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At least 19 recordsLinked to original sources
PubMed1992

Occupational dimethylformamide exposure. 1. Diffusive sampling of dimethylformamide vapor for determination of time-weighted average concentration in air.

A diffusive sampling method with water as absorbent was examined in comparison with 3 conventional methods of diffusive sampling with carbon cloth as absorbent, pumping through National Institute of Occupational Safety and Health (NIOSH) charcoal tubes, and pumping through NIOSH silica gel tubes to measure time-weighted average concentration of dimethylformamide (DMF). DMF vapors of constant concentrations at 3-110 ppm were generated by bubbling air at constant velocities through liquid DMF followed by dilution with fresh air. Both types of diffusive samplers could either absorb or adsorb DMF in proportion to time (0.25-8 h) and concentration (3-58 ppm), except that the DMF adsorbed was below the measurable amount when carbon cloth samplers were exposed at 3 ppm for less than 1 h. When both diffusive samplers were loaded with DMF and kept in fresh air, the DMF in water samplers stayed unchanged for at least for 12 h. The DMF in carbon cloth samplers showed a decay with a half-time of 14.3 h. When the carbon cloth was taken out immediately after termination of DMF exposure, wrapped in aluminum foil, and kept refrigerated, however, there was no measurable decrease in DMF for at least 3 weeks. When the air was drawn at 0.2 l/min, a breakthrough of the silica gel tube took place at about 4,000 ppm.min (as the lower 95% confidence limit), whereas charcoal tubes could tolerate even heavier exposures, suggesting that both tubes are fit to measure the 8-h time-weighted average of DMF at 10 ppm.

Air Pollutants, Occupational↗
PubMed1992

Occupational dimethylformamide exposure. 2. Monomethylformamide excretion in urine after occupational dimethylformamide exposure.

The relationship between the 8-h time-weighted average (TWA) intensity of exposure to N,N-dimethylformamide (DMF) vapor (with little possibility of skin contact with liquid DMF) and the subsequent excretion of N-monomethylformamide (MMF) precursor in shift-end urine samples was examined in 116 workers exposed to DMF and 92 workers exposed to DMF in combination with toluene. Urinary MMF level was examined also in 42 non-exposed subjects. The TWA vapor concentration in breathing zone air of each worker was successfully measured by means of a recently developed diffusive sampler in which water was used as an absorbent. The examination of gas chromatographic (GC) conditions for MMF determination showed that the formation of MMF was not saturated when the injection port temperature was set at 200 degrees C, reached a plateau at 250 degrees C, and showed no additional increase at 300 degrees C. There was a linear relationship between DMF in air and MMF in urine with a regression equation of y = 1.65 x + 1.69 (r = 0.723, P less than 0.01), where y is MMF (unit; mg/l, uncorrected for urine density) in urine and x is DMF (ppm) in air, when only those exposed to DMF were selected, and the injection port temperature was set at 250 degrees C. From this equation, it was possible to estimate that about 10% of the DMF absorbed will be excreted into urine as the MMF precursor. The slope of the regression line was significantly smaller among those exposed to DMF and toluene in combination as compared with those with DMF exposure only.

Adult↗
PubMed1992

Occupational dimethylformamide exposure. 3. Health effects of dimethylformamide after occupational exposure at low concentrations.

A factory survey was conducted in a plant where N,N-dimethylformamide (DMF) was in use during the production of polyurethane plastics and related materials. In all, 318 DMF-exposed workers (195 men and 123 women) and 143 non-exposed controls (67 men and 76 women) were examined for time-weighted average exposure (to DMF and other solvents by diffusive sampling), hematology, serum biochemistry, subjective symptoms, and clinical signs. Most of the exposed workers were exposed only to DMF, whereas others were exposed to a combination of DMF and toluene. DMF exposure in the former group was up to 7.0 ppm (geometric mean on a workshop basis), whereas it was up to 2.1 ppm in combination with 4.2 ppm toluene. Both hematology and serum biochemistry, results (including aspartate and alanine aminotransferases, gamma-glutamyl transpeptidase and amylase) were essentially comparable among the 3 groups. There was, however, a dose-dependent increase in subjective symptoms, especially during work, and in digestive system-related symptoms such as nausea and abdominal pain in the past 3-month period. The prevalence rate of alcohol intolerance complaints among male (assumedly) social drinkers was also elevated in relation to DMF dose.

