Tobacco Smoke Exposure Biomarkers

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enter Researchers at Berkeley Lab have shed light on the cellular mechanisms linking exposure to thirdhand smoke THS with oxidative stress, DNA damage and cancer risk. They have also identified a biomarker of THS exposure that is absent in cases of secondhand smoke SHS exposure, making the biomarker especially useful in establishing THS exposure and risk.

THS refers to tobacco smoke pollutants remaining on skin, clothing, furniture and other surfaces after tobacco has been smoked. It also includes the secondary pollutants formed when residual tobacco smoke pollutants react with other compounds in the environment. Parent s who stop smoking incur health benefits, model non-smoking and quitting to children and stop exposure to SHS in the home, car and other locations. Effective systems are needed to increase parental smoking cessation and implement home smoking restrictions. We propose preliminary studies to evaluate a novel intervention to accomplish these objectives.

We hypothesize that a clinic system that routinely measures and reports levels of tobacco toxicants tobacco-specific carcinogens, nicotine and cotinine found in the urine of children exposed to SHS will 1 increase provider delivery of tobacco treatment, 2 increase parental participation in tobacco treatment, 3 increase parental smoking cessation and 4 reduce childhood exposure to secondhand smoke.

We propose formative work among healthcare providers and parents to develop the intervention and to pilot test the effects of the intervention on providers and parents.

We will conduct focus groups among staff to identify training needs, develop methods to integrate the intervention with office practice and assess barriers to implementation. We will also conduct focus groups among parents to assess willingness to provide urine specimens, optimal feedback format and reactions to biomarker data. Results from focus groups will be used to develop the experimental treatment protocol.

We will test the intervention in a two-group randomized pilot study in the University of Minnesota Primary Care Clinic. We will recruit 80 children age with a parent who smokes. We will provide brief behavioral counseling in healthy lifestyle options to all parents. One provider team will implement the experimental intervention in 40 parent-child pairs and the other team will serve as the control.

Children who see providers in the experimental group will provide a urine sample to test for nitrosamines a tobacco-specific carcinogen , nicotine and cotinine. We will communicate laboratory results to providers using the electronic medical record and incorporate these results in parental tobacco counseling designed to promote smoking cessation and home smoking restrictions.

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The primary outcome will be provider delivery of smoking cessation treatment. We will also measure effects on parental engagement in treatment, smoking cessation and institution of home smoking restrictions in both the experimental and control groups. The research team brings extensive experience with novel tobacco interventions, health services research and biomarker assessment to the project. Routine documentation of tobacco toxicants in children's urine has potential to dramatically alter clinical care for families at risk from smoking.

FDA Resources. Associations between white blood cell count, lung function, respiratory illness and mortality: the Busselton Health Study. Eur Respir J 13 5 — Carcinogenesis 16 9 — Cancer Epidemiol Biomarkers Prev 2 3 — A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 9 — Int J Cancer 81 1 — Larynx cancer risk in relation to glutathione S-transferase M1 and T1 genotypes and tobacco smoking.

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J Natl Cancer Inst 87 14 — Variation in DNA repair is a factor in cancer susceptibility: a paradigm for the promises and perils of individual and population risk estimation? Carcinogenesis 6 5 — Decline of DNA damage and other biomarkers in peripheral blood following smoking cessation. Increase in circulating products of lipid peroxidation F2-isoprostanes in smokers. Smoking as a cause of oxidative damage.

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Med Hypotheses 42 4 — Biochemical evidence of a chronic abnormality in platelet and vascular function in healthy individuals who smoke cigarettes. Circulation 76 1 :6— Early and late weight gain following smoking cessation in the Lung Health Study. Am J Epidemiol 9 — Prognostic value of coronary electron-beam computed tomography for coronary heart disease events in asymptomatic populations.

Am J Cardiol 85 8 — Double-blind study on the effect of cigarette smoking on the chromosomes of human peripheral blood lymphocytes in vivo. Mutat Res 92 1—2 — Increased levels of the nicotine metabolite cotinine in schizophrenic smokers compared to other smokers. Biol Psychiatry 42 1 :1—5. Cytochrome P 2E1 polymorphism as a risk factor for lung cancer: in relation to p53 gene mutation.

