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PubMed1982

Grain elevator workers show work-related pulmonary function changes and dose-effect relationships with dust exposure.

The purpose of this study was to determine whether grain handlers underwent work-related changes in their pulmonary function and, if so, to examine the dose-effect relationships with dust exposure. The pulmonary function of grain handlers was measured at the beginning and end of work shifts over a period of one week, during which their exposure to dust was measured daily. The results showed changes indicative of a within-day obstructive change, in addition to a small restrictive defect occurring over the course of a week. Civic outside labourers who were examined as a control group showed a similar within-week obstructive change without any associated restriction of lung volume. The data on the grain handlers were also used to examine the dose-effect relationships of dust exposure, both on baseline pulmonary function and on within-day changes in these measurements. The baseline flow rates of workers who did not wear a mask were found to vary inversely with their average exposure to respirable dust. In addition, the flow rates underwent a within-day decrease that varied directly with their corresponding exposure to respirable dust and was unrelated to mask wearing. The median of the slopes for this relationship indicated that 50% of the subjects had a decrease of at least 923 ml/s in the value of their Vmax50%VC for each 1 mg/m3 increase in the concentration of respirable dust. Non-respirable dust did not have a measurable effect either on the baseline or the within-day changes in pulmonary function. The acute changes were unaffected by age, duration of employment, or extent of smoking.

Adult↗
PubMed1984

Comparison of radiographic appearances with associated pathology and lung dust content in a group of coalworkers.

The pathology and dust content of lungs from 261 coalminers in relation to the appearances of their chest radiographs taken within four years of death were examined. Radiological opacities of coalworkers' pneumoconiosis were more profuse the more dust was retained in lungs. Among the men who had mined low rank coal--that is, with a relatively high proportion of ash--the increase in profusion was most closely related to the ash component of the dust, whereas in men who had mined high rank coal both coal and ash increased in the lungs in relation to radiological profusion. The fine p type of opacity was found to be associated with more dust and a higher proportion of coal and less ash than the nodular r opacity, and was also more likely to be associated with emphysema. The pathological basis of the different types of opacity found on the radiographs of coalminers related to the number, size, and nodularity of the dust lesions. Larger fibrotic lesions were likely to appear as r opacities, whereas fine reticular dust deposition was most likely to present as p opacities, q opacities showing a mixture of appearances. The study has shown that the composition of dust retained in the lung, as well as its amount, makes an important contribution to the radiographic appearances of pneumoconiosis. In particular, the r type of lesion on the radiograph of a low rank coalminer indicates the possibility of a silicotic like lesion.

Coal Mining↗
PubMed1985

Ventilatory responses of normal subjects to flax dust inhalation: the protective effect of autoclaving the flax.

A homogeneous batch of dew retted hackled flax was divided into two portions. One was untreated and the other was steamed for 45 minutes at 125 degrees C in three pressure/vacuum cycles in an autoclave. Dust was collected when the two flaxes were separately processed by industrial doubler and stapler machines. From untreated flax 7.2 g of dust was collected per kilogram of flax after two processing operations. From the steamed flax 4.4 g of flax was obtained per kilogram after four operations. A method was devised to disperse the dust in a room to produce dust levels similar to those encountered in a dusty mill (4.5-5.7 mg/m3). Twelve normal volunteers from the managerial staff of the linen industry of Northern Ireland inhaled the dust over six hour periods. With the untreated flax decreases were obtained in mean forced expiratory measurements of 7.6% in FEV1 and 4.5% in FVC (p less than 0.01). A double blind crossover comparison of similar levels of untreated and steamed flax dusts showed 30% less impairment of the forced expirations with steamed than with untreated flax (p less than 0.05). If these responses reflect the long term airway effects of flax dust then the steaming of flax may help in reducing byssinosis.

Adult↗
PubMed1989

Inflammatory responses in lungs of rats inhaling coalmine dust: enhanced proteolysis of fibronectin by bronchoalveolar leukocytes.

