Environmental factors: Toxic fume inhalation, tobacco, dust, and aerosols[5]
Chronic Bronchitis: may be caused by smoking, air pollutants, occupational exposures, and genetic factors
Smoking
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.[6][7] Exposure to cigarette smoke is measured in pack-years, the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking.[8] The likelihood of developing COPD increases with age and cumulative smoke exposure. Almost all life-long smokers will develop COPD.[9]
Occupational Exposures
Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry, and chemicals such as cadmium, isocyanates, and fumes from welding, have been implicated in the development of airflow obstruction, even in nonsmokers.[10] 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.[11] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking.[12]
Air Pollution
Studies in many countries reveal that people who live in large cities have a higher rate of COPD compared to people who live in rural areas.[13] 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 performed. 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) suggest that 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.[14]
Genetics
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.[15] 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 approximately 2% of cases of COPD. In this condition, the body does not make enough of the protein alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by proteaseenzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.[16]
The cause of acute bronchitis depends on several factors including season of the year (winter and fall), vaccination level, age and immune status of the patient.
↑Jonsson JS, Sigurdsson JA, Kristinsson KG, Guthnadóttir M, Magnusson S (1997). "Acute bronchitis in adults. How close do we come to its aetiology in general practice?". Scand J Prim Health Care. 15 (3): 156–60. PMID9323784.
↑Boivin G, Abed Y, Pelletier G, Ruel L, Moisan D, Côté S, Peret TC, Erdman DD, Anderson LJ (2002). "Virological features and clinical manifestations associated with human metapneumovirus: a new paramyxovirus responsible for acute respiratory-tract infections in all age groups". J. Infect. Dis. 186 (9): 1330–4. doi:10.1086/344319. PMID12402203.
↑Louie JK, Hacker JK, Gonzales R, Mark J, Maselli JH, Yagi S, Drew WL (2005). "Characterization of viral agents causing acute respiratory infection in a San Francisco University Medical Center Clinic during the influenza season". Clin. Infect. Dis. 41 (6): 822–8. doi:10.1086/432800. PMID16107980.
↑Wenzel RP, Fowler AA (2006). "Clinical practice. Acute bronchitis". N. Engl. J. Med. 355 (20): 2125–30. doi:10.1056/NEJMcp061493. PMID17108344.
↑Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN0-07-146633-9.CS1 maint: Multiple names: authors list (link)
↑Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (2006). "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID16611654. Unknown parameter |month= ignored (help)CS1 maint: Multiple names: authors list (link)