Asthma among workers in healthcare settings: role of disinfection with quaternary ammonium compounds.

INTRODUCTION: An increased incidence of asthma has been reported among healthcare workers. The role of quaternary ammonium compounds (QACs), commonly used in cleaning/disinfection products, has not been clearly defined. The aim of this study was to analyse associations between asthma and occupational exposure to disinfectants, especially QACs. METHODS: The study was performed on a stratified random sample of the various healthcare departments of 7 healthcare settings. The study included: questionnaire, physical examination and specific IgE assays. Occupational exposure assessment was performed by means of a work questionnaire, workplace studies and a review of products ingredients. Data were analysed by logistic regression. RESULTS: Response rate was 77%; 543 workers (89% female) participated; 37.1% were registered nurses (RNs), 16.4% auxiliary nurses (ANs), 17.3% cleaners; 32.8% were atopic. 335 participants were exposed to QACs. Nursing professionals reported a significantly higher risk of reported physician-diagnosed asthma and, for RNs, of nasal symptoms at work than administrative staff working in healthcare sector. This risk was particularly marked during disinfection tasks and when exposure to QACs. Exposure to QACs increased significantly the risk of reported physician-diagnosed asthma and nasal symptoms at work (adjusted OR = 7.5 and 3.2, respectively). No significant association was found with other exposures such as latex glove use, chlorinated products/bleach or glutaraldehyde. CONCLUSION: RNs and ANs presented a higher risk of reported asthma than administrative staff. The highest risk was associated with tasks involving dilution of disinfection products by manual mixing, suggesting possible exposure to repeated peaks of concentrated products known to be strong respiratory irritants. Workplace interventions should be conducted to more clearly determine QAC exposure and improve disinfection procedures.

Repeated inhalation of low doses of cat allergen that do not induce clinical symptoms increases bronchial hyperresponsiveness and eosinophil cationic protein levels.

The aim of this study was to investigate whether repeated exposure to subclinical doses of cat allergens, not inducing asthma symptoms, could affect eosinophil cationic protein (ECP) levels in bronchoalveolar lavage (BAL) or in peripheral blood, without the appearance of clinical symptoms. Twelve patients with mild asthma, all sensitized to cats and not exposed to cat allergen at home, underwent a series of inhalations of cat allergen or placebo for 8 days over 2 weeks. A methacholine challenge was performed before and after the allergen and saline exposures, and BAL and blood were sampled for ECP measurements and eosinophil counts. No patients experienced asthma symptoms. However, PD20 methacholine (geometric mean) decreased significantly from 263 microg before to 126 microg after inhalation of allergen. Inhalation of saline did not induce any significant change in PD20. The change in log PD20 before and after cat allergen exposure was statistically different from the change in log PD20 before and after saline. Median ECP levels in BAL and serum increased significantly after allergen exposure, from 0.8 to 3.1 microg/l (p<0.02) and from 15.9 to 31.4 microg/l (p<0.05), respectively. No change was observed after saline inhalations. The change in BAL and serum ECP levels was statistically significant compared to that in the control group. The number of eosinophils did not change, however, nor did IL-5 and RANTES levels in BAL and serum. In conclusion, our results show that (1) exposure of asthma patients to repeated low doses of allergen, which did not provoke any clinical symptoms, is capable of inducing a local eosinophil activation associated with an increase in nonspecific bronchial hyperresponsiveness and (2) the increase in serum ECP levels due to eosinophil activation precedes the occurrence of asthma symptoms and may thus be a marker of allergen exposure in allergic asthma.

[Occupational asthma]. / Asthmes professionnels.

Occupational asthma is specifically induced by repeated exposure to substances in the work place. Diagnosis requires using the results of numerous tests, and a challenge test is the most appropriate to establish the diagnosis of occupational asthma due to chemical agents. Agents responsible for occupational asthma may be of animal or vegetable origin, or may be chemical agents. The pathophysiological mechanisms of occupational asthma are not well known. It is probable that immunologic mechanisms play an important role, in particular in occupational asthma due to glycoproteins. An important feature of occupational asthma is the relationship to chemical substances, for which the mechanisms are often still hypothetical. From the legal viewpoint, a recent law holds the promise of better compensation for those who are afflicted.

