Search PubMed⌕ Search

Biomedical subjects

J G de Monchy

Publications and source records attributed to J G de Monchy.

At least 19 recordsLinked to original sources

Factors affecting FEV1 in workers with potroom asthma after their removal from exposure.

OBJECTIVE: In this study the relationship has been studied between exposure time and potential prognostic factors and FEV1 percent predicted (FEV1-% pred) in workers with potroom asthma, after their transfer from exposure to exposure-free departments. METHODS: Between 1970 and 1990 in a Dutch aluminium-production plant, 179 workers had been diagnosed as having potroom asthma. We carried out a follow-up study (n = 122) in the population still present at the factory 5 years after their relocation to an exposure-free department. In this study population, we examined the relationship between FEV1-% pred at follow-up, and exposure time: the time interval between start of exposure and diagnosis. To correct for confounding factors, we included age, pre-employment FEV1-% pred, allergy, medical treatment, and smoking in the analysis. RESULTS: The mean FEV1-% pred at follow-up was within the normal range (90.3, SD 13.5). Long exposure time was significantly associated with a low FEV1-% pred at follow-up (P = 0.0046). Adjustment was necessary for pre-employment FEV1-% pred and current smoking as confounding factors. CONCLUSION: Long duration of exposure is a factor affecting FEV1 in workers with potroom asthma. The results of this study give support for additional preventive measures to be taken, such as early recognition of work-related respiratory complaints and repeated education.

Aluminum↗

Resistance of activated human Th2 cells to NO-induced apoptosis is mediated by gamma-glutamyltranspeptidase.

Activation-induced death of inflammatory cells (AICD) has an important function in immune maintenance. Type 1 Th cells are known to be more susceptible to AICD than Th2 cells. In the current study we examined whether NO-induced apoptosis also preferentially eliminates Th1 cells over Th2 cells. Naive human Th lymphocytes (CD4(+)CD45RO(-)) were activated in vitro for 1 week in the presence of IL-12 plus anti-IL-4 or IL-4 plus anti-IL-12 to generate Th1- and Th2-polarized cultures respectively. Cultures were exposed to the NO donors Spermine-nonoate (Sper) and DPTA-nonoate to study NO-induced apoptosis. We found that NO preferentially induced apoptosis in Th1-polarized cells as demonstrated by Annexin staining in the presence of 10 microM Sper (70 +/- 16 versus 23 +/- 4.4% in Th2 cells P: < 0.01) and by DioC6 staining (38 +/- 10 versus 11 +/- 5% in Th2 cells, P: < 0.01). The mechanism of NO-induced apoptosis in Th1/Th2-polarized cells was distinct from AICD and Fas-induced apoptosis. Differential sensitivity between Th1- and Th2-polarized cultures originated at the level of intracellular glutathione (GSH) metabolism. GSH levels were higher in Th2 cells (1.6 +/- 0.2-fold Th1, P: < 0.01). High intracellular GSH in Th2-polarized cells did not account for reduced susceptibility to NO per se, since the inhibition of gamma-glutamyltrans-peptidase (gamma-GT), which is involved in GSH import, sensitized Th2 cells to NO-induced apoptosis without GSH depletion. Therefore, higher activity of gamma-GT in Th2 cells (2.1 +/- 0.4-fold Th1, P: < 0.001) specifically protects Th2 cells against NO-induced apoptosis. Preferential NO-induced elimination of human Th1 cells at sites of inflammation may thus select Th2 cells and contribute to immune deviation.

Apoptosis↗

Follow-up study of workers in a nylon carpet yarn plant after remedial actions taken against a contaminated humidification system.

