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PubMed1998

Formaldehyde-related textile allergy: an update.

Part I of this study explores whether clothing today contains formaldehyde levels likely to cause contact allergy in formaldehyde-allergic patients. Part II of this study examines whether current reactions to textiles may be due to allergy to textile resins and whether individuals with formaldehyde-related textile allergy will react to the newer low formaldehyde resins used in the textile industry. Part I: free formaldehyde was measured in 16 fabric specimens produced in the US and overseas. Additionally, since the textile industry has moved to the use of newer methods for measuring fabric formaldehyde content, the newer methodology was compared with the older methods used in the medical literature. Part II: 10 subjects with known textile contact allergy were patch tested to available Chemotechnique textile resins and 6 new low-formaldehyde resins used by the textile industry. Part I: 8 fabric specimens yielded no detectable formaldehyde and 7 specimens yielded <200 ppm free formaldehyde, using Schiff's reagent and Merck testing methods. 1 specimen showed approximately 2000 ppm formaldehyde, as measured by the Merck test, but only 24 ppm free formaldehyde when retested by the method described in Japanese Law #112. Part II: all subjects reacted strongly to formaldehyde and DMDHEU (the predominant resin currently used in textiles). 6 subjects reacted to EUMF. 2 subjects had mild reactions to the newer low-formaldehyde resins and 1 to the non-formaldehyde Fixapret NF. Our results suggest that most clothing today yields free formaldehyde levels unlikely to cause contact allergy in formaldehyde-allergic individuals. Japanese method #112 is the recommended methodology to measure free formaldehyde in future studies. DMDHEU may now represent the main cause of textile allergy and may be a better screen than EUMF for this problem. Newer resins yielding fabrics with <75 ppm free formaldehyde may cause occasional reactions, but are more likely to be tolerated by individuals with textile contact allergy. Treatment of these individuals should be directed at identification of reliable sources of garments utilizing these newer resins.

Adult↗
PubMed2002

Conversion and toxicity characteristics of formaldehyde in acetoclastic methanogenic sludge.

An unadapted mixed methanogenic sludge transformed formaldehyde into methanol and formate. The methanol to formate ratio obtained was 1:1. Formaldehyde conversion proceeded without any lag phase, suggesting the constitutive character of the formaldehyde conversion enzymes involved. Because the rate of formaldehyde conversion declined at increased formaldehyde additions, we hypothesized that some enzymes and/or cofactors might become denatured as a result of the excess of formaldehyde. Furthermore, formaldehyde was found to be toxic to acetoclastic methanogenesis in a dual character. Formaldehyde toxicity was partly reversible because once the formaldehyde concentration was extremely low or virtually removed from the system, the methane production rate was partially recovered. Because the degree of this recovery was not complete, we conclude that formaldehyde toxicity was partly irreversible as well. The irreversible toxicity likely can be attributed to biomass formaldehyde-related decay. Independent of the mode of formaldehyde addition (i.e., slug or continuous), the irreversible toxicity was dependent on the total amount of formaldehyde added to the system. This finding suggests that to treat formaldehyde-containing waste streams, a balance between formaldehyde-related decay and biomass growth should be attained.

Acetates↗
PubMed1992

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

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

Animals↗
PubMed1984

Effect of acetaldehyde and cyanamide on the metabolism of formaldehyde by hepatocytes, mitochondria, and soluble supernatant from rat liver.

