Effects of long term exposure to occupational noise on textile industry workers' lung function.

UNLABELLED: Vibroacoustic disease is a pathology caused by long occupational exposure to large pressure amplitude and low frequency noise. It is a systemic disease, with evolvement of respiratory structures. The exposure workers to this noise of textile industry may favour alterations in lung function. We studied 28 women working more than ten years in cotton-mill rooms to evaluate their lung function, including Spirometry, forced oscillation technique (I.O.S.) and Diffusion capacity. These results were compared with those of 30 women of similar ages not exposed to similar noise and not presenting respiratory disease. Statistical significance (P<0.05) was found with FEV25, R5 and Delta Rs5-Rs20. There was a resistance frequency dependence in 36% of the population exposed to noise, not statistically confirmed. Neither restriction nor changes in diffusing capacity where detected. CONCLUSION: The analysis of global alterations of lung function parameters suggests small airways aggression by noise. However we cannot definitively exclude the influence of cotton dust inhalation in itself which effects could be increased by the loss of ciliated cells and impairment of airways clearance caused by noise.

Tubular kidney damage and centrilobular liver injury after intratracheal instillation of dimethyl selenide.

Accidental inhalation of selenium (Se) derivatives, such as dimethyl selenide (DMSe), has been associated with damage of respiratory tissues. However, systemic effects of inhaled Se have not been thoroughly established. We have investigated whether mouse kidney and liver show cellular pathology as a result of a single intratracheal instillation of two different doses of DMSe (0.05 and 0.1 mg Se/kg BW). The animals were sacrificed 1, 7, 14, and 28 days after either 1 of the 2 DMSe treatments; samples were studied by light microscopy. Instillation of the low DMSe dose resulted in acute and transient tubular disease of the kidney expressed by swelling and vacuolation of epithelial cells of proximal tubules; in some mice, tubular necrosis was observed. After 14 days of the DMSe treatment, these lesions were ameliorated and, by day 28, the kidney tubular epithelium depicted a normal morphology. The same low dose of DMSe caused sustained damage to centrilobular hepatocytes characterized by swollen and vacuolized liver cells. After the instillation of the high DMSe dose, the mice presented sustained liver and kidney focal necrosis. Our data suggest that inhalation of DMSe results in: (i) acute tubular injury of the kidney and damage to centrilobular liver cells and (ii) this systemic pathology induced by DMSe is a dose-dependent phenomenon.

Acute pulmonary inflammation induced by lung overloading with selenium particles: leukocyte response and in situ detection of selenium at high resolution.

The kinetics of the acute inflammatory response of the lung was triggered in CD-1 mice by a single intratracheal instillation of a large amount of Se (10 mg); it was studied by quantitative cytology of bronchoalveolar lavage samples, light microscopy, and scanning electron microscopy coupled with x-ray elemental microanalysis. Bronchoalveolar lavage leukocytes were mostly neutrophils and increased from 12 to 24 h of Se treatment and decreased at 72 h. Only less than half of the granulocytes showed ingested Se particles; in contrast, virtually all BAL macrophages contained Se particles. Scanning electron microscopy coupled with X-ray elemental microanalysis revealed that the intracellular Se particles were heterogeneous in size (diameters from 0.4 and up to 14 microm), and that Se inclusions were sometimes accumulated at a pole of the cell. At 72 h after instillation of the particles, Se-loaded alveolar macrophages were migrated in the interstitial space of the alveoli. Se-positive regions had a focal distribution in the lung; accumulation of inflammatory cells erased the alveolar architecture of these areas of the deep lung. Our data indicates that Se overloading of the lung results in: (1) an acute inflammatory response that is dominated by neutrophils; (2) early removal of Se done mostly by alveolar macrophages, and (3) formation of focal areas of invasion of the lung parenchyma by inflammatory infiltrates.

In vivo ingestion of heavy metal particles of Se, Hg and W by murine macrophages. A study using scanning electron microscopy coupled with X-ray microanalysis.

Several heavy metals that are currently employed in industry may become polluters of work and natural environments. As particulate matter, heavy metals are suitable for entering the human body through the respiratory and digestive systems. They often end up inside phagocytes; the size of the microscopic particles modulates both their phagocytosis, and the physiology of macrophages. Here we have adopted an experimental model to investigate the ingestion of particles of three industrial heavy metals (Se, Hg, W) by murine peritoneal macrophages in vivo. The phagocytes were studied by scanning electron microscopy coupled with X-ray elemental microanalysis (SEM-XRM), a method that allows specific identification of Se, W and Hg in cells at high resolution. We found that Hg that was taken up by macrophages was organized into small, round particles (0.31 +/- 0.14 microm). This was in contrast with the larger size of intracellular particles of Se (2.37 +/- 1.84 microm) or W (1.75 +/- 1.34 microm). Ingested particles of Se and W, but not Hg, often caused bulging of the cell surface of macrophages. We conclude that particulate matters of Se, W and Hg are organized in particles of different size inside macrophages. This size difference is likely to be associated with distinct phlogistic activities of these heavy metals, Se and W causing a milder inflammatory reaction than Hg.