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At least 19 recordsLinked to original sources
PubMed1978

Hapten-specific respiratory hypersensitivity in guinea pigs.

Respiratory hypersensitivity to small chemical determinants (haptens) was produced in guinea pigs by repeatedly exposing the animals to aerosols of hapten-ovalbumin conjugates. In this way, reactivity toward p-azobenzenearsonate and p-tolyl isocyanate was induced. Carrier (ovalbumin)-specific respiratory reactions were not produced. Hapten-specific respiratory hypersensitivity was accompanied by the production of hapten-specific antibodies. The method for inducing hapten-specific hypersensitivity can be applied to screen various industrial chemicals for their sensitizing abilities toward the respiratory tract.

Animals↗
PubMedDate not supplied

[The hypersensitive respiratory system in childhood].

Aetiological factors and mechanisms of bronchial hyperreactivity are discussed. The hypothesis of increased permeability of the bronchial mucosa--caused by either endogenous or exogenous stimuli--as the most plausible explanation for the connection between hyperreactivity and childhood asthma bronchiale is emphasized. Finally, unspecific inhalative provocation tests for proof of bronchial hyperreactivity, its indications and contraindications as well as the criteria of judgement are mentioned.

Airway Resistance↗
PubMed2002

Occupational respiratory hypersensitivity in dental personnel.

OBJECTIVE: The aim was to study the causes of respiratory hypersensitivity in dental personnel based on the statistics of the Finnish Register of Occupational Diseases (FROD; 1975-1998) and the patient material of the Finnish Institute of Occupational Health (FIOH; 1990-1998). METHODS: Details about the cases of respiratory hypersensitivity were compiled from the FROD. The occupational rhinitis diagnoses studied at the FIOH were based on work-related symptoms and a change in the status of the nasal mucosa during challenge testing; and the diagnosis of occupational asthma based on reactions in challenge testing, or on IgE positivity and peak flow monitoring at work and during days off. RESULTS: A total of 64 cases of occupational respiratory diseases (ORDs) was diagnosed in dental personnel during 1975 to 1998 according to the FROD; two cases in 1975 to 1989, and 62 in 1990 to 1998. Twenty-eight cases were of occupational asthma (18 caused by methacrylates), 28 occupational rhinitis (six caused by methacrylates), seven allergic alveolitis and one organic dust toxic syndrome (ODTS). The non-acrylate-material diagnosed in 1990-1998 at the FIOH comprised three cases of asthma and one of rhinitis caused by chloramine-T (sodium- N-chlorine- p-toluene sulphonamide); as well as one case of asthma, seven cases of rhinitis, and two cases of combined rhinitis and conjunctivitis caused by natural rubber latex (NRL). Furthermore, one case of occupational rhinitis caused by Nobetec containing colophony was diagnosed. The incidence rate (IR) of ORD increased from 0 in 1988 to a peak of 105.1 new cases per 100,000 working years in 1995. During the last observation year, i.e. 1998, the IR was 55 new cases per 100,000 workers. The IR in dental personnel was lower than in the whole working population in Finland up until 1992, but since then has been greater than in the whole population, peaking in 1995 when the IR of dental personnel was 2.55 times greater than in the whole population. CONCLUSION: The present study shows the increasing frequency of respiratory hypersensitivity among dental personnel. Besides methacrylates, important causes of respiratory hypersensitivity are NRL and chloramine-T.

Adult↗
PubMed2005

Assessing the potential to induce respiratory hypersensitivity.

Acute and repeat dose inhalation studies have been an important part of the safety assessment of drugs, chemicals, and other products throughout the world for many years. It is known that damage to the respiratory tract can be triggered either by nonspecific irritation or by specific immune-mediated pathogenesis, and it is acknowledged that traditional inhalation studies are not designed to address fully the impact of the latter. It is also recognized that different types of immune-mediated responses can be triggered by different classes of compounds and that some immune reactions in the lung are life threatening. As such, it is important to understand as fully as possible the basis for the immune-mediated damage to the lung in order to characterize adequately the risks of individual chemicals or proteins. It is against this background that a review of the methods used to assess the potential for immune-mediated respiratory hypersensitivity was conducted. The primary objectives of this review are to discuss appropriate methods for identifying and characterizing respiratory hypersensitivity hazards and risks; and to identify key data gaps and related research needs with respect to respiratory hypersensitivity testing. The following working definition of respiratory hypersensitivity was formulated: a hypersensitivity response in the respiratory tract precipitated by a specific immune response, mediated by multiple mechanisms, including IgE antibody. Because of the importance played by various classes of compounds, the subsequent sections of this review will consider protein-specific, chemical-specific, and drug-specific aspects of respiratory hypersensitivity.