Chronic exposure to coalmine dust is associated with the accumulation of inflammatory leukocytes in the bronchoalveolar region of the lung and, in the long term, with fibrosis and emphysema of the lung parenchyma. Degradation of connective tissue by inflammatory leukocytes has been implicated in the parenchymal damage that precedes the development of fibrotic or emphysematous lesions in the lung. The ability of inflammatory leukocytes obtained by bronchoalveolar lavage from rats inhaling coalmine dust to degrade fibronectin in vitro was assessed. The animals were exposed to an airborne mass concentration of dust similar to the maximum permissible level in United Kingdom collieries. The bronchoalveolar lavage cell population showed changes with duration of dust exposure; there were increases in the total number of leukocytes and in the percentage of polymorphonuclear leukocytes, and the macrophage component of the lavage became increasingly activated, as assessed by the ability of these cells to spread on glass. In addition, degradation of a radiolabelled fibronectin matrix by the coalmine dust exposed bronchoalveolar leukocytes increased with duration of dust exposure. Thus exposure to airborne coalmine dust causes an influx of inflammatory leukocytes to the alveolar region. These cells have enhanced ability to degrade fibronectin and this may be important in subsequent disease development.

Animals↗
PubMed1990

Combined effect of silica dust and tobacco smoking on mortality from chronic obstructive lung disease in gold miners.

A sample of 2209 white South African gold miners aged 45-54 between 1968-71, who started mining exposure during 1936-43, was investigated from 1968-71 to 30 December 1986. The effect of silica dust and tobacco smoking on mortality from chronic obstructive lung disease (COLD) was assessed. The relative risk (RR) for dust exposure before 1950 was estimated as 2.5 (95% confidence interval (CI) 1.5-4.2), for 10 units of 1000 particle-years. The combined effect of dust exposure before 1950 and years of cigarette smoking on mortality from COLD was best estimated by the multiplicative model, indicating that the two exposures act synergistically. All those that died of the disease were smokers. According to the estimates of attributable risk about 5% of the deaths from COLD were from the effect of dust, 34% were from smoking, and 59% were from the combined effect of dust and smoking. In conclusion, the results indicate that workers exposed to silica dust who smoke are at higher risk of dying from COLD than smokers not exposed to silica dust, as the two exposures act synergistically in causing COLD.

Aged↗
PubMed1992

Assessment of the permissible exposure level to manganese in workers exposed to manganese dioxide dust.

The prevalence of neuropsychological and respiratory symptoms, lung ventilatory parameters, neurofunctional performances (visual reaction time, eye-hand coordination, hand steadiness, audioverbal short term memory), and several biological parameters (calcium, iron, luteinising hormone (LH), follicle stimulating hormone (FSH), and prolactin concentrations in serum, blood counts, manganese (Mn) concentration in blood and in urine) were examined in a group of workers (n = 92) exposed to MnO2 dust in a dry alkaline battery factory and a matched control group (n = 101). In the battery plant, the current exposure of the workers to airborne Mn was measured with personal samplers and amounted on average (geometric mean) to 215 and 948 micrograms Mn/m3 for respirable and total dust respectively. For each worker, the lifetime integrated exposure to respirable and total airborne Mn dust was also assessed. The geometric means of the Mn concentrations in blood (MnB) and in urine (MnU) were significantly higher in the Mn exposed group than in the control group (MnB 0.81 v 0.68 microgram/100 ml; MnU 0.84 v 0.09 microgram/g creatinine). On an individual basis, MnU and MnB were not related to various external exposure parameters (duration of exposure, current exposure, or lifetime integrated exposure to airborne Mn). On a group basis, a statistically significant association was found between MnU and current Mn concentrations in air. No appreciable difference between the exposed and the control workers was found with regard to the other biological measurements (calcium, LH, FSH, and prolactin in serum). Although the erythropoietic parameters and serum iron concentration were in the normal range for both groups, there was a statistically significant trend towards lower values in the Mn exposed workers. The prevalences of reported neuropsychological and respiratory symptoms, the lung function parameters, and the audioverbal short term memory scores did not differ between the control and exposed groups. The Mn workers, however, performed the other neurofunctional tests (visual reaction time, eye-hand coordination, hand steadiness) less satisfactorily than the control workers. For these tests, the prevalences of abnormal results were related to the lifetime integrated exposure to total and respirable Mn dust. On the basis of logistic regression analysis it may be inferred that an increased risk of peripheral tremor exists when the lifetime integrated exposure to Mn dust exceeds 3575 or 730 micrograms Mn/m3 x year for total and respirable dust respectively. The results clearly support a previous proposal by the authors to decrease the current time weighted average exposure to Mn dust.

