Histological, Histochemical, Immunohistochemical and Morphometric Study of Adult Male Albino Rat s Lung Following Exposure to Air Pollution

Introduction: Exposure to air pollution is associated with increased respiratory and cardiovascular morbidity, although the underlying mechanisms are unclear. Thus the way of assessing the effects of inhalation of whole mixtures from defined sources as tobacco smoke and car exhaust need to be considered more. Aim of the Work: To investigate using histological, histochemical, immunohistochemical and morphometric study, the harmful effects of tobacco smoke and car exhaust on adult male albino rats lung and the influence of arrest of these air pollutants. Materials and Methods: Thirty adult male albino rats were randomly divided into three groups: control group, tobacco exposed group, and car exhaust exposed group. Rat s general condition and behavior were noticed and they were weighed at the beginning of research and at the time of sacrifice. Paraffin sections were prepared for histological, histochemical, immunohistochemical using marker.CD44 and morphometric study and statistical analysis were done. Results: Rats exposed to tobacco smoke or car exhaust showed significant decrease in body weight more intensified after car exhaust which remained significantly less than control rats after arrest of exposure. Histological, histochemical, immunohistochemical and morphometric changes were more exaggerated after car exhaust than after tobacco exposure. Rats showed pulmonary congestion, extravasation of blood in lung alveoli, perivascular infiltration and thickened interalveolar septa, obliteration of most alveoli and subsequently compensatory emphysematous changes. There was increased deposition of collagen fibers and apparent increase in mucopolysaccharides and immunohistochemical reaction CD44. Arrest of exposure to either tobacco smoke, or car exhaust caused partial recovery which was less ameliorated after car exhaust. Conclusion: These results provide evidence that air pollution from either tobacco smoke or car exhaust are risky factors for parenchymal lung damage and marked thickening of the interalveolar walls. Partial recovery was observed after arrest of tobacco smoke better than after car exhaust.