SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Acute intoxication by methylene chloride has primarily been reported from occupational settings. However, it may occur through domestic exposure, by the use of aerosol sprays, degreasers and paint removers. We describe an unusual case of an accidental domestic methylene chloride intoxication through the use of aerosol spray, resulting in an HbCO of 30%.
Various groups including the Occupational Safety and Health Administration, Environmental Protection Agency, and Consumer Product Safety Commission have expressed concern over methylene chloride and its possible effects on human health. A group of employees exposed to relatively high levels of methylene chloride (average = 475 ppm 8-hour time-weighted average) for greater than 10 years were compared to a similar nonexposed group of employees for selected health parameters. All were participants in an employee health monitoring program. Selected questions evaluating cardiac and neurologic health effects revealed no differences between the two groups. Likewise, hematologic assessment also revealed no clinically significant differences between the two groups for SGOT(AST), SGPT(ALT), total bilirubin, and hematocrit. Therefore, it appears that chronic exposure to even high levels of methylene chloride produces no difference in symptoms or adverse health effects in this population as judged by selected liver, cardiac, and neurologic health parameters.
Nephrotoxic reaction occurred after inhalation exposure to methylene chloride. This exposure is associated with acute renal failure, myoglobinuria, hypocomplementemia, and liver enzyme elevations. Pathologic specimens, both light and electron microscopic, demonstrate renal tubular damage. We conclude that methylene chloride may have potential as both a hepatotoxic and nephrotoxic agent when inhaled at high concentrations over an extended period of time.
The fat content of the body was calculated in 12 healthy male subjects aged 21 to 35 years by means of hydrostatic weighing and anthropometric estimation of skeletal weight. The subjects were exposed to a concentration of 2,600 mg of methylene chloride per cubic meter of inspired air (750 ppm) for 1 h while performing work at an intensity of 50 W on a bicycle ergometer. The uptake in the organism was measured continuously with the Douglas bag technique. The amount of methylene chloride absorbed correlated highly with degree of obesity and body weight. Needle biopsy specimens of subcutaneous adipose tissue were taken from the buttocks before exposure and 0, 1, 2, 3 and 4 h after exposure. The mean yield of tissue from the 72 biopsies was 25 mg. The concentration of methylene chloride in the adipose tissue was determined by gas chromatography, using a headspace method. The mean concentration was 10.2 mg/kg 1 h after exposure and 8.4 mg/kg after 4 h. There was a wide distribution around the mean values. In the six slim subjects the concentration in the adipose tissue during the 4 h after exposure was on an average twice that of the six more obese subjects. On the other hand, in spite of lower concentrations, the obese subjects had a greater calculated amount of methylene chloride in the total fat depots of the body. Two subjects were studied about 22 h after exposure, the concentration in subcutaneous adipose tissue being 1.6 and 1.7 mg/kg, respectively, at that time.
The pharmacokinetics of the solvent methylene chloride have been studied using a physiologically based model that was developed for iv administrations to mice. Subsequently, the model was expanded to simulate pharmacokinetic behavior in mice and rats following single and repeated oral exposures. Through computer simulations, how different dosing variables, such as dose vehicle and exposure route, could influence the time course of methylene chloride concentrations at potentially critical sites of toxicity was examined. With this technique, methods of quantifying tissue exposure as it relates to externally applied doses was sought. In this way pharmacokinetic models help investigators design experiments that lead to more appropriate and reliable toxicologic assessment studies.
A long-term study was conducted to determine the possible chronic toxicity and oncogenicity of methylene chloride. Rats and hamsters were exposed by inhalation to 0, 500, 1500, or 3500 ppm of methylene chloride for 6 hr per day, 5 days a week, for 2 years. No exposure-related cytogenetic effects were present in male or female rats exposed to 500, 1500, or 3500 ppm. Females rats exposed to 3500 ppm had an increased mortality rate while female hamsters exposed to 1500 or 3500 ppm had decreased mortality rates. Carboxyhemoglobin values were elevated in rats and hamsters exposed to 500, 1500, or 3500 ppm with the percentage increase in hamsters greater than in rats. Minimal histopathologic effects were present in the livers of rats exposed to 500, 1500, or 3500 ppm. Decreased amyloidosis was observed in the liver and other organs in hamsters exposed to 500, 1500 or 3500 ppm. While the number of female rats with a benign tumor was not increased, the total number of benign mammary tumors was increased in female rats in an exposure-related manner. This effect was also evident in male rats in the 1500- and 3500-ppm exposure groups. Finally, male rats exposed to 1500 or 3500 ppm had an increased number of sarcomas in the ventral neck region located in or around the salivary glands. Therefore, in this 2-year study, some effects were observed in male and female rats exposed to 500, 1500, or 3500 ppm of methylene chloride. In contrast, hamsters exposed to the same exposure concentrations had less extensive spontaneous geriatric changes, decreased mortality (females), and lacked evidence of definite target organ toxicity.
