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PubMed2006

Adsorptive stripping voltammetric determination of netilmicin in the presence of formaldehyde.

A linear sweep adsorptive stripping voltammetric method for the determination of netilmicin in the presence of formaldehyde has been proposed for the first time. In the presence of 3.0 x 10(-3) g ml(-1) formaldehyde, netilmicin exhibits a sensitive cathodic peak at -1.30 V (vs. the saturated calomel electrode, SCE) in a medium of Britton-Robinson buffer (pH 8.7) with a scan rate of 100 mV s(-1) after a preconcentration period of 120 s at -1.10 V (vs. SCE). The peak current showed a linear dependence on the netilmicin concentration over the range 4.2 x 10(-9)-1.0 x 10(-7) g ml(-1). The achieved limits of detection and quantitation were 1.0 x 10(-10) and 3.3 x 10(-10) g ml(-1) netilmicin, respectively. It was deduced from the experiments that the amine-aldehyde condensation product formed between netilmicin and formaldehyde is mainly responsible for the appearance of the peak. The electrochemical behavior of netilmicin in the presence of formaldehyde has been studied. The method was applied to the direct determination of netilmicin in injectable formulations and spiked human urine and serum samples.

Adsorption↗
PubMed2004

Biofiltration of waste gases containing a mixture of formaldehyde and methanol.

Several biofilters and biotrickling filters were used for the treatment of a mixture of formaldehyde and methanol; and their efficiencies were compared. Results obtained with three different inert filter bed materials (lava rock, perlite, activated carbon) suggested that the packing material had only little influence on the performance. The best results were obtained in a biotrickling filter packed with lava rock and fed a nutrient solution that was renewed weekly. A maximum formaldehyde elimination capacity of 180 g m(-3) h(-1) was reached, while the methanol elimination capacity rose occasionally to more than 600 g m(-3) h(-1). Formaldehyde degradation was affected by the inlet methanol concentration. Several combinations of load vs empty bed residence time (EBRTs of 71.9, 46.5, 30.0, 20.7 s) were studied, reaching a formaldehyde elimination capacity of 112 g m(-3) h(-1) with about 80% removal efficiency at the lowest EBRT (20.7 s).

Air Pollutants↗
PubMed1996

Application of formaldehyde for treatment of hemorrhagic radiation-induced proctitis.

Radiation-induced proctitis with hemorrhage is not a common complication of radiotherapy to the pelvis for carcinoma. In the most severe forms, massive hemorrhage may necessitate repeated transfusions and inpatient treatment. In severe cases medical treatment has not been proved effective. Surgery may lead to serious complications and is technically difficult. Six patients who showed a hemorrhagic radiation-induced proctitis have been treated as outpatients with application of formaldehyde 4%. In four cases the bleeding ceased after the first formaldehyde application; two patients continued to bleed, but another application of formaldehyde 3 weeks later definitively controlled the hemorrhage. Follow-up evaluation at 12 months showed in each case that the hemorrhage was controlled and treated. There were no complications, such as burns or late stenoses of the deep layers of the rectum. This inexpensive technique is well tolerated by the patient, gives good long-term results, and is available at every hospital. Local application of formaldehyde 4% to the rectum may be the treatment of choice for hemorrhagic radiation-induced proctitis.

Administration, Topical↗
PubMed1996

[An example for stepwise reduction of work site-induced formaldehyde exposure in pathology].

Occupational formaldehyde exposure in pathology depends on the efficiency of the ventilation system in use and may reach concentrations considerably above the current threshold limit values. The reduction of formaldehyde exposure by stepwise improvement of the ventilation system at a pathologist's workplace is presented as an example in this paper. Assessment of formaldehyde concentration by personal air sampling at a workplace originally equipped with a hood ventilation system resulted in values of up to 4 ml/m3 in the pathologist's breathing zone. Lowering the ventilation inlet to the working level by connecting the hood to a suction unit via a flexible hose resulted in an effective reduction of formaldehyde exposure to values of about 0.5 ml/m3. This simple and low-cost technical improvement had some uncomfortable side effects, such as current noise and wind chill, which could only be overcome by installing ventilated work tables according to modern technical standards.

