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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction 11 Exposure and Biomarker Assessment in Humans The evaluation of potential reduced-exposure agents (PREPs) has to be defined in the context of the outcome of interest (e.g., individual or population reduction in risk and disease type) and compared to an appropriate baseline (i.e., nonsmokers, former smokers, current smokers in the context of host susceptibility and previous level of smoke exposure). Tobacco exposure can be measured in the aggregate at the level of the entire population (e.g., through the measurement of tobacco sales or reported consumption in population-based surveys) and related to disease incidence or change in mortality rates. These methodologies are considered descriptive epidemiological tools that are useful in generating hypotheses and/or validating public health strategies, marketing programs, and so forth. Exposure can also be measured at the level of the individual through biomarker measurements. This type of assessment within epidemiological studies can be used for hypothesis generation or testing. A range of methodologies and assays can be used for assessing exposure, as well as a range of assays for assessing host susceptibilities to exposure. The evaluation of a PREP can include four components: (1) external exposure measurements, (2) internal exposure measurements, (3) biomarkers estimating the biologically effective dose (Perera, 1987), and (4) biomarkers of potential harm (see Figure 11–1). The definitions of each are provided in Table 11–1 and explained further herein. There have been different definitions of types of exposure assessments used previously, but more recent understandings of biomarker uses and limitations, as
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction FIGURE 11–1 Assessing potential harm reduction products. NOTE: Dashed lines indicate hypothetical indirect relationship. Solid lines indicate mechanistic direct relationship. SOURCE: Modified with permission from Committee on Biological Markers of the National Research Council, 1987.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction TABLE 11–1 Exposure and Biomarker Assessment Definitions Exposure or Biomarker Assessmenta Definition External exposure marker A tobacco constituent or product that may reach or is at the portal of entry to the body Biomarker of exposure A tobacco constituent or metabolite that is measured in a biological fluid or tissue that has the potential to interact with a biological macromolecule; sometimes considered a measure of internal dose Biologically Effective Dose (BED) The amount that a tobacco constituent or metabolite binds to or alters a macromolecule; estimates of the BED might be performed in surrogate tissues Biomarker of potential harm A measurement of an effect due to exposure; these include early biological effects, alterations in morphology, structure, or function, and clinical symptoms consistent with harm; also includes “preclinical changes” aCategories and definitions reflect concept that the critical exposure is at the level of a biological macromolecule, so that exposure for this discussion is not limited to a measurement at the portal of entry to the body. well as different approaches needed for PREP evaluation lead to a need for clarification and redefinition. The latter three measurements improve upon the first by quantifying exposure at the cellular level to characterize low-dose exposures or low-risk populations, providing a relative contribution of individual chemical carcinogens from complex mixtures and estimating total burden of a particular exposure where there are many sources (Vineis and Porta, 1996). In assessing PREPs through biomarkers, understanding the biological effects of a wide range of exposures will be important. Within the context of this chapter, exposure at the level of the cell and critical macromolecules is considered with greater weight, rather than the traditional view of exposure at the portal of entry into a person. Biomarkers are intuitively more informative and better disease risk markers when measured in the target tissue through biopsies (e.g., oral mucosa, lung, bladder). However, biomarker assays are technically limited, and target tissue can be difficult to obtain, especially in nondiseased smokers. Therefore, biomarker assays have been developed for surrogate tissues and fluids (e.g., expired breath, saliva, blood, urine). While these are technically simpler to use and easier to collect, the ability to prove a
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction 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? predictive value for the potential harm reduction is more difficult. It should be noted that the biomarkers discussed in this chapter refer to either target or surrogate tissue or fluid assays, but that the biologically effective dose refers to the assessment of a mechanistically relevant biomarker only in the target organ. The following factors should be considered when evaluating measurements for predicting or determining the effects of a PREP. Table 11–2 summarizes these factors and Table 11–3 provides an overview of available measures to predict the effects. Type of measurement. Measurements are defined within four general categories—namely, external exposure, biomarkers of exposure, biomarkers estimating the biologically effective dose, and biomarkers of
