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PubMed1992

Use of physical chemistry and in vivo exposure to investigate the toxicity of formaldehyde bound to carbonaceous particles in the murine lung.

Knowledge about the health effects of exposure to formaldehyde associated with automotive emissions is of pivotal importance in the risk assessment of this agent. Mobile sources emit many combustion-derived pollutants, including formaldehyde, in association with respirable carbon particles. Because it is hydrophilic, most of the inhaled formaldehyde is absorbed in the upper respiratory tract. However, if the organic vapor is adsorbed on respirable particles, formaldehyde may be deposited in the deep lung with the inhaled particles and may be available to interact adversely with cells along the lung parenchyma. On the respiratory surface, the alveolar macrophage phagocytic system plays the pivotal role in defending the lung against infectious agents. Susceptibility to respiratory infections is a relevant and sensitive indicator of the adverse effects of air pollution because acute and chronic exposures to a variety of air pollutants have been shown to decrease pulmonary antibacterial defenses. The goal of this research was to investigate whether exposure to formaldehyde decreases resistance to respiratory infections through dysfunctions of the alveolar macrophage phagocytic system. The study also explored whether interactions between formaldehyde and respirable carbon black particles alter susceptibility to respiratory infections and impairment of alveolar macrophage phagocytosis by delivering adsorbed formaldehyde to the deep lung with the inhaled particles. A carbon black, Regal GR, was used in these studies as a surrogate for the carbonaceous core of Diesel particulate matter. This material was selected to represent the worst-case scenario because the carbon black was expected to adsorb formaldehyde strongly. To accomplish this goal, mice were exposed to formaldehyde and to carbon black and formaldehyde combinations; increased susceptibility to respiratory infections was quantified by alveolar macrophage-dependent intrapulmonary killing of Staphylococcus aureus after an inhalation challenge with the bacterium. The salient findings of the bactericidal studies are as follows: Fifteen parts per million (ppm)* formaldehyde impaired the intrapulmonary killing of S. aureus when exposure followed the bacterial challenge. One ppm formaldehyde impaired the intrapulmonary killing of S. aureus when exposure preceded and was continued after the bacterial challenge. Coexposures to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde, or 10 mg/m3 carbon black and 5 ppm formaldehyde after the bacterial challenge had no effect on the intrapulmonary killing of S. aureus. Preexposure for four hours per day for four days to target concentrations of 3.5 mg/m3 carbon black and 2.5 ppm formaldehyde had no effect on the intrapulmonary killing of S. aureus when the assay was performed one day after the cessation of exposure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Mast cell response to formaldehyde. 1. Modulation of mediator release.

To examine the effects of the atmospheric pollutant formaldehyde on functionally distinct mast cells, peritoneal mast cells (PMC), intestinal mucosal mast cells (IMMC) and mouse bone-marrow-derived mast cells (BMMC) were incubated with various concentrations of formaldehyde. Pretreatment for 30 min with up to 100 micrograms/ml formaldehyde was not cytotoxic to mast cells. Formaldehyde (1-10 micrograms/ml) alone induced low levels of histamine release (< 10%) from IMMC and BMMC. Antigen-induced histamine release was significantly increased in both PMC pretreated with low concentrations of formaldehyde (5-20 micrograms/ml) and BMMC pretreated with 10 micrograms/ml formaldehyde but decreased in PMC pretreated with a higher concentration (100 micrograms/ml) of formaldehyde. By contrast, antigen-induced histamine release was decreased in IMMC pretreated with formaldehyde in a dose-dependent manner. Histamine release stimulated with A23187 was also increased in PMC pretreated with a low concentration (10 micrograms/ml) of formaldehyde but decreased in those pretreated with a higher concentration (100 micrograms/ml) of formaldehyde. Pretreatment with 10 micrograms/ml formaldehyde significantly enhanced beta-hexosaminidase release from PMC stimulated with antigen or A23187. Compared to sham-treated PMC, PMC pretreated with formaldehyde expressed a markedly depressed natural cytotoxicity for the tumor target WEHI-164 (an assay of tumor necrosis factor alpha activity). These results suggest that formaldehyde modifies various mast cell functions through alterations in cellular metabolism. Such effects may be important in respiratory and other diseases associated with formaldehyde exposure.

