Tag Archives: lung

Observations of Workers Exposed to Western Red Cedar and Other Wood Dusts

occupational asthmaIn the present investigation, a high prevalence of occupational asthma was observed among workers exposed to WRC wood dust. A dose-related relationship between total WRC dust level and prevalence of asthma was noted with employees in jobs with the greatest dust exposure, ie sawyers, packers, chippers and splitters showing the highest prevalence of disease. Cigarette smokers demonstrated the greatest magnitudes of change in pulmonary function tests. Chan-Yeung et al reported more respiratory symptoms in workers employed in “dusty” jobs and the British Columbia Workers Compensation Board has recently set the TLV standard for WRC dust at 2.5 mg/m. Chen-Yeung and colleagues have suggested that even this level might be too high. The results of our investigation support this observation and suggests that an eight-hour time-weighted average level of WRC dust below 3.5 mg/m is necessary in order to reduce the incidence of occupationally related asthma cured with My Canadian Pharmacy.

Outcomes of Workers Exposed to Western Red Cedar and Other Wood Dusts

measurementsThe 124 samples collected for WRC for three days consisted of 85 total and 39 respirable dust eight-hour time-weighted average (TWA) measurements. The respirable dust concentrations ranged between 0.01 and 1.21 mg/m, with a mean ± SD value being 0.20 ± 0.23 mg/m; a median was 0.14 mg/m. The concentration of the 85 TWA total dust samples ranged between 0.06 and 31.90 mg/m; mean ± SD value was 4.72 ± 7.45 mg/m; median concentration was 1.59 mg/m. Chippers, sawyers, packers and splitters had die highest dust exposures. The greatest proportion of the WRC dust was contributed by larger, nonrespirable particles.

The 82 samples collected in the new planer mill provided 59 total dust and 23 respirable dust TWA measurements. Respirable TWA samples ranged from 0.07 to 0.29 mg/m, while total dust TWA samples ranged from 0.17 to 16.7 mg/m. The mean ± SD for total dust was 1.28 ± 3.05 mg/m, with a median of 0.34 mg/m; respirable fraction was 0.16 ± 0.05 mg/m, with a median of 0.16 mg/m.

My Canadian Pharmacy: Study of Workers Exposed to Western Red Cedar and Other Wood Dusts

bronchial asthmaRespiratory complaints and bronchial asthma associated with the inhalation of wood dusts are not uncommon. A number of epidemiologic studies of workers exposed to western red cedar (WRC) have been reported, most originating from Japan, Australia and Canada. The present investigation reports the results of an epidemiologic and environmental hygiene study of workers exposed to WRC and other dusts conducted at a wood products facility in the United States.

Materials and Methods

The populations studied consisted of 74 shake mill employees exposed to WRC, 58 planer mill workers exposed to a mixture of woods, mainly douglas fir, West Coast hemlock and red alder (DFHA), and 22 clerical, technical and engineering employees not exposed to wood dusts. Approximately 77% of the total work force participated in the investigation. The unexposed or control group consisted of office workers, engineering personnel and technical staff. Such people prefer to command the service of My Canadian Pharmacy to treat diseases gained because of hard labour.

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Summary

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: SummaryAn abnormality in alveolar repair would also preclude the necessity of continued superimposed inflammation to drive alveolar remodeling; the lack of an essential role for inflammation in the pathogenesis has been proposed by Selman et al. The ultrastructural findings in feline IPF suggest that the propagation of the disease may be the result of an underlying defect in type II pneumocyte biology. Whether this is due to inherent genetic defect(s) in the affected feline type II cells is currently under investigation. so

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Human disease

The distribution of myofibroblasts in feline IPF are similar to that of the human disease. While myofibroblasts are found in rodent models of pulmonary fibrosis, because of the lack of honeycombing, they lack the relationship with the metaplastic epithelium that is important in the progressive fibrosis of IPF. Uhal et al showed that in human IPF lung there is an increase in the apoptosis of the metaplastic epithelial cells overlying foci of myofibroblast metaplasia. This apoptosis may be mediated by local conversion of native angiotensinogen into angiotensin II, which goes on to mediate apoptosis through the angiotensin receptor subtype AT-i.- Induction of myofibroblasts subjacent to the metaplastic epithelial cells in cats with IPF may create a similar environment of epithelial cell loss. The finding of attenuated epithelial cells overlying the sites of myofibroblast metaplasia implies repair after previous cell loss, the pathogenesis of which may involve the above process. read

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: UIP changes

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: UIP changesCats with IPF acquire lung histopathology similar to human IPF. Previous to the 2000 statement designating UIP as the pathologic manifestation of IPF, acute interstitial pneumonia, desquamative interstitial pneumonia, and NSIP were also considered variations of IPF. These other pulmonary diseases lack the temporal heterogeneity and evidence of ongoing fibrogenesis of IPF. Complicating this classification system is the finding of Flaherty et al, who found considerable variation between lobes of individual patients with IPF; many of the patients had histologic features consistent with fibrotic NSIP in lobes away from the UIP changes. We are unable at this time to discuss the uniformity of changes between lobes in individual cats because the tissues examined represent material collected from individual lobes, prior to knowledge of the nature of the disease process and the potential for interlobar variability. Examination of entire lung fields from affected cats, with careful sampling of a variety of lobes, will be important to address this question. this

