Carcinogen Biomarkers Research Articles

Dietary creatine and carcinogenic biomarkers in adult population.

Background: Several reports suggest potential cytotoxic effects of creatine, possibly due to its role in facilitating the formation of food-borne chemical carcinogenic compounds. Aim: This cross-sectional study aims to investigate the relationship between creatine consumption and various carcinogenic biomarkers in blood and urine among individuals aged 18 years and older, utilizing data from the 2013-2014 National Health and Nutrition Examination Survey (NHANES). Methods: Daily creatine intake was assessed using the Dietary Data databases, which were compiled from individual in-person 24-h food recall interviews. The concentrations of carcinogenic compounds (heterocyclic amines, acrylamide, and formaldehyde) were extracted from NHANES 2013-2014 Laboratory Data database. Results: The final analysis included 1763 adult respondents, of whom 907 (51.4%) were female. The mean daily creatine intake was 0.83 ± 0.77 grams (95% CI, from 0.80 to 0.87). Regression analysis revealed no significant relationship between daily creatine intake and most carcinogenic biomarkers, except for a significant correlation (Model 1) between creatine intake and acrylamide levels (B = -3.999, ß = -0.088, p = 0.05). Model 2 (demographics) confirmed a significant relationship between daily creatine intake and circulating acrylamide (B = -3.490, ß = -0.077, p = 0.02), as well as for blood levels of glycidamide (B = -2.992, ß = -0.068, p = 0.05) and urinary 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (B = 0.190, ß = 0.088, p = 0.03). However, no correlation between creatine consumption and any carcinogenic biomarkers remained significant after adjusting for nutritional factors (Model 3) (p > 0.05). Conclusion: In conclusion, the consumption of dietary creatine may be considered safe and not associated with increased levels of above carcinogens in the general population.

Understanding the mediation effects of cigarettes per day on time to first cigarette and carcinogen biomarkers: National Health and Nutrition Examination Survey 2015-2016.

Previous research indicates that cigarette smokers with a time to first cigarette (TTFC) of less than 30 minutes after waking up had significantly higher levels of carcinogen biomarkers compared to those with a TTFC of more than 30 minutes. The mediation (potential mediator: cigarettes smoked per day) between TTFC and carcinogen biomarkers, remains unclear and has yet to be established. Multivariable linear regression models were used to estimate adjusted geometric means (GMs) and ratios of GMs for urine biomarkers of VOCs by smokers' TTFC status (≤30 vs >30 min). Further, data from the NHANES 2015-2016 special sample were analyzed to assess the mediation between TTFC (exposure) and carcinogen biomarkers, including urine metabolites of polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs), and cadmium. Cigarette smokers with a short TTFC (≤30 min) presented significantly higher concentrations in 8 out of 17 urine metabolites of VOCs examined compared to smokers with TTFC >30 min. The association between exposure and carcinogen biomarkers was not mediated by CPD. Cigarette smokers with a short TTFC (≤30 min) had significantly higher levels in VOCs, PAHs, and cadmium, but the association was not mediated by cigarettes smoked per day.

Recent studies on metabolism, DNA adducts, and biomarkers of tobacco carcinogens

Recent studies on metabolism, DNA adducts, and biomarkers of tobacco carcinogens

Pan-cancer characterization of ncRNA synergistic competition uncovers potential carcinogenic biomarkers.

Non-coding RNAs (ncRNAs) act as important modulators of gene expression and they have been confirmed to play critical roles in the physiology and development of malignant tumors. Understanding the synergism of multiple ncRNAs in competing endogenous RNA (ceRNA) regulation can provide important insights into the mechanisms of malignant tumors caused by ncRNA regulation. In this work, we present a framework, SCOM, for identifying ncRNA synergistic competition. We systematically construct the landscape of ncRNA synergistic competition across 31 malignant tumors, and reveal that malignant tumors tend to share hub ncRNAs rather than the ncRNA interactions involved in the synergistic competition. In addition, the synergistic competition ncRNAs (i.e. ncRNAs involved in the synergistic competition) are likely to be involved in drug resistance, contribute to distinguishing molecular subtypes of malignant tumors, and participate in immune regulation. Furthermore, SCOM can help to infer ncRNA synergistic competition across malignant tumors and uncover potential diagnostic and prognostic biomarkers of malignant tumors. Altogether, the SCOM framework (https://github.com/zhangjunpeng411/SCOM/) and the resulting web-based database SCOMdb (https://comblab.cn/SCOMdb/) serve as a useful resource for exploring ncRNA regulation and to accelerate the identification of carcinogenic biomarkers.