Tobacco Smoke Exposure Biomarkers - CRC Press Book

Anticancer Res 17 1B — Detection of DNA adducts by high-performance liquid chromatography with electrochemical detection. Carcinogenesis 10 5 — Smoking, alcohol consumption, and leukocyte counts. Am J Clin Pathol 1 — A metabolite of the tobacco-specific lung carcinogen 4- methylnitrosamino 3-pyridyl butanone in the urine of hospital workers exposed to environmental tobacco smoke. Cancer Epidemiol Biomarkers Prev 7 3 — Impact of inherited polymorphisms in glutathione S-transferase M1, microsomal epoxide hydrolase, cytochrome P enzymes on DNA, and blood protein adducts of benzo a pyrene-diolepoxide.

Cancer Epidemiol Biomarkers Prev 7 8 — Validity of self-reported smoking: a review and meta-analysis. American Journal of Public Health 84 7 : — Binding of polycyclic aromatic hydrocarbons to DNA: comparison with mutagenesis and tumorigenesis. J Toxicol Environ Health 6 5— 6 — Cancer Epidemiol Biomarkers Prev 7 4 — Perera FP. Molecular cancer epidemiology: a new tool in cancer prevention.

J Natl Cancer Inst 78 5 — The leukocyte count and risk of lung cancer. Cancer 69 3 — Phillips DH. Detection of DNA modifications by the 32P-postlabelling assay. Mutat Res 1—2 :1— Correlation of DNA adduct levels in human lung with cigarette smoking. Nature — DNA damage by tobacco smoke and some antiblastic drugs evaluated using the Comet assay.

Toxicol Lett 2—3 — The influence of age, sex and smoking habits on the background level of fish-detected translocations. Prevost V, Shuker DE. Cigarette smoking and urinary 3-alkyladenine excretion in man. Chem Res Toxicol 9 2 — Identification of patients at increased risk of first unheralded acute myocardial infarction by electron-beam computed tomography. Circulation 8 — The effects of age and lifestyle factors on the accumulation of cytogenetic damage as measured by chromosome painting. Mutat Res 1—6 — Covalent DNA damage in tissues of cigarette smokers as determined by 32P-postlabeling assay.

J Natl Cancer Inst 81 5 — Tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in women stratified by age. Circulation 86 5 — Rebbeck TR. Cancer Epidemiol Biomarkers Prev 6 9 — Reddy MV, Randerath K. Nuclease P1-mediated enhancement of sensitivity of 32P-postlabeling test for structurally diverse DNA adducts.

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Adv Clin Chem. ; doi: / Epub Nov 4. Biomarkers of tobacco smoke exposure. Mattes W(1), Yang X(2), Orr MS(3). Environ Health Perspect. May; Suppl Biomarkers of environmental tobacco smoke exposure. Benowitz NL(1). Author information: (1) Division.

Carcinogenesis 7 9 — Short-term smoking reduction is associated with reduction in measures of lower respiratory tract inflammation in heavy smokers. Eur Respir J 3 7 — Pharmacogenetics 8 2 — Stereoselective metabolism of - benzo[a]pyrene-7,8-diol by human lung microsomes and peripheral blood lymphocytes: effect of smoking.

Carcinogenesis 13 6 — Identification of an NAD P H:quinone oxidoreductase polymorphism and its association with lung cancer and smoking. Pharmacogenetics 5 4 — Formation of polycyclic aromatic hydrocarbon-DNA adducts in peripheral white blood cells during consumption of charcoal-broiled beef.

Carcinogenesis 11 7 — Cancer Res 54 6 — Genotypes of glutathione transferase M1 and P1 and their significance for lung DNA adduct levels and cancer risk. Carcinogenesis 18 7 — Interlaboratory comparison of antisera and immunoassays for benzo[a]pyrene-diol-epoxide-I-modified DNA. Carcinogenesis 9 7 — Carcinogenesis 19 5 — High frequency of K-ras codon 12 mutations in bronchoalveolar lavage fluid of patients at high risk for second primary lung cancer.

Clin Cancer Res 3 3 — Seeman P. Dopamine receptors. Psycopharmacology; 4th Generation of Progress. Cancer risk and low-penetrance susceptibility genes in gene-environment interactions. J Clin Oncol 18 11 — Dopamine D4 receptors and the risk of cigarette smoking in African-Americans and Caucasians.

Cancer Epidemiol Biomarkers Prev 7 6 — Increased formation of oxidative DNA damage, 8-hydroxydeoxyguanosine, in human livers with chronic hepatitis. Cancer Res 54 12 — Sidransky D. Nucleic acid-based methods for the detection of cancer. Simpson AJ.