Formaldehyde can be metabolized primarily by two different pathways, one involving oxidation by the low-Km mitochondrial aldehyde dehydrogenase, the other involving a specific, glutathione-dependent, formaldehyde dehydrogenase. To estimate the roles played by each enzyme in formaldehyde metabolism by rat hepatocytes, experiments with acetaldehyde and cyanamide, a potent inhibitor of the low-Km aldehyde dehydrogenase were carried out. The glutathione-dependent oxidation of formaldehyde by 100,000g rat liver supernatant fractions was not affected by either acetaldehyde or by cyanamide. By contrast, the uptake of formaldehyde by intact mitochondria was inhibited 75 to 90% by cyanamide. Acetaldehyde inhibited the uptake of formaldehyde by mitochondria in a competitive fashion. Formaldehyde was a weak inhibitor of the oxidation of acetaldehyde by mitochondria, suggesting that, relative to formaldehyde, acetaldehyde was a preferred substrate. In isolated hepatocytes, cyanamide, which inhibited the oxidation of acetaldehyde by 75 to 90%, produced only 30 to 50% inhibition of formaldehyde uptake by cells as well as of the production of 14CO2 and of formate from [14C]formaldehyde. The extent of inhibition by cyanamide was the same as that produced by acetaldehyde (30-40%). In the presence of cyanamide, acetaldehyde was no longer inhibitory, suggesting that acetaldehyde and cyanamide may act at the same site(s) and inhibit the same formaldehyde-oxidizing enzyme system. These results suggest that, in rat hepatocytes, formaldehyde is oxidized by cyanamide- and acetaldehyde-sensitive (low-Km aldehyde dehydrogenase) and insensitive (formaldehyde dehydrogenase) reactions, and that both enzymes appear to contribute about equally toward the overall metabolism of formaldehyde.

Acetaldehyde↗
PubMed1992

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

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

Animals↗
PubMed1997

Comparison of inhaled formaldehyde dosimetry predictions with DNA-protein cross-link measurements in the rat nasal passages.

Kimbell and coworkers (Toxicol, Appl. Pharmacol, 121, 253-263, 1993) developed a computational fluid dynamics (CFD) model of a F344 rat nasal passage to quantify local wall mass flux (uptake rate) of inhaled chemical. To simulate formaldehyde uptake, Kimbell et al. assumed that mass transfer of formaldehyde from the air into the nasal lining was fast and complete. This was approximated in the CFD model by setting the formaldehyde concentration at the airway walls to zero. Experimental confirmation of formaldehyde mass-flux predictions is desirable if the CFD model is to be used for predicting formaldehyde dosimetry. The purpose of this study was to see if the CFD model predictions of formaldehyde mass flux are consistent with laboratory data on formaldehyde dosimetry. In this study, a mathematical model of the nasal lining was modified to link CFD dosimetry predictions for inhaled formaldehyde with measured tissue disposition of inhaled gas. This model treats the nasal lining as a single, well-stirred compartment, accounts for formaldehyde reaction via saturable and first-order pathways, and allows comparison of model-predicted DNA-protein cross-links (DPX) with regional DPX measured in formaldehyde-exposed rats. Effective Michaelis-Menten kinetic parameters (Vmax = 3040 microM/min and Km = 59 microM) and a pseudo-first-order rate constant for elimination of formaldehyde by nonsaturable pathways (kf = 6 min-1) were estimated (fit) using an average mass flux derived from experimentally measured uptake of formaldehyde. DPX predictions obtained using the estimated kinetic parameters and linking the CFD model to the nasal-lining model compared well with experimentally measured DPX. The close correlation between predicted and measured DPX in the rat nasal passage supports the CFD model predictions of formaldehyde mass flux at the level of resolution provided by the experimental data.

Administration, Inhalation↗
PubMed1996

The effects of mercaptoethanol-formaldehyde on tissue fixation and protein retention.

