Data from Research Priorities, Measures, and Recommendations for Assessment of Tobacco Use in Clinical Cancer Research
Stephanie R. LandBenjamin A. TollCarol M. MoinpourSandra A. MitchellJamie S. OstroffDorothy K. HatsukamiSonia A. DuffyEllen R. GritzNancy A. RigottiThomas H. BrandonSheila A. PrindivilleLinda SarnaRobert A. SchnollRoy S. HerbstPaul M. CinciripiniScott J. LeischowCarolyn M. DreslerMichael C. FioreGraham Warren
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<div>Abstract<p>There is strong evidence that cigarette smoking causes adverse outcomes in people with cancer. However, more research is needed regarding those effects and the effects of alternative tobacco products and of secondhand smoke, the effects of cessation (before diagnosis, during treatment, or during survivorship), the biologic mechanisms, and optimal strategies for tobacco dependence treatment in oncology. Fundamentally, tobacco is an important source of variation in clinical treatment trials. Nevertheless, tobacco use assessment has not been uniform in clinical trials. Progress has been impeded by a lack of consensus regarding tobacco use assessment suitable for cancer patients. The NCI-AACR Cancer Patient Tobacco Use Assessment Task Force identified priority research areas and developed recommendations for assessment items and timing of assessment in cancer research. A cognitive interview study was conducted with 30 cancer patients at the NIH Clinical Center to evaluate and improve the measurement items. The resulting Cancer Patient Tobacco Use Questionnaire (C-TUQ) includes “Core” items for minimal assessment of tobacco use at initial and follow-up time points, and an “Extension” set. Domains include the following: cigarette and other tobacco use status, intensity, and past use; use relative to cancer diagnosis and treatment; cessation approaches and history; and secondhand smoke exposure. The Task Force recommends that assessment occur at study entry and, at a minimum, at the end of protocol therapy in clinical trials. Broad adoption of the recommended measures and timing protocol, and pursuit of the recommended research priorities, will help us to achieve a clearer understanding of the significance of tobacco use and cessation for cancer patients. <i>Clin Cancer Res; 22(8); 1907–13. ©2016 AACR</i>.</p></div>Keywords:
Tobacco smoke
Charnley total hip arthroplasty has been demonstrated to provide good clinical results and a high rate of implant survivorship for twenty years and longer. Most long-term series are not large enough to stratify the many demographic factors that influence implant survivorship. The purpose of this study was to analyze the effects of demographic factors and diagnoses on the long-term survivorship of the acetabular and femoral components used in Charnley total hip arthroplasty.Two thousand primary Charnley total hip arthroplasties (1689 patients) were performed at one institution from 1969 to 1971. Patients were contacted at five-year intervals after the arthroplasty. Twenty-five years after the surgery, 1228 patients had died and 461 patients were living. Hips that had not had a reoperation, revision or removal of a component for any reason, or revision or removal for aseptic loosening were considered to have survived. Survivorship data were calculated with use of the method of Kaplan and Meier. Patients were stratified by age, gender, and underlying diagnosis to determine the influence of these factors on implant survivorship.The twenty-five year rates of survivorship free of reoperation, free of revision or removal of the implant for any reason, and free of revision or removal for aseptic loosening were 77.5%, 80.9% and 86.5%, respectively. The twenty-five-year survivorship free of revision for aseptic loosening was poorer for each decade earlier in life at which the procedure was performed; this survivorship ranged from 68.7% for patients who were less than forty years of age to 100% for patients who were eighty years of age or older. Men had a twofold higher rate of revision for aseptic loosening than did women.Age, gender, and underlying diagnosis all affected the likelihood of long-term survivorship of the acetabular and femoral components used in Charnley total hip arthroplasty.
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Survivorship data can be effectively summarized using the shape and scale parameters of the Weibull frequency distribution. The shape parameter controls the rate of change of the age—specific mortality rate and, therefore, the general form of the survivorship curve. Estimates of shape and scale parameters and their confidence intervals can be easily calculated and used to compare survivorship curves of different populations.
