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Comparison of formaldehyde emission from building finishing materials at various temperatures in under heating system; ONDOL.

UNLABELLED: The objective of this research was to investigate the effect of various temperatures, room, 37 and 50 degrees C, on formaldehyde emission from floor materials, such as laminate and plywood floorings, and furniture materials, such as MDF and particleboard veneered with decorative paper foil, by desiccator's method. The temperature conditions were set up by, measuring the temperature in a Korean under heating system. To maintain an indoor air temperature of 20 degrees C, the temperature of the flooring surface was about 37 degrees C and the temperature of the cement mortar was 50 degrees C. The initial formaldehyde emission of the laminate flooring and plywood flooring was 1.44 and 0.63 mg/l, and for MDF and particleboard it was 4.73 and 4.95 mg/l, respectively. Floor materials were under E1 grade while furniture materials were under E2 grade in terms of formaldehyde emission. Because of the under heating system, the flooring materials were exposed to 37 and 50 degrees C, while the furniture materials mostly existed at room temperature. At 37 and 50 degrees C, the formaldehyde emission level of the flooring materials was already under 0.3 ppm (F level by JIS A 1460, application possibility without area limit) after 10 days and the emission had decreased further (0.03-0.10 mg/l) after 28 days. These levels are not injurious to the human body and will not cause sick house syndrome (SHS). The problem, however, is the furniture materials such as MDF and particleboard. As these materials are not exposed to high temperature (50 degrees C in this experiment) in living condition, it was still E2 grade of formaldehyde emission level at room temperature remained even after 28 days. Although there will be variations with the volume of furniture materials and the indoor conditions, furniture materials are the principal cause of indoor air quality pollution in Korean with the under heating system. PRACTICAL IMPLICATIONS: Koreans spend most of their time sitting on ONDOL (heated) floors, with their buttocks always in contact with the floor surface. The flooring materials are exposed to high temperatures (37-50 degrees C) why the effect of bake-out is rapid. The emission of formaldehyde from furniture materials are more important for the IAQ because usually MDF and particleboard of E2 grade are being used as furniture materials in Korea.

Air Pollution, Indoor↗

Adsorption of formaldehyde by various surfaces during gaseous decontamination.

Study of the effect of atmospheric relative humity (RH) on the adsorption of paraformaldehyde-generated formaldehyde gas on various surfaces and the effect of the adsorbed formaldehyde on the death rate of bacterial spores showed that increasing the RH caused a corresponding increase of formaldehyde levels on all surfaces. The amount peaked at 83% RH. The levels obtained at 100% RH were slightly below those at 83% RH. Cotton cloth had a much greater affinity for the gas at all RH than either glass or stainless steel. The death rate of bacterial spores on surfaces containing adsorbed formaldehyde was high for the first hour after removal from the formaldehyde atmosphere but decreased rapidly thereafter. This held true for both cotton and glass surfaces. Also, formaldehyde levels of 15 to 27 mug/ml of nutrient broth caused inhibition of bacterial growth, but levels above 27 mug/ml rendered broth sterile.

Adsorption↗

Properties of pertussis toxin mutant PT-9K/129G after formaldehyde treatment.

Formaldehyde treatment is a method routinely used to detoxify diphtheria, tetanus, and pertussis toxins as well as other molecules suitable for vaccine production. To investigate whether chemical detoxification alters the immunological properties of vaccine components, we have treated the pertussis toxin mutant PT-9K/129G with formaldehyde and tested the properties of the resulting molecules. Very low concentrations of formaldehyde stabilize the molecule without affecting the physicochemical and immunological parameters. Increasing doses of formaldehyde abolish the mitogenic and hemagglutinating activities of PT-9K/129G. At the same time, the molecule loses the ability to be recognized by a monoclonal antibody specific for a major protective epitope on the S1 subunit of pertussis toxin and its affinity for anti-pertussis toxin polyclonal antibodies is also reduced. In marked contrast, the ability of PT-9K/129G to be recognized by human T-cell clones is not affected by Formalin treatment. In vivo, the formaldehyde-treated molecules induce amounts of specific antibodies comparable with those of untreated molecules but significantly lower levels of toxin-neutralizing antibodies. Furthermore, the formaldehyde-treated molecules also show a reduced protective activity in the intracerebral challenge assay.