Alteration of genome-wide DNA methylation in non-uranium miners induced by high level radon exposure.

In China, according to statistics about underground non-uranium mine radon levels, 15% exceed the national standard intervention level of 1000Bq/m3, and some mines may exceed 10,000Bq/m3. The relationship between radon exposure in underground miners and lung cancer has already been established, but the mechanisms and biological processes underlying it are poorly understood. In order to identify the genome-wide DNA methylation profile associated with long-term radon exposure, we performed the Infinium Human Methylation 850K BeadChip measurement in whole blood samples obtained from 15 underground non-uranium miners and 10 matched aboveground control workers. Radon concentrations in the air of workplaces and living environments were measured by CR-39 radon detectors, and annual effective doses were calculated using the detection data. Under the high radon concentration with an average value of 12,700Bq·m-3, a total of 165 significant differentially methylated positions (127 hypermethylated sites and 38 hypomethylated sites) annotated to 71 genes were identified in underground miners (|Δβ| ≥ 0.10, p<0.05), and the average DNA methylation level of 165 DMPs was significantly higher than that of the control workers. Most DMPs were found on chromosome 1, and approximately one-quarter of them were located in genomic promoter regions. Through bioinformatics analysis and pyrosequencing validation, five candidate genes differentially methylated by radon, including TIMP2, EMP2, CPT1B, AMD1 and SLC43A2 were identified. GO and KEGG analysis implicated that long term radon exposure could induce the lung cancer related biological processes such as cell adhesion and cellular polarity maintenance. Our study provides evidence for the alterations of genome-wide DNA methylation profiles induced by long-term high level radon exposure, and new insights into searching for carcinogenic biomarkers of high radon exposure in future studies.

Highly sensitive detection of carcinogenic biomarkers MCF-7 using graphene oxide-based SPR biosensor

In this paper, we propose the enhance sensing performance-based surface plasmon resonance (SPR) biosensor using silver (Ag), silicon nitride (Si3N4), and graphene oxide (GO). Here in, we describe the theoretical analysis of SPR biosensors for the detection of six types of cancer biomarkers (HeLa, Jurkat, PC12, MDA-MB-231, and MCF-7) using the transfer matrix method (TMM) and a comparative study is made on the basis of their sensing performances (sensitivity, detection accuracy, quality factor). We conclude that enhancement in sensing parameters for different cancer cells. Also, we performed numerical analysis using the finite element method (FEM). This biosensor shows better performance parameters for different cancer cells. Our biosensor shows good performance for different types of proposed cancer biomarkers. It is 172 deg./RIU (skin cancer), 199 deg./RIU (cervical cancer), 205 deg./RIU (blood cancer), 225 deg./RIU (adrenal cancer), 245 deg./RIU (breast cancer (type-1)), and 259 deg./RIU (breast cancer (type-II)), respectively. Our proposed biosensor shows better sensing performances in comparison to the other reported works. It may potential applications for different types of cancerous cell with enhanced performances.

Thymoquinone ameliorates acrylamide-induced reproductive toxicity in female rats: An experimental study.

