Naghash Mahdokht, Calafat Antonia M, Poustchi Hossein, Wang Lanqing, Roshandel Gholamreza, Botelho Julianne Cook, Kamangar Farin, Boffetta Paolo, Abnet Christian C, Freedman Neal D, Malekzadeh Reza, Etemadi Arash
Tehran University of Medical Sciences, Tehran, Iran.
Centers for Disease Control and Prevention, Atlanta, GA, United States.
Cancer Epidemiol Biomarkers Prev. 2025 Jun 5. doi: 10.1158/1055-9965.EPI-25-0126.
Opium consumption is carcinogenic, but the impact of route of use (smoking vs. ingestion) on exposure to potential proposed carcinogens is understudied.
As a nested study within Golestan Cohort Study, we gathered comprehensive histories of teriak (raw opium), shireh (refined opium sap), and tobacco use, by validated questionnaires and selected 100 long-term opium users (50 exclusively ingesting and 50 exclusively smoking), 15 cigarette smokers, and a reference sample using neither. We analyzed spot urine samples for seven hydroxy-polycyclic aromatic hydrocarbons (OH-PAH) and cotinine. PAH biomarker concentrations were creatinine-corrected to account for urinary dilution and adjusted for demographic factors and opium use patterns using multivariable linear regression models to evaluate associations between the route of opium use and PAH biomarker concentrations.
After excluding opium users who reported no tobacco use but had discordant cotinine concentrations, PAH biomarker concentrations were significantly higher in opium users than the reference sample. Smoking opium was associated with substantially elevated PAH biomarker concentrations compared with ingestion, particularly for Σ2,3-hydroxyphenanthrene (5-fold increase) and 3-hydroxyfluorene (4.5-fold increase). For Σ2,3-hydroxyphenanthrene, concentrations exceeded those of cigarette smokers. No difference was observed between teriak and shireh use. Only among opium smokers, PAH biomarker concentrations decreased by time since last use but remained consistently higher than the reference sample.
Opium consumption, regardless of type and route, exposes individuals to PAHs, with greater concentrations of select PAH biomarkers observed for smoking compared to ingestion.
Considering the route of opium use in exposure and cancer risk assessments is crucial.
吸食鸦片具有致癌性,但使用途径(吸烟与摄入)对潜在致癌物暴露的影响尚未得到充分研究。
作为戈勒斯坦队列研究中的一项嵌套研究,我们通过经过验证的问卷收集了关于鸦片膏(生鸦片)、鸦片汁(精制鸦片液)和烟草使用的全面历史信息,并选择了100名长期鸦片使用者(50名仅摄入鸦片者和50名仅吸食鸦片者)、15名吸烟者以及一个既不使用鸦片也不吸烟的对照样本。我们分析了即时尿样中的七种羟基多环芳烃(OH-PAH)和可替宁。PAH生物标志物浓度经肌酐校正以考虑尿液稀释情况,并使用多变量线性回归模型对人口统计学因素和鸦片使用模式进行调整,以评估鸦片使用途径与PAH生物标志物浓度之间的关联。
在排除那些报告不使用烟草但可替宁浓度不一致的鸦片使用者后,鸦片使用者的PAH生物标志物浓度显著高于对照样本。与摄入鸦片相比,吸食鸦片与PAH生物标志物浓度大幅升高相关,尤其是对于Σ2,3-羟基菲(增加5倍)和3-羟基芴(增加4.5倍)。对于Σ2,3-羟基菲,其浓度超过了吸烟者。在使用鸦片膏和鸦片汁之间未观察到差异。仅在吸食鸦片者中,PAH生物标志物浓度自上次使用后随时间下降,但仍始终高于对照样本。
无论鸦片的类型和使用途径如何,吸食鸦片都会使个体暴露于多环芳烃中,与摄入相比,吸食鸦片时某些PAH生物标志物的浓度更高。
在暴露和癌症风险评估中考虑鸦片的使用途径至关重要。