[Asthma and household chemical pollutants (with the exception of tobacco)]. / Asthme et polluants chimiques domestiques (à l'exception du tabac).

The relationship between allergens in a domestic environment and asthma has been extensively studied and it is only recently that studies have suggested the possibility of the role of chemical pollutants in the internal environment in the genesis of asthma. The pollutants studied are oxides of nitrogen (nitrogen dioxide NO2), volatile organic components (COV), formaldehyde, ozone (O3) and sulphur dioxide (SO2). The level of nitrogen dioxide in the interior of houses may be greater than those met outside. Normal values are 400 mcg per metre3 per hour and 150 mcg per metre3 in twenty four hours. In asthmatics challenge test to nitrogen dioxide and epidemiological studies suggest that internal nitrogen dioxide is capable of provoking asthmatic crises either by a direct pollutant effect or by potentialising the allergenic crises either by a direct pollutant effect or by potentialising the allergenic response of the bronchi. COV and formaldehyde are liberated by urea formaldehyde foams and by chipboard furniture. The levels of COV and formaldehyde inside a house may be up to 10 times higher than those outside. COV and formaldehyde perhaps would have an effect on the bronchi in asthmatics at significant levels which are rarely found in the domestic environment. Ozone is an external pollutant. However, from 5-80% of the external concentrations may be found inside some locations. Thus, in certain conditions which are relatively rare, the interior concentrations of dwelling places may attain levels which are capable of inducing, in healthy subjects who are sensitive to ozone, a drop in the FEV1. As regards asthmatics, only experimental work has been able to show any bronchospastic effect of ozone, either by a direct effect on the bronchi or by the potentiation of a bronchial response to allergens. It would be convenient to perform some epidemiological studies to determine if there is a relationship between exposure to ozone internally and to bronchial changes. The concentrations of SO2 inside houses increases when coal is burnt. The levels provoking a bronchial reaction are much greater than those found inside houses. The data and the literature which is mostly recent seems to stress the role of NO2 ozone and SO2 as a factor which might favour asthmatic crises induced by allergens in atopic subjects. However, other studies will be necessary to confirm the initial data.

[Experimental studies of the effects of atmospheric pollutants]. / Etudes expérimentales des effets des polluants atmosphériques.

Experimental studies in man are an indispensable complement to epidemiological studies and experimental studies on animals. They aim at understanding the mechanisms of action of the main pollutants and at knowing their thresholds of triggering of the acute effects on the respiratory system. The studies made in man involve controlled exposure to different atmospheric pollutants, with measurement of the functional respiratory repercussions, studies of modification of the cells in broncho-alveolar lavage, as well as experimental protocols that combine inhalation of allergen and exposure to atmospheric pollutants by allergic subjects. The main results that are available are reported to distinguish those from normal subjects and those who are allergic. More recent protocols are based on exposure to concentrations that are close to atmospheric concentrations or those that are met in work places. The main data in the literature are reported in this journal and concern SO2 acid aerosols, dioxides of nitrogen, ozone and diesel particles. Pathogenic hypotheses concerning the undesirable effects of atmospheric pollutants on the respiratory system are considered.

[Occupational asthma in an agricultural setting]. / L'asthme professionnel en milieu agricole.