Animals↗

Growth of Pseudomonas C on C1 compounds: enzyme activites in extracts of Pseudomonas C cells grown on methanol, formaldehyde, and formate as sole carbon sources.

Pseudomonas C can grow on methanol, formaldehyde, or formate as sole carbon source. It is proposed that the assimilation of carbon by Pseudomonas C grown on different C1 growth substrates proceeds via one of two metabolic pathways, the serine pathway or the allulose pathway (the ribose phosphate cycle of formaldehyde fixation). This contention is based on the distribution of two key enzymes, each of which appears to be specifically involved in one of the assimilation pathways, glycerate dehydrogenase (serine pathway) and hexose phosphate synthetase (allulose pathway). The assimilation of methanol in Pseudomonas C cells appears to occur via the allulose pathway, whereas the utilization of formaldehyde or formate in cells grown on formaldehyde or formate as sole carbon sources appears by the serine pathway. When methanol is present together with formaldehyde or formate in the growth medium, the formaldehyde or formate is utilized by the allulose pathway.

Alcohol Oxidoreductases↗

Novel formaldehyde-activating enzyme in Methylobacterium extorquens AM1 required for growth on methanol.

Formaldehyde is toxic for all organisms from bacteria to humans due to its reactivity with biological macromolecules. Organisms that grow aerobically on single-carbon compounds such as methanol and methane face a special challenge in this regard because formaldehyde is a central metabolic intermediate during methylotrophic growth. In the alpha-proteobacterium Methylobacterium extorquens AM1, we found a previously unknown enzyme that efficiently catalyzes the removal of formaldehyde: it catalyzes the condensation of formaldehyde and tetrahydromethanopterin to methylene tetrahydromethanopterin, a reaction which also proceeds spontaneously, but at a lower rate than that of the enzyme-catalyzed reaction. Formaldehyde-activating enzyme (Fae) was purified from M. extorquens AM1 and found to be one of the major proteins in the cytoplasm. The encoding gene is located within a cluster of genes for enzymes involved in the further oxidation of methylene tetrahydromethanopterin to CO(2). Mutants of M. extorquens AM1 defective in Fae were able to grow on succinate but not on methanol and were much more sensitive toward methanol and formaldehyde. Uncharacterized orthologs to this enzyme are predicted to be encoded by uncharacterized genes from archaea, indicating that this type of enzyme occurs outside the methylotrophic bacteria.

Amino Acid Sequence↗

Mortality among a cohort of garment workers exposed to formaldehyde: an update.

AIMS: To evaluate the mortality experience of 11 039 workers exposed to formaldehyde for three months or more in three garment plants. The mean time weighted average formaldehyde exposure at the plants in the early 1980s was 0.15 ppm but past exposures may have been substantially higher. METHODS: Vital status was updated through 1998, and life table analyses were conducted. RESULTS: Mortality from all causes (2206 deaths, standardised mortality ratio (SMR) 0.92, 95% CI 0.88 to 0.96) and all cancers (SMR 0.89, 95% CI 0.82 to 0.97) was less than expected based on US mortality rates. A non-significant increase in mortality from myeloid leukaemia (15 deaths, SMR 1.44, 95% CI 0.80 to 2.37) was observed. Mortality from myeloid leukaemia was greatest among workers first exposed in the earliest years when exposures were presumably higher, among workers with 10 or more years of exposure, and among workers with 20 or more years since first exposure. No nasal or nasopharyngeal cancers were observed. Mortality from trachea, bronchus, and lung cancer (147 deaths, SMR 0.98, 95% CI 0.82 to 1.15) was not increased. Multiple cause mortality from leukaemia was increased almost twofold among workers with both 10 or more years of exposure and 20 years or more since first exposure (15 deaths, SMR 1.92, 95% CI 1.08 to 3.17). Multiple cause mortality from myeloid leukaemia among this group of workers was also significantly increased (8 deaths, SMR 2.55, 95% CI 1.10 to 5.03). CONCLUSIONS: Results support a possible relation between formaldehyde exposure and myeloid leukaemia mortality. Previous epidemiological studies supporting a relation between formaldehyde exposure and leukaemia mortality have been primarily of formaldehyde exposed professional groups, not formaldehyde exposed industrial workers. Limitations include limited power to detect an excess for rare cancers such as nasal and nasopharyngeal cancers and lack of individual exposure estimates.

