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PubMed1985

Monitoring of formaldehyde in air.

Any one of several monitoring methods, depending on requirement and circumstance, can be used to measure employee exposure to formaldehyde. Ordinarily, monitoring at DuPont is performed by sampling with impingers containing 1% aqueous sodium bisulfite or with silica gel tubes. The collected formaldehyde is measured spectrophotometrically after reaction with chromotropic acid. Results from studies on a selected number of formaldehyde monitoring methods reveal that reliable methods are available for area and personnel monitoring over both short term and long term. Accurate results are obtained from short-term monitoring (15 min at 1 L/min) with impingers of formaldehyde concentrations as low as 0.14 ppm. The current studies show that long-term monitoring (8 hr at 0.5 L/min) can be performed accurately at concentrations as low as 0.05 ppm. Accurate results also are obtained from short-term monitoring (15 min at 500 mL/min) with silica gel tubes of concentrations as low as 0.11 ppm formaldehyde; the lower limit established in the current studies for long-term monitoring (8 hr at 30 mL/min) is 0.15 ppm. Passive monitors provide the most convenient means of obtaining 8-hour time-weighted average (TWA) data. The Pro-Tek Formaldehyde Badge was demonstrated to reliably monitor formaldehyde concentrations varying from 0-0.5 ppm or 0-3 ppm. All of these methods satisfy the NIOSH criterion for acceptability that all results fall within +/- 25% of the true value at the 95% confidence level. Investigation of the Lion Formaldemeter disclosed that instantaneous and accurate (+/- 5%) measurement of formaldehyde in air can be made over a concentration range of 0.3-5 ppm in the absence of other substances that are oxidizable in its fuel cell detector.

Air Pollutants, Occupational↗

PubMed1986

Effect of the pH value when treating concentrate protein with formaldehyde on protein protection in the rumen.

Nine samples of soybean extracted meal were treated by fumigation in plastic bag with 0.5 g formaldehyde/100 g crude protein, the pH ranging from 2.1 to 10.7. The studies showed that with rising pH (x) the proportion of totally bound (y1, % of formaldehyde amount used) and irreversibly bound (y2) formaldehyde increased (y1 = 77.7 + 1.56x, y2 = 28.2 + 2.04x), whilst the reversible proportion remained constant (45.4% of formaldehyde amount used). The lysine detectable (g/16 g N) after HCl hydrolysis was reduced due to pH raising (y = 101 - 0.67x). Solubility and fermentability of the soybean protein in the rumen were found to rise though. Consequently, the formaldehyde content of the protein was positively correlated with the content of soluble N and fermentable N, respectively, and negatively correlated with the lysine content. These experimental results allow to conclude that the desired protein protection to be attained by treating soybean extracted meal with formaldehyde, is greatly influenced by the respective pH value. To reach maximum protection of the protein against microbial degradation in the rumen (N degradation after 12 hours incubation less than or equal to 20% of total N), the pH value should be below 5. The contents of totally, reversibly or irreversibly bound formaldehyde does not allow any conclusion regarding the protein protection attained. The apparently increased binding rate of formaldehyde is presumably due to the fact that here the reaction stops at the stage of methylol formation (molar proportion 1:1). Under the conditions of acid protein hydrolysis for lysine determination, the released formaldehyde obviously reacts irreversibly with the E-NH2 group of lysine.

Animals↗

PubMed2004

Influence of formaldehyde impurity in polysorbate 80 and PEG-300 on the stability of a parenteral formulation of BMS-204352: identification and control of the degradation product.

The purpose of this study was to identify a degradation product formed in the clinical parenteral formulation of BMS-204352, investigate the role of excipients in its formation, and develop a strategy to minimize/control its formation. The degradant was identified as the hydroxy methyl derivative (formaldehyde adduct, BMS-215842) of the drug substance based upon liquid chromatography/mass spectroscopy (LC/MS), liquid chromatography/mass spectroscopy/mass spectroscopy (LC/MS/MS), nuclear magnetic resonance (NMR), and chromatographic comparison to an authentic sample of hydroxymethyl degradation product, BMS-215842. An assay method for the detection of formaldehyde based on HPLC quantitation of formaldehyde dinitrophenylhydrazone was developed to quantitate its levels in various Polysorbate 80 and PEG 300 excipient lots. A direct relationship between the levels of formaldehyde in the excipients and the formation of the hydroxymethyl degradant was found. To confirm the hypothesis that the formaldehyde impurity in these two excipients contributed to the formation of the hydroxymethyl degradant, several clinical formulation lots were spiked with formaldehyde equivalent to 1, 10, and 100 mg/g of BMS-204352. A correlation was found between the formaldehyde level and the quantity of the hydroxymethyl degradant formed upon storage at 5 and 25 degrees C. From these experiments, a limit test on the formaldehyde content in polysorbate 80 and PEG 300 can be set as part of a strategy to limit the formation of the degradation product.

