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Biomedical subjects

J Thorn

Publications and source records attributed to J Thorn.

At least 19 recordsLinked to original sources

Upper airway inflammation in waste handlers exposed to bioaerosols.

AIMS: To examine work associated upper airway inflammation in 31 waste handlers, and to correlate these findings with personally monitored exposure to different bioaerosol components. METHODS: Cell differentials, interleukin 8 (IL-8), myeloperoxidase (MPO), and eosinophilic cationic protein (ECP) were examined in NAL (nasal lavage), and swelling of the nasal mucosa was determined by acoustic rhinometry before work start on Monday and the following Thursday. Bioaerosol exposure was determined by personal full shift exposure measurements on Monday, Tuesday, and Wednesday and analysed for total bacteria, fungal spores, endotoxin, and beta(1-->3)-glucans. RESULTS: The increased percentage of neutrophils from Monday (28%) to Thursday (46%) correlated with increases in ECP (r(S) = 0.71, p < 0.001) and MPO (r(S) = 0.38, p < 0.05), and showed a close to significant correlation with nasal swelling (r(S) = -0.55, p = 0.07). The Thursday levels of neutrophils, MPO, and IL-8 were associated with the exposure to fungal spores (range 0-2.0 x 10(6)/m(3)) and endotoxin (range 4-183 EU/m(3)) measured the day before, and the median exposure to beta(1-->3)-glucans (range 3-217 ng/m(3)), respectively (r(S) = 0.47-0.54, p < 0.01). Swelling of the nasal mucosa was associated with the fungal spore and beta(1-->3)-glucan exposure (r(S) = 0.58-0.59, p < 0.05). CONCLUSION: These results are based on a relatively small population, and conclusions must be drawn with care. The results suggested that a moderate exposure to fungal spores, endotoxins, and beta(1-->3)-glucans during waste handling induced upper airway inflammation dominated by neutrophil infiltration and swelling of the nasal mucosa.

Adolescent↗

Airway inflammation in waste handlers exposed to bioaerosols assessed by induced sputum.

Work-associated lower airway inflammation in waste collectors was examined by induced sputum and correlated with the bioaerosol exposure. Organic waste collectors (n=25) underwent induced sputum collection and spirometry before work on Monday and the following Thursday. Total cells, cell differentials, interleukin (IL)-8 and eosinophilic cationic protein were determined. Personal full-shift exposure measurements were performed Monday, Tuesday and Wednesday and analysed for total bacteria, fungal spores, endotoxins and beta(1-3)-glucans. The percentage of neutrophils (46-58%) and the IL-8 concentration (1.1-1.4 ng x mL(-1)) increased from Monday to Thursday. Forced expiratory volume in one second (FEV1) was significantly reduced on Thursday, and the decrease in FEV1/forced vital capacity correlated with the increase in the percentage of neutrophils. The median exposure to endotoxin (range 7-180 EU x m(-3)) and beta(1-3)-glucan (range 5-220 ng x m(-3)) was correlated with the increase in IL-8. Bioaerosol exposure during waste collection induced an inflammatory response in the lower airways, characterised by neutrophils and interleukin-8 secretion, that influenced the lung function. The inflammatory response was related to microbial components in the bioaerosol and was more pronounced for endotoxin than beta(1-3)-glucan exposure. No associations were found for mould spores or bacteria.

Aerosols↗

Mould exposure at home relates to inflammatory markers in blood.

