Dibromomethane

CAS RN:74-95-3

Health Effects

0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) DESCRIPTION: Metal fume fever is an illness produced by the inhalation of metal oxide fumes. These oxides are produced by heating various metals such as cadmium, zinc, magnesium, copper, antimony, nickel, cobalt, manganese, tin, lead, beryllium, silver, chromium, aluminum, selenium, iron, and arsenic. However, the most common metals implicated are zinc and copper. It is an occupational disease among individuals who weld, heat or cut galvanized metals. NOTE: This document deals only with metal fume fever. Please see documents for individual metals and/or metal compounds when necessary to obtain information regarding other toxic effects.
    • B) TOXICOLOGY: The exact mechanism of meal fume fever is not known but it is thought to be secondary to a cytokine-mediated immune response. The inhalation of the metal oxide fumes injuring the cell lining of airways is thought to be the precipitating event that leads to a systemic reaction.
    • C) EPIDEMIOLOGY: Metal fume fever most often occurs among welders with several hundred cases reported to the United States poison centers every year and thousands of cases that likely occur annually in the US.
    • D) WITH POISONING/EXPOSURE
      • 1) Symptoms of metal fume fever are generally described as a flu-like illness. Complaints include fever, chills, nausea, vomiting, abdominal pain, respiratory difficulties, fatigue, joint pain, and muscle aches. Classically, the onset of metal fume fever symptoms is rapid, occurring within 3 to 10 hours of exposure. Initial symptoms may include a metallic taste associated with throat irritation, dyspnea, and a feeling of thirst. This is then followed by a low-grade fever, chills, myalgias, arthralgias, malaise, fatigue, and a nonproductive cough. These may be accompanied by excessive sweating, shaking chills, nausea, vomiting, and headaches. Symptoms are self-limiting and usually resolve within a day or two (but may take longer). There can be subsequent temporary tolerance to the metal oxide fumes that may go away after 1 to 2 days after last exposure.
0.2.3 VITAL SIGNS
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0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: Dichloromethane (methylene chloride) is used as a solvent in the chemical industry. In household products, it is used as paint remover, aerosol propellant, urethane foam, and degreaser.
    • B) TOXICOLOGY: Similar to other halogenated solvents, an acute high concentration exposure can cause CNS depression and respiratory depression. Dichloromethane is a tissue irritant, and a high concentration inhalation may cause mucous membrane irritation, pulmonary edema, and hemorrhage. It is metabolized to carbon monoxide (CO) and large exposures can lead to elevated carboxyhemoglobin concentrations. When heated to decomposition, dichloromethane releases toxic phosgene, hydrogen chloride gas, and chlorine gas.
    • C) EPIDEMIOLOGY: Poisoning is rare and most often occurs by the inhalational route. Rarely, intentional ingestions have been reported. Systemic poisoning after dermal exposure is unusual since dichloromethane evaporates quickly.
    • D) WITH POISONING/EXPOSURE
      • 1) MILD TO MODERATE TOXICITY: Drowsiness, somnolence, skin and mucous membrane irritation, abdominal pain if ingested, and nausea and vomiting.
      • 2) SEVERE TOXICITY: Severe effects include significant CNS depression, corrosive injury of the gastrointestinal tract, and pancreatitis. Hepatotoxicity, renal injury leading to renal failure may be seen, but are not common. Elevated carboxyhemoglobin levels may develop in significant poisoning. Severe inhalational injury is associated with pulmonary edema and hemorrhage. Hypotension and hypertension have been reported after a large, deliberate ingestion. Cardiac dysrhythmias and cardiac depression have been linked to chronic exposure with dichloromethane. Delirium and seizures may be seen.
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Exposure to fumes causes eye irritation. Direct contact or immersion may cause burns to the cornea or oral mucosa.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Methylene chloride may cause occupational heart disease. Inhalation of methylene chloride may exacerbate angina in persons with preexisting cardiac disease.
      • 2) Angina, myocardial infarction, and cardiac arrest associated with methylene chloride inhalation developed in one patient. Hypotension, hypertension, and tachycardia have been reported after ingestion of methylene chloride.
0.2.6 RESPIRATORY
  • 0.2.6.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Pulmonary irritation and cough may develop after inhalation exposure. Pulmonary edema is rarely reported. Respiratory failure may develop secondary to CNS depression in severe exposures. Goodpasture's syndrome has been associated with one case of occupational exposure.
