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PubMed1982

Determination of formaldehyde in biological tissues by gas chromatography/mass spectrometry.

A quantitative method is described for the determination of formaldehyde in biological tissues by stable isotope dilution using gas chromatography/mass spectrometry. (13C2H2)Formaldehyde is used as the isotopic diluent. After tissue homogenization, derivatization is carried out in situ with pentafluorophenylhydrazine, followed by extraction and analysis using selected ion monitoring. The sensitivity of the technique is higher than that of conventional methods of formaldehyde analysis, enabling endogenous formaldehyde to be quantitatively analyzed in tissues, even in samples as small as 20 mg wet weight. The effects of exposure to airborne formaldehyde or to airborne methyl chloride on the formaldehyde concentrations of several tissues of Fischer-344 rats are reported.

Animals↗
PubMed1984

Occupational formaldehyde exposure and increased nasal cancer risk in man.

A comprehensive data linkage system for the detailed investigation of occupational cancer has newly been established in the Danish Cancer Registry, providing employment histories back until 1964. Based on this system a study of 839 cases of cancer of the nasal cavities, sinuses and rhinopharnyx and 2,465 cancer controls diagnosed in Denmark during the period 1970-1982 was conducted. Histories of exposure to formaldehyde, wood-dust and 10 other specified compounds or procedures, were assessed by industrial hygienists unaware of the case-control status of the cancer patients under study. Some 4.2% of the male and 0.1% of the female controls had been exposed to formaldehyde. A statistically significant excess risk (p less than 0.05) for carcinoma of the nasal cavity and sinuses among males with a history of exposure to formaldehyde (RR = 2.8), wood-dust (RR = 2.5) and paint lacquer and glue (RR = 2.1) was found. When adjustment was made for wood-dust exposure the relative risk associated with formaldehyde was reduced to 1.6, which is not significantly in excess of 1.0, although still compatible with a 3- to 4-fold increase in risk using conventional 95% confidence limits. The joint action of exposure to wood-dust and formaldehyde was in accordance with an additive effect. The excess risk of sino-nasal cancer with exposure to paint, lacquer and glue remained statistically elevated after adjustment for contemporary exposure to wood-dust and formaldehyde.

Air Pollutants, Occupational↗
PubMed1987

Subchronic (13-week) inhalation toxicity study of formaldehyde in rats.

Male and female albino Wistar rats were exposed to concentrations of 0, 1, 10 or 20 ppm formaldehyde vapour during 6 h/day, 5 days/wk for 13 weeks. Treatment-related changes observed at 20 ppm included in both sexes: stared coats, uncoordinated locomotion and excitation during the first 30 minutes of each exposure, yellowing of the fur, growth retardation, a decreased level of plasma protein, severe and extensive karatinized stratified squamous metaplasia of the nasal respiratory epithelium, and focal degeneration and squamous metaplasia occasionally accompanied by keratinization of the olfactory epithelium; in males only; increased activities of plasma aspartate amino transferase (ASAT), alanine amino transferase (ALAT) and alkaline phosphatase (ALP) and squamous metaplasia of the laryngeal epithelium. Lesions seen at 10 ppm included yellowing of the fur and moderate squamous metaplasia of the nasal respiratory epithelium. The only change observed in three out of twenty 1 ppm exposed animals that might or might not be treatment-related was minimal focal epithelial hyperplasia and squamous metaplasia of the respiratory epithelium lining the nasal septum and maxillary turbinates. No histopathological evidence of hepatotoxicity was detected in any of the formaldehyde-treated groups. An in vivo/in vitro cell proliferation study showed an increase in [3H]-thymidine labeling index of the respiratory epithelium lining the nasoturbinates of rats exposed to 10 or 20 ppm formaldehyde on three successive days, whereas at the 1 ppm level the labeling index was similar to that of controls. It was concluded that under the conditions of the present 13-week inhalation study, formaldehyde at concentrations up to 10 ppm was not hepatotoxic to rats. At the 20 ppm formaldehyde level, a slight effect on the liver of male rats cannot be completely excluded. The study was inconclusive with respect to 1 ppm formaldehyde being a cytotoxic or a no-cytotoxic effect level for the nasal epithelium.