Living in damp buildings has been associated with airway symptoms, suspected to be due to inflammatory reactions. The relationship between home exposure to mould and signs of inflammation was, therefore, studied. Nonsmoking subjects with a high (G-high, > 4.0 ng x m(-3), n = 17) or low (G-low, < 2.0 ng x m(-3), n = 18) amount of airborne beta(1 --> 3)-D-glucan, an indicator of mould biomass, in the home were recruited. Blood samples were analysed for granulocytic enzymes, T-cell subsets and the secretion of cytokines from in vitro incubated peripheral blood mononuclear cells (PBMCs). In the G-high group, the proportion of cytotoxic T-cells (CD8+S6F1+) was lower and secretion of tumour necrosis factor-alpha from PBMCs higher than in the G-low group. There were no significant differences in secretion of interferon gamma and interleukin (IL)-4 from PBMCs between the two groups. Among nonatopic subjects, the ratio between interferon gamma and IL-4 was significantly higher in the G-high group than in the G-low group and was related to the amount of beta(1 --> 3)-D-glucan in the home. No significant differences were found regarding secretion of IL-10 or IL-Ibeta from PBMCs, eosinophil cationic protein or myeloperoxidase in serum, or differential cell counts in blood. The effects found on inflammatory markers in relation to beta(1 --> 3)-D-glucan in the home suggest upregulation of some parts of the inflammatory/immunological system due to mould exposure.

Adult↗

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.

Central Nervous System Diseases↗

Health effects among employees in sewage treatment plants: A literature survey.

BACKGROUND: Over the years, there have been regular reports in the media of work-related symptoms among employees at sewage treatment plants. Concern has spread among employees over the lack of knowledge of risk agents' symptoms, and diseases in that environment. This paper reviews the investigations of health risks in employees working in the sewage treatment plants. METHODS: A literature search was performed with the search terms; sewage, waste water, health effects, infection, and health hazards. Articles on health effects in relation to sewage were selected. RESULTS: Work in sewage water plants can involve exposure to different types of microorganisms and chemicals. The bacterial exposure is dominated by bacteria that naturally occur in nature. However, different bacteria and viruses that give rise to infections can be present in this environment and thus there exists a risk of infection, especially of hepatitis A. Investigations suggest that gastrointestinal tract symptoms are more common among employees at sewage treatment plants than among controls. Respiratory symptoms, fatigue, and headache have also been reported in several investigations. The cause of the symptoms is unknown, although certain data suggest that they are caused by inflammation. The results suggest that endotoxin in Gram-negative bacteria may be one of the causative agents. As regards cancer, some studies report an increased risk of stomach cancer and a few studies report an increased risk of cancer in the larynx, liver or, prostate or of leukemia. The spread of the cancers over a multitude of organs does not support a hypothesis of causality with agents commonly found in sewage treatment plants. CONCLUSIONS: Further investigations are needed to determine the work-related effects and ascertain the causal agents.

Cause of Death↗

The inflammatory response in humans after inhalation of bacterial endotoxin: a review.

There is increasing evidence that diseases caused by organic dusts are mainly of an inflammatory nature. Among the many agents present in organic dusts, bacterial endotoxin is a major candidate for the inflammatory reaction. The purpose of this paper was to review the inflammatory response in humans after inhalation of bacterial endotoxin (lipopolysaccharide, LPS) in order to improve the understanding of symptoms and reactions found among persons exposed to endotoxin-containing organic dusts. It has been reported that inhalation of LPS causes changes in forced expiratory volume in one second (FEV1), and forced vital capacity (FVC). At the alveolar level, inhalation of LPS can induce changes in the diffusion capacity. Activation and migration of neutrophils are major effects of acute LPS inhalation. Changes in mediators of inflammation, such as eosinophilic cationic protein (ECP), myeloperoxidase (MPO), interleukin-8 (IL-8), IL-1beta, tumor necrosis factor alpha (TNFalpha) and C-reactive protein (CRP) in the airways and/or blood, have also been found. Inhalation of 30-40 microg LPS seems to be a threshold level for inducing clinical symptoms and lung function changes in healthy subjects. The threshold dose for inducing changes in blood neutrophils may be less than 0.5 microg LPS. In conclusion, available data regarding the responses to LPS inhalation challenges demonstrate a local and a systemic inflammatory response at lower doses of LPS, while higher inhaled doses are required to elicit significant clinical and lung function responses. Future inhalation studies on LPS need to focus on relevant diagnostic tools for the inflammatory reaction among persons exposed to endotoxin-containing organic dusts and to evaluate whether the large variation between individuals in the response to organic dusts or endotoxin could be due to differences in the molecular mechanisms responsible for the toxicity of the agent.

