Jörgen Thorn

Airways inflammation and glucan exposure among household waste collectors

A field study was made on 17 workers collecting unsorted household waste, eight workers collecting organic/nonorganic separated waste, and 24 controls. Measurements of airborne endotoxin and (1-->3)-beta-D-glucan were made in their working environments. Examinations consisted of a questionnaire for symptoms, spirometry, airway responsiveness, and blood and sputum sampling for determination of cell counts, eosinophilic cationic protein (ECP), and myeoloperoxidase (MPO). A higher proportion of waste collectors reported diarrhea, congested nose, and unusual tiredness as compared to controls. The number of blood lymphocytes was higher among waste collectors and were dose-related to the amount of airborne (1-->3)-beta-D-glucan at the workplaces. The amount of ECP and the number of macrophages were lower in sputum among waste collectors as compared with controls. The results suggest that certain dusts from household waste may cause airway inflammation as well as general symptoms, and the effects were associated with higher (1-->3)-beta-D-glucan levels.

Inflammatory response after inhalation of bacterial endotoxin assessed by the induced sputum technique.

BACKGROUND Organic dusts may cause inflammation in the airways. This study was performed to assess the usefulness of the induced sputum technique for evaluating the presence of airways inflammation using inhaled endotoxin (lipopolysaccharide) as the inducer of inflammation. METHODS To characterise the inflammatory response after inhalation of endotoxin, 21 healthy subjects inhaled 40 μg lipopolysaccharide and were examined before and 24 hours after exposure. Examinations consisted of a questionnaire for symptoms, spirometric testing, blood sampling, and collection of induced sputum using hypertonic saline. Eleven of the subjects inhaled hypertonic saline without endotoxin exposure as controls. Cell counts, eosinophilic cationic protein (ECP), and myeloperoxidase (MPO) were determined in blood and sputum. RESULTS A significantly higher proportion of subjects reported respiratory and general symptoms after endotoxin inhalation. MPO and the number of neutrophils in the blood were higher and spirometric values were decreased after the lipopolysaccharide challenge. In the sputum MPO, ECP, and the numbers of neutrophils and lymphocytes were higher after the lipopolysaccharide challenge. No significant differences were found after the inhalation of hypertonic saline compared with before, except for a significantly lower number of lymphocytes in the sputum. CONCLUSIONS The results support previous studies that inhaled endotoxin causes an inflammation at the exposure site itself, as well as general effects. Sampling of sputum seems to be a useful tool for assessing the presence of airways inflammation, and the inhalation of hypertonic saline used to induce sputum did not significantly interfere with the results found after inhalation of lipopolysaccharide.

Work related symptoms among sewage workers: a nationwide survey in Sweden

Aims: To assess the risk for work related symptoms among sewage workers in Sweden using a postal questionnaire. Methods: All municipalities in Sweden were contacted and asked to provide addresses of sewage workers and controls. Controls were recruited among other municipal workers not exposed to sewage, such as workers in drinking water plants and gardeners. A questionnaire was sent to the subjects and after two reminders, the response rate was 74% among sewage workers and 59% among controls. Results: Significantly increased risks for airway symptoms, chronic bronchitis, and toxic pneumonitis, as well as central nervous system symptoms such as headache, unusual tiredness, and concentration difficulties were found among the sewage workers compared with controls. Furthermore, an increased risk for non-specific work related gastrointestinal symptoms was found among the sewage workers; an increased risk for joint pains, related to pains in more than four joints but not with loading, was also found. Conclusions: The results of this questionnaire survey show an increased risk for airway, gastrointestinal, and general symptoms such as joint pains and central nervous system symptoms among sewage workers. Clinical investigations are needed to determine the cause of the reported symptoms among sewage workers, and further field studies are required to assess the causal agents.

Inhalation of (1-->3)-beta-D-glucan causes airway eosinophilia.

BACKGROUND: Moulds are present in a variety of environments and aerosols of fungal spores are generated when mouldy materials are handled. Molds contain (1-->3)-beta-D-glucan, a polyglucose which is present in the cell wall of fungi, certain bacteria and plants. AIM: This study was undertaken to investigate the cellular inflammatory response in the lung after inhalation of (1-->3)-beta-D-glucan and bacterial endotoxin. METHODS: Guinea pigs were exposed daily to an aerosol of pure (1-->3)-beta-D-glucan and pure endotoxin for five weeks. Lung lavage and lung interstitial cell preparations were done and the inflammatory cells counted. Histological sections were prepared from the trachea. RESULTS: There was an increase in eosinophil numbers in lung lavage, lung interstitium, and the airway epithelium of animals exposed to (1-->3)-beta-D-glucan. In animals simultaneously exposed to endotoxin, there was no increase in eosinophils. In the lung interstitium, (1-->3)-beta-D-glucan exposure caused an increase in lymphocytes, which was not found after endotoxin exposure. Endotoxin exposure caused an increase in neutrophils and macrophages in lung lavage, which was not found after (1-->3)-beta-D-glucan exposure. CONCLUSIONS: The results support previous findings that (1-->3)-beta-D-glucan causes a different response in the airways as compared to endotoxin. Endotoxin modulated the increase in eosinophils caused by (1-->3)-beta-D-glucan exposure, suggesting a complex interaction between the microbial cell wall components.

