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PubMed1986

Initiation of in vitro cell transformation by formaldehyde and acetaldehyde as measured by attachment-independent survival of cells in aggregates.

The ability of formaldehyde and acetaldehyde to initiate transformation of a rat kidney cell line has been studied using a newly developed two-stage in vitro cell transformation assay. The assay is based on measurements of attachment-independent survival of cells in aggregates. Short treatment with non-cytotoxic doses of formaldehyde and acetaldehyde did not affect survival of the cells in the aggregate assay system. However, when the aldehyde treatment was followed by exposure of the cells to the tumor promoters TPA and PDD, a considerable increase in the number of viable cells was observed. On a molar basis, formaldehyde was about 100 times more potent than acetaldehyde in initiation of cell transformation. The data showed that cells derived from aggregates of cultures treated with formaldehyde or acetaldehyde followed by exposure to TPA possessed a considerably higher ability to form colonies in soft agar than untreated control cells.

Acetaldehyde↗
PubMed1988

Identification of spinacine as the principal reaction product of gamma-casein with formaldehyde in cheese.

Formaldehyde is added to milk in the production of grana cheese as an antimicrobial agent. In order to study the fate of the formaldehyde, a grana cheese preparation was made using 14C-labelled formaldehyde. The 14C-activity in the cheese was found to be mainly associated with the caseins, but it was not uniformly distributed among the different fractions (alpha s, beta- and gamma-caseins). gamma-Casein, separated by electrophoresis, was the most reactive component showing the highest specific activity. In the gamma-casein fractions, 99% of 14C-activity was associated with the basic amino acids. The only radioactive reaction product present in the gamma-casein fraction was identified by HPTLC and by an amino acid analyser to be spinacine, a condensation product of formaldehyde and histidine. Using the same method, other unknown radioactive products, of much less relevance, were detected in the total casein hydrolysate.

Caseins↗
PubMed1992

Methylamine metabolism to formaldehyde by vascular semicarbazide-sensitive amine oxidase.

The capacity of the vascular enzyme, semicarbazide-sensitive amine oxidase (SSAO), to metabolize methylamine to the potentially toxic product, formaldehyde, was tested using rat aortic homogenates and purified porcine aortic SSAO. Formaldehyde production in incubations of enzyme source with methylamine (1 mM) was detected by high performance liquid chromatography and product was confirmed by desorption chemical ionization mass spectrometry (DCI-MS). Inhibitor studies using the specific SSAO inhibitor semicarbazide and the monoamine oxidase inhibitor pargyline indicate that SSAO is responsible for metabolism of methylamine to formaldehyde. These results suggest the possibility that elevated methylamine found in several pathologic states (such as uremia and diabetes mellitus), or generated from exogenous sources, could result in overproduction of formaldehyde in tissues with high SSAO activity, especially blood vessels.

Amine Oxidase (Copper-Containing)↗
PubMed1988

Nasal tumours in rats after short-term exposure to a cytotoxic concentration of formaldehyde.

Male Wistar rats were exposed to 0, 10 or 20 ppm formaldehyde vapour for 4, 8 or 13 weeks (6 h/day; 5 days/week), and were then observed for periods up to 126 weeks. Transient growth retardation occurred in both test groups. Death rate was not noticeably affected by formaldehyde. Despite recovery periods of at most 126 weeks, the nasal respiratory and olfactory epithelium of many rats of the 20 ppm group exhibited non-neoplastic histopathological changes. Similar but much less severe changes of the respiratory epithelium were seen in a small number of rats of the 10 ppm group; the olfactory epithelium was not visibly affected in rats of this group. Nasal tumours considered to be induced by formaldehyde were seen only in the 20 ppm group and mainly in rats that had been exposed for 13 weeks, the incidence being 4.5% (6/132). These tumours comprised 3 squamous cell carcinomas, 1 carcinoma in situ and 2 polypoid adenomas, all originating from respiratory epithelium. It was concluded that rat nasal respiratory epithelium severely damaged by formaldehyde vapour often does not regenerate and in some cases develops tumours.

