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PubMed1986

Mortality among industrial workers exposed to formaldehyde.

A historical cohort study evaluated the mortality experience of 26,561 workers employed in 10 formaldehyde-producing or -using facilities. Approximately 600,000 person-years of follow-up accrued as workers were followed to January 1, 1980. Estimates of historical exposure to formaldehyde by job were developed by project industrial hygienists using monitoring data available from participating plants, comments from long-term workers, and comprehensive monitoring data specifically collected for this study. Mortality from all causes combined was about as expected [standardized mortality ratio (SMR) = 96] based on mortality rates of the general U.S. population. Significantly fewer deaths occurred from infective and parasitic diseases (SMR = 51) and from accidents (SMR = 72) than expected. Cancer overall was not related to formaldehyde exposure. Workers exposed to formaldehyde had slight excesses for Hodgkin's disease and cancers of the lung and prostate gland, but these excesses were not consistently related to duration of or average, cumulative, or peak formaldehyde exposure levels. Recent animal studies found nasal cancer among rats exposed to formaldehyde, but no excess of this tumor occurred in this study. Mortality from brain cancer and leukemia among these industrial workers was not excessive in contrast to reported excesses among professional groups (e.g., anatomists, embalmers, and pathologists) with exposure to formaldehyde. Although there was a deficit for cancer of the buccal cavity and pharynx, mortality from certain subsites, i.e., the nasopharynx and oropharynx, was elevated. These subsites did not, however, show a consistently rising risk with level of exposure. These data provide little evidence that mortality from cancer is associated with formaldehyde exposure at levels experienced by workers in this study.

Adult↗
PubMed1985

Canine antibodies against formaldehyde-dog serum albumin conjugates: induction, measurement, and specificity.

Formaldehyde-dog serum albumin (F-DSA) conjugates were prepared as soluble haptenized proteins. The F-DSA reacted with rabbit anti-DSA. Change in electrophoretic migration of F-DSA as compared with DSA demonstrated conjugation. The more rapid migration toward the anode of F-DSA implied deletion of positive charges on DSA by conjugation with formaldehyde. F-DSA was antigenic for dogs when given intravenously as solution or subcutaneously in Freund's complete adjuvant. Intravenously administered formaldehyde resulted in an anti-F-DSA response, presumably caused by F-DSA forming in vivo. Canine IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay. Canine anti-F-DSA has specificity for neither formaldehyde nor DSA alone, as determined by inhibition analysis, indicating that the antigenic determinant of F-DSA for dogs is a combination of formaldehyde and a new antigenic determinant formed on DSA. Immediate-type hypersensitivity occurred transiently in dogs immunized intravenously with formaldehyde or F-DSA. Finally, exposure of DSA to formaldehyde either in vivo or in vitro results in alteration of DSA molecules and an immune response to that altered DSA as well as to commercial DSA. Such results have previously been seen with formaldehyde in rabbits or with glutaraldehyde by other investigators.

Animals↗
PubMed1982

Formaldehyde asthma: challenge exposure levels and fate after five years.

Because of current concern regarding possible adverse health effects of formaldehyde, we have reinvestigated two renal dialysis unit nurses shown to have formaldehyde asthma by inhalation provocation tests in 1973 and 1975, respectively. Their original tests were repeated and the formaldehyde levels generated (previously unknown) were measured. One nurse had not worked with formaldehyde since 1976 and had had no further symptoms. Her 1981 test (15-minute exposure to 6 parts per million [ppm] formaldehyde) provoked no asthmatic response. The other nurse had continued to work with formaldehyde, though under much improved conditions, and mild intermittent attacks of asthma had continued. Her test (five-minute exposure to 3 ppm formaldehyde) provoked a late asthmatic reaction similar to that observed in 1975. We conclude that in sensitized subjects specific late asthmatic reactions may be provoked by brief exposures to formaldehyde at about the current Occupational Safety and Health Administration standard (3 ppm); and that while asthmatic responsiveness may persist with continuing low levels of intermittent exposure, it may be lost following complete cessation of exposure.

