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PubMed1982

Sensitive formaldehyde determination with Nash's reagent and a 'tryptophan reaction'.

The widely applied Nash-method and its modifications have unsatisfactory specificity and restricted sensitivity for the determination of small amounts of formaldehyde. A method using small volumes of reaction mixtures with low background absorbance is described; this method avoids dilution during the protein denaturation step by the use of trichloroacetic acid. Alternatively a 'tryptophan-sulfuric acid-iron' reaction takes advantage of high specificity for formaldehyde detection. A more economical and sensitive variant is described including trichloroacetic acid precipitation of protein. The sensitivity and specificity of the colour development reaction of the 'tryptophan-sulfuric acid-iron' reaction appears to be superior to the Nash-modification. However the detection of formaldehyde by the NASH method can also be amplified by subsequent extraction and concentration of the reaction product diacetyl-dihydrolutidine into n-amyl alcohol so that a formaldehyde amount of few nanomoles can be determined. The application of these methods is recommended in cases of formaldehyde formation in small amounts such as in cell cultures or when kinetic data at low substrate concentrations and slow turnover rates have to be measured.

Animals↗
PubMed1983

Testing the mutagenicity of malondialdehyde and formaldehyde by the Drosophila mosaic and the sex-linked recessive lethal tests.

The mutagenicities of malondialdehyde and formaldehyde were tested by screening each for genetic mosaics of Drosophila melanogaster and by the Muller-5 test for sex-linked recessive lethal mutations. For comparison, the effects of X-rays were also assayed by the above technique. Malondialdehyde, a degradation product of polyunsaturated fatty acids, was found to be a weak mutagen by the above criteria; it induced point mutations and chromosome exchanges at low frequency, as proved by the mosaic test, but failed to induce detectable sex-linked lethality. Formaldehyde was more mutagenic than malondialdehyde; beside induction of mosaic spots it induced sex-linked recessive lethal mutations, but only in the larval testes of Drosophila. Formaldehyde also induced disintegration of the clones. Formaldehyde treatment (feeding larvae with formaldehyde-containing food for about 4 days) was 5 times more mutagenic than malondialdehyde treatment and 5 times less effective than irradiation by 1000 R of X-rays. Wing mosaicism offers a more sensitive way to detect mutagenesis as compared with eye mosaicism. It is suggested that aldehyde-induced mosaic spots derive from mitotic recombination and point mutations.

Animals↗
PubMed1991

Detection of stable epitopes on formaldehyde-detoxified Pasteurella multocida toxin by monoclonal antibodies.

Progressive atrophic rhinitis in pigs can be prevented by vaccination of pregnant sows with formaldehyde-detoxified preparations of either crude extract of toxigenic Pasteurella multocida or purified P. multocida toxin (PMT). The protective value of a vaccine is expected to be related to its content of detoxified immunogenic PMT, but previously described methods for detection of PMT cannot be used for the quantification of formaldehyde-detoxified PMT. In contrast to the epitopes on PMT recognized by previously produced anti-PMT monoclonal antibodies (mAbs), two of the epitopes recognized by mAbs developed in this study showed a significant stability after treatment with formaldehyde under conditions relevant for production of vaccines. When analysed in a sandwich ELISA based on these two mAbs, the titre of a preparation of PMT, detoxified by treatment with 1% (w/v) formaldehyde for 48 h at 20 degrees C, decreased by less than 30% when compared to the titre of native PMT. A close relationship between the amount of formaldehyde-treated PMT in a vaccine determined by the sandwich ELISA and its immunogenic properties in mice was observed.

Animals↗
PubMed1996

The effect of formaldehyde, hydrogen peroxide and genetic detoxification of pertussis toxin on epitope recognition by murine monoclonal antibodies.