Adolescent↗
PubMed1990

Alteration of lacto-series glycolipid glycosyltransferase activities in human colonic adenocarcinoma DLD-1 cells after culture in N,N-dimethylformamide-containing medium.

Human colonic adenocarcinoma DLD-1 cells were grown under conditions which induce characteristics of differentiated cells using medium containing 0.8% N,N-dimethylformamide in order to study alterations in glycosphingolipid glycosyltransferase activities during this process. Analysis of biosynthetic reactions involved in lacto-series antigen synthesis revealed no changes in the specific activities of either beta 1----4galactosyltransferase or alpha 1----3/4fucosyltransferase with N,N-dimethylformamide treatment. However, a dramatic decrease of from 14- to 20-fold in the beta 1----3N-acetylglucosaminyltransferase activity was observed in the treated cells. This enzyme catalyzes the rate-limiting step in lacto-series core chain synthesis. This is consistent with the pattern of regulation of lacto-series antigen expression found to occur during oncogenesis in human colonic mucosa (Holmes EH, Hakomori S, Ostrander GK: J Biol Chem 262:15649, 1987). Total glycolipids from untreated and N,N-dimethylformamide-treated cells were isolated and subjected to TLC immunostain analysis and solid phase radioimmunoassay with a series of monoclonal antibodies specific for lacto-series-based carbohydrate antigens. A decrease of about 2-fold or less in the quantity of lacto-series antigens was observed as a consequence of N,N-dimethylformamide treatment in both neutral glycolipid and ganglioside fractions. The results suggest that only very low levels of beta 1----3N-acetylglucosaminyltransferase activity are required for the steady state expression of significant levels of lacto-series based glycolipids and that modulation of its activity levels by N,N-dimethylformamide treatment in DLD-1 cells represents a convenient in vitro system for studying aspects of regulation of lacto-series antigen expression.

Adenocarcinoma↗
PubMed1990

Triple combination of retinoic acid plus actinomycin D plus dimethylformamide induces differentiation of human acute myeloid leukaemic blasts in primary culture.

Differentiation induction therapy provides an alternative for treatment of acute myeloid leukaemia (AML) patients who are either unsuitable for or unresponsive to conventional cytotoxic chemotherapy. The effect of a triple combination of retinoic acid (RA) + actinomycin D (Act-D) + dimethylformamide (DMF) on differentiation of blasts from 24 AML patients was studied. Non-adherent mononuclear cells were seeded at a concentration of 5 x 10(5) cells/ml in 24-well tissue-culture plates containing RPMI 1640 culture medium with 20% fetal calf serum, 10% autologous serum and 10% 5637-conditioned medium and incubated with 10(-6) M retinoic acid, 5 nM actinomycin D and/or 100 mM dimethylformamide alone and in combination with each other for 6 days at 37 degrees C in a humidified incubator and an atmosphere containing 5% CO2. The triple combination of 10(-6) M retinoic acid + 5 nM actinomycin D + 100 mM dimethylformamide induced 90% of the blasts from 22 of the 24 AML patients to differentiate. The combination of N-methylformamide (a compound similar to dimethylformamide) with cyclophosphamide significantly increased the in vivo activity with no concomitant increase in its reversible hepatotoxicity. Since several polar compounds related to dimethyl-formamide, e.g. hexamethylene bisacetamide and N-methylformamide, are currently undergoing phase II clinical trials, it may be feasible to combine one of these with retinoic acid and/or actinomycin D in the treatment of AML patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Identification by proton NMR of N-(hydroxymethyl)-N-methylformamide as the major urinary metabolite of N,N-dimethylformamide in mice.

Urine samples from mice which had received N,N-dimethylformamide were investigated by high field 1H-NMR spectroscopy. The most prominent signals in the N-CH3 region had chemical shifts identical with those of N,N-dimethylformamide (delta 2.85, 3.01) and N-(hydroxymethyl)-N-methylformamide (delta 2.91, 3.05). Resonances downfield of delta 7.5 (from formyl protons) also coincided with those of the reference formamides. When [14C]methyl-labelled N,N-dimethylformamide was injected and urine samples investigated by radio thin layer chromatography, the major area of radioactivity corresponded to the Rf of N-(hydroxymethyl)-N-methylformamide. Dimethylamine and methylamine were found to be minor metabolites of N,N-dimethylformamide.

