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PubMed1979

A dual effect of formaldehyde on the inwardly rectifying potassium conductance in skeletal muscle.

1. The inwardly rectifying potassium conductance of the membrane of frog sartorius muscle fibres is greatly reduced by treatment of muscles for 30 min with a solution containing formaldehyde (10 mM). 2. A transient increase in the conductance of the inward rectifier is observed early during formaldehyde action. 3. Analysis of the biphasic time course of the conductance changes, as determined under controlled voltage conditions, suggests that treatment with formaldehyde alters simultaneously, but in opposite ways, two factors that determine the conductance of the inward rectifier. 4. The linear component of the current-voltage relation, which dominates the relation at strongly positive potentials, is not affected while the above changes occur. But on prolonged exposure to formaldehyde the leak conductance increases. 5. The effects of formaldehyde on the inward rectifier are reversible on prolonged superfusion with normal Ringer solution. 6. The slight inward rectification remaining after most of the extracellular K is replaced by Rb, is similarly reduced by treatment with formaldehyde. 7. The results are interpreted in terms of the chemical properties of formaldehyde and present views of the mechanisms of inward rectification.

Animals↗
PubMed1978

Formaldehyde incorporation by a new methylotroph (L3).

A number of bacterial strains have been isolated and investigated in our search for a promising organism in the production of single-cell protein from methanol. Strain L3 among these isolates was identified as an obligate methylotroph which grew only on methanol and formaldehyde as the sole sources of carbon and energy. The organism also grew well in batch and chemostat mixed-substrate cultures containing methanol, formaldehyde, and formate. Although formate was not utilized as a sole carbon and energy source, it was readily taken up and oxidized by either formaldehyde- or methanol-grown cells. The organism incorporated carbon by means of the ribulose monophosphate pathway when growing on either methanol, formaldehyde, or various mixtures of C1 compounds. Its C1-oxidation enzymes included phenazine methosulfate-linked methanol and formaldehyde dehydrogenase and a nicotinamide adenine dinucleotide-linked formate dehydrogenase. Identical inhibition by formaldehyde of the first two dehydrogenases suggested that they are actually the same enzyme. The organism had a rapid growth rate, a high cell yield in the chemostat, a high protein content, and a favorable amino acid distribution for use as a source of single-cell protein. Of special interest was the ability of the organism to utilize formaldehyde via the ribulose monophosphate cycle.

Alcohol Oxidoreductases↗
PubMed2004

Positive and negative transcriptional regulators of glutathione-dependent formaldehyde metabolism.

A glutathione (GSH)-dependent pathway is used for formaldehyde metabolism by a wide variety of prokaryotes and eukaryotes. In this pathway, S-hydroxymethylglutathione, produced by the reaction of formaldehyde with the thiolate moiety of glutathione, is the substrate for a GSH-dependent formaldehyde dehydrogenase (GSH-FDH). While expression of GSH-FDH often increases in the presence of metabolic or exogenous sources of formaldehyde, little is known about the factors that regulate this response. Here, we identify two signal transduction pathways that regulate expression of adhI, the gene encoding GSH-FDH, in Rhodobacter sphaeroides. The loss of the histidine kinase response regulator pair RfdRS or the histidine kinase RfdS increases adhI transcription in the absence of metabolic sources of formaldehyde. Cells lacking RfdRS further increase adhI expression in the presence of metabolic sources of formaldehyde (methanol), suggesting that this negative regulator of GSH-FDH expression does not respond to this compound. In contrast, mutants lacking the histidine kinase response regulator pair AfdRS or the histidine kinase AfdS cannot induce adhI expression in the presence of either formaldehyde or metabolic sources of this compound. AfdR stimulates activity of the adhI promoter in vitro, indicating that this protein is a direct activator of GSH-FDH expression. Activation by AfdR is detectable only after incubation of the protein with acetyl phosphate, suggesting that phosphorylation is necessary for transcription activation. Activation of adhI transcription by acetyl-phosphate-treated AfdR in vitro is inhibited by a truncated RfdR protein, suggesting that this protein is a direct repressor of GSH-FDH expression. Together, the data indicate that AfdRS and RfdRS positively and negatively regulate adhI transcription in response to different signals.