Air Pollutants, Occupational↗
PubMed1999

Assessment of total exposure to phenol-formaldehyde resin glue in plywood manufacturing.

OBJECTIVE: Respiratory and dermal exposure to phenol-formaldehyde resin-glue components used in plywood manufacturing were assessed. METHODS: Formaldehyde and phenol were monitored in the workplace air. Formaldehyde was measured both in the breathing zones of the workers and at stationary sampling sites. Phenol was used as a marker agent for dermal exposure due to its near-nonvolatility at the temperatures occurring during the present study and to its ready absorption through the skin, causing systemic exposure in addition to local skin rashes. Sampling and analytical methods were developed to measure the dermal exposure to phenol. Sampling was accomplished with whole-body dosimetry using Tyvek coveralls and cotton gloves. In addition, a liquid chromatography method was developed for the analysis of phenol from dermal exposure samples. RESULTS: As expected, formaldehyde was noted to be the major compound causing respiratory exposure. When exposure assessment was done on the basis of air samples collected both at stationary sampling sites and in the breathing zones of the workers the agreement between the results obtained was good. The dermal sampling revealed that the workers were exposed to phenol, but the risk for toxic effects was slight due to the low concentrations of urinary phenol. CONCLUSIONS: We conclude that it is possible to use the stationary sampling method for the assessment of respiratory exposure in a plywood factory instead of the usually more complicated breathing-zone sampling. This study also demonstrates the importance of taking dermal exposure into account, at least due to the ability of the resins to cause skin rashes, in assessment of the exposure to chemicals in plywood manufacturing.

Administration, Cutaneous↗
PubMed1984

Irreversible ATP depletion caused by low concentrations of formaldehyde and of calcium-chelator esters in intact human red cells.

Calcium chelators which can be incorporated inside small cells without disruption have become useful tools to investigate the role of intracellular ionized calcium in the processes of cell activation and signal-effect mediation. In experiments designed to investigate further Ca2+ pump function in chelator-loaded human red cells we found that the chelator-loading procedure itself caused delayed Ca2+-pump inhibition when pump function was explored by increasing the intracellular Ca2+ levels with the aid of the divalent cation ionophore A23187. Ca2+-pump inhibition was found to be secondary to ATP-depletion, and ATP-depletion, in turn, could be attributed to formaldehyde, which was released during the hydrolytic incorporation of free chelator, from the cleavage of the four ester groups which anchor it to cell membranes on addition to cell suspensions. The evidence suggests that the formaldehyde released stays largely within the cells. Formaldehyde, in concentrations of up to 20 mmol/l cells had no direct effects on Ca2+ transport in red cells, other than through ATP depletion. Procedures to circumvent the difficulties arising from the formaldehyde effects are outlined and discussed.

Adenosine Triphosphate↗
PubMed1983

Production of formaldehyde and acetone by hydroxyl-radical generating systems during the metabolism of tertiary butyl alcohol.

t-Butyl alcohol is not a substrate for alcohol dehydrogenase or for the peroxidatic activity of catalase and, therefore, it is used frequently as an example of a non-metabolizable alcohol. t-Butyl alcohol is, however, a scavenger of the hydroxyl radical. The current report demonstrates that t-butyl alcohol can be oxidized to formaldehyde plus acetone by hydroxyl radicals generated from four different systems. The systems studied were: (a) two chemical systems, namely, the iron catalyzed oxidation of ascorbic acid and the Fenton reaction between H2O2 and iron; (b) an enzymatic system, the coupled oxidation of xanthine by xanthine oxidase; and (c) a membrane-bound system, NADPH-dependent microsomal electron transfer. The oxidation of t-butyl alcohol appeared to be mediated by hydroxyl radicals, or by a species with the oxidizing power of the hydroxyl radical, because the production of formaldehyde plus acetone was (a) inhibited by competing scavengers of the hydroxyl radical; (b) stimulated by the addition of iron-EDTA; and (c) inhibited by catalase. The last observation suggests that H2O2 served as the precursor of the hydroxyl radical in all three systems. A possible mechanism is hydrogen abstraction to form the alkoxyl radical [CH3)3-C-O.), spontaneous fission of the alkoxyl radical to produce acetone and the methyl radical (CH3.), interaction of the methyl radical with O2 to form the methyl peroxy radical (CH300.), and decomposition of the later to formaldehyde. These results extend the alcohol oxidizing capacity of the microsomal alcohol oxidizing system to a tertiary alcohol. Since t-butyl alcohol is not a substrate for alcohol dehydrogenase or catalase, the ability of microsomes to oxidize t-butyl alcohol lends further support for a role for hydroxyl radicals in the microsomal alcohol oxidation system. In view of the production of formaldehyde, and the reactivity as well as further metabolism of this aldehyde, caution should be used in interpreting experiments in which t-butyl alcohol is used as a presumed "non-metabolizable" alcohol. t-Butyl alcohol may be a valuable probe for the detection of hydroxyl radicals in intact cells and in vivo.

