Light Smokers Research Articles

Pooled analysis of the HLA-DRB1 by smoking interaction in Parkinson disease.

Inflammatory response plays an important role in Parkinson disease (PD). Previous studies have reported an association between human leukocyte antigen (HLA)-DRB1 and the risk of PD. There has also been growing interest in investigating whether inflammation-related genes interact with environmental factors such as smoking to influence PD risk. We performed a pooled analysis of the interaction between HLA-DRB1 and smoking in PD in 3 population-based case-control studies from Denmark and France. We included 2,056 cases and 2,723 controls from 3 PD studies (Denmark, France) that obtained information on smoking through interviews. Genotyping of the rs660895 polymorphism in the HLA-DRB1 region was based on saliva or blood DNA samples. To assess interactions, we used logistic regression with product terms between rs660895 and smoking. We performed random-effects meta-analysis of marginal associations and interactions. Both carrying rs660895-G (AG vs AA: odds ratio [OR] = 0.81; GG vs AA: OR = 0.56; p-trend = 0.003) and ever smoking (OR = 0.56, p < 0.001) were inversely associated with PD. A multiplicative interaction was observed between rs660895 and smoking using codominant, additive (interaction parameter = 1.37, p = 0.005), and dominant (interaction parameter = 1.54, p = 0.001) genetic models without any heterogeneity (I² = 0.0%); the inverse association of rs660895-(AG+GG) with PD seen in never smokers (OR = 0.64, p < 0.001) disappeared among ever smokers (OR = 1.00, p = 0.99). Similar interactions were observed when we investigated light and heavy smokers separately. Our study provides the first evidence that smoking modifies the previously reported inverse association of rs660895-G with PD, and suggests that smoking and HLA-DRB1 are involved in common pathways, possibly related to neuroinflammation. Ann Neurol 2017;82:655-664.

Intent to quit, quit attempts, and perceived health risk reduction among African American, Latino, and White nondaily and daily smokers in the United States

ABSTRACTObjective: Ethnic and racial differences in smoking patterns and behaviors have been well documented and most African American and Latino smokers are nondaily or light smokers. However, differences within smoking levels are understudied. Our primary aim was to determine whether there are racial and ethnic differences among African American, Latino, and White nondaily, light daily, and moderate to heavy daily smokers on (1) perceived health risk reduction, (2) intentions to quit, and (3) past year quit attempts.Design: Smokers were recruited through an online research panel for a cross-sectional survey (n = 2376). Sampling quotas were used to obtain equal numbers of African American, Latino, and White nondaily and daily smokers.Results: African American (59.6%) and Latino (54%) nondaily smokers were more likely than White nondaily smokers (45%) to currently limit their cigarettes per day (cpd) as a perceived health risk reduction strategy (p < 0.05). African American nondaily smokers were more likely than Latino and White nondaily smokers (p < 0.05) to limit their smoking in the past year as a perceived health risk reduction strategy (range: 0 ‘never’ to 5 ‘always’; Means = 3.2, 2.9, 3.0, standard deviations [SD] = 1.1, 1.1, 1.2, respectively). African American nondaily smokers (15%) were more likely than either Latinos (7.8%) or Whites (8.5%) to intend to quit in the next 30 days (p < 0.01). African American (61.6%) and Latino (60.3%) nondaily smokers were more likely than Whites (49%) to have made a quit attempt in the past year (p < 0.01). Fewer racial and ethnic differences were found among daily smokers.Conclusions: Racial and ethnic group differences were more pronounced among nondaily smokers compared to light daily smoker and moderate to heavy daily smokers. Smoking level is an important consideration in understanding racial and ethnic variation in perceived health risk reduction and cessation-related behaviors.

Finding a place for ceritinib in the landscape of ALK-positive nonsmall cell lung cancer

The ALK fusion oncogene was first identified in non-small cell lung cancer (NSCLC) in 2007 (1). It has been identified in approximately 3–7% of NSCLC cases, and more commonly in younger patients, and non- or light smokers. The central nervous system (CNS) is the most common site of disease progression, with many incidences of brain metastases diagnosed at disease onset. In the last 10 years, the discovery of ALK rearrangements has led to the rapid emergence of various ALK inhibitors, many developed in response to ALK resistance mutations that develop to crizotinib and to improve responses in the CNS.