Aldehyde Oxidoreductases↗
PubMed2004

Multiple formaldehyde oxidation/detoxification pathways in Burkholderia fungorum LB400.

Burkholderia species are free-living bacteria with a versatile metabolic lifestyle. The genome of B. fungorum LB400 is predicted to encode three different pathways for formaldehyde oxidation: an NAD-linked, glutathione (GSH)-independent formaldehyde dehydrogenase; an NAD-linked, GSH-dependent formaldehyde oxidation system; and a tetrahydromethanopterin-methanofuran-dependent formaldehyde oxidation system. The other Burkholderia species for which genome sequences are available, B. mallei, B. pseudomallei, and B. cepacia, are predicted to contain only the first two of these pathways. The roles of the three putative formaldehyde oxidation pathways in B. fungorum LB400 have been assessed via knockout mutations in each of these pathways, as well as in all combinations of knockouts. The resulting mutants have the expected loss of enzyme activities and exhibit defects of varying degrees of severity during growth on choline, a formaldehyde-producing substrate. Our data suggest that all three pathways are involved in formaldehyde detoxification and are functionally redundant under the tested conditions.

Aldehyde Oxidoreductases↗
PubMed1982

Proportional mortality patterns among chemical plant workers exposed to formaldehyde.

To examine the possible health risks associated with occupational exposure to formaldehyde a proportional mortality analysis was conducted on deaths occurring between 1950 and 1976 among 136 men who had been employed a month or more in one of five formaldehyde-related areas of a large chemical producing plant located in Springfield, Massachusetts, USA. Overall, no statistically significant excesses or deficits in proportional mortality were observed among the formaldehyde-exposed group based on comparisons with both United States men and men from the local county area. In addition, no important differences in mortality were observed among this group when comparisons were made with 456 male decedents from the same plant who had not had a month or more of formaldehyde exposure. Within the calendar period examined, no deaths from sinonasal cancer were observed among the chemical workers studied nor was mention made on any death certificate of sinonasal cancer as a contributory cause of death. No important excesses, trends, or patterns in cancer mortality were observed among white male formadelhyde-exposed workers when consideration was given to age and time period of death, type and duration of formaldehyde exposure, and the lapse period from the onset of the first formaldehyde-related job assignment. Although certain limitations of this study do not allow definite conclusions to be drawn, the results indicate no trends or patterns in proportional mortality that could be directly linked to exposures to formaldehyde.

Adult↗
PubMed1997

Changes in respiratory function after one and three hours of exposure to formaldehyde in non-smoking subjects.

OBJECTIVE: To determine the changes in respiratory function within one hour and three hours of exposure to formaldehyde and investigate the relation between exposure to formaldehyde and acute changes in respiratory function. METHOD: Respiratory function of 50 non-smoking medical students exposed to formaldehyde in a gross anatomy laboratory were compared with respiratory function of 36 non-exposed, non-smoking physiotherapy students. Formaldehyde concentrations were measured in the breathing zone of each exposed subject and in the general work environment. RESULTS: Formaldehyde concentrations in the breathing zone of exposed subjects generally exceeded recommended standards. On average, the variables of respiratory function of both the exposed and the control subjects increased significantly within one hour and from one to three hours after exposure. The increase in respiratory function of the exposed subjects was significantly less than that of the control subjects. There was no meaningful correlation between concentration of formaldehyde in the breathing zone and changes in the respiratory function of exposed subjects. CONCLUSION: As the increase in the respiratory function of the subjects can be attributable to normal diurnal variation, the significantly lower increase in respiratory function of the exposed group than in the control group is probably due to exposure to formaldehyde. The results of this study do not, however, support a dose-response relation.

Adult↗
PubMed2000

Occupational exposure to formaldehyde and wood dust and nasopharyngeal carcinoma.