Acetone↗
PubMed1988

Effect of glutathione depletion on aminopyrine and formaldehyde metabolism.

In previous studies, diethylmaleate (DEM)- and phorone-induced hepatic glutathione (GSH) depletion in rats was accompanied by impaired evolution of 14CO2 from the N-14C-labeled methyl groups of aminopyrine, which in turn was attributed to impaired generation of formaldehyde, its subsequent oxidation to formate, or to some combination of both. In the present study, l-buthionine sulfoximine (BSO)-induced hepatic GSH depletion was also accompanied by decreased evolution of CO2 from aminopyrine, but the extent of the fall in CO2 was less than that induced by DEM or phorone, even though the decrease in hepatic GSH was comparable with all three GSH-lowering compounds. Incubation of freshly prepared normal hepatic microsomes in vitro with the GSH-lowering agents resulted in impaired aminopyrine-N-demethylase (APDM) activity with inhibition by phorone greater than DEM greater than BSO. By contrast, hepatic microsomes prepared from rats pretreated with these compounds had normal APDM activity. 14CO2 evolution from i.p. administered [14C]formaldehyde was not impaired by any of the GSH-lowering compounds. Thus, assessment of APDM activity and formaldehyde metabolism did not unequivocally establish the mechanism(s) by which CO2 evolution from aminopyrine is depressed by DEM, phorone and BSO, although low GSH is likely to impair metabolism of formaldehyde formed in liver after demethylation of aminopyrine. Quantitative differences in the degree of depression of CO2 evolution suggest that at least DEM and phorone exert an additional inhibitory effect by a GSH-independent mechanism. This may involve inhibition of aminopyrine-N-demethylase activity.

Aminopyrine↗
PubMed1996

Role of tachykinin and bradykinin receptors and mast cells in gaseous formaldehyde-induced airway microvascular leakage in rats.

We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde. Extravasation of Evans blue dye into airway tissues was used as an index of airway microvascular leakage. Leakage of dye in the trachea and main bronchi increased significantly in a concentration-dependent fashion after 10 min inhalation of formaldehyde (5-45 parts per million (ppm)). The airway response induced by 10 min inhalation of 15 ppm formaldehyde (trachea: 119.5 +/- 13.9 ng/mg, n = 7; main bronchi: 139.6 +/- 7.9 ng/mg, n = 7) was abolished by the administration of CP-99,994 (3 and 6 mg/kg i.v.), but not by the administration of HOE 140 (0.65 mg/kg i.v.) nor ketotifen (1 mg/kg i.v.). The increase in vascular permeability induced by formaldehyde in the rat airway was mediated predominantly by NK1 receptor stimulation. Activation of bradykinin receptors and mast cells did not appear to play an important role in this airway response.

Animals↗
PubMed1978

Formaldehyde-induced appearance of septate junctions between digestive vacuoles.