Animals↗
PubMed1989

Assimilation of methylamine by Paracoccus denitrificans involves formaldehyde transport by a specific carrier.

Assimilation of methylamine by Paracoccus denitrificans involves the following enzymes: a periplasmic methylamine dehydrogenase, a formaldehyde transport system, cytoplasmic formaldehyde and formate dehydrogenase. Formaldehyde transport follows saturation kinetics with a high substrate affinity (Km = 7 microM), and is severely inhibited by iodoacetate, cyanide and p-trifluoromethoxy carbonylcyanide phenylhydrazone. Expression of the formaldehyde carrier is regulated by the carbon source.

Adenosine Triphosphate↗
PubMed1983

An open-ended rat tracheal implant model: toxic effects of formaldehyde on the respiratory epithelium.

An open-ended rat tracheal implant model was developed to permit quantitative and repetitive exposure of respiratory epithelia to test substances of a variety of physical forms. To investigate the acute toxicity of formaldehyde with this new model, tracheas were exposed to formaldehyde solutions twice a week, for up to 12 weeks. At the higher formaldehyde concentrations (1.0, 0.6, 0.3%) the tracheal lumens became obstructed by granulation tissue. At the lower concentrations (0.2, 0.1, 0.01%), the appearance of flattened and atrophic epithelium as well as hyperplasia and squamous metaplasia were observed. The extent of these epithelial alterations was, for the most part, formaldehyde dose-dependent.

Animals↗
PubMed1985

Absence of embryotoxic effects of formaldehyde after percutaneous exposure in hamsters.

Pregnant hamsters were treated by topical application of formaldehyde solution on day 8, 9, 10 or 11 of gestation. Fetuses recovered on day 15 were weighed, measured, and examined for teratogenic effects of formaldehyde exposure. The resorption rate was increased in the treated groups, but formaldehyde treatment did not significantly affect weight or length, nor did any malformations which could be related to treatment appear. It was concluded that fetal risk due to maternal topical exposure to formaldehyde is minimal in this model system.

Animals↗
PubMed1995

Increased oxidation of ethylene glycol to formaldehyde by microsomes after ethanol treatment: role of oxygen radicals and cytochrome P450.

The production of ferryl-type oxidants by microsomes from ethanol-fed rats and pair-fed controls was determined by assaying for the production of formaldehyde from ethylene glycol. Microsomes from the ethanol-fed rats were more reactive than controls in oxidizing ethylene glycol. Catalase was a powerful inhibitor for this reaction, superoxide dismutase was slightly inhibitory and hydroxyl radical scavengers had no effect. These results suggest an important role for H2O2, but not O2-. or .OH in the overall pathway for oxidizing ethylene glycol to formaldehyde. The production of H2O2 by microsomes was increased after ethanol treatment, the extent of increase corresponding to the increase in oxidation of ethylene glycol. A variety of inhibitors and ligands of cytochrome P450, including miconazole, diethyldithiocarbamate, tryptamine, and 4-methylpyrazole, inhibited formaldehyde production by both microsomal preparations. Anti-cytochrome P4502E1 IgG also inhibited the reaction with both microsomal preparations and prevented the increase caused by ethanol treatment. These results indicate that microsomes from ethanol-treated rats are more reactive than pair-fed controls in generating ferryl-type oxidants and that increased production of H2O2 by cytochrome P4502E1 plays a role in the elevated oxidation of ethylene glycol to formaldehyde.

Animals↗
PubMed2006

Formaldehyde assay by capacitance versus voltage and impedance measurements using bi-layer bio-recognition membrane.