Adult↗
PubMed1995

[Microbial resistance to formaldehyde. III> Dependence of the microbial effect on Staphylococcus aureus, Enterococcus faecium and spores of Bacillus stearothermophilus on temperature].

Temperature dependence of microbicidal efficacy of formaldehyde was examined with suspension tests (pH 7.0). Test germs were Staphylococcus aureus, Enterococcus faecium and spores of Bacillus stearothermophilus. The methodology was nearly the same as in previous investigations (5, 7). At given exposure periods and temperatures formaldehyde concentrations necessary to produce a microbicidal effect of log (N/N0) = -4.0 (concentrations of equal efficacy) were determined. N and N0 represent the numbers of colony-forming units in suspensions with and without formaldehyde, respectively. On rectangular graphic representation with the reciprocal value of absolute temperature on the abscissa and with the logarithm of the formaldehyde concentration on the ordinate, the formaldehyde concentrations of equal efficacy fitted straight lines. Lines referring to different exposure periods nearly paralleled each other. With increasing exposure periods the steepness of the lines decreased slightly. This effect was most pronounced with Staphylococcus aureus as a test germ. The ratio of formaldehyde concentrations of equal efficacy for exposure periods of 120 minutes at 20 degrees C and 30 degrees C, respectively, was 3.1:1 with Staphylococcus aureus, and 2.8:1 with Enterococcus faecium. The corresponding ratio obtained with spores of Bacillus stearothermophilus and referring to 60 degrees C and 70 degrees C, respectively, was 3.6:1. The logarithms of these ratios decreased with temperature in the same measure as the pertinent absolute temperatures increased. On the basis of the previously presented three-dimensional model of the relations between concentration, period of action and efficacy of microbicidal agents, it could be shown that deviations of the results from a linear and parallel course reflect an inconstant concentration exponent. When low formaldehyde concentration, long exposure period and "high" temperature coincide, the efficacy of formaldehyde is lower than calculated for a linear and parallel course of the relation.

Drug Resistance, Microbial↗
PubMed1994

[Contamination of waters by formaldehyde].

The high toxicity of formaldehyde and its relatively high number of release sources called for extensive studies for elucidating its sources and the degree of contamination of waters in Poland with this compound. In the study formaldehyde was determined in community sewage, industrial sewage and precipitations in the street, as well as in surface waters, waters taken for supplying networks and drinking waters. It was tried also to establish the possible influence of meteorological factors on formaldehyde presence in surface waters. Formaldehyde was determined by the colorimetric method with chromotropic acid after previous distillation of the analysed samples of waters and sewage. It was found in these studies that the main source of contamination of surface waters with formaldehyde are community sewage and industrial sewage. In summer the concentration of formaldehyde in these waters was higher than in winter. It is stressed that the maximal values of these concentrations in studied waters were above the acceptable value, even several times. Despite this unfavourable situation it was found that in tap water obtained from rivers this contamination was negligible, and after treatment it contained practically no formaldehyde. Thus formaldehyde in drinking water is not a health risk for the population.

Environmental Monitoring↗
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↗
PubMed1996

Correlation of regional and nonlinear formaldehyde-induced nasal cancer with proliferating populations of cells.

Formaldehyde induces nonlinear, concentration-related increases in nasal epithelial cell proliferation and squamous cell carcinomas (SCC) in rats. A formaldehyde carcinogenicity study was conducted in which a major end point was correlation of cell proliferation indices with sites of formaldehyde-induced SCC. A poor correlation in certain sites led to incorporation of the number of cells in each site into the correlation. Rats were exposed (6h/day, 5 days/week) to formaldehyde (0, 0.7, 2, 6, 10 or 15 ppm) for up to 24 months with interim sacrifice time points at 3, 6, 12, and 18 mo. A unit length labeling index (ULLI; S-phase nuclei/mm basement membrane) was determined for specific nasal regions in addition to a population-weighted ULLI (PWULLI). The PWULLI was defined as the product of regional ULLI and total number of nasal epithelial cells in the respective site. Nasal SCC sites of origin were mapped. Formaldehyde induced SCC in a highly nonlinear fashion, with no observed effect at the level of 2 ppm, a minimal response at 6 ppm, and a sharp increase at 10 and 15 ppm. The tumor incidence was 1, 22, and 47% at 6, 10 and 15 ppm, respectively. ULLI was significantly (P<0.05) increased at 10 and 15 ppm but not at the lower concentrations. There was a good correlation between PWULLI and regional tumor incidence (R(2) = 0.88), while the correlation of regional SCC with ULLI was relatively poor (R(2) = 0.46). We conclude that target cell population size and sustained increases of cell proliferation in these populations, determined by differences in regional airflow-driven formaldehyde binding to DNA dose to these sites, coupled with the known nonlinear kinetics of formaldehyde binding to DNA, can together account for the nonlinearity and site specificity of formaldehyde-induced nasal SCC in rats.