Animals↗
PubMed1985

Mercapturates in the urine of persons exposed to N,N-dimethylformamide.

N,N-dimethylformamide, a nucleophilic aprotic dipolar solvent, has multipurpose uses, especially in the manufacture of plastics. Its acute toxicity for mammals is low; it is hepatotoxic. Vapors are absorbed by the lungs, in the liquid form it causes cutaneous maceration and is rapidly absorbed through the skin. In the organism it is primarily metabolized to N-monomethylformamide, to a lesser extent to formamide. Urine of individuals exposed to N,N-dimethylformamide was newly found to have higher levels of thioethers, most likely mercapturates, as yet of unknown chemical structure. The correlation between the urinary concentrations of mercapturates (y) and N-monomethylformamide (x) can be expressed by equation y = 4.93 + 0.58 x, with the coefficient of correlation r = 0.90. Part of N,N-dimethylformamide metabolites is likely to react with biopolymers, part of it is excreted as metabolic end products, i.e. carbon dioxide, water and urea. Breakdown to mercapturates may implicate N,N-dimethylformamide as being a potential carcinogen.

Acetylcysteine↗
PubMed1988

The effects of dimethylformamide on the interaction of the estrogen receptor with estradiol.

The study of the mechanism of interaction of antiestrogens with the estrogen receptor is complicated by the limited solubility of these compounds and their nonspecific, hydrophobic interactions with proteins in estrogen receptor preparations and with the glass or plastic wall of the test tube. The organic solvent dimethylformamide increases the solubility of these compounds in aqueous solution and interferes with hydrophobic interactions with solid phases and thereby reduces their loss from the solution. For these reasons some investigators use dimethylformamide in the antiestrogen-estrogen receptor binding assay. In this study we report that dimethylformamide interferes with the estrogen receptor's binding kinetics and the estradiol-induced activation of the estrogen receptors, and inactivates the receptor.

Allosteric Regulation↗
PubMed1984

Reversal by L-cysteine of the growth inhibitory and glutathione-depleting effects of N-methylformamide and N,N-dimethylformamide.

N-Methylformamide and N,N-dimethylformamide, which can induce differentiation in selected malignant cell lines, are known to increase doubling times, inhibit clonigenicity in agar, and to effect responses against particular human colon carcinomas in vivo. At concentrations which inhibit growth and clonigenicity, N-methylformamide (170 mM) and N,N-dimethylformamide (103 mM) deplete total intracellular glutathione levels of DLD-1 Clone A human colon carcinoma cells in a dose and time dependent manner. In the presence of 0.5 mM 1-cysteine, both the growth and glutathione levels of polar-solvent treated DLD-1 Clone A cells are restored. 1-Cysteine also reverses the inhibition of clonigenicity mediated by NMF. The mechanism of action of N-methylformamide and N,N-dimethylformamide against this cell line, at least in vitro, is therefore related to its effects on cysteine/glutathione metabolism. Furthermore, this evidence suggests that glutathione plays a key role in regulating the growth of these cells.

Antineoplastic Agents↗
PubMed1992

Induction of myogenic differentiation in human rhabdomyosarcoma cells by ionising radiation, N,N-dimethylformamide and their combination.

Differentiation-inducing ability of gamma-radiation, N,N-dimethylformamide and their combination has been tested on human rhabdomyosarcoma RMZ-RC2 clone cells. Ionising radiation at 2-5 Gy doses induced a more differentiated morphology, with the appearance of an increased proportion of multinuclear myotube-like cells, and a significant increase in myosin-positive and multinuclear cells. Radiation appeared to act by inducing de novo differentiated elements. N,N-dimethylformamide was able to induce an increased myosin expression, but did not affect multinuclear cell proportion. The combined treatment (ionising radiation and N,N-dimethylformamide) resulted in an additive increase in the proportion of myosin-positive cells, approaching 25-35%, but de novo differentiated elements were not increased above the levels obtained with irradiation alone.

Cell Differentiation↗
PubMed1976

Molecular weight of an extremely hydrophobic protein, zein, in dimethylformamide and in formamide.

