AUTHORS: Lemus R; Abdelghani AA; Akers TG; Horner WE

AUTHOR AFFILIATION: Department of Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA 70112, USA.

SOURCE: Rev Environ Health 1998 Jan-Jun;13(1-2):91-8

CITATION IDS: PMID: 9718624 UI: 98384736

ABSTRACT: An indoor air quality survey was conducted in Southern Louisiana to determine levels of airborne formaldehyde. Gas chromatography analyses of 419 air samples collected from 53 houses revealed levels of formaldehyde ranging from non-detectable to 6.60 mg/m3. Seventy four percent (312/419) of the samples had detectable amounts of airborne formaldehyde. Of the 312 positive samples, approximately 60% exceeded the American Society of Heating, Refrigeration, and Air Conditioning Engineers (ASHRAE) guideline of 0.123 mg/m3. The highest number of samples exceeding the formaldehyde benchmark were collected in winter. It would appear that in some Southern Louisiana houses, a high level of formaldehyde could serve as a potential upper respiratory irritant.

AUTHORS: Georghiou PE; Winsor L; Sliwinski J; Shirtliffe CJ

SOURCE: IARC Sci Publ 1993;(109):251-5

CITATION IDS: PMID: 8514355 UI: 93293268

MAIN MESH HEADINGS: Air Pollution, Indoor/*analysis, Environmental Monitoring/*methods, Formaldehyde/*analysis

ADDITIONAL MESH HEADINGS: Environmental Monitoring/instrumentation, Reproducibility of Results, Toluidines

AUTHORS: Georghiou PE; Winsor L; Sliwinski JF; Shirtliffe CJ

SOURCE: IARC Sci Publ 1993;(109):245-50

CITATION IDS: PMID: 8514354 UI: 93293267

MAIN MESH HEADINGS: Air Pollution, Indoor/*analysis, Environmental Monitoring/*methods, Formaldehyde/*analysis

ADDITIONAL MESH HEADINGS: Environmental Monitoring/instrumentation, Reproducibility of Results, Toluidines

AUTHORS: Koeck M; Pichler-Semmelrock FP; Schlacher R

AUTHOR AFFILIATION: Office for Information of Environment Protection, University of Graz, Austria.

SOURCE: Cent Eur J Public Health 1997 Sep;5(3):127-30

CITATION IDS: PMID: 9386898 UI: 98048139

ABSTRACT: As part of a long-term study of indoor air pollution, formaldehyde concentrations were determined in 792 apartments following complaints by inhabitants. Measurements were carried out using Draeger tubes as well as the acetyl acetone method. In 157 apartments, HCHO concentrations of more than 0.1 ppm, exceeding the recommended standard values for indoor air concentrations, were determined. The concentrations determined tended to decrease over time. As far as they were caused by furnishings, they were limited to the spaces where these furnishings were installed. In older-style prefabricated houses with foam-filled particle-board wall systems, concentrations of more than 1.0 ppm were determined. In spite of legal regulations governing the release of formaldehyde from substances, preparations and products containing formaldehyde which have been in existence in Austria since 1990, this substance must still be considered as a possible factor of indoor pollution in causing feelings of ill-health.

AUTHORS: Meyer B; Hermanns K

SOURCE: J Air Pollut Control Assoc 1985 Aug;35(8):816-21

CITATION IDS: PMID: 4045002 UI: 86009241

MAIN MESH HEADINGS: Air Pollutants/*analysis, Formaldehyde/*analysis

ADDITIONAL MESH HEADINGS: Ventilation

AUTHORS: Liu KS; Huang FY; Hayward SB; Wesolowski J; Sexton K

AUTHOR AFFILIATION: California Indoor Air Quality Program, Air and Industrial Hygiene Laboratory, California Department of Health Services, Berkeley 94704- 9980.

SOURCE: Environ Health Perspect 1991 Aug;94:91-4

CITATION IDS: PMID: 1954947 UI: 92063946

ABSTRACT: 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.

AUTHORS: Smith DL; Bolyard M; Kennedy ER

SOURCE: Am Ind Hyg Assoc J 1983 Feb;44(2):97-9

CITATION IDS: PMID: 6837445 UI: 83175403

MAIN MESH HEADINGS: Formaldehyde/*analysis

ADDITIONAL MESH HEADINGS: Charcoal, Chemistry, Drug Stability, Specimen Handling

AUTHORS: Triebig G; Schaller KH; Beyer B; Muller J; Valentin H

AUTHOR AFFILIATION: Institute of Occupational and Social Medicine and Polyclinic of Occupational Diseases, University Erlangen-Nuremberg, F.R.G.

SOURCE: Sci Total Environ 1989 Mar;79(2):191-5

CITATION IDS: PMID: 2727671 UI: 89266867

ABSTRACT: The results of formaldehyde determinations in the air at various workplaces in the period 1980-1988 are presented. The airborne concentrations varied between less than 0.01 and 10.9 mg m-3 (mean 0.7 mg m-3). For ambient air monitoring, active sampling and capillary gas chromatography are reliable and sensitive methods. Formic acid excretion in urine is an unspecific and insensitive biological indicator for monitoring low-dose formaldehyde exposure.