Drug Hypersensitivity↗
PubMed1996

Environmental factors and respiratory hypersensitivity: experiences from studies in Eastern and Western Europe.

Allergy and respiratory hypersensitivity are the end results of an interaction in genetically susceptible individuals, exposure to allergens and adjuvant factors. The incidence of allergic disease (but not respiratory hypersensitivity) is higher in urban than in rural areas and in Western industrialised countries than in the formerly socialist countries of Eastern Europe. It appears to be caused by factors encountered in early childhood. Tobacco smoke is by far the most important single environmental risk factor that has been identified so far. Other risk factors include air pollution such as NO2, SO2 and ozone, and modern, tightly isolated and poorly ventilated houses. However, even if all known environmental factors are added, this could only partly explain the increasing prevalence of these diseases. Therefore, other, unknown factors associated with 'Western lifestyle' must be looked for.

Adult↗
PubMed1996

Environmental chemicals relevant for respiratory hypersensitivity: the indoor environment.

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.

Air Pollution, Indoor↗
PubMed1998

Occupational respiratory hypersensitivity caused by preparations containing acrylates in dental personnel.

BACKGROUND: Allergic contact dermatitis caused by acrylate compounds is common in dental personnel; they also often complain of work-related respiratory or conjunctival symptoms. OBJECTIVE: The aim of the present study was to report the cases of acrylates induced respiratory hypersensitivity in dental personnel diagnosed in Finland during the last 6 years. METHODS: Occupational asthma, rhinitis, laryngitis and pharyngitis cases were diagnosed according to patient history, PEF monitoring, and a work-simulating provocation test. RESULTS: Twelve cases of respiratory hypersensitivity caused by acrylates diagnosed in dental personnel (six dentists and six dental nurses) in 1992-97 are reported. During this period one case of conjunctivitis and one of laryngitis have been published separately. Nine cases of occupational asthma, two rhinitis cases, and one laryngitis case were verified according to the challenge tests with dental acrylate compounds (acrylates, methacrylates and epoxy acrylates). Only three patients had positive skin-prick test reactions to common environmental allergens, and none reacted to acrylates in the skin-prick tests. Five patients had an elevated total IgE (>110 kU/L). PEF follow-up showed an occupational effect in all examined eight patients with diagnosed asthma. The mean duration of exposure to acrylates was 22 years, and the duration of respiratory symptoms 8 years. CONCLUSIONS: The results indicate that acrylates constitute an important hazard for dental workers. The mechanism of respiratory hypersensitivity is still unknown, and it is probably not IgE-mediated.

Acrylates↗
PubMed1994

Assessment of respiratory hypersensitivity in guinea-pigs sensitized to diphenylmethane-4,4'-diisocyanate (MDI) and challenged with MDI, acetylcholine or MDI-albumin conjugate.