Adolescent↗
PubMed1997

Does occupational exposure to brown coal dust cause a decline in lung function?

OBJECTIVES: To determine if the rate of change in forced expiratory volume in one second (FEV1) in subjects with high exposure to Latrobe Valley brown coal dust was significantly greater than the rate of change among subjects with low exposure. METHODS: A retrospective dynamic cohort design with variable time windows. This study was conducted over a period of 14 years from 1980 to 1994 and used data collected by the State Electricity Commission (SEC) Lung Function Unit for an asbestos surveillance programme. The subjects were exposed to low, medium, or high levels of coal dust. Basic spirometry with wedge bellows spirometers was used to assess lung function. A general linear model (GLM) was used to assess the effects of smoking and exposure to coal dust upon the change in forced expiratory volume in one second (FEV1) while adjusting for age and height. RESULTS: The mean (95% confidence interval (95% CI) rate of decline in FEV1 was 40 (36 to 44) ml/year. Age was a significant predictor of change. A significant effect was found for smoking (P = 0.02) and for exposure to coal dust (P = 0.008). The only significant difference with exposure to coal dust was between the high and mixed exposure categories. CONCLUSION: There is no convincing evidence of excessive decline in FEV1 with exposure to coal dust > 0.75 mg/m3. The absence of a dose response relation provides some evidence against a causal relation. On the basis of this study, reduction of the exposure standards currently applied to brown coal dust in the Victorian electricity industry is not warranted to prevent respiratory disease.

Age Factors↗
PubMed2001

Dust exposure and impairment of lung function at a small iron foundry in a rapidly developing country.

OBJECTIVES: A cross sectional prospective study was carried out among iron foundry workers (exposed) and soft drink bottling and supply company workers (unexposed) to assess their occupational exposure to ambient respiratory dust in their work environment and its effect on their lung function profile. PARTICIPANTS: Lung function was measured in 81 exposed and 113 unexposed workers. Personal respirable dust concentrations were measured for all the exposed and the unexposed workers. Information on respiratory signs and symptoms was also collected from the participants. RESULTS: Among the exposed workers, midexpiratory flow (FEF25-75), forced expiratory volume in 1 second (FEV1), peak expiratory flow (PEF), FEV1/FVC, and FEV1/VC ratios were significantly lower whereas the vital capacity (VC) and forced vital capacity (FVC) were non-significantly higher. Job at the iron foundry was a significant predictor of lung function. Exposure to high concentration of respirable dust at the iron foundry was also a significant predictor. Workers working in high exposure areas (general works, furnace, continuous casting areas, and fabrication workshop) had lower lung function values than workers in medium and low exposure areas. Smoking did not enhance the effects of exposure to dust on lung function. CONCLUSIONS: Exposure to respirable dust was higher among the iron foundry workers; and among these, general, furnace, rolling mill, and fabrication workers had higher exposures to dust than did workers in continuous casting, the mechanical workshop, and the bottling plant. Job type and exposure to dust were significant predictors of lung function. Implementation of industrial hygiene and proper and efficient use of personal protection equipment while at work could help to protect the respiratory health of industrial workers.

Case-Control Studies↗
PubMed2005

Inhalation of stable dust extract prevents allergen induced airway inflammation and hyperresponsiveness.