AUTHORS: Wiglusz R; Sitko E; Jarnuszkiewicz I

AUTHOR AFFILIATION: Department of Toxicology and Biochemistry, Institute of Maritime and Tropical Medicine, Gdynia.

SOURCE: Bull Inst Marit Trop Med Gdynia 1991;42(1-4):51-6

CITATION IDS: PMID: 1844846 UI: 93250459

ABSTRACT: The contamination of indoor air by formaldehyde (CH2O) is a serious hygienic problem. One of the potential sources of formaldehyde release may be furnishing fabrics. The study was conducted to evaluate the effect of ageing on textiles (17.5 months), air temperature (25-45 degrees C) and relative air humidity (RH) (45-85%) on the CH2O release rate from 6 kinds of drapers and furniture coverings. The emission was determined in small glass chambers (13.08 dm3) under controlled conditions: at one air exchange per hour and load factor 1 m2/m3. Results of these studies indicated that effect of textile ageing on CH2O emission was different for each fabric tested. The increase of temperature and RH within the ranges studied multiplied the rate of CH2O release. The drapers and covering fabrics tested, in the production of which textile dressing containing CH2O compounds was used, may remain a source of formaldehyde emission for several months.

AUTHORS: Buckler GF

SOURCE: Imprint 1994 Apr-May;41(3):60-5, 93

CITATION IDS: PMID: 7927422 UI: 95012319

MAIN MESH HEADINGS: *Air Pollution, Indoor

ADDITIONAL MESH HEADINGS: Human, Risk Factors

AUTHORS: Stock TH; Mendez SR

SOURCE: Am Ind Hyg Assoc J 1985 Jun;46(6):313-7

CITATION IDS: PMID: 4014007 UI: 85248161

ABSTRACT: A survey of indoor air quality under warm weather conditions, in a variety of Houston area residences not selected in response to occupant complaints, revealed a distribution of indoor formaldehyde concentrations ranging from less than 0.008 ppm to 0.29 ppm, with an arithmetic mean of 0.07 ppm. Approximately 15% of the monitored residences had concentrations greater than 0.10 ppm. Formaldehyde levels were observed to depend on both age of dwelling and the structural classification of the residence. These factors are not independent and reflect the influence of more fundamental variables, such as the rate of exchange of indoor and outdoor air and the overall emission potential of indoor materials. The results of this survey suggest that considerable population exposures to excess (greater than 0.10 ppm) formaldehyde concentrations may occur in the residential environment, indicating the need for improved control strategies.

AUTHORS: Lemus R; Abdelghani AA; Akers TG; Horner WE

AUTHOR AFFILIATION: Department of Environmental Health Sciences, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA 70112, USA.

SOURCE: Rev Environ Health 1998 Jan-Jun;13(1-2):91-8

CITATION IDS: PMID: 9718624 UI: 98384736

ABSTRACT: An indoor air quality survey was conducted in Southern Louisiana to determine levels of airborne formaldehyde. Gas chromatography analyses of 419 air samples collected from 53 houses revealed levels of formaldehyde ranging from non-detectable to 6.60 mg/m3. Seventy four percent (312/419) of the samples had detectable amounts of airborne formaldehyde. Of the 312 positive samples, approximately 60% exceeded the American Society of Heating, Refrigeration, and Air Conditioning Engineers (ASHRAE) guideline of 0.123 mg/m3. The highest number of samples exceeding the formaldehyde benchmark were collected in winter. It would appear that in some Southern Louisiana houses, a high level of formaldehyde could serve as a potential upper respiratory irritant.

AUTHORS: Krakowiak A; Gorski P; Pazdrak K; Ruta U

AUTHOR AFFILIATION: Department of Occupational Diseases, Nofer Institute of Occupational Medicine, Lodz, Poland.

SOURCE: Am J Ind Med 1998 Mar;33(3):274-81

CITATION IDS: PMID: 9481426 UI: 98142425

ABSTRACT: The aim of the study was to characterize the mechanism of formaldehyde (FM)-induced nasal and bronchial response in asthmatic subjects with suspected FM allergy. Ten subjects purported to have FM rhinitis and asthma and 10 healthy subjects submitted to an inhalation provocation in an exposure chamber with FM at a dose of 0.5 mg/m3 over 2 hr. Spirometry at rest and following bronchial provocation with histamine (PC20) were recorded before and after FM inhalation. In addition, FM- specific serum IgE antibodies were measured and cellular, biochemical, and mediator changes were assessed in nasal lavage before, and immediately after, provocation and at 4 hr and 24 hr later. Provocation with FM caused only transient symptoms of rhinitis in both groups. None of the subjects supposed to have occupational asthma developed clinical symptoms of bronchial irritation. No specific IgE antibodies to FM were detected in persons with occupational exposure to FM. No differences in the nasal response to FM were found between subjects reporting to have occupational allergic respiratory diseases and healthy subjects (P > 0.05). In summary, inhaled formaldehyde at a level as low as 0.5 mg/m3 did not induce a specific allergic response either in the upper or in the lower part of the respiratory tract. Moreover, there is no difference in nasal response to FM in asthmatic subjects occupationally exposed to FM and healthy subjects.

AUTHORS: Montanaro A

AUTHOR AFFILIATION: Division of Allergy and Clinical Immunology, Oregon Health Sciences University, Portland 97201-3098, USA.