Administration, Inhalation↗

Adult-onset asthma is associated with self-reported mold or environmental tobacco smoke exposures in the home.

BACKGROUND: In recent years, we have gained better knowledge about the influence of indoor environments on respiratory symptoms and asthma. The purpose of this study was to examine certain exposures in the home environment and the risk of adult-onset asthma. METHODS: A nested case-referent study of adult-onset asthma was performed in a random population sample (n = 15813), aged 20-50 years. Cases for the study included subjects reporting "physician-diagnosed" asthma (n= 174). The referents (n = 870) were randomly selected from the whole population sample. The case-referent sample was investigated with a comprehensive mailed questionnaire about exposures in the home environment, asthma, respiratory symptoms, smoking habits, and atopy. Odds ratios (OR) with 95% confidence intervals (CI) were calculated while controlling for age, sex, smoking, and atopy. RESULTS: Increased adjusted OR for asthma were associated with exposure to molds (OR 2.2, 95%, CI 1.4-3.5), environmental tobacco smoke (OR 2.4, 95%, CI 1.4-4.1), and the presence of a wood stove (OR 1.7, 95% CI 1.2-2.5). CONCLUSIONS: This population-based case-referent study indicates that self-reported domestic exposures to molds or environmental tobacco smoke can be associated with adult-onset asthma.

Adult↗

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.

Administration, Inhalation↗

Effects after inhalation of (1-->3)-beta-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.

Adjuvants, Immunologic↗

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.

Air Pollutants, Occupational↗

Consultant appraisals. With due respect.

Consensus is needed on which management competencies should be included in doctors' appraisals. One trust employed management consultants to find out the views of senior doctors, managers, directors and patients. Common themes included concern for standards, effective use of information, openness, integrity and insight. The results will be used to guide future recruitment.

Clinical Competence↗

Airways inflammation among workers in a paper industry.

Exposure to organic dusts may cause airways inflammation in a large proportion of exposed persons. Most studies have relied on questionnaires and spirometry for diagnosis. To assess the possibility of determining the presence of inflammation using clinical diagnostic procedures, a study was undertaken among workers in a paper industry. Participants were 83 workers and 44 controls. Airborne endotoxin and (1-->3)-beta-D-glucan levels at the worksites were determined. The effects of this exposure were evaluated using a questionnaire, spirometry and measurements of airway responsiveness (methacholine) and levels of eosinophil cationic protein (ECP), myeloperoxidase (MPO), and C-reactive protein (CRP) in serum. The workers had a decreased baseline forced expiratory volume in one second (FEV1) and an increased airway responsiveness compared with controls. The concentrations of ECP and MPO were elevated compared with controls. There was a relation between exposure to endotoxin and (1-->3)-beta-D-glucan and airway responsiveness as well as ECP levels, when controlling for age, sex, smoking habits, atopy and asthma. The results suggest an increased prevalence of subjective respiratory symptoms, and an increased airway responsiveness among exposed workers. There was also a relationship between the serum concentration of eosinophil cationic protein and airway responsiveness. Taken together, the results suggest the presence of airways inflammation in the workers.

Adult↗

The incidence of systemic side-effects following subconjunctival Mydricaine no. 1 injection.

PURPOSE: To investigate the cardiovascular response to the subconjunctival injection of 0.25 ml of Mydricaine No. 1 during vitrectomy surgery. METHODS: Pulse and blood pressure were recorded at 5 min intervals before and following the subconjunctival injection of Mydricaine No. 1 in a group of 49 sequential patients undergoing vitrectomy surgery under general anaesthetic during a 6 month period. These responses were compared with a sequential and similar group of 35 patients during the following 6 months. RESULTS: Ten patients in the group administered Mydricaine, but no patients in the control group, developed a sinus tachycardia of > 100 beats/min for more than 10 min which was attributable to the mydriatic regime used. The occurrence of this response was not predictable based on the patients' age, weight or the presence of conjunctival erythema. The magnitude and temporal course of the tachycardia observed were variable. Blood pressure recordings showed no clinically significant changes during the tachycardias. CONCLUSION: Twenty per cent of patients administered 0.25 ml of Mydricaine No. 1 subconjunctivally develop a significant sinus tachycardia following injection. This response is unpredictable and all patients given Mydricaine should be monitored carefully after injection.

