Chronic bronchitis risk factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Overview

Common risk factors in the development of chronic bronchitis include cigarette smoking, air pollution, genetic factors, increasing age, male gender, allergy, and repeated airway infections.

Risk Factors

The most potent risk factor for development of chronic bronchitis is smoking. Other risk factors include: environmental exposures, genetic susceptibility, air pollution and respiratory infections.

Cigarette smoking

Genetic factors can influence the severity of smoking effect on airways.^[1]^[2]

Occupational exposure

Dusts, gases, fumes, or organic antigens can contribute to increased airways responsiveness.^[3]^[2]^[4]

Genetic factors

Alpha-1 antitrypsin (AAT) deficiency is the leading genetic risk factor for developing chronic bronchitis.^[3]^[2]^[5] Some novel risk factors such as, small nucleotide polymorphisms and gene clusters, are assumed to be involved in developing chronic airway diseases.^[6]

Developmentally abnormal lungs

Frequent childhood infection may cause scarring of lungs, decrease elasticity, thereby increasing risk for COPD.

References

↑ PIERCE JA, HOCOTT JB, EBERT RV (1961). “The collagen and elastin content of the lung in emphysema”. Ann. Intern. Med. 55: 210–22. PMID 13735539.
↑ ^2.0 ^2.1 ^2.2 Raherison C, Girodet PO (2009). “Epidemiology of COPD”. Eur Respir Rev. 18 (114): 213–21. doi:10.1183/09059180.00003609. PMID 20956146.
↑ ^3.0 ^3.1 Mehta GR, Mohammed R, Sarfraz S, Khan T, Ahmed K, Villareal M, Martinez D, Iskander J, Mohammed R (2016). “Chronic obstructive pulmonary disease: A guide for the primary care physician”. Dis Mon. 62 (6): 164–87. doi:10.1016/j.disamonth.2016.03.002. PMID 27087562.
↑ Jeffery PK (2000). “Comparison of the structural and inflammatory features of COPD and asthma. Giles F. Filley Lecture”. Chest. 117 (5 Suppl 1): 251S–60S. PMID 10843939.
↑ Gadek JE, Fells GA, Crystal RG (1979). “Cigarette smoking induces functional antiprotease deficiency in the lower respiratory tract of humans”. Science. 206 (4424): 1315–6. PMID 316188.
↑ Han MK, Agusti A, Calverley PM, Celli BR, Criner G, Curtis JL, Fabbri LM, Goldin JG, Jones PW, Macnee W, Make BJ, Rabe KF, Rennard SI, Sciurba FC, Silverman EK, Vestbo J, Washko GR, Wouters EF, Martinez FJ (2010). “Chronic obstructive pulmonary disease phenotypes: the future of COPD”. Am. J. Respir. Crit. Care Med. 182 (5): 598–604. doi:10.1164/rccm.200912-1843CC. PMID 20522794.

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[pmid13735539-1] PIERCE JA, HOCOTT JB, EBERT RV (1961). “The collagen and elastin content of the lung in emphysema”. Ann. Intern. Med. 55: 210–22. PMID 13735539.

[pmid20956146-2] 2.0 ^2.1 ^2.2 Raherison C, Girodet PO (2009). “Epidemiology of COPD”. Eur Respir Rev. 18 (114): 213–21. doi:10.1183/09059180.00003609. PMID 20956146.

[pmid27087562-3] 3.0 ^3.1 Mehta GR, Mohammed R, Sarfraz S, Khan T, Ahmed K, Villareal M, Martinez D, Iskander J, Mohammed R (2016). “Chronic obstructive pulmonary disease: A guide for the primary care physician”. Dis Mon. 62 (6): 164–87. doi:10.1016/j.disamonth.2016.03.002. PMID 27087562.

[pmid10843939-4] Jeffery PK (2000). “Comparison of the structural and inflammatory features of COPD and asthma. Giles F. Filley Lecture”. Chest. 117 (5 Suppl 1): 251S–60S. PMID 10843939.

[pmid316188-5] Gadek JE, Fells GA, Crystal RG (1979). “Cigarette smoking induces functional antiprotease deficiency in the lower respiratory tract of humans”. Science. 206 (4424): 1315–6. PMID 316188.

[pmid20522794-6] Han MK, Agusti A, Calverley PM, Celli BR, Criner G, Curtis JL, Fabbri LM, Goldin JG, Jones PW, Macnee W, Make BJ, Rabe KF, Rennard SI, Sciurba FC, Silverman EK, Vestbo J, Washko GR, Wouters EF, Martinez FJ (2010). “Chronic obstructive pulmonary disease phenotypes: the future of COPD”. Am. J. Respir. Crit. Care Med. 182 (5): 598–604. doi:10.1164/rccm.200912-1843CC. PMID 20522794.

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