[The importance of diffusing capacity as a complementary study to plethysmography in smokers].

Unlabelled: This study comprised 194 male and female heavy smokers or ex-smokers (>or= 1 pack-year) aged between 20 and 82, whose symptoms varied. Cases were only selected from patients with normal whole-body plethysmography. Subjects with any significant pathology and occupational risk factors were excluded from the study.

[Respiratory epithelia in Wistar rats born in low frequency noise plus varying amounts of additional exposure].

Earlier studies of Wistar rat respiratory epithelia exposed to low frequency noise (LFN) (< or =500 Hz, including infrasound) showed that LFN effects trauma on the respiratory tract. In rats gestated and born in LFN environments, trauma was still treated in accordance with 86/609/EC. Respiratory epithelial fragments were prepared for light and scanning/transmission electron microscopy.

[Respiratory epithelia in Wistar rats after 48 hours of continuous exposure to low frequency noise].

Previous studies show that exposure to low frequency noise (LFN) (< or =500 Hz, including infrasound) produces irreversible lesions in Wistar rat respiratory epithelia. Recovery periods for LFN-induced lesions have thus become an object of interest. Changes in the respiratory epithelia of Wistar rats after continuous short-term exposure to LFN are described.

Respiratory epithelia in Wistar rats.

Morphofunctional changes of respiratory epithelia became the object of intense study in Wistar rats after previous research showed that occupationally-simulated exposure to low frequency noise (500 Hz, including infrasound) induced irreversible lesions in these tissues. Aspects of normal respiratory epithelia in rats are lacking in the literature, and are the object of this report. Ten Wistar rats were kept in silence, fed standard rat food, and had unrestrained access to water (treated in accordance with 86/609/CE).

Noise and the respiratory system.

Noise-induced pulmonary pathology is still an issue that is regarded with much suspicion despite the significant body of evidence demonstrating that acoustic phenomena target the respiratory tract. The goal of this review paper is threefold: a) to describe acoustic phenomena as an agent of disease, and the inadequacies of current legislation regarding noise-induced, non-auditory pathology; b) to trace how the interest in noise-induced pulmonary pathology emerged within the scope of studies on vibroacoustic disease; and c) to bring to light other studies denouncing noise as an agent of disease that impinges on the respiratory tract. As concluding remarks, future perspectives in LFN-related research will be discussed.