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PubMed1985

Seasonal formaldehyde concentrations in an office building.

The objective of this investigation was to determine if there was a seasonal effect on formaldehyde emissions from paneling and shelving in a one story office building. Measurement of formaldehyde was done by standard impinger sampling techniques using 1% bisulfate absorbing solution and by using a dry diffusional formaldehyde monitor. Results show a definite seasonal trend for formaldehyde concentrations by either monitoring method. The formaldehyde concentrations for warm weather are about twice as great as those in cold weather. In addition the dry diffusional monitor concentrations determined were consistently low compared to impinger sampling.

Air Pollutants, Occupational↗

PubMed1985

Residential formaldehyde sampling--current and recommended practices.

The usefulness of test results in assessing the health hazard potential of residential formaldehyde exposures depends in great measure on the accuracy and reliability of sampling/analysis methods employed, the protocol used in collecting samples, sampling objectives, and an understanding of residential formaldehyde dynamics and their relationship to environmental variables. Active sampling and analysis methods including detector tubes, the impinger/chromotropic acid method, the impinger/pararosaniline method, and the CEA continuous monitor are reviewed as to advantages and limitations for residential sampling. Passive dosimeter methods including the Dupont Pro-Tec Badge, 3M Monitor, Air Quality Research, Inc. Passive Formaldehyde Kit, and Envirotech, Inc. Dosimeter are also reviewed. Sampling considerations for one-time formaldehyde sampling using the impinger/chromotropic acid method are discussed in detail, including pre-sampling closure of residences, maintenance of a standard indoor temperature both before and during sampling, the undesirability of sampling during cold, dry winter weather, sample number, sampling location, height and duration, environmental measurements during sampling, source identification and sample storage. A model formaldehyde sampling protocol based on the impinger/chromotropic acid method is described.

Air Pollutants↗

PubMed1990

An evaluation of the effect of source and concentration on three methods for the measurement of formaldehyde in indoor air.

Three methods for measuring formaldehyde (HCHO) in indoor air were evaluated under field and laboratory conditions using different sources and concentrations of formaldehyde in air. Two impinger methods (the chromotropic acid method and modified pararosaniline method) and the Draeger short-term detector tube method (with and without activation tubes) were compared when sampling for formaldehyde from a particle board box, formalin solution, and a conventional home. Concentrations of formaldehyde ranged from 0.05-0.5 ppm in air. All samples were collected independently using personal sampling pumps and a Draeger bellows pump. The results indicate that the Draeger tube method using an activation tube gives lower results than either of the impinger methods. Without using an activation tube (concentrations greater than 0.5 ppm), the Draeger tube method was comparable to the two impinger methods. In addition, there are indications that the chromotropic acid method gives different results than the modified pararosaniline method, depending on the source of formaldehyde. The modified pararosaniline method indicated higher results than the chromotropic acid method when sampling from a particle board++ box but not from a formalin source. Overall analytical precision for each method of analysis was good.

Air Pollutants↗

PubMed1996

Worker exposure to endotoxin, phenolic compounds, and formaldehyde in a fiberglass insulation manufacturing plant.

Worker exposures in a fiberglass wool insulation manufacturing plant were studied. The plant used a continuous process and operated at full production during a six-week study. Area samples were used to characterize spatial variability of contaminant levels. Repeated personal samples were used to characterize the distribution and to explore within- and between-worker variability of exposures. The greatest potential for exposure to each of the contaminants was restricted to specific areas of the plant. Area geometric mean concentrations were 1 to 390 ng/m3 for endotoxin and 22 to 414 micrograms/m3 for formaldehyde. There was considerable within-area variation of endotoxin (geometric standard deviation [GSD] 2.6 to 5.5) and formaldehyde (GSD 2.0 to 4.5). Concentrations of phenolic compounds were correlated with endotoxin and were influenced by a relatively high limit of detection. The ranges of personal GM exposures across homogeneous groupings were smaller than the range for the corresponding areas (endotoxin 5.8 to 36.4 ng/m3; formaldehyde 18.1 to 67.4 micrograms/m3). Variability in personal exposure was high. Individual GSDs ranged up to 10, with the mean individual GSD of 3.4 for endotoxin, and up to 12 with mean 3.7 for formaldehyde. Suggested thresholds for acute respiratory effects of endotoxin exposure were frequently exceeded (46% of 8-hr personal samples > 10 ng/m3, 7% > 100 ng/m3). No personal samples exceeded the Occupational Safety and Health Administration permissible exposure level or the American Conference of Government Industrial Hygienists' threshold limit value for formaldehyde; however, 34% were greater than 60 micrograms/m3 and 11% were greater than 120 micrograms/m3. Thus, exposures fell in a range where important exposure-response relationship could be examined.

