Marijuana Smoking and the Risk of Head and Neck Cancer: Pooled Analysis in the INHANCE Consortium


Autoria(s): BERTHILLER, Julien; LEE, Yuan-Chin Amy; BOFFETTA, Paolo; WEI, Qingyi; STURGIS, Erich M.; GREENLAND, Sander; MORGENSTERN, Hal; ZHANG, Zuo-Feng; LAZARUS, Philip; MUSCAT, Joshua; CHEN, Chu; SCHWARTZ, Stephen M.; ELUF NETO, Jose; WUNSCH FILHO, Victor; KOIFMAN, Sergio; CURADO, Maria Paula; MATOS, Elena; FERNANDEZ, Leticia; MENEZES, Ana; DAUDT, Alexander W.; FERRO, Gilles; BRENNAN, Paul; HASHIBE, Mia
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

19/10/2012

19/10/2012

2009

Resumo

Background: Marijuana contains carcinogens similar to tobacco smoke and has been suggested by relatively small studies to increase the risk of head and neck cancer (HNC). Because tobacco is a major risk factor for HNC, large studies with substantial numbers of never tobacco users could help to clarify whether marijuana smoking is independently associated with HNC risk. Methods: We pooled self-reported interview data on marijuana smoking and known HNC risk factors on 4,029 HNC cases and 5,015 controls from five case-control studies within the INHANCE Consortium. Subanalyses were conducted among never tobacco users (493 cases and 1,813 controls) and among individuals who did not consume alcohol or smoke tobacco (237 cases and 887 controls). Results: The risk of HNC was not elevated by ever marijuana smoking [odds ratio (OR), 0.88; 95% confidence intervals (95% Cl), 0.67-1.16], and there was no increasing risk associated with increasing frequency, duration, or cumulative consumption of marijuana smoking. An increased risk of HNC associated with marijuana use was not detected among never tobacco users (OR, 0.93; 95% Cl, 0.63-1.37; three studies) nor among individuals who did not drink alcohol and smoke tobacco (OR, 1.06; 95% Cl, 0.47-2.38; two studies). Conclusion: Our results are consistent with the notion that infrequent marijuana smoking does not confer a risk of these malignancies. Nonetheless, because the prevalence of frequent marijuana smoking was low in most of the contributing studies, we could not rule out a moderately increased risk, particularly among subgroups without exposure to tobacco and alcohol. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1544-51)

NIH, National Cancer Institute[R03CA113157]

NIH, National Cancer Institute[R01CA048896]

NIH, National Cancer Institute[R01DE012609]

NIH, National Cancer Institute[P01CA068384]

NIH, National Cancer Institute[K07CA104231]

NIH, National Cancer Institute[P50CA90388]

NIH, National Cancer Institute[R01DA11386]

NIH, National Cancer Institute[R03CA77954]

NIH, National Cancer Institute[T32CA09142]

NIH, National Cancer Institute[U01CA96134]

NIH, National Cancer Institute[R21ES011667]

NIH, National Cancer Institute[R01ES11740]

NIH, National Cancer Institute[R01CA100264]

University of California at Los Angeles Jonsson Comprehensive Cancer Center

Fondo para la Investigacion Cientifica y Tecnologica (FONCyT) (Argentina)

IMIM (Barcelona)

FAPESP Fundacao de Amparo a Pesquisa no Estado de Sao Paulo[01/01768-2]

European Commission[TC18-CT97-0222]

Identificador

CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, v.18, n.5, p.1544-1551, 2009

1055-9965

http://producao.usp.br/handle/BDPI/22428

10.1158/1055-9965.EPI-08-0845

http://dx.doi.org/10.1158/1055-9965.EPI-08-0845

Idioma(s)

eng

Publicador

AMER ASSOC CANCER RESEARCH

Relação

Cancer Epidemiology Biomarkers & Prevention

Direitos

restrictedAccess

Copyright AMER ASSOC CANCER RESEARCH

Palavras-Chave #SQUAMOUS-CELL CARCINOMA #HUMAN-PAPILLOMAVIRUS #CANNABIS USE #TOBACCO #CIGARETTE #TAR #Oncology #Public, Environmental & Occupational Health
Tipo

article

original article

publishedVersion