Animals↗

PubMed1976

[Microbial resistance to formaldehyde. I. Comparative quantitative studies in some selected species of vegetative bacteria, bacterial spores, fungi, bacteriophages and viruses].

The resistence of different microorganisms to formaldehyde was determined. As test objects served gram-negative and gram-positive vegetative germs (Klebsiella pneumoniae, Pseudomonas aeruginosa, Salmonella paratyphi-B, Staphylococcus aureus, Streptococcus faecalis), bacterial spores (Bacillus cereus, Bacillus pumilus, Bacillus stearothermophilus, Bacillus subtilis), fungi (Aspergillus niger, Candida albicans), bacteriophages (Escherichia coli phages, T1, T2, T3), and viruses (adenovirus, poliomyelitis virus, vaccinia virus). For the studies, suspensions of germs were exposed at identical temperature (20 degrees C) and pH (7.0). The microbicidal effect of formaldehyde was measured by the decrease of the proportion of germs capable of multiplication in the suspension (lg (N/N0); where: N0 equals initial number of germs capable of multiplication; N equals number of germs capable of multiplication after exposure to formaldehyde). For all germs the dependence of the microbicidal effect on the concentration of formaldehyde was determined. In all experiments, the duration of exposure was two hours. Pseudomonas aeruginosa, Klebsiella pneumoniae, and Salmonella paratyphi-B were found to be more susceptible than Staphylococcus aureus (vf. Fig. 1 A). The strains of Pseudomonas aeruginosa used were widely varying as to their susceptibility. To obtain equal microbicidal effects, concentrations of formaldehyde almost three times as high had to be used for the most resistant strain than were necessary for the most susceptible strain of Pseudomonas aeruginosa. All strains of Klebsiella pneumoniae examined were found to have an identical resistence to formaldehyde. Streptococcus faecalis was even more resistant to formaldehyde than Staphylococcus aureus. In the case of Streptococcus faecalis, a concentration of formaldehyde about three times as high had to be used to obtain microbicidal effects of identical magnitude. For the killing of Candida albicans cells concentrations of formaldehyde not higher than those needed for the killing of vegetative gram-negative bacteria were necessary. The conidia of Aspergillus niger were found to be more resistant than the cells of Candida albicans but did not require any higher concentrations than for the killing of Staphylococcus aureus (see Fig. 1 B). In the case of bacterial spores, a special phenomenon was observed. If the spores had been exposed to a temperature of 80 and 95 degrees C, respectively (depending on the species involved) for one or two hours following exposure to formaldehyde, a considerably higher number of spores was found to be capable of germination and colony formation than without such treatment (heat activation: cf. Fig. 2A and Fig. 2B). The spores of Bacillus cereus had only a relatively low resistance to formaldehyde. To reduce the proportion of the spores capable of colony formation to 1/10000, a 2.9% formaldehyde concentration was necessary without heat activation and one of 10.8% with heat activation...

Adenoviridae↗

PubMed1991

Regional increases in rat nasal epithelial cell proliferation following acute and subchronic inhalation of formaldehyde.