The study compared the effects of mercaptoethanol-formaldehyde and formaldehyde alone, on tissue fixation and protein retention in human and mouse tissues. Shrinkage of tissues and the penetration rate of the fixatives were assessed. The cross-linking ability of the fixatives was determined by viscometry, sodium dodecyl sulphate-polyacrylamide gel electrophoresis, and spectrophotometry, using bovine serum albumin and human haemoglobin. Tissues fixed in buffered 0.0025% mercaptoethanol-4% formaldehyde showed good nuclear and cytoplasmic detail, better than those fixed in buffered 4% formaldehyde. There was no significant difference in shrinkage. A mixture of 0.0025% mercaptoethanol-4% formaldehyde penetrated faster into adult liver than 4% formaldehyde. The mean penetration rate (+/-SE) or coefficient of diffusibility of 0.0025% mercaptoethanol-4% formaldehyde into adult liver was 1.32 +/- 0.01 and that of 4% formaldehyde was 1.12 +/- 0.06 (p < 0.04). Both fixatives diffused more rapidly into mouse liver than into human liver. The cross-linking ability of mercaptoethanol-formaldehyde depends on the concentration of the fixative and the time of fixation. Bovine serum albumin (15%) and 0.1% mercaptoethanol alone formed a gel, whilst electrophoresis showed monomers in the supernatant. Mercaptoethanol (0.1%) also rapidly decreased the absorption at 420 nm, suggesting denaturation. It seems that mercaptoethanol increases the number of thiol groups available to form cross-links with formaldehyde. This study demonstrated that mercaptoethanol-formaldehyde fixed and cross-linked tissues better than formaldehyde at 3 h and 4 h, but not at 1 h and 2 h. The most effective concentration of mercaptoethanol for tissue fixation in 4% formaldehyde is 0.0025%.

Animals↗
PubMed1990

Formaldehyde in drinking water: comparative hazard evaluation and an approach to regulation.

Formaldehyde, a widely used industrial chemical to which humans are ubiquitously exposed, presented cause for concern when it was demonstrated to be carcinogenic in laboratory animals. Risk assessment protocols subsequently applied to formaldehyde are of questionable validity in light of the results of recent mechanistic investigations of biological responses to formaldehyde. Further, the hazard of ingested formaldehyde is not addressed in current assessment protocols. This paper addresses the potential human health risks accompanying low-level exposure to formaldehyde as a contaminant in drinking water. In this exposure scenario, noncarcinogenic risk from inhalation of formaldehyde from drinking water is evaluated through knowledge of the metabolism and biological effects of formaldehyde exposure. Noncarcinogenic risk from ingestion of formaldehyde in drinking water is evaluated from the perspective gained by comparison with dietary sources of formaldehyde. Carcinogenic risk to humans is evaluated in light of recent investigations into the mechanisms underlying biological responses to formaldehyde exposure. Finally, based on a comparison of ingestion of formaldehyde in drinking water with ingestion of naturally occurring formaldehyde in foods, a comparative hazard approach to formaldehyde regulation is offered as a supplement to the rigid evaluation protocols currently used.

Animals↗
PubMed2005

Determination of formaldehyde levels in 100 furniture workshops in Ankara.

One of the airborne pollutants in wood products industry is formaldehyde, which may pose some health effects. Therefore this study is conducted to determine formaldehyde levels in 100 furniture-manufacturing workshops in Ankara and also to determine the symptoms, which may be related with formaldehyde exposure among the workers. Indoor formaldehyde levels ranged from 0.02 ppm to 2.22 ppm with a mean of 0.6 +/- 0.3 ppm. Outdoor formaldehyde levels also ranged from 0.0 ppm to 0.08 ppm with a mean of 0.03 +/- 0.03 ppm. Formaldehyde levels were higher in workplaces located at basement than in workplaces located at or above ground level (p < 0.01). An association was found between indoor formaldehyde levels and the types of fuel used (p < 0.05). The levels were higher in workplaces where only sawdust was used for heating, than in workplaces where wood, coal, and sawdust are used (p = 0.02). An association was found between runny nose and indoor formaldehyde levels (p = 0.03). Formaldehyde levels were lower in workplaces where employees had no symptoms than in those where employees had 4 or more symptoms (p = 0.02). Of 229 employees 57 subjects (24.9%) work under the formaldehyde levels of 0.75 ppm and above. Thus, approximately one fourth of the employees in workplaces are working in environments with formaldehyde levels exceeding those permitted by Occupational Safety and Health Administration (OSHA). The employees working in small-scale furniture workshops are at risk of formaldehyde exposure. Measures, such as improved ventilation, have to be taken in these workplaces, in order to decrease the formaldehyde levels.

Age Distribution↗
PubMed2003

[Formaldehyde exposure levels and exposure control measures during an anatomy dissecting course].