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Every tetraeffective cause of mortality and survivorship negatively and positively affects mortality and negatively and positively affects survivorship. There is previous evidence of tetraeffective causes of mortality and survivorship, and strong rationales suggest that every cause of mortality and survivorship is tetraeffective. Here I elucidate and explain that every tetraeffective cause of mortality and survivorship combines corresponding at least one cause-specific mortacause and at least one cause-specific vitacause; “mortacause” refers here to a cause-specific component that positively affects mortality and negatively affects survivorship, and “vitacause” refers to a cause-specific component that positively affects survivorship and negatively affects mortality. I show tetraeffective causes, mortacauses, and vitacauses in results of multivariable regression analyses of effects of age, lifespan, contemporary aggregate size, lifespan aggregate size, and historical time humans’ and medflies’ mortality and survivorship. In these analyses I specify tetraeffective causes, mortacauses, and vitacauses with sign(β 1 ) = - sign(β 2 ) , where respective corresponding β 1 and β 2 denote respective first and second variable-specific regression coefficients. Thus tetraeffective causes, mortacauses, and vitacauses of mortality and survivorship are hereby defined, identified, named, recognized, elucidated, conceptualized, specified, explained, and demonstrated.
Cancer Survivorship
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In their study in this issue of Hospital Pediatrics, Mahabee-Gittens et al1 compared tobacco smoke exposure (TSE) based on parental self-report in a convenience sample of pediatric patients who were hospitalized with TSE based on biochemical confirmation with levels of child salivary cotinine, a biomarker of nicotine. The study revealed poor sensitivity and specificity of parental self-report of TSE (reported in the electronic health record [EHR]), compared with measured cotinine levels. Only 67% of patients with positive cotinine levels were identified as having TSE by parental self-report, as documented in the EHR. In contrast, 77% of children with parental report of TSE who were hospitalized had positive cotinine levels. The authors concluded that almost 40% of children were misclassified in the EHR as not having TSE.What accounts for the differences between parental self-report of TSE and biochemical measurement of salivary cotinine? The authors suggest several possibilities, including (1) their use of enzyme-linked immunosorbent assay to measure cotinine levels, which is not as sensitive as other methods; (2) the screening questions in the EHR were nonspecific, with a prompt for the nurse or physician to assess "tobacco smoke exposure" or "smokers in the home"; (3) overly general screening questions that did not determine the type of tobacco product, location, amount, and frequency of exposure.Indeed, the way parents are asked about TSE may significantly impact responses: Groner et al2 determined sensitivity and specificity and correlation with hair nicotine levels for a variety of tobacco screening questions. They concluded that a "one size fits all" approach was insufficient and recommended universal biochemical screening for TSE.2 In several other studies, parental report was found to underestimate children's TSE when compared with cotinine levels.3,4 By contrast, Wilson et al5 found no differences between parental report and cotinine levels measured in children seen in a pediatric emergency department.Why is screening for TSE so important? Despite the decreasing prevalence of cigarette smoking among adults (now at 14.0% nationally), 37.9% of children 3 to 11 years old are exposed to tobacco smoke.6,7 With the rise in popularity of electronic cigarettes, also known as vapes and known by brand names such as JUUL, clinicians should also recognize the harms and inquire about potential secondhand aerosol exposure.8 This study reveals the opportunity to improve screening for all forms of TSE and to consider both universal and targeted screening and interventions. The authors conclude that universal tobacco screening should be performed, either by performing child cotinine-level testing when feasible or by "standardized and expanded TSE screening and counseling." We agree.Although a single, perfect, validated, universal screening question to determine child TSE is elusive, asking "Does anyone who lives in your home or who cares for your child smoke tobacco?" was shown in Groner et al2 to have a sensitivity of 74% and a positive predictive value of 88% when compared with measuring hair nicotine levels. The American Academy of Pediatrics (AAP), in the article "Clinical Practice Policy to Protect Children From Tobacco, Nicotine and Tobacco Smoke," recommends asking in a standardized method.9 Although child cotinine-level testing may be more sensitive in picking up TSE, many institutions may not have access to cotinine-level testing that is sensitive enough for TSE.The focus of this study was on improved screening for TSE, but the ultimate goal of identifying TSE among children who are hospitalized is to provide interventions to parents, caretakers, and patients who use tobacco products. Multiple organizations, including the National Academy of Medicine, the American Medical Association, and the AAP, recommend identification and treatment of tobacco use in health care settings, and the AAP specifically recommends providing tobacco-use treatment of parents and caretakers.9 The AAP article "Clinical Practice Policy to Protect Children From Tobacco, Nicotine, and Tobacco Smoke" provides pediatric health care providers with guidance and recommendations on the basis of the 5 A's (ask, advise, assess, assist, and arrange).9 Additional information can be accessed on the AAP Julius B. Richmond Center of Excellence Web site: https://www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/Richmond-Center/Pages/default.aspx.Universal screening for TSE should be performed for all pediatric patients who are hospitalized. How that is best accomplished may vary by institution, but the ultimate goal should not: all tobacco users should be identified and offered treatment.