Association of Preventive Maintenance Therapy Compliance and Peri-Implant Diseases: A Cross-Sectional Study.

This study aims to investigate association between peri-implant maintenance therapy (PIMT) and the frequency of peri-implant diseases and to further identify factors that contribute to failure of PIMT compliance. A cross-sectional study on patients who were healthy and partially edentulous was conducted. They were grouped in the following categories according to PIMT compliance: 1) regular compliers (RC) (≥2 PIMT/year); 2) erratic compliers (EC) (<2 PIMT/year); and 3) non-compliers (NC) (no PIMT). Radiographic and clinical analyses were carried out including probing depth (PD), plaque index (PI), bleeding on probing (BOP), mucosal redness (MR), suppuration (SUP), keratinized mucosa dimension, and marginal bone loss. A multiple logistic regression model was estimated at implant and patient level to obtain adjusted odds ratios (ORs) and to control possible confounding effects among variables. Overall, 206 implants in 115 patients fulfilled inclusion criteria. At patient level, it was shown that association between compliance and peri-implant condition was statistically significant (P = 0.04). Compliance was associated with 86% fewer conditions of peri-implantitis. The probability of PIMT compliance was substantially associated with frequency of peri-implantitis (OR = 0.13, P = 0.01). Patients with a history of periodontal disease multiplied their probability of being EC (versus NC) 4.23 times with respect to not having a history of periodontal disease (P = 0.02). Moreover, light smokers significantly resulted to be NC compared with RC (P = 0.04) and EC (P = 0.02). Nevertheless, mucositis was not found to be statistically associated with level of compliance. In addition, PD, PI, BOP, MR, and SUP varied significantly according to PIMT compliance and peri-implant condition. Peri-implant maintenance compliance ≥2 PIMT/year seems to be crucial to prevent peri-implantitis in healthy patients. Furthermore, history of periodontal disease and disease severity, as well as its extent and a smoking habit, appear to be factors that influence the compliance risk profile (NCT02789306).

Lung Cancer Mortality Associated With Smoking and Smoking Cessation Among People Living With HIV in the United States

Lung cancer has become a leading cause of death among people living with human immunodeficiency virus (HIV) (PLWH). Over 40% of PLWH in the United States smoke cigarettes; HIV independently increases the risk of lung cancer. To project cumulative lung cancer mortality by smoking exposure among PLWH in care. Using a validated microsimulation model of HIV, we applied standard demographic data and recent HIV/AIDS epidemiology statistics with specific details on smoking exposure, combining smoking status (current, former, or never) and intensity (heavy, moderate, or light). We stratified reported mortality rates attributable to lung cancer and other non-AIDS-related causes by smoking exposure and accounted for an HIV-conferred independent risk of lung cancer. Lung cancer mortality risk ratios (vs never smokers) for male and female current moderate smokers were 23.6 and 24.2, respectively, and for those who quit smoking at age 40 years were 4.3 and 4.5. In sensitivity analyses, we accounted for nonadherence to antiretroviral therapy (ART) and for a range of HIV-conferred risks of death from lung cancer and from other non-AIDS-related diseases (eg, cardiovascular disease). Cumulative lung cancer mortality by age 80 years (stratified by sex, age at entry to HIV care, and smoking exposure); total expected lung cancer deaths, accounting for nonadherence to ART. Among 40-year-old men with HIV, estimated cumulative lung cancer mortality for heavy, moderate, and light smokers who continued to smoke was 28.9%, 23.0%, and 18.8%, respectively; for those who quit smoking at age 40 years, it was 7.9%, 6.1%, and 4.3%; and for never smokers, it was 1.6%. Among women, the corresponding mortality for current smokers was 27.8%, 20.9%, and 16.6%; for former smokers, it was 7.5%, 5.2%, and 3.7%; and for never smokers, it was 1.2%. ART-adherent individuals who continued to smoke were 6 to 13 times more likely to die from lung cancer than from traditional AIDS-related causes, depending on sex and smoking intensity. Due to greater AIDS-related mortality risks, individuals with incomplete ART adherence had higher overall mortality but lower lung cancer mortality. Applying model projections to the approximately 644 200 PLWH aged 20 to 64 in care in the United States, 59 900 (9.3%) are expected to die from lung cancer if smoking habits do not change. Those PLWH who adhere to ART but smoke are substantially more likely to die from lung cancer than from AIDS-related causes.