The evaporation of formaldehyde from cadavers can produce high exposures among students and instructors. A possible causal role for formaldehyde has been considered likely for tumor of the nasopharynx and the nasal cavities in human beings. Due to this reason, Japan Ministry of Education, Culture, Sports, Science and Technology (MEXT) has set a guideline, which includes--decrease in gaseous formaldehyde in gross anatomy dissection laboratories and a guide to medical students about the toxicity of formaldehyde and protective method to avoid damages to skin, mucous, membrane, etc, in 2002. To understand what effective plans should be regarding the awareness of students about this notification, this study measured the gaseous formaldehyde concentrations in the anatomy dissection room and also analyzed the formaldehyde-related symptoms, and frequency of using protective measures. The study was conducted over a period of 3 months during the anatomy dissection exercise. We found that immediately after removing the cadavers' plastic covering, formaldehyde concentrations in the dissection room increased sharply. The concentration reached a peak point of 0.62 ppm after 10 minutes of starting of the class. This was much above the recommended level of 0.5 ppm set by Japan Society for Occupational Health. After 30 minutes of achieving the peak the formaldehyde level started decreasing gradually to a level of 0.11 ppm. Formaldehyde-related symptoms were observed in 59% of students. They had experienced symptoms of irritation of eyes, nose, throat, airways, skin, and headache during the course. Ocular discomfort was found significantly higher in the contact lenses users compared to the spectacle users or the normal eye sight group. Although, the guidelines about toxicity of formaldehyde and its protective measures to prevent damages to skin, mucous membrane etc. were informed to every student, only 52% of the students used both the mask containing activated carbon and the rubber gloves in every practical class without fail. Environmental Health Criteria 89 of International Program of Chemical Safety states, "It must be regarded that formaldehyde fluid is not absorbed directly into tissues through the skin". So the students may be allowed in some cases to touch the cadaver, treated by formaldehyde content fixative, by bare hands to understand the feel of certain organs and tissues. These results support that the rules of health supervision including necessity to use of protective measures, monitoring of indoor air formaldehyde etc. should be adhered by students and instructors in anatomy dissection room during the practical class.

Air Pollution, Indoor↗
PubMed2004

[Validation of a method for discrimination of formaldehyde processing in textile products].

It is important to investigate a cause of formaldehyde contamination exceeding a regulation limit value in a textile product. If formaldehyde was released from a textile product itself by treatment or processing with formaldehyde, an administrative guidance is given to a manufacture. On the other hand, when the formaldehyde migrated from other textile products or a furniture stand during displaying, an improvement instruction is performed to the store. Iwama et al. [Ann. Rep. Nagoya City Public Res. Inst., 42, 11-16 (1996)] developed a method for distinguishing fabric processing and migration by additional hydrolytic extraction using hydrochloric acid solution. This study was to confirm the reliability and stability of the method for knowing formaldehyde processing on textiles. Five laboratories evaluated three samples: unprocessed textile, processed textile and unprocessed but formaldehyde-migrated textile. For a processed textile sample, amounts of formaldehyde increased by additional extractions with acidic solution, so all laboratories judged that the sample had been treated with formaldehyde. In the cases of the other two samples, such increases were not observed in the extracts using acidic solution. All laboratories reported that these samples were not processed using formaldehyde but had absorbed a different level of formaldehyde by migration. In a series of experiments, the judgement about the existence of formaldehyde processing or migration is comparatively consistent among all laboratories. This validation study concluded that the distinguishing method adopting additional extractions with acidic solution is useful to find formaldehyde processing of textile, and to deal with processing and migration separately as a cause of formaldehyde contamination.

Consumer Product Safety↗
PubMed1996

Formaldehyde replaces glutaraldehyde in porcine bioprosthetic heart valves.