0.2.7 NEUROLOGIC
  • 0.2.7.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Headache and light-headedness are common after inhalation. Psychomotor performance is impaired with acute exposure. Syncope, CNS depression and coma may develop with more severe exposure. CNS excitation including seizures may also occur.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Nausea and vomiting are common after inhalation exposure. Gastrointestinal ulceration and bleeding and pancreatitis have been reported after ingestion.
0.2.9 HEPATIC
  • 0.2.9.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Elevated liver enzyme levels rarely occur.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Renal effects are rare. Hematuria, acute tubular necrosis and the development of Goodpasture's syndrome have been associated with exposure to methylene chloride.
0.2.13 HEMATOLOGIC
  • 0.2.13.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Methylene chloride is metabolized to carbon monoxide. Carboxyhemoglobin as high as 50% are reported, and levels may continue to rise for several hours after exposure has ceased. The apparent half-life of carboxyhemoglobin is prolonged to 13 hours because of ongoing production of carboxyhemoglobin.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Skin irritation, pain, numbness and mild burns may develop with acute exposure. Severe burns may develop with prolonged exposure or immersion. Systemic effects can result from absorption through the skin.
0.2.18 PSYCHIATRIC
  • 0.2.18.1 ACUTE EXPOSURE
    • A) Delirium with auditory and visual hallucinations is rare but has been reported after chronic exposure.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Methylene chloride was not found to be teratogenic in mice and rabbits. It crosses the placenta, and is found in breast milk, and has been associated with increased spontaneous abortion. However, few reproductive effects are seen in rats.
0.2.21 CARCINOGENICITY
  • 0.2.21.1 IARC CATEGORY
    • A) IARC Carcinogenicity Ratings for CAS75-09-2 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
      • 1) IARC Classification
        • a) Listed as: Dichloromethane (methylene chloride)
        • b) Carcinogen Rating: 2A
      • 1) The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
  • 0.2.21.2 HUMAN OVERVIEW
    • A) Methylene chloride has been classified as probably carcinogenic to humans (Group
    • 2A) by IARC following a systematic review and evaluation.
  • 0.2.21.3 ANIMAL OVERVIEW
    • A) Methylene chloride is considered to be a confirmed animal carcinogen; divergent results have been obtained in rodent studies.
0.2.22 GENOTOXICITY
  • A) Results concerning the genotoxicity of methylene chloride have been conflicting in vivo and in vitro. It is generally mutagenic and can cause DNA breaks and chromosomal aberrations.
The information contained in the Truven Health Analytics Inc. products is intended as an educational aid only. All treatments or procedures are intended to serve as an information resource for physicians or other competent healthcare professionals performing the consultation or evaluation of patients and must be interpreted in view of all attendant circumstances, indications and contraindications. The use of the Truven Health Analytics Inc. products is at your sole risk. These products are provided "as is" and "as available" for use, without warranties of any kind, either express or implied. Truven Health Analytics Inc. makes no representation or warranty as to the accuracy, reliability, timeliness, usefulness or completeness of any of the information contained in the productsAdditionally, Truven Health ANALYTICS INC. makes no representation or warranties as to the opinions or other service or data you may access, download or use as a result of use of the Truven Health ANALYTICS INC. products. All implied warranties of merchantability and fitness for a particular purpose or use are hereby excluded. Truven Health Analytics Inc. does not assume any responsibility or risk for your use of the Truven Health Analytics Inc. products.
0.2.1 SUMMARY OF EXPOSURE
  • 0.2.1.1 ACUTE EXPOSURE
    • A) USES: In the past, bromides were widely used both as a sedative and an antiepileptic agent in the United States, and they are still used as sedatives in some areas of the world. It is still found as a bromide salt in many medications. The major source of bromide exposure in humans in the United States is the presence of bromide residues in food. Bromine-containing fumigants are extensively used in horticulture and in post-harvest treatments, but the amounts are too minimal to cause toxicity. Contaminated well water may be a source of bromide exposure.
    • B) PHARMACOLOGY: Bromide ion causes secondary anion potentiation of gamma-aminobutyric acid (GABA) channels in the CNS. GABA receptors are complexed with chloride channels. Available bromide ions, due to their smaller hydrated diameter, diffuse more readily through cellular channels, producing a hyperpolarized post-synaptic membrane, which potentiates the action of GABA, an inhibitory neurotransmitter.
    • C) TOXICOLOGY: With chronic exposure, the bromide ion displaces chloride from plasma, extracellular fluid, and, to some extent, from cells. The kidneys increase the elimination of chloride ions in an attempt to maintain a constant total halide concentration. Central nervous system function is progressively impaired, presumably through a membrane-stabilizing effect. A toxic concentration can be reached very rapidly when the intake of chloride is reduced.