Acrylamide (AA) is a carcinogenic compound that causes severe reproductive impairments and represents a high environmental risk factor. Thymoquinone (TQ) has a unique antioxidant activity and has been widely used as a protective agent against various types of toxicity. To evaluate the protective effects of TQ against AA-induced reproductive toxicity in female rats. In this experimental study, 40 female albino rats (120-150 gr, 8-10 wk) were sorted into 4 groups, (n = 10/each), vehicle group (received a daily oral administration of 0.5 ml saline [9%]); AA group (received a daily oral administration with freshly prepared AA, 20 mg/kg body weight) for 21 days which is less than the lethal dose LD of AA in rats (20 mg/kg body weight); AA+TQ group (received a daily oral administration of TQ, 10 mg/kg body weight) after AA intoxication for 21 days, and TQ group (received a daily oral administration of TQ only, 10 mg/kg body weight) for 21 consecutive days. Reproductive hormones, carcinogenic biomarkers, and oxidative stress markers were measured. The histological assessment showed the protective effect of TQ against AA-induced ovarian injury. Network pharmacology analysis and molecular docking approach were carried out to determine the binding affinity of TQ with cyclooxygenase 2. TQ administration significantly enhanced the functional capacity of the ovary at hormones, oxidative biomarkers, and tumor markers at a significant level of p 0.001. Besides, TQ protects the ovary of AA-treated rats from the severe degeneration effect. TQ showed a promising protective effect against AA-induced reproductive toxicity in female rats.

Pan-cancer landscape of the RUNX protein family reveals their potential as carcinogenic biomarkers and the mechanisms underlying their action

BackgroundThe RUNX family of transcription factors plays an important regulatory role in tumor development. Although the importance of RUNX in certain cancer types is well known, the pan-cancer landscape remains unclear.Materials and MethodsData from The Cancer Genome Atlas (TCGA) provides a pan-cancer overview of the RUNX genes. Hence, herein, we performed a pan-cancer analysis of abnormal RUNX expression and deciphered the potential regulatory mechanism. Specifically, we used TCGA multi-omics data combined with multiple online tools to analyze transcripts, genetic alterations, DNA methylation, clinical prognoses, miRNA networks, and potential target genes.ResultsRUNX genes are consistently overexpressed in esophageal, gastric, pancreatic, and pan-renal cancers. The total protein expression of RUNX1 in lung adenocarcinoma, kidney renal clear cell carcinoma (KIRC), and uterine corpus endometrial carcinoma (UCEC) is consistent with the mRNA expression results. Moreover, increased phosphorylation on the T14 and T18 residues of RUNX1 may represent potential pathogenic factors. The RUNX genes are significantly associated with survival in pan-renal cancer, brain lower-grade glioma, and uveal melanoma. Meanwhile, various mutations and posttranscriptional changes, including the RUNX1 D96 mutation in invasive breast carcinoma, the co-occurrence of RUNX gene mutations in UCEC, and methylation changes in the RUNX2 promoter in KIRC, may be associated with cancer development. Finally, analysis of epigenetic regulator co-expression, miRNA networks, and target genes revealed the carcinogenicity, abnormal expression, and direct regulation of RUNX genes.ConclusionsWe successfully analyzed the pan-cancer abnormal expression and prognostic value of RUNX genes, thereby providing potential biomarkers for various cancers. Further, mutations revealed via genetic alteration analysis may serve as a basis for personalized patient therapies.

Comparison of Carcinogen Biomarkers in Smokers of Menthol and Nonmenthol Cigarettes: The 2015-2016 National Health and Nutrition Examination Survey Special Sample.

The US FDA announced its commitment to prohibiting menthol as a characterizing flavor in tobacco. The relationship between cigarette menthol and exposure to toxic substances in mainstream tobacco smoke is not well characterized. Data from the National Health and Nutrition Examination Survey (NHANES) 2015 to 2016 special sample were used to study markers of 26 harmful and potentially harmful constituents (HPHC) in tobacco smoke. These include urine metabolites of polycyclic aromatic hydrocarbons (PAH), volatile organic compounds (VOC), and heavy metals in exclusive menthol (n = 162) and nonmenthol (n = 189) cigarette smokers. Urine metabolites of 7 PAHs, 15 VOCs, and 4 heavy metal biomarkers were compared by menthol status. Multivariable analyses were conducted on creatinine-adjusted concentrations. There were no significant differences in cotinine levels or in 22 of 26 HPHCs. Among the urine metabolites of PAHs, the levels of 1-hydroxyphenanthrene were about 16% lower in menthol smokers. Among the urine metabolites of VOCs, menthol cigarette smokers presented significantly lower concentrations of acrylamide, N,N-dimethylformamide, and acrylonitrile. Menthol and nonmenthol smokers presented similar levels of heavy metals. Menthol did not affect the levels of cotinine and the nicotine metabolite ratio in urine. Menthol and nonmenthol cigarettes deliver similar levels of most HPHCs. Findings on toxicity are similar for menthol and nonmenthol cigarettes.