The effect of detoxification of pertussis toxin (PT) for vaccine usage by either genetic manipulation, hydrogen peroxide or formaldehyde treatment on epitope recognition by a large collection of murine monoclonal pertussis toxin antibodies (PT MAbs) was assessed in a solid-phase and a soluble phase enzyme-linked immunosorbent assay (ELISA). The MAb binding patterns were found to be different in the two assays as the immobilization step appeared to cause conformational alterations in the native as well as the toxoided forms of PT. According to the solid-phase ELISA, genetic, hydrogen peroxide and 0.35% formaldehyde detoxification of PT resulted in reduced epitope binding in 2.9, 31.4 and 78.1% of the MAbs, respectively. In the soluble-phase ELISA, in which the MAbs were allowed to react with the toxoids or native toxin in solution, the percentages of MAbs showing decreased binding activity were 9.1, 50.0 and 71.4%, respectively. Stabilization of native PT and the genetically inactivated PT by 0.035% formaldehyde reduced the epitope binding activity in 50.0 and 8.7% of the MAbs, respectively. Increased antibody binding in the soluble-phase ELISA was observed in some of the toxoids: this ranged from 0% in the 0.35% formaldehyde-treated PT to 13.6% in the hydrogen peroxide-treated and 27.3% in the genetically detoxified PT. Regarding the effects of detoxification on epitopes recognized by PT-neutralizing MAbs in the soluble-phase ELISA, we found that treatment of PT with either 0.035%, 0.35% formaldehyde or hydrogen peroxide induced impairment of epitope binding in 72.7, 81.8 and 45.5% of the MAbs, respectively. In the genetically inactivated PT, the epitopes recognized by the neutralizing MAbs either appeared to remain intact or to show increased MAb binding activity. The epitope-binding patterns of several PT MAbs with mouse-protective properties varied considerably and were shown to be dependent on the detoxification procedure employed. The relevance of epitope alterations on PT as a vaccine component is discussed. The results of the present study may have important implications for future quality assessment of PT for use in acellular pertussis vaccines.

Animals↗
PubMed1989

Two-year drinking-water study of formaldehyde in rats.

Formaldehyde was administered in the drinking-water to groups of 70 male and 70 female Wistar rats for up to 24 months. Survivors of subgroups of ten rats/sex/group each were killed after 12 or 18 months. The mean formaldehyde doses administered were 0, 1.2, 15 or 82 mg/kg body weight/day for males, and 0, 1.8, 21 or 109 mg/kg/day for females. There were no adverse effects on general health, survival or haematological or clinical chemistry parameters. Body weight and food intake were decreased in the high-dose group. Liquid intake was decreased by 40% in the high-dose group in both sexes in comparison with the controls. There was a slight temporary increase in the density of urine, whereas there was a tendency towards lower urine production in the high-dose group. The relative kidney weights were increased in the high-dose females. Gross examination at autopsy revealed a raised and thickened limiting ridge of the forestomach in most high-dose rats. In addition, several rats in the high-dose group showed irregular mucosal thickenings in the fore- and/or glandular stomach. Treatment-related histopathological gastric changes seen in most of the animals of the high-dose group included papillary epithelial hyperplasia frequently accompanied by hyperkeratosis and focal ulceration in the forestomach and focal chronic atrophic gastritis, occasionally accompanied by ulceration and/or glandular hyperplasia, in the glandular stomach. A higher incidence and/or degree of renal papillary necrosis occurred in the high-dose rats. From this study it appeared that the 'no-observed-adverse-effect level' of formaldehyde was 15 and 21 mg/kg body weight/day for male and female rats, respectively. Oral administration of formaldehyde at doses of 82 and 109 mg/kg/day to male and female rats, respectively, caused severe damage to the gastric mucosa but did not result in gastric tumours or tumours at other sites. The study did not provide any evidence of carcinogenicity of formaldehyde after oral administration.

Administration, Oral↗
PubMed1981

Initiation of C3H/10T1/2 cell transformation by formaldehyde.

The effects of formaldehyde were evaluated in the C3H/10T1/2 Cl 8 cell transformation system. Treatment of the cells with 0.1-2.5 micrograms/ml for formaldehyde alone did not result in significant rates of transformation. If formaldehyde treatment was followed by continuous treatment with 0.1 microgram/ml of the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), transformed foci were produced. Methanol and formic acid lacked significant transforming activity under either treatment regimen. The results suggest that formaldehyde is an initiating agent for C3H/10T1/2 Cl 8 transformation. The fact that some compounds may act solely as initiators should be considered when this transformation system is used to study chemicals which may interact with cells by mechanisms similar to that of formaldehyde.

Animals↗
PubMed1985

Percutaneous absorption of formaldehyde in rats.

As formaldehyde is used as a preservative in cosmetic products, its dermal absorption from an O/W-cream was studied using rats. [14C]Formaldehyde as a tracer, together with non-labelled formaldehyde, was incorporated into a cream at a total concentration of 0.1%. Approx. 5% of the applied radioactivity was absorbed percutaneously within 48 h. Higher values were not found under occlusive conditions. The labelled substance was excreted primarily in urine and exhaled air. Further radioactivity was found in the carcass. Based on these results, a rough approximation was attempted of the amount of formaldehyde which could penetrate human skin after the application of a formaldehyde-containing cosmetic.

Animals↗
PubMed2005

Simultaneous nitrification and formaldehyde biodegradation in an activated sludge unit.