OBJECTIVES: To investigate whether occupational exposures to formaldehyde and wood dust increase the risk of nasopharyngeal cancer (NPC). METHODS: A multicentered, population based case-control study was carried out at five cancer registries in the United States participating in the National Cancer Institute's SEER program. Cases (n=196) with a newly diagnosed NPC between 1987 and 1993, and controls (n=244) selected over the same period from the general population through random digit dialing participated in structured telephone interviews which inquired about suspected risk factors for the disease, including a lifetime history of occupational and chemical exposure. Histological type of cancer was abstracted from clinical records of the registries. Potential exposure to formaldehyde and wood dust was assessed on a job by job basis by experienced industrial hygienists who were blinded as to case or control status. RESULTS: For formaldehyde, after adjusting for cigarette use, race, and other risk factors, a trend of increasing risk of squamous and unspecified epithelial carcinomas was found for increasing duration (p=0.014) and cumulative exposure (p=0.033) but not for maximum exposure concentration. The odds ratio (OR) for people cumulatively exposed to >1.10 ppm-years was 3.0 (95% confidence interval (95% CI) 1.3 to 6.6) compared with those considered unexposed. In analyses limited to jobs considered definitely exposed, these trends became stronger. The associations were most evident among cigarette smokers. By contrast, there was no association between potential exposure to formaldehyde and undifferentiated and non-keratinising carcinomas. There was little evidence that exposure to wood dust increased risk of NPC, as modest crude associations essentially disappeared after control for potential exposure to formaldehyde. CONCLUSIONS: These results support the hypothesis that occupational exposure to formaldehyde, but not wood dust, increases risk of NPC. This association seems to be specific to squamous cell carcinomas. Established cohorts of workers exposed to formaldehyde and wood dust should continue to be monitored for NPC and other respiratory cancers. Future studies of NPC should take into account histological type in assessing risk from environmental and host factors.

Adolescent↗
PubMed1998

Toxicity of formaldehyde to human oral fibroblasts and epithelial cells: influences of culture conditions and role of thiol status.

The toxicity of formaldehyde, a monomer released from certain polymeric dental materials, was studied in cultured human oral fibroblasts and epithelial cells. The influences of growth conditions were evaluated for both cell types, as well as the role of the internal and external thiol states. A one-hour exposure to formaldehyde decreased the colony-forming efficiency (CFE) of both cell types in a concentration-dependent manner, although the toxicity varied up to 100-fold with the conditions. Clearly, the presence of serum and the thiol cysteine counteracted the toxicity in fibroblasts. Similarly, pituitary extract and cysteine, or a mixture of amino acids and ethanolamines, counteracted the formaldehyde toxicity in serum-free cultures of epithelial cells. In contrast, a growth-promoting surface matrix of fibronectin and collagen did not influence the formaldehyde toxicity, as shown by both the CFE assay and a dye reduction assay. Further, a short-term change to the various growth media per se with or without the supplements serum or cysteine did not significantly alter the CFE. Analysis of the thiol state demonstrated significant differences between epithelial cells and fibroblasts, i.e., comparatively lower cellular levels of the free low-molecular-weight thiols glutathione and cysteine in fibroblasts. This result correlated to significantly higher formaldehyde toxicity in the fibroblasts than in the epithelial cells. Taken together, the results indicated the cytoprotective function of both intracellular and extracellular thiols toward formaldehyde, as well as the usefulness of thiol-free and chemically defined conditions for toxicity assessments in oral epithelial cells and fibroblasts. We conclude that the combined use of a controlled external milieu and the presumed target cell type may be advantageous in evaluations of oral toxicity mechanisms or the toxic potency of dental materials, particularly those which, like formaldehyde, may react with thiols or amines.

Biological Assay↗
PubMed1975

Denaturation of deoxyribonucleic acid in situ effect of formaldehyde.

