<P> A number of other factors are less closely linked to COPD . The risk is greater in those who are poor, although if this is due to poverty itself or other risk factors associated with poverty, such as air pollution and malnutrition, is not clear . Tentative evidence indicates those with asthma and airway hyperreactivity are at increased risk of COPD . Birth factors such as low birth weight may also play a role, as do a number of infectious diseases, including HIV / AIDS and tuberculosis . Respiratory infections such as pneumonia do not appear to increase the risk of COPD, at least in adults . </P> <P> An acute exacerbation (a sudden worsening of symptoms) is commonly triggered by infection or environmental pollutants, or sometimes by other factors such as improper use of medications . Infections appear to be the cause of 50 to 75% of cases, with bacteria in 30%, viruses in 23%, and both in 25% . Environmental pollutants include both poor indoor and outdoor air quality . Exposure to personal smoke and secondhand smoke increases the risk . Cold temperature may also play a role, with exacerbations occurring more commonly in winter . Those with more severe underlying disease have more frequent exacerbations: in mild disease 1.8 per year, moderate 2 to 3 per year, and severe 3.4 per year . Those with many exacerbations have a faster rate of deterioration of their lung function . Pulmonary emboli (blood clots in the lungs) can worsen symptoms in those with pre-existing COPD . Signs of PE in COPD include pleuritic chest pain and heart failure without signs of infection . </P> <P> COPD is a type of obstructive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and inability to breathe out fully (air trapping) exist . The poor airflow is the result of breakdown of lung tissue (known as emphysema) and small airways disease (known as obstructive bronchiolitis). The relative contributions of these two factors vary between people . Severe destruction of small airways can lead to the formation of large air pockets--known as bullae--that replace lung tissue . This form of disease is called bullous emphysema . </P> <P> COPD develops as a significant and chronic inflammatory response to inhaled irritants . Chronic bacterial infections may also add to this inflammatory state . The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells . Those who smoke additionally have Tc1 lymphocyte involvement and some people with COPD have eosinophil involvement similar to that in asthma . Part of this cell response is brought on by inflammatory mediators such as chemotactic factors . Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors . The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow, and finally, poor absorption and release of respiratory gases . General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood . </P>

British sign in english and type of disease