OBJECTIVE: To investigate the effectiveness of remedial actions taken against a contaminated humidification system, after an outbreak of humidifier disease in a nylon carpet yarn plant. METHODS: Two and 6 years after modification, a follow-up investigation of a stratified (age, smoking habits) sample of exposed (n = 75) and non-exposed (n = 56) workers was carried out. Outcome-parameters were: respiratory symptoms, spirometry, skin tests and serology with various humidifier fungi. In addition, the yearly incidence of work-disability because of chronic respiratory disease during the 2 years before, and 11 years after the modification was compared. RESULTS: At follow-up, exposed workers, who remained at the same workplace no longer had significantly more frequent chronic respiratory symptoms. The prevalence of positive serology was still higher (P < 0.05) in exposed workers after 2 years, but at the 6 year follow-up investigation, the difference was no longer significant. Prevalence of positive skin tests after 2 years no longer differed from that of the non-exposed workers. Slopes (ml/years) of the graphs of forced vital capacity (FVC) and one-second forced expiratory volume (FEV1) during the 6 year follow-up after the first investigation did not differ between exposed and non-exposed workers, both before and after adjustment for age, smoking habits and results of skin tests and serology before modification. Before modification, exposed workers with a positive late skin test had a lower FVC than non-exposed workers. After 6 years of follow-up their FVC was still lower, but the difference was no longer significant. There were no indications of selective loss to follow-up. After remedial actions no new cases of humidifier disease occurred. Moreover, the yearly incidence of work-disability in this plant because of chronic respiratory disease, decreased from 1.30% to 0.27% compared with a decrease from 0.30% to 0. 12% in other synthetic fibre plants. CONCLUSION: Follow-up investigation of exposure-effects demonstrated the effectiveness of remedial actions taken against a contaminated humidification system.

Adolescent↗

Exposure and acute exposure-effects before and after modification of a contaminated humidification system in a synthetic-fibre plant.

OBJECTIVE: Follow-up study of exposure and acute exposure-effects after modification to steam humidification of a contaminated cold water system which had caused an outbreak of humidifier fever in a synthetic-fibre plant. METHODS: Before and after modification of the system aerobiological measurements were performed. Concentrations of fungi and bacteria, in colony forming units (cfu) per m3, were measured by stationary air sampling with an Andersen sampler. Endotoxin levels (pg/m3) were determined by Limulus Amoebocyte Lysate (LAL) assay in pooled dust from personal air sampling. An indication of exposure levels of oil-mist was obtained by monitoring with a direct reading optical photometer. Changes as acute exposure-effects in spirometry and white blood cell count, during an afternoon shift were compared in exposed and non-exposed workers before and after modification. RESULTS: Measured levels of fungi, total bacteria, Gram-negative bacteria and endotoxins both before and after modification were below levels which would be expected to be associated with the exposure-effects. However, after modification, we found that the statistically significant differences in levels of bacteria and endotoxins with a department without humidification no longer existed. Mean oil-mist concentrations were below 1 mg/m3, with short-time peak exposure during certain tasks of up to 5 mg/m3. Before modification, in exposed workers there was significantly more decline of spirometry, and more increase of white blood cell count during the first afternoon shift, compared with non-exposed workers. In exposed workers, the white blood cell count increase was positively associated with decline of spirometry. After modification, differences between exposed and non-exposed workers no longer existed. CONCLUSION: Follow-up investigation of acute exposure-effects demonstrated the effectiveness of remedial actions taken against a contaminated humidification system. Follow-up of exposure-effects in particular is recommended when there is doubt about the interpretation of exposure measurements.

Bacteria↗

Effects of budesonide and formoterol on eosinophil activation induced by human lung fibroblasts.

