<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.tobaccoinduceddiseases.com/feeds/latestarticles/journal?quantity=&amp;format=rss&amp;version=">
        <title>Tobacco Induced Diseases - Latest Articles</title>
        <link>http://www.tobaccoinduceddiseases.com</link>
        <description>The latest research articles published by Tobacco Induced Diseases</description>
        <dc:date>2012-02-02T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/10/1/1" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/13" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/12" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/11" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/10" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/9" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/8" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/7" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/6" />
                                <rdf:li rdf:resource="http://www.tobaccoinduceddiseases.com/content/9/1/5" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/10/1/1">
        <title>Varenicline as a smoking cessation aid in a Greek population: a subanalysis of an observational study</title>
        <description>Background:
Greece has the highest proportion of smokers in the European Union with 42% of Greeks admitting that they smoke, based on a 2009 survey. This post-hoc analysis of a prospective, observational study evaluated the effectiveness and safety profile of the smoking cessation aid varenicline, as well as potential predictors of quit success in a Greek population.
Methods:
Participants were prescribed varenicline according to the recommendations of the European Summary of Product Characteristics (1 mg twice daily). The 7-day point prevalence of abstinence at Week 12 was determined based on verbal reporting using a nicotine use inventory. Abstinence was confirmed by carbon monoxide measurements of exhaled air at the last visit of the study. The safety profile of varenicline was also assessed.
Results:
At baseline, the Greek subsample (n=196) had a mean age of 42.6 years, with 54.6% of them being men. Participants had a smoking history of 23.5 years and a Fagerstrom Test for Nicotine Dependence total score of 6.6. After 12 weeks of varenicline therapy, 70.4% (95% CI, 64.0-76.7) of all participants had quit smoking. This increased to 86.2% among participants who had taken the study medication for 80% of the planned number of treatment days. Age was a significant predictor of quit success. The most frequently observed treatment-emergent adverse event was nausea, occurring in 13.3% of participants.
Conclusions:
In this &apos;real-world&apos; observational study, 70.4% of Greek smokers successfully quit smoking after 12 weeks of varenicline therapy, providing support that varenicline is an effective smoking cessation medication. Further studies with longer follow-up are warranted.Trial Registration: www.clinicaltrials.gov (unique identifier: NCT00669240).</description>
        <link>http://www.tobaccoinduceddiseases.com/content/10/1/1</link>
                <dc:creator>Christina Gratziou</dc:creator>
                <dc:creator>Konstantinos Gourgoulianis</dc:creator>
                <dc:creator>Paraskevi Argyropoulou Pataka</dc:creator>
                <dc:creator>Georgia Sykara</dc:creator>
                <dc:creator>Michael Messig</dc:creator>
                <dc:creator>Sunil Raju</dc:creator>
                <dc:source>Tobacco Induced Diseases 2012, null:1</dc:source>
        <dc:date>2012-02-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-10-1</dc:identifier>
                                <prism:require>/content/figures/1617-9625-10-1-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2012-02-02T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/13">
        <title>Cigarette ignition propensity, smoking behavior, and toxicant exposure: A natural experiment in Canada</title>
        <description>Background:
This study used a &quot;pre-post&quot; research design to measure the impact of the Canadian reduced ignition propensity law on cigarette toxicity and smoking behavior among Canadian smokers.MethodThe study was conducted in Ontario, Canada over a ten-month period in 2005-2006, consisting of 4 laboratory visits (baseline N=61, final N=42). At Visit 1, questionnaire data and biospecimens were collected. During the following 24 hours, participants smoked 5 cigarettes ad libitum through a topography recording device and collected their cigarette butts. Visit 2 consisted of a questionnaire and smoking one cigarette to measure laboratory topography values.  After ten months, these procedures were repeated.
Results:
Generalized estimating equations, with law status (pre and post) as a fixed within-subject factor, were used to determine changes in behavior and biomarker exposure. Overall, there were no significant differences in smoking topography, breath carbon monoxide, and saliva cotinine pre-post law (p&gt;0.3). However, analyses revealed a significant increase in the summed concentrations of hydroxyfluorene metabolites (p = 0.013, 22% increase), hydroxyphenanthrene metabolites (p = 0.061, 17% increase), and 1-hydroxypyrene in urine (p = 0.018, 24% increase).