BACKGROUND: Recent epidemiological studies have shown that growing up on a traditional farm provides protection from the development of allergic disorders such as hay fever and allergic asthma. We present experimental evidence that substances providing protection from the development of allergic diseases can be extracted from dust collected in stables of animal farms. METHODS: Stable dust was collected from 30 randomly selected farms located in rural regions of the Alps (Austria, Germany and Switzerland). The dust was homogenised with glass beads and extracted with physiological sodium chloride solution. This extract was used to modulate immune response in a well established mouse model of allergic asthma. RESULTS: Treatment of mice by inhalation of stable dust extract during sensitisation to ovalbumin inhibited the development of airway hyperresponsiveness and airway eosinophilia upon challenge, as well as the production of interleukin 5 by splenocytes and of antigen specific IgG(1) and IgE. Dust extract also suppressed the generation of human dendritic cells in vitro. The biological activity of the dust extract was not exclusively mediated by lipopolysaccharide. CONCLUSIONS: Stable dust from animal farms contains strong immune modulating substances. These substances can interfere with the development of both cellular and humoral immunity against allergens, thus suppressing allergen sensitisation, airway inflammation, and airway hyperresponsiveness in a murine model of allergic asthma.

Allergens↗
PubMed1997

Lung cancer in relation to exposure to silica dust, silicosis and uranium production in South African gold miners.

BACKGROUND: A nested case-control study for lung cancer was performed on a cohort of 2260 South African gold miners in whom an association between exposure to silica dust and risk of lung cancer was previously reported. The objective was to investigate an expanded set of risk factors and also cancer cell type. METHODS: The 78 cases of lung cancer found during the follow up period from 1970 to 1986 were matched with 386 controls. Risk of lung cancer was related to smoking, exposure to silica dust, incidence of silicosis, and uranium production and the uranium content of the mine ore. RESULTS: The risk of lung cancer was associated with tobacco smoking, cumulative dust exposure, duration of underground mining, and with silicosis. The best predictive model included pack years of cigarette consumption (adjusted relative risk (RR) = 1.0 for < 6.5 pack years, 3.5 (95% confidence interval (CI) 0.7 to 16.8) for 6.5-20 pack years, 5.7 (95% CI 1.3 to 25.8) for 21-30 pack years, and 13.2 (95% CI 3.1 to 56.2) for more than 30 pack years) and silicosis (RR = 2.45 (95% CI 1.2 to 5.2)). No association was found with uranium production. The lung tumour cell type distribution was 40.3% small cell carcinoma, 38.8% squamous cell, 16.4% adenocarcinoma, and 4.5% large cell carcinoma. Small and large cell cancer combined were associated with exposure to dust. CONCLUSIONS: The results cannot be interpreted definitively in terms of causal association. Possible interpretations are: (1) subjects with high dust exposure who develop silicosis are at increased risk of lung cancer; (2) high levels of exposure to silica dust on its own is important in the pathogenesis of lung cancer and silicosis is coincidental; and (3) high levels of silica dust exposure may be a surrogate for the exposure to radon daughters.

Adenocarcinoma↗
PubMed2005

Clinical and pathological responses of weaned pigs to atmospheric ammonia and dust.

Nine hundred and sixty weaned pigs were exposed for five weeks to controlled concentrations of atmospheric ammonia and dust in a single, multifactorial experiment. The treatments were a mean dust concentration of either 1.2, 2.7, 5.1 or 9.9 mg/m3 (inhalable fraction) and a mean ammonia concentration of either 0.6, 10.0, 18.8 or 37.0 ppm, concentrations representative of commercial conditions. The experiment was carried out over two years and the pigs were used in eight batches, each consisting of five lots of 24 pigs. Each treatment combination was replicated once, and an additional control lot (nominally 0 mg/m3 dust and 0 ppm ammonia) was included in each batch. The dust concentration was the same in the other four lots in each batch in which the four concentrations of ammonia were used; thus, the split-plot design was more sensitive to the effects of ammonia than dust. The groups of pigs were kept separately in five rooms in a purpose-built facility, and the pollutants were injected continuously into the air supply. Ammonia was supplied from a pressurised cylinder, and the endogenous dust in each room was supplemented by an artificial dust manufactured from feed, barley straw and faeces, mixed by weight in the proportions 5:1:4; its ingredients were oven-dried, milled and mixed, and then resuspended in the air supply. The health of the pigs was assessed in terms of general pathology, respiratory tract pathology, and the microbiology of the nasal cavity, trachea and lung. In each batch, postmortem examinations were carried out on 40 pigs after five weeks' exposure to the pollutants and on 30 pigs two weeks later to test for carryover and recovery--a total of 560 pigs. These examinations revealed minimal gross pathology and widespread minor pathological changes of little significance. The pigs' turbinate and lung scores were low and unaffected by exposure to pollutants. All the putative bacterial pathogens, with the exception of toxigenic Pasteurella multocida type D, were isolated from the respiratory tract of the pigs of both ages, but there were no differences between the effects of the different concentrations of pollutants.

