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Biomedical subjects

T Sandström

Publications and source records attributed to T Sandström.

At least 55 records · Page 3Linked to original sources
PubMed1999

Efficiency of automotive cabin air filters to reduce acute health effects of diesel exhaust in human subjects.

OBJECTIVES: To evaluate the efficiency of different automotive cabin air filters to prevent penetration of components of diesel exhaust and thereby reduce biomedical effects in human subjects. Filtered air and unfiltered diluted diesel exhaust (DDE) were used as negative and positive controls, respectively, and were compared with exposure to DDE filtered with four different filter systems. METHODS: 32 Healthy non-smoking subjects (age 21-53) participated in the study. Each subject was exposed six times for 1 hour in a specially designed exposure chamber: once to air, once to unfiltered DDE, and once to DDE filtered with the four different cabin air filters. Particle concentrations during exposure to unfiltered DDE were kept at 300 micrograms/m3. Two of the filters were particle filters. The other two were particle filters combined with active charcoal filters that might reduce certain gaseous components. Subjective symptoms were recorded and nasal airway lavage (NAL), acoustic rhinometry, and lung function measurements were performed. RESULTS: The two particle filters decreased the concentrations of diesel exhaust particles by about half, but did not reduce the intensity of symptoms induced by exhaust. The combination of active charcoal filters and a particle filter significantly reduced the symptoms and discomfort caused by the diesel exhaust. The most noticable differences in efficacy between the filters were found in the reduction of detection of an unpleasant smell from the diesel exhaust. In this respect even the two charcoal filter combinations differed significantly. The efficacy to reduce symptoms may depend on the abilities of the filters investigated to reduce certain hydrocarbons. No acute effects on NAL, rhinometry, and lung function variables were found. CONCLUSIONS: This study has shown that the use of active charcoal filters, and a particle filter, clearly reduced the intensity of symptoms induced by diesel exhaust. Complementary studies on vehicle cabin air filters may result in further diminishing the biomedical effects of diesel exhaust in subjects exposed in traffic and workplaces.

Acute Disease↗
PubMed1999

Bronchoalveolar inflammation after exposure to diesel exhaust: comparison between unfiltered and particle trap filtered exhaust.

OBJECTIVES: Air pollution particulates have been identified as having adverse effects on respiratory health. The present study was undertaken to further clarify the effects of diesel exhaust on bronchoalveolar cells and soluble components in normal healthy subjects. The study was also designed to evaluate whether a ceramic particle trap at the end of the tail pipe, from an idling engine, would reduce indices of airway inflammation. METHODS: The study comprised three exposures in all 10 healthy never smoking subjects; air, diluted diesel exhaust, and diluted diesel exhaust filtered with a ceramic particle trap. The exposures were given for 1 hour in randomised order about 3 weeks apart. The diesel exhaust exposure apperatus has previously been carefully developed and evaluated. Bronchoalveolar lavage was performed 24 hours after exposures and the lavage fluids from the bronchial and bronchoalveolar region were analysed for cells and soluble components. RESULTS: The particle trap reduced the mean steady state number of particles by 50%, but the concentrations of the other measured compounds were almost unchanged. It was found that diesel exhaust caused an increase in neutrophils in airway lavage, together with an adverse influence on the phagocytosis by alveolar macrophages in vitro. Furthermore, the diesel exhaust was found to be able to induce a migration of alveolar macrophages into the airspaces, together with reduction in CD3+CD25+ cells. (CD = cluster of differentiation) The use of the specific ceramic particle trap at the end of the tail pipe was not sufficient to completely abolish these effects when interacting with the exhaust from an idling vehicle. CONCLUSIONS: The current study showed that exposure to diesel exhaust may induce neutrophil and alveolar macrophage recruitment into the airways and suppress alveolar macrophage function. The particle trap did not cause significant reduction of effects induced by diesel exhaust compared with unfiltered diesel exhaust. Further studies are warranted to evaluate more efficient treatment devices to reduce adverse reactions to diesel exhaust in the airways.

Adult↗
PubMed1999

The effects of regular inhaled formoterol, budesonide, and placebo on mucosal inflammation and clinical indices in mild asthma.