Conclusion:
While the results suggest no change in topography variables, data showed increases in exposure to three PAH biomarkers following reduced ignition propensity implementation in Canada.  These findings suggest that human studies should be considered to evaluate policy impacts.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/13</link>
                <dc:creator>Kristie June</dc:creator>
                <dc:creator>David Hammond</dc:creator>
                <dc:creator>Andreas Sjodin</dc:creator>
                <dc:creator>Zheng Li</dc:creator>
                <dc:creator>Lovisa Romanoff</dc:creator>
                <dc:creator>Richard O'Connor</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:13</dc:source>
        <dc:date>2011-12-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-13</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-13-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>13</prism:startingPage>
        <prism:publicationDate>2011-12-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/12">
        <title>Smoking, white blood cell counts, and TNF system activity in Japanese male subjects with normal glucose tolerance. </title>
        <description>Background:
Cigarette smokers have increased white blood cell (WBC) counts and the activation of tumor necrosis factor (TNF). The effect of smoking on WBC counts and TNF system activity, however, has not been separately investigated yet.Subjects and MethodsOne hundred and forty-two Japanese male subjects with normal glucose tolerance were recruited. They were stratified into two groups based on the questionnaire for smoking: one with current smokers (n = 48) and the other with current non-smokers (n = 94). Whereas no significant differences were observed in age, BMI, high molecular weight (HMW) adiponectin, and TNF-&#945; between the two groups, current smokers had significantly higher soluble TNF receptor 1 (sTNF-R1) (1203 &#177; 30 vs. 1116 &#177; 21 pg/ml, p = 0.010) and increased WBC counts (7165 &#177; 242 vs. 5590 &#177; 163/&#956;l, p &lt; 0.001) and lower HDL cholesterol (55 &#177; 2 vs. 60 &#177; 1 mg/dl, p = 0.031) as compared to current non-smokers. Next, we classified 48 current smokers into two subpopulations: one with heavy smoking (Brinkman index &#8805; 600) and the other with light smoking (Brinkman index &lt; 600).
Results:
Whereas no significant difference was observed in age, BMI, HMW adiponectin, WBC counts and TNF-&#945;, sTNF-R1 and sTNF-R2 were significantly higher in heavy smoking group (1307 &#177; 44 vs. 1099 &#177; 30 pg/ml, p &lt; 0.001; 2166 &#177; 86 vs. 827 &#177; 62 pg/ml, p = 0.005) than in light smoking group, whose sTNF-R1 and sTNF-R2 were similar to non-smokers (sTNF-R1: 1116 &#177; 15 pg/ml, p = 0.718, sTNF-R2; 1901 &#177; 32 pg/ml, p = 0.437). In contrast, WBC counts were significantly increased in heavy (7500 &#177; 324/&#956;l, p &lt; 0.001) or light (6829 &#177; 352/&#956;l, p = 0.001) smoking group as compared to non-smokers (5590 &#177; 178/&#956;l). There was no significant difference in WBC counts between heavy and light smoking group (p = 0.158).
Conclusion:
We can hypothesize that light smoking is associated with an increase in WBC counts, while heavy smoking is responsible for TNF activation in Japanese male subjects with normal glucose tolerance.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/12</link>
                <dc:creator>Naoya Watanabe</dc:creator>
                <dc:creator>Mitsuo Fukushima</dc:creator>
                <dc:creator>Ataru Taniguchi</dc:creator>
                <dc:creator>Takahide Okumura</dc:creator>
                <dc:creator>Yoshio Nomura</dc:creator>
                <dc:creator>Fusanori Nishimura</dc:creator>
                <dc:creator>Sae Aoyama</dc:creator>
                <dc:creator>Daisuke Yabe</dc:creator>
                <dc:creator>Yoshio Izumi</dc:creator>
                <dc:creator>Ryoichi Otsubo</dc:creator>
                <dc:creator>Yoshikatsu Nakai</dc:creator>
                <dc:creator>Shoichiro Nagasaka</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:12</dc:source>
        <dc:date>2011-11-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-12</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-12-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>12</prism:startingPage>
        <prism:publicationDate>2011-11-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/11">
        <title>Toward Improved Statistical Methods for Analyzing 
Cotinine-Biomarker Health Association Data 
</title>
        <description>Background:
Serum cotinine, a metabolite of nicotine, is frequently used in research as a biomarker of recent tobacco smoke exposure. Historically, secondhand smoke (SHS) research uses suboptimal statistical methods due to censored serum cotinine values, meaning a measurement below the limit of detection (LOD).