The simultaneous removal of formaldehyde and ammonium in a lab-scale activated sludge unit was investigated. The unit was operated at a hydraulic retention time of 2.4 days with an ammonium concentration in the influent of 350 mg NH4+-N/L, maintaining the ammonium loading rate at 0.15 g NH4+-N/Ld during the operation time. However, the applied organic loading rate was increased stepwise by increasing the formaldehyde concentration from 26 up to 3168 mg/L, corresponding to 0.01-1.40 g COD/Ld. High formaldehyde removal efficiencies, around 99.5% (+/-0.38), were maintained at all the formaldehyde concentrations. Ammonium removal was also very high during the operation period, around 99.9% (+/-0.01). The ammonium concentration in the effluent was lower than 0.1 mg NH4+-N/L at all applied organic loading rates, indicating that there was no inhibition of nitrification by formaldehyde.

Ammonia↗
PubMed2004

Effect of prolonged exposure to low concentrations of formaldehyde on the corticotropin releasing hormone neurons in the hypothalamus and adrenocorticotropic hormone cells in the pituitary gland in female mice.

We examine the effect on the hypothalamus-pituitary-adrenal gland (HPA) axis of prolonged exposure to low levels of formaldehyde in female C3H/He mice, using immunocytochemical and RT-PCR methods. Two groups of female mice were exposed to differing concentrations (0, 80, 400, 2000 ppb) of formaldehyde inhalation for 16 h/day, 5 days/week, for 12 weeks. The corticotropin releasing hormone (CRH)-immunoreactive (ir) neurons in the hypothalamus were then examined, together with the adrenocorticotropin hormone (ACTH)-ir cells and ACTH mRNA in the pituitary. One group comprised sham control mice. The other group was made allergic by injection of ovalbumin (OVA) and alum prior to exposure to formaldehyde, since most sick building syndrome (SBS) sufferers are women with allergic disease. These animals were further exposed to aerosolized OVA as a booster four times during the exposure period. Our results showed a dose-dependent increase in the number of CRH-ir neurons in the non-allergy (NAG) group. A similar pattern was found in ACTH-ir cells and ACTH mRNA. The allergy (AG) model group showed an increase in basal levels of all markers of HPA activity. Moreover, the AG mice appeared to respond to the lowest concentration of formaldehyde, and all indices of HPA activity were reduced at the highest concentrations of formaldehyde. These results relate to an important clinical issue and also have implications in the broader area of HPA regulation. We conclude that our experimental system may be a suitable animal model for SBS and/or multiple chemical sensitivity (MCS).

Adrenocorticotropic Hormone↗
PubMed2005

Kinetic analysis of photocatalytic oxidation of gas-phase formaldehyde over titanium dioxide.

Degradation of formaldehyde with different initial concentration over titanium dioxide was carried out in a photocatalytic reactor. Photocatalytic rates were well described by the simplified Langmuir-Hinshelwood model. The kinetic analysis shows that the apparent first-order reaction coefficient is lower and half-life of photocatalysis is longer for low concentration than for high concentration formaldehyde. A network formation model of the photocatalytic products was established. Experimental results and analysis demonstrate that carbon dioxide concentration and carbon monoxide concentration in gas phase vary exponentially with the illumination time and may be even higher than gas-phase formaldehyde concentration if there is much pre-adsorbed formaldehyde in adsorption equilibrium on catalysts before illumination. Carbon monoxide is found to be one of the by-products during formaldehyde photooxidation.

Catalysis↗
PubMed2004

Levels and determinants of formaldehyde, acetaldehyde, and acrolein in residential indoor air in Prince Edward Island, Canada.

This study was undertaken to determine the concentrations of formaldehyde, acetaldehyde, and acrolein in air samples taken in some Canadian houses and to determine the association between aldehyde levels and housing characteristics. Concentrations of formaldehyde, acetaldehyde, and acrolein were measured in 59 homes in Prince Edward Island, Canada, during the winter of 2002. Housing characteristics were documented through inspection and by interviews of occupants. Formaldehyde, acetaldehyde, and acrolein concentrations ranged from 5.5 to 87.5 microg/m(3) (median, 29.6 microg/m(3)), from 4.4 to 79.1 microg/m(3) (median, 18.9 microg/m(3)), and from 0.1 to 4.9 microg/m(3) (median, 0.9 microg/m(3)), respectively. Formaldehyde levels were elevated in homes built after 1970. Acetaldehyde and acrolein levels were elevated in homes inhabited by at least one smoker and in homes built 1970--1985 and were correlated with absolute humidity and carbon dioxide, two variables likely to be surrogates for lower air exchange rates. In conclusion, lower air exchange rates appear to be important determinants of formaldehyde, acetaldehyde, and acrolein levels in homes. These data also confirm that smoking is a significant source of acetaldehyde and acrolein and indoor air.