Animals↗
PubMed1992

Cytogenetic analysis of pulmonary lavage and bone marrow cells of rats after repeated formaldehyde inhalation.

Cytogenetic analyses were conducted on bone marrow and pulmonary lavage cells from rats that received repeated inhalation exposures to formaldehyde. Male Sprague-Dawley rats were exposed to 0, 0.5, 3, or 15 ppm formaldehyde for 6 h per day, 5 days per week, for 1 and 8 weeks. There was no significant increase in chromosomal abnormalities in the bone marrow cells of formaldehyde-exposed rats relative to controls. There was a statistically significant increase in chromosomal aberrations in the pulmonary lavage cells from rats that inhaled 15 ppm. There were 7.6 and 9.2% of the scored pulmonary lavage cells that had aberrations following 1 and 8 weeks, respectively, of 15 ppm formaldehyde exposure (with control levels of 3.5 and 4.8%, respectively). The predominant damage seen was chromatid breaks. These findings indicate that marginal but statistically significant genotoxic effects could be detected locally in lung alveolar macrophages, but not distally in bone marrow, following repeated formaldehyde exposures only at a high concentration that is carcinogenic to rats. The biological significance of this effect is uncertain since formaldehyde is not considered to be a lung carcinogen in rats.

Administration, Inhalation↗
PubMed1996

A rapid formaldehyde assay using purpald reagent: application under periodation conditions.

Measurement of formaldehyde is encountered in a broad range of applications including the wine and alcohol industry and environmental pollution surveillance. In carbohydrate structural chemistry, frequent use is made of formaldehyde by periodate oxidation of terminal vicinal diols. Popular methods for the detection of formaldehyde use reagents such as chromotropic acid (4,5-dihydroxynaphthalene-2,7-disulfonic acid) or acetylacetone. The chromotropic acid method requires heating of the sample under strongly acidic conditions, which is undesirable in many applications. The acetylacetone method yields a yellow color product, and is less specific and sensitive (Mimura et al., J. Hyg. Chem. 22, 39-41, 1976). The reaction of formaldehyde with Purpald (4-amino-3-hydrazino-5-mercapto-1,2,4-triazole) works under alkaline conditions at room temperature, and the sensitivity is superior to other methods. The color development by this reagent, however, requires oxidation of the adduct with hydrogen peroxide, air oxygen, or dilute periodate. We found that low levels of periodate, commonly used to oxidize specifically terminal vicinal diols to yield formaldehyde, are compatible with color development with the Purpald reagent. We have investigated the conditions required for use of the Purpald reagent, especially in conjunction with periodate oxidation reactions. We have used the assay either in test tubes or with microplates, attaining sensitivity of as little as 1 nmol formaldehyde.

Chromatography, Gel↗
PubMed2002

An international collaborative study on a method for determination of formaldehyde in veterinary vaccines.

An international collaborative study of a quantitative colorimetric method for determination of formaldehyde in veterinary vaccines was conducted on a series of replicate, blinded veterinary vaccine products by 15 laboratories in three regions: North America, Europe and Japan. Participants conducted determinations using a modification of a method from the European Pharmacopoeia, a colorimetric method based on the reaction of formaldehyde with methylbenzothiazolone hydrazone hydrochloride. For this study, three licensed vaccine products containing formaldehyde were revialed, randomly numbered, tested for uniformity and distributed by one of the participating laboratories through regional coordinators to collaborators. One of the revialed products was spiked with a known amount of formaldehyde and included in the test series. Results along with all raw data were returned to the distributing laboratory for consolidation and statistical treatment. For the modified method spike recovery was 101% and reproducibility (inter-laboratory variation expressed as relative standard deviation) ranged from 18.0 to 8.0% for respective formaldehyde concentrations of 0.28 to 1.07 g/l. Based on the study, the method was proposed by the Biologicals Working Group of the International Cooperation on Harmonization of Technical Requirements for Registration of Veterinary Medicinal Products (VICH) as a candidate for the VICH Guideline standard method for residual formaldehyde.