SOURCE: Clin Rev Allergy Immunol 1997 Summer;15(2):187-203

CITATION IDS: PMID: 9315411 UI: 97461044

MAIN MESH HEADINGS: Bronchial Hyperreactivity/*chemically induced

ADDITIONAL MESH HEADINGS: Air Pollutants/adverse effects, Bronchial Hyperreactivity/epidemiology, Bronchial Hyperreactivity/etiology, Bronchitis/chemically induced, Environmental Exposure/adverse effects, Formaldehyde/adverse effects, Human, Irritants/adverse effects, Occupational Diseases/chemically induced, Occupational Diseases/immunology, Respiratory Hypersensitivity/chemically induced, Respiratory Hypersensitivity/etiology, Respiratory Hypersensitivity/immunology, Tobacco Smoke Pollution/adverse effects

AUTHORS: Collins JJ; Acquavella JF; Esmen NA

AUTHOR AFFILIATION: Monsanto Company, St. Louis, Mo. 63167, USA.

SOURCE: J Occup Environ Med 1997 Jul;39(7):639-51

CITATION IDS: PMID: 9253725 UI: 97397686

ABSTRACT: In this study, we summarize 47 epidemiologic studies related to formaldehyde exposure and use meta-analytic techniques to assess findings for cancers of the lung, nose/nasal sinuses, and nasopharynx. Our analyses indicate that workers with formaldehyde exposure have essentially null findings for lung cancer and a slight deficit of sinonasal cancer. Nasopharyngeal cancer rates were elevated moderately in a minority of studies. Most studies, however, did not find any nasopharyngeal cancers, and many failed to report their findings. After correcting for underreporting, we found a meta relative risk of 1.0 for cohort studies. Case-control studies had a meta relative risk of 1.3. Our review of the exposure literature indicated that the nasopharyngeal cancer case-control studies represented much lower and less certain exposures than the cohort studies. We conclude that the available studies do not support a causal relation between formaldehyde exposure and nasopharyngeal cancer. This conclusion conflicts with conclusions from two previous meta-analyses, primarily because of our consideration of unreported data.

AUTHORS: Akbar-Khanzadeh F; Mlynek JS

AUTHOR AFFILIATION: Medical College of Ohio, Department of Occupational Health, Toledo 43699-0008, USA.

SOURCE: Occup Environ Med 1997 May;54(5):296-300

CITATION IDS: PMID: 9196449 UI: 97339895

ABSTRACT: OBJECTIVE: To determine the changes in respiratory function within one hour and three hours of exposure to formaldehyde and investigate the relation between exposure to formaldehyde and acute changes in respiratory function. METHOD: Respiratory function of 50 non-smoking medical students exposed to formaldehyde in a gross anatomy laboratory were compared with respiratory function of 36 non-exposed, non-smoking physiotherapy students. Formaldehyde concentrations were measured in the breathing zone of each exposed subject and in the general work environment. RESULTS: Formaldehyde concentrations in the breathing zone of exposed subjects generally exceeded recommended standards. On average, the variables of respiratory function of both the exposed and the control subjects increased significantly within one hour and from one to three hours after exposure. The increase in respiratory function of the exposed subjects was significantly less than that of the control subjects. There was no meaningful correlation between concentration of formaldehyde in the breathing zone and changes in the respiratory function of exposed subjects. CONCLUSION: As the increase in the respiratory function of the subjects can be attributable to normal diurnal variation, the significantly lower increase in respiratory function of the exposed group than in the control group is probably due to exposure to formaldehyde. The results of this study do not, however, support a dose-response relation.

AUTHORS: Ziem G; McTamney J

AUTHOR AFFILIATION: Occupational and Environmental Medicine, Baltimore, Maryland, USA.

SOURCE: Environ Health Perspect 1997 Mar;105 Suppl 2:417-36

CITATION IDS: PMID: 9167975 UI: 97311258

ABSTRACT: Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.

AUTHORS: Dearman RJ; Smith S; Basketter DA; Kimber I

AUTHOR AFFILIATION: Zeneca Central Toxicology Laboratory, Macclesfield, Cheshire, UK.

SOURCE: J Appl Toxicol 1997 Jan-Feb;17(1):53-62

CITATION IDS: PMID: 9048228 UI: 97200293

ABSTRACT: Characteristic cytokine secretion profiles, consistent with the selective activation of discrete functional subpopulations of T helper (Th) cells, have been demonstrated following repeated topical exposure of mice to chemical contact or respiratory allergens. Draining lymph node cells (LNC) derived from animals treated with the respiratory allergen trimellitic anhydride (TMA; 10%) expressed high levels of the Th2 cytokines interleukins 4 and 10, but little of the Th1 cell product interferon gamma. Under conditions of exposure of equivalent immunogenicity with respect to LNC proliferation, the contact allergen 2,4-dinitrochlorobenzene (DNCB) provoked the converse pattern of cytokine secretion. The purpose of the present investigations was to examine dose-response relationships with respect to cytokine production with a wider range of chemical allergens. In each case, cytokine secretion patterns were compared with those observed with LNC prepared from animals exposed concurrently to TMA or DNCB. Despite some inter- experimental variation in the absolute amounts of cytokines produced, DNCB- and TMA-activated LNC invariably expressed Th1- and Th2-type patterns, respectively. At all concentrations tested, the contact allergens isoeugenol and formaldehyde stimulated a Th1-type cytokine secretion profile, whereas a Th2-type pattern was induced following exposure to the chemical respiratory allergens cyanuric chloride and diphenylmethane diisocyanate. These data demonstrate that divergent cytokine secretion profiles characterize immune responses to different classes of chemical allergen and suggest that it may be possible, in a single integrated assay, to identify and classify chemical allergens as a function of induced cytokine production patterns.

