Myocardial fibrosis in rats exposed to low frequency noise.

UNLABELLED: Low frequency noise (LFN) characterized by large pressure amplitude (> or =90 dB SPL) and low frequency bands (< or =500 Hz) can lead to structural and ultrastructural modifications in the extracellular matrix of several tissues, with an abnormal proliferation of collagen and development of fibrosis. It is not known whether LFN induces similar structural alterations in the ventricular myocardium of rats. OBJECTIVE: The aim of this study was to evaluate and measure the myocardial fibrosis induced by LFN. METHODS: Two groups of rats were considered: group A with 26 rats continuously exposed to LFN during a period of 3 months; group B with 20 control rats.The hearts were sectioned from the ventricular apex to the atria and the mid-ventricular fragment was selected. Chromotrope-aniline blue (CAB) staining was used for histological observation. The measurement of fibrosis was performed using the computer image analysis Image J software. RESULTS: Histological observation with CAB staining showed the presence of collagen deposition between the cardiomyocytes. Fibrosis increased 97.5%, 81.5% and 83.7%, respectively, in the left ventricle, interventricular septum and right ventricle, in exposed rats (P <0.001).The ratio fibrosis/muscle in left ventricle, interventricular septum and right ventricle was significantly higher in LFN exposed rats (P< 0.001). CONCLUSIONS: Our study demonstrates a significant myocardial fibrosis induced by low frequency noise in rats. Our results reinforce the need for further experimental and clinical investigations concerning the effects of low frequency noise on the heart.

Histomorphometric evaluation of the coronary artery vessels in rats submitted to industrial noise.

INTRODUCTION: Industrial noise (IN) is characterized by high intensity and a wide spectrum of wavelengths that induce physical vibration on the body structures. This effect, resulting from the low-frequency sound waves, can lead to pathological alterations in the extracellular matrix with an abnormal proliferation of collagen and development of tissue fibrosis, in the absence of an inflammatory process. OBJECTIVE: The aim of this study was to evaluate the modifications of the arterial coronary vessels in Wistar rats submitted to IN. METHODS: Two groups of rats were considered: group A with 20 rats exposed to IN during a maximum period of 7 months; group B with 20 rats as age-matched controls.The hearts were sectioned from the ventricular apex to the atria and the mid-ventricular fragment was selected. Haematoxylin-eosin and Masson's trichrome staining were used for histological observation. Histomorphometric evaluation of the coronary vessels was performed using the computer image analysis ImageJsoftware. The mean lumen-to-vessel wall (L/W) and media vessel wall-to-perivascular tissue (W/P) ratios were calculated in each group. RESULTS: Histological evaluation showed a prominent perivascular tissue with fibrotic development in the absence of inflammatory cells in group A. Histomorphometric analysis showed that the mean L/W was 0.7297 and 0.6940 in group A and B, respectively. The mean W/P ratio was 0.4923 and 0.5540 in group A and B, respectively, being higher in the control group (P <0.01). CONCLUSIONS: There are perivascular structural modifications in arterial coronary vessels. Our results show a significant development of periarterial fibrosis induced by industrial noise in the rat heart.

Exposure to industrial wideband noise increases connective tissue in the rat liver.

Rats were daily exposed (eight hours/day) for a period of four weeks to the same high-intensity wideband noise that was recorded before in a large textile plant. Histologic observation of liver sections of the rats was used to perform quantitative comparison of hepatic connective tissue (dyed by Masson trichromic staining) between the noise-exposed and control animals. For that, we have photographed at random centrolobular areas of stained rat liver sections. We found that noise exposure resulted in significant enhancement in the area of collagen-rich connective tissue present in the centrolobular domain of the rat liver. Our data strengthen previous evidence showing that fibrotic transformation is a systemic effect of chronic exposure of rodents and humans to industrial wideband noise.

Chronic exposure of rats to occupational textile noise causes cytological changes in adrenal cortex.

Chronic exposure to industrial noise and its effects on biological systems. Occupational exposure to noise may result in health disorders. Our aim was to evaluate the effects of chronic exposure to high-intensity noise of textile industry cotton rooms on the adrenal morphology. The environmental noise of a cotton-mill room from a large textile factory of Northern Portugal was recorded and reproduced by an adopted electroacoustic setup in a sound-insulated animal room where the rats were housed. The sounds were reproduced at the original levels of approximately 92 dB, which was achieved by equalization and distribution of sound output in the room. Wistar rats were submitted to noise exposure, in the same time schedule as employed in textile plants. After one, three, five, and seven months, the adrenals were collected and analyzed by light microscopy. Analyzed by multivariate analysis of variance and post hoc Bonferroni correction for multiple comparisons of the means between the groups. Noise exposure induced time-dependent changes in adrenal cortex, with decrease of zona fasciculata (ZF) and increase of zona reticularis volumes, together with a significant depletion of lipid droplet density in ZF cells of exposed rats, in comparison to control rats. Chronic exposure of rats to textile industry noise triggers cytological changes in the adrenals that suggest the existence of a sustained stress response.