Chlorine↗
PubMed1998

Pathways for transcriptional activation of a glutathione-dependent formaldehyde dehydrogenase gene.

The widespread occurrence of glutathione-dependent formaldehyde dehydrogenases (GSH-FDH) suggests that this enzyme serves a conserved function in preventing the cytogenetic and potentially lethal interaction of formaldehyde with nucleic acids, proteins and other cell constituents. Despite this potential role of GSH-FDH, little is known about how its expression is regulated. Here, we identify metabolic and genetic signals that activate transcription of a GSH-FDH gene (adhI) in the bacterium Rhodobacter sphaeroides. Activity of the adhI promoter is increased by both exogenous formaldehyde and metabolic sources of this toxin. Elevated adhI promoter activity in DeltaGSH-FDH mutants implicates formaldehyde or the glutathione adduct that serves as a GSH-FDH substrate, S-hydroxymethylglutathione, as a transcriptional effector. From studying adhI expression in different host mutants, we find that the photosynthetic response regulator PrrA and the trans-acting spd-7 mutation increase function of this promoter. The behavior of a nested set of adhI::lacZ fusions indicates that activation by formaldehyde, PrrA and spd-7 requires only sequences 55 bp upstream of the start of transcription. A working model is presented to explain how GSH-FDH expression responds to formaldehyde and global signals generated from the reduced pyridine nucleotide produced by the activity of this enzyme.

Aldehyde Oxidoreductases↗
PubMed1993

Changes in nasal lavage fluid due to formaldehyde inhalation.

The aim of the study was to characterize the nature of the formaldehyde-induced nasal response consisting in symptoms of rhinitis and changes in nasal lavage fluid. Eleven healthy subjects and nine patients with specific skin sensitization were provoked in a toxicological chamber with formaldehyde at a dose of 0.5 mg/m3 over 2 h. Nasal lavage was performed prior to and immediately after provocation and 4 and 18 h later. Provocation with formaldehyde caused transient symptoms of rhinitis and prolonged changes in nasal washings. There were increases in the number and proportion of eosinophils and elevated albumin and total protein levels in nasal lavage fluid 4 and 18 h after provocation. No difference in the nasal response to formaldehyde was found between patients with skin sensitization and healthy subjects. These data confirm the irritative effects of formaldehyde and are also suggestive of nonspecific proinflammatory properties when formaldehyde is inhaled at a low (0.5 mg/m3) dose.

Albumins↗
PubMed1990

Different types of formaldehyde-oxidizing dehydrogenases in Nocardia species 239: purification and characterization of an NAD-dependent aldehyde dehydrogenase.

Three different dehydrogenases able to oxidize formaldehyde were found in the Gram-positive methylotroph, Nocardia sp. 239: an NAD-dependent aldehyde dehydrogenase (NA-ADH), and NAD- and factor-dependent formaldehyde dehydrogenase (FD-FDH), and a dye-linked aldehyde dehydrogenase (DL-ADH). The ratio of the activities observed for the two NAD-linked enzymes varied with growth conditions: batch-wise grown cells had nearly the same activities for both enzymes; in fed batch-wise grown cells (methanol limitation) only FD-FDH was detected. The latter is clearly involved in formaldehyde oxidation, since the enzyme and the factor were found only in methanol-grown cells and the enzyme is specific for formaldehyde. In contrast, the two aldehyde dehydrogenases may have significance for aldehyde dissimilation in general, since both activities could also be demonstrated in ethanol-grown cells (but not in glucose-grown cells) and higher aldehydes are even better substrates than formaldehyde. NA-ADH was purified to homogeneity. The enzyme seems to be a homotetramer since it showed a relative molecular mass of 200,000 and the denaturated form of 55,000. Other characteristics are as follows: the enzyme showed substrate inhibition for the aldehydes tested; optimal activity was found at pH 9.2; the reverse reaction was not observed; the enzyme was specific for NAD; GSH, K+, or NH4+ addition did not stimulate formaldehyde oxidation; the order of NAD and substrate addition to the enzyme was not important; several compounds able to block SH groups were inhibitory. Comparison with NAD-linked aldehyde dehydrogenases from Gram-negative bacteria showed that the Nocardia enzyme is distinct from the enzyme of Pseudomonas putida (EC 1.2.1.46) and of Hyphomicrobium X.