Animals↗
PubMed1998

Epidoxoform: a hydrolytically more stable anthracycline-formaldehyde conjugate toxic to resistant tumor cells.

The recent discovery that the formaldehyde conjugates of doxorubicin and daunorubicin, Doxoform and Daunoform, are cytotoxic to resistant human breast cancer cells prompted the search for hydrolytically more stable anthracycline-formaldehyde conjugates. Doxoform and Daunoform consist of two molecules of the parent drug bound together with three methylene groups, two forming oxazolidine rings and one binding the oxazolidines together at their 3'-amino nitrogens. The 4'-epimer of doxorubicin, epidoxorubicin, reacts with formaldehyde at its amino alcohol functionality to produce a conjugate, Epidoxoform, in 59% yield whose structure consists of two molecules of epidoxorubicin bound together with three methylene groups in a 1, 6-diaza-4,9-dioxabicyclo[4.4.1]undecane ring system. The structure was established from spectroscopic data and is consistent with products from reaction of simpler vicinal trans-amino alcohols with formaldehyde. Epidoxoform hydrolyzes at pH 7.3 to an equilibrium mixture with dimeric and monomeric epidoxorubicin-formaldehyde conjugates without release of formaldehyde or epidoxorubicin. The hydrolysis follows the rate law (A if B) if C + D where A (Epidoxoform) is in rapid equilibrium with B, and B is in slow equilibrium with C and D. The forward rate constant for A/B going to C+D gives a half-life of approximately 2 h at 37 degrees C. At equilibrium the mixture is stable for at least 2 days. At pH 6.0, hydrolysis proceeds with first-order kinetics to epidoxorubicin and formaldehyde with a half-life of 15 min at 37 degrees C. Epidoxoform and epidoxorubicin plus formaldehyde react with the self-complementary DNA octamer (GC)4 to yield five drug-DNA adducts which have structures analogous to the doxorubicin-DNA adducts from reaction of Doxoform with (GC)4. Epidoxoform is 3-fold more toxic to MCF-7 human breast cancer cells and greater than 120-fold more toxic to MCF-7/ADR resistant cells than epidoxorubicin. Epidoxoform in equilibrium with its hydrolysis products is greater than 25-fold more toxic to resistant cells with respect to epidoxorubicin.

Antibiotics, Antineoplastic↗
PubMed2005

Hydrothermal carbon-carbon bond formation and disproportionations of C1 aldehydes: formaldehyde and formic acid.

