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Official websites use. Share sensitive information only on official, secure websites. Corresponding author: Name: Dr. Wolfe St. The incidence of oropharyngeal and oral tongue cancers have increased over the last twenty years which parallels increased use of marijuana among individuals born after Pooled analysis of individual-level data from nine case-control studies from the U. Self-reported information on marijuana smoking, demographic, and behavioral factors was obtained from 1, oropharyngeal cases, oral tongue cases, and 7, controls. Compared with never marijuana smokers, ever marijuana smokers had an elevated risk of oropharyngeal adjusted odds ratio \[aOR\]: 1. The risk of oropharyngeal cancer remained elevated among never tobacco and alcohol users. Sensitivity analysis adjusting for potential confounding by HPV exposure attenuated the association of marijuana use with oropharyngeal cancer aOR: 0. These results suggest that the association of marijuana use with Head and Neck Carcinoma may differ by tumor site. The associations of marijuana use with oropharyngeal and oral tongue cancer are consistent with both possible pro- and anti-carcinogenic effects of cannabinoids. Additional work is needed to rule out various sources of bias, including residual confounding by HPV infection and misclassification of marijuana exposure. Head and neck squamous cell carcinomas, which include cancers of the oral cavity, oropharynx, and larynx, are the sixth most common cancers worldwide with an estimated annual burden of , deaths and , incident cases 1. In addition to traditional risk factors, such as tobacco and alcohol use, human papillomavirus HPV infection has recently been established as a major etiologic factor for a subset of Head and Neck Squamous Cell Carcinomas—cancers arising from the oropharynx, including the base of tongue, tonsil, and other parts of the pharynx 2. The incidence of a majority of head and neck cancer subsets i. While increases in oropharyngeal cancer incidence are attributed to increased acquisition of oral HPV through changes in sexual behaviors among recent birth cohorts 7 , the reasons underlying increasing oral tongue cancer incidence are largely unknown. Notably, HPV infection is not currently believed to play a major role in the etiology of oral tongue cancers 8. Marijuana use has significantly increased among individuals born after 9 , 10 , raising the hypothesis of a role of marijuana use as a risk factor for oropharyngeal and oral tongue cancer development A recent case-control study reported that marijuana use was strongly associated with increased risk of HPV-positive oropharyngeal cancer Conversely, a case-control study of HNSCC demonstrated an inverse association of marijuana use on cancers of the oral cavity However, epidemiologic studies that have examined the association of marijuana use with Head and Neck Squamous Cell Carcinomas have been inconsistent 14 — We therefore investigated the association of marijuana use with risk of oropharyngeal and oral tongue cancers in a large pooled analysis consisting of 9 case-control studies that were part of the International Head and Neck Cancer Epidemiology INHANCE consortium. Oropharyngeal cancer outcomes included tumors of the oropharynx C Oral tongue cancer included tumors of the dorsal surface C Characteristics of the individual studies included in the pooled data are presented in Supplemental Table 1. All studies matched controls to cases on age and sex. Anonymized data from individual studies were pooled; each data item was checked for illogical or missing values; inconsistencies were resolved by local site All studies included in this analysis collected data on lifetime marijuana use from cases and controls, including duration of use and frequency of use. For these later five studies the lifetime average frequency of marijuana use was calculated by weighting the frequency of each specific period by the duration of that period relative to the total years of marijuana use. Four out of the nine studies Latin America, Tampa, Los Angeles, and North Carolina — defined marijuana use specifically as smoking marijuana whereas the remaining five studies defined marijuana use in any form. All studies collected information on tobacco use including ever vs. In six out of nine studies Seattle — \[Schwartz\], Seattle-LEO \[Vaughan\], North Carolina — , Los Angeles, Houston, and Boston ever smoking cigarettes was defined as anyone smoking at least cigarettes in their lifetime. For each study, pack-years was directly calculated by multiplying the number of cigarettes smoked by the age of initiation and cessation of smoking i. Cigar and Pipe use was defined as ever vs. One study Boston defined ever pipe use as ever smoking 12 ounces of tobacco and cigar use as smoking one cigar per week for at least one year. Alcohol consumption was defined as ever vs. Ever use of alcohol