In situ denaturation of nuclear deoxyribonucleic acid (DNA) is studied by use of acridine orange to differentially stain native versus denatured DNA, and a flow-through cytofluorometer for measurements of cell fluorescence. Thermal- or acid-induced DNA denaturation is markedly influenced by formaldehyde. Two mechanisms of the formaldehyde action are distinguished. If cells are exposed to the agent during heating, DNA denaturation is facilitated, most likely by the direct action of formaldehyde as a "passive" denaturing agent on DNA. If cells are pretreated with formaldehyde which is then removed, DNA resistance to denaturation increases, presumably due to chromatin cross-linking. It is believed that both effects occur simultaneously in conventional techniques employing formaldehyde to study DNA in situ, and that the extent of each varies with the temperature and cell type (chromatin condensation). Thus, profiles of DNA denaturation of cells heated with formaldehyde do not represent characteristics of DNA denaturation in situ; DNA denaturation under these conditions is modulated by the reactivity of chromatin components with formaldehyde rather than by DNA interactions with the macromolecules of nuclear mileu.

Acridines↗
PubMed1989

Formaldehyde-amine fixatives for immunocytochemistry of cultured Xenopus myocytes.

Although formaldehyde is commonly used in immunocytochemical studies, this fixative can cause distortions in cell structure. We tested the possibility that adducts of formaldehyde and primary amines could be used as improved fixatives for immunolabeling studies of cultured cells. A variety of primary amines were reacted with formaldehyde and applied to cultured Xenopus muscle cells, after which the cultures were labeled for immunofluorescence. Amine-formaldehyde fixatives improved structural preservation of the myocytes as compared with formaldehyde alone. The extent of improvement depended on the amine tested; the best results were obtained using cyclohexylamine. Immunofluorescence localization of a variety of antigens was better in myocytes fixed with cyclohexylamine-formaldehyde than in cells fixed with formaldehyde alone. In addition, the fixative provided good ultrastructural preservation of cytoskeletal structures and permitted immunogold labeling for alpha-actinin by use of pre-embedding labeling techniques.

Actinin↗
PubMed2002

Domestic exposure to formaldehyde significantly increases the risk of asthma in young children.

Concern has arisen in recent years about indoor air pollution as a risk factor for asthma. Formaldehyde exposure was examined in relation to asthma among young children (between 6 months and 3 yrs old) in a population-based control study carried out in Perth, Western Australia, between 1997-1999. An association between exposure to formaldehyde and asthma in young children has been suggested. Cases (n=88), whose parents were recruited at Princess Margaret Hospital Accident and Emergency Dept (Perth, Western Australia), were children discharged with asthma as the primary diagnosis. Controls (n=104), who were children in the same age group without asthma diagnosed by a doctor, were identified from birth records through the Health Dept of Western Australia (Perth, Western Australia). Health outcomes for the children were studied using a respiratory questionnaire and skin-prick tests. Formaldehyde, average temperature and relative humidity were measured on two occasions, winter (July-September 1998) and summer (December 1998-March 1999) in the child's bedroom and in the living room. The study found seasonal differences in formaldehyde levels in the children's bedrooms and living rooms with significantly greater formaldehyde exposure during the summer period for case and control subjects. The generalised estimating equation model showed that children exposed to formaldehyde levels of > or = 60 microg x m(-3) are at increased risk of having asthma. The results suggest that domestic exposure to formaldehyde increases the risk of childhood asthma.

Age Factors↗
PubMed2003

Glutaraldehyde-induced and formaldehyde-induced allergic contact dermatitis among dental hygienists and assistants.