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Third-hand smoke
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For species of conservation concern, ecologists often need to estimate potential population growth rates with minimal life history data. We use a survivorship database for captive mammals to show that, although survivorship scale (i.e., longevity) varies widely across mammals, survivorship shape (i.e., the age-specific pattern of mortality once survivorship has been scaled to maximum longevity) varies little. Consequently, reasonable estimates of population growth rate can be achieved for diverse taxa using a model of survivorship shape along with an estimate of longevity. In addition, we find that the parameters of survivorship shape are related to taxonomic group, a fact that may be used to further improve estimates of survivorship when full life history data are unavailable. Finally, we compare survivorship shape in captive and wild populations of the same species and find higher adult survivorship in captive populations but no corresponding increase in juvenile survivorship. These differences likely reflect a convolution of true differences in captive vs. wild survivorship and the difficulty of observing juvenile mortality in field studies.
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Vital rates
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A specification of mortality or survivorship provides respective explicit details about mortality's or survivorship's relationships with one or more other variables (e.g., age, sex, etc.). Previous studies have discovered and analyzed diverse specifications of mortality or survivorship; these discoveries and analyses suggest that additional specifications of mortality or survivorship have yet to be discovered and analyzed. In consistency with previous research, multivariable limited powered polynomials regression analyses of mortality and survivorship of selected humans (Swedes, 1760–2008) and selected insects (caged medflies) show age-specific, historical-time-specific, environmental-context-specific, and sex-specific mortality and survivorship. These analyses also present discoveries of hitherto unknown lifespan-specific, contemporary-aggregate-size-specific, and lifespan-aggregate-size-specific mortality and survivorship. The results of this investigation and results of previous research help identify variables for inclusion in regression models of mortality or survivorship. Moreover, these results and results of previous research strengthen the suggestion that additional specifications of mortality or survivorship have yet to be discovered and analyzed, and they also suggest that specifications of mortality and survivorship indicate corresponding specifications of frailty and vitality. Furthermore, the present analyses reveal the usefulness of a multivariable limited powered polynomials regression model-building approach. This article shows that much has yet to be learned about specifications of mortality or survivorship of diverse kinds of individuals in diverse times and places.
Cancer Survivorship
Vitality
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Cook DG, Strachan DP . Parental smoking and prevalence of respiratory symptoms and asthma in school age children. Thorax1997 Dec; 52 : 1081 –94. [OpenUrl][1][Abstract][2] Question In school age children, is exposure to parental (environmental) tobacco smoke associated with an increased risk of asthma and respiratory symptoms? Studies were identified with Medline and Embase searched to April 1997 using the terms tobacco smoke pollution; passive, second hand, involuntary, parent, maternal, mother, paternal, father or household; and smok—with various endings, tobacco or cigarette. Bibliographies of relevant studies were also reviewed. Studies were selected if they evaluated school age children (5–16 y) and both exposure to parental tobacco smoke and respiratory symptoms or asthma were assessed. Data were extracted on year of publication, country of study, population characteristics including age, symptoms … [1]: {openurl}?query=rft.jtitle%253DThorax%26rft.stitle%253DThorax%26rft.aulast%253DCook%26rft.auinit1%253DD.%26rft.volume%253D52%26rft.issue%253D12%26rft.spage%253D1081%26rft.epage%253D1094%26rft.atitle%253DHealth%2Beffects%2Bof%2Bpassive%2Bsmoking.%2B3.%2BParental%2Bsmoking%2Band%2Bprevalence%2Bof%2Brespiratory%2Bsymptoms%2Band%2Basthma%2Bin%2Bschool%2Bage%2Bchildren%26rft_id%253Dinfo%253Adoi%252F10.1136%252Fthx.52.12.1081%26rft_id%253Dinfo%253Apmid%252F9516904%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/ijlink?linkType=ABST&journalCode=thoraxjnl&resid=52/12/1081&atom=%2Febnurs%2F1%2F3%2F86.atom
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Survivorship data by general age-class are reviewed for 30 species of turtles representing nine families. Survivorship varies significantly across age-classes, with mortality generally inversely related to age (type III survivorship). Survivorship also varies significantly across habitat types, with marine and terrestrial turtles exhibiting higher survivorship early in life than freshwater turtles. Marine turtles also tend to have the lowest survivorship as adults. The implications of these findings for the evolution of marine and terrestrial turtles form ancestral freshwater forms are discussed.
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