Abstract
(Englisch)
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The objectives of the project are to provide knowledge for the prevention of waste dust related disease through co-ordination and optimisation of different ongoing research projects. The specific objectives are: 1) to identify causative agents and the pathological reactions caused by these; 2) to develop measurement strategies to assess the exposure and the risk of disease; 3) to evaluate 'no reaction' limit threshold based on dose response relationships established by both epidemiological and experimental data; 4) to develop improved diagnostic criteria and methods for an early detection of inflammatory disease; and 5) to develop information material on disease risks and protection measures for groups engaged in waste handling.
The contributions of the Swiss group consist in studying risk exposures among industrial compost workers (CW). The project is organised in 3 overlapping phases. The initial phase consist in an epidemiological survey to define the prevalence and the symptom profile among CW in relation with their exposure to organic dust. The objectives of phases two and three are to assess in exposed CW dust induced inflammation both in vivo and in vitro. For this purpose, two groups of CW with and without work related symptoms have been recruited. The presence of airways responsiveness will be measured both in on the work place and after inhalation challenge tests with selected antigens. Exposure measurements in terms of endotoxin and (1®3)-b-D-glucan will be made by using personal samplers provided by collaborative groups [GOT and WAG]. The clinical examinations will be completed by in vitro evaluation of inflammation and of the immune reactivity to various compost dust components. Serological mediators (ECP, CRP) will be used as well as cellular reactivity tests (lymphocyte stimulation, mediator release: PAF, leucotriènes (LTC/LTD/LTE4), TNF-a, IL-5, IL-10, and cytokine profile of Th1 or Th2 responses).
Phases two and three are under way. The first phase of the project has been completed. 205 CW (89.3%) from 88 of the 110 major composting plants in Switzerland participated in this study. An excess of symptoms of sneezing, nasal irritation and dry cough, as well as skin reactions, was reported among the CW as compared to a standard cohort of persons not exposed to organic dust. >25% of all CW complained of persistent respiratory problems. Prevalence was directly related with exposure frequency. >42% of the CW also complained of reacting to compost dust, and 26.7% had symptom scores compatible with bronchial hyperreactivity.
The contributions of the Swiss group to this project consisted in studying risk exposures among industrial compost workers (CW). In the initial phase, an epidemiological survey defined the prevalence and the symptom profile among professional CW in Switzerland employed in industrial composting plants. An excess of symptoms of sneezing, nasal irritation and dry cough, as well as skin reactions, was reported among the CW as compared to a standard cohort of non-exposed persons. >25% of all CW complained of persistent respiratory problems. >42% of the CW also complained of reacting to compost dust, and 26.7% reported symptom scores compatible with an existing bronchial or mucosal hyper-reactivity. The prevalence of these symptoms was directly related with exposure frequency and job position. With the second and third phases, dust-induced inflammation was assessed; both with in vivo and in vitro analysis, in a selected group of exposed CW.
Results and conclusions: Inhalation of CE and Af induced an increase on BHR in respectively 5/11 and 2/11 CW but no immediate changes in spirometric values. Inhalation of 50 mg LPS in CV did not induce any significant change in spirometric parameters, thought 3 had a moderate increase in BHR and > 60% had systemic symptoms. 5/11 CW had a significant change in lung values with a lowered threshold tolerance to LPS. 2 more developed an increase of BHR and one had moderate systemic symptoms (fever). Only 2 CW were absolutely tolerant to this maximal inhalation dose having had no bronchial and no systemic responses. One CW developed a severe ODTS-like syndrome less than an hour after the cumulated inhalation of 5.5 mg LPS but with no respiratory symptoms. PAF-acether release was found to correlate the best with the results of bronchial provocation tests.
Discussion and conclusions:
The investigations undertaken in this study have shown that CW have an abnormal response to LPS exposure, both in vivo and in vitro. Rylander and colleagues had suggested that 50 mg LPS corresponded to the threshold for inducing clinical symptoms, whereas Michel and collaborators had found that 20 mg LPS did not induce any symptoms in normal non exposed subjects. In this project, we used the same material and inhalation equipment as [BRU]. When compared to the standard group of non-exposed persons studied by [BRU] in the first year of this project, the group of CW studied had a very high degree of sensitivity and bronchial response to LPS. While none of the [BRU] volunteers tested with 50 mg LPS showed a significant change in spirometric parameters and only three had a moderate increase in BHR, 5 among the ten CW tested had a significant change in lung values and 2 more developed an increase of BHR. Only 2 CW were absolutely tolerant to this maximal inhalation dose having had no bronchial and no systemic responses. One CW developed a severe ODTS-like syndrome less than an hour after the cumulated inhalation of 5.5 mg LPS. The two first CW had a FEV1 fall > 20% already after 5.5 mg LPS, two more after 13 mg cumulated inhalation of LPS, the last remaining CW which a consecutive FEV1 fall > 20% reacted only after 50.5 5 mg LPS.
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