Aldehyde Oxidoreductases↗
PubMed1981

Formaldehyde mutagenesis in the nematode Caenorhabditis elegans.

We have found that formaldehyde is capable of inducing mutations in the nematode Caenorhabditis elegans. 4 concentrations of formaldehyde were tested. At a concentration of 1%, formaldehyde is lethal to the nematode, and 0.01% formaldehyde did not induce any mutations in approx. 60 000 tested chromosomes. 2 concentrations of formaldehyde, 0.1% and 0.07%, were found to be mutagenic, inducing both point mutations and deficiencies in the unc-22 region of linkage group IV. 4 of the point mutations have been demonstrated to be alleles of the unc-22 gene and have been mapped within the locus. 2 of the putative deficiencies have been confirmed. Each spans the unc-22 gene and at least 2 other genes in the region. A rough estimate of the forward mutation frequency using 0.1% formaldehyde in this region is 3 X 10(-5), while for 0.07% the frequency is 2 X 10(-4).

Alleles↗
PubMed1987

The effect of formaldehyde exposure upon the mononuclear phagocyte system of mice.

The vapors of formaldehyde have been reported to represent a potential health hazard, resulting in an increased incidence of carcinomas of the nasal turbinates in experimental animals. To determine the potential role of alterations in the mononuclear phagocyte system (MPS) induced by inhalation of formaldehyde, we studied the systemic effects of exposure upon macrophages. Specifically, we examined the effects of formaldehyde exposure upon development of the MPS by use of an established system of quantitative objective markers, which characterizes and classifies populations of murine macrophages into several developmental stages. Exposure of mice to 15 ppm of formaldehyde for 6 hr daily for 3 weeks did not alter the number or impair the function of resident peritoneal macrophages, although this exposure increased (approximately twofold) competence for release of H2O2 from the macrophages. Furthermore, formaldehyde exposure did not alter the tumoricidal activation or differentiation of macrophages produced by the defined stimulant MVE-2. The data thus indicate that exposure of mice to formaldehyde can induce selective systemic alterations in the function of the MPS for H2O2 production, a change which has been shown in other studies to increase the frequency of mutagenesis.

Acid Phosphatase↗
PubMed1985

Clinical evaluation of patients with complaints related to formaldehyde exposure.

Formaldehyde is a very widely used chemical in our present society and one with which every physician has had a first-hand experience in his early days of training in the anatomy laboratory. The National Institute of Occupational Safety and Health lists 52 occupations that expose people to formaldehyde. In recent years, however, the increasing use of formaldehyde resins in the production of building materials such as particleboard and urea-formaldehyde foam insulation has resulted in exposures of large numbers of people in nonoccupational settings. Consumer products such as cosmetics, cigarettes, textiles, furniture, draperies, and preservatives release formaldehyde. It is present in the outdoor atmosphere from products of combustion and automobile exhaust and likewise in the home from such things as gas cooking. These more widespread and increased exposures have resulted in concern regarding potential health effects. Therefore, it is likely that physicians have or will encounter patients who wish evaluations of a present or potential health effect from formaldehyde. This article is for the purpose of providing assistance in such evaluation.

Acute Disease↗
PubMed1984

Technical aspects of gaseous formaldehyde as a sterilant.