The importance of RET -directed therapy in patients with RET- rearranged non-small cell lung cancer

Non-small cell lung cancer (NSCLC) has been recognized as a heterogeneous set of diseases according to oncogenic gene alterations level, such as sensitizing EGFR mutations, ALK rearrangements, or ROS1 rearrangements (1). Specific molecularly targeted therapies are effective in NSCLC patients harboring sensitizing EGFR mutations, ALK or ROS1 rearrangements, with response rates of approximately 60% and median progression-free survival of over 10 months (2-4). RET is a proto-oncogene that codes for a transmembrane protein belonging to the receptor tyrosine kinases family (5). In 2012, RET rearrangements were identified as new oncogenic alterations occurring in 1% to 2% of patients with NSCLC (6-9). It is reported that RET rearrangements has tumor-driving activity in vitro and in vivo . RET can partner with different genes in NSCLC, and KIF5B is the most common fusion partner in NSCLC. To date, several other genes including CCDC6, NCOA, TRIM33, CUX1, KIAA1468, KIAA1217, and FRMD4A, have been identified as other fusion partners of RET in NSCLC patients. RET rearrangements tend to be found in younger patients, female, never or former light smokers, and in patients with lung adenocarcinomas (10). A few case reports reported that cabozantinib and vandetanib, which are multi-targeted tyrosine kinase inhibitor exhibiting RET kinase activity, have antitumor activity in patients with RET -rearranged NSCLC (11-13).

Cigarette smoking associated with chronic pancreatitis: a case control study in China

BackgroundChronic pancreatitis (CP) is a long-term inflammatory disease affecting the pancreas. No studies are currently available associating cigarette smoking with CP in Chinese mainland population. This study aims to assess the evidence for tobacco smoking as a risk factor for CP and to find the dose-response relationship between them precisely in Chinese mainland population.MethodsThis retrospective study enrolled Chinese patients with CP and control patients at the Peking Union Medical College Hospital from 1983 to 2008. Demographic and clinical data were collected, and Chi-square (χ2) test and a Cox proportional hazards regression model were used for statistical analysis. This study evaluated whether cigarette smoking is a risk factor for CP in 346 patients and 346 healthy controls (CP group: 267 males, 79 females; control group: 270 males, 76 females) with mean ages of 49 and 49.2 years, respectively.ResultsIn the CP group, 46.8% were smokers, and 41% were drinkers. Heavy smokers (≥ 20 cigarettes/d), who were either male (P = 0.03) or older than 30 years (P = 0.045), or males older than 30 years (P = 0.021), were significantly more prone to CP than light smokers. CP patients, regardless of their gender, who had smoked for more than 30 years and were without biliary disease had a significantly higher risk to develop CP compared with health control group (OR = 2.35, 95% CI: 1.106–4.973, P = 0.026). There was no statistically significant association between smoking duration of less than 30 years and the risk of CP regardless of gender, age, or biliary disease.ConclusionsCigarette smoking is an important risk factor for CP in the Chinese population and correlates with risk factors, such as age, gender, biliary disease, and alcohol consumption. In conclusion, cigarette smoking is an important risk factor for CP in the Chinese subpopulation.

Intercalating and maintenance gefitinib plus chemotherapy versus chemotherapy alone in selected advanced non-small cell lung cancer with unknown EGFR status