The present study was designed to observe the effects of 8 wk of treatment with formoterol (Foradil) 24 microgram, budesonide 400 microgram, and matched placebo inhaled twice a day on inflammatory indices in the bronchial mucosa of 64 patients with mild atopic asthma. Biopsies were obtained at the start and 1 wk before stopping a 9-wk period of treatment, and inflammatory cell numbers were assessed in the submucosa and epithelium by immunohistochemistry. Regular formoterol significantly reduced the number of submucosal mast cells, with a similar trend for eosinophils but not activated T cells. A subgroup analysis conducted in biopsies with >= 10 eosinophils per mm2 revealed a significant reduction in eosinophil numbers when compared with both pretreatment baseline (p < 0.01) and changes after placebo (p < 0.01). Parallel, but less pronounced, effects were observed on mast cell but not on CD25(+) T cell numbers. There was no effect of any of the three treatments on BAL levels of mast cell or eosinophil mediators. We conclude that regular treatment with inhaled formoterol reduces rather than increases inflammatory cells in the mucosa of asthmatic patients. It is possible that these cellular effects of formoterol may contribute to the therapeutic efficacy of this drug when used regularly in the treatment

Administration, Inhalation↗
PubMed1999

Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide.

Nitrogen dioxide (NO2) is a common indoor and outdoor air pollutant that may induce deterioration of respiratory health. In this study the effects of repeated daily exposure to NO2 on airway antioxidant status, inflammatory cell and mediator responses, and lung function were examined. Healthy nonsmoking subjects were exposed under controlled conditions to air (once) and to 2 ppm of NO2 for 4 h on four consecutive days. Lung function measurements were made before and immediately after the end of each exposure. Bronchoscopy with endobronchial biopsies, bronchial wash (BW), and bronchoalveolar lavage (BAL) was carried out 1.5 h after the air exposure and after the last exposure to NO2. Repeated NO2 exposure resulted in a decrease in neutrophil numbers in the bronchial epithelium. The BW revealed a twofold increase in content of neutrophils (p < 0.05) and a 1.5-fold increase in myeloperoxidase (MPO) (p < 0.01) indicative of both migration and activation of neutrophils in the airways. After the fourth NO2 exposure, antioxidant status of the airway fluid was unchanged. Significant decrements in FEV1 and FVC were found after the first exposure to NO2, but these attenuated with repeated exposures. Together, these data indicate that four sequential exposures to NO2 result in a persistent neutrophilic inflammation in the airways, whereas changes in pulmonary function and airway antioxidants are resolved. We conclude that NO2 is a proinflammatory air pollutant under conditions of repeated exposure.

Adult↗
PubMed1999

Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers.

Several epidemiologic studies have demonstrated a consistent association between levels of particulate matter (PM) in the ambient air with increases in cardiovascular and respiratory mortality and morbidity. Diesel exhaust (DE), in addition to generating other pollutants, is a major contributor to PM pollution in most places in the world. Although the epidemiologic evidence is strong, there are as yet no established biological mechanisms to explain the toxicity of PM in humans. To determine the impact of DE on human airways, we exposed 15 healthy human volunteers to air and diluted DE under controlled conditions for 1 h with intermittent exercise. Lung functions were measured before and after each exposure. Blood sampling and bronchoscopy were performed 6 h after each exposure to obtain airway lavages and endobronchial biopsies. While standard lung function measures did not change following DE exposure, there was a significant increase in neutrophils and B lymphocytes in airway lavage, along with increases in histamine and fibronectin. The bronchial biopsies obtained 6 h after DE exposure showed a significant increase in neutrophils, mast cells, CD4+ and CD8+ T lymphocytes along with upregulation of the endothelial adhesion molecules ICAM-1 and VCAM-1, with increases in the numbers of LFA-1+ cells in the bronchial tissue. Significant increases in neutrophils and platelets were observed in peripheral blood following DE exposure. This study demonstrates that at high ambient concentrations, acute short-term DE exposure produces a well-defined and marked systemic and pulmonary inflammatory response in healthy human volunteers, which is underestimated by standard lung function measurements.

Adult↗
PubMed1999

Interleukin-5 production by human airway epithelial cells.