A novel formaldehyde sensitive biosensor based on bacterial formaldehyde dehydrogenase (FDH) as a bio-recognition element has been developed. The bio-recognition membrane had bi-layer architecture and consisted of FDH, cross-linked with albumin, and of the cofactor NAD at a high concentration level (first layer). The second layer was a negatively charged Nafion membrane, which prevented a leakage of negatively charged NAD molecules from the bio-membrane. As transducers, gold electrodes SiO(2)/Si/SiO(2)/Ti/Au and electrolyte-insulator-semiconductor Si/SiO(2) (EIS) structures have been used. Changes in capacitance and impedance properties of the bio-recognition membrane have been used for monitoring formaldehyde concentration in a bulk solution. It has been shown that formaldehyde can be detected within a concentration range from 1 microM to 20mM depending on the type of transduction used, with a detection limit of 1 and 100 microM for gold-based and EIS-based transducers, respectively.

Aldehyde Oxidoreductases↗
PubMed2006

On-line detection of atmospheric formaldehyde by a conductometric biosensor.

Atmospheric formaldehyde (CH(2)O) was detected under continuous flow conditions by an on-line system comprising of a wet scrubber for a continuous transfer of the pollutant to an aqueous solution, a micro-reactor containing immobilized formaldehyde dehydrogenase (FDH) and a conductometric transducer. By this system atmospheric formaldehyde concentrations in the range 0.05-2 ppm were detected with a sensitivity of 20 microS/ppm. In this concentration range the immobilized enzyme oxidized all the sampled formaldehyde molecules to formic acid, avoiding cumbersome calibration procedures. The operational stability of the biosensor was at least 3 months, working continuously 10 h/day at room temperature.

Air Pollutants↗
PubMed2005

Adsorption of gaseous formaldehyde and carboxylic acids by ammonium-ion-exchanged alpha-zirconium phosphate.

Ammonium-ion-exchanged alpha-Zr(HPO(4))(2)H(2)O (alpha-ZrP) was obtained as a single phase with the interlayer distance of 9.4 A by the ion-exchange of proton with ammonium ion. The ammonium ion-exchanged alpha-ZrP could adsorb ill-smelling gases, such as formaldehyde and carboxylic acids (formic acid, acetic acid, propionic acid, and butyric acid). The adsorption amounts of carboxylic acids increased in the order, butyric acid<propionic acid<acetic acid<formic acid, whereas the adsorption amount of formaldehyde was the same as that of butyric acid. It was cleared that the adsorbed formaldehyde was partially decomposed to formic acid and methanol by self oxidation-reduction reaction in the interlayer region as evidenced by solid-state NMR. Thereby the interlayer distance after the adsorption of formaldehyde expanded to 14.4 A. In the case of formic acid, it was cointercalated into the interlayer region, and the interlayer distance expanded to 11.1 A. On the other hand, the interlayer distance of the other carboxylic acid-adsorbed compounds decreased to 7.6 A due to release by the evacuation.

Acetic Acid↗
PubMed2005

The fabrication and characterization of a formaldehyde odor sensor using molecularly imprinted polymers.

The fabrication and characterization of odor sensors based on molecularly imprinted polymers is reported as the first case of imprinting formaldehyde. A quartz crystal microbalance is employed as a sensitive apparatus of a sensor for the determination of odor formaldehyde. An equation is deduced to characterize the interaction between molecularly imprinted films and the template. A linear relationship between the frequency shifts and the concentration of analyte in the range of 1.25 to 14.25 microM is found. The detection limit is about 20.5 microM. The sensor can selectively distinguish gaseous formaldehyde. It is envisaged that this novel and handy method could be employed to determine formaldehyde gas in the atmosphere.

Air Pollution↗
PubMed2005

The effect of endogenous formaldehyde on the rat aorta endothelial cells.