AUTHORS: Wieslander G; Norback D; Bjornsson E; Janson C; Boman G

AUTHOR AFFILIATION: Department of Occupational and Environmental Medicine, Uppasala University, University Hospital, Sweden.

SOURCE: Int Arch Occup Environ Health 1997;69(2):115-24

CITATION IDS: PMID: 9001918 UI: 97155204

ABSTRACT: As a part of the worldwide European Community Respiratory Health Survey, possible relations between asthma and emissions from newly painted indoor surfaces were studied. The participants (n = 562) answered a self-administered questionnaire, with questions on symptoms and indoor exposures, including indoor painting, during the last 12 months. The participants also underwent a structured interview, spirometry, peak flow measurements at home (PEF), methacholine provocation test for bronchial hyper-responsiveness (BHR), and skin prick tests. In addition, serum concentration of eosinophilic cationic protein (S-ECP), blood eosinophil count (B-EOS), and total immunoglobulin E (S-IgE) were measured. Current asthma was defined as a combination of BHR and at least one asthma-related symptom (wheezing and attacks of breathlessness). The information gathered on indoor painting was compared with exposure measurements of formaldehyde and volatile organic compounds (VOC) performed in a selected sample of the dwellings (n = 62). Relations between exposures, asthma and clinical signs were calculated by multiple linear or logistic regression, adjusting for possible influence of age, gender and tobacco smoking. The prevalence of asthma was increased among subjects with domestic exposure to newly painted surfaces (OR = 1.5; 95% CI 1.0-2.4), particularly newly painted wood details (OR = 2.3; 95% CI 1.2-4.5) and kitchen painting (OR = 2.2; 95% CI 1.1-4.5). Moreover, blood eosinophil concentrations were significantly elevated among subjects living in newly painted dwellings. A significantly increased prevalence of symptoms related to asthma, but not BHR, was observed in relation to workplace exposure to newly painted surfaces. The indoor concentration of aliphatic compounds (C8-C11), butanols, and 2,2,4-trimethyl 1,3- pentanediol diisobutyrate (TXIB) was significantly elevated in newly painted dwellings. The total indoor VOC was about 100 micrograms/m3 higher in dwellings painted in the last year. A significant increase in formaldehyde concentration was observed in dwellings with newly painted wood details. Our results indicate that exposure to chemical emissions from indoor paint is related to asthma, and that some VOCs may cause inflammatory reactions in the airways. To improve asthma management, and to counteract the increasing frequency of asthma, the significance of the indoor environment should not be neglected. Our study suggests that the contribution of emissions from paint to indoor concentrations of formaldehyde and VOCs should be as low as possible.

AUTHORS: Dearman RJ; Moussavi A; Kemeny DM; Kimber I

AUTHOR AFFILIATION: Zeneca Central Toxicology Laboratory, Macclesfield, Cheshire, UK.

SOURCE: Immunology 1996 Dec;89(4):502-10

CITATION IDS: PMID: 9014813 UI: 97167124

ABSTRACT: Chemical allergens of different types, those that cause in humans allergic contact dermatitis or occupational asthma induce in mice divergent immune responses characteristic, respectively, of T-helper 1 (Th1)- and Th2-type cell activation. Such responses are associated with the development of different cytokine secretion patterns by draining lymph node cells (LNC), such that contact allergens stimulate vigorous interferon-gamma (IFN-gamma) production, but little secretion of the Th2 cytokines interleukin-4 and interleukin-10 (IL-4 and IL-10), whereas the converse pattern is provoked by respiratory allergens. Using selective depletion with antibody and complement we have here examined the relative contribution of CD4+ and CD8+ T lymphocytes to the cytokine secretion patterns of draining LNC isolated from mice sensitized to chemical allergens. Mice received repeated topical applications of respiratory allergens, trimellitic anhydride (TMA) or diphenylmethane diisocyanate (MDI), or of contact allergens 2,4- dinitrochlorobenzene (DNCB) or formaldehyde. Thirteen days following the initiation of exposure the production by draining LNC of IL-10, IFN- gamma and mitogen (concanavalin A)-inducible IL-4 was measured by enzyme-linked immunosorbent assay (ELISA) after various periods of culture. It was found that the high levels of IL-4 and IL-10 secretion stimulated by TMA or MDI, and the lower levels of these cytokines induced by DNCB or formaldehyde, were in all cases dependent upon the presence of CD4- cells. In contrast, the comparatively high concentrations of IFN-gamma observed following exposure to contact allergens were found to be derived from CD4+ cells, and in the case of DNCB from CD8+ cells also. The low levels of IFN-gamma induced by treatment with TMA or MDI were associated largely or wholly with CD8+ cells. These data indicate that the type 2 cytokine responses induced to different extents by both contact and respiratory chemical allergens are almost exclusively a function of CD4+ cells, but that IFN-gamma is produced by either CD4+ cells in the case of contact allergens or largely by CD8+ cells in the case of chemical respiratory allergens.