Effects after inhalation of (1→ 3)-β-D-glucan in healthy humans

BACKGROUND AND AIM: This study was performed to assess the effects of an exposure to a pure (1-->3)-beta-D-glucan, a cell wall component of fungi, plants and certain bacteria. METHODS: Twenty-one healthy subjects inhaled saline or (1-->3)-beta-D-glucan suspended in saline in a random, double-blind, cross-over design. They were examined before exposure and 24 and 72h afterwards with spirometry, blood sampling and collection of induced sputum. Differential cell counts and eosinophilic cationic protein (ECP) were determined in blood and sputum, and myeloperoxidase (MPO), tumour necrosis factor-alpha (TNF-alpha), and interleukin (IL)-8 and IL-10 were determined in sputum supernatants. TNF-alpha was determined after cultivation of blood mononuclear cells. RESULTS: In sputum, inhalation of saline caused a significant increase in ECP and TNF-alpha. (1-->3)-beta-D-Glucan inhalation caused a further increase in these cytokines, although not statistically significantly different from the increase induced by inhalation of saline alone. In blood, the number of eosinophils was significantly decreased 72 h after the challenge with (1-->3)-beta-D-glucan. This effect was not found after the inhalation of saline alone. TNF-alpha production from stimulated blood mononuclear cells was significantly decreased 72 h after the (1-->3)-beta-D-glucan inhalation as compared with the increase induced by saline inhalation. CONCLUSIONS: The results suggest that (1-->3)-beta-D-glucan causes a different type of response as compared with inflammatory agents such as bacterial endotoxin that cause a neutrophil-dominated inflammatory response.

Effects after inhalation of (1-->3)-beta-D-glucan and relation to mould exposure in the home.

BACKGROUND: Damp conditions indoors favour the growth of microorganisms, and these contain several agents that may cause inflammation when inhaled. Moulds contain a polyglucose in their cell wall, defined as (1-->3)-beta-D-glucan, exhibiting effects on inflammatory cells. AIM: The aim of the present study was to evaluate whether an inhalation challenge to purified (1-->3)-beta-D-glucan (grifolan) in humans could induce effects on inflammatory markers in blood, and to evaluate whether the reactions were related to the home exposure to (1-->3)-beta-D-glucan. METHODS: Seventeen subjects in homes with high levels of airborne (1-->3)-beta-D-glucan (G-high) and 18 subjects in homes with low levels of (1-->3)-beta-D-glucan (G-low) underwent two randomised, double-blind inhalation challenges, one to (1-->3)-beta-D-glucan suspended in saline and one to saline alone. A blood sample was taken before and after the challenges, and differential cell count, granulocyte enzymes in serum and the secretion of cytokines from peripheral blood mononuclear cells (PBMC) were measured. RESULTS: Inhalation challenge with (1-->3)-beta-D-glucan induced a decrease in the secretion of tumour necrosis factor alpha from endotoxin-stimulated PBMC in the G-high group as well as in the G-low group. In the G-high group, the inhalation of (1-->3)-beta-D-glucan induced an increase in blood lymphocytes that was significantly different from the saline-induced effect. CONCLUSIONS: The results suggest that an inhalation challenge to (1-->3)-beta-D-glucan has an effect on inflammatory cells and this effect may be related to a chronic exposure to moulds at home.

Person-centred care after acute coronary syndrome, from hospital to primary care — A randomised controlled trial☆ ,★

AIM To evaluate if person-centred care can improve self-efficacy and facilitate return to work or prior activity level in patients after an event of acute coronary syndrome. METHOD 199 patients with acute coronary syndrome < 75 years were randomly assigned to person-centred care intervention or treatment as usual and followed for 6 months. In the intervention group a person-centred care process was added to treatment as usual, emphasising the patient as a partner in care. Care was co-created in collaboration between patients, physicians, registered nurses and other health care professionals and documented in a health plan. A team-based partnership across three health care levels included transparent knowledge about the disease and medical state to achieve agreed goals during recovery. Main outcome measure was a composite score of changes in general self-efficacy ≥ 5 units, return to work or prior activity level and re-hospitalisation or death. RESULTS The composite score showed that more patients (22.3%, n=21) improved in the intervention group at 6 months compared to the control group (9.5%, n=10) (odds ratio, 2.7; 95% confidence interval: 1.2-6.2; P=0.015). The effect was driven by improved self-efficacy ≥ 5 units in the intervention group. Overall general self-efficacy improved significantly more in the intervention group compared with the control group (P=0.026). There was no difference between groups on re-hospitalisation or death, return to work or prior activity level. CONCLUSION A person-centred care approach emphasising the partnership between patients and health care professionals throughout the care chain improves general self-efficacy without causing worsening clinical events.

