title: HIV infection is associated with an increased risk for lung cancer, independent of smoking.
abstract: BACKGROUND
  Human immunodeficiency virus (HIV)-infected persons have an elevated risk for lung cancer, but whether the increase reflects solely their heavy tobacco use remains an open question.
  
  
  METHODS
  The Acquired Immunodeficiency Syndrome (AIDS) Link to the Intravenous Experience Study has prospectively observed a cohort of injection drug users in Baltimore, Maryland, since 1988, using biannual collection of clinical, laboratory, and behavioral data. Lung cancer deaths were identified through linkage with the National Death Index. Cox proportional hazards regression was used to examine the effect of HIV infection on lung cancer risk, controlling for smoking status, drug use, and clinical variables.
  
  
  RESULTS
  Among 2086 AIDS Link to the Intravenous Experience Study participants observed for 19,835 person-years, 27 lung cancer deaths were identified; 14 of the deaths were among HIV-infected persons. All but 1 (96%) of the patients with lung cancer were smokers, smoking a mean of 1.2 packs per day. Lung cancer mortality increased during the highly active antiretroviral therapy era, compared with the pre-highly active antiretroviral therapy period (mortality rate ratio, 4.7; 95% confidence interval, 1.7-16). After adjusting for age, sex, smoking status, and calendar period, HIV infection was associated with increased lung cancer risk (hazard ratio, 3.6; 95% confidence interval, 1.6-7.9). Preexisting lung disease, particularly noninfectious diseases and asthma, displayed trends for increased lung cancer risk. Illicit drug use was not associated with increased lung cancer risk. Among HIV-infected persons, smoking remained the major risk factor; CD4 cell count and HIV load were not strongly associated with increased lung cancer risk, and trends for increased risk with use of highly active antiretroviral therapy were not significant.
  
  
  CONCLUSIONS
  HIV infection is associated with significantly increased risk for developing lung cancer, independent of smoking status.
authors.affiliation: Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA. gkirk@jhsph.edu
authors.forename: Gregory D
authors.initials: GD
authors.lastname: Kirk
authors.forename: Christian
authors.initials: C
authors.lastname: Merlo
authors.forename: Peter
authors.initials: P
authors.lastname: O' Driscoll
authors.forename: Shruti H
authors.initials: SH
authors.lastname: Mehta
authors.forename: Noya
authors.initials: N
authors.lastname: Galai
authors.forename: David
authors.initials: D
authors.lastname: Vlahov
authors.forename: Jonathan
authors.initials: J
authors.lastname: Samet
authors.forename: Eric A
authors.initials: EA
authors.lastname: Engels
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D002277:Carcinoma / Q000453:epidemiology* / Q000209:etiology / Q000401:mortality; D015331:Cohort Studies; D005260:Female; D006678:HIV / Q000187:drug effects; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D008175:Lung Neoplasms / Q000453:epidemiology* / Q000209:etiology / Q000401:mortality; D008297:Male; D008396:Maryland / Q000453:epidemiology; D008875:Middle Aged; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects; D014030:Tobacco, Smokeless