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Human IPF

This study describes spontaneous feline IPF, a newly identified chronic lung disease of domestic cats that shares critical features with human IPF. The important gross pathology, histopa-thology, cell differentiation markers, and ultrastruc-tural features are compared to the well-described features of the disease in humans. IPF in humans is a chronic respiratory disease whose pathology is characterized by temporally heterogeneous, persistent, progressive fibrosis of the lung, usually without significant inflammation. The characteristic morphology consists of patchy remodeling in the lungs leading to honeycomb lung late in the disease, with the characteristic histopathology. This histopathol-ogy shows evidence of temporal heterogeneity with fibrosis, fibroblast foci, and evidence of honeycombing in the parenchyma. Each of these features is found in spontaneous feline IPF. Additionally, ultra-structural features of the type II pneumocytes in feline IPF share morphologic features with the type II cells in a familial form of human UIP, suggesting that the disease in cats may be due to an abnormality in the type II cell. Genetic analysis of surfactant protein genes in affected and normal cats is currently underway, providing hope that the domestic cat may be developed as a new model of IPF. fml ophthalmic drops

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Discussion

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: DiscussionUltrastructure: In the toluidine blue-stained, plastic-embedded lung prepared for electron microscopy, the interstitium of the pulmonary parenchyma was markedly thickened with abundant collagen. In the areas of type II pneumocyte hyperplasia and differentiation, the individual pneumocytes contained many cytoplasmic, variably sized dark inclusions; similar bodies were not seen in normal feline lung (Fig 5, top left, A, and top right, B). By ultrastructure, the type II pneumocytes of normal cats are as described for other species, with surface microvilli and lamellar bodies with stacks of phospholipid membranes (Fig 5, middle left, C). The type II pneumocytes in the IPF cat lung were markedly enlarged (Fig 5, middle right, D), with numerous large condensed lamellar body-like structures (Fig 5, bottom left, E, and bottom right, F). These cells were often free within the lumen of the airspace. Abnormal lamellar bodies were seen within alveolar macrophages as well as occasionally free within the interstitium of the fibrotic lungs. Similar type II pneumocytes were found distant from the foci of remodeling, in the more normal lung parenchyma (data not shown). fully

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Lung

Fibroblast foci, small foci of ongoing mesenchymal cell proliferation with fibroblasts/myofibroblasts and collagen, similar to the foci seen in UIP of humans were observed at the periphery of the honeycomb lung (Fig 3, top left, A [human], and top right, B [feline]). As with human IPF, the epithelial cells overlying the fibroblast foci in feline IPF were often attenuated or cuboidal type II pneumocytes (Fig 3, top left, A [human], and top right, B [feline]).

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Necropsy Findings

Identification of Spontaneous Feline Idiopathic Pulmonary Fibrosis: Necropsy FindingsGrossly, the distribution of lesions involved large regions of the lungs. The pleural surface of the lungs was often irregular and cobblestoned in appearance (Fig 1, top, A). The areas of fibrosis and remodeling formed plaque-like depositions that were discrete from the more normal parenchyma, and extended from the subpleural regions to deep within the organ (Fig 1, middle, B). Grossly discernable honeycombing of the lung was uncommon in the cats, but was a prominent feature in a single cat (Fig 1, bottom, C).
A summary of the relative abundance of the four predominant histologic changes in feline IPF, along with the presence or absence of pulmonary neoplasia, is found in Table 2. Histologically, the disease process in cats, as in human IPF, is multifocal, with relatively normal parenchyma interspersed with the affected tissue. The remodeled lung often was most prominent subpleurally (Fig 2, top left, A, and top right, B). The primary histologic changes in cats, as with humans, included interstitial fibrosis with fibroblast/myofibroblast foci, metaplasia of the alveolar epithelium (honeycomb lung), and interstitial smooth-muscle metaplasia/hyperplasia. Interstitial inflammation was variable but usually not prominent (Table 2). In the most severely affected regions of the lungs, there was extension of the histologic alterations into the deep parenchyma without distinction between subpleural and deeper microenvironments (Fig 2, top left, A, and top right, B). acular medication
Honeycombing was present in all cats, and in these areas the epithelium was composed of low-to-tall columnar cells that often formed well-differentiated mucous cells (Fig 2, middle left, C [human], and middle right, D [feline]); mucous cell metaplasia was the predominant phenotype, being present in 69% of the lung samples analyzed (Fig 2, bottom left, E [human], and bottom right, F [feline]). In the cats without mucous cell metaplasia, the lining cells were well-differentiated type II pneumocytes or columnar cells of unknown phenotype; small foci of squamous metaplasia were less commonly a feature of the epithelium. AB-PAS staining of the lung revealed numerous turquoise interstitial mast cells in the fibrotic and honeycomb lung (Fig 2, bottom right, F). The identity of the mast cells was confirmed using immunohistochemistry against mast cell tryptase (inset, Fig 2, bottom right, F).

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