Air Pollutants, Occupational↗

PubMed2005

Exposure to low molecular weight isocyanates and formaldehyde in foundries using hot box core binders.

Emissions from a chemical core binder system (Hot Box) based on a formaldehyde-carbamide resin have been investigated. The binder is used in some Swedish die-casting foundries. During core-making and casting, low molecular monoisocyanates, in particular methyl isocyanate (MIC) and isocyanic acid (ICA), were identified. Exposure to air concentrations of MIC, ICA and formaldehyde were subsequently determined in all Swedish foundries using the Hot Box binder, and involved three brass and one grey iron foundry. The survey was carried out in the winter period of 2001, and involved core-makers, casters and fettlers in the brass foundries, whereas only core-makers were included in the grey iron foundry. For each worker, four to five short-term samples of isocyanates (n = 298) and one 8 h sample of formaldehyde (n = 64) were collected during one shift for 15 die-casters, 39 core-makers and 10 other workers in the foundry. The air concentrations of the MIC short-term samples varied between <4 and 68 microg m(-3), with corresponding ICA levels between <4 and 280 microg m(-3). Calculated 8 h time weighted average air concentrations of MIC, based on short-term samples for each individual, varied between <4 and 31 microg m(-3); for ICA the corresponding levels varied from <4 to 190 microg m(-3). The formaldehyde time weighted average concentration levels ranged from 14 to 1600 microg m(-3), and the Swedish occupational exposure limit (600 microg m(-3)) was exceeded only in 3% of the samples. In general, the core-makers were exposed to higher average formaldehyde levels compared to the casters, the latter being more exposed to monoisocyanates. During core-making and die-casting, low molecular monoisocyanates, in particular MIC and ICA, were identified. Compared to the American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value-time weighted average (TLV-TWA) for MIC, the exposures were low. The lack of toxicological and human data for ICA and the relatively high air concentrations call for medical examination and preventive measures in production, ventilation and the use of personal safety equipment in the investigated foundries.

Air Pollutants, Occupational↗

PubMed1984

Formaldehyde as a possible mutagenic metabolite of N-nitrodimethylamine and of other agents which are suggested to yield non-alkylating species in vitro.

N-Nitramines are biologically active compounds of environmental significance. In this study the suggested bioactivation of N- nitrodimethylamine via oxidation at the methyl-group was confirmed, as was indicated by formaldehyde liberation. N- Nitrodimethylamine and formaldehyde as well as the suggested metabolites, N- nitrohydroxymethylmethylamine and N- nitromethylamine were tested for mutagenicity in histidine auxotrophic Salmonella typhimurium strains in a variety of conditions. N- Nitrodimethylamine was mutagenic only in S. typhimurium TA 100 after pre-incubation with bacteria and a complete metabolizing mixture containing 9000 g liver supernatant and NADPH-regenerating cofactors. N- Nitrohydroxymethylmethylamine and formaldehyde were approximately equally mutagenic without the metabolizing mixture in TA 100 and TA 98, but not in TA 1535. The addition of the 9000 g supernatant of homogenized liver increased the yield of his+ revertants induced by the two compounds. N- Nitromethylamine was not mutagenic with or without the metabolic activation system. The results suggest that formaldehyde is possibly the mutagenically active intermediate formed during in vitro metabolism of N- nitrodimethylamine . Furthermore the participation of formaldehyde as the mutagenic intermediate of other non-alkylating N-nitro and N-nitroso compounds is demonstrated.