Both alpha zein purified from a commericial preparation and beta zein prepared fresh from corn are soluble in the nonaqueous solvents formamide and dimethylformamide; in this regard zein resembles water soluble proteins such as insulin, ribonuclease, and lysozyme. On the basis of osmotic pressure measurements made in both formamide and dimethylformamide, alpha zein has a number average moleular weight of 21000-24000 daltons and shows no tendency to aggregate or dissociate. Beta zein exists in an aggregated state (dimer and higher forms) in dimethylformamide. Formamide dissociates the beta zein dimer into monomer units but aggregation to higher species occurs with increasing protein concentration.

Binding Sites↗
PubMed1985

Elevated growth factor levels in transformed mouse embryo cells treated with N,N-dimethylformamide.

The transformed mouse embryo fibroblast cell line AKR-MCA, produces several transforming growth factor (TGF) activities which can be identified in cell extracts and serum-free conditioned medium. Treatment of these transformed cells with 1% N,N-dimethylformamide resulted in a more normal phenotype and an increased level of TGFs in cell extracts and conditioned medium. In addition, an 11-fold increase in an epidermal growth factor receptor-competing activity was observed in cell extracts and conditioned medium compared to control untreated cells. Fractionation of the conditioned medium on Bio-Gel P-100 showed that the same size classes of TGFs were present in N,N-dimethylformamide-treated as well as untreated cells. The increased EGF-receptor-competing activity was eluted in two peaks at Mr 6500 and Mr 4000. The Mr 6500 peak did not coelute with a TGF peak in the N,N-dimethylformamide-treated cells.

Animals↗
PubMed1979

N,N-dimethylformamide-induced alteration of cell culture characteristics and loss of tumorigenicity in cultured human colon carcinoma cells.

Human colon carcinoma cell lines established in this laboratory were treated in vitro with N,N-dimethylformamide. This polar solvent caused morphological changes in the cells as well as alterations in their growth properties. Untreated cells had cloning efficiencies of up to 77% in soft agar; treatment with N,N-dimethylformamide resulted in a complete loss of clonogenicity in semisolid medium. Growth in the presence of the polar solvent also effected a marked reduction in the tumorigenicity of the cells. Ten of ten nude mice that received a s.c. inoculum of 1 X 10(6) untreated cells developed tumors histologically similar to colonic adenocarcinomas in 10 to 14 days, whereas nine of ten nude mice inoculated with 1 X 10(6) treated cells have shown no sign of tumor 3 to 6 months postinjection. Removal of the polar solvent from the culture medium was accompanied by the reappearance of tumorigenicity and the original cell culture characteristics. Therefore, it appears that N,N-dimethylformamide can reversibly effect the reversion of cultured human colon carcinoma cells to less malignant cell types.

Animals↗
PubMedDate not supplied

Monitoring of industrial exposure to dimethylformamide by analysis of alveolar air.

The occupational exposure to Dimethylformamide was studied by testing the environmental and alveolar air of 8 workers, at hourly intervals, during the workshift. The correlations between alveolar and environmental concentrations of Dimethylformamide turned out to be statistically significant at all the intervals studied, except at the 4th hour when the correlation was not significant. In six out of the eight workers studied, the correlation between alveolar and environmental concentrations was statistically significant. Only in two workers was the correlation not significant. On the basis of the slope of the regression line between all the data, the alveolar concentration of Dimethylformamide turned out to correspond to 27,8% of the environmental concentration.

Air Pollutants, Occupational↗
PubMed1976

Affinity chromatography of 3 alpha-hydroxysteroid dehydrogenase from Pseudomonas testosteroni. Use of N,N-dimethylformamide to prevent hydrophobic interactions between the enzyme and the ligand.

1. The 3alpha-hydroxysteroid: NAD+-oxidoreductase (EC 1.1.1.50) from Pseudomonas testosteroni (ATCC 11996) has been purified by affinity chromatography on Sepharose 4B using glycocholic acid as ligand covalently bound through its carboxyl group to the ethylenediamine spacer. 2. The attachment of the enzyme to the substrate-containing matrix is greatly enhanced by the presence of NAD+ suggesting that this enzyme has a compulsory ordered mechanism where NAD+ binds to the enzyme before the steroid. 3. A NAD+-independent interaction between the enzyme and the ligand was also found. This interaction was mainly hydrophobic and interfered with the NAD+-dependent binding. The NAD+-independent interaction was reduced by N,N-dimethylformamide. 4. By using the affinity column in the presence of 10% N,N-dimethylformamide, highly purified enzyme, as judged from polyacrylamide gel electrophoresis, could be obtained in one step from crude bacterial extracts.