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The natural somatic mutation frequency and human carcinogenesis. Adv Cancer Res — Association between the p21 codon 31 A1 arg allele and lung cancer. Hum Hered 46 4 — Carcinogenesis 13 10 — Human urine mutagenicity study comparing cigarettes which burn or primarily heat tobacco. Mutat Res 1 :1—9.

Hum Mutat 15 1 — Speit G, Hartmann A. The comet assay single-cell gel test. A sensitive genotoxicity test for the detection of DNA damage and repair. Methods Mol Biol — Mutagen sensitivity as a biological marker of lung cancer risk in African Americans. Case-control study of the D2 dopamine receptor gene and smoking status in lung cancer patients. J Natl Cancer Inst 90 5 — Stellman SD, Garfinkel L. Lung cancer risk is proportional to cigarette tar yield: evidence from a prospective study.

Prev Med 18 4 — Metabolic activation, DNA adducts, and H-ras mutations in human neoplastic and non-neoplastic laryngeal tissue. J Cell Biochem Suppl 17F— High-density lipoprotein concentrations increase after stopping smoking. Does passive smoking impair endothelium-dependent coronary artery dilation in women? J Am Coll Cardiol 31 4 — Longitudinal relation between smoking and white blood cells. Am J Epidemiol 8 — A molecular epidemiological case-control study of lung cancer.

Cancer Epidemiol Biomarkers Prev 4 4 — Molecular and genetic damage from environmental tobacco smoke in young children. Cancer Epidemiol Biomarkers Prev 8 5 — Early endothelial dysfunction in adults at risk from atherosclerosis: different responses to L-arginine. J Am Coll Cardiol 32 1 — DHHS U. Department of Health and Human Services. Washington, DC: U. Biological effect markers for exposure to carcinogenic compound and their relevance for risk assessment.

Crit Rev Toxicol 28 5 — Influence of smoking habits on the frequencies of structural and numerical chromosomal aberrations in human peripheral blood lymphocytes using the fluorescence in situ hybridization FISH technique. Mutagenesis 10 6 — Polycyclic aromatic hydrocarbon-DNA adducts in lung tissue from lung cancer patients. Carcinogenesis 11 9 — Assessing outcome in smoking cessation studies.

Psychological Bulletin 1 — Genetically based N-acetyltransferase metabolic polymorphism and low-level environmental exposure to carcinogens. Vineis P, Porta M. Causal thinking, biomarkers, and mechanisms of carcinogenesis. J Clin Epidemiol 49 9 — Vutuc C, Kunze M. Tar yields of cigarettes and male lung cancer risk.

J Natl Cancer Inst 71 3 — Serum cholesterol and subsequent risk of cancer: results from the BUPA study. Br J Cancer 59 6 — Gender difference in smoking effect on chromosome sensitivity to gamma radiation in a healthy population. Radiat Res 1 — Benzo a pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer. DNA repair and aging in basal cell carcinoma: a molecular epidemiology study. Relation between tobacco use and urinary excretion of thromboxane A2 and prostacyclin metabolites in young men. Circulation 83 5 — Correlation of DNA adducts in blood mononuclear cells with tobacco carcinogen-induced damage in human lung.

Cancer Res 55 21 — Cancer Epidemiol Biomarkers Prev 6 2 — Early age at smoking initiation and tobacco carcinogen DNA damage in the lung. J Natl Cancer Inst 91 7 — Smoking and lung cancer: risk as a function of cigarette tar content.

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Prev Med 17 3 — High frequency of K-ras mutations in normal appearing lung tissues and sputum of patients with lung cancer. Int J Cancer 63 6 — Yamasaki E, Ames BN. Concentration of mutagens from urine by absorption with the nonpolar resin XAD cigarette smokers have mutagenic urine. Glutathione S-transferase M1 genotype affects aminobiphenyl-hemoglobin adduct levels in white, black and Asian smokers and nonsmokers. Cancer Epidemiol Biomarkers Prev 4 8 — Cumulative tar exposure. A new index for estimating lung cancer risk among cigarette smokers. Cancer 70 1 — Despite overwhelming evidence of tobacco's harmful effects and pressure from anti-smoking advocates, current surveys show that about one-quarter of all adults in the United States are smokers.

This audience is the target for a wave of tobacco products and pharmaceuticals that claim to preserve tobacco pleasure while reducing its toxic effects. Clearing the Smoke addresses the problems in evaluating whether such products actually do reduce the health risks of tobacco use. Within the context of regulating such products, the committee explores key questions:. This book looks at the types of products that could reduce harm and reviews the available evidence for their impact on various forms of cancer and other major ailments. It also recommends approaches to governing these products and tracking their public health effects.