Air Pollutants↗
PubMed1994

Extracellular matrix synthesis by coal dust-exposed type II epithelial cells.

Although integrity of the alveolar basement membrane may influence progression of lung injury induced by inhaled particulates, little is known about direct effects of coal dusts on the alveolar epithelium or its extracellular matrix (ECM). Effects of dust on synthesis of cell and ECM proteins by type II cells (T2P) was thus investigated. Three coal dusts (anthracite no. 867; bituminous no. 1451 and no. 1361) and mine dust MIT-3, of respirable size, were studied as a function of dose and time over 3 days of primary T2P culture. On day 1, 750 micrograms/ml of 867 were required to increase relative synthesis of ECM proteins (ECM/cell). MIT-3, 1451, and 1361 were without effect. By day 3, 867 or MIT-3 increased ECM/cell 60-100% at 300 micrograms/ml; 1451 produced modest, dose-dependent stimulation, whereas 1361 remained without effect. None of the dusts caused significant cytotoxicity. The results show dose- and time-dependent effects of well-characterized coal and mind dusts to modify partitioning of newly synthesized proteins into the ECM and suggest that coal dust exposure may modulate structure or function of the subepithelial basement membrane.

Animals↗
PubMed1994

Grain dust-induced airflow obstruction and inflammation of the lower respiratory tract.

To investigate the relationship between the physiologic and biologic effects of grain dust inhalation, we exposed 15 nonsmoking, nonasthmatic, nonatopic male grain handlers to buffered saline and aqueous corn dust extract by inhalation challenge in a crossover study. The inhalation challenges to buffered saline and corn dust extract were separated by at least 14 d. Compared with buffered saline, inhalation of corn dust extract resulted in significant airflow obstruction, which was observed within 30 min of exposure and persisted for 5 h. Inhalation of corn dust extract resulted in an acute inflammatory response characterized by higher concentrations of neutrophils (p = 0.001), IL-1 beta (p = 0.001), IL-1RA (p = 0.001), IL-6 (p = 0.001), IL-8 (p = 0.001), and TNF-alpha (p = 0.04) in bronchoalveolar lavage (BAL) fluid. mRNA levels specific for IL-1 beta, IL-1RA, IL-6, and IL-8 from cells present in the BAL fluid were significantly greater after challenge with corn dust extract than after challenge with buffered saline. Importantly, no significant differences were observed in the concentration of lymphocytes or eosinophils in the BAL fluid following inhalation of corn dust extract, and the concentrations of histamine and 15-HETE were similar in BAL fluid after the two challenges. The maximal percentage decrease in FEV1 was significantly associated with the absolute neutrophil concentration in the BAL fluid (p = 0.001), as well as the concentration of TNF-alpha (p = 0.03), IL-1 beta (p = 0.005), IL-1RA (p = 0.001), IL-6 (p = 0.001), and IL-8 (p = 0.001) in the BAL fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Cotton dust produces an increase in intraepithelial mucosubstances in rat airways.