BACKGROUND: Research has found that among health care workers, dental personnel are especially likely to have reactions to glutaraldehyde and formaldehyde. METHODS: The authors conducted patch test evaluations with a voluntary cohort of randomly recruited, healthy dental hygienists, or DHs, and dental assistants, or DAs, and nondental professionals to determine the incidence of glutaraldehyde-induced and formaldehyde-induced allergic contact dermatitis, or ACD; the potential for coreactivity between glutaraldehyde and formaldehyde; and the correlation between training methods in safe handling of sterilizing solutions and the sensitivity to glutaraldehyde and formaldehyde among DHs and DAs. RESULTS: The researchers enrolled 101 DHs and DAs and 51 nondental professionals in the study. All except one DH/DA subject were female. The dental subjects' mean age was 34.3 +/- standard deviation of 10.7 years; the nondental subjects', 33.8 +/- 11.0 years. DHs and DAs had worked in their profession for a mean of 11.0 +/- 9.3 years. Among the dental professionals, 80 (79.2 percent) had had a known exposure to cold sterilizing solutions, while the remainder were unable to provide a known history of exposure. Eleven (10.9 percent) dental professionals had clear reactions to glutaraldehyde, four (4.0 percent) were questionably allergic to glutaraldehyde, and two (2 percent) were definitively allergic to formaldehyde. One (2 percent) control subject had a reaction to glutaraldehyde, and one other (2 percent) had a reaction to formaldehyde. CONCLUSIONS AND CLINICAL: IMPLICATIONS: The authors found a statistically significant disparity in the rates of glutaraldehyde sensitivity among healthy DHs and DAs versus healthy control subjects (10.9 percent versus 2 percent reactively; P = .02). They found no evidence of cross-reactivity between glutaraldehyde and formaldehyde. The preponderance of reactions among the DHs and DAs suggests that their present safety practices are largely ineffective in protecting against sensitization to glutaraldehyde in sterilizing solutions.

Adult↗
PubMed2000

Effects of intravenous administration of formaldehyde on platelet and coagulation variables in healthy horses.

OBJECTIVES: To assess safety and determine effects of IV administration of formaldehyde on hemostatic variables in healthy horses. ANIMALS: 7 healthy adult horses. PROCEDURE: Clinical signs and results of CBC, serum biochemical analyses, and coagulation testing including template bleeding time (TBT) and activated clotting time (ACT) were compared in horses given a dose of 0.37% formaldehyde or lactated Ringer's solution (LRS), IV, in a 2-way crossover design. In a subsequent experiment, horses received an infusion of 0.74% formaldehyde or LRS. In another experiment, horses were treated with aspirin to impair platelet responses prior to infusion of formaldehyde or LRS. RESULTS: Significant differences were not detected in any variable measured between horses when given formaldehyde or any other treatment. Infusion of higher doses of formaldehyde resulted in adverse effects including muscle fasciculations, tachycardia, tachypnea, serous ocular and nasal discharge, agitation, and restlessness. CONCLUSIONS AND CLINICAL RELEVANCE: Intravenous infusion of formaldehyde at doses that do not induce adverse reactions did not have a detectable effect on measured hemostatic variables in healthy horses.

Animals↗
PubMedDate not supplied

Histological changes in the nasal mucosa in rats after long-term exposure to formaldehyde and wood dust.

Wood dust is a well known nasal carcinogen in man, as formaldehyde is in rats. In certain occupational environments, combined exposure to wood dust and formaldehyde is common. Little is known about the effects of this combination. A pilot study was performed on four groups of Sprague-Dawley rats: one exposed to wood dust (25 mg/m3), another to formaldehyde (12.4 ppm) and a third to both wood dust and formaldehyde; the fourth group served a control group. After 104 weeks of exposure the nose and lungs were examined histologically. One well differentiated squamous cell carcinoma was found in the formaldehyde group. Squamous cell metaplasia was found significantly more often among the formaldehyde-exposed rats. Squamous cell metaplasia with dysplasia was most frequently observed, however, in the group exposed to both formaldehyde and wood dust. There were also significantly more rats with pulmonary emphysema in the groups exposed to wood dust than in the other groups.

Animals↗
PubMed1993

Interactions of hydroxyl radicals with tris (hydroxymethyl) aminomethane and Good's buffers containing hydroxymethyl or hydroxyethyl residues produce formaldehyde.

The production of formaldehyde from tris(hydroxymethyl) aminomethane(Tris) by interaction with hydroxyl radicals(.OH) was studied, since the reaction mixture from the Fenton reaction performed in Tris/HCl buffer was found to be color-developed by colorimetric determination of formaldehyde. The absorption spectrum of chromogens was identical to that of authentic formaldehyde. Color development, which required the presence of Tris, hydrogen peroxide and cupric ions in the Fenton reaction mixture, was inhibited by the addition of hydroxyl radical scavengers such as glucose or hyaluronic acid. These results indicated that formaldehyde was produced when Tris interacted with .OH. With structures similar to Tris, Good's buffers were also found to produce formaldehyde by interaction with .OH. Analysis of formaldehyde derived from these buffers may provide a simple and convenient assay for detecting .OH generation. In evaluating effects of .OH on the biological system in Tris/HCl buffer or certain Good's Buffers, .OH loss may be due to interactions of .OH with these buffers. The formaldehyde produced as a result of such interactions may affect biological systems.

