Association of tobacco dependence and quit attempt duration with Rasch-modeled withdrawal sensitivity using retrospective measures

Aim   To examine whether Rasch modeling would yield a unidimensional withdrawal sensitivity measure correlating with factors associated with successful smoking cessation.
Design   The psychometric Rasch modeling approach was applied to estimate an underlying latent construct (withdrawal sensitivity) in retrospective responses from 1644 smokers who reported quitting for 3 or more months at least once.
Setting   Web-based, passcode-controlled self-administered computerized questionnaire.
Participants   Randomly selected convenience sample of 1644 adult members of an e-mail invitation-only web panel drawn from consumer databases.
Measurements   Lifetime Tobacco Use Questionnaire, assessing tobacco use across the life-span, including demographics and respondent ratings of the severity of withdrawal symptoms experienced in respondents' first and most recent quit attempts lasting 3 or more months.
Findings   Rasch-modeled withdrawal sensitivity was generally unidimensional and was associated with longer periods of smoking cessation. One latent variable accounted for 74% of the variability in symptom scores. Rasch modeling with a single latent factor fitted withdrawal symptoms well, except for increased appetite, for which the fit was marginal. Demographic variables of education, gender and ethnicity were not related to changes in sensitivity. Correlates of greater withdrawal sensitivity in cessation attempts of at least 3 months included younger age at first quit attempt and indicators of tobacco dependence.
Conclusion   The relationship between tobacco dependence symptoms and Rasch-model withdrawal sensitivity defines further the relationship between sensitivity and dependence. The findings demonstrate the utility of modeling to create an individual-specific sensitivity measure as a tool for exploring the relationships among sensitivity, dependence and cessation.     

The interaction of glutathione S-transferase M1-null variants with tobacco smoke exposure and the development of childhood asthma

Background The glutathione S -transferase M1 (GSTM1)-null variant is a common copy number variant associated with adverse pulmonary outcomes, including asthma and airflow obstruction, with evidence of important gene-by-environment interactions with exposures to oxidative stress.
Objective To explore the joint interactive effects of GSTM1 copy number and tobacco smoke exposure on the development of asthma and asthma-related phenotypes in a family-based cohort of childhood asthmatics.
Methods We performed quantitative PCR-based genotyping for GSTM1 copy number in children of self-reported white ancestry with mild to moderate asthma in the Childhood Asthma Management Program. Questionnaire data regarding intrauterine (IUS) and post-natal, longitudinal smoke exposure were available. We performed both family-based and population-based tests of association for the interaction between GSTM1 copy number and tobacco smoke exposure with asthma and asthma-related phenotypes.
Results Associations of GSTM1-null variants with asthma ( P =0.03), younger age of asthma symptom onset ( P =0.03), and greater airflow obstruction (reduced forced expiratory volume in 1 s / forced vital capacity, P =0.01) were observed among the 50 children (10% of the cohort) with exposure to IUS. In contrast, no associations were observed between GSTM1-null variants and asthma-related phenotypes among children without IUS exposure. Presence of at least one copy of GSTM1 conferred protection.
Conclusion These findings support an important gene-by-environment interaction between two common factors: increased risk of asthma and asthma-related phenotypes conferred by GSTM1-null homozygosity in children is restricted to those with a history of IUS exposure.     

Chronic pancreatitis and extrapancreatic cancer A retrospective study among 181 patients with chronic pancreatitis

Summary The relationship between chronic pancreatitis (CP) and extrapancreatic cancer has been debated in the recent years. In prospective studies, it has been found that pancreatic cancer develops in 0–5% of patients with chronic pancreatitis. Many papers describe an increased relative risk for developing extrapancreatic cancer in patients suffering from chronic pancreatitis. In this study including 181 patients with CP, we found 14 patients with extrapancreatic cancer (three of these had two different types of cancer). No patient had pancreatic cancer. It was found that the respiratory airways and upper gastrointestinal tract were the dominating locations (five and four cases, respectively), but also genital and hemolymphopoietic cancers were represented (four and two cases, respectively). Two patients had metastatic cancer with unknown primary tumor. The patients with cancer tended to be older than those without cancer. The patients with CP had a 2.43 times greater risk of developing cancer than the general Danish population (age and sex standardized comparison). The relatively large number of cancers in the upper gastrointestinal tract and respiratory airways suggest that tobacco and alcohol may be responsible, as these organs have the highest exposure to these compounds, which are well known carcinogens.     

Tobacco smoke exposure, wheeze, and atopy

We investigated the effect of in utero and postnatal environmental tobacco smoke (ETS) exposure on respiratory symptoms and atopy in the first 3 years of life in children at high risk of allergic disease (both parents atopic). Three hundred and sixty-nine children were followed from birth and reviewed at ages 1 and 3 years (respiratory questionnaire, skin testing). Parental smoking questionnaires were administered, and plasma cotinine in cord and peripheral blood (at age 1 year) was measured (capillary column gas-liquid chromatography). Wheezing starting in the first year of life was significantly more common in children of smoking mothers (54.2% vs. 39.5%, P = 0.017), but not wheezing starting after age 1 year (10.8% vs. 10.9%, smoking and nonsmoking mothers, P = 0.99). Detectable cord cotinine was not associated with wheeze. More frequent wheeze in infancy was significantly more common in those with detectable 1-year cotinine (e.g., wheeze without colds, 17.8% vs. 5.6%, P = 0.02; wheeze most days, 6.5% vs. 0%, P = 0.04). ETS exposure was not associated with atopy. In the multivariate regression analysis, maternal smoking during pregnancy and/or in the first year of life remained associated with wheeze in the first year of life (odds ratio, 1.88; 95% confidence interval, 1.14-3.12; P = 0.01). ETS exposure in "high-risk" infants increases the risk of wheezing starting in the first year of life, but not after age 1 year. However, ETS exposure has little or no effect on the development of atopy. Measurement of plasma cotinine was no more useful than tobacco exposure assessment by questionnaire in our cohort.     

