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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.
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.
Background Chronic exposure to industrial noise is known to affect biological systems, namely, by inducing fibrosis in the absence of inflammatory cells. In rat hearts exposed to this environmental hazard, we have previously found myocardial and perivascular fibrosis. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (<20 Hz), whose effects on the heart are unknown. We evaluated the morphological changes induced by IFS in rat coronaries in the presence and absence of dexamethasone. Methods Adult Wistar rats were divided into three groups: group A (GA)—IFS (<20 Hz, 120 dB)-exposed rats for 28 days treated with dexamethasone; group B (GB)—IFS-exposed rats; group C (GC)—age-matched controls. The midventricle was prepared for observation with an optical microscope using 100× magnification. Thirty-one arterial vessels were selected (GA 8, GB 10, GC 13). The vessel caliber, thickness of the wall, and perivascular dimensions were quantified using image J software. Mann–Whitney and Kruskal–Wallis tests were used to compare the groups for lumen-to-vessel wall (L/W) and vessel wall-to-perivascular tissue (W/P) ratios. Results IFS-exposed rats exhibited a prominent perivascular tissue. The median L/W and median W/P ratios were 0.54 and 0.48, 0.66 and 0.49, and 0.71 and 0.68, respectively, in GA, GB, and GC. The W/P ratio was significantly higher in GC compared with IFS-exposed animals (P=.001). The difference was significant between GC and GB (P=.008) but not between GC and GA. Conclusion IFS induces coronary perivascular fibrosis that differs under treatment with corticosteroid.
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.
Chronic exposure to excessive noise may cause systemic disorders, in addition to the well-established damage to hearing (Melamed HW DO, 1996; Nicholas HWWDO, 1998). Noise-related disorders have been identified in exposed workers and to the concept of Vibroacoustic Disease (VAD) (Castelo Branco and Rodriguez, 1999).Textile workers show increased frequency of respiratory infections (Simpson HW DO, 1998; Raza HW DO, 1999). We have investigated whether the bronchial epithelium undergoes any cytological change in animals chronically exposed to cotton-mill-room noise. To perform quantitative cytology of the bronchial epithelium of noise-exposed and control rats we have used scanning electron microscopy (SEM). 0DWHULDOVV DQGG 0HWKRGV Thirty-five rats were divided into 4 experimental groups and submitted to different periods of noise exposure, ranging from 1 to 7 months, according to an occupationally simulated time schedule (8 hours/day; 5 days/week with weekends in silence). The different groups of noise-exposed rats were sacrificed after 1, 3, 5 and 7 months of exposure to cotton-mill-noise. The remaining 20 Wistar rats were used as age-matched controls and sacrificed when they were 3, 5, 7 and 9 months old. The rats were sacrificed by a lethal intravenous injection of sodium-pentobarbital (40 mg/kg) and the left lung excised and processed for SEM. The samples were fixed LQQWRWRRin a solution of 3% glutaraldehyde in 0.1 M phosphate buffer, pH 7.2, washed in several changes of 5% sucrose in 0.1 M phosphate buffer, pH 7.2, dehydrated, critical point-dried and coated with gold-palladium (Oliveira HWW DO, 2002a).Random SEM micrographs of the samples were obtained at a magnification of 1000. Ten micrographs were made of each sample; a total area of 0.11 mm 2 of the bronchial epithelium was used for quantitative analysis of each sample. The relative area of the bronchial surface that was coated by ciliated cells, secretory cells, brush cells or other unidentifiable cells was determined with the help of a transparent grid of 20 points, spaced 4 cm from each other, that was superimposed on the printed micrographs (Oliveira HW DO, 2002a,b). The numerical values of the relative area of the pleura that showed microvilli were calculated using the following formula: total points of ciliated or other cell types/total points of the grid inside the micrograph. 5HVXOWVVSEM micrographs were randomly taken of the bronchial lining of both noise–exposed and control groups of rats. Based on these micrographs, we have determined the relative area occupied by the several cells types that make up the luminal surface of the bronchi.). In control rats, we found an increase with age (from 3 to 9 months) of the relative area occupied by ciliated cells on the bronchial lining. In fact, 7 and 9 months old animals had a larger proportion of the bronchial surface covered by ciliated cells than what was observed in younger control rats (3 and 5 months old animals). Chronic exposure of rats to textile-mill noise inhibited this enhancement in the cilia-coated area of bronchi. This phenomenon was also observed after 7 months of noise exposure of the animals. Therefore, it can be concluded that
Scanning electron microscopy (SEM) was used to investigate whether chronic exposure to noise modifies pleural morphology. Rats were submitted to 8-h/day schedule of noise that is similar to the working hours at cotton-mill rooms. Morphometry of the area occupied by microvilli on the pleural surface showed a decrease in microvilli after 3 months of rat exposure to noise. The reduction of microvilli was 10% after 3 months of noise exposure (reaching 20% after 7 months of noise treatment) and is consistent with pleural effusions found in some of the patients working in noise-polluted environments.