BACKGROUND: Source reduction, defined as chemical, equipment and process changes that intervene in an industrial process to eliminate or reduce hazards, has not figured as a front-line strategy for the protection of workers' health. Such initiatives are popular for environmental protection, but their feasibility and effectiveness as an industrial hygiene approach have not been well described. METHODS: We investigated four cases of source reduction as a hazard prevention strategy in Massachusetts companies that had used methylene chloride, an occupational carcinogen, for cleaning and adhesive thinning. Three cases were retrospective and one was prospective, where the researchers assisted with the source reduction process change. Data were collected using qualitative research methods, including in-depth interviews and site visits. RESULTS: Motivated by environmental restrictions, a new worker health standard, and opportunity for productivity improvements, three companies eliminated their use of methylene chloride by utilizing available technologies and drop-in substitutes. Aided by technical assistance from the investigators, a fourth case dramatically reduced its use of methylene chloride via process and chemistry changes. While the companies' evaluations of potential work environment impacts of substitutes were not extensive, and in two cases new potential hazards were introduced, the overall impact of the source reduction strategy was deemed beneficial, both from a worker health and a production standpoint. CONCLUSION: The findings from these four cases suggest that source reduction should be considered potentially feasible and effective for reducing or eliminating the potential hazards of methylene chloride exposure. Especially when faced with a hazard that is both an environmental and worker health concern, companies may chose to change their processes rather than rely on local exhaust ventilation equipment or personal protective equipment that might not be as effective, might transfer risk and/or not be integrated with financial goals. However, technical assistance sensitive to environmental and health and safety impacts as well as production issues should be provided to guide companies' source reduction efforts.
STATEMENT OF PROBLEM: A durable repairing system for denture base fracture is desired to avoid recurrent fracture. Purpose. This study evaluated the strength and modulus of elasticity of repaired acrylic specimens reinforced with various processes. MATERIAL AND METHODS: Transverse strength and modulus of elasticity of repaired acrylic denture base specimens were evaluated with a 3-point bending test and compared with a heat-polymerized control. Autopolymerizing acrylic resin was used with woven metal fiber and glass fiber with and without methylene chloride surface treatment (n = 6 per group). The specimens were cut in half and fixed in a metal mold to obtain a space for placing the repairing resin. A cavity was prepared when metal or glass fiber was used. All specimens were stored in 37 degrees C distilled water for 48 hours before the test. All data were statistically analyzed with 1-way ANOVA, and differences among groups were analyzed with Fisher test (P< or =.05). RESULTS: The mean value of the transverse strength for the control was 87.2 MPa. The specimens repaired by glass fiber with methylene chloride surface treatment exhibited the highest transverse strength (96.8 MPa), which was significantly higher than that of the control (P< or =.05). The elastic modulus of the specimens repaired by glass fiber with methylene chloride surface treatment (4189.3 MPa) was significantly greater than that of the control (2683.7 MPa) at a 95% level of confidence. The values of transverse strength and elastic modulus were highest when the surface treatment was combined with a reinforcing glass fiber. CONCLUSION: Reinforcement with glass fiber and methylene chloride pretreatment produced transverse strength and a modulus of elasticity higher than the control.
Explore the source record for details and available documents.
A 29-year-old man working in a closed room was exposed to methylene chloride. 2 days later he developed acute renal failure and hepato-cellular damage. Despite the fact that methylene chloride is usually considered nontoxic, fatal cases have been described. It should be stressed that a good history, especially in those who work with materials of low toxicity, can explain complex clinical pictures, allowing proper treatment to be started. Our patient was treated by hemodialysis and recovered completely without residual hepatic damage.
A GC assay was developed that quantitates methanol and methylene chloride at the lowest detectable levels for this mode of analysis. A statistical limit of detection was determined for both methanol and methylene chloride. This method is sensitive and reliable for detecting possible residues of these solvents on film-coated tablets.
A large male employee population with continuous low level work exposures to methylene chloride for up to 30 years was examined for mortality experience using non-concurrent prospective and proportionate mortality techniques. Mortality of the study group was consistent with industrial controls and less than the New York State general population. Life table analysis of the 1964 methylene chloride exposed cohort was followed through 1976 and demonstrated age group specific probabilities or 13 year survivorship equal to or better than that of three control male populations: Kodak Park, New York State, and United States.