Guinea-pigs were sensitized to monomeric diphenylmethane-4,4'-diisocyanate (MDI) by two intradermal injections (1-10% MDI, injection volumes of 50-100 microliters/day, on days 0, 2 and 4) or by a single brief high-concentration inhalation exposure (135 or 360 mg/m3, 15 min). Starting with day 21 following sensitization the animals were subjected to inhalation-challenge exposures (30 min) with non-irritating and irritating concentrations of the hapten (MDI). MDI-challenge concentrations ranged from 3.4 +/- 0.9 to 60 +/- 14.3 mg/m3 air. In some groups guinea-pigs were also challenged with acetylcholine (ACh) aerosol or the MDI-guinea pig serum albumin (GPSA) conjugate. Experimental findings indicated that from intradermally sensitized animals an immediate onset respiratory hypersensitivity response could only be elicited with concentrations exceeding the irritant threshold concentration for MDI, i.e. with concentrations greater than approximately 20 mg/m3 air. Guinea-pigs challenged with the MDI-GPSA conjugate (35.3 +/- 2.8 mg/m3 air) also experienced a weak immediate-type respiratory hypersensitivity response. An increased non-specific airway hyper-responsiveness following ACh-challenge was only observed from animals challenged with approximately 60 mg MDI/m3 air. The histopathological evaluation of lungs and lung-associated lymph nodes revealed an association of the increase in eosinophilic granulocytes and concentration of MDI used for challenge exposures. It appeared, in most instances, that this influx was more pronounced in animals sensitized with MDI as compared with concurrent controls challenged with the same MDI concentration. Guinea-pigs sensitized by a single 15-min inhalation exposure to either 135 or 360 mg MDI/m3 air were challenged sequentially with 12 +/- 2.1 mg MDI/m3 air, ACh and MDI-GPSA conjugate. Following the inhalation-induction, an airway hyper-responsiveness was elicited both after challenge with MDI and with the MDI-GPSA conjugate. The influx of eosinophilic granulocytes was more pronounced from animals sensitized by inhalation when compared with guinea-pigs sensitized intradermally and challenged with the same concentration of MDI. Thus, experimental findings suggest that elicitation of respiratory hypersensitivity is concentration-dependent and that challenge concentrations should slightly exceed the threshold concentration for irritation (approximately 20 mg/m3). Sensitization by inhalation increased the susceptibility to irritant stimuli and thus confounds the selection of the most appropriate concentration for challenge. However, the combined assessment of specific pathologic features such as airway eosinophilia and the evaluation of several breathing parameters during hapten- and ACh-challenge make it easier to distinguish effects caused by irritation and respiratory hypersensitivity.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1995

A murine model for assessing the respiratory hypersensitivity potential of chemical allergens.

Using equimolar quantities of 2 chemical allergens, toluene diisocyanate (TDI), noted for its ability to cause respiratory hypersensitivity, and dinitrochlorobenzene (DNCB), noted for its dermal sensitizing activity, the mouse was evaluated as a possible model to indicate respiratory hypersensitivity. A previously published procedure (Garssen et al. (1989) Immunology 68, 51-58) was followed whereby chemicals were applied epicutaneously to the shaved flank of BALB/c mice. Eight days later, animals were challenged by intranasal application of the chemical. The lungs were evaluated at 48 h. Both TDI and DNCB elicited mild mononuclear inflammatory cuffing around pulmonary vasculature. No reaction was noted around pulmonary airways. Sera, drawn 48 h following the intranasal challenge with chemical allergen, were evaluated for total IgE, hapten-specific IgE and IgG, and for IL-2, IL-4, IL-5, IL-6, and interferon gamma. Animals exposed to TDI demonstrated decreased total IgE and the presence of TDI-specific IgG. Cytokine levels were unchanged in both groups. These results indicate that in this mouse model, total serum IgE and the production of hapten-specific IgG antibodies distinguished a respiratory from a contact sensitizing chemical. Further comparison of the serologic response of mice to these two classes of chemicals is required to determine if the murine model can be used to predict dermal versus respiratory sensitizing activity of chemical allergens.

Administration, Intranasal↗
PubMed1996

The role of the gastrointestinal tract in the development of respiratory hypersensitivities.

Adverse reactions to foods may sometimes cause symptoms from the respiratory tract, including bronchial obstruction and rhinitis. The true prevalence is not known. In adults, it has been estimated to be about 1% of asthmatic patients or less. This would correspond to a prevalence of about 2-4 in 10,000 of the general population. The prevalence in children is higher, as IgE mediated food allergy is more common in this age group than in adults. The most common foods causing immunologically mediated reactions include milk, egg, fish, crustaceans, nuts, wheat, soy, peanut, peas and other legumes. In addition certain food additives, e.g. sulphites, may rarely be incriminated in respiratory hypersensitivity via adverse reactions with unknown mechanisms. A double-blind placebo controlled food challenge (DBPCFC) is the only way to conclusively confirm a relationship between the ingestion of a certain food item and a reaction in the respiratory tract.

Adult↗
PubMed1999

Respiratory hypersensitivity to diphenylmethane-4,4'-diisocyanate in guinea pigs: comparison with trimellitic anhydride.