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Visit NAP. Looking for other ways to read this? No thanks. Page Share Cite. TABLE 11—2 Measurements Used For Assessing Harm Reduction Products Factor Comment Type of measurement Types of measurements that can be used include external exposure assessment, biomarkers of exposure, biomarkers that represent the biologically effective dose, and biomarkers of potential harm. Depending on the context, the PREP, and the outcome of interest, different measurements might be more appropriate, although it is likely that a combination will be needed Target tissue and outcome effect Is the measurement used for detecting effects in target or surrogate tissues, and is this a measurement of pathogenesis?

Dose-response data Measurements must have a dose-response relationship that is understood on a mechanistic basis. Biomarker should be able to demonstrate effects from exposure over the range of human experience, so that it can show exposure reduction from a PREP Harm reduction in dose-response data Biomarker should be able to predict a decrease in disease incidence after exposure is reduced Specificity Is the measurement specific for a tobacco product constituent, or does is also measure exposures from nontobacco products?

Sensitivity Is the measurement sensitive enough to measure what it is supposed to measure in humans within the possible exposure ranges? Validation Are there sufficient data to show that the assay is reproducible? TABLE 11—4 External Exposure Assessment a Category Variables Used in Literature Related to a Disease Outcome b Strengths Limitations FTC machine method Tar yield Nicotine yield Individual smoke constituent yield Yes Standardized method for yields Little relationship to actual human experience Subject smoking history Cigarettes per day Years of smoking Age of initiation Recall of inhalation depth Usual type of cigarette smoked Quitting attempts Cumulative tar exposure Yes Inexpensive assessment; generally considered reliable, except in some circumstances listed in limitations Recall is subject to self-perceptions of risk.

Thus, not sufficiently reliable in harm reduction studies Smoking Topography Puff duration Puffs per cigarette Interpuff interval Puff volume No Direct measure of inhalation exposure per cigarette. Can be used to assess effects of cigarette brand switching Measurement performed in artificial environment a References are not provided in this table but can be found in the text of this and disease-related chapters. Short-term marker only Yes except when using NRT Yes addiction only Well validated; can be measured easily in urine, plasma saliva, or hair.

Useful for environmental tobacco smoke Short-term marker only. At higher levels of smoking, dose-response relationship is less clear and there is wide overlap among smokers Yes except when using NRT NDA Allows for assessment of nicotine metabolism Low levels. No benefit over cotinine. Levels vary over the day No Yes Measures cumulative, although short-term exposure to several cigarettes Requires blood draw and special handling.

Saliva easy to obtain Many dietary sources. Adducts found in all tissues, including heart and blood vessels Cannot identify adducts so mechanistic studies are problematic Yes No Yes Can be measured in any tissue and assays are available that are sufficiently sensitive Low sensitivity and technical difficulties make assay use limited in large-scale studies. Diet might be greater contributor than smoking Yes No NDA Can be measured in any tissue; has some specificity for smoking if no known occupational exposure Low sensitivity makes assay use limited in large-scale studies Yes Yes NDA Can be measured in any tissue, although methodology has low sensitivity.

Biomarkers for Detection of Thirdhand Smoke Exposure 2014-060

Highly specific for smoking Low sensitivity makes assay use limited in large-scale studies Yes No NDA Can be measured in any tissue Assay has large interlaboratory variation; it is easy to introduce oxidative damage into laboratory assay; low sensitivity makes assay use limited in large-scale studies Yes No Not available Sufficient sensitivity to use for ETS Technically difficult Yes No NDA Can be measured in any tissue Low sensitivity makes assay use limited in large-scale studies.

Specific to Tobacco Related to a Disease Risk c Strengths Limitations No Yes Indicates acquired changes in susceptibility; related to DNA-adduct levels Technically difficult to assess in large epidemiological studies No Yes Indicates acquired changes in susceptibility; related to DNA-adduct levels Technically difficult to assess in large epidemiological studies No NDA Indicates acquired changes in susceptibility; provides analysis of what is likely to be critical part of carcinogenesis Technically difficult No NDA Reflects integrated measure of multiple genotypes, provides complex data potentially usable for rapid identification of important risk factors Difficult to perform; relationship to disease risk is technically difficult to prove; requires extensive laboratory validation; RNA and protein microarray assays are expensive; large-scale studies are needed; refined bioinformatic analysis required No Yes Can be done in blood as surrogate tissue.