Short-term studies (9 days) in the rat have demonstrated that formaldehyde-induced nasal epithelial lesions are associated with increases in surface epithelial cell proliferation rates. The present studies were designed, in part, to investigate cell proliferation rates in the nasal epithelium of rats exposed to formaldehyde for a longer duration in order to determine if correlations exist between (1) the concentration-response in cell proliferation rate with the previously published formaldehyde bioassay tumor response; (2) sites of increased cell proliferation and the regions of the nasal passages that exhibit formaldehyde-induced cytotoxicity; and (3) sites of increased cell proliferation and the regions of the rat nasal passages previously determined to be most susceptible to neoplasia (i.e., the lateral meatus and nasal septum of the anterior nasal passages). Another important endpoint of this study was to provide data for a comparison of formaldehyde-induced responses in rats with previous findings in rhesus monkeys. Fischer-344 rats were exposed to 0, 0.7, 2, 6, 10, or 15 ppm formaldehyde for up to 6 weeks and pulse labeled with tritiated thymidine prior to each scheduled termination. Exposure to formaldehyde at 6 ppm or higher induced site-specific lesions in the nasal respiratory epithelium and was associated with increases in cell proliferation rate which remained statistically elevated throughout the 6 weeks. While a direct correlation between sites susceptible to formaldehyde-induced nasal cancer and increased cell proliferation was not evident, results from the present studies did demonstrate a clear correlation between sites of cellular injury and increases in cell proliferation and a concentration-dependent response which correlated with the previously published formaldehyde bioassay tumor response. Furthermore, this work demonstrated that formaldehyde-induced responses in rats exposed to 6 ppm were morphologically similar to those reported in the rhesus monkey; however, the distribution of lesions between the two species differed significantly.

Administration, Inhalation↗

PubMedDate not supplied

Formaldehyde-related antibodies in hemodialysis patients.

In a study of anti-N-like antibodies, we tested sera from 93 hemodialysis patients for hemagglutination reactions with untreated and formaldehyde-treated reagent red blood cells. Six of 22 sera from patients who had been dialyzed with formaldehyde-sterilized membranes had anti-N-like activity and 20 (91%) specifically agglutinated formaldehyde-treated red blood cells. Sera from 71 patients dialyzed with disposable membranes neither had anti-N-like activity nor agglutinated formaldehyde-treated red blood cells. The agglutination of formaldehyde-treated red blood cells by sera from hemodialysis patients was unrelated to MNU phenotypes and, therefore, identified a second serologic specificity, provisionally termed "anti-formaldehyde." "Anti-formaldehyde" was absorbed by and eluted from NN red blood cells as well as from formaldehyde-treated red blood cells regardless of MNU phenotype. All eluates and sera containing anti-N-like activity also agglutinated formaldehyde-treated red blood cells, typically after the addition of anti-human serum. These findings are consistent with the hypothesis that anti-N-like reactions of hemodialysis patients' sera represent cross reactions of formaldehyde related antibodies with N antigens of normal red blood cells.

Absorption↗

PubMed1992

Lung cancer mortality among industrial workers exposed to formaldehyde: a Poisson regression analysis of the National Cancer Institute Study.

The Formaldehyde Institute (FI) sponsored additional Poisson regression analysis of lung cancer mortality data from the joint National Cancer Institute (NCI)/FI cohort study of workers exposed to formaldehyde to investigate the previously reported effects of plant and latency period and to assess the impact of short-term workers (under 1 yr employment) on the results. There were 242 lung cancer deaths in this cohort of 20,067 white male workers. With OCMAP software, lung cancer death rates for the white males in this cohort were computed by plant, age, calendar time, and job type for several time-dependent formaldehyde exposures, including formaldehyde exposure in the presence of 12 selected co-exposures: ammonia (AM), antioxidants (AN), asbestos (AS), carbon black (CB), dyes/inks/pigments (DY), hexamethylenetetramine (HX), melamine (ME), particulates (PT), phenol (PH), plasticizers (PL), urea/urea compounds (UR), wood dust (WD), and a composite co-exposure (X5) involving AN, HX, ME, PH, and UR.A 1.6-fold increase in lung cancer risk was found, beginning approximately 16-20 yr after first employment in the study plants with no evidence of a differential effect of latency between hourly and salaried workers or among the various categories of formaldehyde exposure as measured by cumulative average intensity or length of exposure. The statistically significant heterogeneity in lung cancer risk among the 10 plants could not be explained by interplant differences in cumulative or average intensity of exposure to formaldehyde, either without regard to co-exposures or in the presence of any of the 12 co-exposures considered individually. Plant was not a statistically significant predictor of lung cancer risk when cumulative exposure to the composite X5 was included in the model, suggesting that some component of X5, or a correlate, could at least partly account for the overall heterogeneity. No significant associations were found for cumulative, average, or length of exposure to formaldehyde without regard to co-exposure, but positive associations were found for cumulative exposure to formaldehyde in the presence of several co-exposures (AN, HX, ME, PH, and UR). For workers who were never exposed to any of 10 co-exposures associated with an increased lung cancer risk, there was a decreasing pattern of estimated lung cancer risk ratios relative to cumulative formaldehyde exposure. Similar patterns were seen when the analysis was restricted to the long-term workers. Analysis of the internal cohort rates corroborates previous analyses of NCI/FI cohort data in that significant positive associations were found between the risk of lung cancer and cumulative exposure to formaldehyde in the presence of several of the same co-exposures. No such associations were found in the absence of these co-exposures.