Tissue biopsies from (1) some chronic inflammatory diseases, (2) a necrotic tumoral process, (3) normal human lymphatic ganglia, and (4) two congenital diseases of the adrenal cortex were selected for study. A block from each biopsy was fixed in glutaraldehyde-paraformaldehyde; a second block was fixed in 10% formaldehyde. In all cases septate junctions between digestive vacuoles did occur in phagocytic cells and some adrenal cortex cells fixed in formaldehyde. These junctions were similar to those reported recently for malakoplakia phagocytes. Consistently, they were not found to attach organelles other than lysosomes derivatives. Both phagocytes and adrenal cortex cells in the material fixed in glutaraldehyde-paraformaldehyde did not display adhesive specializations between digestive vacuoles. This suggests that the septate junctions described herein are artifactuous structures induced by formaldehyde. There is, however, a certain degree of specificity of cells having the capability of developing these septate junctions. It is assumed that the coating material of digestive organelles in phogocytes and some other cells would be responsible for both cell specificity and organelle specificity of the formaldehyde-induced septate junctions.

Adrenal Cortex↗
PubMed1986

Responses of the nasal mucociliary apparatus of F-344 rats to formaldehyde gas.

The nasal mucociliary apparatus is an important component of the airway defenses. Studies were undertaken to determine the nature and distribution of acute effects of inhaled formaldehyde on the nasal mucociliary apparatus of male F-344 rats using whole body exposures. Formaldehyde exposures ranged from a single 6-hr period up to multiple 6-hr exposures daily for 3 weeks, with exposure concentrations of 15, 6, 2, 0.5, and 0 ppm. Within 1 hr of the last exposure, the rats were killed and the nasal passages examined for effects on nasal mucociliary function. Exposure to 15 ppm formaldehyde induced inhibition of mucociliary function in specific regions of the nose, and mucostasis was generally more extensive than ciliastasis. These effects, which were initially confined to the anterior regions of the nose, became progressively more extensive for up to 2 weeks of exposure with only very slight progression during the third week. Inhibition of mucociliary function was much less severe with 6 ppm, minimal at 2 ppm, and not detected in rats following exposure to 0.5 ppm. The distribution of epithelial lesions, identified by histopathology, correlated well with the distribution of defective mucociliary function, but mucociliary function was a more sensitive indicator of toxicity. Localized defects in mucociliary function represent a potentially important consequence of exposure to formaldehyde.

Animals↗
PubMed1989

Antibody production in rats after long-term exposure to formaldehyde.

Sprague-Dawley rats were vaccinated with pneumococcal polysaccharide antigens and tetanus toxoid to evaluate the immunologic effects of long-term formaldehyde exposure. The antibody response to vaccination was measured 3 to 4 weeks later by enzyme-linked immunosorbent assay. An IgG response to pneumococcal polysaccharides and to tetanus toxoid was found in both the formaldehyde-exposed group and a control group of rats not exposed to formaldehyde. The IgM response to tetanus toxoid was significant in both groups but neither group showed a significant IgM response to pneumococcal polysaccharides. There were thus no signs of impaired B-cell function in rats exposed to a high concentration (12.6 ppm) of formaldehyde for nearly 2 years.

Animals↗
PubMed1990

Histochemical localization of formaldehyde dehydrogenase in the rat.