AUTHORS: Nair RS; Dudek BR; Grothe DR; Johannsen FR; Lamb IC; Martens MA; Sherman JH; Stevens MW

AUTHOR AFFILIATION: Monsanto Company, St Louis, MO 63167, USA.

SOURCE: Food Chem Toxicol 1996 Nov-Dec;34(11-12):1139-45

CITATION IDS: PMID: 9119327 UI: 97240237

ABSTRACT: Monsanto employs several pragmatic approaches for evaluating the toxicity of mixtures. These approaches are similar to those recommended by many national and international agencies. When conducting hazard and risk assessments, priority is always given to using data collected directly on the mixture of concern. To provide an example of the first tier of evaluation, actual data on acute respiratory irritation studies on mixtures were evaluated to determine whether the principle of additivity was applicable to the mixture evaluated. If actual data on the mixture are unavailable, extrapolation across similar mixtures is considered. Because many formulations are quite similar in composition, the toxicity data from one mixture can be extended to a closely related mixture in a scientifically justifiable manner. An example of a family of products where such extrapolations have been made is presented to exemplify this second approach. Lastly, if data on similar mixtures are unavailable, data on component fractions are used to predict the toxicity of the mixture. In this third approach, process knowledge and scientific judgement are used to determine how the known toxicological properties of the individual fractions affect toxicity of the mixture. Three examples of plant effluents where toxicological data on fractions were used to predict the toxicity of the mixture are discussed. The results of the analysis are used to discuss the predictive value of each of the above mentioned toxicological approaches for evaluating chemical mixtures.

AUTHORS: Wantke F; Focke M; Hemmer W; Tschabitscher M; Gann M; Tappler P; Gotz M; Jarisch R

AUTHOR AFFILIATION: Dermatologic and Pediatric Allergy Clinic, Vienna, Austria.

SOURCE: Allergy 1996 Nov;51(11):837-41

CITATION IDS: PMID: 8947343 UI: 97102971

ABSTRACT: 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.

AUTHORS: Becher R; Hongslo JK; Jantunen MJ; Dybing E

AUTHOR AFFILIATION: National Institute of Public Health, Department of Environmental Medicine, Oslo, Norway.

SOURCE: Toxicol Lett 1996 Aug;86(2-3):155-62

CITATION IDS: PMID: 8711767 UI: 96326734

ABSTRACT: The allergenic constituents of non-industrial indoor environments are predominantly found in the biologic fraction. Several reports have related biological particles such as mites and their excreta, dander from pets and other furred animals, fungi and bacteria to allergic manifestations including respiratory hypersensitivity among the occupants of buildings. Also, bacterial cell-wall components and the spores of toxin-producing moulds may contribute to the induction of hypersensitivity, but the relevance for human health is not yet determined. The knowledge regarding hypersensitivity and asthmatic reactions after exposure to chemical agents is primarily based on data from occupational settings with much higher exposure levels than usually found in non-industrial indoor environments. However, there is evidence that indoor exposure to tobacco smoke, some volatile organic compounds (VOC) and various combustion products (either by using unvented stoves or from outdoor sources) can be related to asthmatic symptoms. In some susceptible individuals, the development of respiratory hypersensitivity or elicitation of asthmatic symptoms may also be related to the indiscriminate use of different household products followed by exposure to compounds such as diisocyanates, organic acid anhydrides, formaldehyde, styrene and hydroquinone. At present, the contribution of the indoor environment both to the development of respiratory hypersensitivity and for triggering asthmatic symptoms is far from elucidated.

AUTHORS: Hilton J; Dearman RJ; Basketter DA; Scholes EW; Kimber I

AUTHOR AFFILIATION: Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK.

SOURCE: Food Chem Toxicol 1996 Jun;34(6):571-8

CITATION IDS: PMID: 8690318 UI: 96319744

ABSTRACT: Formaldehyde causes upper respiratory tract irritation and has been reported in some investigations to be a cause of occupational allergic asthma. The data are equivocal, however, and it has proved difficult to confirm that exposure to formaldehyde induces respiratory sensitization or provokes the production of specific immunoglobulin E (IgE) antibody. In this study the sensitizing properties of formaldehyde were examined experimentally. This chemical elicited strong positive responses in three independent methods for the prospective identification of contact sensitizing chemicals-the guinea pig maximization test, the occluded patch test of Buehler and the murine local lymph node assay. In contrast, in a novel predictive test method for assessment of respiratory sensitization potential-the mouse IgE test-formaldehyde at the same test concentrations was negative. Furthermore, formaldehyde induced in mice a pattern of cytokine secretion by draining lymph node cells inconsistent with the stimulation of IgE antibody responses or respiratory sensitization. These data indicate that, although formaldehyde is a potent contact allergen, it lacks a significant potential to cause sensitization of the respiratory tract.

AUTHORS: Priha E; Liesivuori J; Santa H; Laatikainen R

AUTHOR AFFILIATION: Tampere Regional Institute of Occupational Health, Finland.

SOURCE: Chemosphere 1996 Mar;32(6):1077-82

CITATION IDS: PMID: 8920592 UI: 97078025

ABSTRACT: Formaldehyde is a well known toxic air impurity affecting the upper respiratory tract. It rapidly forms methylene glycol in water. Reactions of the hydrated formaldehyde with nasal mucus were studied by C-13 NMR spectroscopy. In the NMR spectra methylene glycol dominated and only minor signals from possible reactions were observed. This finding suggests that nasal mucus effectively protects nasal epithelium against formaldehyde.

AUTHORS: Roto P; Sala E

AUTHOR AFFILIATION: Tampere Regional Institute of Occupational Health, Finland.

SOURCE: Am J Ind Med 1996 Mar;29(3):275-77

CITATION IDS: PMID: 8833780 UI: 96430656

ABSTRACT: Formaldehyde is commonly accepted to be an allergen and irritant. However, specifically diagnosed occupational respiratory diseases caused by formaldehyde are relatively rare. Occupational laryngitis was diagnosed in a 47-year-old dairy foreman. He had been exposed for 9 years to formaldehyde emitted from a milk-packing machine situated underneath his office. His exposure level varied considerably. Under normal process conditions, the measured formaldehyde level was 0.03 mg/m3. The patient was examined by different specialists over 1 1/2 years. It was concluded that he had psychogenic dysphonia. However, a specific laryngeal provocation test with formaldehyde carried out at the Finnish Institute of Occupational Health was positive. His laryngitis was so serious that he was pensioned. During the 3 years of follow-up his condition gradually worsened. He now reacts especially to tobacco smoke and other air impurities known to contain formaldehyde.

AUTHORS: Wantke F; Demmer CM; Tappler P; Gotz M; Jarisch R

AUTHOR AFFILIATION: Dermatological and Paediatric Allergy Clinic, Vienna, Austria.

SOURCE: Clin Exp Allergy 1996 Mar;26(3):276-80

CITATION IDS: PMID: 8729664 UI: 96362858

ABSTRACT: BACKGROUND: Children attending a primary school showed symptoms such as headache, cough, rhinitis and epistaxis. Assessment of specific IgE to formaldehyde gave positive results in some children. OBJECTIVE: Was IgE- mediated sensitization as well as symptoms in children associated with formaldehyde exposure at school? METHODS: Sixty-two 8-year-old children attending three forms at a primary school were investigated. Indoor formaldehyde concentrations were measured in classrooms of both schools (one frame construction with particleboard used extensively as panelling vs a brick building) which were consecutively attended. Assessment of specific IgE to formaldehyde was done in all children. Children were transferred to a brick building and 3 months later specific IgE to formaldehyde in pupils showing initially elevated radioallergosorbent test (RAST) values reassessed. In all children symptoms were evaluated by questionnaire before and 3 months after changing school. RESULTS: In the school panelled with particleboard the World Health Organization (WHO) threshold for formaldehyde of 0.050 ppm was crossed in two classrooms (0.075 ppm and 0.069 ppm) whereas in one classroom 0.043 ppm was found. RAST classes of > or = 2 were found in three children, two of them attending the classroom with 0.075 ppm formaldehyde. Elevated RAST classes of > or = 1.3 were found in another 21 pupils. Thirty-eight pupils as well as 19 control children showed RAST classes in the normal range of < or = 1.2. Headache, nose bleeding, rhinitis, fatigue, cough, dry nasal mucosa and burning eyes were found in the affected children. There was a good correlation between symptoms and the formaldehyde concentrations in the classrooms. However, elevated IgE levels to formaldehyde did not correlate with symptoms. Formaldehyde concentrations in the classrooms of the brick built school were 0.029 ppm, 0.023 ppm and 0.026 ppm. After transferral specific IgE to formaldehyde decreased significantly from 1.7 +/- 0.5 to 1.2 +/- 0.2 (P < 0.002) as did the incidence of symptoms. CONCLUSION: Gaseous formaldehyde, besides its irritant action, leads to IgE-mediated sensitization. As children are more sensitive to toxic substances than adults, threshold levels for indoor formaldehyde should be reduced for children.

AUTHORS: Smedley J

SOURCE: Clin Exp Allergy 1996 Mar;26(3):247-9

CITATION IDS: PMID: 8729659 UI: 96362853

MAIN MESH HEADINGS: Formaldehyde/*adverse effects, Respiratory Hypersensitivity/*chemically induced

ADDITIONAL MESH HEADINGS: Adult, Asthma/chemically induced, Asthma/immunology, Child, Child, Preschool, Environmental Exposure, Formaldehyde/immunology, Haptens/immunology, Human, IgE/biosynthesis, IgE/immunology, Occupational Exposure, Respiratory Hypersensitivity/immunology

AUTHORS: Schenker MB; Jacobs JA

AUTHOR AFFILIATION: Department of Community and International Health, University of California at Davis, USA.