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.

Arrest in ciliated cell expansion on the bronchial lining of adult rats caused by chronic exposure to industrial noise.

Workers chronically exposed to high-intensity/low-frequency noise at textile plants show increased frequency of respiratory infections. This phenomenon prompted the herein investigation on the cytology of the bronchial epithelium of Wistar rats submitted to textile noise. Workplace noise from a cotton-mill room of a textile factory was recorded and reproduced in a sound-insulated animal room. The Wistar rats were submitted to a weekly schedule of noise treatment that was similar to that of the textile workers (8h/day, 5 days/week). Scanning electron microscopy (SEM) was used to compare the fine morphology of the inner surface of the bronchi in noise-exposed and control rats. SEM quantitative cytology revealed that exposure to noise for 5-7 months caused inhibition in the natural expansion of the area occupied by ciliated cells on the bronchial epithelium as adult rats grow older. This difference between noise-exposed and age-matched control rats was statistically significant (P<0.05) and documents that the cytology of the rat bronchial epithelium is mildly altered by noise exposure. The decrease in the area of bronchial cilia may impair the mucociliar clearance of the respiratory airways and, thus, increase vulnerability to respiratory infection.

Mercury intake by inflammatory phagocytes: in vivo cytology of mouse macrophages and neutrophils by X-ray elemental microanalysis coupled with scanning electron microscopy.

Phagocytes remove and store mercury (Hg) that enters the body. Macrophages and granulocytes respond in opposite ways to Hg: macrophages loose cell viability, and neutrophils become protected from apoptosis. We have investigated the cytology of early intake of Hg by macrophages and neutrophils after a short period (2-4 min) of in vivo exposure to HgCl2. The two types of phagocytes were attracted either to a subcutaneous air pouch or to the peritoneal cavity of BALB/c mice by in situ BSA injection. BSA caused, 72 hours later, inflammatory exudates where neutrophils (air-pouch cavity) or macrophages (peritoneal cavity) were the predominant cell type. A lethal dose of HgCl2 (25 mg) was then injected in the two inflammatory cavities. The mice died 2-4 min later and the cell exudates were harvested and studied by scanning electron microscopy coupled with X-ray elemental microanalysis (SEM-XRM). More than half of the phagocytes showed ingested Hg; a higher percentage of macrophages (around 70%) than neutrophils (around 50%) were positive for the metal. Intracellular particles of Hg were spheroid and presented a small diameter (less than 20 nm). They could be seen in large numbers inside phagocytes (up to 20-30 Hg dots per cell); they were scattered throughout the cytoplasm of the cells. The ability of phagocytes to ingest Hg increased as the BSA-induced inflammation progressed. We conclude that (i) Hg is quickly ingested as small particles by phagocytes; (ii) endocytosis of Hg increases with the degree of activation of phagocytes; and (iii) phagocytes internalize Hg by pinocytosis.

Chronic exposure of rats to cotton-mill-room noise changes the cell composition of the tracheal epithelium.

The work environment of cotton mill rooms of modern textile plants is characterized by noise pollution. We have taped and reproduced this noisy environment to study its effects on experimentally exposed rats. Because we have previously documented that chronic noise causes alterations in the respiratory epithelium, we have focused our investigation on the morphology of the tracheal lining. Wistar rats were exposed to the textile-type noise from 1 up to 7 months, with an average 40 hours weekly exposure of the animals. The rats were sacrificed monthly and the tracheas were studied by scanning electron microscopy (SEM) to quantify the areas of the airway lining that were covered by ciliated, serous or other cells of the epithelium. We found that noise exposure of the rats caused a significant loss of tracheal ciliated cells; an increased density of serous cells on the epithelium balanced this change. This modification of the rat trachea was already established after 1 month of noise treatment of the animals; it did not change significantly throughout the 7-month course of the herein investigation. Loss of ciliated cells was more intense in areas of the tracheal epithelium located between the regions of cartilage rings. We conclude that the ciliated cell is an elective target for damage caused on the respiratory epithelium by the workplace noise occurring in cotton mill rooms. This modification of the respiratory epithelium is likely to impair clearance of the airways since this function depends on the activity of ciliated cells.

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.