Adolescent↗

Occupational exposure to formaldehyde and histopathological changes in the nasal mucosa.

To study the cytotoxic effect of formaldehyde on the human nasal mucosa 75 men with occupational exposure to formaldehyde or to formaldehyde and wood dust, were examined, looking particularly at early signs of irritative effects and histopathological changes in the nasal mucosa. All men underwent a medical examination and a nasal biopsy specimen was examined by a pathologist and graded from 0-8 according to the morphological changes. A high frequency of nasal symptoms, mostly a running nose and crusting, was related to exposure to formaldehyde. Only three men had a normal mucosa; the remainder had loss of cilia and goblet cell hyperplasia (11%) and squamous metaplasia (78%); in six cases (8%) there was a mild dysplasia. The histological grading showed a significantly higher score when compared with unexposed contents (2.9 v 1.8). There was no dose response relation, no malignancies, and no difference in the histological score between those exposed to formaldehyde or to formaldehyde and wood dust.

Environmental Exposure↗

Six year follow up of lung function in men occupationally exposed to formaldehyde.

The long term effects of formaldehyde on the respiratory tract have been investigated in a group of 164 workers exposed daily to the chemical during the production of urea formaldehyde resin, together with 129 workers not exposed to free formaldehyde. Exposure was classified as high (corresponding to an eight hour time weighted exposure of more than 2.0 ppm), medium (0.6 to 2.0 ppm), or low (0.1 to 0.5 ppm). Twenty five per cent of workers had had high exposure at some time and 17% moderate exposure. Both the exposed and unexposed groups had an annual assessment that included lung function. The proportion with self reported respiratory symptoms was similar in the two groups, 12% and 16% reporting breathlessness on hurrying and 26% and 20% wheezing. The initial forced expiratory volume in one second (FEV1) was within 0.5 l (approximately one standard deviation (SD)) of the predicted value (by age and height) in 65% of the exposed and 59% of unexposed workers and more than 0.5 l below the predicted value in 9% of exposed and 11% of unexposed workers. The mean decline in FEV1 was 42 ml a year (SD 45) in the exposed group and 41 ml a year in the unexposed group (SD 40 ml a year). The rate of decline showed the expected association with smoking in the unexposed group, but in the exposed group the mean rate of decline in the never smokers was similar to that in current smokers. There were, however, relatively few never smokers and considerable variation in the rates of decline. In the exposed group no association was found between the rate of decline and indices of exposure to formaldehyde. Thus there is no evidence from this study of an excess of respiratory symptoms or decline in lung function in the workers exposed to formaldehyde. The similar rate of decline of FEV1 however in never smokers and smokers of the exposed group is consistent with findings of other studies for workers exposed to formaldehyde and to toluene di-isocyanate.

Adolescent↗

Mortality among chemical workers in a factory where formaldehyde was used.

OBJECTIVES: An independent and updated historical cohort mortality study was conducted among chemical plant workers to investigate further an association between exposures to formaldehyde and particulates and cancers of the nasopharynx and lung reported in an earlier National Cancer Institute study of the same plant. METHODS: Subjects were 7359 workers who were first employed between 1941 and 1984 in a factory in Wallingford, Connecticut where formaldehyde was used. Vital status was determined on 31 December 1984 for 96% of the cohort and death certificates were obtained for 93% of 1531 known deaths. Exposures of individual workers were estimated quantitatively for formaldehyde, product particulates, and non-product particulates, and qualitatively for pigment. Statistical analyses focused on 6039 white men in 1945-84. Cohort data that could not have been included in the National Cancer Institute study were also analysed separately. RESULTS: Mortality among long term workers (employed > or = 1 y) was generally similar to or more favourable than that of the general population, and there was little evidence of a relation between either rates of lung cancer or standardised mortality ratios (SMRs) and several measures of exposure to formaldehyde, particulates, and pigment. For several causes including lung cancer, death rates among short term workers (employed < 1 y) were significantly increased. Short term workers did not seem to differ from long term workers for the exposures considered. Among all white men, a significant SMR of 550 (local comparison) for nasopharyngeal cancer (NPC) was based on the same four index cases identified in the earlier study of this plant. Only one case of nasopharyngeal cancer had any appreciable exposure to formaldehyde. No new cases of nasopharyngeal cancers were found among the cohort data that could not have been included in the National Cancer Institute study--that is, extended observation time and additional study members. CONCLUSIONS: Among workers employed for at least one year, this study provides little evidence that the risk of lung cancer is associated with exposure to formaldehyde alone or in combination with particulates or pigment. The significant increases in both the rates and SMRs for lung cancer seem to be primarily a phenomenon of short term workers, but the possibility remains that unmeasured occupational or non-occupational factors may have played a part.