Animals↗

PubMed1999

Simultaneous determination of formaldehyde and methylglyoxal in urine: involvement of semicarbazide-sensitive amine oxidase-mediated deamination in diabetic complications.

The deamination of methylamine and aminoacetone by semicarbazide-sensitive amine oxidase (SSAO) produces formaldehyde and methylglyoxal, respectively, which have been presumed to be involved in diabetic complications. A high-performance liquid chromatography procedure using 2,4-dinitrophenylhydrazine (DNPH) as a derivatizing agent is developed to determine endogenous formaldehyde, methylglyoxal, malondialdehyde, and acetaldehyde. The devised DNPH method is sensitive enough to analyze aldehyde levels in urine. An increase in the excretion of formaldehyde, methylglyoxal, and malondialdehyde is confirmed in streptozotocin-induced diabetic rats. Following the chronic administration of methylamine, the urinary levels of both formaldehyde and malondialdehyde (a product from lipid peroxidation) are found to be substantially increased. A potent selective SSAO inhibitor, (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride (MDL-72974A), reduced the formation of formaldehyde, methylglyoxal, and malondialdehyde. The increase of the cytotoxic aldehyde levels as a result of increased SSAO-mediated deamination may occur in some pathological conditions.

Amine Oxidase (Copper-Containing)↗

PubMed1993

Sources of discrepancies between a job exposure matrix and a case by case expert assessment for occupational exposure to formaldehyde and wood-dust.

Two methods used for retrospective evaluation of occupational exposures, a case by case assessment by expert and the application of a job exposure matrix (JEM), are compared using occupational histories collected for a case-control study on sinonasal cancer. The objective was to identify the main sources of discrepancies and to contribute to an optimal use of a JEM for population-based case-control studies. Comparisons were based on job periods, and were performed separately for two substances: formaldehyde and wood-dust. Job periods were classified according to the category of exposure assigned by the matrix, and to the probability and level of exposure assessed by the study expert. The sources of discrepancies were examined for job periods probably or definitely exposed according to the JEM and unexposed for the expert, or unexposed in the JEM and probably or definitely exposed to medium or high level for the expert. Such discrepancies were observed for 8% of the job periods for formaldehyde and 3% of the job periods for wood-dust. The agreement between the two approaches was better for wood-dust than for formaldehyde. The relative importance of different sources of discrepancies was not the same for formaldehyde and wood-dust. For formaldehyde a substantial part of the discrepancies was due to disagreements between the study expert and the matrix experts, which were mostly differences in threshold limits between 'not exposed' and 'definitely exposed at a low level'. Differences between experts' opinions did not explain the discordances observed for wood-dust. The presence of additional information in the questionnaire was an important source of discrepancy for the two substances.(ABSTRACT TRUNCATED AT 250 WORDS)

Case-Control Studies↗

PubMed2001

In vitro reaction of formaldehyde with fenfluramine: conversion to N-methyl fenfluramine.

Embalming is common, and it can create problems for the forensic scientist if a drug has been the cause death and this drug is also reactive toward the embalming fluid. Previous studies have focused on the tricyclic amines nortriptyline and desipramine. In the presence of formaldehyde, a typical component of embalming fluid, either of these two compounds can be rapidly converted to their methylated derivatives amitriptyline and imipramine, respectively. We have begun a larger project designed to determine the reactivity and reactions of a wide range of drugs with formaldehyde. We report here our results from fenfluramine, which, like the tricyclic amines, is reactive towards formaldehyde and is converted into its N-methyl derivative. The rate of conversion is dependent upon pH and formaldehyde concentration. Up to 100% conversion in 24 h was observed. In addition, we have also devised a simplified procedure for monitoring this process that may be useful for others working in this area. Finally, we note that the reactions of fenfluramine studied here and of amines in general with formaldehyde need to be considered when performing postmortem/postembalming forensic analysis.