BACKGROUND AND AIMS OF THE STUDY: In the production of porcine bioprostheses, the initial glutaraldehyde treatment is often followed by a short incubation in formaldehyde to ensure sterility of the valve. It is assumed that the glutaraldehyde cross links are stable and that the formaldehyde step does not alter the glutaraldehyde incorporated. The objective of this study was to determine whether the formaldehyde interacts with the tissue to cause changes in the glutaraldehyde composition. MATERIALS AND METHODS: Two methods of tissue treatment were investigated: (i) fresh porcine leaflet tissue was treated with glutaraldehyde, followed by storage in formaldehyde, (ii) tissue processed in glutaraldehyde and transferred to formaldehyde for six hours was returned to glutaraldehyde for storage. The content of the two aldehydes was estimated by high performance liquid chromatography (HPLC), using an adaptation of the method developed by Hughes et al, which measures the acid labile Schiff bases formed between the collagen and the aldehyde. RESULTS: The initial content of glutaraldehyde in the tissue declined from 63 +/- 10 nmol/mg dry weight to 21 +/- 4 nmol/mg dry weight when the leaflets were placed in formaldehyde for 24 hours. The initial uptake of formaldehyde was 800 +/- 144 nmol/mg dry weight after 24 hours and this declined to 370 +/- 33 nmol/mg dry weight over a 16 week period of storage in formaldehyde. By this stage, the level of glutaraldehyde had decreased to 2.4 +/- 0.2 nmol/mg dry weight. There was a sharp decline in the glutaraldehyde concentration from 89 +/- 6 nmol/mg dry weight to 14 +/- 1 nmol/mg dry weight when the tissue was placed in 4% formaldehyde solution for six hours. The formaldehyde uptake was 770 +/- 54 nmol/mg dry weight. After return to 0.625% glutaraldehyde solution the formaldehyde concentration declined whilst the glutaraldehyde concentration initially increased. CONCLUSIONS: These results show that the formaldehyde reacts with the epsilon amino groups of lysine which had not reacted with glutaraldehyde, probably for steric reasons; and that formaldehyde replaces some glutaraldehyde in the tissue by a mass action effect. The tissue concentration of both aldehydes subsequently declined over the study period.

Animals↗
PubMed1993

Formaldehyde-induced airway hyperreactivity in vivo and ex vivo in guinea pigs.

Human exposure to formaldehyde is extensive, in both the indoor and the outdoor environment. The airways are clearly an important site of action of formaldehyde. Although many previous studies have examined the effect of formaldehyde in the upper respiratory tract, it remains controversial whether this compound can affect the lower respiratory tract. To determine whether formaldehyde induces airway hyperreactivity, guinea pigs were exposed to formaldehyde or filtered air (sham control) for 2 or 8 hr. Airway smooth muscle responsiveness was evaluated in vivo and ex vivo. Specific pulmonary resistance and airway reactivity (to infused acetylcholine) increased with formaldehyde exposure. Formaldehyde exposure caused bronchoconstriction and hyperreactivity at lower concentrations when exposure duration was extended from 2 to 8 hr. Exposure to > or = 0.3 ppm formaldehyde for 8 hr was sufficient to produce a significant increase in airway reactivity, while similar effects only occurred after > 9 ppm formaldehyde for 2 hr. Formaldehyde exposure also heightens airway smooth muscle responsiveness to acetylcholine (or carbachol) ex vivo. These effects occurred with no evidence of epithelial damage or inflammation up to 4 days after formaldehyde exposure. Thus, at concentrations relevant to environmental exposure, formaldehyde, a common indoor air pollutant, alters airway smooth muscle reactivity in guinea pigs. These findings suggest that the duration of exposure is important to the induction of airway hyperreactivity and that prolonged, low-level exposures may generate abnormal physiological responses in the airways not detectable after acute exposures.

Animals↗
PubMed1986

Inhibition of the low-Km mitochondrial aldehyde dehydrogenase by diethyl maleate and phorone in vivo and in vitro. Implications for formaldehyde metabolism.