Carcinogenic biomarkers of exposure in the urine of heated tobacco product users associated with bladder cancer: A systematic review.

To identify biomarkers of exposure present in Heated Tobacco Products (HTPs) users' urine which are associated with bladder cancer and to compare quantitative biomarker levels to those seen in combustible cigarette users. A systematic literature review was conducted in December 2020 with no date limits. Relevant studies that reported quantitative urinary biomarker of exposure in HTP users were included. Biomarkers and their parent compounds were classified by carcinogenicity according to the International Agency for Research on Cancer Monographs and were cross-referenced with the Collaborative on Health and the Environment Toxicant and Disease Database to determine associations with bladder cancer. Our literature search identified 561 articles and 30 clinical trial reports. 11 studies met inclusion criteria. These studies identified 29 biomarkers of exposure present in HTP users' urine, which reflect exposure to 21 unique parent compounds. Of these parent compounds, 14 are carcinogens and 10 have a known link to bladder cancer. HTP users' biomarkers of exposure were present at lower levels than combustible cigarette users but higher than never-smokers. Biomarkers of exposure to bladder carcinogens are present in the urine of HTP users. While levels of these biomarkers appear to be lower than combustible cigarette users, chronic urothelial exposure to bladder carcinogens is concerning and degree of bladder cancer risk remains unknown. Further long-term study is needed to elucidate the bladder cancer risk of HTP use.

MP38-08 BIOMARKERS OF EXPOSURE ASSOCIATED WITH BLADDER CANCER RISK PRODUCED BY HEAT-NOT-BURN DEVICES COMPARED TO COMBUSTIBLE CIGARETTES

You have accessJournal of UrologyBladder Cancer: Epidemiology & Evaluation I (MP38)1 Sep 2021MP38-08 BIOMARKERS OF EXPOSURE ASSOCIATED WITH BLADDER CANCER RISK PRODUCED BY HEAT-NOT-BURN DEVICES COMPARED TO COMBUSTIBLE CIGARETTES Andrew James, Chris Svendsen, Richard Matulewicz, Elizabeth Moreton, Ibardo Zambrano, Roman Sosnowski, Daniel Schatz, Omar El Shahawy, Scott Sherman, Terry Gordon, and Marc Bjurlin Andrew JamesAndrew James More articles by this author , Chris SvendsenChris Svendsen More articles by this author , Richard MatulewiczRichard Matulewicz More articles by this author , Elizabeth MoretonElizabeth Moreton More articles by this author , Ibardo ZambranoIbardo Zambrano More articles by this author , Roman SosnowskiRoman Sosnowski More articles by this author , Daniel SchatzDaniel Schatz More articles by this author , Omar El ShahawyOmar El Shahawy More articles by this author , Scott ShermanScott Sherman More articles by this author , Terry GordonTerry Gordon More articles by this author , and Marc BjurlinMarc Bjurlin More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000002053.08AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Heat-Not-Burn (HNB) devices are FDA approved as alternatives to combustible cigarettes as they either heat a nicotine-free liquid which then passes through tobacco, or directly heats tobacco to less than 350°C, and therefore do not combust. Specifically, IQOS (I-Quit-Ordinary-Smoking)(Phillip Morris International) is a device marketed to significantly reduce the production of harmful and potentially harmful chemicals compared to combustible cigarettes. These products, which are unfamiliar to most urologists, may produce bladder cancer-linked carcinogenic biomarkers of exposure (BoE) during smoking similar to combustible cigarettes. We reviewed the literature to assess bladder cancer-related toxicant and carcinogen exposures from HNB devices compared to combustible cigarettes. METHODS: A systematic literature search was performed (PROSPERO #CRD42021227973) using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and included PubMed, Embase, Scopus, ClinicalTrials.gov and Cochrane Central Register of Controlled Trials (CENTRAL) to assess BoE in HNB devices compared to combustible cigarettes. BoE are measures of exposure to harmful and potentially harmful constituents within alternative tobacco products.BoE were classified according to the International Agency for Research on Cancer (IARC) Monographs on the Evaluation of Carcinogenic Risks to Humans and cross referenced using the Collaborative on Health and the Environment, Toxicant and Disease Database to determine a link to bladder cancer, grouped by strength of evidence. Quantity of BoE was assessed based on a 5 point scale. RESULTS: Our search identified 591 articles of which 16 met final inclusion criteria and were included for analysis. These studies described 37 different BoE toxicants of which11 are carcinogenic BoE (IARC Group 1 Carcinogenic to humans) including 7 that are linked to bladder cancer (Table). Specifically, HNB devices produced pyrene, 4-aminobiphenyl, naphthalene, fluorene, phenanthrene, O-toluidine, and 2-naphthylamine, all of which have a strong association to bladder cancer, although at lower levels than combustible cigarettes (Quantity of BoE was 1.0 vs 3.3, respectively). CONCLUSIONS: HNB products produce carcinogenic BoE with a strong link to bladder cancer. Long-term implications of risk to these carcinogens are unknown but concerning, given the similarities to combustible cigarette smoke and its established relationship with bladder cancer. Source of Funding: MAB is funded by grant 550KR221903 © 2021 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 206Issue Supplement 3September 2021Page: e695-e696 Advertisement Copyright & Permissions© 2021 by American Urological Association Education and Research, Inc.MetricsAuthor Information Andrew James More articles by this author Chris Svendsen More articles by this author Richard Matulewicz More articles by this author Elizabeth Moreton More articles by this author Ibardo Zambrano More articles by this author Roman Sosnowski More articles by this author Daniel Schatz More articles by this author Omar El Shahawy More articles by this author Scott Sherman More articles by this author Terry Gordon More articles by this author Marc Bjurlin More articles by this author Expand All Advertisement Loading ...