Chemical Industry↗

Occupational asthma due to formaldehyde.

Bronchial provocation studies on 15 workers occupationally exposed to formaldehyde are described. The results show that formaldehyde exposure can cause asthmatic reactions, and suggest that these are sometimes due to hypersensitivity and sometimes to a direct irritant effect. Three workers had classical occupational asthma caused by formaldehyde fumes, which was likely to be due to hypersensitivity, with late asthmatic reactions following formaldehyde exposure. Six workers developed immediate asthmatic reactions, which were likely to be due to a direct irritant effect as the reactions were shorter in duration than those seen after soluble allergen exposure and were closely related to histamine reactivity. The breathing zone concentrations of formaldehyde required to elicit these irritant reactions (mean 4.8 mg/m3) were higher than those encountered in buildings recently insulated with urea formaldehyde foam, but within levels sometimes found in industry.

Adult↗

Importance of fixation in immunohistochemistry: use of formaldehyde solutions at variable pH for the localization of tyrosine hydroxylase.

Adequate fixative in immunohistochemistry requires not only a rapid and total immobilization of the antigen, but also a sufficient preservation of its immunoreactivity and maintenance of its accessibility to the immunochemical reagents for localization. Thus, the optimal fixation condition for a specific antigen necessitates a compromise between these opposing variables and can be determined by the preparation of a series of tissues with a progressively increasing degree of fixation. Unless the results of localization using such a series is available, one must be satisfied with adequate but less than optimal results. In the present study, this principle is demonstrated using the localization of tyrosine hydroxylase in the dopaminergic system with formaldehyde as the fixative. The rate and degree of fixation with formaldehyde was shown to be highly pH dependent. By perfusing the tissue with formaldehyde at pH 6.5 (where the rate of fixation is extremely slow) it is possible to rapidly distribute the fixative homogeneously into the tissue. By suddenly changing to a formaldehyde perfusate of higher pH, the cross-linking reaction is rapidly increased. This two-step fixation procedure provides a means of obtaining a rapid and uniform immobilization of the antigen, so that its translocation can be avoided. The final degree of fixation is controlled by the duration and pH of the second fixative solution. The results obtained by increasing the pH of the second solution demonstrated that complete fixation of tyrosine hydroxylase in the dopaminergic system with formaldehyde maybe obtained using a very basic formaldehyde solution (pH 11) while still retaining immunoreactivity of the enzyme. The localization that was achieved at lower pH appeared adequate until it was compared to the results obtained by perfusion at pH 11 in the second step.

Animals↗

Pharyngeal cancer mortality among chemical plant workers exposed to formaldehyde.

OBJECTIVES: To assess the possible relationship between formaldehyde exposure and mortality risk from pharyngeal cancer (PC), in particular nasopharyngeal cancer (NPC). METHODS: Subjects were 7328 workers employed at a plastics-producing plant (1941-1984). Vital status for 98% of the cohort and cause of death for 95% of 2872 deaths were determined. Reconstructed exposures to formaldehyde, particulates and pigment were used to compute several exposure measures. Standardized mortality ratios (SMRs) were computed for several demographic, work history and formaldehyde exposure variables. In a nested case-control study, seven cases of NPC and 15 cases of other PC were matched on race, sex, age and year of birth to four controls from the cohort. Among interviewed subjects, lifetime smoking history was determined using respondents or proxies for all but one control subject. RESULTS: Statistically significant 2.23-fold and fivefold excesses for PC and NPC, respectively, were observed. Fivefold range NPC excesses were observed for both short ( < 1 year) and long-term workers and were concentrated among workers hired during 1947-1956. Only three NPC cases were exposed to formaldehyde for longer than one year, and each had low average intensity of formaldehyde exposure (0.03-0.60 ppm). Only a few exposure measures revealed some evidence of an association with all PC or NPC. For all PC combined, adjustment for smoking and year-of-hire in the case-control study generally corroborated findings from the cohort study. CONCLUSIONS: Overall, the pattern of findings suggests that the large, persistent nasopharyngeal and other PC excesses observed among the Wallingford workforce are not associated with formaldehyde exposure, and may reflect the influence of nonoccupational risk factors or occupational risk factors associated with employment outside the Wallingford plant.