Interleukin (IL)-5 is a pleiotropic cytokine that exhibits biologic activity on cells of diverse hemopoieitic lineages. IL-5 enhances mediator release from human basophils and plays a pivotal role in the chemoattraction, proliferation, differentiation, survival, and activation of eosinophils. Th2- and Tc2-like T cells, mast cells, basophils, and eosinophils are the known cellular sources of this cytokine. Using a sensitive and novel reverse transcription-polymerase chain reaction enzyme-linked immunosorbent assay system, we found that IL-5 messenger RNA (mRNA) was constitutively expressed in bronchial biopsies obtained from healthy individuals, and that the levels of IL-5 mRNA expression decreased 1. 5 h after exposure to 0.12 ppm ozone for 2 h. Because the oxidative effects of ozone are confined to the epithelial cell surface and it is known that ozone induces epithelial damage and shedding, we hypothesized that epithelial cells might be a source of IL-5 mRNA. We demonstrate here that both transformed human bronchial epithelial cell lines (A549 and 16HBE14o-) and primary human bronchial and nasal epithelial cells grown in culture constitutively express IL-5 mRNA, which is upregulated on stimulation with tumor necrosis factor (TNF)-alpha. Culture supernatants derived from A549 cells exposed to TNF-alpha and interferon-gamma demonstrated detectable levels of IL-5 protein, and immunostaining of bronchial biopsies obtained from healthy human airways revealed the presence of IL-5 protein localized to the bronchial epithelium. To our knowledge, this is the first report demonstrating IL-5 production by human airway epithelial cells. This observation provides further evidence for the role of airway epithelium in regulating airway immune responses, in particular enhancing chemotaxis, activation, and survival of eosinophils, which could play an important role in the pathogenesis of bronchial asthma.

Adult↗
PubMed1999

Ozone-induced lung function decrements do not correlate with early airway inflammatory or antioxidant responses.

This study sought to clarify the early events occurring within the airways of healthy human subjects performing moderate intermittent exercise following ozone challenge. Thirteen healthy nonsmoking subjects were exposed in a single blinded, crossover control fashion to 0.2 parts per million (ppm) O3 and filtered air for 2 h, using a standard intermittent exercise and rest protocol. Lung function was assessed pre- and immediately post-exposure. Bronchoscopy was performed with endobronchial mucosal biopsies, bronchial wash (BW) and bronchoalveolar lavage (BAL) 1.5 h after the end of the exposure period. Respiratory tract lining fluid (RTLF) redox status was assessed by measuring a range of antioxidants and oxidative damage markers in BW and BAL fluid samples. There was a significant upregulation after O3 exposure in the expression of vascular endothelial P-selectin (p<0.005) and intercellular adhesion molecule-1 (p<0.005). This was associated with a 2-fold increase in submucosal mast cells (p<0.005) in biopsy samples, without evidence of neutrophilic inflammation, and a decrease in BAL fluid macrophage numbers (1.6-fold, p<0.005), with an activation of the remaining macrophage subset (2.5-fold increase in % human leukocyte antigen (HLA)-DR+ cells, p<0.005). In addition, exposure led to a 4.5-fold and 3.1-fold increase of reduced glutathione (GSH) concentrations, in BW and BAL fluid respectively (p<0.05), with alterations in urate and alpha-tocopherol plasma/RTLF partitioning ratios (p<0.05). Spirometry showed reductions in forced vital capacity (p<0.05) and forced expiratory volume in one second (p<0.01), with evidence of small airway narrowing using forced expiratory flow values (p<0.005). Evidence was found of O3-induced early adhesion molecule upregulation, increased submucosal mast cell numbers and alterations to the respiratory tract lining fluid redox status. No clear relationship was demonstrable between changes in these early markers and the lung function decrements observed. The results therefore indicate that the initial lung function decrements are not predictive of, or causally related to the O3-induced inflammatory events in normal human subjects.

Adult↗
PubMed1999

Antioxidant consumption and repletion kinetics in nasal lavage fluid following exposure of healthy human volunteers to ozone.