Adult↗

PubMed1992

A survey of formaldehyde in shampoos and skin creams on the Danish market.

To evaluate the exposure of the general population to formaldehyde from the use of cosmetic products, as well as to monitor whether cosmetic products comply with national regulations, 285 shampoos, creams, etc., were analysed for formaldehyde. Identification and determination of formaldehyde was performed by the EEC method for the analysis of formaldehyde in cosmetic products. It was shown that 29.5% of the products investigated contained 0.001%-0.147% total formaldehyde. In 10 of the products (3.5%), total formaldehyde content was > 0.05%. 8 of these products contained > 0.05% free formaldehyde. None of these products was labelled 'contains formaldehyde'. 17 of the products investigated were declared to contain specific formaldehyde-releasers. Formaldehyde could not be detected (detection limit 0.001%) in cosmetic products that were declared to contain Bronidox/Bronopol.

Chromatography, High Pressure Liquid↗

PubMed1992

Structural determinants for alcohol substrates to be oxidized to formaldehyde by rat liver microsomes.

Glycerol can be oxidized to formaldehyde by rat liver microsomes and by cytochrome P450. The ability of other alcohols to be oxidized to formaldehyde was determined to evaluate the structural determinants of the alcohol which eventually lead to this production of formaldehyde. Monohydroxylated alcohols such as 1- or 2-propanol did not produce formaldehyde when incubated with NADPH and microsomes. Geminal diols such as 1,3-propanediol, 1,3-butanediol, or 1,4-butanediol also did not yield formaldehyde. However, vicinal diols such as 1,2-propanediol or 1,2-butanediol produced formaldehyde. With 1,2-propanediol, the residual two-carbon fragment was found to be acetaldehyde, while with 1,2-butanediol, the residual three-carbon fragment was propionaldehyde. Oxidation of 1,2-propanediol to formaldehyde plus acetaldehyde involved interaction with an oxidant derived from H2O2 plus nonheme iron, since production of the two aldehydic products was completely prevented by catalase or glutathione plus glutathione peroxidase and by chelators such as desferrioxamine or EDTA. The oxidant was not superoxide or hydroxyl radical. Product formation was fivefold lower when NADH replaced NADPH, and was inhibited by substrates, ligands, and inhibitors of cytochrome P450. A charged glycol such as alpha-glycerophosphate (but not the geminal beta-glycerophosphate) was readily oxidized to formaldehyde, suggesting that interaction of the glycol with the oxidant was occurring in solution and not in a hydrophobic environment. These results indicate that the carbon-carbon bond between 1,2-glycols can be cleaved by an oxidant derived from microsomal generated H2O2 and reduction of non-heme iron, with the subsequent production of formaldehyde plus an aldehyde with one less carbon than the initial glycol substrate.

Acetaldehyde↗

PubMedDate not supplied

[Behaviour of DNA-RNase A complex in the presence of formaldehyde].