A Novel Luminescent Metal‐Organic Framework as a Remarkable Sensor for Detecting Aristolochic Acids in Biological Fluids

AbstractAbstract: Aristolochic acids (AAs) have caused widespread concern as highly nephrotoxic and carcinogenic substances. Therefore, it is essential to explore a simple and feasible method to detect AAs for disease prevention and clinical diagnosis. In this work, we designed and synthesized a novel luminescent metal organic framework (Zn‐MOF), which has excellent structural stability and fluorescence stability. Notably, the luminescent Zn‐MOF exhibits strong blue emission owing to ligand‐centered electronic transitions, while being capable as a selective sensor for the quantitative detection of AAs in biological fluids with low detection limit. The fluorescence analysis method, possessing the advantages of reliability and high accuracy, further demonstrated that Zn‐MOF has potential applications in monitoring the carcinogen biomarker AAs. Moreover, a paper‐based sensor has been devised by depositing Zn‐MOF on filter paper, which provides a novel strategy for visual, rapid, and on‐site AAs detection with the naked eye.

Systems Medicine Design for Triple-Negative Breast Cancer and Non-Triple-Negative Breast Cancer Based on Systems Identification and Carcinogenic Mechanisms.

Triple-negative breast cancer (TNBC) is a heterogeneous subtype of breast cancers with poor prognosis. The etiology of triple-negative breast cancer (TNBC) is involved in various biological signal cascades and multifactorial aberrations of genetic, epigenetic and microenvironment. New therapeutic for TNBC is urgently needed because surgery and chemotherapy are the only available modalities nowadays. A better understanding of the molecular mechanisms would be a great challenge because they are triggered by cascade signaling pathways, genetic and epigenetic regulations, and drug–target interactions. This would allow the design of multi-molecule drugs for the TNBC and non-TNBC. In this study, in terms of systems biology approaches, we proposed a systematic procedure for systems medicine design toward TNBC and non-TNBC. For systems biology approaches, we constructed a candidate genome-wide genetic and epigenetic network (GWGEN) by big databases mining and identified real GWGENs of TNBC and non-TNBC assisting with corresponding microarray data by system identification and model order selection methods. After that, we applied the principal network projection (PNP) approach to obtain the core signaling pathways denoted by KEGG pathway of TNBC and non-TNBC. Comparing core signaling pathways of TNBC and non-TNBC, essential carcinogenic biomarkers resulting in multiple cellular dysfunctions including cell proliferation, autophagy, immune response, apoptosis, metastasis, angiogenesis, epithelial-mesenchymal transition (EMT), and cell differentiation could be found. In order to propose potential candidate drugs for the selected biomarkers, we designed filters considering toxicity and regulation ability. With the proposed systematic procedure, we not only shed a light on the differences between carcinogenetic molecular mechanisms of TNBC and non-TNBC but also efficiently proposed candidate multi-molecule drugs including resveratrol, sirolimus, and prednisolone for TNBC and resveratrol, sirolimus, carbamazepine, and verapamil for non-TNBC.