was defined as either greater than four or more drinks in a year Seattle — \[Schwartz\] and Baltimore \[HOTSPOT\] , greater than or equal to one drink per week for greater than or equal to one year Tampa and Houston , greater than either one Latin America or four drinks per month North Carolina — , or ever consumed in a lifetime Boston. Total alcohol consumption i. Total alcohol consumption was treated as a continuous variable in all analyses. Given that all the case-control studies included in this analysis utilize incident cases derived from open and dynamic populations, the odds ratio estimated in this study approximates the relative risk. To control for heterogeneity in effects across study, study indicator was included as a random effects intercept term in all regression models. We tested for heterogeneity across study using a log likelihood ratio test for the goodnesss of fit of the model with and without a product term for marijuana use and study. The Tampa study was excluded from analyses on duration and frequency of marijuana use because there were insufficient cases and controls in each category of marijuana use. For subjects with missing data on education level 82 cases and controls , multiple imputation analysis was performed. Analysis excluding individuals with missing educational status demonstrated similar associations of marijuana use with cancer data not shown. Tobacco and alcohol use is a recognized risk factor for both oropharyngeal and oral tongue cancers and is strongly correlated with marijuana use 23 , In addition, the additive interaction of tobacco and alcohol use on the association of marijuana use with cancer outcomes was also tested through estimation of the Relative Excess Risk due to Interaction RERI using a generalized linear model Because sexual behaviors which increase the likelihood of HPV exposure and marijuana use could be highly correlated, we conducted two separate analyses to evaluate the potential confounding effects of HPV on the observed associations of marijuana use with risk of oropharyngeal cancer. First, analyses were stratified by HPV 16 L1 serologic status. Second, given the absence of either detailed information on oral sexual behaviors or oral HPV status in a majority of studies, we utilized external information to indirectly adjust the marijuana-oropharyngeal cancer association for confounding by HPV using the methods described by Steenland and Greenland 26 See Statistical Appendix. The observed marijuana-oropharyngeal cancer association was then divided by the bias factor to estimate an adjusted OR which accounted for confounding by HPV. The studies included in this analysis primarily collected information on marijuana use using interviewer or self-administered questionnaires. Therefore, differential misclassification of the reporting of marijuana use between cancer cases and controls is a possibility. To estimate the potential effect of reporting bias, simple probabilistic sensitivity analyses were conducted based on methods previously described 29 , Sensitivity and specificity estimates used in this analysis were derived from the literature on misreporting of marijuana use in a variety of populations 31 , There were 1, oropharyngeal cancer cases from nine studies with the majority from Houston Compared to controls, oropharyngeal cancer cases were more likely to be male Oropharyngeal cancer cases were more likely than controls to ever use tobacco products ICD After adjusting for demographic factors, tobacco and alcohol use, the risk of oropharyngeal cancer was significantly elevated among ever marijuana users aOR: 1. However, there was significant heterogeneity of these associations by study-site for ever marijuana use Figure 1. Models adjusted for age continuous , sex, race white vs. Hispanic vs. Some high school vs. High school graduate vs. Technical school, some college vs. Study was included as a random intercept. The positive association of marijuana use and oropharyngeal cancer could potentially be explained by increased consumption of tobacco and alcohol, known risk factors for oropharyngeal cancer, among marijuana users as compared to non-users. HPV 16 L1 antibody status was available in 4 of the 9 studies Boston, Houston, Latin America, and Seattle \[Schwartz\] making up oropharyngeal cancer cases and 2, controls. The adjusted association of marijuana use with oropharyngeal cancer prior to considering HPV antibody status in these four studies was null aOR: 0. Among individuals seronegative for HPV16 L1 antibodies, ever marijuana use was associated with significantly decreased risk of oropharyngeal cancer aOR: 0. In contrast, among HPV16 seropositive individuals ever marijuana use was positively, but not significantly associated with oropharyngeal cancer aOR: 1. On an additive scale, the relative odds was significant higher among HPV 16 seropositive individuals only among ever marijuana users RERI: 2. We then performed