Chromatography, High Pressure Liquid↗

PubMed2001

Stability of benzodiazepines in formaldehyde solutions.

Benzodiazepine-type drugs are used in the treatment of a number of pathologic disorders, but they may be implicated in forensic toxicology cases because of their abuse potential. Occasionally, it becomes necessary to measure drug levels following exposure to formaldehyde (postembalming or after tissue storage) if drug involvement was not previously suspected. Virtually no information exists on the decomposition of benzodiazepines in the presence of formaldehyde (the active ingredient in many embalming fluids), yet formaldehyde is known to be highly reactive, particularly with nitrogen-containing compounds. In order to evaluate the effects of formaldehyde on benzodiazepines, 10 benzodiazepine drugs were exposed to various concentrations of formaldehyde and various pH conditions (to simulate potential postembalming conditions), and the decomposition of each drug was measured by high-performance liquid chromatography over a 30-day period. The decomposition rates of all but one of the benzodiazepines were accelerated (to differing degrees) by formaldehyde as compared to controls, and this decomposition was in several cases both pH and formaldehyde concentration dependent. Thus, forensic examiners must be particularly cautious when attempting to determine benzodiazepine concentrations postembalming because the compound may have reacted with formaldehyde to form other products not inherently obvious analytically. Determination of these reaction products will serve to provide alternate analytes, allowing for establishment of accurate conclusions during forensic analyses.

Anti-Anxiety Agents↗

PubMed1996

Formaldehyde and phenol exposure during an anatomy dissection course: a possible source of IgE-mediated sensitization?

The sensitizing potency of formaldehyde and phenol exposure during 4 weeks of an anatomy dissection course was assessed in 45 medical students. Specific IgE against formaldehyde by RAST and by ELISA and specific IgE against phenol by ELISA were assessed before and after the course. At the start of the course, symptoms, type I allergy, respiratory diseases, and smoking habits were noted. At the end of the course, only symptoms experienced during the dissection lessons were assessed. Indoor formaldehyde levels were measured continuously. The mean indoor formaldehyde level was 0.124 +/- 0.05 ppm, with a minimum of 0.059 ppm and a maximum of 0.219 ppm. Specific IgE against formaldehyde or phenol was found in none of the subjects at the beginning of the course, and no student showed specific IgE against formaldehyde or phenol after the course. Assessment of primarily irritant symptoms during the lesson revealed itch and paraesthesia of hands in 33/45 students (P < 0.00005), headache in 15/45 students, burning eyes in 13/45 students (P < 0.02), dizziness in 8/45 students (P < 0.008), sneezing in 4/45 students, epistaxis in 2/45 students, and shortness of breath in 1/45 students. According to our data, 1-month exposure to formaldehyde and phenol during an anatomy dissection course does not induce specific IgE against formaldehyde or phenol.

Adolescent↗

PubMed1994

Cell proliferation and formaldehyde-induced respiratory carcinogenesis.

Formaldehyde is a nasal carcinogen in the rat but the cancer risk this chemical poses for humans remains to be determined. Formaldehyde induces nonlinear, concentration-dependent increases in nasal epithelial cell proliferation and DNA-protein cross-link formation following short-term exposure. Presented in this review are results from a mechanistically based formaldehyde inhalation study in which an important endpoint was the measurement of cell proliferation indices in target sites for nasal tumor induction. Male Fischer 344 rats were exposed to 0, 0.7, 2, 6, 10, or 15 ppm formaldehyde for up to 2 years (6 hr/day, 5 day/week). Statistically significant increases in cell proliferation were confined to the 10 and 15 ppm groups, which remained elevated throughout the study. The concentration-dependent increases in cell proliferation correlated strongly with the tumor response curve, supporting the proposal that sustained increases in cell proliferation are an important component of formaldehyde carcinogenesis. The nonlinearity observed in formaldehyde-induced rodent nasal cancer is consistent with a high-concentration effect of regenerative cell proliferation of the target organ coupled with the genotoxic effects of formaldehyde. Cell kinetic data from these studies provide important information that may be utilized in the assessment of risk for humans exposed to formaldehyde.