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction potential harm. Placing a measurement solely within one category may not be possible. The external exposure assessment category is limited to those methods that are not detected by an assay using a body fluid or part. Although some external exposure methods might be poor predictors of disease risk and hence also poor measures for assessing a new product (e.g., the Federal Trade Commission [FTC] method described below), others might be strongly associated with disease risk and might therefore be better (e.g., cigarettes per day). While some external exposure assessments might be useful for harm reduction risk assessments (e.g., smoking history), they should not be used alone in assessing harm reduction because the predictive power for disease is not sufficient without corroborative biomarker data. Biomarkers of exposure are assayed in a body fluid (including exhaled air) or tissue that measures a constituent of tobacco smoke, tobacco-related products, or metabolites, where the constituent is not bound to a biomolecule. These biomarkers include unmetabolized compounds (e.g., carbon monoxide [CO], serum nicotine, carcinogen levels in serum or internal organs), biomarkers of exposure to individual cigarettes (e.g., incremental increases in exhaled CO or serum nicotine), and metabolites in any body fluid (e.g., cotinine in serum or urine, carcinogen metabolites in urine). Biomarkers assessing the biologically effective dose are those considered mechanistically related to disease outcomes (e.g., carcinogen-DNA adducts in the target tissue). Surrogate biologically effective doses, once validated, estimate a biological effect in a target organ (e.g., hemoglobin adducts or white blood cell carcinogen-DNA adducts). These biomarkers are in theory best able to link exposure (external and internal) to disease outcomes. Biomarkers of potential harm can reflect early or late damage (e.g., loss of heterozygosity in sputum, background mutations in nondiseased tissues, reactive airway disease, arrhythmias, premalignant lesions, mutations in premalignant lesions, chromosomal aberrations in smoking-damaged epithelium, hypermethylation of genes, atherosclerosis). In this context, potential harm implies that the assay might or might not reflect actual harm and that some change in physiological function, for example, might not represent a harmful effect. Target tissue and outcome relationship. A biomarker assay should be shown to be relevant to the outcome of interest. Besides having a mechanistic relationship to pathogenesis, data should be available to determine the predictive capacity for disease and disease reduction. This validation includes supportive evidence that the assay reflects harm reduction, such as might be done in an experimental cell culture or animal study. Assays that measure the effects in target tissue would generally have the greatest weight to support the use of a PREP. Sometimes, the target tissue effect
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction TABLE 11–3 Methods for PREP Assessment Category Type of Measurement Target vs. Surrogate Examples External exposure External exposure assessment Neither Questionnaire data, FTC yield Biomarker of exposure Internal dose Target tissue Polycyclic aromatic hydrocarbon in lung tissue Surrogate tissue Urinary measurement of tobacco constituent or metabolite, exhaled CO, carboxyhemoglobin, urinary mutagenicity Biologically effective dose Biologically effective dose Target tissue Carcinogen-DNA adducts in human lung tissue, exfoliated bladder cells, or oral mucosa Surrogate tissue Carcinogen-DNA or hemoglobin adducts; DNA adducts; lipid peroxidation Biomarker of potential harm Early biological and genetic effects Target tissue Changes in RNA or protein expression, somatic mutations, and LOH in normally or abnormally appearing tissue; change in methylation or gene control; mitochondrial mutations, mRNA expression arrays, or proteomics Alterations in morphology, structure, or function Target tissue Osteoporosis, hypertension, cough, hyperplasia, dysplasia, lipids, blood coagulant pathways, mRNA expression arrays, or proteomics Surrogate assays Surrogate tissue Leukocytosis; HPRT mutations; chromosomal aberrations; circulating lymphocytes; mRNA or protein expression via microarrays in cultured blood cells Effect modifiers Measures of interindividual variation Neither Genetic polymorphisms for genes involved in disease pathways Target Enzyme induction of metabolizing enzymes NOTE: HPRT=hypoxanthine phosphoribosyltransferase; LOH=loss of heterozygosity.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction Strengths Limitations Inexpensive Does not reflect actual internal doses Provides integrated measure of external exposure and smoking behavior Expensive; may not be specific for tobacco products; does not necessarily reflect biologically effective dose; tissue may be difficult to access; may be difficult to validate as a risk marker for disease Easily accessible; provides integrated measure of external exposure and smoking behavior; metabolites reflect host capacity for metabolism and clearance May not be specific for tobacco products; does not necessarily reflect biologically effective dose; may be difficult to validate as a risk marker for disease Reflects integrated measure of external exposure, smoking behavior, metabolic activation, DNA repair capacity, cell-cycle control, and capacity for