Formaldehyde dehydrogenase (FDH) activity has been demonstrated biochemically in the olfactory and respiratory mucosae and in the liver of the rat, but the cellular localization of this enzyme has not been investigated. A histochemical procedure was developed to permit cellular localization of FDH. This allowed us to examine the relationship between distribution of FDH and formaldehyde-induced toxicity. Cold-processed glycol methacrylate embedded tissues were used to localize FDH activity in the rat respiratory tract, kidney, liver, and brain. Five- or ten-micrometer tissue sections were incubated in a reaction mixture containing formaldehyde (HCHO), glutathione (GSH), NAD+, nitroblue tetrazolium, pyrazole, and disulfiram. A blue formazan precipitate was formed at the site of FDH activity. Epithelial cell cytoplasm of both the respiratory and the olfactory mucosae of the nose stained for FDH, and olfactory sensory cell nuclei were also positive. Underlying Bowman's and seromucous glands were weakly positive. The lung had FDH activity located mainly in the Clara cells of the airways, with only diffuse weak activity in the lung parenchyma. Liver had activity in the cytoplasm of the hepatocytes, while in the kidney FDH was most prominent in the brush border of the P2 segment of the proximal tubules. Brain white matter stained strongly for FDH, while in gray matter only the neuropil exhibited weak activity. Corresponding tissue sections were stained for sulfhydryls; these sections indicated that GSH is likely to be present in all cells with FDH activity. For the respiratory tract these results demonstrate distinct differences between the location of FDH activity and previously reported nonspecific aldehyde dehydrogenase activity in the nose (M. S. Bogdanffy, H. W. Randall, and K. T. Morgan, 1986, Toxicol. Appl. Pharmacol. 82, 560-567). While high aldehyde dehydrogenase activities were found in tissues with low toxicities due to acetaldehyde exposure and vice versa, FDH activity was observed in tissues whether or not they exhibited a toxic response to inhaled HCHO. While not able to account for the localized toxicity of HCHO, the presence of FDH and glutathione in the epithelial layer of the nasal cavity presents a barrier to inhaled formaldehyde at low concentrations and may partially explain the observed nonlinearity of HCHO toxicity.

Administration, Inhalation↗
PubMed1992

Additional stabilization of penicillin G acylase-agarose derivatives by controlled chemical modification with formaldehyde.

We have tested the effect of chemical modifications with formaldehyde on the activity/stability of immobilized derivatives of the enzyme penicillin G acylase (PGA). These derivatives were previously stabilized through enzyme-support multipoint covalent attachment. We carried out very different chemical treatments of our derivatives by testing the effect of different variables which control the intensity and the nature of these amine-formaldehyde reactions. The variables tested were: formaldehyde concentration, pH, time, and temperature. We also developed a colorimetric titration of the free amine groups on immobilized PGA in order to evaluate the extension of the reaction between formaldehyde and the amine groups of the enzyme. As a consequence of these studies, we have been able to get additional stabilizations of our previously stabilized-immobilized derivatives: e.g. a factor of 24-fold was achieved in terms of stabilization against irreversible thermal inactivation. The integrated effect of additional chemical modification plus previous multipoint covalent attachment has allowed us to prepare PGA derivatives which are 50,000 more thermostable than native PGA as well as most of the commercial PGA derivatives.

Amines↗
PubMed1984

Frog palate mucociliary apparatus: structure, function, and response to formaldehyde gas.

The upper respiratory tract mucociliary apparatus represents one of the first defenses against inhaled noxious materials. The frog palate has been widely used as a model to investigate the mode of action of this apparatus and to study its response to irritant gases. Video analysis was used here for the determination of mucus flow rate and flow patterns, ciliary beat frequency, and the nature of ciliary activity in the in vitro frog palate preparation. The results of studies of time-lapse video recordings were used in conjunction with light microscopic and ultrastructural morphologic investigations to determine functional interactions between cilia, the epiphase, and the periciliary fluid. It was concluded that the cilia enter the epiphase during the effector stroke, that waves may be produced on the under surface of this layer, and that the periciliary fluid is less viscous than, and moves in the same direction as, the epiphase. The response of the frog palate mucociliary apparatus to formaldehyde gas was also studied using an in vitro exposure system. There were distinct concentration-related responses to formaldehyde with initial stimulation, and at higher concentrations, subsequent inhibition of mucociliary function. Stimulation of mucus flow rate was due to increased ciliary activity, while inhibition of flow, which preceded ciliastasis, was attributed to direct effect of formaldehyde on the superficial mucus layer. Ciliastasis on the other hand was considered to provide evidence that the formaldehyde had penetrated the mucus layer and induced direct toxic effects on the underlying epithelial cells.

Animals↗
PubMed1991

Covalent binding of inhaled formaldehyde to DNA in the respiratory tract of rhesus monkeys: pharmacokinetics, rat-to-monkey interspecies scaling, and extrapolation to man.