Embalming↗

PubMed2000

Induction and repair of formaldehyde-induced DNA-protein crosslinks in repair-deficient human cell lines.

We have previously shown that the alkaline Comet assay (single cell gel electrophoresis) in a modified version is a sensitive test for the detection of formaldehyde-induced DNA-protein crosslinks (DPC). Our results also indicated that formaldehyde-induced DPC are related to the formation of chromosomal effects such as micronuclei and sister chromatid exchanges. To better understand the genetic consequences of formaldehyde-induced DPC we have now investigated the induction and removal of DPC in relationship to the formation of micronuclei in normal and repair-deficient human cell lines. We did not find significant differences between normal cells, a xeroderma pigmentosum (XP) cell line and a Fanconi anaemia (FA) cell line with respect to the induction and removal of DPC. However, the induction of micronuclei was enhanced in both repair-deficient cell lines, particularly in XP cells, under the same treatment conditions. Comparative investigations with the DNA-DNA crosslinker mitomycin C (MMC) revealed a delayed removal of crosslinks and enhanced induction of micronuclei in both repair-deficient cell lines. FA cells were found to be particularly hypersensitive to micronucleus induction by MMC. In contrast to the results with formaldehyde, induction of micronuclei by MMC occurred at much lower concentrations than the effects in the Comet assay. Our results suggest that more than one repair pathway can be involved in the repair of crosslinks and that disturbed excision repair has more severe consequences with regard to the formation of chromosomal aberrations after formaldehyde treatment than has disturbed crosslink repair.

Cell Line↗

PubMed2000

The specificity of protein-DNA crosslinking by formaldehyde: in vitro and in drosophila embryos.

Formaldehyde crosslinking has been widely used to study binding of specific proteins to DNA elements in intact cells. However, previous studies have not determined if this crosslinker preserves the bona fide pattern of DNA binding. Here we show that formaldehyde crosslinking of Drosophila embryos maps an interaction of the transcription factor Zeste to a known target element in the Ultrabithorax promoter. This data agrees broadly with previous mapping of the same Zeste binding sites by in vivo UV crosslinking, though the formaldehyde method does give a low, possibly artifactual signal on other DNA fragments that is not detected by the UV method. We also demonstrate, using an in vitro assay, that formaldehyde crosslinking accurately reflects the DNA binding specificities of both Zeste and a second transcription factor, Eve. The crosslinking reagent methylene blue is shown to preserve DNA binding specificity in vitro as well. Our results suggest that crosslinking by formaldehyde, and possibly also by methylene blue, provide an accurate guide to the interaction of proteins with their high affinity target sites in cells.

Animals↗

PubMed2001

Formaldehyde release from ground root canal sealer in vitro.

The formaldehyde release from three different ground root canal sealer materials was examined. Ten specimens each of AH26, Amubarut, and N2 were stored under dry conditions for 6 months. An amount of approximately 100 to 200 mg ground material was obtained from each sample by using a round bur and stored for 10 min in distilled water. The formaldehyde concentration of the immersion water was determined by high-performance liquid chromatography. The mean formaldehyde release per mg material was 6.6 (+/-2.5) microg for AH26 and 8.3 (+/-1.0) microg for Amubarut. A lower formaldehyde release was detectable by our method from the N2 samples (0.3 +/- 0.1 microg/g; p < 0.0001). In conclusion formaldehyde release from ground root canal material is low, although a risk of an allergic reaction in susceptible patients cannot be excluded.

Bismuth↗

PubMed1988

Reanalysis of lung cancer mortality in a National Cancer Institute study on mortality among industrial workers exposed to formaldehyde.