indirect adjustment of the OR for the association of ever marijuana use and oropharyngeal cancer diagnosis for confounding by oral HPV infection status Table 4. These analyses indicated that, under plausible assumptions of the difference in oral HPV prevalence by marijuana use status and the association of HPV infection with oropharyngeal cancer risk, confounding by oral HPV infection could potentially explain the observed association of marijuana use with oropharyngeal cancer risk OR indirect adjustment : 0. Assuming an odds ratio of JAMA Sensitivity analyses that corrected for differential misclassification in which there was greater under-reporting of marijuana exposure reduced sensitivity among cases strengthened the association with oropharyngeal cancer, whereas greater under-reporting among controls attenuated the association Supplemental Table 4. In contrast, correction for non-differential misclassification resulted in a slight strengthening of the association of marijuana with oropharyngeal cancer. Lastly, analyses that excluded both base of tongue and tonsil cancers, subsets of oropharynx cancers that are strongly associated with HPV infection, resulted in an attenuation of the odds ratios and loss of statistical significance OR ever vs. There were oral tongue cancer cases from five studies with the majority from Houston As compared to controls, oral tongue cancer cases were more likely to be female Oral tongue cancer cases were more likely to ever use of tobacco products After adjustment for demographic factors, tobacco and alcohol use, the risk of oral tongue cancer was significantly reduced i. These associations remained significant when these exposure metrics were treated as continuous on either an absolute or logarithmic scale or defined based on the means of the each category for each variable Supplemental Table 2. Sensitivity analyses that corrected for differential misclassification in which there was greater under-reporting of marijuana exposure reduced sensitivity among cases attenuated the association with oral tongue cancer whereas greater under-reporting among controls strengthened the association Supplemental Table 4. Correction for non-differential misclassification resulted in a slight attenuation of the association of marijuana with oral tongue cancer. The rising incidence of oropharyngeal and oral tongue cancers over the last twenty years has paralleled trends of increasing use of marijuana among individuals born after 4 , 11 , Therefore, we initially hypothesized that marijuana use could, in part, have contributed to the rising incidence of these cancers. Using pooled data from 9 case-control studies that contributed to the INHANCE consortium, we found evidence of a possible positive association of marijuana use with oropharyngeal cancer and a negative association with oral tongue cancer.. Our findings of a positive association of marijuana use and oropharyngeal cancer while in agreement with two prior studies 12 , 20 contrasts with findings from five studies that showed no association 14 — 16 , 18 , The possibility of a true association of marijuana use with oropharyngeal cancer risk was supported in the present study by the consistency of the observed associations with multiple measures of marijuana use including ever use, duration and frequency of use and was unaffected across strata of smoking and drinking. However, the inconsistent association across studies in this pooled analysis combined with an attenuation in the association after adjustment for smoking and drinking make the effect of residual and unmeasured confounding highly plausible. Differential exposure to HPV infection among marijuana smokers as compared to non-smokers could be one source of potential confounding to explain the association of marijuana use with oropharyngeal cancer, as marijuana users engage more frequently in risky sexual behaviors leading to higher rates of sexually transmitted infections 34 , We had serologic information on HPV 16 from four studies. Unfortunately, the association of marijuana use and oropharyngeal cancer among these four studies was not representative of all the studies included in the pooled analysis, although stratified analyses among these four studies by HPV 16 L1 serostatus revealed a modest positive association of ever and long duration marijuana use oropharyngeal cancer among seropositive individuals. Therefore, we attempted to estimate the potential confounding effect of HPV on this association using plausible estimates of the association of HPV infection on oropharyngeal cancer risk as well as differences in oral HPV prevalence by marijuana usage. This approach revealed a substantial and nearly complete attenuation of the association of marijuana use with oropharyngeal cancer risk. These data suggest that the positive association of marijuana use and oropharyngeal cancer may be dependent on exposure to HPV. In lieu of more definitive information