Formaldehyde can be oxidized primarily by two different enzymes, the low-Km mitochondrial aldehyde dehydrogenase and the cytosolic GSH-dependent formaldehyde dehydrogenase. Experiments were carried out to evaluate the effects of diethyl maleate or phorone, agents that deplete GSH from the liver, on the oxidation of formaldehyde. The addition of diethyl maleate or phorone to intact mitochondria or to disrupted mitochondrial fractions produced inhibition of formaldehyde oxidation. The kinetics of inhibition of the low-Km mitochondrial aldehyde dehydrogenase were mixed. Mitochondria isolated from rats treated in vivo with diethyl maleate or phorone had a decreased capacity to oxidize either formaldehyde or acetaldehyde. The activity of the low-Km, but not the high-Km, mitochondrial aldehyde dehydrogenase was also inhibited. The production of CO2 plus formate from 0.2 mM-[14C]formaldehyde by isolated hepatocytes was only slightly inhibited (15-30%) by incubation with diethyl maleate or addition of cyanamide, suggesting oxidation primarily via formaldehyde dehydrogenase. However, the production of CO2 plus formate was increased 2.5-fold when the concentration of [14C]formaldehyde was raised to 1 mM. This increase in product formation at higher formaldehyde concentrations was much more sensitive to inhibition by diethyl maleate or cyanamide, suggesting an important contribution by mitochondrial aldehyde dehydrogenase. Thus diethyl maleate and phorone, besides depleting GSH, can also serve as effective inhibitors in vivo or in vitro of the low-Km mitochondrial aldehyde dehydrogenase. Inhibition of formaldehyde oxidation by these agents could be due to impairment of both enzyme systems known to be capable of oxidizing formaldehyde. It would appear that a critical amount of GSH, e.g. 90%, must be depleted before the activity of formaldehyde dehydrogenase becomes impaired.

Acetaldehyde↗
PubMed1996

The role of the outer membrane in formaldehyde tolerance in Escherichia coli VU3695 and Halomonas sp. MAC.

To investigate the mechanism of formaldehyde tolerance in Gram-negative bacteria, two formaldehyde-tolerant strains, Escherichia coli VU3695 and Halomonas sp. MAC (DSM 7328), and formaldehyde-sensitive revertants obtained by ethidium bromide or novobiocin treatment were studied. The presence of high levels of formaldehyde dehydrogenase activity alone proved insufficient to confer tolerance to high formaldehyde concentrations, as shown by high activity displayed by formaldehyde-sensitive revertants of Halomonas MAC. Moreover, formaldehyde-tolerant strains also proved to be tolerant to high concentrations of acetaldehyde and glutaraldehyde, which are not oxidized by formaldehyde dehydrogenase. Treatment with sublethal concentrations of EDTA rendered the resistant strains highly sensitive to formaldehyde without affecting the activity of formaldehyde dehydrogenase. Comparison of the outer membrane proteins of formaldehyde-resistant strains with those of their sensitive revertants showed the presence of at least one additional high molecular mass protein in the tolerant strains. It is concluded that formaldehyde tolerance in the bacteria studied depends on the composition and structure of the outer membrane.

Acetaldehyde↗
PubMed1989

Measurement of specific IgE antibodies in individuals exposed to formaldehyde.

Using an in-vitro test, the presence of formaldehyde-specific IgE antibodies was investigated in sera from four groups of individuals exposed to formaldehyde by different routes and concentrations. Group (A) 28 subjects living or working in rooms or places where formaldehyde-containing construction materials were used; (B) 18 subjects occupationally exposed to relatively high concentrations of formaldehyde; (C) 12 paramedic employees working in a renal dialysis unit where formaldehyde-sterilized dialysers were being used; and (D) 28 subjects undergoing haemodialysis with these formaldehyde-sterilized dialysers. Formaldehyde-specific IgE antibodies could be detected in only one of the 86 serum samples. This particular sample was from a worker occupationally exposed to formaldehyde (group (B], but who did not show any work-related symptoms. In two pools of control sera from unexposed subjects no specific IgE antibodies to formaldehyde were detected. It is concluded that exposure to formaldehyde, even in relatively high concentrations, rarely evokes the production of specific IgE antibodies. The presence of these specific antibodies is not necessarily attended by allergic symptoms. On the other hand, the symptoms supposed to be related to formaldehyde exposure and reported in this study by 24 out of 28 subjects in group (A), and some of the subjects in groups (B) and (C), cannot be attributed to an IgE-mediated sensitization to formaldehyde.