Epidermal growth factor receptor tyrosine-kinase inhibitors (EGFR-TKIs) are standard treatment for advanced non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutation. However, EGFR mutation testing is not attainable in approximately 20% of patients. The current study examined intercalating and maintaining gefitinib treatment in stage IIIB/IV non-squamous NSCLC, never or former light smoking patients with unknown EGFR mutation status. Briefly, 219 patients who achieved stable disease (SD) with gemcitabine (1250 mg/m2) plus carboplatin (5 AUC) were randomized at 1:1 ratio to continue chemotherapy (n = 110) or intercalating gefitinib (250 mg/day on days 15–25 of each cycle until disease progress (n = 109). Progression-free survival (PFS) was 9.7 vs. 4.2 month in the gefitinib vs. control arm (HR: 0.41, 95% CI: 0.31–0.56; P < 0.001). Overall survival (OS) was also longer in the gefitinib arm (20.1 vs. 15.4 months; HR: 0.68; 95% CI 0.48–0.97; P = 0.0323). Adverse events, including diarrhea, dermal reaction and thrombocytopenia, were more common in the gefitinib arm. In conclusion, intercalating and maintenance gefitinib treatment is a viable option for advanced NSCLC patients with unknown EGFR mutation status in subpopulations with high EFGR mutation rate.

Genetic polymorphisms in CYP2A6 are associated with a risk of cigarette smoking and predispose to smoking at younger ages

Nicotine is the main component of cigarettes that causes addiction, which is considered a complex disease, and genetic factors have been proposed to be involved in the development of addiction. The CYP2A6 gene encodes the main enzyme responsible for nicotine metabolism. Depending on the study population, different genetic variants of CYP2A6 associated with cigarette smoking have been described. Therefore, we evaluated the possible association between SNPs in CYP2A6 with cigarette smoking and nicotine addiction-related variables in Mexican mestizo smokers. We performed a genetic association study comparing light smokers (LS, n=349), heavy smokers (HS, n=351) and never-smokers (NS, n=394). SNPs rs1137115, rs4105144, rs1801272 and rs28399433 were genotyped in the CYP2A6 gene. We found that the A allele of rs1137115 (OR=1.41) in exon 1 of CYP2A6 and the T allele of rs4105144 (OR=1.32) in the 5′ UTR of the gene are associated with the risk of cigarette smoking (p<0.05); rs1137115 affects the level of alternative splicing, resulting in a CYP2A6 isoform with low enzymatic activity, whereas rs4105144 is likely to be in a binding site for the transcription factor for glucocorticoids receptor (GR) and regulates the expression of CYP2A6. In addition, having a greater number of risk alleles (rs1137115 (A), rs4105144 (T) and rs28399433 (G)) is associated with a younger age at onset. The present study shows that in Mexican mestizos, the analyzed SNPs confer greater risk in terms of consumption and age of onset.

Detection of Lung Cancer and EGFR Mutation by Electronic Nose System

IntroductionEarly detection of lung cancer (LC) has been well established as a significant key point in patient survival and prognosis. New highly sensitive nanoarray sensors for exhaled volatile organic compounds that have been developed and coupled with powerful statistical programs may be used when diseases such as LC are suspected. Detection of genetic aberration mutation by nanoarray sensors is the next target. MethodsBreath samples were taken from patients who were evaluated for suspicious pulmonary lesions. Patients were classified as those with benign nodules, as patients with LC with or without the EGFR mutation, and according to their smoking status. Breath prints were recognized by nanomaterial-based sensor array, and pattern recognition methods were used. ResultsA total of 119 patients participated in this study, 30 patients with benign nodules and 89 patients with LC (16 with early disease and 73 with advanced disease). Patients with LC who harbored the EGFR mutation (n = 19) could be discriminated from those with wild-type EGFR (n = 34) with an accuracy of 83%, sensitivity of 79%, and specificity of 85%. Discrimination of early LC from benign nodules had 87% accuracy and positive and negative predictive values of 87.7 and 87.5% respectively. Moderate discrimination (accuracy of 76%) was found between LC of heavy smokers and that of never-smokers or distant past light smokers. ConclusionsBreath analysis could discriminate patients with LC who harbor the EGFR mutation from those with wild-type EGFR and those with benign pulmonary nodules from those patients with early LC. A positive breath print for the EGFR mutation may be used in treatment decisions if tissue sampling does not provide adequate material for definitive mutation analysis.

Evaluation of baseline frequency of sister chromatid exchanges in an Italian population according to age, sex, smoking habits, and gene polymorphisms.