Improved prediction of COPD in at-risk patients using lung function pre-screening in primary care : a real-life study and cost-effectiveness analysis.

BACKGROUND The importance of identifying chronic obstructive pulmonary disease (COPD) at an early stage is recognised. Improved and easily accessible identification of individuals at risk of COPD in primary care is needed to select patients for spirometry more accurately. AIMS To explore whether use of a mini-spirometer can predict a diagnosis of COPD in patients at risk of COPD in primary care, and to assess its cost-effectiveness in detecting patients with COPD. METHODS Primary care patients aged 45-85 years with a smoking history of >15 pack-years were selected. Data were collected on the Clinical COPD Questionnaire (CCQ), Medical Research Council (MRC) dyspnoea scale and smoking habits. Lung function (forced expiratory volume in 1 and 6 s; FEV1 and FEV6, respectively) was measured by mini-spirometer (copd-6), followed by diagnostic standard spirometry (COPD diagnosis post-bronchodilation ratio of FEV1 to forced vital capacity (FVC) <0.7). Time consumed was recorded. Univariate logistic regression and receiver operating characteristic (ROC) curves were used. RESULTS A total of 305 patients (57% females) of mean (SD) age 61.2 (8.4) years, mean (SD) total CCQ 1.0 (0.8) and mean (SD) MRC 0.8 (0.8) were recruited from 21 centres. COPD was diagnosed in 77 patients (25.2%) by standard diagnostic spirometry. Using the copd-6 device, mean (SD) FEV1/FEV6 was 68 (8)% in patients with COPD and 78 (10)% in patients without COPD. Sensitivity and specificity at a FEV1/FEV6 cut-off of 73% were 79.2% and 80.3%, respectively. The area under the ROC curve was 0.84. Screening with the copd-6 device significantly predicted COPD. Gender, CCQ, and MRC were not found to predict COPD. CONCLUSIONS Using the copd-6 as a pre-screening device, the rate of COPD diagnoses by standard diagnostic spirometry increased from 25.2% to 79.2%. Although the sensitivity and specificity of the copd-6 could be improved, it might be an important device for prescreening of COPD in primary care and may reduce the number of unnecessary spirometric tests performed.

Seasonal variations in exposure to microbial cell wall components among household waste collectors

BACKGROUND Collection, separation, and composting of household waste generates organic dusts that may contain the inflammagenic agent endotoxin and (1-->3)-beta-D-glucan, a cell wall component of fungi, plants and certain bacteria. In previous studies, waste collectors have reported a greater number of or more severe symptoms in the summer. To further elucidate whether a seasonal variation in exposure could support previous findings of the presence of symptoms during summer months, a study was performed to assess exposures to airborne (1-->3)-beta-D-glucan and endotoxin during different seasons among household waste collectors handling compostable waste. METHODS Measurements were made of the amounts of airborne (1-->3)-beta-D-glucan and endotoxin using personal sampler equipment in two household waste collectors handling compostable waste. Measurements were made every second week from September 1998 to January 2000. RESULTS The amounts of airborne endotoxin were low during the study period. The amount of airborne (1-->3)-beta-D-glucan was higher during the warm season, and there was a relationship between exposure levels of (1-->3)-beta-D-glucan and outdoor temperature. CONCLUSIONS The results suggest that household waste collectors handling compostable waste can be exposed to airborne (1-->3)-beta-D-glucan, especially during the warm season, when more symptoms have been reported among waste collectors, according to previous studies. This cannot be interpreted as a causal relationship as household waste may contain several agents that could cause effects. Further studies are needed to explore such relationships.

Management of chronic obstructive pulmonary disease (COPD) in primary care: a questionnaire survey in western Sweden

AIM To assess the primary care management of chronic obstructive pulmonary disease (COPD) in relation to COPD guidelines. METHOD A postal questionnaire was sent out to all Primary Health Care Centres (PHCCs) in western Sweden (n=232). The response rate was 75%. RESULTS A majority of the PHCCs had a nurse and physician responsible for COPD care. They used spirometry equipment regularly, but only 50% reported that they calibrated it at least weekly. Less than 30% of the PHCCs reported access to a dietician, occupational therapist or physiotherapist. There was a structured smoking cessation program in 50% of the PHCCs. Larger PHCCs were more likely to use spirometry equipment regularly and to have specific personnel for COPD care. CONCLUSION There is a need to establish structured programs for COPD care including smoking cessation programs for COPD patients with special trained staff. Larger PHCCs have a better infrastructure for providing guideline-defined COPD care.