Nicotine therapeutic benefits: Difference between revisions

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*However, smokers who develop HP have been shown to have a more severe course and higher mortality.

**Citation: Chandra D, Cherian SV. Hypersensitivity Pneumonitis. [Updated 2023 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499918/

===2007: [https://academic.oup.com/qjmed/article-abstract/100/4/233/2258683?redirectedFrom=fulltext Extrinsic allergic alveolitis: incidence and mortality in the general population]===

*We identified 271 incident cases of EAA (mean age at diagnosis 57 years, 51% male). Between 1991 and 2003, the incident rate for EAA was stable at ∼0.9 cases per 100 000 person-years. In comparison to the 1084 general population controls, patients with EAA were less likely to smoke (odds ratio 0.56, 95%CI 0.39–0.81), but had a marked increase in the risk of death (hazard ratio 2.98, 95%CI 2.05–4.33).

**Citation: M. Solaymani-Dodaran, J. West, C. Smith, R. Hubbard, Extrinsic allergic alveolitis: incidence and mortality in the general population, QJM: An International Journal of Medicine, Volume 100, Issue 4, April 2007, Pages 233–237, https://doi.org/10.1093/qjmed/hcm008

===2002: [https://www.atsjournals.org/doi/10.1164/rccm.200210-1154OC Inhibitory Effect of Nicotine on Experimental Hypersensitivity Pneumonitis In Vivo and In Vitro]===

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*Results of this study show that nicotine reduces the alveolar inflammatory response to S. rectivirgula antigen and affects some AM (stimulated with LPS or S. rectivirgula) functions in vitro. This influence could be, at least in part, responsible for the protection that smokers have against development of HP. Because nicotine is effective in the treatment of ulcerative colitis, it could also be of interest in the treatment of HP and other pulmonary inflammatory diseases.

**Citation: Blanchet MR, Israël-Assayag E, Cormier Y. Inhibitory effect of nicotine on experimental hypersensitivity pneumonitis in vivo and in vitro. Am J Respir Crit Care Med. 2004 Apr 15;169(8):903-9. doi: 10.1164/rccm.200210-1154OC. Epub 2003 Dec 30. PMID: 14701707.

===1977: [https://pmc.ncbi.nlm.nih.gov/articles/PMC470791/ Extrinsic allergic alveolitis: a disease commoner in non-smokers.]===

*In the literature of extrinsic allergic alveolitis non-smokers predominate in those papers in which smoking habits are recorded (Hapke et al., 1968; Schlueter et al., 1969; Schofield et al., 1976). Studies of the prevalence of precipitating antibodies against Micropolyspora faeni in farmers have shown that they are detected significantly more often in non-smokers than in smokers (Morgan et al., 1975).

**Citation: Warren CP. Extrinsic allergic alveolitis: a disease commoner in non-smokers. Thorax. 1977 Oct;32(5):567-9. doi: 10.1136/thx.32.5.567. PMID: 594937; PMCID: PMC470791.

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@@ Line 702: / Line 702: @@
 *However, smokers who develop HP have been shown to have a more severe course and higher mortality.
 **Citation: Chandra D, Cherian SV. Hypersensitivity Pneumonitis. [Updated 2023 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499918/
+===2007: [https://academic.oup.com/qjmed/article-abstract/100/4/233/2258683?redirectedFrom=fulltext Extrinsic allergic alveolitis: incidence and mortality in the general population]===
+*We identified 271 incident cases of EAA (mean age at diagnosis 57 years, 51% male). Between 1991 and 2003, the incident rate for EAA was stable at ∼0.9 cases per 100 000 person-years. In comparison to the 1084 general population controls, patients with EAA were less likely to smoke (odds ratio 0.56, 95%CI 0.39–0.81), but had a marked increase in the risk of death (hazard ratio 2.98, 95%CI 2.05–4.33).
+**Citation: M. Solaymani-Dodaran, J. West, C. Smith, R. Hubbard, Extrinsic allergic alveolitis: incidence and mortality in the general population, QJM: An International Journal of Medicine, Volume 100, Issue 4, April 2007, Pages 233–237, https://doi.org/10.1093/qjmed/hcm008
 ===2002: [https://www.atsjournals.org/doi/10.1164/rccm.200210-1154OC Inhibitory Effect of Nicotine on Experimental Hypersensitivity Pneumonitis In Vivo and In Vitro]===
@@ Line 707: / Line 711: @@
 *Results of this study show that nicotine reduces the alveolar inflammatory response to S. rectivirgula antigen and affects some AM (stimulated with LPS or S. rectivirgula) functions in vitro. This influence could be, at least in part, responsible for the protection that smokers have against development of HP. Because nicotine is effective in the treatment of ulcerative colitis, it could also be of interest in the treatment of HP and other pulmonary inflammatory diseases.
 **Citation: Blanchet MR, Israël-Assayag E, Cormier Y. Inhibitory effect of nicotine on experimental hypersensitivity pneumonitis in vivo and in vitro. Am J Respir Crit Care Med. 2004 Apr 15;169(8):903-9. doi: 10.1164/rccm.200210-1154OC. Epub 2003 Dec 30. PMID: 14701707.
+===1977: [https://pmc.ncbi.nlm.nih.gov/articles/PMC470791/ Extrinsic allergic alveolitis: a disease commoner in non-smokers.]===
+*In the literature of extrinsic allergic alveolitis non-smokers predominate in those papers in which smoking habits are recorded (Hapke et al., 1968; Schlueter et al., 1969; Schofield et al., 1976). Studies of the prevalence of precipitating antibodies against Micropolyspora faeni in farmers have shown that they are detected significantly more often in non-smokers than in smokers (Morgan et al., 1975).
+**Citation: Warren CP. Extrinsic allergic alveolitis: a disease commoner in non-smokers. Thorax. 1977 Oct;32(5):567-9. doi: 10.1136/thx.32.5.567. PMID: 594937; PMCID: PMC470791.
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