To obtain information on the real-time events occurring within human respiratory tract lining fluids (RTLFs) during ozone exposure, sequential nasal lavage was performed on 13 human volunteers exposed on separate occasions to 0.2 parts per million O3 and filtered air (2-h exposures, with intermittent exercise). Nasal lavage was performed and blood samples obtained at four time points throughout each exposure: pre-exposure (Pre-E), 1 h into exposure (1h-E), immediately post-exposure (0h-PE) and 1 h post-exposure (1h-PE). Endobronchial mucosal biopsies were obtained at 1.5 h-post exposure (1.5h-PE). Nasal RTLF neutrophilia was not apparent during, or 1.5 h after, 03 exposure. Furthermore, activation of the pre-existing neutrophil population did not occur. Airway permeability was not altered by this 03 exposure regimen. Sequential lavage resulted in significant washout of RTLF ascorbic acid, reduced glutathione, extracellular superoxide dismutase and myeloperoxidase at 1h-E, 0h-PE and 1.5h-PE relative to baseline Pre-E values. In contrast, RTLF uric acid (UA), total protein and albumin concentrations did not display washout kinetics. Of the antioxidants examined, only UA was clearly depleted by 03, concentrations, falling by 6.22 micromol x L(-1) at 1h-E, compared with 1.61 micromol x L(-1) (p<0.01) during control air exposure. The establishment of a new pseudo-steady-state concentration of RTLF UA (70% of Pre-E values) during the second hour of O3 exposure was coincident with a small but significant increase in plasma UA concentration (19.27 (O3) versus 1.95 micromol x L(-1) (air), p<0.05). These data demonstrate that inhalation of 0.2 parts per million 03 results in the depletion of nasal respiratory tract lining fluid uric acid and that this regional loss of uric acid leads to a small increase in plasma uric acid concentration. Whilst the reaction of uric acid with inspired 03 may confer protection locally, the role of upper airway uric acid as a sink for inhaled O3 is not supported by these findings.

Adult↗
PubMed1998

Are symptoms of obstructive sleep apnoea syndrome related to bronchitic symptoms or lung function impairment? Report from the Obstructive Lung Disease in Northern Sweden Study.

To investigate whether the high prevalence of symptoms related to obstructive sleep apnoea syndrome (OSAS) in a bronchitic cohort is correlated with the bronchitic symptoms or lung function impairment we examined two cohorts with bronchitic symptoms (n = 357 and 82) and a reference group who had reported no respiratory symptoms in a previous survey in 1986 (n = 140). The study was a part of the Obstructive Lung Disease in Northern Sweden Study and included clinical examination and lung function tests. Although lung function measured as FEV1 percentage predicted was correlated with bronchitic symptoms we found that bronchitic symptoms and body mass index but not lung function impairment were correlated with symptoms related to obstructive sleep apnoea. According to our findings it was the various bronchitic symptoms such as longstanding cough, wheezing, sputum production and chronic productive cough that were correlated with OSAS symptoms. This might be due to increased upper airway swelling or increased upper airway resistance, and lung function impairment does not seem to be responsible for the high prevalence of symptoms related to obstructive sleep apnoea in this bronchitic cohort.

Body Mass Index↗
PubMed1998

Effects of 0.2 ppm ozone on biomarkers of inflammation in bronchoalveolar lavage fluid and bronchial mucosa of healthy subjects.

Short-term exposure to ozone at peak ambient levels induces neutrophil influx and impairs lung function in healthy humans. In order to investigate the mechanisms contributing to neutrophil recruitment and to examine the role of T-cells in the acute inflammatory response, we exposed 12 healthy humans to 0.2 parts per million (ppm) of ozone and filtered air on two separate occasions for 2 h with intermittent periods of rest and exercise (minute ventilation = 30 L x min(-1)). Fibreoptic bronchoscopy was performed 6 h after the end of exposures. Total protein, tryptase, histamine, myeloperoxidase, interleukin (IL)-8 and growth-related oncogene-alpha (Gro-alpha) were measured and total and differential cell counts were performed in bronchoalveolar lavage (BAL) fluid. Flow cytometry was performed on BAL cells to study total T-cells, T-cell receptors (alphabeta and gammadelta), T-cell subsets (CD4+ and CD8+ cells) and activated T-cell subsets (CD25+). Using immunohistochemistry, neutrophils, mast cells, total T-cell numbers, T-cell subsets, CD25+ T-cells and leukocyte endothelial adhesion molecules including P-selectin, E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 were quantified in the bronchial biopsies. Paired samples were available from nine subjects. Following ozone exposure there was a threefold increase in the proportion of polymorphonuclear neutrophils (PMNs) (p=0.07) and epithelial cells (p=0.05) in BAL fluid. This was accompanied by increased concentrations of IL-8 (p=0.01), Gro-alpha (p=0.05) and total protein (p=0.058). A significant positive correlation was demonstrated between the two chemokines and proportion of PMNs in BAL fluid. After ozone exposure there was a significant decrease in the CD4/CD8 ratio (p=0.05) and the proportion of activated CD4+ (p=0.01) and CD8+ T-cells (p=0.04). However, no significant changes were demonstrable in any of the inflammatory markers studied in the biopsies. Short-term exposure of healthy humans to 0.2 ppm ozone induced a neutrophil influx in peripheral airways at 6 h post exposure, but no apparent inflammatory response in proximal airways. This response seems to be mediated at least in part by interleukin-8 and growth-related oncogene-alpha.