Redesign of ultrasensitive and robust RecA gene circuit to sense DNA damage.

SummarySOS box of the recA promoter, PVRecA from Vibrio natriegens was characterized, cloned and expressed in a probiotic strain E. coli Nissle 1917. This promoter was then rationally engineered according to predicted interactions between LexA repressor and PVRecA. The redesigned PVRecA‐AT promoter showed a sensitive and robust response to DNA damage induced by UV and genotoxic compounds. Rational design of PVRecA coupled to an amplification gene circuit increased circuit output amplitude 4.3‐fold in response to a DNA damaging compound mitomycin C. A TetR‐based negative feedback loop was added to the PVRecA‐AT amplifier to achieve a robust SOS system, resistant to environmental fluctuations in parameters including pH, temperature, oxygen and nutrient conditions. We found that E. coli Nissle 1917 with optimized PVRecA‐AT adapted to UV exposure and increased SOS response 128‐fold over 40 h cultivation in turbidostat mini‐reactor. We also showed the potential of this PVRecA‐AT system as an optogenetic actuator, which can be controlled spatially through UV radiation. We demonstrated that the optimized SOS responding gene circuits were able to detect carcinogenic biomarker molecules with clinically relevant concentrations. The ultrasensitive SOS gene circuits in probiotic E. coli Nissle 1917 would be potentially useful for bacterial diagnosis.

Alteration of DNA methylation induced by PM2.5 in human bronchial epithelial cells.

This current study explored the effects of fine particulate matter (PM2.5) on deoxyribonucleic acid methylation in human bronchial epithelial cells. Human bronchial epithelial cells were exposed to PM2.5 for 24h after which, deoxyribonucleic acid samples were extracted, and the differences between methylation sites were detected using methylation chips. Subsequent gene ontology functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed for the differential methylation sites. Functional epigenetic modules analysis of the overall differential methylation site interactions was also conducted. A total of 127 differential methylation sites in 89 genes were screened in the PM2.5 10μg/ml group, of which 55 sites demonstrated increased methylation, with methylation levels decreasing in a further 72 sites. Following an exposure of 50μg/ml PM2.5, a total of 238 differentially methylated sites were screened in 168 genes, of which methylation levels increased in 127 sites, and decreased in 111. KEGG analysis showed that the top 10 enrichment pathways predominantly involve hepatocellular carcinoma pathways and endometrial cancer pathways, whereas functional epigenetic modules analysis screened eight genes (A2M, IL23A, TPIP6, IL27, MYD88, ILE2B, NLRC4, TNF) with the most interactions. Our results indicate that exposure to PM2.5 for 24h in human bronchial epithelial cells induces marked changes in deoxyribonucleic acid methylation of multiple genes involved in apoptosis and carcinogenesis pathways, these findings can provide a new direction for further study of PM2.5 carcinogenic biomarkers.

A Cross-Sectional Study on Benzene Exposure in Pediatric Age and Parental Smoking Habits at Home.