apoptosis Difficult to measure and validate as a disease risk marker, predictive value for disease risk is insufficiently studied, more commonly reflects internal dose to a target macromolecule rather than disease risk Does not require invasive procedures, greater amount of tissue is generally available; more likely to be used in an epidemiological setting Relationship to disease risk is not fully established Assessment of mechanistic pathway leading to disease Tissue difficult to obtain; technically difficult; relationship to disease risk difficult to establish; harmful effects may already be present; bioinformatics with which to process information not yet available Greater ability to identify risk for disease with marker Tissue difficult to obtain; late effects where harm has already occurred; bioinformatics with which to process information not yet available Easily accessible; provides integrated measure of external exposure and smoking behavior; metabolites reflect host capacity for metabolism and clearance Relationship to target organ effect is difficult to prove; specificity for tobacco product needs to be proved; bioinformatics not yet available Reflects lifetime response to exposure; high throughput possible Candidate gene approach will typically study many polymorphisms that are not related to disease risk Integrated assessment of how prior exposures or genetic traits affect exposures and harm Tissue technically difficult to obtain; laboratory validation difficult
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction might also be a surrogate for an effect in other tissues, and a surrogate tissue assay might reflect effects in multiple organs. Dose-response data for harm. Assays that have a demonstrable dose-response relationship to actual disease outcomes is important for assessing a PREP and, if they do not, it should be shown to have a dose-response relationship to a biomarker of potential harm relevant to a disease pathway. The mechanistic basis for the relationship should be well understood in order to make meaningful interpretations of data used to assess a PREP. For example, assays that demonstrate a dose-response relationship between smoking and DNA damage in epithelial cells of a target organ could be useful. Methods assessing tobacco exposure as a complex mixture would have greater weight than a single component exposure. Dose-response data for harm reduction. Assays that show a reduction in harm after reducing exposure to tobacco smoke or a tobacco product constituent would have the greatest weight, where the experimental design uses an initial dose level for a specific duration of time followed by exposure to a lower level at a later time. The intent is to simulate the effects of a person’s switching from one level of exposure to another level of exposure. Importantly, the effects of the biomarker should be measurably different over the range of human exposures, so that the assessment can predictably measure the effects of exposure reduction from a PREP. Currently, there are some biomarker assays that have been assessed in former smokers or smoking cessation trials. These biomarker studies that indicate measurable decreases in effect can provide some information about the utility of markers for assessing exposure reduction. Included in this are half-life data, which must be measured and taken into account when evaluating a tobacco-related PREP. Methods assessing tobacco exposure as a complex mixture would have greater weight than a single component exposure. Specificity. Consideration should be given to whether the effect is specific to a constituent of tobacco smoke or a tobacco product, or whether the method also measures exposure from other sources. Higher degrees of specificity are useful, although in some cases the method might be useful for assessing exposures from multiple sources other than tobacco in order to provide an understanding about relative contributions. Assays that are specific for tobacco’s complex chemical mixture and those that are specific for a chemical or chemical class both have utility, but the former would have greater weight if appropriately validated, because persons are exposed simultaneously to all of the constituents. Validating assays for complex effects is more difficult because they may have less specificity for tobacco.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction Sensitivity. The assay must be sufficiently sensitive to measure what it is supposed to measure in the human tissue of interest. This is especially problematic in measuring low-level effects, for example, in assessing the effects of environmental tobacco smoke (ETS) exposure. Validation. It is critical that biomarkers for assessing PREPs be well validated in the laboratory. Validation includes proof that the assay measures what it claims to measure and that it is reproducible. Sensitivity, specificity, and predictive value are all important to consider. EXTERNAL EXPOSURE ASSESSMENT: THE FTC METHOD AND QUESTIONNAIRE DATA External exposure markers attempt to measure the amount of a tobacco smoke or tobacco product constituent that may enter at a portal to the body. However, these predictors generally do so without regard to most interindividual differences in smoking behavior and cellular processes. There are several types of external exposure assessment, some of which are listed in Table 11–4. A common way to assess potential exposure to tobacco smoke is by