A formaldehyde-produced fixation of defects caused by a despiralizing action of a protein was studied in the case of DNA-RNAase A complex. The concentration of the defects fixed was measured by kinetic formaldehyde method (KF-method). It was shown that following processes take place in the complex in the presence of formaldehyde: (a) fixation of defects; (b) unwinding of DNA; (c) inactivation of the protein. The rates of all these processes depend on the concentration of formaldehyde, phi. At formaldehyde concentrations above some critical value phic the protein is inactivated before the defects are fixed. At phi less than phic the protein inactivation proceeds more slowly than the fixation of defects; at sufficiently low formaldehyde concentration no inactivation of protein occurs practically during the fixation time (20 min). The number of new defects formed during the time of fixation is linear with the formaldehyde concentration in the region where no inactivation of the protein occurs. Therefore the initial concentration of defects can be determined through an extrapolation to zero concentration of formaldehyde. On the basis of the data obtained a method is proposed for the evaluation of the number of defects in DNA caused by the despiralizing action of proteins. A model is proposed describing the behaviour of the complexes of DNA with despiralizing proteins in the presence of formaldehyde.

DNA↗

PubMed1976

[The formaldehyde content in fish in relation to anemia in mink (author's transl)].

The fish-induced anemia in mink is an alimentary disease produced by feeding high amounts of some raw marine fishes. The anemiogenic properties of the fish has been related mainly to its content of the iron binding agent-trimethylaminoxide. The aim of the present investigation was to examine how far formaldehyde could also play a part as an anemiogenic factor. The content of formaldehyde has been analysed in all species of raw, cold stored fish known to be used in mink food and in a few samples of ready made food (Table II). The content of formaldehyde varied within wide limits from 12 to 105 ppm, but none of the measured contents reached the high values obtained by Costly (1970). The mean values of formaldehyde in gutted coalfish, fillet waste of coal fish, cod and haddock prepared for the feeding experiments, were all close to 50 ppm. 175 female mink and 632 mits were tested during the whole of the breeding period from 15.2-30.6, 80 per cent of the diet (page 1) was fish products with and without supplements of formaldehyde. Amounts from 200 to 50 ppm were tried (Table I). The supplement of 200 ppm formaldehyde had an appetite-decreasing and anemiogenic effect, but the supplement of 50 ppm, i.e. a formaldehyde content up to the highest value observed in fillet waste, had no effect on appetite or hemoglobin synthesis neither in females nor in kits. This content of formaldehyde did not counteract the anti-anemiogenic effect of iron glutamate. The fish-induced anemia occurred in mink thus appears unaffected by the quantities of formaldehyde found in fish diets to fur bearing animals. Triox must be regarded as the dominant anemiogenic factor in raw fish diets.

Anemia↗

PubMed1979

[Formaldehyde in hair shampoos].

In most hair shampoos commercially available in Western Germany formaldehyde or formaldehyde liberating substances serve as efficient preservatives especially in shampoos of the lower price group. Besides, PHB-ester, mercury containing substances and since recently brome compounds are used for this purpose. We observed a 15 year old patient who developed an allergic contact dermatitis from formaldehyde in a hair shampoo. However, compared to the widespread opportunities of exposure allergic contact dermatitis caused by hair shampoos is not very frequent. For this rarity of formaldehyde dermatitis caused by shampoos the short period of application and the low concentration because of the high dilution and perhaps the low contact dermatitis reactivity of the scalp are responsible. After all only two out of thirtyone thoroughly questioned patients, who had acquired a professional formaldehyde sensitivity elsewhere, reported a contact dermatitis caused by shampoos, which by the way appeared in the orbital region as typical. Probably allergic contact dermatitis from formaldehyde in shampoos will be expected in patients with a formaldehyde sensitivity acquired formerly elsewhere, especially professionally. To those patients formaldehyde free hair shampoos should be recommended. The declaration of formaledehyde in cosmetics, which will be legally obligatory in Germany in 1979, will be valuable for finding out the alternate products free of formaldehyde.

Adolescent↗

PubMed1992

Allergic contact dermatitis from formaldehyde resins in permanent press clothing: an underdiagnosed cause of generalized dermatitis.