Methods:
We compared commonly used methods for analyzing censored serum cotinine data using parametric and non-parametric techniques employing data from the 1999-2004 National Health and Nutrition Examination Surveys (NHANES). To illustrate the differences in associations obtained by various analytic methods, we compared parameter estimates for the association between cotinine and the inflammatory marker homocysteine using complete case analysis, single and multiple imputation, &quot;reverse&quot; Kaplan-Meier, and logistic regression models.
Results:
Parameter estimates and statistical significance varied according to the statistical method used with censored serum cotinine values. Single imputation of censored values with either 0, LOD or LOD/&#8730;2 yielded similar estimates and significance; multiple imputation method yielded smaller estimates than the other methods and without statistical significance. Multiple regression modelling using the &quot;reverse&quot; Kaplan-Meier method yielded statistically significant estimates that were larger than those from parametric methods.
Conclusions:
Analyses of serum cotinine data with values below the LOD require special attention. &quot;Reverse&quot; Kaplan-Meier was the only method inherently able to deal with censored data with multiple LODs, and may be the most accurate since it avoids data manipulation needed for use with other commonly used statistical methods. Additional research is needed into the identification of optimal statistical methods for analysis of SHS biomarkers subject to a LOD.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/11</link>
                <dc:creator>Tulay Koru-Sengul</dc:creator>
                <dc:creator>John Clark</dc:creator>
                <dc:creator>Lora Fleming</dc:creator>
                <dc:creator>David Lee</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:11</dc:source>
        <dc:date>2011-10-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-11</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-11-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2011-10-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/10">
        <title>Interest in technology-based and traditional smoking cessation programs among adult smokers in Ankara, Turkey</title>
        <description>Background:
Little is known about the demand for smoking cessation services in settings with high smoking prevalence rates. Furthermore, acceptability of text messaging and Internet as delivery mechanisms for smoking cessation programs in non-developed countries is under-reported. Given the cost effectiveness of technology-based programs, these may be more feasible to roll out in settings with limited public health resources relative to in-person programs.Findings148 adult smokers took part in a community-based survey in Ankara, Turkey. Two in five (43%) respondents reported typically smoking their first cigarette within 30 minutes of waking. Many participants expressed a desire to quit smoking: 27% reported seriously thinking about quitting in the next 30 days; 53% reported at least one quit attempt in the past year. Two in five smokers wanting to quit reported they were somewhat or extremely like to try a smoking cessation program if it were accessible via text messaging (45%) or online (43%).
Conclusions:
Opportunities for low-cost, high-reach, technology-based smoking cessation programs are under-utilized. Findings support the development and testing of these types of interventions for adult smokers in Turkey.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/10</link>
                <dc:creator>Michele Ybarra</dc:creator>
                <dc:creator>A.Tulay Bagci Bosi</dc:creator>
                <dc:creator>Nazmi Bilir</dc:creator>
                <dc:creator>Jodi Holtrop</dc:creator>
                <dc:creator>Josephine Korchmaros</dc:creator>
                <dc:creator>A.K. Salih Emri</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:10</dc:source>
        <dc:date>2011-08-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-10</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-10-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2011-08-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/9">
        <title>Tobacco retailer density surrounding schools and youth smoking behaviour: a multi-level analysis</title>
        <description>Background:
Youth smoking prevention should be a public health priority. It is not only vital to prevent youth from smoking but also to prevent non-smoking youth from becoming susceptible to smoking. Past research has examined factors associated with youth&apos;s susceptibility to become a future smoker, but research has yet to examine tobacco retailer density and susceptibility to smoking among never smokers. The objectives of this study are to examine how tobacco retailer density surrounding schools and social smoking influences are associated with smoking susceptibility among youth of never smokers, and occasional and daily smoking among youth of current smokers.