Adult↗
PubMed1998

Nasal cavity lining fluid ascorbic acid concentration increases in healthy human volunteers following short term exposure to diesel exhaust.

To determine if diesel exhaust (DE) exposure modifies the antioxidant defense network within the respiratory tract lining fluids, a randomized, single blinded, crossover control study using nasal lavage and flexible video bronchoscopy with bronchial and bronchoalveolar lavage was performed. Fifteen healthy, non-smoking, asymptomatic subjects were exposed to filtered air or diluted diesel exhaust (300mg m(-3) particulates, 1.6ppm nitrogen dioxide) for one hour on 2 separate occasions, at least three weeks apart. To examine the kinetics of any DE-induced antioxidant reactions, nasal lavage fluid and blood samples were collected prior to, immediately after, and 5 1/2 hours post exposure. Bronchoscopy was performed 6 hours after the end of DE exposure. Ascorbic acid, uric acid and reduced glutathione (GSH) concentrations were determined in nasal, bronchial, bronchoalveolar lavage and plasma samples. Malondialdehyde (MDA) and protein carbonyl concentrations were determined in plasma and bronchoalveolar lavage samples. Nasal lavage ascorbic acid concentration increased 10-fold during DE exposure [1.02 (0.26-2.09) Vs 7.13 (4.66-10.79) micromol/L(-1)], but returned to basal levels 5.5 hours post-exposure [0.75 (0.26-1.51) micromol/L(-1)]. There was no significant effect of DE exposure on nasal lavage uric acid or GSH concentration. DE exposure did not influence plasma, bronchial wash, or bronchoalveolar lavage antioxidant concentrations and no change in MDA or protein carbonyl concentrations were found. The physiological response to acute DE exposure is an increase in the level of ascorbic acid in the nasal cavity. This response appears to be sufficient to prevent further oxidant stress in the respiratory tract of normal individuals.

Adult↗
PubMed1997

Impaired pulmonary function in patients with hemorrhagic fever with renal syndrome.

Pulmonary and cardiac functions were investigated in 13 patients hospitalized with nephropathia epidemica, a European form of hemorrhagic fever with renal syndrome. As compared with reference values, the patients' diffusion capacity for carbon monoxide was decreased (P = .002) and pulmonary clearance of inhaled technetium-99m-labeled diethylenetriamine pentaacetic acid was increased (P = .002). In four of 11 patients, arterial blood gas analysis disclosed a reduction in partial pressure of O2 (< 10 kPa) and oxygen saturation (< 94%). In three of 13 patients, chest radiography revealed interstitial infiltrates or pleural effusions. Lung volumes and expiratory flow rates of the patients were not significantly changed. By electrocardiography and echocardiography, no significant cardiac dysfunction was demonstrable. The pulmonary dysfunction was best explained by an alveolocapillary lesion. The two hantavirus-caused clinical syndromes, hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, may be pathophysiologically more similar than appears from the clinical presentations.

Adult↗
PubMed1997

Incidence of asthma in adults--report from the Obstructive Lung Disease in Northern Sweden Study.

Incidence studies offer a better opportunity to study risk factors for asthma than do prevalence studies. However, regular prospective follow-ups of large cohorts are difficult to perform, and that is why direct measurement of the incidence rate of asthma is almost impossible. Thus, cross-sectional follow-up studies of defined cohorts can be used to provide data on incidence. In 1986, a postal questionnaire survey on respiratory symptoms and diseases was performed in the northernmost province of Sweden. The population sample comprised all subjects born in 1919-20, 1934-5, and 1949-50 in eight representative areas of the province, which comprises 25% of the total area of Sweden. Completed answers were given by 5698 subjects (86%) of the 6610 subjects invited to the study. In 1992, the cohort was invited to a follow-up survey during the same season as in 1986, and 6215 subjects were traced. Of the 5393 subjects who answered the questionnaire, 4932 had participated in the 1986 survey, or 87% of those who participated in 1986. For the period 1986-92, the cumulative incidences of asthma were 4.9 and 5.0%, respectively, as assessed by the questions, "Have you ever had asthma?" and "Have you been diagnosed as having asthma by a physician?" Thus, the results indicate a mean annual cumulative incidence of asthma of 0.8%. After correction of the results for subjects who were diagnosed as having asthma in the clinical part later in the 1986 study, the mean annual cumulative incidence of asthma was found to be 0.5%. Risk factors were family history of asthma (OR 3.46) and current and former smoking, while female sex was a strong trend.

