**3.1.8 Dietary factors**

Observational studies strongly suggest that dietary factors, such as a higher intake of vitamin C and other antioxidants(carotenoids,Vitamin E,lutein, flavanoids) are significantly associated with better lung function(ATS,2010). Some dietary elements like fruits and vegetables(antioxidants), fish(omega-3 polyunsaturated fatty acids) and Vitamin D seem protective while processed foods like cured meats(nitrites) may be deleterious for lung function preservation(ATS,2010).

## **3.1.9 Tuberculosis**

Pulmonary tuberculosis can lead to scarring and accelerated decline in lung function(Hnizdo et al.,2000 as cited in Shapiro SD,2010). Some population-based surveys(PLATINO and PREPOCOL) reported strong association between previous tuberculosis and a greater risk of COPD(Caballero et al.,2008; Menezes et al.,2007 as cited in Shapiro SD,2010).

#### **3.1.10 Intravenous drug abuse**

Emphysema is prevalent in approximately 2% of intravenous drugs abusers which can be attributed to pulmonary vascular damage possibly from the insoluble filler. Bullous cysts

Current Overview of COPD with Special Reference to Emphysema 123

antiproteinase imbalance lead to inflammatory cell recruitment, proteolytic injury to the extracellular matrix (ECM), and cell death. Alveolar walls become perforated and later due to incomplete and disorderly repair, become obliterated with coalescence of small distinct air spaces into abnormal and much larger air spaces, which is the pathological hallmark of emphysema (Shapiro & Ingenito,2005 as cited in Shapiro SD,2010). Emphysema has been classically described with absence of interstitial fibrosis to differentiate from restrictive lung diseases. However, scarring of the small airway subepithelial space and collagen

Various subtypes of emphysema have been described based on location and distribution of the lesions in the acinus (Pipavath et al.,2009 as cited in Shapiro SD,2010). In most patients, however, the process within the lung will be heterogeneous and in advanced stages,

Strongly associated with smoking, it begins in the respiratory bronchioles and spreads peripherally, primarily involving the upper and posterior parts of lungs(Leopold & Gough,1957;Thurlbeck,1991 as cited in Shapiro SD,2010). Focal emphysema, a form of centriacinar emphysema, occurs in persons with heavy exposure to inert dust such as coal

Involves the entire alveolus uniformly and is predominant in the lower half of the lungs(Snider et al.,1962;Thurlbeck,1963,1976 as cited in Shapiro SD,2010). It is observed in

It usually involves the distal airway structures, alveolar ducts, and alveolar sacs around the septae of the lungs or pleura(Hogg & Timens,2009;Kim et al.,1991 as cited in Shapiro SD,2010). Apical and giant bullae described in this subtype may lead to spontaneous

It is commonly seen as an inconsequential lesion adjacent to scars but may be extensive arising as a complication of fibrosing diseases such as tuberculosis, silicosis, and sarcoidosis (Reid & Simon,1962;Thurlbeck,1991 as cited in Shapiro SD,2010). The spaces have dense fibrous walls and are mostly lined by bronchiolar epithelium(Akashi et al.,2009 as cited in

Bullae are marked focal dilation of respiratory air spaces that may result from coalescence of adjacent areas of severe panacinar emphysema, or from a ball-valve effect in the bronchi

accumulation around larger disrupted air spaces has been noted in emphysema.

distinction becomes blurred. The following three patterns of emphysema are noted:

**4.2.1 Centriacinar (centrilobular, proximal acinar) emphysema** 

dust (Morgan & Seaton,1984 as cited in Shapiro SD,2010).

**4.2.2 Panacinar emphysema** 

Shapiro SD,2010).

**4.3.2 Bullae** 

patients with homozygous A1PI deficiency.

**4.2.3 Paraseptal (distal acinar) emphysema** 

pneumothorax or compression of adjacent lung tissue.

**4.3 Other pathologic variants mimicking emphysema 4.3.1 Air space enlargement with pulmonary fibrosis** 

are found in upper lobes of cocaine or heroin abusers whereas basilar and panacinar emphysema are associated with methadone and methylphenidate injections.

#### **3.1.11 Immune deficiency syndromes**

Human immunodeficiency virus (HIV) infection was found to be a risk factor for COPD, independent of confounding variables(Crothers et al.,2006 as cited in Shapiro SD,2010). Apical and cortical bullous lung damage occurs in autoimmune deficiency syndrome and *Pneumocystis carinii* infection.