Published evidence demonstrates successful induction and elicitation of respiratory hypersensitivity in guinea pigs by the known human respiratory allergens trimellitic anhydride (TMA) and diphenylmethane-4,4'-diisocyanate (MDI). From these data it is apparent that TMA-related respiratory hyperresponsiveness can be elicited readily in guinea pigs upon inhalation challenge with the free chemical. Despite the interlaboratory variability in methodological procedures used for the sensitization as well as elicitation of response and the wide range of concentrations of TMA employed for challenge exposures (6-57 mg/m(3) air), TMA had been unequivocally identified as a benchmark respiratory sensitizer by measurements of the respiratory rate during challenge. The protocols were duplicated to examine the respiratory sensitizer MDI. In intradermally sensitized guinea pigs, changes in immediate-onset-like respiratory response were observed when MDI challenge concentrations exceeded approximately 30 mg MDI/m(3) air. Collective experimental evidence suggests that the respiratory responses observed upon challenge with TMA were markedly more pronounced and easier to identify than those recorded following challenge with MDI or MDI conjugate. In contrast to TMA, irritant concentrations of MDI had to be used to elicit any respiratory response and the differentiation of irritant and allergic responsiveness became increasingly difficult. Despite the absence of unequivocal changes in breathing patterns upon MDI challenge, MDI-sensitized animals displayed elevated anti-MDI immunoglobulin G1 (IgG1) antibodies, and a significant influx of eosinophilic granulocytes in the bronchial wall and lung-associated lymph nodes. Therefore, it is believed that the robustness of this animal model to identify low-molecular-weight agents as respiratory sensitizer is increased when several endpoints are considered. These are (1) positive respiratory response upon challenge with the hapten, and if negative, also challenge with the conjugate of the hapten; (2) an influx of eosinophilic granulocytes; and (3) increased specific IgG1 response. Furthermore, it appears that particles in the range of approximately 2-6 microm evoke more consistent respiratory response upon challenge exposure than particles in the 1-2 microm range.

Administration, Inhalation↗
PubMed1996

Exposure to environmental chemicals relevant for respiratory hypersensitivity: global aspects.

Trends of air pollutant concentrations that influence the incidence of respiratory diseases and might be influential for respiratory hypersensitivity are presented and discussed. Data for these trends are collected in UNEP/WHO's Global Environmental Monitoring System GEMS/Air which recently has been revitalized and redirected to become a tool for providing the information necessary for rational air quality management. Data are interpreted with respect to WHO's most recent air quality guidelines, which are an update of the air quality guidelines for Europe published in 1987. A WHO study on the global disease burden and the contribution of air pollution to it is discussed and global estimates of mortality resulting from air pollution through sulphur dioxide and suspended particulate matter, by different economic regions, are given. Starting from the air quality guidelines still valid at the time of publication of the update, about 460,000 excess deaths globally are due to suspended particulate matter and about 370,000 to sulphur dioxide.

Air Pollutants↗
PubMed2002

Respiratory hypersensitivity to trimellitic anhydride in Brown Norway rats: evidence for different activation pattern of immune cells following topical and respiratory induction.

The elicitation of respiratory allergy in animal models is exquisitely complex and interpretation of results from different laboratories cannot readily be compared due to variability in testing protocols, biomarkers and techniques used to identify 'positive' responses. On the one hand, guinea-pigs have been proposed as a good model with which to study allergic and irritant bronchial hyperresponsiveness. On the other hand, considerable efforts have been made to develop animal models that take the immunological mechanisms into account to reduce the complexity as well as duration of the guinea-pig assays. In principle, local skin reactions can easily be determined by the local lymph node assay (LLNA) introduced by Kimber and Weisenberger. In contrast to lung sensitization there are already simplified and reliable models available to test for and discriminate contact sensitizers from skin irritants, i.e. the modified local lymph node assay IMDS (integrated model for the differentiation of skin reactions). Modifications of this assay verified that methods other than radioactive labelling may be comparably sensitive, and that it is possible to eliminate 'false positive' results induced by irritants (IMDS). Thus, we asked whether there could be a similar simplified model like the modified LLNA or IMDS for investigations of respiratory allergens. Therefore, we analysed immune reactions induced by the dermal and respiratory route, respectively. Analyses of the draining lymph nodes of the lung and the ear were carried out before and after challenge via the pulmonary tract. The results clearly support that (1) the reactions in the lung draining lymph nodes could be used as early indicators of respiratory sensitization, and (2) the specificity of the immune competent cells seem to be dependent of the route of administration during induction.

Administration, Inhalation↗
PubMed2006

Modern approaches to therapeutic vaccination as treatment for type 1 respiratory hypersensitivity (allergy) treatment.