measuring the yield of tobacco smoke constituents. One attempt to estimate delivered doses is the method adopted by the Federal Trade Commission in 1967. It was intended to provide a standardized estimate of tar and nicotine yield by cigarette brand, simulating a cursory observation of human smoking behavior. A cigarette is inserted into a smoking machine and lit, puffs are taken through a syringe (35 ml over 2 seconds, every 60 seconds) until the cigarette is “smoked” to a fixed length. Particulates are collected on a filter and weighed. Nicotine is assayed separately. Tar is measured as total particulate matter less nicotine, other alkaloids, and water. Although the machine provides yield data that can be used to compare one cigarette to another, this information has limited usefulness for understanding human exposure because people do not smoke cigarettes as the machine does due to different smoking behaviors. Smokers also can affect cigarette filter performance by covering ventilation holes in the filter with their lips or fingers, which would increase yields in vivo. Although FTC yields might define a comparative range of actual exposures, there is a wide overlap of actual to predicted yields among types of cigarettes (i.e., low, medium, and high yields), where smokers of low-nicotine cigarettes might have higher nicotine levels than those who smoke brands with higher FTC yields (Byrd et al., 1998, 1995). Altering the FTC method to simulate puffs and times for actual smokers results in
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction TABLE 11–4 External Exposure Assessmenta Category Variables Used in Literature Related to a Disease Outcomeb 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. Reporting is variable depending on context, such as smoking cessation program or where recall bias might exist in epidemiology studies. Known limitations for persons who are switching brands or altering smoking behavior; also not sufficiently reliable in smoking cessation studies. 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 aReferences are not provided in this table but can be found in the text of this and disease-related chapters. bAny report related to a disease outcome where the report is plausible but has not necessarily been replicated.
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Clearing the Smoke: Assessing the Science Base for Tobacco Harm Reduction higher exposures to tar and specific carcinogens (e.g., tobacco-specific nitrosamines and benzo[a]pyrene) (Djordjevic et al., 2000; Fischer et al., 1989; Hoffman and Hoffman, 1997). For example, using modified protocols to stimulate human smoking behavior, the medium-yield (0.9–1.2 mg nicotine per cigarette) and low-yield (0.8 mg nicotine per cigarette) cigarettes deliver similar amounts of tar per day, although by FTC method measured per cigarette yields of tar, benzo[a]pyrene (BaP), and tobacco-specific nitrosamines (TSNAs) were higher in the former (Djordjevic et al., 2000). As cigarettes with different designs are developed and marketed, an assumption that the FTC method of estimating yields will be comparable to existing products is premature. Over the last 30 years, data from surveys have been an important tool in the assessment of tobacco exposure among individuals and the population. They have been an effective means of tracking patterns of tobacco use and the societal perceptions that ultimately influence consumption. Individual exposure can be assessed through the measurement of the number of cigarettes smoked per day, duration of smoking, types or brands of cigarettes smoked (e.g., “tar” delivery, filter type, type of tobacco, mentholation), and age at initiation (IARC, 1986; Kaufman et al., 1989; La Vecchia et al., 1990; Lubin et al., 1984; Stellman and Garfinkel, 1989; U.S. DHHS, 1988; Vutuc and Kunze, 1983; Wilcox et al., 1988; Zang and Wynder, 1992). Lifetime exposures can be estimated by calculating pack-years (average packs per day multiplied by number of years smoked) or cumulative tar exposure (Zang and Wynder, 1992). A more detailed description of the most common surveys in use is presented in Table 11–5. Most analyses indicate that self-report validity among adults is good (Patrick et al., 1994). Certain limitations, however, are evident in this type of exposure assessment (Giovino, 1999; U.S.DHHS, 1994). First, sampling errors may occur in any study in which generalizations are made from a selected population sample. One example is the over- or underrepresentation of certain groups, especially those that exhibit significant tobacco use or have differing smoking behavior. In fact, there is a built-in exclusion in many of the major surveillance tools of various segments of the population, such as the institutionalized mentally ill, prisoners, and those in areas of inadequate telephone coverage. Errors in response must be considered including memory errors, nonresponse errors, and misclassifications and inconsistencies in reporting. The validity of self-reported responses can be influenced by many factors (Velicer et al., 1992), particularly the respondent’s perception of privacy (Giovino, 1999). This is especially a concern among adolescents in the home setting and among groups that have increased pressure to abstain or to quit, including pregnant women, adolescents, and patients with heart or lung disease. One
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Representative terms from entire chapter: