Chronic obstructive pulmonary disease causes

Chronic obstructive pulmonary disease (COPD), is most often due to tobacco smoking; but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites. In the United States, tobacco use is a key factor in the development and progression of COPD, but asthma, exposure to air pollutants in the home and workplace, genetic factors, and respiratory infections also play a role. In the developing world, indoor air quality is thought to play a larger role in the development and progression of COPD than it does in the United States.

The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.^[1][2] Exposure to cigarette smoke is measured in pack-years,^[3] the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extra-pulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand.^[4]

Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, iso-cyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in non-smokers.^[5] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.^[6] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.^[7]

Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas.^[8] Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women.^[9]

Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.^[10] The genetic differences that make some peoples’ lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.^[11]

There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking.^[12] Many individuals with COPD who have stopped smoking have active inflammation in the lungs.^[13] The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.^[13] This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.^[13][14][15]

A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.^[7] It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.

• Abnormal activity of tissue inhibitors of metalloproteinase (TIMP-1)
• Age
• Alpha-1-antitrypsin deficiency
• Asthma (controversial)
• Atopy
• Bronchopulmonary dysplasia
• Cadmium
• Cigarette smoking
• Decreased function of microsomal epoxide hydrolase
• Decreased function of microsomal epoxide hydrolase
• Decreased glutathione levels
• Decreased glutathione S-transferase P1 activity
• Deficiency of antioxidant vitamins
• Environmental air pollution such as coal, grain
• Excess elastase
• First-degree relatives severe premature COPD
• Fumes from welding
• Gender (controversial)
• Genetic influences
• Heredity
• History of childhood respiratory infections
• Increased airway responsiveness
• Increased Matrix metalloproteinases (MMP)-2 (gelatinase A)
• Increased Matrix metalloproteinases (MMP)-8 (Collagenase 2)]]
• Increased Matrix metalloproteinases ( MMP)-9 (gelatinase B)]]
• Isocyanates
• Low socioeconomic status
• Metalloproteinase dysregulation
• Occupation pollution exposure to dusts and chemicals
• Pulmonary tuberculosis
• Second hand smoking
• Several gene polymorphisms of Transforming growth factor beta 1
• Several SNPs (Several gene polymorphisms) of the leptin receptor (LEPR) gene
• Silicosis
• Sulfur dioxide
• Tumor necrosis factor-alpha (TNF-a) gene polymorphisms
• Use of biomass fuels for cooking
• Vitamin C deficiency
• Vitamin E deficiency
• Zanamivir

http://www.cdc.gov/copd/index.htm

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