The incidence of respiratory and other allergies has increased dramatically in many countries over the last few decades. Drug treatment is symptomatic and has a minimal effect on the underlying immunological dysfunction. This disease process may, however, be modified by allergy vaccination, which is typically applied by injecting increasing strengths of the offending allergens. Its use has been fairly limited owing to long injection schedules involving many visits to the physician, occasional local or systemic side effects, perceived limited efficacy and poor compliance. A greater understanding of the immunological mechanisms involved in allergy vaccination has led recently to the development of new generations of products with properties that address some of these issues, and these advances are likely to increase the successful use of the therapy.

Allergens↗
PubMed1996

Environmental factors and respiratory hypersensitivity: the Americas.

Diverse environmental exposure profiles exist in the Americas because of widely different climates, ambient pollutants, and bioaerosols in these continents. This paper reviews selected studies from the Americas that support the broad hypothesis that environmental factors contribute to respiratory hypersensitivity. Processes influenced by environmental factors include primary immunologic sensitization, the development and exacerbation of specific immunologic diseases and the activation of nonspecific mechanisms with tissue inflammation, injury and remodeling. Endpoints resulting from these processes include respiratory symptoms, diseases such as asthma, with measures of disease severity including medication use and hospitalization rates, and death due to cardiorespiratory disease. Studies associate sensitization rates to specific allergens with environmental factors such as humidity and indices of allergen exposure. Regional variation occurs with exposure to outdoor source pollutants such as ozone, but varies by household to bioaerosols such as dust mite, cat or cockroach allergen. Indoor allergens are associated with asthma while outdoor allergens are associated with allergic rhinitis. In a national survey, the atopic sensitization rate in the USA increased with urban residence (defined as towns of population > 2500) and varied by region. Controlled human challenge studies show that ozone increases the response of allergic subjects to allergen. Increased ambient photochemical pollution concentrations, of which ozone is an important component, are associated with increased emergency room visits for asthma in cities such as Toronto, New York, Atlanta, and Mexico City. In Sao Paolo, Brazil, mortality due to childhood respiratory disease was influenced by the ambient levels of NO2. Epidemiologic studies including the recent meta-analysis of a large, longitudinal study population associate ambient concentrations of particulate matter < 10 microns and respiratory symptoms, disease severity and increased cardiorespiratory deaths. Toxicology studies show that individual variation in responsiveness is important in nonspecific inflammatory responses to irritant pollutants such as ozone and environmental tobacco smoke. These studies indicate that environmental factors influence primary allergen sensitization, secondary allergic responses, the activation of nonspecific inflammatory responses, and the severity of respiratory diseases, including asthma.

Adolescent↗
PubMed1976

Uptake and catabolism of antigen by alvelar macrophages of dogs with respiratory hypersensitivity. Processing of antigen by alveolar macrophages.

The ability of alveolar macrophages of dogs to bind and metabolize two antigens was studied. The antigens were ragweed antigen E (AgE) and keyhole limpet haemocyanin (KLH). These antigens were chosen because of the availability of dogs with respiratory hypersensitivity to them and because they are of very different molecular weights. It was shown that: (1) antigen processing was identical using macrophages from hypersensitive as compared with normal dogs; (2) in comparison with AgE, much more of the higher molecular weight antigen, KLH, was bound to macrophages and much less degraded during subsequent incubation, leaving a greater proportion of the antigen bound to the cell membrane; (3) respiratory cells which had taken up AgE at 0 degrees C instead of 37 degrees C and were then incubated at 37 degrees C were much more active in catabolizing bound antigen with consequently less membrane bound antigen remaining; (4) increases in catabolism of bound AgE were also found in cells from relatively recently lavaged animals; (5) there was no evidence that cytophilic antibody contributed to the uptake of AgE.

Animals↗
PubMed1996

The role of the skin in the development of chemical respiratory hypersensitivity.

Certain chemicals are known to cause occupational respiratory allergy associated with symptoms of pulmonary distress, including asthma and rhinitis. While there is no doubt that inhalation represents an important route of exposure for the development of sensitization to the inducing allergen, there is evidence that effective sensitization of the respiratory tract may result also from dermal contact with the chemical. The mechanisms relevant to the stimulation of respiratory sensitization following cutaneous exposure to chemical allergens and implications for the prevention of occupational asthma are considered here.

Administration, Cutaneous↗