Animals↗

PubMed1996

Plasmid-mediated formaldehyde resistance in Escherichia coli: characterization of resistance gene.

The formaldehyde resistance mechanisms in the formaldehyde-resistant strain Escherichia coli VU3695 were investigated. A large (4.6-kb) plasmid DNA fragment encompassing the formaldehyde resistance gene was sequenced. A single 1,107-bp open reading frame encoding a glutathione- and NAD-dependent formaldehyde dehydrogenase was identified and sequenced, and the enzyme was expressed in an in vitro assay and purified. Amino acid sequence homology studies showed 62.4 to 63.2% identity with class III alcohol dehydrogenases isolated from horse, human, and rat livers. We demonstrated that the resistance mechanism in the formaldehyde-resistant strain E. coli VU3695 and in other formaldehyde-resistant members of the family Enterobacteriaceae is based on the enzymatic degradation of formaldehyde by a formaldehyde dehydrogenase.

Aldehyde Oxidoreductases↗

PubMed1992

Mast cell response to formaldehyde. 2. Induction of stress-like proteins.

Previously we established that immediately after pretreatment with low concentrations (5-10 micrograms/ml) of formaldehyde antigen- and ionophore-induced histamine secretion was enhanced from peritoneal mast cells (PMC) isolated from rats infected with Nippostrongylus brasiliensis. In contrast to immediately following pretreatment with low concentrations of formaldehyde, 3 h after a 30-min treatment with formaldehyde (10, 50 and 100 micrograms/ml) antigen-induced histamine secretion from PMC was significantly depressed, and 35S-methionine incorporation was also decreased. To further explore the effects of formaldehyde on mast cells, we investigated protein biosynthesis of PMC following formaldehyde treatment and compared this with the effects of hydrogen peroxide (H2O2) or heat treatment. One- and two-dimensional SDS-PAGE were used to assess the effects. Formaldehyde treatment induced the synthesis of 70- and 72-kD stress-like proteins in rat PMC. Pretreatment of PMC with 50 microM H2O2 and heat (45 degrees C) also induced proteins with the same molecular weight. Two-dimensional SDS-PAGE analysis established that formaldehyde-induced 70-kD proteins had the same pI values as 70-kD heat shock proteins previously observed in mammalian cells. These results suggest that formaldehyde, H2O2 and heat shock induce stress proteins in rat PMC. It will be important to establish whether or not these stress proteins are responsible for the functional alterations observed in the mast cells.

Animals↗

PubMed2000

Simulation modeling of the tissue disposition of formaldehyde to predict nasal DNA-protein cross-links in Fischer 344 rats, rhesus monkeys, and humans.

Formaldehyde inhalation causes formation of DNA-protein cross-links (DPX) in the nasal mucosa of Fischer 344 (F344) rats and rhesus monkeys. DPX are considered to be part of the mechanism by which cytotoxic and carcinogenic effects of formaldehyde in laboratory animals are exerted, and DPX data have been used as a measure of tissue dose in cancer risk assessments for formaldehyde. Accurate prediction of DPX concentrations in humans is therefore desirable. The goal of this work was to increase confidence in the prediction of human DPX by refining earlier models of formaldehyde disposition and DPX kinetics in the nasal mucosa. Anatomically accurate, computational fluid dynamics models of the nasal airways of F344 rats, rhesus monkeys, and humans were used to predict the regional flux of formaldehyde to the respiratory and olfactory mucosa. A previously developed model of the tissue disposition of formaldehyde and of DPX kinetics was implemented in the graphical simulation tool SIMULINK and linked to the regional flux predictions. Statistical optimization was used to identify parameter values, and good simulations of the data were obtained. The parameter estimates for rats and monkeys were used to guide allometric scale-up to the human case. The relative levels of nasal mucosal DPX in rats, rhesus monkeys, and humans for a given inhaled concentration of formaldehyde were predicted by the model to vary with concentration. This modeling approach reduces uncertainty in the prediction of human nasal mucosal DPX resulting from formaldehyde inhalation.