SOURCE: Tuber Lung Dis 1996 Feb;77(1):4-18

CITATION IDS: PMID: 8733408 UI: 96297267

ABSTRACT: Organic solvents are widely used in industrial processes and found in many common household products. Exposures to solvents are common in both idustrialized and industrializing countries. While organic solvents exposure is well known to produce central nervous system toxicity, hepatic, renal and dermatologic injury, the respiratory effects of solvent exposure are poorly documented. Several recent population-based epidemiologic studies have found an independent association of occupational solvent exposure with respiratory symptoms, impaired pulmonary function or respiratory disease, but interpretation of these studies is limited by self-reported exposure data. Animal studies have demonstrated adverse effects in both the conducting and the respiratory airways, although often at very high exposure levels. Human chamber studies have most consistently reported irritation of the eyes, nose and throat without evidence of airway hyper-responsiveness. Case series have observed obstructive and restrictive effects in patients with high level inhalational exposures to solvents, particularly formaldehyde, but occupational epidemiologic studies have not consistently demonstrated changes in pulmonary function. Finally, mortality studied have not found increased mortality rates from respiratory disease in occupations associated with solvent use. In general, solvents have been demonstrated to cause mucosal irritation of the eyes and upper airways, but studies of pulmonary impairment following exposure have been limited and inconsistent. Solvent-mediated respiratory toxicity is biologically plausible, but further research is needed to better characterize exposures and to elucidate the specific mechanisms associated with injury.

AUTHORS: Smedley J; Coggon D

AUTHOR AFFILIATION: MRC Environmental Epidemiology Unit, Southampton General Hospital, UK.

SOURCE: Occup Med (Oxf) 1996 Feb;46(1):33-6

CITATION IDS: PMID: 8672791 UI: 96271903

ABSTRACT: Seventy-eight National Health Service occupational health departments were invited to take part in an audit of health surveillance for employees exposed to respiratory sensitising agents. Most of the departments had responsibility for workers using glutaraldehyde, formaldehyde, methyl methacrylate and X-ray processing chemicals, but the extent to which health surveillance was provided for these employees varied. Many departments had no written policies for surveillance, and the methods used were often unnecessarily labour intensive. Only a minority of departments had made arrangements for communicating the collective results of screening to employees, failure to do so indicating a breach of statutory duty. There were major discrepancies between departments in criteria for excluding employees from work with respiratory sensitising agents. Occupational physicians caring for hospital staff should discuss and establish guidelines for effective surveillance of people working with the commonly encountered sensitisers.

AUTHORS: Cassee FR; Arts JH; Groten JP; Feron VJ

AUTHOR AFFILIATION: Toxicology Division, TNO Nutrition and Food Research Institute, Zeist, The Netherlands.

SOURCE: Arch Toxicol 1996;70(6):329-37

CITATION IDS: PMID: 8975631 UI: 96253325

ABSTRACT: Sensory irritation of formaldehyde (FRM), acrolein (ACR) and acetaldehyde (ACE) as measured by the decrease in breathing frequency (DBF) was studied in male Wistar rats using nose-only exposure. Groups of four rats were exposed to each of the single compounds separately or to mixtures of FRM, ACR and/or ACE. Exposure concentrations of the mixtures were chosen in such a way that summation of the effects of each chemical would be expected not to exceed 80% reduction of the breathing frequency. FRM, ACR and ACE appeared to act as sensory irritants as defined by Alarie (1966, 1973). With FRM and ACR desensitization occurred, whereas with ACE the breathing frequency gradually decreased with increasing exposure time (up to 30 min). For mixtures, the observed DBF was more pronounced than the DBF for each compound separately, but was less than the sum of the DBFs for the single compounds. A model for three compounds competing for the same receptor was applied to predict the DBF of mixtures of FRM, ACE and ACR. The results also showed that with mixtures no desensitization occurred; in fact, the breathing frequency further decreased in the last 15 min of exposure. These observations were similar to those found for ACE alone, and might have been caused by effects on the upper respiratory tract. The results of the present study allow the conclusion that sensory irritation in rats exposed to mixtures of irritant aldehydes is more pronounced than that caused by each of the aldehydes separately, and that the DBF as a result of exposure to a mixture could well be predicted using a model for competitive agonism, thus providing evidence that the combined effect of these aldehydes is basically a result of competition for a common receptor (trigeminal nerve).

AUTHORS: Norback D; Bjornsson E; Janson C; Widstrom J; Boman G

AUTHOR AFFILIATION: Department of Occupational and Environmental Medicine, Uppsala University, Akademiska sjukhuset, Sweden.