Methods:
Data were collected in 2005-2006 from grade 9 to 12 students attending 76 secondary schools in Ontario, Canada, as part of the SHAPES-On study. A series of multi-level logistic regression analyses were performed to understand how student- and school-level factors are associated with three smoking behaviour outcomes: smoking susceptibility among never smokers, occasional smoking, and daily smoking.
Results:
The number of tobacco retailers surrounding a school was found to be associated with the likelihood of a never smoker being susceptible to future smoking (OR 1.03, 95CI% 1.01, 1.05). We also identified that being surrounded by smoking social influences, specifically family and close friends, can substantially increase the likelihood that never smokers are at risk for future smoking or that youth are already occasional or daily smokers.
Conclusions:
We identified that the number of tobacco retailers surrounding a school was associated with an increased odds of being susceptible to future smoking among male never smokers. Smoking social models surrounding youth also appears to have an important impact on their smoking behaviour regardless of their smoking status. It is important for youth smoking prevention programs to begin early, interrupt youths&apos; susceptibility to future smoking, and focus on subgroups that are at higher risk of smoking. The government should consider the impact of tobacco retailer density on youth smoking behaviour, and be cautious when granting licenses for establishments to sell tobacco products.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/9</link>
                <dc:creator>Wing Chan</dc:creator>
                <dc:creator>Scott Leatherdale</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:9</dc:source>
        <dc:date>2011-07-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-9</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-9-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2011-07-27T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/8">
        <title>Lethal impacts of cigarette smoke in cultured tobacco cells</title>
        <description>Background:
In order to understand and generalize the toxic mechanism of cigarette smoke in living cells, comparison of the data between animal systems and other biological system such as microbial and plant systems is highly beneficial.ObjectiveBy employing the tobacco cells as model materials for cigarette smoke toxicity assay, the impacts of the combustion by-products such as nitrogen oxides could be highlighted as the toxic impacts of the plant-derived endogenous chemicals could be excluded in the plant cells.
Methods:
Cigarette smoke-induced cell death was assessed in tobacco cell suspension cultures in the presence and absence of pharmacological inhibitors.
Results:
Cigarette smoke was effective in induction of cell death. The smoke-induced cell death could be partially prevented by addition of nitric oxide (NO) scavenger, suggesting the role for NO as the cell death mediator. Addition of NO donor to tobacco cells also resulted in development of partial cell death further confirming the role of NO as cell death mediator. Members of reactive oxygen species and calcium ion were shown to be protecting the cells from the toxic action of smoke-derived NO.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/8</link>
                <dc:creator>Masaru Yukihiro</dc:creator>
                <dc:creator>Takuya Hiramatsu</dc:creator>
                <dc:creator>Tomonori Kawano</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:8</dc:source>
        <dc:date>2011-07-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-8</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-8-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2011-07-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/7">
        <title>Regulating duty free sales and tobacco advertising in airports: a call for action</title>
        <description>According to the United Nations&apos; World Tourism Organization, there were an estimated 880 million international travelers in 2009, or roughly 13% of the world&apos;s population. While tobacco remains one of the world&apos;s leading causes of preventable disease and death, prompting numerous governments around the world to implement policies to protect the public&apos;s health from the harm caused by tobacco, many international airports remain exempt from tobacco control restrictions. Tobacco advertising and tobacco sales are largely unregulated in many international airports, exposing hundreds of millions of travelers each year to the tobacco industry&apos;s influence. Consequently, airports may represent one of the last remaining havens for the tobacco industry.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/7</link>
                <dc:creator>Constantine Vardavas</dc:creator>
                <dc:creator>Andrew Seidenberg</dc:creator>
                <dc:creator>Gregory Connolly</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:7</dc:source>