BACKGROUND AND METHODS: Formaldehyde resins have been used to impart wrinkle resistance to clothing fabrics since 1926. After several patients with positive patch tests to formaldehyde resins had been examined, a study was undertaken of the records of all patch tests performed at the University of Louisville Patch Test Clinic and the Allergy Section of the Skin and Cancer Clinic of New York University Medical Center from January 1988 through April 1990 to determine the prevalence of positive patch-test reactions to formaldehyde-based textile resins and the clinical and demographic patterns associated with textile resin allergy. RESULTS: Seventeen patients were identified at the two centers. Twelve were allergic to formaldehyde as well as to formaldehyde textile resins. Several clinical patterns were found, including accentuation of dermatitis in areas of tight clothing, primary occurrence in clothing-covered areas, and a chronic recalcitrant course. Ethylene urea melamine formaldehyde resin was the best screening agent with 14 definite positive reactions and one equivocal reaction. CONCLUSION: Formaldehyde textile resin allergy is more common than has been previously recognized. Patch testing with one or more formaldehyde textile resins is indicated in patients with a particular pattern of dermatitis.

Adult↗

PubMed1992

Mast cell response to formaldehyde. 2. Induction of stress-like proteins.

Previously we established that immediately after pretreatment with low concentrations (5-10 micrograms/ml) of formaldehyde antigen- and ionophore-induced histamine secretion was enhanced from peritoneal mast cells (PMC) isolated from rats infected with Nippostrongylus brasiliensis. In contrast to immediately following pretreatment with low concentrations of formaldehyde, 3 h after a 30-min treatment with formaldehyde (10, 50 and 100 micrograms/ml) antigen-induced histamine secretion from PMC was significantly depressed, and 35S-methionine incorporation was also decreased. To further explore the effects of formaldehyde on mast cells, we investigated protein biosynthesis of PMC following formaldehyde treatment and compared this with the effects of hydrogen peroxide (H2O2) or heat treatment. One- and two-dimensional SDS-PAGE were used to assess the effects. Formaldehyde treatment induced the synthesis of 70- and 72-kD stress-like proteins in rat PMC. Pretreatment of PMC with 50 microM H2O2 and heat (45 degrees C) also induced proteins with the same molecular weight. Two-dimensional SDS-PAGE analysis established that formaldehyde-induced 70-kD proteins had the same pI values as 70-kD heat shock proteins previously observed in mammalian cells. These results suggest that formaldehyde, H2O2 and heat shock induce stress proteins in rat PMC. It will be important to establish whether or not these stress proteins are responsible for the functional alterations observed in the mast cells.

Animals↗

PubMed1992

Possible mechanisms of formaldehyde-induced discomfort in the upper airways.

Occupational exposure to formaldehyde often causes nasal discomfort. The objective of this study was to determine whether chronic exposure to formaldehyde causes annoying symptoms by direct irritation and whether it affects all exposed people (through hyperreactivity in atopic persons, through formaldehyde-induced hyperreactivity also in nonatopic persons, or through an immunologically mediated, immediate type 1 reaction to formaldehyde itself). It was found that about 50% of the studied population of 66 workers occupationally exposed to formaldehyde during formaldehyde production experienced nasal discomfort through hyperreactivity. Atopics were not significantly overrepresented among the persons with occupational nasal symptoms. Two workers with isolated occupational nasal discomfort, and sensitized by long-term inhalation, had a positive radioallergosorbent test for formaldehyde. The conclusion was reached that exposure to formaldehyde should be minimized as much as possible for all people, not only for atopic persons.

Adult↗

PubMed1976

[Control of disinfection with formaldehyde].