Adult↗

Report on the Consensus Workshop on Formaldehyde.

The Consensus Workshop on Formaldehyde consisted of bringing together scientists from academia, government, industry and public interest groups to address some important toxicological questions concerning the health effects of formaldehyde. The participants in the workshop, the Executive Panel which coordinated the meeting, and the questions posed, all were chosen through a broadly based nomination process in order to achieve as comprehensive a consensus as possible. The subcommittees considered the toxicological problems associated with formaldehyde in the areas of exposure, epidemiology, carcinogenicity/histology/genotoxicity, immunology/sensitization/irritation, structure activity/biochemistry/metabolism, reproduction/teratology, behavior/neurotoxicity/psychology and risk estimation. Some questions considered included the possible human carcinogenicity of formaldehyde, as well as other human health effects, and the interpretation of pathology induced by formaldehyde. These reports, plus introductory material on the procedures used in setting up the Consensus Workshop are presented here. Additionally, there is included a listing of the data base that was made available to the panel chairmen prior to the meeting and was readily accessible to the participants during their deliberations in the meeting. This data base, since it was computerized, was also capable of being searched for important terms. These materials were supplemented by information brought by the panelists. The workshop has defined the consensus concerning a number of major points in formaldehyde toxicology and has identified a number of major deficits in understanding which are important guides to future research.

Abnormalities, Drug-Induced↗

An approach to mechanism-based cancer risk assessment for formaldehyde.

The established carcinogenicity of formaldehyde in the rat and suggestive epidemiological evidence that formaldehyde may be a human carcinogen have led to its regulation by U.S. Federal agencies as a probable human carcinogen. These risk assessments have typically been based on tumor data in F344 rats exposed chronically to formaldehyde by inhalation and used the inhaled concentration as a measure of dose and the linearized multistage model (LMS) for dose-response characterization. Low-dose risks estimated with the LMS are thought to be conservative but are also generally acknowledged to be highly uncertain. In this manuscript, we first consider in generic terms how use of chemical-specific data on mechanisms of target tissue dosimetry and the series of tissue responses to the chemical that culminate in tumor formation can lead to more accurate dose-response characterization. A planned mechanism-based risk assessment for formaldehyde is then described. This risk assessment uses data on target tissue dosimetry, size of the target cell population in the rat nasal epithelium, number and size of putative preneoplastic lesions, and tumor incidence. These data establish parameter values for a biologically based, multistage cancer model that is then used to predict cancer risk at low exposure levels. Such work provides insights into the relative roles of formaldehyde-stimulated cell replication and procarcinogenic mutation in tumor formation. Finally, future directions are outlined for research on tissue dosimetry and scaling of the mechanism-based formaldehyde risk model from rats to people.

Animals↗

Irritant effects of formaldehyde exposure in mobile homes.

This paper reports the irritant effects associated with formaldehyde exposures in mobile homes. Week-long, integrated formaldehyde concentrations were measured using passive monitors in summer and winter while the mobile home residents continued their normal activities. Information on acute health problems, chronic respiratory/allergic illnesses, smoking behavior, demographic variables, and time spent at home was obtained on over 1000 individuals during the sampling period. Measured formaldehyde concentrations varied from under the limit of detection (0.01 ppm) to 0.46 ppm. Formaldehyde exposure was estimated for each individual by multiplying the concentration measured in his or her home by the time he or she spent at home. Irritant effects were found to be associated with formaldehyde exposure after controlling for age, sex, smoking status, and chronic illnesses using a logistic procedure. Some of the interaction terms found to be significant indicated that there were synergistic effects between formaldehyde exposure and chronic health problems.

