Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 24: Methylene Chloride Toxicity
Case Study 24: Methylene Chloride Toxicity
Pages 493-511
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From page 493... ...
23 Metabolic conversion of methylene chloride to carbon monoxide may place persons with pre-existing coronary artery disease at increased Ask. 1~ EPA considers methylene chloride to be a probable human carcinogen.
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A complete blood count, chemistry panel, arterial blood gases, and urinalysis are within normal limits. Upon conferring with the emergency physician, you administer sublingual nitroglycerin during electrocardiographic monitoring.
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Exposures to the highest concentrations of methylene chloride are generally occupational; more than a million workers have significant potential for exposure. Nonoccupational exposures may occur through ambient air or groundwater contaminated by facilities that manufacture, use, store, or dispose of methylene chloride, or from consumer products that contain methylene chloride as a solvent, flame retardant additive, orpropellant.
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From page 496... ...
From here it may be ingested in drinking water or inhaled as it volatilizes from the water during activities such as showering and laundering. O Workers and residents near Industrial facilities that produce, use, store, or dispose of methylene chloride have an Increased risk of exposure.
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It is not known if the developing human fetus is at increased risk from the direct effects of unmetabolized methylene chloride. Indirect effects from increased levels of maternal carbon monoxide produced by the metabolism of methylene chloride, however, may have adverse consequences on fetal development.
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The metabolic formation of carbon monoxide and its subsequent binding to hemoglobin, producing carboxyhemoglobin (CO-Hb) , may continue for several hours after cessation of methylene chloride exposure, as fat and other tissues continue to release accumulated amounts of the lipophilic solvent.
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The CNS effects are generally reversible and are thought to be due to methylene chloride abne or in combination with metabolically released carbon monoxide, but not to carbon monoxide alone. Other effects of acute exposure include irritation of the eyes and upper respiratory tract, cardiac effects (myocardial ischemia, dysrhythmia)
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O Persons with coronary artery disease or angina may not ba able to tolerate the added cardiovascular stress brought on by carbon monoxide that Is metabol. Ically released from methylene chloride.
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Like many other organic solvents, methylene chloride can reach the human fetus through the placenta and can enter human breast milk. Maternal carbon monoxide levels may have an effect on the developing fetus.
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The medical history should emphasize the following: family history, particularly coronary artery disease occupational history hobbies or household projects, particularly furniture refinishing, spray painting, paint stripping location of residence and workplace in relation to induslnal facilities source of drinking water supply Signs and Symptoms Acute Exposure Methylene chloride exposures at levels below the odorthreshold for up to 8 hours have produced no adverse health effects in humans. At levels of exposure at or above the odorthreshold, reported effects include the following: euphoria sluggishness light- he adedne ss irritability sleepiness dizziness At exposure levels above 500 ppm, the following may also be present: headache impairment of concentration and coordination loss of balance irritation of eyes, nose, and throat nausea flushing confusion slurred speech ischemic heart pain respiratory distress or failure to maintain the airway during CNS depression pulmonary edema (rare)
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Chronic Exposure Early signs and symptoms of chronic methylene chloride exposure are not well documented, but are likely to reflect CNS depression. The following have been reported by workers with repeated exposure: headache, dizziness, nausea, memory loss, paresthesias in hands and feet, mental and physical fatigue, and loss of consciousness.
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The methylene chloride concentration in exhaled air will generally reflect the amount inhaled at ambient levels up to about 500 ppm. The concentration of carbon monoxide in alveolar air also has been found to correlate with methylene chloride levels in ambient air up to 200 ppm.
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Exposure to about 500 ppm for several hours results in CO-Mb levels as high as 15%. Since many factors can contribute to elevated CO-Mb levels, including exercise, smoking, and exogenous exposure to carbon monoxide, the CO-Mb level may not correspond directly to inhaled levels of methylene chloride.
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It would also be prudent to advise patients with coronary artery disease or angina to avoid all exposure to such products. Chronic Exposure There are no known antidotes to methylene chloride and no methods for enhancing the direct elimination of methylene chloride from the body.
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In 1976, the National Institute for Occupational Safety and Health (NIOSH) recommended a threshold limit value (TLV)
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FOCUS Level Comments ACGIH Air-Workplace 50 ppm NIOSH Air-Workplace N/A OSHA Air-Workplace 500 ppm EPA Air-Environment N/A FDA Cosmetics O Food 10 ppm Advisory; TWA t; to avoid carcinogenic risk Advisory; lowest feasible level Regulation; PEL§ as TWA t Under review; proposal scheduled for June, 1990 Regulation; ban became effective in 1989 Regulation; residual in decaffeinated coffee * ACGIH = American Conference of GovernmentaJ Industrial Hygienists; EPA = Environmental Protection Agency; FDA = Food and Drug Administration; NIOSH = National Institute for Occupational Safety and Health; 0SHA = Occupational Safety and Health Administration t TWA (Time-Weighted Average)
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Atkins EH, Baker EL. Exacerbation of coronary artery disease by occupational carbon monoxide exposure: a report of two fatalities and a review of the literature.
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Cerebral damage due to endogenous chronic carbon monoxide poisoning caused by exposure to methylene chloride. J Soc Occup Med 1979;29:12~.
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From page 511... ...
Continued production of CO-Mb during gradual release of methylene chloride from adipose tissue may lead to prolonged tissue hypoxia, resulting in cardiac ischemia, particularly when coronary artery disease is already present. The other constituents of the paint stripper, mineral spirits and methanol, are also anesthetic agents, but in these concentrations have likely contributed only slightly to your patient's mental confusion.
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