The design of a sterilizer for sterilization of heat sensitive items using gaseous formaldehyde and steam is described. The sterilizer is able to create a constant formaldehyde-steam concentration over a period of at least one hour. It is further able to operate at formaldehyde concentrations close to saturation with only small residues on sterilized plastic materials. The autoclave is used for measurement of formaldehyde solubility in polyolefines and poly(vinyl chloride) being approx. 15 and 250 ppm, respectively, at 70 degrees C and 30 mg HCHO I-1. The diffusion coefficient of formaldehyde in poly(vinyl chloride) is measured and is in the same order of magnitude as for ethylene oxide in poly(methyl methacrylate) i.e. 10(-10) cm2 s-1. Measurements of airborne formaldehyde in front of different sterilizers show that it is possible to design facilities meeting occupational exposure limits.

Diffusion↗
PubMed1994

The role of formaldehyde and S-chloromethylglutathione in the bacterial mutagenicity of methylene chloride.

Methylene chloride was less mutagenic in Salmonella typhimurium TA100/NG-11 (glutathione-deficient) compared to TA100, indicating that glutathione is involved in the activation of methylene chloride to a mutagen in bacteria. In rodents, the pathway of methylene chloride metabolism utilizing glutathione produces formaldehyde via a postulated S-chloromethylglutathione conjugate (GSCH2Cl). Formaldehyde is known to cause DNA-protein cross-links, and GSCH2Cl may act as a monofunctional DNA alkylator by analogy with the glutathione conjugates of 1,2-dihaloalkanes. The lack of sensitivity of Salmonella TA100 towards formaldehyde (Schmid et al., Mutagenesis, 1 (1986) No. 6, 427-431) suggests that GSCH2Cl is responsible for methylene chloride mutagenicity in Salmonella. In Escherichia coli K12 (AB1157), formaldehyde was mutagenic only in the wild-type, a characteristic shared with cross-linking agents, whereas 1,2-dibromoethane (1,2-DBE) was more mutagenic in uvrA cells (AB1886). Methylene chloride, activated by S9 from mouse liver, was mutagenic only in wild-type cells, suggesting a mutagenic role for metabolically derived formaldehyde in E. coli. Mouse-liver S9 also enhanced the cell-killing effect of methylene chloride in the uvrA, and a recA/uvrA double mutant (AB2480) which is very sensitive to DNA damage. This pattern was consistent with formaldehyde damage. However, a mutagenic role in bacteria for the glutathione conjugate of methylene chloride cannot be ruled out by these E. coli experiments because S9 fractions did not increase 1,2-DBE mutagenicity, suggesting lack of cell wall penetration by this reactive species. Rat-liver S9 did not activate methylene chloride to a bacterial mutagen or enhance methylene chloride-induced cell-killing, which is consistent with the carcinogenicity difference between the species.

Animals↗
PubMed1995

DNA-protein crosslink formation in rat nasal epithelial cells by hexamethylphosphoramide and its correlation with formaldehyde production.

Hexamethylphosphoramide (HMPA) is an aprotic polar solvent and nasal carcinogen in rats. The metabolism of HMPA to formaldehyde, another nasal carcinogen in rats, was found to be approximately 6 times greater in microsomes from olfactory tissues than from respiratory tissues (isolated from both male and female rats). HMPA was shown to induce formation of DNA-protein crosslinks (DPXLS) in isolated rat nasal epithelial cells. Using a filter binding assay, we demonstrated that microsomal activation is necessary for HMPA-induced crosslink formation between plasmid DNA and calf thymus histones, presumably through metabolic N-demethylation of HMPA and the formation of formaldehyde. Both formaldehyde production and DPXL formation were inhibited by pre-incubation of nasal mucosal extracts with metyrapone, an inhibitor of cytochrome P-450. Significant dose-dependent increases in DPXL formation were observed in respiratory and olfactory epithelial cells exposed to > or = 0.5 and 1 mM HMPA, respectively, for 3 h at 37 degrees C. This resulted in DPXL accumulation at 18-20% higher levels than untreated cells. Increases in DPXL formation in rat nasal epithelial cells cultured with 1 mM HMPA were inhibited by over 70% by co-administration of metyrapone. These data suggest that metabolic liberation of formaldehyde from HMPA is involved in the mechanism of HMPA-induced nasal carcinogenesis. Comparative studies showed formaldehyde to be more potent than HMPA in the induction of DPXL in nasal epithelium. However, induction of tumor formation after two years at 50 ppb HMPA and 6 ppm formaldehyde show the former to be active at several-fold lower concentrations. Therefore, other mechanisms are likely to be involved in HMPA nasal carcinogenesis.