Increased SCEs frequencies in human lymphocytes are an indicator of spontaneous chromosome instability and could be influenced by different exogenous and endogenous factors. In this study, we evaluated the influence of age, sex, smoking habits, and genetic polymorphisms on the background levels of SCEs in peripheral blood lymphocytes. Two hundred-thirty healthy Italian subjects were recruited. Data about age, sex and smoking habits were recorded. Subjects were also genotyped for GSTT1, GSTM1, GSTP1 A/G, CYP1A1 Ile/Val, CYP2C19 G/A, ERCC2/XPD Lys751Gln, XRCC1 Arg194ATrp, XRCC1 Arg399Gln, and XRCC1Arg208His gene polymorphisms. The frequency of SCEs/cell was 5.15±1.87, with females showing a significantly higher SCEs value with respect to males (5.36±2.10 and 4.82±1.39, respectively). Smokers showed significantly increased levels of SCEs with respect to nonsmokers (5.93±1.75 and 4.70±1.79, respectively) whereas no differences were observed between heavy and light smokers. Age correlated with the RI value (P=.01) but not with the SCEs frequency (P=07), although the 31-40 age group showed a significantly lower SCEs frequency with respect to the other age groups. A significant association was also found between GSTP2C19-AA, GSTT1-null, GSTM1-null, ERCC2/XPD Gln751Gln, and XRCC1 His208His genotypes, and higher frequencies of SCEs. We describe the association between some phase I, phase II, and DNA-repair gene polymorphisms with increased SCEs frequencies, reinforcing the importance of genetic analysis in biomonitoring studies. Sex and age were found to be important endogenous factors that affect the level of genomic damage and the replicative capacity of cells, respectively.

Accuracy and utility of an epigenetic biomarker for smoking in populations with varying rates of false self-report.

Better biomarkers to detect smoking are needed given the tremendous public health burden caused by smoking. Current biomarkers to detect smoking have significant limitations, notably a short half-life for detection and lack of sensitivity for light smokers. These limitations may be particularly problematic in populations with less accurate self-reporting. Prior epigenome-wide association studies indicate that methylation status at cg05575921, a CpG residue located in the aryl hydrocarbon receptor repressor (AHRR) gene, may be a robust indicator of smoking status in individuals with as little as half of a pack-year of smoking. In this study, we show that a novel droplet digital PCR assay for measuring methylation at cg05575921 can reliably detect smoking status, as confirmed by serum cotinine, in populations with different demographic characteristics, smoking histories, and rates of false-negative self-report of smoking behavior. Using logistic regression models, we show that obtaining maximum accuracy in predicting smoking status depends on appropriately weighting self-report and cg05575921 methylation according to the characteristics of the sample being tested. Furthermore, models using only cg05575921 methylation to predict smoking perform nearly as well as those also including self-report across populations. In conclusion, cg05575921 has significant potential as a clinical biomarker to detect smoking in populations with varying rates of accuracy in self-report of smoking behavior.

Prevalence and correlates of light and non-daily smoking in Brazil: Results from a nationwide representative survey

BackgroundThe research of light (≤10 cigarettes per day) and non-daily smokers in developing countries including Brazil is scarce despite the high prevalence of these groups among smokers and health risks associated to low-level smoking. ObjectiveTo describe health and smoking characteristics of Brazilian adult light and non-daily smokers. MethodsWe analyzed data from the 2013 Brazilian National Health Research survey (n=48,282). ResultsThe prevalence of current manufactured cigarette smoking in the total sample was 12.4%. Among these smokers, 12.8% were non-daily smokers (NDS), 47.4% were light smokers (LS) and 39.8% were moderate/heavy smokers (MHS). Bivariate analysis showed that non-daily smoking was associated with higher odds of poor self-rated health, binge drinking and lung diseases compared to never smokers (ORs=1.2; 5.9 and 1.9). Light smoking was associated with higher odds of poor self-rated health, binge drinking, depression, use of sleeping pills and lung diseases (ORs=1.3; 4.3; 1.4; 1.2 and 2.0). After controlling for sex and age, non-daily smoking was associated with lung disease (OR=2.2) and light smoking with depression and lung diseases (ORs=1.3 and 1.8). Smoking levels were associated with living with same-level smokers in bivariate and multivariate analyses. ConclusionA large proportion of smokers in Brazil are light and non-daily smokers, carrying substantial health risks related to tobacco use. Longitudinal research is needed to provide further evidence of associations found in this study. Public health policies must take the different smoking patterns into consideration to effectively target all smokers and reduce the harmful consequences of tobacco worldwide.