        <dc:date>2011-06-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-7</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-7-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2011-06-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/6">
        <title>Trends in Smokeless Tobacco Use in the US Workforce: 1987-2005 </title>
        <description>The primary aim was to examine whether increasing workplace smoking restrictions have led to an increase in smokeless tobacco use among US workers. Smokeless tobacco exposure increases the risk of oral cavity, esophageal, and pancreatic cancers, and stroke. The prevalence of smokeless tobacco use decreased from 1987-2000, except among men 25-44. While smokeless tobacco use has declined in the general population, it may be that the prevalence of smokeless tobacco use has increased among workers due to workplace smoking restrictions, which have been shown to have increased over the years. Using the most current nationally representative National Health Interview Survey (NHIS) data, we examined whether increasing workplace smoking restrictions have led to an increase in smokeless tobacco use among US workers (n = 125,838). There were no significant changes in smokeless tobacco use prevalence from 1987-2005 (pooled prevalence = 3.53%); rates also were lower in smoke free workplaces. Worker groups with high rates of smokeless tobacco use included farm workers (10.51%) and blue collar workers (7.26%). Results indicate that smokeless tobacco prevention strategies targeting particular worker groups are warranted.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/6</link>
                <dc:creator>Noella Dietz</dc:creator>
                <dc:creator>David Lee</dc:creator>
                <dc:creator>Lora Fleming</dc:creator>
                <dc:creator>William LeBlanc</dc:creator>
                <dc:creator>Kathryn McCollister</dc:creator>
                <dc:creator>Kristopher Arheart</dc:creator>
                <dc:creator>Evelyn Davila</dc:creator>
                <dc:creator>Alberto Caban-Martinez</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:6</dc:source>
        <dc:date>2011-06-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-6</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-6-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2011-06-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.tobaccoinduceddiseases.com/content/9/1/5">
        <title>Reduction in Oxidatively Generated DNA Damage Following Smoking Cessation</title>
        <description>Background:
Cigarette smoking is a known cause of cancer, and cancer may be in part due to effects of oxidative stress. However, whether smoking cessation reverses oxidatively induced DNA damage unclear. The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.
Methods:
Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial and provided blood samples from which leukocyte DNA was extracted and assessed for 3 DNA lesions (thymine glycol modification [d(TgpA)]; formamide breakdown of pyrimidine bases [d(TgpA)]; 8-oxo-7,8-dihydroguanine [d(Gh)]) via liquid chromatography tandem mass spectrometry (LC-MS/MS). Change in lesions over time was assessed using generalized estimating equations, controlling for gender, age, and treatment condition.
Results:
Overall time effects for the d(TgpA) (&#967;2(3) = 8.068, p &lt; 0.045), d(PfpA) (&#967;2(3) = 8.477, p &lt; 0.037), and d(Gh) (&#967;2(3) = 37.599, p &lt; 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed smoking cessation. The d(TgpA) and d(PfpA) lesions show relatively greater rebound at Week 16 compared to the d(Gh) lesion (88% of baseline for d(TgpA), 64% of baseline for d(PfpA), vs 46% of baseline for d(Gh)).
Conclusions:
Overall, results from this analysis suggest that cigarette smoking contributes to oxidatively induced DNA damage, and that smoking cessation appears to reduce levels of specific damage markers between 30-50 percent in the short term. Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.</description>
        <link>http://www.tobaccoinduceddiseases.com/content/9/1/5</link>
                <dc:creator>Harold Box</dc:creator>
                <dc:creator>Richard O'Connor</dc:creator>
                <dc:creator>Helen Patrzyc</dc:creator>
                <dc:creator>Herbert Iijima</dc:creator>
                <dc:creator>Jean Dawidzik</dc:creator>
                <dc:creator>Harold Freund</dc:creator>
                <dc:creator>Edwin Budzinski</dc:creator>
                <dc:creator>K Michael Cummings</dc:creator>
                <dc:creator>Martin Mahoney</dc:creator>
                <dc:source>Tobacco Induced Diseases 2011, null:5</dc:source>
        <dc:date>2011-05-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1617-9625-9-5</dc:identifier>
                                <prism:require>/content/figures/1617-9625-9-5-toc.gif</prism:require>
                <prism:publicationName>Tobacco Induced Diseases</prism:publicationName>
        <prism:issn>1617-9625</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2011-05-12T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>