SOURCE: Occup Environ Med 1995 Jun;52(6):388-95

CITATION IDS: PMID: 7627316 UI: 95353437

ABSTRACT: OBJECTIVES--As a part of the worldwide European Community respiratory health survey, possible relations between symptoms of asthma, building characteristics, and indoor concentration of volatile organic compounds (VOCs) in dwellings were studied. METHODS--The study comprised 88 subjects, aged 20-45 years, from the general population in Uppsala, a mid-Swedish urban community, selected by stratified random sampling. Room temperature, air humidity, respirable dust, carbon dioxide (CO2), VOCs, formaldehyde, and house dust mites were measured in the homes of the subjects. They underwent a structured interview, spirometry, peak expiratory flow (PEF) measurements at home, methacholine provocation test for bronchial hyperresponsiveness, and skin prick tests. In addition, serum concentration of eosinophilic cationic protein (S-ECP), blood eosinophil count, and total immunoglobulin E (S-IgE) were measured. RESULTS--Symptoms related to asthma were more common in dwellings with house dust mites, and visible signs of dampness or microbial growth in the building. Significant relations were also found between nocturnal breathlessness and presence of wall to wall carpets, and indoor concentration of CO2, formaldehyde, and VOCs. The formaldehyde concentration exceeded the Swedish limit value for dwellings (100 micrograms/m3) in one building, and CO2 exceeded the recommended limit value of 1000 ppm in 26% of the dwellings, showing insufficient outdoor air supply. Bronchial hyperresponsiveness was related to indoor concentration of limonene, the most prevalent terpene. Variability in PEF was related to two other terpenes; alpha- pinen and delta-karen. CONCLUSION--Our results suggest that indoor VOCs and formaldehyde may cause asthma-like symptoms. There is a need to increase the outdoor air supply in many dwelling, and wall to wall carpeting and dampness in the building should be avoided. Improved indoor environment can also be achieved by selecting building materials, building construction, and indoor activities on the principle that the emission of volatile organic compounds should be as low as reasonably achievable, to minimise symptoms related to asthma due to indoor air pollution.

AUTHORS: Koltai PJ

AUTHOR AFFILIATION: Section of Pediatric Otolaryngology, Albany Medical College, NY 12208.

SOURCE: Otolaryngol Head Neck Surg 1994 Jul;111(1):9-11

CITATION IDS: PMID: 8028949 UI: 94301720

ABSTRACT: The impact of the environment on the upper respiratory tract of children has become an issue of recent interest. Sulfur dioxide causes nasal congestion in children as well as an increase in both mast cells and lymphocytes in nasal lavage fluids. Chlorpheniramine blocks the effect of sulfur dioxide on the nasal mucosa. Ozone exposure results in nasal congestion, increased levels of histamine, neutrophils, eosinophils, and mononuclear cells in nasal lavage fluid. No data are available on the effects of nitrogen dioxide or wood-burning stoves on the upper respiratory tracts of children. Formaldehyde in sufficient concentrations causes upper airway irritation; however, no data are available on its long-term effects. Detriments in air quality cause adverse changes in the lower respiratory tracts of susceptible individuals. The effects on the upper respiratory tract are more difficult to document. There may be a causal relationship, but definitive proof of whether air pollution results in significant increases in pediatric otitis media, sinusitis, rhinitis, and pharyngitis has yet to be demonstrated.

AUTHORS: Franco G

AUTHOR AFFILIATION: Cattedra di Medicina del lavoro dell'Universita degli studi di Modena, Italy.

SOURCE: Monaldi Arch Chest Dis 1994 Jun;49(3):239-42

CITATION IDS: PMID: 8087123 UI: 94372968

ABSTRACT: This review deals with some of the emerging events that are assuming increasing relevance as work-related respiratory diseases (indoor air pollution and sick building syndrome, respiratory toxicity of formaldehyde, pollutant-induced asthma, dental technician lung diseases, lung cancer from diesel exhaust, environmental silicosis). The industrial hygienist's role in recognition, evaluation, and control of health hazards is stressed as an essential contribution to both prevention and diagnosis of occupational lung disease.

AUTHORS: Kriebel D; Sama SR; Cocanour B

AUTHOR AFFILIATION: Department of Work Environment, University of Massachusetts, Lowell 01854.

SOURCE: Am Rev Respir Dis 1993 Dec;148(6 Pt 1):1509-15

CITATION IDS: PMID: 8256892 UI: 94079087

ABSTRACT: Epidemiologic studies of irritants are difficult to perform using standard epidemiologic methods for several reasons, including the reversible nature of the health outcomes, the selection of sensitive individuals from the study population, and the wide heterogeneity in normal responses to irritants. This study examined the feasibility of using repeated measurements of peak expiratory flow (PEF) and reported symptoms to study respiratory irritants and their effects in students exposed to formaldehyde during a clinical anatomy laboratory course. We studied 24 physical therapy students dissecting cadavers for 3 h per week over a 10-wk period. Formaldehyde exposures in the breathing zone ranged from 0.49 to 0.93 ppm (geometric mean +/- geometric SD, 0.73 +/- 1.22). Irritant symptoms increased strongly over the course of the average laboratory period, but this effect was stronger at the beginning than at the end of the semester. PEF measured before each laboratory session declined over the semester by an average of about 10 L/min (2% of baseline), a trend that was statistically significant in random-effects regression models. After 14 wk away from the laboratory, the group's mean baseline PEF had returned to its preexposure level. Mean PEF also declined over each laboratory period, although this effect was attenuated over the course of the semester. Other important predictors of cross-laboratory PEF decrements were asthma and reporting throat irritation during the laboratory. It appears that mild irritant effects can be detected in naive subjects using a repeated monitoring design and relatively simple instrumentation.

AUTHORS: Wilhelmsson B; Holmstrom M

AUTHOR AFFILIATION: Department of Oto-Rhino-Laryngology, Vasteras Central Hospital, Sweden.

SOURCE: Scand J Work Environ Health 1992 Dec;18(6):403-7

CITATION IDS: PMID: 1485166 UI: 93134357

ABSTRACT: 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.