Adult↗
PubMed1997

The inflammatory effects of 2 ppm NO2 on the airways of healthy subjects.

Nitrogen dioxide (NO2) is a free radical and a common oxidant in polluted air. Here we present data on the time course of inflammation after NO2 exposure, as reflected in bronchial biopsy and airway lavage specimens. Healthy, nonsmoking subjects were exposed to air or 2 ppm NO2 for 4 h in random order on separate occasions. Endobronchial biopsies, bronchial washing (BW), and bronchoalveolar lavage (BAL) were done at 1.5 h (n = 15) or 6 h (n = 15) after exposure. In BW, exposure to NO2 induced a 1.5-fold increase in interleukin-8 (IL-8) (p < 0.05) at 1.5 h and a 2.5-fold increase in neutrophils (p < 0.01) at 6 h. In BAL fluid (BALF), small increases were observed in CD45RO+ lymphocytes, B-cells, and natural killer (NK) cells only. Immunohistologic examination of bronchial biopsy specimens showed no signs of upregulation of adhesion molecules, and failed to reveal any significant changes in inflammatory cells at either time point after NO2 exposure. In summary, NO2 induced a neutrophilic inflammation in the airways that was detectable in BW at 6 h after NO2 exposure. The increase in neutrophils could be related to the enhanced IL-8 secretion observed at 1.5 h after exposure. The absence of adhesion-molecule upregulation or cellular inflammation in mucosal biopsy specimens indicates that the major site of inflammation following exposure to NO2 may be in the smaller airways and not in the alveoli.

Adult↗
PubMed1997

Differential inhibition of inflammatory cytokine release from cultured alveolar macrophages from smokers and non-smokers by NO2.

Human alveolar macrophages (AMs) obtained from smokers and non-smokers by bronchoalveolar lavage (BAL) were subjected to various concentrations of NO2 in an inverted monolayer exposure model. Culture supernatants were collected 4 h after the exposure and assayed for secreted TNF-alpha, IL-1 beta, IL-8 and MIP-1 alpha. The steady state levels of the mRNAs for these cytokines were also analysed in the cells. The adherence of BAL cells to plastic prior to exposure to the gas elevated the steady state mRNA levels of all four cytokines tested in smoker's cells and that of TNF-alpha and IL-1 beta, but not IL-8 (MIP-1 alpha not tested), in non-smoker's cells. Interestingly, adherent cells from non-smokers released circa 15-, 3-, 1.5- and 3-fold the amounts of IL-1 beta, IL-8, TNF-alpha and MIP-1 alpha, respectively, than smoker's cells during control incubation or exposure to air. A 20 min exposure to NO2 (5 or 20 p.p.m.) did not increase the secretion of any of the cytokines from either cell type. In contrast, NO2 caused a concentration-dependent inhibition of the secretion of all cytokines except IL-1 beta from smoker's cells. Additionally, NO2 greatly diminished the release of all cytokines in response to further treatment with lipopolysaccharide (LPS). In contrast, only the secretion of TNF-alpha from non-smoker's cells was inhibited by the gas in a concentration-dependent manner, whilst LPS-induced secretion of the cytokines was not affected by the gas. The steady state levels of the respective mRNAs for each of the cytokines were not significantly affected in smoker's cells by exposure to NO2, except for a negative, dose-dependent trend in the case of TNF-alpha. Nitrogen dioxide also failed to elevate the levels of the mRNAs in non-smoker's cells but, again, tended to diminish the levels, particularly of IL-1 beta mRNA. However, exposure to the gas inhibited LPS-induced accumulation of cytokine mRNAs in smoker's cells only. The data suggest that macrophage-derived cytokine mediators of the sepsis response may not play a role in the generation of NO2-induced inflammation in the human lung. Conversely, the gas seems to non-specifically inhibit the release and/or production of cytokines, particularly from smoker's cells, at the post-transcriptional level, and impairs the ability of the cells to increase the transcription and release of the cytokines in response to bacterial LPS. The fact that NO2 seriously impaired the already diminished capacity of smoker's cells to release several important pro-inflammatory cytokines, both under control conditions and in response to LPS, strongly suggest that the inhalation of NO2 in cigarette smoke may contribute to impairing host defence against infection in the lung.

