Elevated risk of lung cancer among people with AIDS

Chaturvedi, Anil Ka; Pfeiffer, Ruth Mb; Chang, Leonarda; Goedert, James Ja; Biggar, Robert Ja; Engels, Eric Aa

AIDS:
doi: 10.1097/QAD.0b013e3280118fca
Epidemiology and Social
Abstract

Background and objectives: Lung cancer is a common malignancy among people with AIDS (PWA). Lung cancer risk was compared between PWA and the general population and its relationship with immunosuppression was assessed. The likelihood that excess risk is explained by a high prevalence of smoking was also investigated.

Methods: Records on adolescent and adult PWA (N = 397 927) were linked with cancer registries in 11 US regions. Cancer risk was assessed for the period 60 months before to 60 months after AIDS onset, with specific emphasis on the period 4–27 months after onset. Observed incidence was compared with general population rates and rates from a lung cancer prediction model for smokers.

Results: Compared with the general population, lung cancer risk among PWA was elevated overall [n = 1489 cases; standardized incidence ratio (SIR), 3.8; 95% confidence interval (CI), 3.6–4.1] and in the 4–27 months after AIDS (n = 393 cases; SIR, 2.9; 95% CI, 2.6–3.2). In the 4–27 months after AIDS, risk was significantly elevated for all demographic subgroups, and was especially high among young PWA (SIRs for ages 15–29 years, 10.4; 30–39 years, 6.3; 40–49 years, 3.7). Lung cancers generally presented at an advanced stage. Risk was not associated with CD4 cell counts at AIDS (Ptrend = 0.36). Under plausible smoking assumptions, observed incidence was significantly higher than predicted among 40–49 and 50–59-year-old men with AIDS (observed/predicted = 5.03 and 1.43, respectively) and 40–49-year-old women with AIDS (observed/predicted = 1.88), but not among older PWA.

Conclusion: Lung cancer risk was substantially elevated among PWA. Smoking could not entirely account for the observed elevation, especially among younger adults, suggesting a role for additional co-factors.

Author Information

From the aViral Epidemiology Branch, USA

bBiostatistics Branch, Division of Cancer Epidemiology and Genetics. National Cancer Institute, Rockville, Maryland, USA.

Received 21 July, 2006

Revised 16 September, 2006

Accepted 4 October, 2006

Correspondence to Anil K. Chaturvedi, PhD, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, EPS 7072, Rockville, MD 20852, USA. e-mail: chaturva@mail.nih.gov

© 2007 Lippincott Williams & Wilkins, Inc.