Animals↗
PubMed1984

Endocytosis of formaldehyde-denatured serum albumin by nonparenchymal liver cells in vitro.

The uptake and degradation of 125I-labeled formaldehyde-denatured serum albumin in nonparenchymal rat liver cells were studied in vitro. Nonparenchymal cells bound formaldehyde-denatured serum albumin at two types of binding site, one with a high affinity and one a low affinity. The number of high affinity binding sites was approx. 10(5) per cell and the association constant, Ka 10(8) M-1. Inhibition of protein synthesis with cycloheximide did not affect the uptake and degradation of formaldehyde-denatured serum albumin suggesting reutilization of the binding sites. The presence of monensin-reduced uptake and degradation to less than 10% of control values. Pronase treatment of nonparenchymal liver cells completely abolished the uptake and degradation of the ligand. The uptake mechanism was not specific for formaldehyde-denatured serum albumin. Unlabeled acetylated, as well as malondialdehyde treated, serum albumin reduced the uptake of 125I-labeled formaldehyde-denatured serum albumin as effectively as unlabeled formaldehyde-denatured serum albumin itself.

Animals↗
PubMed1992

Radiolysis of aqueous formaldehyde relevant to cometary environments.

The radiation chemistry of aqueous solutions of formaldehyde was studied in order to obtain an insight into the possible role of ionizing radiation on cometary environments. Aqueous solutions of 1.0 mol dm-3 formaldehyde were exposed to gamma-radiation in the dose range from 0.01 to 1200 kGy at 298 K. The radiation chemical yield of decomposition of formaldehyde was determined to be: G(-CH2(OH)2)-26.3 +/- 1.2. The high radiation chemical yield of decomposition was explained by a chain reaction initiated by the radical CH(OH)2 with formaldehyde. Computer fitting of the experimental data gives k(CH(OH)2 + CH2(OH)2)- 8.0xl0(1) dm3 mol-1 s-1. In the computer treatment of experimental findings we used 54 equations to consider the radiolysis of water and 11 reactions for the radiolysis of aqueous formaldehyde. Based on previous estimates of the total dose of ionizing radiation that comets have accumulated over 4.6 billion years, we predict a radiation damage-depth curve of formaldehyde in comet nuclei.

Cobalt Radioisotopes↗
PubMed1988

Evaluation of the oral toxicity of acetaldehyde and formaldehyde in a 4-week drinking-water study in rats.

A subacute oral toxicity study of acetaldehyde and formaldehyde was carried out in rats. Groups of ten male and ten female 5-wk-old rats received one of the aldehydes in the drinking-water for a period of 4 wk, acetaldehyde being given at dose levels of 25, 125 and 675 mg/kg body weight/day and formaldehyde at dose levels of 5, 25 and 125 mg/kg body weight/day. A group of 20 males and 20 females served as controls and received unsupplemented drinking-water ad lib. An additional group of ten males and ten females was given unsupplemented drinking-water in an amount equal to the amount of liquid consumed by the group given the top dose of formaldehyde. Food and liquid intake were decreased in the groups on the top dose of both acetaldehyde and formaldehyde. Hyperkeratosis of the forestomach, observed only in the top-dose rats, was the only adverse effect of acetaldehyde detected. Effects of formaldehyde, also observed only in the top-dose group, were yellow discoloration of the fur, decreased protein and albumin levels in the blood plasma, thickening of the limiting ridge and hyperkeratosis in the forestomach, and focal gastritis in the glandular stomach. It was concluded that in this study the no-observed-adverse-effect levels of acetaldehyde and formaldehyde were 125 and 25 mg/kg body weight/day, respectively.

Acetaldehyde↗