The results of an historical cohort study of mortality among individuals occupationally exposed to formaldehyde were announced in 1986 by Blair et al (JNCI 1986; 76:1071-1084). The study was a joint undertaking of the National Cancer Institute and the Formaldehyde Institute, and concluded, ". . .this large multiplant cohort study provided little evidence to suggest that formaldehyde exposure affected the mortality experience of these industrial workers." However, there were concerns by a number of workers that the design and analysis of the study had possibly masked an existing occupational hazard. Analyzing time-integrated exposure to formaldehyde without simultaneously considering length of exposure and comparing mortality of formaldehyde workers to mortality of the general population could have masked an increase in cancer risks because of the healthy worker effect. A copy of the data of the study was obtained from the principal investigator and reanalyzed. We find a significantly increased risk for all cancers and for lung cancer as a function of cumulative exposure when workers with higher levels of exposure are compared with those with little or no exposure while simultaneously considering length of exposure. When the risk ratio (RR) for lung cancer at less than or equal to 0.1 ppm cumulative exposure (CX) is taken as 1.0, the lung cancer RR for CX of 0.1 to 0.5 ppm is 1.41 (1.20 to 1.66), the RR for CX of 0.5 to 2.0 ppm is 1.73 (1.42 to 2.11), and the RR for CX greater than or equal to 2.0 is 1.70 (1.32 to 2.18). Hourly workers have a significantly higher RR than salaried workers (RR = 1.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Mortality of iron foundry workers: IV. Analysis of a subcohort exposed to formaldehyde.

In the final phase of the mortality study of workers at an automotive iron foundry, a subset (N = 3929) of the original cohort of 8147 men, consisting of those exposed to formaldehyde during the period from January 1960 through May 1987, was analyzed. In addition to the external US population, an internal population (N = 2032), consisting of men who had worked in the same foundry during the same time period but not in formaldehyde-exposed jobs, was also used as a referent. Follow-up continued through December 31, 1989. Smoking status was ascertained for 65.4% of the exposed and for 55.1% of the unexposed cohorts. Detailed work histories and evaluation of occupational exposures by an industrial hygienist enabled us to categorize cumulative formaldehyde and silica exposures. Standardized mortality ratios were used to compare the mortality experience of the exposed cohort with the US population and, because of concerns about the healthy worker effect, with an occupational referent population. Relative risks for race, formaldehyde exposure status, smoking status, and silica exposure level were estimated by fitting a Poisson regression model to four causes of death: cancers of the buccal cavity and pharynx, lung cancer, diseases of the respiratory system, and emphysema. No association between formaldehyde exposure and deaths from malignant or nonmalignant diseases of the respiratory system was found. Cigarette smoking and silica exposure were found to be significantly associated with deaths attributed to lung cancer and disease of the respiratory system.

Adolescent↗

PubMed2003

Benchmark dose risk assessment for formaldehyde using airflow modeling and a single-compartment, DNA-protein cross-link dosimetry model to estimate human equivalent doses.

Formaldehyde induced squamous-cell carcinomas in the nasal passages of F344 rats in two inhalation bioassays at exposure levels of 6 ppm and above. Increases in rates of cell proliferation were measured by T. M. Monticello and colleagues at exposure levels of 0.7 ppm and above in the same tissues from which tumors arose. A risk assessment for formaldehyde was conducted at the CIIT Centers for Health Research, in collaboration with investigators from Toxicological Excellence in Risk Assessment (TERA) and the U.S. Environmental Protection Agency (U.S. EPA) in 1999. Two methods for dose-response assessment were used: a full biologically based modeling approach and a statistically oriented analysis by benchmark dose (BMD) method. This article presents the later approach, the purpose of which is to combine BMD and pharmacokinetic modeling to estimate human cancer risks from formaldehyde exposure. BMD analysis was used to identify points of departure (exposure levels) for low-dose extrapolation in rats for both tumor and the cell proliferation endpoints. The benchmark concentrations for induced cell proliferation were lower than for tumors. These concentrations were extrapolated to humans using two mechanistic models. One model used computational fluid dynamics (CFD) alone to determine rates of delivery of inhaled formaldehyde to the nasal lining. The second model combined the CFD method with a pharmacokinetic model to predict tissue dose with formaldehyde-induced DNA-protein cross-links (DPX) as a dose metric. Both extrapolation methods gave similar results, and the predicted cancer risk in humans at low exposure levels was found to be similar to that from a risk assessment conducted by the U.S. EPA in 1991. Use of the mechanistically based extrapolation models lends greater certainty to these risk estimates than previous approaches and also identifies the uncertainty in the measured dose-response relationship for cell proliferation at low exposure levels, the dose-response relationship for DPX in monkeys, and the choice between linear and nonlinear methods of extrapolation as key remaining sources of uncertainty.