Can be measured in persons without cancer Very nonspecific; relationship to target organ is not established; significant lack of specificity and wide overlap between smokers and nonsmokers No NDA Facile assay Lack of specificity No No Easy to do in blood as surrogate tissue. Can be measured in persons without cancer Very nonspecific; relationship to target organ is not established; predictivity for disease risk not established.

Significant lack of specificity and wide overlap between smokers and nonsmokers No NDA Similar lesions observed in cancer Technically complex; relationship to cancer risk unknown No NDA Facile assay in blood Relationship to target tissue or blood unknown. Significant confounders exist No Yes Easy to measure; intraindividual differences may be important for the individual Both interindividual and intraindividual differences are significant.

Substantial confounders exist, and many persons are on medications No No Minimally invasive Very nonspecific No NDA Pathogenically related to disease Does not distinguish levels of smoking. Specific to Tobacco Related to a Disease Risk c Strengths Limitations No No Platelet activation in vivo might be pathophysiologically related to cardiac artery thrombosis Technically difficult to use for large numbers of subjects. Smoking increases platelet counts No Yes Can be a surrogate marker for several processes including atherosclerosis and thrombosis Relationship to disease uncertain, although alterations in levels are linked epidemiologically to disease.

Wide interindividual and intraindividual variation and large number of confounders No No Can reflect both cardiac and respiratory disease risk Insensitive; wide interindividual differences No NDA Provides different types of data with single procedure Bronchoscopy is too invasive for large epidemiological studies No NDA Provides different types of data with single procedure Bronchoscopy is too invasive for large epidemiological studies Yes NDA May be specific to tobacco smoke Requires invasive test; short half-life No NDA May be measured in urine, bronchioalveolar lavage, and serum Substantial number of confounders No Yes Widely available Low sensitivity for mild disease.

Specific to Tobacco Related to a Disease Risk c Strengths Limitations No Yes Data collection is easy Nonspecific; numerous confounders No Yes Both a biomarker for metabolism and an important outcome for some people Some people perceive weight loss as a benefit of smoking, despite significant adverse effects associated with smoking a Selected examples; list is not all-inclusive. Login or Register to save! Within the context of regulating such products, the committee explores key questions: Does the use of such products decrease exposure to harmful substances in tobacco?

Is decreased exposure associated with decreased harm to health? Are there surrogate indicators of harm that could be measured quickly enough for regulation of these products? What are the public health implications? Stay Connected! Harm reduction in dose-response data. Are there sufficient data to show that the assay is reproducible? Polycyclic aromatic hydrocarbon in lung tissue.

Early biological and genetic effects. Alterations in morphology, structure, or function. Measures of interindividual variation. Genetic polymorphisms for genes involved in disease pathways. Enzyme induction of metabolizing enzymes. Does not reflect actual internal doses. Provides integrated measure of external exposure and smoking behavior.

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Relationship to disease risk is not fully established. Assessment of mechanistic pathway leading to disease. Greater ability to identify risk for disease with marker. Reflects lifetime response to exposure; high throughput possible. Tissue technically difficult to obtain; laboratory validation difficult.

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Variables Used in Literature. Tar yield Nicotine yield Individual smoke constituent yield. Little relationship to actual human experience. Cigarettes per day Years of smoking Age of initiation Recall of inhalation depth Usual type of cigarette smoked Quitting attempts Cumulative tar exposure. Puff duration Puffs per cigarette Interpuff interval Puff volume. Measurement performed in artificial environment. Civilian, noninstitutionalized adults over age 18; children by proxy. Noninstitutionalized adults over age Noninstitutionalized civilian population over age University of Michigan Survey Research Center.

Eighth, tenth, and twelfth grade students. Household interview with responses typed directly in laptop computer; annual. Excludes homeless not in shelters, military personnel, prisoners, hospital patients Data: cigarette, chewing tobacco, cigar, and pipe use since Oversampling of black American and Hispanic populations.

Computer-assisted telephone interviews; annual. Added smokeless tobacco use questions in State level. Approximately 40, participants between and Personal interview with physical exam and blood tests; periodic. Serum cotinine measurements Oversampling of children 1—5years, adults over age 60, black Americans, and Mexican Americans. Approximately 25, participants in Household interview; self-administered through a computer; annual. State level Oversampling of black Americans, Hispanic Americans, and youth.

Approximately 50, students from public and private high schools. Classroom based; self-administered; annual.