Air Pollutants↗
PubMed1985

Contact allergy to phenol-formaldehyde resins.

Adverse reactions to phenol-formaldehyde resins include depigmentation, irritant dermatitis, chemical burns and allergic contact dermatitis. Allergic contact dermatitis from phenol-formaldehyde resin has mainly been ascribed to resins based on paratertiary-butyl phenol and formaldehyde, and such a resin is included in the ICDRG standard patch test series. When 1220 patients were patch tested with this resin as well as with 2 other phenol-formaldehyde resins, based on phenol and formaldehyde, 26 patients were positive to at least 1 resin. The figures for positive reactions to paratertiary-butyl phenol-formaldehyde resin and the 2 other resins were 0.8%, 1.0% and 3.0% (440 tested subjects), respectively. Therefore, a battery of phenol-formaldehyde resins should be used for screening purposes, since patch testing with the paratertiary-butyl phenol-formaldehyde resin is not sufficient to identify patients with contact allergy to phenol-formaldehyde resins. Several of the 26 patients were patch tested with the basic substances phenol, formaldehyde and paratertiary-butyl phenol, but only 1 positive reaction to formaldehyde was noted. The sensitizing capacity of 2-methylol phenol, 4-methylol phenol and 2,4,6-trimethylol phenol, all 3 compounds being possible ingredients of resins based on phenol and formaldehyde, was demonstrated; 5 of 14 resin positive patients reacted to at least 1 of these methylol phenols.

Chemical Phenomena↗
PubMed2003

[Effects of formaldehyde on germ cells of male mice].

General toxicity and genetic materials damage of formaldehyde on germ cells in different stages was studied. In order to discover the toxicity mechanism of formaldehyde on germ cells and the biomarkers of effect after the presence of damage in germ cells and the estimation index, the relationships between the damage of germ cells and the MDA, SDH activity and Cu and Zn. in testicle tissue were investigated. Male mice exposed to formaldehyde by i.p. for 5 days. Formaldehyde doses were: 0.20 mg/kg, 2.00 mg/kg, 20.00 mg/kg. Mice were killed at the 6th day and the 14th day. HE staining was used to study the pathological changes happened in testicle tissue. In order to study the changes in sperm, the sperms and the abnormality of the sperm's heads were observed. In order to study the damage of the genetic material in the germ cells, the frequencies of sister chromosome exchanges and the frequencies of MN cells were studied. MDA was measured by MDA diagnosis box. Copper and zinc were determined by FAAS. US was used to determine the SDH activity in serum and testicle tissue. The results showed that: The main pathological changes in testicle tissue of formaldehyde groups were degeneration; The sperm quantity was decreased and the sperm heads deformation ratio was increased in all formaldehyde groups; There were a significant increase of MN ratio in early spermatogenic cells and SCE ratio in medial and high dose groups; The MDA in testicle tissue significant increased in high dose group. The SDH activity in testicle tissue was declined in all formaldehyde groups; There were a significant decline of copper and zinc in testicle tissue in high dose group. It is suggested that: Formaldehyde could induce genetic materials in spermatogone, primary spermatocyte and caused degeneration and necrosis in secondary spermatocyte, spermatogenic cell, sperm; The damage of LPO, decline of copper and zinc and SDH activity in mice's testicle tissue could be caused by formaldehyde; The effect of lipid peroxidation may be one of the toxicity mechanisms of formaldehyde on genetic materials; SDH is the biomarkers of effect after the toxicity effects induced by formaldehyde on germ cells appeared; Testing the sperm heads deformation ratio is the estimation index that can be used to judge the general toxicity of germ cells and the damage on their genetic materials of formaldehyde.

Animals↗