Administration, Inhalation↗

PubMed1990

A study of conventional formaldehyde fumigation methods.

The currently recommended methods for the formaldehyde fumigation of rooms have been studied with the aid of an instrument designed to monitor the temperature, humidity and formaldehyde concentration. The results show that although the procedures are generally effective as measured by microbiological methods the conditions within the areas treated are not those expected from calculations based on the room volume and the amount of formaldehyde used. The measured formaldehyde levels in particular are much lower than predicted and indicate that formaldehyde vapour may be effective at lower concentrations than previously supposed.

Bacillus↗

PubMed1985

A comparison of the antimicrobial activities of noxythiolin and formaldehyde solutions.

The availability of a rapid and highly specific polarographic method of analysis for formaldehyde enabled investigation of the rate of formaldehyde release from noxythiolin solutions and actual concentrations of formaldehyde in solutions during clinical use and storage. The antimicrobial activity of noxythiolin solutions, equivalent pure formaldehyde solutions and N-methylthiourea individually or in combination was examined against standard bacteriological strains and clinical isolates. Several interesting observations were made. Clinical isolates were found to be relatively susceptible to noxythiolin in contrast to laboratory strains. The growth phase of the organism radically affects activity, early exponential phase cells being susceptible to 1.0% noxythiolin. Levels of formaldehyde detected in fresh noxythiolin solutions are extremely low and would not appear to be solely responsible for the antimicrobial activity observed.

Bacteroides fragilis↗

PubMed1976

The study of DNA-RNA-polymerase complexes by kinetic formaldehyde method.

A modification of the kinetic formaldehyde method has been proposed providing a possibility for locally denatured regions (defects) formed in DNA preincubated with RNA polymerase (in the absence of nucleoside triphosphates) to be detected. This modification consists in a previous fixation of DNA-enzyme complex with small concentrations of formaldehyde, which do not induce formation of defects in DNA alone. The method has been calibrated under the conditions favourable to RNA synthesis. Studies of the effect of the fixation conditions on the number of defects in DNA interacting with RNA polymerase have shown that the number of defects is constant with formaldehyde fixation concentration between 0.05% and 0.3-0.5% and with fixation time between 2 min and 100 min. The dependence of the number of defects in DNA on RNA polymerase concentration at low ionic strength (0.05 M KCl) is presented by a curve with a plateau. From the initial linear part of the curve it has been found that the enzyme bound to DNA as a monomer. At the excess of the enzyme the mean number of nucleotide pairs between defects is 400-500. Increase of ionic strength results in decrease of the number of defects in DNA. The number of defects depends on temperature of preincubation of the complex. There were no defects in DNA at temperatures below 20 degrees C. At temperatures above 30 degrees C the number of defects reaches saturation. A sharp transition occurs in the range of temperatures between 20 degrees C and 30 degrees C. Analysis of the experimental and literature data, concerning the interaction of formaldehyde and amino acid methylol derivatives with DNA bases, leads to the conclusion that the mechanism of the formation of defects in helical DNA most likely consists in its unwinding or sharp weakening upon binding of RNA polymerase, prior to addition of formaldehyde.

Binding Sites↗