Chromatography, Affinity↗
PubMed1990

Clinical and pathological characteristics of hepatotoxicity associated with occupational exposure to dimethylformamide.

The clinical characteristics, laboratory results, and liver biopsy findings of seven workers with toxic liver injury associated with exposure to several solvents, including substantial levels of the widely used solvent dimethylformamide, are presented. Three patients had short exposure (less than 3 months), four long exposure (greater than 1 year). Among those with brief exposure, symptoms included anorexia, abdominal pain, and disulfiram-type reaction. Aminotransferases were markedly elevated with the ratio of alanine aminotransferase to aspartate aminotransferase always greater than 1. Liver biopsy showed focal hepatocellular necrosis and microvesicular steatosis with prominence of smooth endoplasmic reticulum, complex lysosomes, and pleomorphic mitochondria with crystalline inclusions. Among workers with long exposure, symptoms were minimal and enzyme elevations modest. Biopsies showed macrovesicular steatosis, pleomorphic mitochondria without crystalloids, and prominent smooth endoplasmic reticulum, but no evidence of persisting acute injury or fibrosis. Abnormal aminotransferases in both groups may persist for months after removal from exposure, but progression to cirrhosis in continually exposed workers was not observed. We conclude that exposure of these workers to solvents, chiefly dimethylformamide, may result in two variants of toxic liver injury with subtle clinical, laboratory, and morphological features. This may be readily overlooked if occupational history and biopsy histology are not carefully evaluated.

Adult↗
PubMed1990

Liver injury in workers exposed to dimethylformamide.

An apparent epidemic cluster of toxic liver disease was reexamined among workers exposed to the solvent dimethylformamide. A demographically similar but unexposed group from a preemployment population was used for comparison. Analysis, after data transformation of the liver transaminases, revealed significant differences between the two populations with respect to the serum glutamic pyruvic transaminase and the ratio of serum glutaminic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio of serum glutamic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio less than 1 may be suggestive of toxic liver disease. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver disease. Dimethylformamide was almost certainly the causative agent of the original epidemic. The use of preemployment populations as a source of unexposed subjects in the analysis of occupational clusters is recommended, especially in the scenario of relatively acute, and highly prevalent, occupational diseases.

Adult↗
PubMed1988

Liver disease associated with occupational exposure to the solvent dimethylformamide.

STUDY OBJECTIVE: to characterize an outbreak of liver disease among workers in a fabric coating factory; and to determine the outbreak's cause and natural history and strategies for clinical recognition, treatment, and prevention. DESIGN: clinical-epidemiological investigation. SETTING: academic medical center, Occupational Medicine Clinic, and worksite. PATIENTS: fifty-eight of sixty-six workers participated in the study. All had standard liver function tests at least once. Forty-six workers completed a questionnaire; 27 had more extensive clinical evaluation for recognized liver abnormalities. RESULTS: a plant-wide outbreak of liver disease was recognized after a new employee presented with signs and symptoms of hepatitis. Evaluation of the worksite showed that dimethylformamide, a widely used industrial solvent and known hepatotoxin, was being used to coat fabric in poorly ventilated areas without appropriate skin protection. No other major hepatotoxic exposure was identified. Overall, 36 of 58 (62%) workers tested had elevations of either aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels. Enzyme abnormalities occurred almost exclusively in production workers (35 of 46 were abnormal), whereas only 1 of 12 nonproduction workers showed any elevations in enzyme levels (P less than 0.0001). Serologic tests excluded known infectious causes of hepatitis in all but 2 workers and changes characteristic of toxic liver injury were confirmed by histologic examinations of biopsy specimens from 4 workers. The ratio of AST to ALT levels was one or less in all but 1 worker. After modification of work practices and removal of workers most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms in most patients were seen, although some patients showed persistent elevations of enzyme levels. CONCLUSIONS: an outbreak of toxic liver disease has been associated with exposure to dimethylformamide in the workplace. The diagnosis of toxic liver disease was established by the clinical histories, negative viral serologies, an enzyme pattern of ALT levels being greater than AST levels, epidemiologic data on coworkers, and liver biopsy specimens. The high prevalence of unsuspected liver enzyme abnormalities in these workers suggests that occupational liver disease may occur more frequently than is generally recognized.

Adolescent↗