After the introduction of the smoke-free legislation, household smoking has become the major source of environmental tobacco smoke (ETS) exposure for children. In our previous research, we found a strong association between urinary unmodified benzene (u-UB) levels and passive smoking exposure related to the home smoking policies (HSP). The aim of the study is to further investigate the impacts of several factors on ETS-exposure in childhood by using u-UB as tobacco-related carcinogen biomarker of exposure. Two cross-sectional studies were performed on the same target population of our previous research, in summer and winter season of the years 2017 and 2018, respectively. A questionnaire and a head space–solid phase micro-extraction/gas chromatography-mass spectrometry (HS-SPME/GC-MS) analytical method were used as investigative procedures. The improvement found in smoking habits, when compared to our previous surveys, reduced the levels of u-UB in children. However, significant differences related to the high number of smokers and smoked cigarettes, in total and at home, still persist. These differences are more relevant in the winter season. Finally, the only effective way for making homes completely smokefree is to develop public health policies for encouraging people to quit or drastically reduce smoking.

Abstract A012: Comparison of NNAL exposure and menthol cigarette use among Black smokers

Abstract Introduction: In the U.S., there is little information available on gender differences in menthol cigarette smoking use among Black smokers. NNAL, has been studied as a carcinogenic biomarker of tobacco and second-hand smoker exposure. Total NNAL was analyzed to compare gender differences in NNAL exposure and menthol cigarette use among Black smokers. Method: Urine samples were collected from 117 current smokers who self-reported as persons of African descent and participated in the Cancer Prevention Project of Philadelphia. Participants completed overall health and wellness questionnaires that included information on tobacco use. Samples were analyzed for NNAL using an ultra-performance liquid chromatography with tandem mass spectrometry along with urinary creatinine for NNAL normalization and urine flow correction. We compared mean NNAL concentrations and tobacco metabolism phenotype and menthol cigarette use by gender. Results: Our preliminary results are reported for 48 current smokers, 20 males and 28 females. The majority were daily smokers (males, 80%, females 68%). The majority of participants reported using mentholated cigarettes (total 63%, males 76.9% vs. females 54.6%, p=0.508). Tobacco exposure based on mean NNAL concentrations was higher but not significantly different between males (268 pg/mg creatinine ± 498 SD) and females (159 pg/mg creatinine ± 121 SD; p=0.645, Wilcoxon rank-sum test). Similarly tobacco exposure based on number of cigarettes per day was not (males 7.2 ± 6.6 cig/day vs. females 10.5 ± 7.8 cig/day, p= 0.139 Wilcoxon rank-sum test). Of those who reported use of filtered or mentholated cigarettes there was no significant difference according to sex (p&amp;gt;0.05). Mean NNAL was higher in Black men who smoked mentholated cigarettes compared to Black women but did not reach statistical significance (p = 0.598, Wilcoxon rank-sum test). The majority of smokers were poor metabolizers of tobacco (total 60%, males 60%, females 61%, p=0.261). For those who reported use of mentholated cigarettes there was no significant difference in metabolizer phenotype between males and females (p=0.655). Conclusion: As expected Blacks more often report using mentholated cigarettes and there was no significant difference between males and females for tobacco exposure and metabolism. Our analyses are ongoing as we investigate these findings to address gender differences and health disparities among smokers of African descent in a larger study sample. Citation Format: Denise Gibbs, Elizabeth Blackman, Yin-Ming Kuo, Andrew Andrews, Karthik Devarajan, Camille Ragin. Comparison of NNAL exposure and menthol cigarette use among Black smokers [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr A012.

Electronic cigarettes and bladder cancer - a game-changer?

Electronic cigarette (e-cigarette) use has risen rapidly over the past decade, despite limited knowledge of the risk of carcinogenesis and broader health implications. A recent systematic review summarizes the current evidence on carcinogen biomarkers in the urine of e-cigarette users. The findings warrant consideration and indicate that further insights are urgently needed.