    • D) EPIDEMIOLOGY: Bromide poisoning is rare and, when it does occur, is generally secondary to chronic ingestion rather than acute overdose.
    • E) WITH POISONING/EXPOSURE
      • 1) ACUTE: Bromide poisoning following acute ingestion is rare. Acute effects may include nausea, vomiting, gastric irritation, CNS depression, coma, hypotension, tachycardia, and respiratory distress.
      • 2) CHRONIC: Ingestion of chronic, excessive amounts may produce a toxic syndrome called "bromism", which is characterized by behavioral changes, hallucinations, psychosis, ataxia, irritability, headache, and confusion. Other symptoms of chronic bromide toxicity include: anorexia, weight loss, constipation, slurred speech, anemia, bromoderma (an erythematous, nodular, or acneiform rash over the face and possibly the entire body), bullous or pustular eruptions on the skin, toxic epidermal necrolysis, musculoskeletal pain, lethargy, and liver enzyme abnormalities. Fever may be seen in up to 25% of cases of chronic ingestion. Chronic intoxication usually develops over 2 to 4 weeks or longer.
0.2.3 VITAL SIGNS
  • 0.2.3.1 ACUTE EXPOSURE
    • A) Fever may occur with chronic intoxication.
0.2.4 HEENT
  • 0.2.4.1 ACUTE EXPOSURE
    • A) Pupils may be normal, miotic or mydriatic. Nystagmus is common.
0.2.5 CARDIOVASCULAR
  • 0.2.5.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Tachycardia and hypotension have occurred with acute intoxication.
0.2.7 NEUROLOGIC
  • 0.2.7.1 ACUTE EXPOSURE
    • A) Acute intoxication can result in CNS depression and coma.
    • B) Chronic effects may include behavioral changes, irritability, confusion, muscular weakness, anorexia, ataxia, lethargy, abnormal reflexes, and slurred speech.
0.2.8 GASTROINTESTINAL
  • 0.2.8.1 ACUTE EXPOSURE
    • A) Nausea and vomiting occur following acute or chronic ingestion. Anorexia and weight loss may occur with chronic intoxication.
0.2.10 GENITOURINARY
  • 0.2.10.1 ACUTE EXPOSURE
    • A) Acute renal failure is rare. Incontinence may develop with chronic intoxication.
0.2.12 FLUID-ELECTROLYTE
  • 0.2.12.1 ACUTE EXPOSURE
    • A) Spuriously elevated chloride level and low anion gap are characteristic of bromism, due to laboratory interference by the bromide ion.
0.2.14 DERMATOLOGIC
  • 0.2.14.1 ACUTE EXPOSURE
    • A) WITH POISONING/EXPOSURE
      • 1) Bromide toxicity is associated in about 25% of cases with the development of bromoderma, an erythematous, nodular or acneiform rash over the face and possibly the entire body. One case of toxic epidermal necrolysis has been reported.
0.2.18 PSYCHIATRIC
  • 0.2.18.1 ACUTE EXPOSURE
    • A) Chronic bromism has been associated with toxic psychosis resembling paranoid schizophrenia, personality changes, and mania with paranoid delusions.
0.2.20 REPRODUCTIVE HAZARDS
  • A) Bromides cross the placenta and may be detected in the milk of nursing mothers. Case reports suggest that prenatal exposure may cause growth retardation, craniofacial abnormalities and developmental delay.
The information contained in the Truven Health Analytics Inc. products is intended as an educational aid only. All treatments or procedures are intended to serve as an information resource for physicians or other competent healthcare professionals performing the consultation or evaluation of patients and must be interpreted in view of all attendant circumstances, indications and contraindications. The use of the Truven Health Analytics Inc. products is at your sole risk. These products are provided "as is" and "as available" for use, without warranties of any kind, either express or implied. Truven Health Analytics Inc. makes no representation or warranty as to the accuracy, reliability, timeliness, usefulness or completeness of any of the information contained in the productsAdditionally, Truven Health ANALYTICS INC. makes no representation or warranties as to the opinions or other service or data you may access, download or use as a result of use of the Truven Health ANALYTICS INC. products. All implied warranties of merchantability and fitness for a particular purpose or use are hereby excluded. Truven Health Analytics Inc. does not assume any responsibility or risk for your use of the Truven Health Analytics Inc. products.
Find more information on this substance at: Hazardous Substances Data Bank , TOXMAP , TOXNET , PubMed