Hydrothermal reaction pathways and kinetics of C1 (carbon-one) aldehydes, formaldehyde (HCHO) and formic acid (HCOOH = HOCHO), are studied at 225 degrees C without and with hydrochloric acid (HCl) up to 0.6 M (mol dm(-3)). Reactions unveiled are the following: (i) the self-disproportionation forming methanol and formic acid, a redox reaction between two formaldehydes, (ii) the cross-disproportionation forming methanol and carbonic acid, a redox reaction between formaldehyde and formic acid, and (iii) the acid-catalyzed C-C bond formation producing glycolic acid (HOCH2COOH) as a precursor of the simplest amino acid, glycine. Reaction iii is a hydrothermally induced chemical evolution step from C1 aldehydes, formaldehyde and formic acid. Disproportionations i and ii are found to proceed even without base catalysts unlike the classical Cannizzaro reaction. Acid catalyzes the self-disproportionation (i) and the C-C bond formation (iii), but retards the cross-disproportionation (ii). The rate constants of noncatalyzed and acid/base-catalyzed paths for reactions i, ii, and iii are given additively as 2 x 10(-4) + (2 x 10(-3))[H+], 10(-4) + 10(3)[OH-], and (2 x 10(-3))[H+] M(-1) s(-1), respectively; the concentrations of proton [H+] and hydroxide ion [OH-] are expressed in M. The rate constant of the noncatalytic (neutral) cross-disproportionation is 1 order of magnitude larger than that of the self-disproportionation. The reaction pathways are controlled on the basis of the kinetic analysis to make the glycolic acid and methanol productions dominant by tuning the concentrations of formaldehyde, formic acid, and HCl. The conversion to glycolic acid reaches approximately 90% when formaldehyde, HCl, and formic acid are mixed in the ratio of 1:2:17. The conversion of formaldehyde to methanol reaches approximately 80% when formic acid is added in excess to formaldehyde.

Journal Article↗
PubMed1994

Detoxification of Formaldehyde by the Spider Plant (Chlorophytum comosum L.) and by Soybean (Glycine max L.) Cell-Suspension Cultures.

The phytotoxicity of formaldehyde for spider plants (Chlorophytum comosum L.), tobacco plants (Nicotiana tabacum L. cv Bel B and Bel W3), and soybean (Glycine max L.) cell-suspension cultures was found to be low enough to allow metabolic studies. Spider plant shoots were exposed to 7.1 [mu]L L-1 (8.5 mg m-3) gaseous [14C]-formaldehyde over 24 h. Approximately 88% of the recovered radioactivity was plant associated and was found to be incorporated into organic acids, amino acids, free sugars, and lipids as well as cell-wall components. Similar results were obtained upon feeding [14C]formaldehyde from aqueous solution to aseptic soybean cell-suspension cultures. Serine and phosphatidylcholine were identified as major metabolic products. Spider plant enzyme extracts contained two NAS+-dependent formaldehyde dehydrogenase activities with molecular mass values of about 129 and 79 kD. Only the latter enzyme activity required glutathione as an obligatory second cofactor. It had an apparent Km value of 30 [mu]M for formaldehyde and an isoelectric point at pH 5.4. Total cell-free dehydrogenase activity corresponded to 13 [mu]g formaldehyde oxidized h-1 g-1 leaf fresh weight. Glutathione-dependent formaldehyde dehydrogenases were also isolated from shoots and leaves of Equisetum telmateia and from cell-suspension cultures of wheat (Triticum aestivum L.) and maize (Zea mays L.). The results obtained are consistent with the concept of indoor air decontamination with common room plants such as the spider plant. Formaldehyde appears to be efficiently detoxified by oxidation and subsequent C1 metabolism.

Journal Article↗
PubMed1993

Effect of urine pH and ascorbic acid on the rate of conversion of methenamine to formaldehyde.

The kinetics of conversion of methenamine to the active form formaldehyde were studied in pooled urine samples at 37 degrees in the pH range 4.9-6.5. Using a method for the determination of both formaldehyde and unhydrolyzed methenamine, the rate of formaldehyde formation in urine was found to be apparent first order and was pH dependent. Bactericidal concentrations of formaldehyde (> 28 micrograms ml-1) were achieved in 3 h in urine of pH 6.0 containing methenamine at 750 micrograms ml-1. There was no difference in the in vitro rate of conversion of methenamine to formaldehyde between the urine collected from normal subjects and the urine from subjects administered ascorbic acid. The rates of degradation of the mandelate and hippurate salts in buffer systems of various pH values did not differ significantly from those of methenamine base in urine adjusted to the same pH. The half-life of methenamine conversion to formaldehyde increased approximately 20 times from 20 h at pH 5.0 to about 400 h at pH 6.5. The data suggest that unless the urine is maintained below pH 6 only a small fraction of methenamine would be converted daily to formaldehyde and, thus, may explain the need for large doses of this drug in patients.