Occupational exposure to endotoxin-contaminated organic dusts is associated with a variety of adverse pulmonary effects, including chronic bronchitis and sputum production. We have previously demonstrated in F344 rats that inhaled endotoxin rapidly induces an increase in the volume of stored intraepithelial mucosubstances (Vs) in the respiratory tract. The present study examined whether endotoxin-contaminated cotton dust can produce a similar increase in Vs in this animal model. Rats were exposed to air or 1.5 to 15.0 mg/m3 cotton dust for 2 h/d for 3 d. Twenty-four hours after the final exposure, the nasal cavity and lungs were fixed in formalin and the presence of Alcian blue/periodic acid-Schiff-staining mucosubstances determined by morphometry. Exposure to cotton dust produced concentration-dependent changes in Vs in the nasal septum and intrapulmonary airways. Statistically significant increases in Vs were observed in the epithelial lining of the nasal septum of animals exposed to 5.3 and 14.5 mg/m3 cotton dust (equivalent to 2.8 and 8.9 micrograms/m3 endotoxin). Vs in the intrapulmonary airways was also significantly increased at these concentrations. No significant changes were observed in the nasal septum or intrapulmonary airways after exposure to 1.8 mg/m3 cotton dust. These results are consistent with the hypothesis that endotoxin may contribute to the increase in human cases of chronic bronchitis reported in occupational settings in which endotoxin-contaminated dusts are encountered.

Animals↗
PubMed2000

(1-->3)-beta-D-glucan and endotoxin in house dust and peak flow variability in children.

House dust-associated bacterial endotoxins have been shown to be associated with asthma severity, and a similar role has been suggested for fungal (1-->3)-beta-D-glucans. In this study the relation between these agents and peak expiratory flow (PEF) variability was investigated in 148 children 7 to 11 yr of age of whom 50% had self- or parent-reported chronic respiratory symptoms. All children self-monitored twice daily their PEF for a period of 16 wk. Dust samples were collected from mattresses and from living room and bedroom floors, and endotoxin and (1-->3)-beta-D-glucan were measured in dust extracts. The relations with mean daily PEF variability (Ampl%mean) were investigated by linear regression analysis, adjusting for dust mite allergen levels, presence of pets, and type of floor cover. In unadjusted analyses the levels of both endotoxin and (1--> 3)-beta-D-glucan per square meter of living room floor were significantly associated with PEF-variability (but not when expressed per gram of sampled dust), particularly in atopic children with asthma symptoms. Adjusted analyses showed the same association for (1--> 3)-beta-D-glucan but not for endotoxin. Although no associations were found with microbial agent levels in bedroom floor or mattress dust, high levels of (1-->3)-beta-D-glucan in living room floor dust apparently increase PEF variability in asthmatic children.

Air Pollution, Indoor↗
PubMed1982

Preventive measures in house-dust allergy.

To evaluate the effect of preventive measures on the concentration of house-dust mites (Pyroglyphidae), the homes of 23 consecutive patients allergic to house-dust mites and the homes of 75 randomly selected control subjects were studied. Although the patients' homes were cleaned more frequently (p less than 0.0007 for 4 cleaning qualities), greater concentrations of house-dust mites (p = 0.0073) were found in dust from bedroom carpets in the patients' homes than in the homes of the control subjects. A tendency (p less than 0.15) in the same direction was found for mattress surfaces and living room carpets. High absolute humidity of indoor air was related to greater concentrations of house-dust mites. There was a tendency (p less than 0.10) towards higher humidity in the patients' homes than in those of the control subjects. It was concluded that high humidity improves the survival of house-dust mites in homes. Energy saving measures such as installing insulation raises indoor humidity and can lead to an increased incidence and severity of house-dust mite allergy.

Animals↗
PubMed1992

Enhanced generation of free radicals from phagocytes induced by mineral dusts.