Buffers↗
PubMed2001

Occupational asthma due to formaldehyde.

Formaldehyde is a low molecular weight chemical and can elicit acute and chronic health related problems. Most of the inhaled formaldehyde is retained in the upper respiratory tract due to its extraordinary solubility. Therefore, cases of formaldehyde-induced occupational asthma are sporadic despite its widespread use in industrial processes. We herein report upon a case of occupational asthma due to formaldehyde, which was confirmed by workplace challenge including working environmental assessments, and by formaldehyde inhalation challenge using a specially designed closed-circuit apparatus. To investigate the possible involvement of an IgE-mediated mechanism, both in vitro and in vivo tests were done. IgE antibody specific for formaldehyde-human serum albumin conjugate (F-HSA) was not detected by ELISA, and no specific cutaneous reactivity to F-HSA was noted by either skin prick or intradermal test. The patient was diagnosed with formaldehyde-induced occupational asthma not associated with an IgE mediated mechanism.

Adult↗
PubMed1985

Formaldehyde exposure and respiratory and related cancers. A case-referent study among Finnish woodworkers.

A case-referent study was undertaken to investigate the associations between formaldehyde exposure and respiratory and related cancers. Fifty-seven such cancers from a retrospective cohort of male woodworkers formed the case group. They were matched by year of birth with 171 referents. Exposure to formaldehyde was assessed with job-exposure matrices. The median of the time-weighted average concentration was about 1 ppm, and the mean duration of exposure was 10 years among the exposed. Odds ratios (OR) were calculated for formaldehyde exposure (1.44), peak exposure to formaldehyde (1.26), and exposure to formaldehyde-containing wood dust (1.22). None of the values exceeded unity with statistical significance. Allowance was also made for a 10-year period from the onset of exposure. Birth year, cigarette smoking and exposure to wood dust, chlorophenols, pesticides, and terpenes were controlled by stratification. The adjusted ORs did not change appreciably. The highest OR was 1.95 for formaldehyde exposure without allowance for minimum latency, adjusted for exposure to terpenes. No exposure-response relation was observed for the level, duration, or dose (ppm-years) of formaldehyde exposure. The result is nonpositive and may be explained by absence of effect, by too short a follow-up, or by insufficient power for detecting a mild excess risk.

Adult↗
PubMed1998

Role of formaldehyde in direct formation of glycine and serine in bean leaves.

In our early study [2] labelled formaldehyde, glyoxylate, glycine and serine were formed from 14CO2 during 1 min incubation. Continuing the detailed work by unlabelled HCO3- with short (1 min) incubation time in numerous experiments, there were significant changes in the amount of formaldehyde, glyoxylate, glycine and serine. The main product was glycine. In illuminated leaves after HCO3- intake, the formaldehyde content increased. However, in dark in the presence of 5 mM HCO3- the formaldehyde content decreased and the amount of glyoxylate, glycine and serine increased in green leaves. The transamination is improbable as the amount of glutamate and aspartate did not decrease during the glycine and serine formation. The change in the amount of the measured free amino acids and glyoxylate was hindered by (aminooxy)acetic acid (AOA) and amethopterin. AOA, which is an inhibitor of pyridoxal phosphate has no effect on formaldehyde alteration. In the presence of amethopterin which inhibits the activity of tetrahydrofolate the formaldehyde amount increased in dark kept CO2 containing green leaves instead of decreasing. This shows that tetrahydrofolate has a role in glyoxylate formation from formaldehyde and CO2. A direct formation of glycine and serine can be supposed in definite circumstances during photosynthesis, in which pyridoxal phosphate has an important role.

Fabaceae↗