Anti-Infective Agents, Urinary↗
PubMedDate not supplied

Protective effects of omega-3 essential fatty acids against formaldehyde-induced neuronal damage in prefrontal cortex of rats.

The aim of this study was to examine the neurotoxicity of formaldehyde on prefrontal cortex and the protective effects of omega-3 essential fatty acids against these toxic effects. For this purpose, 21 male Wistar rats were divided into three groups. The rats in group I comprised the controls, while the rats in group II were injected every other day with formaldehyde (FA). The rats in group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation. The brains of the rats were removed and the prefrontal cortex tissues were obtained from all brain specimens. Some of the prefrontal cortex tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels. The remaining prefrontal cortex tissue specimens were used for light microscopic and immunohistochemical evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Furthermore, in the microscopic examination of this group, formation of apoptotic bodies, pycnotic cells, and apoptotic cells including nuclear fragmentation and membrane budding were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels were detected in the rats administered omega-3 fatty acids while exposed to formaldehyde. Additionally, cellular damage caused by formaldehyde was decreased, and structural appearance was similar to that of the control rats in this group. The biochemical and histological findings observed in all groups were also confirmed by immunohistochemical evaluation. It was determined that formaldehyde-induced neuronal damage in prefrontal cortex was prevented by administration of omega-3 essential fatty acids.

Animals↗
PubMedDate not supplied

Melatonin prevents formaldehyde-induced neurotoxicity in prefrontal cortex of rats: an immunohistochemical and biochemical study.

This study was undertaken to investigate the protective effects of melatonin against formaldehyde-induced neurotoxicity in prefrontal cortex of rats. For this purpose, 21 male Wistar rats were divided into three groups. The rats in Group I were used as a control, while the rats in Group II were injected every other day with formaldehyde. The rats in Group III received melatonin daily while exposed to formaldehyde. At the end of 14-day experimental period, all rats were killed by decapitation. The brains of the rats were removed and the prefrontal cortex tissues were obtained from all brain specimens. Some of the prefrontal cortex tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) levels. The remaining prefrontal cortex tissue specimens were used for immunohistochemical evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels, were significantly increased in rats treated with formaldehyde compared with those of the controls. In the immunohistochemical evaluation of this group, apoptotic cells were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels, were detected in the rats administered melatonin while exposed to formaldehyde. Furthermore, apoptotic changes caused by formaldehyde were decreased in these rats. The results of our study suggest that melatonin treatment prevents formaldehyde-induced neuronal damage in prefrontal cortex.

Animals↗
PubMed2005

Assimilation, dissimilation, and detoxification of formaldehyde, a central metabolic intermediate of methylotrophic metabolism.

Methanol is a valuable raw material used in the manufacture of useful chemicals as well as a potential source of energy to replace coal and petroleum. Biotechnological interest in the microbial utilization of methanol has increased because it is an ideal carbon source and can be produced from renewable biomass. Formaldehyde, a cytotoxic compound, is a central metabolic intermediate in methanol metabolism. Therefore, microorganisms utilizing methanol have adopted several metabolic strategies to cope with the toxicity of formaldehyde. Formaldehyde is initially detoxified through trapping by some cofactors, such as glutathione, mycothiol, tetrahydrofolate, and tetrahydromethanopterin, before being oxidized to CO2. Alternatively, free formaldehyde can be trapped by sugar phosphates as the first reaction in the C1 assimilation pathways: the xylulose monophosphate pathway for yeasts and the ribulose monophosphate (RuMP) pathway for bacteria. In yeasts, although formaldehyde generation and consumption takes place in the peroxisome, the cytosolic formaldehyde oxidation pathway also plays a role in formaldehyde detoxification as well as energy formation. The key enzymes of the RuMP pathway are found in a variety of microorganisms including bacteria and archaea. Regulation of the genes encoding these enzymes and their catalytic mechanisms depend on the physiological traits of these organisms during evolution.