The prevalence of asthma in a farming environment is significant (from 3-7.7% according to various studies). The clinical picture has not been specified. The responsible agents are multiple and polysensitization frequent. Numerous substances of vegetable origin may be a cause, pollens, moulds, cereals, oil and protein producing plants, fibrous textiles, diverse plants and wood, etc. Amongst substances of animal origin the most frequent allergens incriminated are: allergens from mammals (horses, cattle, pigs), allergens from chickens and birds, arthropod allergens, insect allergens. Amongst chemical products those which are at risk to the respiratory system include insecticides, herbicides, fungicides, antibiotics and antiparasites. The diagnosis of the occupational character of asthma is sometimes difficult because of other causes of lung diseases in farm workers. The aetiological diagnosis is achieved by the clinical history, cutaneous tests, a level of specific serum IgE, and bronchial provocation tests which contrary to asthma in the industrial environment are not fundamental to the diagnosis except where chemical products are suspected. The mechanisms are sometimes intricate (IgE dependant mechanisms, non-specific liberation of histamine, activation of complement, intervention of endotoxins and pharmacological mechanisms...). Prevention may be carried out on behalf of the victim (for example wearing filtration masks in dusty work) and also carry out various methods to reduce the level of exposure to the allergen.

HLA class II alleles in isocyanate-induced asthma.

Studying genetic factors that control human immune responsiveness may further our understanding of specific types of asthma in which the role of immune factors is uncertain to date. HLA Class II gene products are involved in the control of immune responses. Therefore, we investigated whether HLA Class II genetic markers contribute to susceptibility or resistance to isocyanate-induced asthma (IAA) in exposed workers. We collected venous blood samples from two groups of unrelated white adults: (1) patients with isocyanate-induced asthma documented by a positive inhalation challenge; and (2) exposed individuals with no history of IAA. The second exon of DQA1, DQB1, DPB1, and DRB genes was selectively amplified by the polymerase chain reaction (PCR) method. HLA typing was carried out by the PCR-RFLP method, which allowed discrimination of most HLA DQA1, DQB1, DPB1, and DRB alleles. No significant difference was found in the distribution of DPB1 alleles between patients and control subjects. Allele DQB1*0503 and allelic combination DQB1*0201/0301 were associated with susceptibility to the disease. Conversely, allele DQB1*0501 and the DQA1*0101-DQB1*0501-DR1 haplotype conferred significant protection to exposed healthy control subjects. Our results are consistent with the hypothesis that immune mechanisms are involved in isocyanate-induced asthma and that specific genetic factors may increase or decrease the risk of developing IAA in exposed workers.

[Occupational asthma: an experimental asthma. Apropos of isocyanate-induced asthma]. / L'asthme professionnel: un asthme expérimental. A propos de l'asthme aux isocyanates.

Isocyanate-induced occupational asthma is a model of experimental asthma related to the environment. Many of its features are identical with those of allergic asthma by sensitization to air-borne allergens. Exposure to isocyanate before the first symptoms of asthma varies from a few weeks to several years. The prevalence of isocyanate-induced asthma has been estimated at 5 to 25%. Atopy is found in less than 30% of the cases. A significant increase of HRBNS can be demonstrated in most patients, but it may be absent. It may also fluctuate with the working periods or after a bronchial provocation test with isocyanate. Elimination of this compound reduces the HRBNS level in only one quarter of the cases. Delayed or biphasic reactions are frequent: 30 to 60% depending of the authors. An early diagnosis followed by total elimination may result in complete cure, but more than 50% of the patients remain symptomatic and with HRBNS. An IgE-dependent mechanism can be demonstrated in about 20% of the cases. The course of isocyanate-induced asthma is interesting in that the same phenomena are probably observed in chronic asthma resulting from repeated exposures to environmental allergens.

Meat wrapper's asthma: identification of the causal agent.

Meat wrapper's asthma is a typical example of occupational asthma due to emissions from chemical products. The authors report three new cases due to the use of the now classic meat packaging techniques in supermarkets. The chemical agents involved were identified. Inhalation tests have been carried out in one patient with the complete wrappings, i.e. the PVC film and the price labels, and separate tests were performed with eight additives of the PVC film, and with phthalic anhydride and di-cyclohexylphthalate emitted from heated price labels. These tests incriminate two products: phthalic anhydride seems to be the principal causal agent and epoxidized soybean oil can be suspected as a secondary agent causing this occupational asthma.