Association of tobacco smoke exposure and respiratory syncitial virus infection with airways reactivity in early childhood.

Exposure to infectious agents and environmental tobacco smoke are thought to induce bronchial hyperresponsiveness (BHR). This study was undertaken to determine the effects of passive exposure to tobacco smoke and respiratory syncitial virus (RSV) lower respiratory infection (LRI) during infancy on the occurrence of BHR in the first 2 years of life. Eighty-six cases of documented RSV (mean age, 188 days) and 78 controls (mean age, 162 days) were enrolled from the clinic and in-patient service of a single hospital. None had a history of prior LRI. Subjects were studied at 6-month intervals up to 19 months of age with a standardized respiratory illness and parental smoking questionnaire, partial expiratory flow-volume curves by the "hug" (rapid thoracic compression) technique, and methacholine challenge. Exposure to maternal and paternal cigarette smoking, maternal history of asthma, and mold exposure were associated with decreased levels of length-corrected maximal flow at functional residual capacity (V'(maxFRC)). RSV-LRI was not related to V'(maxFRC). After adjustment of V'(maxFRC) for these factors, V'(maxFRC) was a significantly and positively correlated with a methacholine concentration provoking a 40% fall in V'(maxFRC) (PC40) and negatively correlated with dose-response slope. After adjustment for V'(maxFRC), there were no independent effects of tobacco smoke exposure or RSV-LRI on methacholine responses. These data do not support a role for RSV as a risk factor for airways reactivity in childhood and indicate that exposure to tobacco smoke affects airways reactivity through its effects on airways.     

Tobacco‐Control Policies in Tobacco‐Growing States: Where Tobacco Was King

Context

The 5 major tobacco-growing states (Kentucky, North Carolina, South Carolina, Tennessee, and Virginia) are disproportionately affected by the tobacco epidemic, with higher rates of smoking and smoking-induced disease. These states also have fewer smoke-free laws and lower tobacco taxes, 2 evidence-based policies that reduce tobacco use. Historically, the tobacco farmers and hospitality associations allied with the tobacco companies to oppose these policies.

Methods

This research is based on 5 detailed case studies of these states, which included key informant interviews, previously secret tobacco industry documents (available at http://legacy.library.ucsf.edu), and media articles. This was supplemented with additional tobacco document and media searches specifically for this article.

Findings

The tobacco companies were particularly concerned about blocking tobacco-control policies in the tobacco-growing states by promoting a pro-tobacco culture, beginning in the late 1960s. Nevertheless, since 2003, there has been rapid progress in the tobacco-growing states’ passage of smoke-free laws. This progress came after the alliance between the tobacco companies and the tobacco farmers fractured and hospitality organizations stopped opposing smoke-free laws. In addition, infrastructure built by National Cancer Institute research projects (COMMIT and ASSIST) led to long-standing tobacco-control coalitions that capitalized on these changes. Although tobacco production has dramatically fallen in these states, pro-tobacco sentiment still hinders tobacco-control policies in the major tobacco-growing states.

Conclusions

The environment has changed in the tobacco-growing states, following a fracture of the alliance between the tobacco companies and their former allies (tobacco growers and hospitality organizations). To continue this progress, health advocates should educate the public and policymakers on the changing reality in the tobacco-growing states, notably the great reduction in the number of tobacco farmers as well as in the volume of tobacco produced.     

The Tobacco Pack Surveillance System: A Protocol for Assessing Health Warning Compliance,Design Features,and Appeals of Tobacco Packs Sold in Low- and Middle-Income Countries

Background

Tobacco remains the world’s leading preventable cause of death, with the majority of tobacco-caused deaths occurring in low- and middle-income countries. The first global health treaty, the Framework Convention on Tobacco Control (FCTC), outlines a set of policy initiatives that have been demonstrated as effective in reducing tobacco use. Article 11 of the FCTC focuses on using the tobacco package to communicate tobacco-caused harms; it also seeks to restrict the delivery of misleading information about the product on the pack.

Objective

The objective of this study was to establish a surveillance system for tobacco packs in the 14 low- and middle-income countries with the greatest number of smokers. The Tobacco Pack Surveillance System (TPackSS) monitors whether required health warnings on tobacco packages are being implemented as intended, and identifies pack designs and appeals that might violate or detract from the communication of harm-related information and undermine the impact of a country’s tobacco packaging laws. The protocol outlined is intended to be applicable or adaptable for surveillance efforts in other countries.

Methods

Tobacco packs were collected in 14 countries during 2013. The intention was, to the extent possible, to construct a census of “unique” pack presentations available for purchase in each country. The TPackSS team partnered with in-country field staff to implement a standardized protocol for acquiring packs from 36 diverse neighborhoods across three cities in each country. At the time of purchase, data on price and place of acquisition of each pack was recorded. The field staff, according to a standardized protocol, then photographed packs before they were shipped to the United States for coding and archiving.

Results

Each pack was coded for compliance with the country-specific health warning label laws, as well as for key design features of the pack and appeals of the branding elements. The coding protocols were developed based upon prior research, expert opinion, and communication theories. Each pack was coded by two independent coders, with consistency of personnel across the project. We routinely measured intercoder reliability, and only retained variables for which a good level of reliability was achieved. Variables where reliability was too low were not included in final analyses, and any inconsistencies in coding were resolved on a daily basis.

Conclusions

Across the 14 countries, the TPackSS team collected 3307 tobacco packs. We have established a publicly accessible, Internet archive of these packs that is intended for use by the tobacco control policy advocacy and research community.