PD50-05 CARCINOGEN BIOMARKERS IN THE URINE OF ELECTRONIC-CIGARETTE USERS AND IMPLICATIONS FOR POTENTIAL BLADDER CANCER

INTRODUCTION AND OBJECTIVE: Use of e-cigarettes has rapidly increased despite unclear longitudinal health effects. Once thought to be a safer alternative to tobacco smoke, it is possible that e-cigarettes expose the user to similar carcinogenic byproducts during the vaping process. These toxicants are metabolized and excreted in the urine and may have oncogenic implications for bladder urothelium. This review characterizes and summarizes known urinary carcinogenic biomarkers in e-cigarette users as they relate to the risk of developing bladder cancer. METHODS: A systematic literature search was performed using PRISMA guidelines. Relevant articles published in peer-reviewed journals that reported on urinary biomarkers in e-cigarettes users were included. Parent compounds and urinary biomarkers were classified according to the International Agency for Research on Cancer Monographs on the Evaluation of Carcinogenic Risks to Humans and cross referenced using the Collaborative on Health and the Environment, Toxicant and Disease Database to determine a link to bladder cancer, grouped by strength of evidence. RESULTS: Our initial search identified 1,385 articles, 22 of which met final inclusion criteria and were included for analysis. In summation, these studies described 40 different parent compounds and 4 metals found in the urine of e-cigarette users. Since each parent compound can be metabolized several different ways, 63 unique toxicant or carcinogenic metabolite biomarkers were identified. Compared to non-user controls, e-cigarette users had higher concentrations of urinary biomarker of several carcinogenic compounds linked to bladder cancer (Table 1). The majority of studies were limited by heterogeneous reporting and a dearth of control subjects who had never smoked. CONCLUSIONS: Biomarkers of carcinogens, several with a strong link to bladder cancer, are present in the urine of e-cigarettes users. The long term implications of urothelial exposure to these toxicants is unknown but concerning given the similarities to tobacco smoke and its established relationship with bladder cancer. Further study on the urologic safety of e-cigarettes is necessary.Source of Funding: National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, through Grant Award Number UL1TR002489 (MAB), and a New York State ECRIP’s award

Carcinogen Biomarkers in the Urine of Electronic Cigarette Users and Implications for the Development of Bladder Cancer: A Systematic Review

ContextUse of electronic cigarettes (e-cigarettes) has rapidly increased despite unclear longitudinal health effects. Once thought to be a safer alternative to tobacco smoke, it is possible that e-cigarettes expose the user to similar carcinogenic byproducts during the vaping process. These toxicants are metabolized and excreted in the urine, and may have oncogenic implications for bladder urothelium. ObjectiveTo characterize and summarize known urinary carcinogenic biomarkers in e-cigarette users as they relate to the risk of developing bladder cancer. Evidence acquisitionA systematic literature search was performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and included PubMed, Embase, Web of Science, and Cochrane Central Register of Controlled Trials (CENTRAL). Relevant articles published in peer-reviewed journals, through January 2019, that reported on urinary biomarkers in e-cigarettes users were included. Parent compounds and urinary biomarkers were classified according to the International Agency for Research on Cancer Monographs on the Evaluation of Carcinogenic Risks to Humans and cross referenced using the Collaborative on Health and the Environment, Toxicant and Disease Database to determine a link to bladder cancer, grouped by strength of evidence. Evidence synthesisOur initial search identified 1385 articles, 22 of which met final inclusion criteria and were included for analysis. In summation, these studies described 40 different parent compounds and four metals found in the urine of e-cigarette users. Since each parent compound can be metabolized several different ways, 63 unique toxicant or carcinogenic metabolite biomarkers were identified. Compared with nonuser controls, e-cigarette users had higher concentrations of urinary biomarkers of several carcinogenic compounds linked to bladder cancer. The majority of studies were limited by heterogeneous reporting and a dearth of control individuals who had never smoked. ConclusionsBiomarkers of carcinogens, several with a strong link to bladder cancer, are present in the urine of e-cigarette users. Long-term implications of urothelial exposure to these toxicants are unknown but concerning, given the similarities to tobacco smoke and its established relationship with bladder cancer. Further study on the urological safety of e-cigarettes is necessary. Patient summaryOur review shows that several carcinogens that have a known link to bladder cancer are present in the urine of electronic cigarette (e-cigarette) users. Further study on the urological safety of e-cigarettes is necessary.