**2. Smoking COPD**

In 1950, smoking was established as a cause of COPD (chronic bronchitis and emphysema) and Fletcher and Peto corroborated its natural history. The relationship between smoking and COPD, probably influenced by genetic determinants poorly understood, is primarily a dose-effect relationship as demonstrated in multiple studies.

Findings have proven smoking cessation disrupts the natural history of COPD, but there are authors who have more controversial opinions about it and assert that in many cases, inflammation persists despite smoking cessation. The perpetuation of inflammation may be related to other factors, bacterial colonization has been proposed.

In the past, it was considered that only 15% of smokers were likely to develop COPD, when in fact it is known that this percentage is near 50% if they survive long enough. This

ERS 1995 FEV1/VC <88% predicted (men) or 89% (woman)

NLHEP 2000 FEV1/FVC or FEV1/ FEV6/<LLN and FEV1<LLN

ATS: American thoracic Society; BTS: British Thoracic Society; VC: Vital capacity; ECCS: European Community for Coal and Steel; ERS: European Respiratory Society; FEV1/ /FVC: ratio of forced expiratory volume in 1s to forced vital capacity; GOLD: Global Initiative for chronic obstructive lung disease; LLN: lower limit of normal (LLN); NICE: National Institute for health and clinical excellence;

There are many diseases or processes that show a FEV1 / FVC post-bronchodilator < 70%,

Although nosological or semantically, definition of COPD as a syndrome is questionable, recently the term has come to be considered by other authors. Table 2 outlines a long list (not exhaustive) of entities that may be associated with airflow obstruction syndrome or COPD. Most of them are common such as pneumoconiosis and other occupational diseases, Airway obstruction in pulmonary tuberculosis, some clinical forms of asthma, etc and other less common such as lymphangioleiomyomatosis, Bronchiolitis obliterans associated with consumption of Sauropus androgynus among others. This chapter will show a list of differential diagnosis, as complete as possible and some clues for the recognition of these

In 1950, smoking was established as a cause of COPD (chronic bronchitis and emphysema) and Fletcher and Peto corroborated its natural history. The relationship between smoking and COPD, probably influenced by genetic determinants poorly understood, is primarily a

Findings have proven smoking cessation disrupts the natural history of COPD, but there are authors who have more controversial opinions about it and assert that in many cases, inflammation persists despite smoking cessation. The perpetuation of inflammation may be

In the past, it was considered that only 15% of smokers were likely to develop COPD, when in fact it is known that this percentage is near 50% if they survive long enough. This

BTS 1997 FEV1/FVC <0.70 and FEV1<80% predicted

NICE 2004 FEV1/FVC <0.70 and FEV1<80% predicted

GOLD 2007 FEV1/FVC<0.70 postbronchodilator

ATS/ERS 2004 FEV1/FVC<0.70 postbronchodilator

Table 1. Spirometry criteria to COPD in some guidelines Society

dose-effect relationship as demonstrated in multiple studies.

related to other factors, bacterial colonization has been proposed.

these processes constitute the great chapter of what we call "disease" COPD.

**Society Year Criteria**

ECCS 1983 FEV1/VC or FEV1/ FVC<LLN

ECCS/ERS 1993 FEV1/VC or FEV1/ FVC<LLN

ATS 1987 FEV1/ FVC<0.75 ATS 1991 FEV1/ FVC<LLN

ATS/ERS 2005 FEV1/VC <LLN

NLHEP: National Lung Health Education Program.

processes vs COPD.

**2. Smoking COPD** 


Table 2. Causes of COPD syndrome

percentage of susceptibility increases if others methods, better than simple spirometry, have been used to detect COPD.

Although transfer of carbon monoxide (DLCO) and computed tomography (CT) with high resolution have demonstrated useful in early diagnosis of emphysema, they are underused.

Disadvantages for Chest CT and other imaging techniques are expensive and irradiation exposure.