Budesonide and formoterol are extensively used in current asthma therapy. Budesonide is known as potent antiinflammatory agent and formoterol also appears to have some antiinflammatory properties. We investigated inhibitory effects of these drugs on eosinophil activation in vitro as induced by fibroblast-conditioned medium (FCM). We measured the modulation of expression of clonal designator (CD)11b and L-selectin with flow cytometry after 4 h or 16 h of culture of eosinophils when budesonide or formoterol was applied either directly to the eosinophils while they were stimulated with FCM (direct method) or when each drug was applied to lung fibroblasts from which conditioned medium was then administered to eosinophils (indirect method). In the direct method, budesonide (10(-)(8) M) inhibited the modulation of CD11b (44 [25th to 75th percentiles: 26 to 66]% of control) and L-selectin (30 [-13 to 48]% of control) only after 16 h, and not after 4 h. Formoterol did not directly inhibit the modulation of eosinophil CD11b and L-selectin expression. In the indirect method, both budesonide and formoterol inhibited lung fibroblast activation, resulting in diminished eosinophil activation after 4 h. Budesonide or formoterol at 10(-)(8) M inhibited upregulation of CD11b to 26 [15 to 40]% and 38 [23 to 46]%, respectively, and inhibited L-selectin shedding to 14 [-3 to 50]% and 27 [2 to 62]%, respectively, of control values. These results show that budesonide inhibits eosinophil activation primarily through effects on lung fibroblasts, presumably by inhibiting production of granulocyte-macrophage colony-stimulating factor. After longer incubation periods, budesonide also directly inhibits eosinophil activation. In contrast, formoterol can inhibit eosinophil activation only via inhibitory effects on lung fibroblasts. We did not observe an additional effect of formoterol, beyond the effects induced by budesonide under any circumstance studied. Lung fibroblasts, in addition to eosinophils, may serve as important target cells for antiinflammatory treatment in asthma.

Adult↗

Clinical effects of air cleaners in homes of asthmatic children sensitized to pet allergens.

BACKGROUND: Exposure to cat and dog allergens is very common in the Western World and is a serious cause of asthma in sensitized subjects. OBJECTIVE: We sought to study the clinical effects of air cleaners in living rooms and bedrooms of asthmatic children sensitized to cat or dog allergens. METHODS: Twenty asthmatic children sensitized to pet allergens (cat/dog) and with an animal at home participated in a double-blind, placebo-controlled, cross-over study in which the effects of air cleaners placed in the living room and bedroom for 3 months were compared with the effects of sham air cleaners. Before and after each study period, lung function, airway hyperresponsiveness (adenosine monophosphate), and peak flow variation were recorded. Cat and dog allergen levels were assessed in the filters of the air cleaners. RESULTS: After a 3-month intervention with active air cleaners, airway hyperresponsiveness decreased significantly, showing a 1.2 doubling dose increase of PC(20 )adenosine (P =.003). Peak flow amplitude also decreased (P =. 045). Substantial amounts of airborne cat and dog allergen were captured by the air cleaners in living rooms and bedrooms as well. Allergen levels in floor dust were not changed. CONCLUSION: In young asthmatic patients sensitized and exposed to pets in the home, application of air cleaners in living rooms and bedrooms was accompanied by a significant improvement in airway hyperresponsiveness and a decrease in peak flow amplitude.

Administration, Inhalation↗

The effect of gas cooking on bronchial hyperresponsiveness and the role of immunoglobulin E.

Some studies have shown an association between gas cooking and respiratory symptoms. This study investigated whether gas cooking affects bronchial responsiveness and whether particular subjects are more sensitive to this effect. Multiple linear regression analysis was performed with the dose-response slope (Percentage fall in forced expiratory volume in one second (FEV1) divided by total dose of methacholine given) as the dependent variable in 1,921 subjects from a random sample of the Dutch population, aged 20-70 yrs. Whether the association was different according to sex, age, total immunoglobulin (Ig)E, specific IgE to inhalant allergens or smoking habits was tested by including interaction terms into the regression model. Subjects who used gas for cooking had a higher prevalence of bronchial hyperresponsiveness (provocative dose causing a 20% fall in FEV1 (PD20) < or = 2 mg) than those who used electricity (21% versus 14%) and this was dependent on the presence of atopy. Especially subjects with total IgE levels in the highest quartile had a significantly higher dose-response slope when using gas for cooking. This was independent of the presence of specific IgE to inhalant allergens. These results show increased bronchial responsiveness with gas cooking, which was only found in subjects with high total immunoglobulin E levels. This suggests that atopic subjects are sensitive to adverse effects of gas cooking on respiratory health.