The reliability of a simple method of formaldehyde disinfection control, based on the colour intensity of End's agar or sulphite agar, was tested in a sealed fume chamber 1.2 cubic metres in size at a constant air temperature (21 degrees C) and at a 40-per-cent or 95-per-cent humidity. The effect of formaldehyde concentration and air humidity was examined, as exerted on bactericidal effectiveness and on the colour intensity of the mentioned media. Air humidity proved to be highly important: together with formaldehyde concentration and exposure time, air humidity is the decisive factor underlying the final effect of disinfection if due temperature is maintained. The intensity of the colouring of End's agar or sulphite agar was found to depend mainly on concentration and slightly on air humidity. Hence it is recommended that this simple control should be used only for the testing of a good sealing of the disinfected space underlying the effect of the active concentration of formaldehyde for the necessary exposure time. End's agar, produced by the Imuna National Corporation, Sarisské Michal'any, gave better results. It is considered necessary for an estimation of formaldehyde disinfection effectiveness to record, at the same time, the humidity and temperature of the air in the disinfected space. In our trials at a 95-per-cent humidity level, E. coli was totally devitalized on carriers disinfected with formaldehyde developed from 25 ml formaline and St. aureus with formaldehyde developed from more than 50 ml formaline per 1 cubic metre of space. When the air humidity level was 40% the total devitalization of the mentioned bacterial strains was not achieved even with formaldehyde concentration developed from 75 ml formaline per 1 cubic metre of space.

Agar↗

PubMed1975

Biochemical aspects of aldehyde fixation and a new formaldehyde fixative.

In this paper, it is assumed that tissue fixation is a process in which the proteins become less soluble and catabolic reactions stop. With this definition in mind, 2.5 and 5% glutaraldehhde and 4% formaldehyde in 0.1 M potassium phosphate buffer, pH 7.4, were compared with a new fixative, bicarbonate-formaldehyde. The following results were obtained. (I) With 2.5 and 5% glutaraldehyde, the solubility of tissue proteins were not decreased unifromly, and tissue glycogen was poorly preserved. (2) 4% formaldehyde in potassium phosphate buffer gave relatively good results. (3) Bicarbonate-formaldehyde decreased the solubility of tissue proteins reliably and preserved tissue glycogen perfectly. Histologically, it yielded excellent results. Since glutaraldehyde alters the properties of proteins substantially (Hopwood, 1972; Habeeb & Hiramoto, 1968), and since the natural appearance of tissues depends on native tissue proteins, formaldehyde-containing fixatives, in particular bicarbonate-formaldehyde, are preferable to glutaraldehyde-containing fixatives for all tissue preparative techniques. However, it is important that the fixation time in formaldehyde is kept short.

Aldehydes↗

PubMed1992

Effect of formaldehyde on the efficiency of hybridization of DNA immobilized on nitrocellulose filters.

We report in this study that under certain conditions formaldehyde interacts with DNA and makes it more efficient for hybridization on nitrocellulose filters. Hybridization signals of formaldehyde-treated DNA are stronger (up to 10 fold) as compared with that of the heat- or alkali-denatured DNA. Various parameters of the DNA-formaldehyde reaction are optimized as follows: (a) 6 x SSC, 10% formaldehyde, 60 degrees C, 20-30 min, reaction volume 10-200 microliters or (b) 6 x SSC, 5% formaldehyde, 98 degrees C, 15 min, reaction volume 10-200 microliters. Treatment of agarose gels after electrophoresis with formaldehyde improved both the transfer of DNA and the efficiency of hybridization. The following conditions are recommended for gel treatment: denaturation in 0.3 N NaOH, 1 M NaCl followed by neutralization with 0.5 M phosphate buffer, pH 7.0, containing 10% formaldehyde at 60 degrees C for 20 min.

Collodion↗

PubMed1992

Perspectives on formaldehyde toxicity: separating fact from fantasy.

Formaldehyde (IUPAC name, methanal) is one of the simplest, most ubiquitous molecules in our environment and troposphere. Exposure to large amounts of formaldehyde can produce a variety of respiratory and dermatologic problems in humans, in both the home and the workplace. However, in spite of anecdotal reports on formaldehyde-induced illness over the past 20 years there is a paucity of data regarding its potential as either an allergen or an antigen in humans. In addition, many of our current impressions about formaldehyde are based on studies of dubious scientific validity. In this review, we discuss the biological and chemical properties of formaldehyde and its presence in materials which we come in contact with, and finally attempt to put in perspective our current understanding of the detrimental effects of formaldehyde on our health, or lack thereof. There is no evidence at present that formaldehyde causes immunological diseases. Finally, and unfortunately, many of the studies have drawn invalid conclusions and are based on poorly controlled anecdotal observations.

Animals↗