Several studies have suggested that pulmonary toxicity to asbestos and silica may be mediated through oxidant-induced cell injury. We have reported recently that surface radicals associated with freshly fractured silica may be an important factor in cell injury and induction of pulmonary disease. Although the generation of oxygenated radicals in dust-cell interactions has been demonstrated, there are no data correlating the toxicity of a dust with the level of oxygen radical generation by the dust during its interaction with phagocytic cells. In the present study, we have investigated the in vitro generation of oxygen free radicals from human neutrophils and rat alveolar macrophages stimulated with freshly fractured silica, aged silica, amosite, crocidolite, chrysotile, and nontoxic dust, barite. Electron spin resonance (ESR) with the aid of a spin trap phenyl-N-tert-butyl nitrone (PBN) was used to measure the oxygen radicals generated during phagocytosis of the dusts. The relative toxicity index and ESR peak heights, on an equal surface area basis and normalized to barite as one, showed a direct relationship. The normalized toxicity indices and peak heights were: silica, 3.5 versus 2; chrysotile, 4 versus 2; crocidolite, 11 versus 8; and amosite, 26 versus 13. Addition of hydroxyl radical scavengers such as catalase, dimethyl sulfoxide, 1,3 dimethyl-2-thiourea (DMTU), sodium benzoate, and mannitol prevented the radical generation. Carmustine, a glutathione reductase-glutathione peroxidase inhibitor, caused a 5-fold increase in the radical generation. These results indicate that a nontoxic dust such as barite generates toxic oxygen radicals at a minimal level that can be quenched by the normal cellular defense system. For toxic dusts such as silica, amosite, chrysotile, and crocidolite, the potential for oxygen radical generation is enhanced by their surface properties, physical dimensions, and the surface-based radical-generating redox sites. The enhanced radical generation may impair the cellular defense system, resulting in cell injury. Use of scavengers, chelators, and potentiating agents suggests the membrane-based oxidase system as the probable primary source of the radical-generating system. The data presented herein suggest the generation of oxygen free radicals as an important primary event in silica- as well as asbestos-induced cell injury.

Animals↗
PubMed1997

Inhalation of swine dust induces cytokine release in the upper and lower airways.

In healthy subjects, acute inhalation of swine dust causes an influx of inflammatory cells into the airways and increased bronchial responsiveness. The exposure may also cause fever and generalized symptoms. It seems likely that proinflammatory cytokines are involved in the response to inhaled swine dust. Nasal and bronchoalveolar lavage (BAL) were performed before, and 7 and 24 h after the start of 3 h exposure to swine dust, during a period of work in a swine confinement building, in 22 healthy subjects. Lavage fluids were analysed with regard to the cellular response and concentrations of interleukin (IL)-1 alpha, IL-1 beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha). Each subject carried personal samplers for exposure measurements. Inhalable dust and airborne endotoxin, 3-hydroxylated (2-OH) fatty acid and muramic acid were measured. Bronchial responsiveness to methacholine was investigated 1-2 weeks before and 7 h after the start of the exposure. Exposure caused fever (> 38 degrees C) in three subjects, and approximately 25% of the subjects experienced symptoms. Bronchial responsiveness to methacholine increased by 3.5 (1.6-4.8) doubling doses (median (25th-75th percentile)). Following exposure, granulocytes increased more than 50 fold in BAL fluid and more than 40 fold in nasal lavage fluid. IL-1 alpha and IL-1 beta increased significantly in BAL fluid (p < 0.05) and nasal lavage fluid (p < 0.01). IL-6 increased 25 fold in BAL and 15 fold in nasal lavage fluid (p < 0.001). TNF-alpha was below detection limit (0.25 ng.L-1) in most subjects before exposure and increased following exposure to 3.8 (2.4-5.7) and 1.3 (0.6-2.3) ng.L-1 in BAL and nasal lavage fluid, respectively, (p < 0.001). Total inhalable dust was 20.5 (14.6-30.0) mg.m-3 and the concentrations of airborne endotoxin, 3-OH fatty acid and muramic acid were 1.2 (0.8-1.4), 3.5 (2.2-4.5) and 0.9 (0.3-1.9) microgram.m-3, respectively. There was a significant correlation between the IL-6 response in BAL fluid and exposure to dust endotoxin activity and 3-OH fatty acids (p < 0.05). Otherwise, no significant correlations were found between exposure and the cytokine response. We conclude that exposure to swine dust causes an intense upper and lower airway inflammation, which involves the proinflammatory cytokines interleukin-1, interleukin-6 and tumour necrosis factor-alpha.

Adult↗