Adult↗

Follow up investigation of workers in synthetic fibre plants with humidifier disease and work related asthma.

OBJECTIVE: To investigate the clinical and sociomedical outcome in patients with various clinical manifestations of humidifier disease and work related asthma after removal from further exposure. METHODS: Follow up investigation (range 1-13 years) of respiratory symptoms, spirometry, airway responsiveness, sickness absence, and working situation in patients with (I) humidifier fever (n = 12), (II) obstructive type of humidifier lung (n = 8), (III) restrictive type of humidifier lung (n = 4), and (IV) work related asthma (n = 22). All patients were working at departments in synthetic fibre plants with microbiological exposure from contaminated humidification systems or exposure to small particles (< 1 micron) of oil mist. RESULTS: At follow up patients with work related asthma were less often symptom free (37%, 7/19) than patients with humidifier disease (I, II, III) (67%, 16/24). Mean forced expiratory volume in one second (FEV1) of patients with obstructive impairment had been increased significantly at follow up but still remained below the predicted value. Mean forced vital capacity (FVC) of patients with initially restrictive impairment had returned to normal values at follow up. Airway hyperresponsiveness at diagnosis persisted in patients with obstructive impairment (II + IV 14/17, but disappeared in patients with humidifier fever (3/3) and restrictive type of humidifier lung (2/2). In patients with obstructive impairment (II + IV), FVC and FEV1 at diagnosis were negatively associated with the duration between onset of symptoms and diagnosis and the number of years of exposure. Those with positive pre-employment history of respiratory disease had a lower FEV1 at diagnosis. Sickness absence due to respiratory symptoms decreased in all groups of patients after removal from further exposure, but this was most impressive in patients with the humidifier lung (II, III) and patients with work related asthma (IV). At follow up 83% of the patients were still at work at the same production site, whereas 11% received a disability pension because of respiratory disease. CONCLUSION: In patients with work related respiratory disease caused by exposure from contaminated humidification systems or oil mist, removal from further exposure resulted in clinical improvement, although, especially in those with obstructive impairment, signs persisted. Because of the possibility of transferring patients to exposure-free departments most patients could be kept at work.

Adult↗

Occurrence of occupational asthma in aluminum potroom workers in relation to preventive measures.

The purpose of this study was to investigate whether preventive measures such as reduction of exposure and the introduction of the histamine provocation test (HPT) as a selection instrument resulted in a lower incidence of potroom asthma (PA) and a longer time lag between the commencement of employment and the occurrence of PA. Between 1970 and 1990, 179 cases of PA were diagnosed. This period was divided into three periods. During period 1 (1970-1975), no exposure data were available. Period 2 (1976-1981) is characterized by known exposure data obtained by means of fluoride determinations in urine. At the beginning of period 3 (1982-1990) the HPT was incorporated into the preemployment medical examination. We computed the incidence density (ID) in the three periods and analyzed the timelag in relation to the year of employment and confounding factors such as age, atopic history, blood eosinophil counts, lung function, smoking habits at preemployment, and exposure level. After introduction of the preemployment HPT the ID decreased, but cases continued to occur (ID 11.6 in period 2 versus 2.5 in period 3). The time lag was did not differ when subjects with bronchial hyperresponsiveness were screened out. The exposure level and an atopic history were factors associated with the period of employment and, therefore, confounded the results. The results of this study support the role of an atopic history as a risk factor for development of PA at lower exposure levels and suggest that potroom exposure not only incites asthmatic symptoms but also acts as an inducer of respiratory disease.

Aluminum↗

Interactions between inhalant allergen extracts and airway epithelial cells: effect on cytokine production and cell detachment.