on tumor HPV infection status among cases and oral HPV infection status among cases and controls, the role of marijuana use as a potential risk factor in oropharyngeal cancer cannot be determined. We observed that marijuana use was strongly inversely associated with oral tongue cancer specifically, which is similar to what has been reported previously among oral cavity cancers in general 9 , 13 , This association remained robust across all marijuana use metrics, was strengthened after adjustment for tobacco and alcohol use, and was consistent across the five studies that had sufficient numbers of cases. Given that a very small fraction of oral cavity cancers are attributed to HPV 8 , it is not surprising that marijuana use remained strongly inversely associated with oral tongue cancer even after adjustment for HPV data not shown. Therefore, this association may reflect a true inverse association of marijuana use on oral tongue cancer. This cannabinoid functions primarily through engagement of specific cell surface receptors CB1, expressed on a range of cell types 36 and CB2 present primarily on a variety of immune cells, particularly those found in the human tonsil Engagement of these receptors on immune cells has been shown to suppress pro-inflammatory cytokine production and enhance anti-inflammatory cytokine production 38 , 39 leading to reduced host immune responses to infectious agents as well as suppression of anti-tumor immunity 40 — As a result, this cannabinoid has been investigated as a potential therapeutic agent in the treatment of glioma, breast and prostate cancers 46 , Interestingly, the anti-tumor effect of this cannabinoid is mediated through the same CB1 and CB2 receptors. This may help explain the differing associations of marijuana smoke with oropharyngeal and oral tongue cancers. Lastly, the presence of other carcinogenic compounds present in marijuana smoke may also play a role in driving the association. Differences in the measurement of marijuana use, study sample recruitment, and measurement of demographic and other risk factors for Head and Neck Squamous Cell Carcinoma across the studies included in this analysis may have contributed to the heterogeneity observed across study sites. However, this heterogeneity was observed only for oropharyngeal cancer and not oral tongue cancer. Nevertheless, we included in our logistic regression models a random-effects term for each study to account for the heterogeneity of the association of marijuana use with oropharyngeal cancer outcomes. Furthermore, we acknowledge the possibility that misclassification in the measurement of marijuana use between cases and controls may explain some of these findings. Misclassification of marijuana exposure due to the use of self-administered or interviewer administered questionnaires has been suggested previously to be significant source of error in the observed association with head and neck cancers 9. Sensitivity analyses that modeled the effects of differential and non-differential misclassification of marijuana exposure demonstrated that correction for misclassification did alter the strength of the association with each cancer outcome Supplementary table 4. Therefore, it cannot be ruled out that either differential or non-differential misreporting of marijuana exposure may explain the observed associations of marijuana use with oropharynx and oral tongue cancers. This pooled analysis of nine case-control studies conducted in the US and Latin America is the largest to date to investigate the relationship of marijuana use specifically with cancers of the oropharynx and oral tongue. The differing associations of marijuana use on oropharyngeal and oral tongue cancers observed in this study provides some epidemiologic support for the biological effect of cannabinoids as both a pro- and anti-carcinogenic agent. However, given the strong association of HPV on orpoharyngeal cancer not measured in this study, the modest attenuated effect of marijuana on these caners may well be explained by confounding by HPV. Additional studies focusing on cannabinoid receptor expression profiles and downstream effector functions across cell types involved in tumorigenesis of these cancers may yield important etiologic information as to the role of marijuana on head and neck cancer risk. This section collects any data citations, data availability statements, or supplementary materials included in this article. As a library, NLM provides access to scientific literature. Cancer Epidemiol Biomarkers Prev. Published in final edited form as: Cancer Epidemiol Biomarkers Prev. 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Issue date Jan. PMC Copyright notice. The publisher's version of this article is available at Cancer Epidemiol Biomarkers Prev. Open in a new tab. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Seattle a. Seattle-LEO b. Drink-Years of alcohol consumption.

Muscat buy marijuana