Acetaldehyde↗
PubMed2006

In vitro model for decontamination of human skin: formaldehyde.

Decontamination of a chemical from skin is often an emergency measure. This study utilized an in vitro model to compare the decontamination capacity of three model decontaminant solutions (tap water, isotonic saline, and hypertonic saline). Human cadaver skin was dosed (approximately 0.25 microg on 3 cm(2) per skin) with radio-labeled [(14)C]-formaldehyde. After a defined exposure time (1, 3, and 30 min post-dosing, respectively), the surface skin was washed three times (4ml per time) with each solution. After washing, the skin was stripped with tape discs twice. Lastly, the wash solutions, strippings, receptor fluid, and remainder of skin were liquid scintillation analyzer counted to determine the amounts of formaldehyde. Additionally, an evaporation test at different exposure times (1min, 3min, 15min, 30min, and 60min, respectively) was conducted to monitor formaldehyde % evaporation. There were no statistical differences among these groups except isotonic saline, at 3min post-exposure (in wash solutions), showed a significantly difference (p<0.05) when compared to tap water. Formaldehyde % evaporation increased linearly with extending application times, and were 7.7%, 13.6%, 19.7%, 24.4%, and 35.9% (1min, 3min, 15min, 30min, and 60min, respectively). This data suggests that isotonic saline may be effective in removing formaldehyde from skin. However, results from this model need validation in vivo. The model may provide a facile and robust method of accelerating knowledge of decontamination mechanism and lead to enhanced efficacy.

Decontamination↗
PubMed2006

Simultaneous determination of formic acid and formaldehyde in pharmaceutical excipients using headspace GC/MS.

Formic acid and its esters, as well as formaldehyde, are trace impurities that are often present in pharmaceutical excipients. These trace impurities can potentially react with amino and/or hydroxyl groups in drugs to form significant levels of degradants. To select the appropriate excipients for a stable formulation, a gas chromatography/mass spectrometry (GC/MS) method was developed and validated for the rapid screening of trace amounts of residual formic acid, its esters and formaldehyde in pharmaceutical excipients. Samples were dissolved or dispersed in acidified ethanol to convert formic acid and formaldehyde to ethyl formate and diethoxymethane, respectively. Identification was conducted using a GC/MS system under scan mode and quantified using a selected ion monitoring (SIM) mode. Evaluation of the mass spectra of ethyl formate and diethoxymethane in the samples indicated that the method is specific. The limits of quantitation of the method were 0.5 ppm for formic acid and 0.2 ppm for formaldehyde. The precision of the method was demonstrated by the acceptable R.S.D. (<or=10%) over a linear range of 0.5-10,000 ppm. The accuracy of the method was within 80-120% over the linearity range. The amounts of formic acid and formaldehyde in commonly used pharmaceutical excipients is reported.

Excipients↗
PubMed2006

Catalytic-kinetic determination of trace amount of formaldehyde by the spectrophotometric method with a bromate-Janus green system.

A new simple and rapid catalytic kinetic method for the determination of trace amount of formaldehyde is described. The method is based on the catalytic effect of formaldehyde on the oxidation of Janus green by bromate in the present of sulfuric acid. The reaction monitored spectrophotometrically by measuring the decrease in absorbance of the reaction mixture at 618 nm. The fixed-time method was used for the first 150 s. For initiation of the reaction, under the optimum conditions, in the concentration range of 0.003-2.5 microg ml(-1) formaldehyde can be determined with a limit of detection 0.0015 microg ml(-1). The relative standard deviation of five replicate measurements is 2.3% for 1.0 microg ml(-1) of formaldehyde. The method was used for the determination of formaldehyde in real samples with satisfactory results.

Azo Compounds↗
PubMed2005

Low-dose exposure of intestinal epithelial cells to formaldehyde results in MAP kinase activation and molecular alteration of the focal adhesion protein paxillin.

We investigated the potential pathophysiological role of non-lethal formaldehyde concentrations on human intestinal epithelial HT-29 cells. Expression levels of actin, tubulin and detectable cytokeratin isoforms 5, 13, 18, 19 and 20 were not affected after 24h of exposure to 1mM formaldehyde. By contrast, cellular organization of cytoskeletal constituents was already changed after 60 min. Within 15 min, formaldehyde induced profound tyrosine phosphorylation of the focal adhesion protein paxillin and of proteins at about 120-130 kDa. Concomitantly, phosphorylation of ERK-1/2 and p38 MAP kinase occurred. Paxillin was not only tyrosine phosphorylated but underwent a sustained molecular weight shift representing serine/threonine phosphorylation that was independent of MAP kinase activity and EGF-R-mediated signalling. Our data show that exposure of intestinal epithelial cells to low-dose formaldehyde is followed by rapid and profound signalling events. The data suggest a modifier role of environmental or endogenous formaldehyde for epithelial cell functions.