BACKGROUND: The factors responsible for inducing or maintaining airway inflammation are poorly understood. Various studies have focussed on the mechanisms leading to allergic airway inflammation in patients with asthma and rhinitis. The observation of local airway inflammation in nonallergic patients with asthma or rhinitis, including those with nasal polyposis, suggest that non-IgE-related mechanisms exist that may lead to airway inflammation. Various lines of evidence suggest that epithelial cells may participate in local inflammation of the airways. OBJECTIVE: This study focused on the interaction of airway epithelial cells with clinically relevant inhalant allergen extracts in vitro. METHODS: Cultures of airway epithelial cells were exposed to mite, Timothy grass pollen, and birch pollen extracts. Production of IL-8, IL-6, monocyte-chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony-stimulating factor and cell detachment were monitored while protease inhibitors and chromatography techniques were applied to identify the factors responsible for these effects. RESULTS: With the mite extracts, cytokine production and cell detachment was largely dependent on protease activity. With the pollen extracts, cytokine production without cell detachment seemed to be independent of protease activity. CONCLUSION: These findings support the view that epithelial cells may contribute to the pathogenesis of airway disease by their interaction with inhalant allergen extracts. Furthermore, allergen extracts may enhance airway inflammation by means other than their IgE-binding activity through both protease-dependent and protease-independent mechanisms.

Allergens↗

Prevalence of sensitization to the storage mites Acarus siro, Tyrophagus putrescentiae, and Lepidoglyphus destructor in allergic patients with different degrees of sensitization to the house-dust mite Dermatophagoides pteronyssinus.

The prevalence of sensitization to the storage mites Acarus siro (AS), Tyrophagus putrescentiae (TP), and Lepidoglyphus destructor (LD) was studied in 250 sera of patients with different degrees of sensitization to the house-dust mite Dermatophagoides pteronyssinus (DP) by measuring IgE binding to extracts of the storage mites. Additionally, allergenic cross-reactivity between DP and the storage mite species was studied by RAST inhibition with five individual sera (and a pool of these sera) with moderate IgE levels to all three storage mites and to DP. Increased serum IgE to storage mites was found in 46% of the 200 patients sensitized to DP. Increased prevalence rates of IgE titers to storage mites were associated with higher IgE levels to DP. In 50 sera without sensitization to DP, only five sera showed increased IgE to one of the storage mites. Extracts of TP almost completely inhibited the IgE binding to AS, and vice versa. DP inhibited IgE binding to all storage mites up to 60%, whereas IgE binding to DP was only minimally inhibited by extracts of storage mites. In conclusion, cosensitization to storage mites is a frequent finding in patients sensitized to DP. Although this is largely the result of cross-reactivity between different mite species, it may nevertheless be of clinical significance in patients exposed to storage mites.

Adult↗

House-dust mite hypersensitivity, eczema, and other nonpulmonary manifestations of allergy.

The pathogenetic role of house-dust mites (HDM) in atopic dermatitis (AD) remains controversial, mainly because there is no common agreement on a provocation test that mimics ordinary exposure to HDM. This is related to the lack of knowledge of the mechanism of how HDM allergens enter the body. Theoretically, there are two possible routes: directly through the epidermis, or by inhalation. In "atopy patch testing", a concentrated HDM suspension is tested on the skin under occlusion. This method is frequently used as a model of the epidermal route. The clinical relevance of this method as a provocation test for AD is discussed. As opposed to atopy patch testing, we describe another method, namely, "allergen inhalation testing", as a model of the respiratory route. Twenty patients with AD underwent bronchial provocations with HDM extract in a double-blind, randomized, placebo-controlled study. In nine out of 20 AD patients, bronchial challenge with HDM evoked skin symptoms. All patients with HDM-induced dermatitis had a history of asthma, and as a group they had a higher mean total log-transformed IgE level than the "negative skin responders". Thus, the respiratory route may be relevant in the provocation of AD in a subset of AD patients and may represent an appropriate model of provocation in these patients. Furthermore, the role of HDM in urticaria and allergic rhinitis is discussed.

Allergens↗