Animals↗

PubMed1986

Contribution of formaldehyde to respiratory cancer.

This article reviews the available data on the carcinogenicity of formaldehyde from experimental and epidemiologic studies and makes recommendations for further research. Two definitive chronic inhalation bioassays on rodents have demonstrated that formaldehyde produces nasal cancer in rats and mice at 14 ppm and in rats at 6 ppm, which is within the domain of present permissible human exposure (8-hr time-weighted average of 3 ppm, a 5 ppm ceiling, and a 10 ppm short-term exposure limit). Biochemical and physiologic studies in rats have shown that inhaled formaldehyde can depress respiration, inhibit mucociliary clearance, stimulate cell proliferation, and crosslink DNA and protein in the nasal mucosa. No deaths from nasal cancer have been reported in epidemiologic studies of cohorts exposed to formaldehyde, but three case-control studies suggest the possibility of increased risk. Although excesses of lung cancer deaths have been observed in some studies at industrial plants with formaldehyde exposure, uncertainties in interpretation limit the evaluation of these findings. Excess cancers of the brain and of lymphatic and hematopoietic tissues have been reported in certain studies of industrial groups and in most studies of formaldehyde-exposed professionals, but whether these excesses are related to formaldehyde exposure is not known. Several properties of formaldehyde pose unique problems for future research: the mechanisms responsible for its nonlinear response; its probable mechanism of carcinogenic action as a cross-linking agent; its formation in tissues as a normal metabolite; its possible action as a promoter and/or a cocarcinogen; and the importance of glutathione as a host defense at low exposure.

Air Pollutants↗

PubMed2005

Hypothalamo-pituitary-adrenal gland axis in mice inhaling toluene prior to low-level long-term exposure to formaldehyde.

We studied the change in the hypothalamo-pituitary-adrenal gland (HPA) axis upon adding prior toluene inhalation to our previous formaldehyde inhalation experiments to determine whether short term exposure to relatively high levels of toluene triggers multiple chemical sensitivity (MCS). Data come from immunocytochemical, morphometrical and RT-PCR measurements. Four groups of adult female mice were exposed to differing concentrations (0, 80, 400, and 2,000 ppb) of formaldehyde for 16 hr/day, 5 days/week for twelve weeks, after the mice were exposed intranasally to 500 ppm toluene per mouse for 6 hr/day, for 3 days. We found that the number of corticotropin releasing hormone (CRH)-immunoreactive (ir) neurons was up-regulated according to the amount of formaldehyde as well as inhalation of formaldehyde alone in our previous experiment. The proportion of adrenocorticotropin hormone (ACTH)-ir cells increased according to the formaldehyde concentration, though there was no significant difference between the 400 and 2,000 groups. The number of ACTH-ir cells was higher in the 400 group than in the other groups (0, 80, and 2,000). Expression of ACTH-mRNA was also up-regulated according to the quantity of formaldehyde. The sinusoid in the anterior pituitary showed more dilatation in the 400 and 2,000 groups than in the control group, especially in the 2,000 group. We propose that exposure to toluene prior to inhalation of formaldehyde has no effect on the HPA axis and as a trigger of MCS, although greater sinusoid dilatation was found in the anterior pituitary gland at higher concentrations of formaldehyde.

Administration, Inhalation↗

PubMed2002

Effects of formaldehyde fixation on equine platelets using flow cytometric methods to evaluate markers of platelet activation.

OBJECTIVE: To investigate the effects of formaldehyde fixation on equine platelets using flow cytometric methods to evaluate markers of platelet activation. SAMPLE POPULATION: Blood samples from 6 Thoroughbreds. PROCEDURE: The degree of fluorescence associated with binding of fluorescein isothiocyanate (FITC)-conjugated anti-human fibrinogen antibody and FITC-annexin V in unactivated and adenosine diphosphate (ADP)-, platelet activating factor (PAF)-, and A23187-activated platelet samples in unfixed and 0.5, 1.0, and 2.0% formaldehyde-fixed samples was assessed by use of flow cytometry. RESULTS: In samples incubated with FITC-anti-human fibrinogen antibody prior to fixation, addition of 2.0% formaldehyde resulted in a 30% increase in total fluorescence in ADP- and PAF-activated samples and a 60% increase in A23187-activated samples. Fixation for 24 hours prior to addition of antibody resulted in reduced fluorescence of samples containing antihuman fibrinogen antibody for all 3 concentrations of formaldehyde in PAF-activated samples. The addition of all 3 concentrations of formaldehyde after incubation with FITC-annexin V resulted in significant increases in fluorescence in unactivated and activated platelet samples. As length of fixation time increased, there was a gradual increase in fluorescence that was significant at 24 hours. CONCLUSIONS: Because fixation with 2.0% formaldehyde results in significant changes in fluorescence in activated platelet samples containing anti-fibrinogen antibody, lower concentrations of formaldehyde should be used to fix equine platelet samples. Formaldehyde-fixed platelet samples should be analyzed within 12 hours of fixation to avoid artifactual increases in fluorescence. Fixation of samples containing FITC-annexin V should be avoided because of significant increases in fluorescence that may interfere with interpretation of results.