Adolescent↗

Formaldehyde in dentistry: a review of mutagenic and carcinogenic potential.

For many years there has been controversy over the value of antimicrobial drugs for intracanal dressings in endodontics. Formocresol, a formaldehyde compound, has evolved as the preferred drug for routine endodontic procedures, as well as pediatric endodontics. The increase in the use of formaldehyde has been complicated by the introduction of paraformaldehyde pastes for filling root canals. Neither of these formulas has ever been standardized. The doses are arbitrary, and the common dose of formocresol has been shown to be many times greater than the minimum dose needed for effect. The efficacy of paraformaldehyde pastes is questionable and remains clouded by inconclusive evidence, conflicting research, inadequate terminology, and a lack of convincing statistical evidence. The clinical use and delivery of formocresol and paraformaldehyde pastes remain arbitrary and unscientific. Formaldehyde has a known toxic mutagenic and carcinogenic potential. Many investigations have been conducted to measure the risk of exposure to formaldehyde; it is clear that formaldehyde poses a carcinogenic risk in humans. There is a need to reevaluate the rationale underlying the use of formaldehyde in dentistry particularly in light of its deleterious effects.

Carcinogens↗

Recent advances in understanding and exploiting the activation of anthracyclines by formaldehyde.

The anthracycline group of compounds are amongst the most effective chemotherapy agents currently in use for cancer treatment. They are generally classified as topoisomerase II inhibitors but also have a variety of other targets in cells. It has been known for some years that the anthracyclines are capable of forming DNA adducts, but the relevance and extent of these DNA adducts in cells and their role in causing cell death has remained obscure. When the adduct structure was solved, it became clear that formaldehyde was an absolute requirement for adduct formation. This led to a renewed interest in the capacity of anthracyclines to form DNA adducts, and there are now several ways in which adduct formation can be facilitated in cells. These involve strategies to provide the requisite formaldehyde in the form of anthracycline-formaldehyde conjugates, and the use of formaldehyde-releasing drugs in combination with anthracyclines. Of particular interest is the new therapeutic compound AN-9 that releases both butyric acid and formaldehyde, leading to efficient anthracycline-DNA adduct formation, and synergy between the two compounds. Targeted formation of adducts using anthracycline-formaldehyde conjugates tethered to cell surface targeted molecules is now also possible. Some of the cellular consequences of these adducts have now been studied, and it appears that their formation can overcome anthracycline-resistance mechanisms, and that they are more efficient at inducing apoptosis than when functioning primarily through impairment of topoisomerase II. The clinical application of the use of anthracyclines as DNA adduct forming agents is now being explored.

Animals↗

Formaldehyde exposure in some educational hospitals of Tehran.

This research was conducted to determine formaldehyde exposure of staffs in pathology laboratories, surgery rooms and endoscopy wards in eight large hospitals of Tehran University of Medical Sciences located at Tehran, Iran. Air sampling have been made by both long and short-term methods. Total numbers of samples were 160 for both methods. Nineteen samples of 160 samples were collected as blank in other non-exposed environments such as administrative sections. The mean (SD) levels of formaldehyde in long-term methods were 0.96 (0.74), 0.25 (0.21) and 0.13 (0.18) ppm, at pathology laboratories, surgery rooms and endoscopy wards, respectively. The results of measurements showed that mean (SD) concentration of formaldehyde in one hour sampling at short intervals were 0.83 (0.29), 0.23 (0.16) and 0.75 (0.25) ppm at pathology labs, surgery rooms and endoscopy wards, respectively. There were significant differences in the mean levels of formaldehyde (long-term) at surgery rooms (p < 0.02) and endoscopy wards (p < 0.005) in eight hospitals of this study. It is concluded that the concentration levels of formaldehyde at pathology laboratories exceeded recommended limit which established by the American Conference of Governmental and Industrial Hygienists ACGIH (TLV-C = 0.3 ppm). It is recommended that local exhaust ventilation should be installed to minimize the contact to formaldehyde in the staffs.

Air Pollutants, Occupational↗