Archaea↗
PubMed2002

Biotransformation of formaldehyde in cultured human bronchus.

Biotransformation of formaldehyde to formic acid was studied to investigate the capacity of human bronchial epithelial cells to detoxicate formaldehyde. Normal human bronchial explants and normal primary bronchial epithelial cells were grown in medium containing 0.5 to 5 mM formaldehyde for up to 48 h. Formic acid was quantitated by analytical isotachophoresis. Explants were cultured with up to 5 mM formaldehyde for 48 h with approximately linear turnover, but at 5 mM the cells showed reduced biotransformation relative to the lower concentrations. The mean K(m) values for explants were 1.4 and 5.1 mM for cells and the mean V(max) values were 3.3 nmol/mg protein.min for the explants and 6.1 nmol/mg protein.min for the cells. By using the same technique with hepatocytes we found K(m) 1.25 mM and V(max) 4.2 nmol/mg protein.min, indicating that human bronchial epithelium cells have formaldehyde biotransforming activity similar to that of hepatocytes. Our results indicate that human bronchial epithelial cells oxidize formaldehyde at a relatively fast rate at concentrations up to 3 mM formaldehyde in the medium over a period up to 48 h.

Biotransformation↗
PubMed2002

The use of noncancer endpoints as a basis for establishing a reference concentration for formaldehyde.

Published studies involving formaldehyde were selected for quality and relevance for determining whether noncancer endpoints could be used to derive a reference concentration for formaldehyde. Chamber studies provided the highest quality data for determining the presence of eye, nose, or throat irritation at a known level of formaldehyde. Some individuals begin to sense irritation at about 0.5 ppm, 5-20% report eye irritation at 0.5 to 1 ppm, and greater certainty for sensory irritation appears at 1 ppm or greater. These levels of formaldehyde do not appear to impact asthmatics even though these individuals are thought to be more sensitive to irritants. Mild, reversible changes in pulmonary function (forced expiratory volume at 1 s and midexpiratory flow) can occur in sensitized individuals at levels approaching 2 ppm. Studies in the manufacturing setting, while confounded by multiple exposures, provide useful information for setting boundaries for sensory irritation or changes in pulmonary function. Community surveys do not provide the specificity nor sensitivity needed to establish a reference concentration. Histological studies of the nasal mucosa suffer significant methodological and technological shortcomings in addition to issues commonly associated with the design of residential and workplace studies. Based on the review of chamber, community, and workplace studies of human exposures to formaldehyde, it is not possible to identify a specific no observed adverse effect level or lowest observed adverse effect level for formaldehyde. Ranges of exposures associated with acute sensory irritation can be derived and do include sensitive subpopulations. However, given the quality and variability of the data, human studies alone, especially those involving sensory irritation, are not adequate to serve as a reference concentration for estimating risk, or lack thereof, for a lifetime of exposure to formaldehyde. Alternative approaches, such as modeling cellular changes observed in animal studies, may be more useful for quantitative risk assessment of noncancer endpoints and should be used as an adjunct to interpreting human sensory studies.

Air Pollutants, Occupational↗
PubMed1987

Experimental toxicology of formaldehyde.

Formaldehyde is a reactive chemical which undergoes spontaneous reactions with various cellular constituents. Mutagenicity data may be interpreted on the background of this behavior. Mice are better able to reduce the irritating effect of formaldehyde than rats and to reduce their ventilation rate when formaldehyde acts on the respiratory tract. Subacute exposure of rats to concentrations higher than 2 ppm inhibits mucociliary clearance of the nasal epithelium and leads to progressive histological and ultrastructural lesions at this site. The occurrence of squamous cell carcinomas of the nasal epithelium of rats after 2 years inhalation of 14.3 ppm formaldehyde (CIIT study) is probably the result of chronic and recurrent local toxicity; this is supported by species differences in susceptibility to the tissue damaging and carcinogenic effect of formaldehyde (rat, mouse, hamster). Data on formaldehyde-DNA interaction further support the argument that a direct risk extrapolation from the formaldehyde effects in rats to those expected for man is not possible.

Animals↗
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↗