Adenosine Diphosphate↗

PubMed1992

Possible mechanisms of formaldehyde-induced discomfort in the upper airways.

Occupational exposure to formaldehyde often causes nasal discomfort. The objective of this study was to determine whether chronic exposure to formaldehyde causes annoying symptoms by direct irritation and whether it affects all exposed people (through hyperreactivity in atopic persons, through formaldehyde-induced hyperreactivity also in nonatopic persons, or through an immunologically mediated, immediate type 1 reaction to formaldehyde itself). It was found that about 50% of the studied population of 66 workers occupationally exposed to formaldehyde during formaldehyde production experienced nasal discomfort through hyperreactivity. Atopics were not significantly overrepresented among the persons with occupational nasal symptoms. Two workers with isolated occupational nasal discomfort, and sensitized by long-term inhalation, had a positive radioallergosorbent test for formaldehyde. The conclusion was reached that exposure to formaldehyde should be minimized as much as possible for all people, not only for atopic persons.

Adult↗

PubMed2003

[The effect of formaldehyde exposure on cytokine production in murine alveolar macrophages].

The vapor of formaldehyde has been reported to represent a potential health hazard, resulting in respiratory dysfunction. To determine the potential role of alterations in the alveolar macrophages induced by inhalation of formaldehyde, we studied the cytokine production of murine alveolar macrophages. Mice were exposed at 0, 2.5, 5, 10 ppm of formaldehyde for 16 hrs daily, respectively. Durations of inhalation were 7, 14, 21 and 28 days. Immediately after the formaldehyde exposure, murine alveolar macrophages were harvested from the mice. 18 hrs after LPS stimulation, the cytokines (IL-4, IL-10, IFN-gamma, TNF-alpha) were measured in the supernatant of cultured murine alveolar macrophages using the ELISA method. No levels of formaldehyde exposure changed these cytokine productions. Either our dose or duration of formaldehyde exposure might not have been enough to produce significant changes of cytokine production of murine alveolar macrophages. Further experiments with low but longer formaldehyde exposure may be needed to understand the effect of formaldehyde on cytokine production.

Animals↗

PubMed1992

Occupational exposure to formaldehyde--OSHA. Response to Court remand; final rule.

By this action, the Occupational Safety and Health Administration (OSHA) hereby amends its existing regulation for occupational exposure to formaldehyde, 29 CFR 1910.1048, in response primarily to a remand by the U.S. Court of Appeals for the D.C. Circuit in UAW v. Pendergrass, 878 F.2d 389 (D.C. Cir. 1989). The final amendments lower the permissible exposure level for formaldehyde from 1 ppm (part per million) as an 8-hour time-weighted average (TWA) to an 8-hour time-weighted average of 0.75 ppm. The amendments also add medical removal protection provisions to supplement the existing medical surveillance requirements for those employees suffering significant eye, nose or throat irritation and for those suffering from dermal irritation or sensitization from occupational exposure to formaldehyde. In addition, certain changes have been made to the standard's hazard communication and employee training requirements. These amendments establish specific hazard labeling requirements for all forms of formaldehyde, including mixtures and solutions composed of 0.1% or greater of formaldehyde in excess of 0.1 ppm. Additional hazard labeling, including a warning that formaldehyde presents a potential cancer hazard, is required where formaldehyde levels, under reasonably foreseeable conditions of use, may potentially exceed 0.5 ppm. The final amendments also provide for annual training of all employees exposed to formaldehyde at levels of 0.1 ppm or higher.

