.