Four cases of serious methylene chloride (dichloromethane) poisoning, including fatalities, in small-scale furniture-stripping shops were reported to the Rocky Mountain Poison and Drug Center between 1984 and 1988. Adequate ventilation systems and use of recommended respirators may seem impractical or overly expensive to the operators of such shops. Twenty-one shops in the metropolitan Denver, Colorado area were surveyed. A half-facepiece respirator with organic vapor cartridges was worn at least part-time in 14 of 21 shops; none was worn in 7. In 10 of 21 shops, workers had experienced dizziness, headache, or nausea when stripping furniture. Current safety practices in small-scale furniture-stripping shops may be inadequate to keep methylene chloride exposure levels in compliance with latest recommendations, and serious or fatal overexposure can occur.
Methylene chloride (MC) has been evaluated for its ability to induce micronucleated polychromatic erythrocytes (MPEs) in the bone marrow of treated mice. Groups of five male and five female C57BL/6J/Alpk mice were exposed, by gavage, to doses of 4000, 2500 and 1250 mg/kg MC in corn oil, the highest dose-level being selected to be the maximum tolerated dose. Bone marrow samples were taken 24, 36, 48 and 72 h after dosing. No significant increases in the incidence of MPEs over controls were observed for any of the test groups, and it is concluded that MC is not clastogenic in this assay.
An excess of self-reported neurological symptoms was found when a group of 46 men exposed to methylene chloride at concentrations below 100 ppm was compared with a non-exposed referent group. A follow-up study was then carried out to see whether there was any evidence of neuropsychological damage in the exposed men. Twenty-nine of the original group participated in this study. Age-matched controls controls were selected from among men working on a similar process but with no exposure to solvents. Each man in the study had a clinical examination; motor conduction velocities were measured in the ulnar and median nerves; an ECG was taken and a psychological test battery was designed to detect minimal brain damage was administered. No evidence was found of long-term damage that could be attributed to exposure to methylene chloride.
Spray-paint inhalation, once a common and inexpensive source of drug abuse, is now rare. Newer organic solvents, such as methylene chloride, were thought to decrease the toxicity of aerosol solvents, but they carry unique toxicities of their own. Methylene chloride toxicity is difficult to diagnose, as early symptoms are similar to those associated with many intoxicants; however, a rising carboxyhemoglobin level, despite removal of the patient from the source of exposure, is pathognomonic. In dealing with industrial exposures or organic aerosol abuse, a carboxyhemoglobin level should be part of the initial diagnostic workup, and treatment with oxygen is mandatory until toxicity resolves.
To assess the potential chronic health effects of methylene chloride, the mortality experience of a maturing 1964 to 1970 cohort of 1,013 hourly men was evaluated through 1984. On average, employees were exposed at a rate of 26 ppm (eight-hour time-weighted average) for 22 years; median latency was 30 years. Compared with the general population, no statistically significant excesses were observed for such hypothesized causes as lung cancer (14 observed v 21.0 expected), liver cancer (0 v 0.8), and ischemic heart disease (69 v 98.1); dose-response relationships based on career methylene chloride exposure and latency were not demonstrated. Among nonhypothesized causes, a significant deficit was reported for total deaths (176 v 253.2). None of the industrial referent comparisons achieved statistical significance. Sufficient power was available to detect relative risks of 1.6 for lung malignancy and 1.3 for ischemic heart disease. In contrast, there was inadequate power to identify meaningful risk levels for hepatic cancer. With 14 combined lung and liver cancer deaths observed v 36.3 predicted (P less than .0001), the mortality estimate projected from a mathematical model derived from an animal bioassay substantially overestimated cancer mortality for these sites. This inconsistency emphasizes the need to incorporate epidemiologic evidence in assessing the human health risks associated with long-term exposure to this widely used solvent.
Mortality findings in a 1964 to 1970 cohort of 1013 hourly-wage men exposed to methylene chloride were substantially unchanged after 4 additional years of observation through 1988. Mean exposure was 26 ppm (8-hour time-weighted average) for 23 years; median follow-up from first exposure was 33 years. A comparison with death rates in both general population and industrial referents showed nonsignificant deficits in observed-expected ratios for such hypothesized causes as lung and liver cancer and ischemic heart disease. Overall mortality from 1964 to 1988 (n = 238) was significantly decreased v both referent groups. The study had 90% power to detect relative risks of 1.7 and 1.3 for lung cancer and ischemic heart disease, respectively; power was inadequate for hepatic cancer. No pancreatic cancer deaths occurred since the 1984 follow-up; eight have been observed v 4.2 expected (P = .13). An analysis of dose response for selected causes of death demonstrated no statistically significant trend according to either career methylene chloride exposure or latency. Similar results were observed when the data were analyzed using Poisson regression modeling.