Drug Labeling↗

PubMed2003

Antagonistic reactions of arginine and lysine against formaldehyde and their relation to cell proliferation, apoptosis, folate cycle and photosynthesis.

1H, 13C NMR, ESMS and MS/MS investigations proved that there is an antagonism in the spontaneous reaction of formaldehyde with L-lysine and L-arginine. L-Arginine can only be hydroxymethylated on the guanidino group in a very fast reaction forming mono-, di-, and trihydroxymethyl arginines (HMA). L-Lysine can be methylated on the epsilon-amino group forming mono-, di-, and trimethyl lysine on physiological pH. Hydroxymethyl arginines are relative stable, isolable products, and can also be formed in biological systems, especially in plants. Significant amounts of hydroxymethyl arginines were identified in the aqueous extract of lyophilized kohlrabi, which can be formed in photosynthesis during CO2 fixation. 14C-Formaldehyde formed in a short-term (10, 30 sec) 14CO2 fixation reaction in Zea mays L. (early maturity variety: Szegedi TC 277) was captured by L-arginine, which occurs in leaves in large amount. Formaldehyde formed during photosynthesis can react not only with the arginine, but with ribulose-1,5-diphosphate present in leaves. In model reactions formaldehyde can react with the 'ene diole' group of ribulose-1,5-diphosphate in the absence of Rubisco enzyme, which is a similar reaction to the addition of formaldehyde to L-ascorbic acid. Hydroxymethyl arginines (HMA) are endogenous formaldehyde carrier molecules transferring the bound formaldehyde to thymidylate synthase enzyme system incorporating it into the folate cycle. HMA can also carry the bound formaldehyde to the cells especially to the tumorous cells (HT29 adenocarcinoma), and cause significant inhibition of cell proliferation and causes apoptosis.

Apoptosis↗

PubMedDate not supplied

Formaldehyde quantitation in air samples by thiazolidine derivatization: factors affecting analysis.

A new method for the determination of trace levels of formaldehyde in air was developed and validated. The method is based on the reaction of formaldehyde with cysteamine to form thiazolidine. Air samples containing trace levels of formaldehyde were prepared from paraformaldehyde. The percent yield of formaldehyde from paraformaldehyde was 85.1 +/- 1.14%. Air samples were bubbled into an aqueous cysteamine trap. Thiazolidine formed from formaldehyde and cysteamine in the trap was determined by gas chromatography with a fused silica capillary column and a nitrogen-phosphorus detector (NPD). The lowest detection level for thiazolidine was 17.2 pg, equivalent to 5.80 pg formaldehyde. The recovery efficiency of trace gas phase formaldehyde in air was greater than 90%. Formaldehyde levels in ambient laboratory air were 48.9-56.2 ppb (v/v).

Air↗

PubMed1989

[Formaldehyde determination in tobacco smoke--studies under experimental and actual conditions].

The estimation of an external exposure to formaldehyde in tobacco smoke requires a reliable analytical method. The gas chromatographic determination of formaldehyde shows in comparison to photometric methods a higher sensitivity and specificity. In the main stream smoke of various kinds of cigarettes the amount of formaldehyde vary between 3.4 micrograms to 8.8 micrograms/cigarette, this is equal to concentration between 2.3 to 6.1 ppm. In the air of lounges in hospitals formaldehyde concentrations up to 0.19 ppm can be detected after smoking of 15 cigarettes over a period of 1.5 h. In kindergartens without tobacco smoke the formaldehyde concentrations in air range from 0.005 to 0.01 ppm. The smoking of 30 cigarettes and one pipe in a non ventilated room over 1.5 h exceeded formaldehyde concentrations between 0.21 to 0.45 ppm. The concentration declines to 0.08 ppm within 2h after termination of smoking. The MAK-value of 0.5 ppm is not exceeded; in contrast to this the indoor limit of 0.1 ppm recommended by the German Bundesgesundheitsamt is exceeded in the vicinity of the smoker. The formaldehyde concentrations in tobacco smoke reported in the older literature can not be confirmed; this is due to the nonspecificity of the photometric methods. On the basis of our results can be concluded that the irritating effects of tobacco smoke to the mucous membranes are the result of the sum of irritating effects caused by several compounds and particles in the smoke and not only the impact of formaldehyde.

Air Pollutants↗