Previous studies have demonstrated endogenous formaldehyde (FA) may be involved in endothelial damage, and may be a potential factor of vulnerability of atherosclerosis. However, the mechanism has not been characterized. The present studies examined DNA-protein cross-links (DPC) formation in rat aorta endothelial cells (RAECs) treated with formaldehyde, hydrogen peroxide (H2O2), or formaldehyde with equal molar concentration of H2O2, which is produced with formaldehyde in the body at the same time. Using a K+/SDS precipitation assay for DPC determination, concentration-dependent increases in DPC formation were observed 1.5 h after treatment of RAECs with 0.01-2mM FA, H2O2, or FA with equal molar concentration of H2O2. Time-dependent increases in DPC formation were also observed at 0.5-4 h time point after treatment of RAECs with 0.05 and 0.1mM FA, or 0.1mM FA with H2O2. The DPC levels reduced after treatment with FA and equal molar concentration of H2O2, compared with treatment with FA alone. FA may be less cytotoxic, as FA alone did not affect the cell viability even treating for 4h, until the treatment concentration reached 2mM. However, H2O2, and FA with H2O2 induced significant decreases of cell viability. These studies suggest that FA and H2O2 may injure endothelial cells synergistically, and low concentration of FA (0.05-0.1) may contribute to the endothelial injury in the body during aging.

Animals↗
PubMed2004

Formaldehyde and urea removal in a denitrifying granular sludge blanket reactor.

Simultaneous formaldehyde biodegradation, urea hydrolysis and denitrification in anoxic batch assays and in a continuous laboratory anoxic reactor were investigated. In batch assays, the initial formaldehyde biodegradation rate was around 0.7 g CH(2)Og VSS(-1)d(-1) and independent of the urea concentration (90- 370 mg N-NH(2)CONH(2)l(-1)). Urea was completely hydrolyzed to ammonium in the presence of 430 mg l(-1) formaldehyde and complete denitrification took place in all cases (125 mg N-NO(-)(3)l(-1)). Formaldehyde removal efficiencies above 99.5% were obtained in a lab-scale denitrifying upflow sludge blanket reactor at organic loading rates between 0.37 and 2.96 kg CODm(-3)d(-1) (625-5000 mg CH(2)Ol(-1)). The urea loading rate was increased from 0.06 to 0.44 kg Nm(-3)d(-1) (100-800 mg N-NH(2)CONH(2)l(-1)) and hydrolysis to ammonium was around 77.5% at all loading rates. The denitrification process was always almost complete (100-800 mg N-NO(3)(-)l(-1)), due to the high COD/N ratio of 6.7 in the influent. A minimum value of 3.5 was found to be required for full denitrification. The composition of the biogas indicated that denitrification and methanogenesis occurred simultaneously in the same unit. A good granulation of the sludge was observed.

Biodegradation, Environmental↗
PubMed2004

Biodegradation and effect of formaldehyde and phenol on the denitrification process.

Formaldehyde and phenol biodegradation during the denitrification process was studied at lab-scale, first in anoxic batch assays and then in a continuous anoxic reactor. The biodegradation of formaldehyde (260 mgl(-1)) as single carbon source and at phenol concentrations ranging from 30 to 580 mgl(-1) was investigated in batch assays, obtaining an initial biodegradation rate around 0.5g CH(2)OgVSS(-1)d(-1). With regard to phenol, its complete biodegradation was only observed at initial concentrations of 30 and 180 mgl(-1). The denitrification process was inhibited at phenol concentrations higher than 360 mgl(-1). Studies were also done using a continuous anoxic upflow sludge blanket reactor in which formaldehyde removal efficiencies above 99.5% were obtained at all the applied formaldehyde loading rates, between 0.89 and 0.14g COD (CH(2)O)l(-1)d(-1). The phenol loading rate was increased from 0.03 to 1.3g COD (C(6)H(6)O)l(-1)d(-1). Phenol removal efficiencies above 90.6% were obtained at phenol concentrations in the influent between 27 and 755 mgl(-1). However, when the phenol concentration was increased to 1010 mgl(-1), its removal efficiency decreased. Denitrification percentages around 98.4% were obtained with phenol concentrations in the influent up to 755 mgl(-1). After increasing phenol concentration to 1010 mgl(-1), the denitrification percentage decreased because of the inhibition caused by phenol.