Adolescent↗

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.

Adult↗

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 micrograms 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.

Administration, Inhalation↗

Airways inflammation and glucan in a rowhouse area.

A study was undertaken in a number of rowhouses, some of which had had previous problems related to dampness and water leakage. The aim of the study was to assess the relation between exposure to airborne (1--> 3)-beta-D-glucan, a cell-wall substance in molds, and airways inflammation. The study involved 75 houses with indoor (1--> 3)-beta-D-glucan levels ranging from 0 to 19 ng/m3. Of 170 invited tenants, 129 (76%) participated in the study. A questionnaire relating to symptoms was used, and measurements were made of lung function and airway responsiveness. Myeloperoxidase (MPO), eosinophilic cationic protein (ECP), and C-reactive protein (CRP) were measured in serum. Atopy was determined with the Phadiatop test. The major findings were a relation between exposure to (1--> 3)- beta-D-glucan and an increased prevalence of atopy, a slightly increased amount of MPO, and a decrease in FEV1 over the number of years lived in the house. The results suggests the hypothesis that exposure to (1--> 3)-beta-D-glucan or molds indoors could be associated with signs of a non-specific inflammation.

Adolescent↗

Quantitative assessment of clinical disease status in primary Sjögren's syndrome. A cross-sectional study using a new classification model.

Quantitative and qualitative assessment of the clinical disease manifestations in 41 primary Sjögren's syndrome (pSS) patients was performed according to a new classification model. Frequencies of subgrouped disease manifestations were as follows: 1) surface exocrine disease: 100%, 2) internal organ exocrine disease: 63%, 3) monoclonal B lymphocyte disease: 5%, 4) inflammatory vascular disease: 71%, 5) non-inflammatory vascular disease: 59%, 6) mediator induced disease: 98%. Summary scores for severity of surface exocrine disease correlated to the summary scores of all other disease manifestations (p = 0.02), to the summary scores of internal organ exocrine disease (p = 0.003), and to the summary scores of mediator induced disease (p = 0.03). Blood leucocyte counts showed significant negative correlations to levels of plasma IgG, serum IgA-RF, IgM-RF, anti-SSA/SSB antibodies, IL-6, and IL-1Ra. We conclude that the model made detailed analysis of the clinical presentation of pSS possible, and thus may assist in elucidating important pathobiological aspect of the disease.

Adult↗

SSCP detection of N-ras promoter mutations in AML patients.

Activation of the N-ras gene via coding region mutations has been previously documented in 25% of patients with acute myeloid leukemia (AML). Since overexpression of normal N-ras is also transforming in vitro, the N-ras promoter of AML patients was analyzed for the presence of promoter mutations that may affect expression of the N-ras gene. Single-stranded conformational polymorphism (SSCP) was used to analyze samples from 26 AML patients and 13 normal subjects. A novel polymorphism at position 390 within the N-ras promoter was observed in both AML patients and normal samples at an overall frequency of 26%. In addition, two of 26 patients had single-base substitutions within protein binding sites that altered the binding of transcription factors to the promoter. One patient had a T-->A mutation at position 520 within an AP-1 binding site; the other had an A-->G mutation at position 409 within a protein binding region adjacent to a Myb binding site. The data suggest that in addition to coding region mutations in the N-ras gene, mutations in the promoter region that could alter regulation of N-ras expression provide an alternative mechanism of involvement of N-ras in AML.

Base Sequence↗