Adult↗
PubMed1997

Terpene exposure and respiratory effects among workers in Swedish joinery shops.

OBJECTIVES: Exposure to monoterpenes (alpha-pinene, beta-pinene and delta 3-carene) in joinery shops was studied in Sweden during the processing of Scot's pine, and the acute respiratory effects among the employees were evaluated. METHODS: A cross-sectional study of 38 workers was carried out in 4 joinery shops. The investigation included personal air sampling of monoterpenes, biological monitoring of metabolites of alpha-pinene in the workers' urine, interviews following a standardized questionnaire, and dynamic spirometry. RESULTS: The personal exposure to monoterpenes in the joinery shops was 10-214 mg/m3. The correlation (correlation coefficient = 0.69) between exposure to alpha-pinene and verbenols (metabolites from alpha-pinene) in urine was relatively good. No acute effects on forced vital capacity or forced expiratory volume during 1 s were detected. The workers had significantly reduced preshift lung function values when compared with the values of a local reference group, even when smokers and ex-smokers were excluded. CONCLUSIONS: Personal exposure to the monoterpenes alpha-pinene, and delta 3-carene in joinery shops may exceed the present Swedish occupational exposure limit of 150 mg/m3 during the winter season when workroom air is commonly recirculated. The determination of metabolites of alpha-pinene (verbenols) in urine can be used as an index of exposure to fumes released during wood-treating processes. The results from the lung function tests indicate chronic rather than acute reactions in the airways. The fact that there were no major changes in lung function over a workshift indicates chronic reaction in the airways.

Adult↗
PubMed1996

Measurements of indoor and outdoor nitrogen dioxide concentrations using a diffusive sampler.

The Willems badge, a short-term diffusion sampler, was used to measure nitrogen dioxide concentrations inside and outside the homes of participants in the European study "PEACE' (Pollution Effects on Asthmatic Children in Europe). The main aim of the study was to determine levels of nitrogen dioxide concentrations both outside and inside children's homes, and to estimate the indoor/outdoor ratios for nitrogen dioxide in an urban area, in comparison with a less urbanized control area. We conducted measurements in 23 homes in Umeå, a city of about 100,000 inhabitants in the northern part of Sweden, in addition to 20 homes in a less urbanized control area situated about 20 km from Umeå. Measurements were made on two different occasions in each home during the period January-March, 1994. The houses were not equipped with any gas appliances. The mean outdoor 24-h concentration in Umeå was 28 micrograms m-3 and the mean indoor concentration was 11 micrograms m-3. The mean indoor: outdoor ratio was 0.44 (s = 0.23). The highest outdoor value, measured in the city centre of Umeå, was 54 micrograms m-3. In the control area the mean ambient 24-h concentration was 12 micrograms m-3, approximately half as high as in the urban area, and the mean indoor concentration was 6 micrograms m-3. The mean indoor: outdoor ratio was 0.67 (s = 0.55). The correlation coefficient between indoor and outdoor concentrations was higher in the control area, r = 0.79 (p < 0.001), in comparison with the urban area, r = 0.43 (p < 0.01). It is concluded that the outdoor as well as the indoor concentrations of nitrogen dioxide were approximately twice as high in Umeå as in the control area. This could be explained by heavier traffic density in Umeå. The mean 24-h concentration outside homes in Umeå was, however, below the 24-h national standard level of 75 micrograms m-3. The higher correlation between indoor and outdoor concentrations, combined with higher indoor: outdoor ratio, in the control area is interpreted as a sign of a lower level of penetration of outdoor air into the houses in the urban area. This was not explained by differences in types of buildings between the two areas, but possibly by differences in air-exchange rates and in habits of ventilating rooms with open windows.

Air Pollutants↗