Biodegradation, Environmental↗
PubMed2004

Formaldehyde and leukemia: an improbable causal relationship.

Formaldehyde has been the subject of numerous toxicological and epidemiological investigations for almost 25 years. Though most toxicology studies have focused on the effects of the chemical on the nasal tract and respiratory system, epidemiology investigations have been more extensive evaluating the association between formaldehyde and cancers not only of the nasal cavities, nasopharynx, and lung, but also of the brain, prostate, pancreas, and hematopoietic system. Recently, three studies have been published which report on the possible association between exposure to formaldehyde and an increased incidence of leukemia, specifically myeloid leukemia. The article summarizes the results of these three studies, evaluates the evidence for causality based on recognized epidemiologic criteria, and provides an assessment that the association between formaldehyde and the increased incidence of leukemia reported in these studies is not plausible.

Carcinogens, Environmental↗
PubMed2006

Inhaled formaldehyde: evaluation of sensory irritation in relation to carcinogenicity.

OBJECTIVES: The critical health effects of formaldehyde exposure include sensory irritation and the potential to induce tumours in the upper respiratory tract. In literature, a concentration as low as 0.24 ppm has been reported to be irritating to the respiratory tract in humans. Nasal tumour-inducing levels in experimental animals seem to be 1-2 orders of magnitude larger. In this paper, the subjectively measured sensory irritation threshold levels in humans are discussed in line with findings obtained in animal experiments. In addition, a Benchmark dose (BMD) analysis of sensory irritation was used to estimate response incidences at different formaldehyde concentrations. METHODS: Data on respiratory irritation and carcinogenicity of formaldehyde were retrieved from public literature and discussed. BMD analysis was carried out on human volunteer studies using the US-EPA BMD software. RESULTS: Subjective measures of irritation were the major data found in humans to examine sensory (eye and nasal) irritation; only one study reported objectively measured eye irritation. On a normalized scale, mild/slight eye irritation was observed at levels 1 ppm, and mild/slight respiratory tract irritation at levels 2 ppm. With the BMD software, it was estimated that at a level of 1 ppm, only 9.5% of healthy volunteers experience 'moderate' (i.e., annoying) eye irritation (95% upper confidence limit). An important factor modulating the reported levels of irritation and health symptoms most probably includes the perception of odour intensity. In several studies, the 0-ppm control condition was missing. From the results of the long-term inhalation toxicity studies in experimental animals, a level of 1 ppm formaldehyde has been considered a NOAEL for nasal injury. CONCLUSIONS: Sensory irritation is first observed at levels of 1 ppm and higher. From both human and animal studies, it was concluded that at airborne levels for which the prevalence of sensory irritation is minimal both in incidence and degree (i.e., <1 ppm), risks of respiratory tract cancer are considered to be negligibly low.

Administration, Inhalation↗
PubMed1997

Induction of glutathione-dependent formaldehyde dehydrogenase activity in Escherichia coli and Hemophilus influenza.

We have examined the induction of glutathione-dependent formaldehyde dehydrogenase (GS-FDH) activity in Escherichia coli and Hemophilus influenza. Formaldehyde was found to induce enzyme activity in both E. coli and H. influenza at concentrations between 0.6 and 20 ppm. Higher formaldehyde concentrations were toxic. Methanol concentrations up to 20% (200,000 ppm) and sodium formate concentrations up to 2% (20,000 ppm) gave negligible amounts of induction. The basic mechanism of induction was probed by inducing GS-FDH activity in the presence of rifampicin to inhibit RNA synthesis or chloramphenicol to inhibit protein synthesis. Both reagents inhibited GS-FDH induction, demonstrating that regulation occurs at the level of transcription. These results indicate that at least one function of GS-FDH in Gram-negative bacteria is to detoxify exogenous formaldehyde encountered in their environment and that GS-FDH inducibility may be a common feature of Gram-negative bacteria.

Aldehyde Oxidoreductases↗