DNA-protein cross-links were formed in the respiratory tract of rhesus monkeys exposed to [14C]formaldehyde (0.7, 2, or 6 ppm; 6 hr). Concentrations of cross-links (pmol/mg DNA) were highest in the mucosa of the middle turbinates; lower concentrations were produced in the anterior lateral wall/septum and nasopharynx. Very low concentrations were found in the larynx/trachea/carina and in the proximal portions of the major bronchi of some monkeys exposed to 6 ppm but not to 0.7 ppm. No cross-links were detected in the maxillary sinuses or lung parenchyma. The pharmacokinetics of cross-link formation in the nose were interpreted using a model in which the rate of formation is proportional to the tissue concentration of formaldehyde. The model includes both saturable and nonsaturable elimination pathways and describes regional differences in DNA binding as having an anatomical rather than a biochemical basis. Using this model, the concentration of cross-links formed in corresponding tissues of different species can be predicted by scaling the pharmacokinetic parameter that depends on minute volume (V) and quantity of nasal mucosal DNA (MDNA). The concentration-response curve for the average rate of cross-link formation in the turbinates, lateral wall, and septum of rhesus monkeys was predicted from that of F-344 rats exposed under similar conditions. There was significant overlap between predicted and fitted curves, implying that V and MDNA are major determinants of the rate of cross-link formation in the nasal mucosa of different species. Concentrations of cross-links that may be produced in the nasal mucosa of adult men were predicted based on experimental data in rats and monkeys. The results suggest that formaldehyde would generate lower concentrations of cross-links in the nasal mucosa of humans than of monkeys, and much lower concentrations in humans than in rats. The rate of formation of DNA-protein cross-links can be regarded as a surrogate for the delivered concentration of formaldehyde. Use of this surrogate should decrease the uncertainty of human cancer risk estimates derived by interspecies extrapolation by providing a more realistic measure of the delivered concentration at critical target sites.

Animals↗
PubMed1983

Formaldehyde risk assessment for occupationally exposed workers.

Formaldehyde has been shown to be carcinogenic in animals and should be considered potentially carcinogenic in humans. The mechanism of action is unknown but formaldehyde is weakly genotoxic and also may act as a late stage carcinogen or promoter. An estimated 1.3 million workers are potentially exposed to formaldehyde through their occupation. Of those exposed workers, about 3.5% were found to be exposed to formaldehyde air concentrations greater than the 3 ppm set by OSHA as a permissible exposure level. Fewer than 12% were exposed to concentrations greater than 1 ppm, but over 88% were exposed to concentrations of 0.5 ppm or more. A quantitative risk assessment, using the multistage low-dose extrapolation model, found the (maximum likelihood) estimate of lifetime risk for excess cancers to be 620 per 100,000 at the OSHA permissible exposure level. The estimated risk is 23 per 100,000 at 1 ppm and 2.8 per 100,000 at 0.5 ppm. Reduction of the OSHA permissible exposure level to 1 ppm would significantly decrease risk with minor economic disruption for most industries involved. However, reduction of risk to levels which have been generally regarded by other regulatory agencies as acceptable, i.e., 10(-5) to 10(-6), would require increased control by all the industries reviewed.

Animals↗
PubMed1989

Do rats comply with EPA policy on cancer risk assessment for formaldehyde?

Formaldehyde has been shown to cause nasal squamous cell carcinomas in the rat following 2-year inhalation exposure. The incidence of this tumor in a historical data base of 16,794 rats was nil, indicating that it is a rare spontaneous tumor. Five different mathematical extrapolation models were applied to the rat nasal tumor data to produce estimates at 10(-4) risk (the size of the historical data base) of between 3.232 and 0.003 ppm formaldehyde depending on the model and choice of maximum likelihood estimate or lower confidence limit values. Assuming that an ambient level of 0.07 ppm formaldehyde exists in a rat house, the multistage linear model did not predict correctly within the observed data. The EPA policy model (multistage third order) was not inconsistent with the observed data (P = 0.259). However, the unit risk, derived from this form of modeling, shows considerable inconsistency, at ambient levels of formaldehyde, when compared to observed incidences of nasal tumors in the general human population. It is proposed that the multistage models are inappropriate, and that caution should be exercised in the extrapolation of highly nonlinear animal tumor data.

Animals↗