Alkaline Phosphatase↗
PubMed2004

A review and meta-analysis of formaldehyde exposure and leukemia.

Most reviews on the carcinogenicity of formaldehyde have focused on cancers of the respiratory tract because these cancer sites were thought to be most biologically plausible. However, two recent updated large industrial studies have found positive associations between some measures of formaldehyde exposure and increased leukemia, although another recent update of a large study did not find any association. We examine 18 epidemiology studies of workers exposed to formaldehyde where leukemia rates were reported. We summarize the findings across studies by using meta-analytic techniques to calculate the meta-relative risk values (mRR), confidence intervals, and heterogeneity of the risk estimates for several study characteristics. We also determine if publication or reporting biases may be affecting the estimates. We found a small increase in rate of leukemia overall among embalmers (mRR = 1.6, 95%CI 1.2-6.0), and pathologists/anatomists (mRR = 1.4, 95%CI 1.0-1.9). Industrial workers, who have been reported to have the highest formaldehyde exposures, had a mRR of 0.9 (95%CI 0.8-1.0). There was increased risk with increasing exposure in two large industrial studies, although the increased risk is one of these studies was not seen when an external comparison group is used. Also, another large industrial study with more highly exposure workers found decreased risk of leukemia among the highest exposed group. The long latency for leukemia deaths observed in the two industrial studies that reported increased risk was not consistent with a chemical carcinogen such as benzene. We found limited evidence of publication or reporting bias. On balance, these data do not provide consistent support for a relationship between formaldehyde exposure and leukemia risk.

Data Interpretation, Statistical↗
PubMed1988

Oxidation of glycerol to formaldehyde by rat liver microsomes.

Rat liver microsomes catalyzed the oxidation of glycerol to a Nash-reactive material in a time- and protein-dependent manner. Omission of the glycerol or the microsomes or any of the components of the NADPH-generating system resulted in almost a complete loss of product formation. Apparent Km and Vmax values for glycerol oxidation were about 18 mM and 2.5 nmol formaldehyde per min per mg microsomal protein. Carbon monoxide inhibited glycerol oxidation indicating a requirement for cytochrome P-450. That the Nash-reactive material was formaldehyde was validated by a glutathione-dependent formaldehyde dehydrogenase positive reaction. These studies indicate that glycerol is not inert when utilized with microsomes or reconstituted mixed function oxidase systems, and that the production of formaldehyde from glycerol may interfere with assays of other substrates which generate formaldehyde as product.

Animals↗
PubMed1998

Formaldehyde derived from dietary aspartame binds to tissue components in vivo.

Adult male rats were given an oral dose of 10 mg/kg aspartame 14C-labelled in the methanol carbon. At timed intervals of up to 6 hours, the radioactivity in plasma and several organs was investigated. Most of the radioactivity found (>98% in plasma, >75% in liver) was bound to protein. Label present in liver, plasma and kidney was in the range of 1-2% of total radioactivity administered per g or mL, changing little with time. Other organs (brown and white adipose tissues, muscle, brain, cornea and retina) contained levels of label in the range of 1/12 to 1/10th of that of liver. In all, the rat retained, 6 hours after administration about 5% of the label, half of it in the liver. The specific radioactivity of tissue protein, RNA and DNA was quite uniform. The protein label was concentrated in amino acids, different from methionine, and largely coincident with the result of protein exposure to labelled formaldehyde. DNA radioactivity was essentially in a single different adduct base, different from the normal bases present in DNA. The nature of the tissue label accumulated was, thus, a direct consequence of formaldehyde binding to tissue structures. The administration of labelled aspartame to a group of cirrhotic rats resulted in comparable label retention by tissue components, which suggests that liver function (or its defect) has little effect on formaldehyde formation from aspartame and binding to biological components. The chronic treatment of a series of rats with 200 mg/kg of non-labelled aspartame during 10 days resulted in the accumulation of even more label when given the radioactive bolus, suggesting that the amount of formaldehyde adducts coming from aspartame in tissue proteins and nucleic acids may be cumulative. It is concluded that aspartame consumption may constitute a hazard because of its contribution to the formation of formaldehyde adducts.

Administration, Oral↗