Alcohol use and smoking as risk factors in chronic pancreatitis. Preliminary data from the Scandinavian Baltic Pancreas Club database

The purpose of this study was to investigate the relationship between the level of tobacco smoking and the clinicopathological features of non-small cell lung cancer (NSCLC) patients, individually for adenocarcinoma (Ad) and squamous cell carcinoma (Sq).We retrospectively reviewed the clinical records of 1825 consecutive lung cancer patients who underwent surgery in our department. Among these, the data sets of 750 Ad patients and 364 Sq patients who received lobectomy or more extensive resection were available.In Ad patients, those who had never smoked (never-smokers) (n = 309) were more likely to be female, to have less advanced stage tumors, and to have a significantly better prognosis than those who had ever smoked (ever-smokers) (n = 441) (5-year OS: never-smokers, 67.9%; ever-smokers, 53.7%, p < 0.0001). In Sq patients, the never-smokers (n = 15) were more likely to be female than the ever-smokers (n = 349). Among ever-smokers, the light-smokers (PY ≤ 30; n = 56) were associated with more female patients, more advanced stage tumors, and significantly worse prognoses than were the heavy smokers (PY > 30; n = 292) (p = 0.0003). The multivariate survival analysis showed that light smoking was related to a worse prognosis compared with heavy smoking (HR = 2.06, 95% CI 1.43–2.98, p = 0.0001).The never-smokers had a significantly better prognosis than ever-smokers among Ad patients, whereas the light-smokers had a significantly worse prognosis than heavy smokers among Sq patients. There may be factors other than tobacco carcinogens that influence the development of Sq in never and/or light smokers.

HUBUNGAN KEBIASAAN MEROKOK DENGAN GANGGUAN POLA TIDUR PADA REMAJA

For some people, smoking has become a necessity of life that can not be abandoned ineveryday life - the day. Results Health Research in 2013, the smoking behavior ofpopulation aged 15 years and over or adolescence is still a decline from 2007 to 2013, islikely to increase from 34.2% in 2007 to 36.2% in 2013.This research uses correlation study with cross sectional approach to determine therelationship of smoking as an independent variable with disruption of sleep patterns inadolescents as the dependent variable. The population in this study were all adultsmokers in the village of Wangkah Gedangan Grogol, Sukoharjo, ie a total of 30adolescent smokers. Researchers using a questionnaire with questions about the amountto 3 point for an overview of smoking and 10 of the questions for the description of sleepdisorders. The data obtained then tabulated tabulation and analyzed using SPSS 16 forWindows.Research result: 1) From the results of this study can be obtained that the majority ofrespondents, a number of 15 (50%) to the category of light smokers, while 9 respondents(30%) to the category of moderate smokers, and 6 respondents (20%) categories ofheavy smokers. 2) The majority of respondents with moderate sleep disorder category,the number of 24 respondents (80%), while 4 respondents (13.3%) with mild sleepdisorder category, and 2 respondents (6.7%) with severe sleep disorder category. Of allrespondents were 30 teenage 100% impaired sleep patterns. 3) Pearson Chi-Square5.513889, where &lt;of α: 0:05. It can be concluded that there is no relationship betweensmoking category by category disruption of sleep patterns. Linear or non smokingcategory to the category of sleep disorders.Keywords: Smoking, disruption of sleep patterns, teen age

Does menthol cigarette use moderate the effect of nicotine metabolism on short-term smoking cessation?

The nicotine metabolite ratio (NMR) has been shown to predict response to the transdermal nicotine patch, such that faster nicotine metabolism is associated with a lower abstinence rate. Menthol cigarette use, versus nonmenthol cigarette use, slows nicotine metabolism and therefore may attenuate the effect of NMR on smoking abstinence. In this study, we evaluated whether cigarette type (menthol vs. nonmenthol) modified the association between NMR and short-term abstinence. This was a secondary analysis examining treatment in the first 8 weeks of 21 mg/day nicotine patch therapy in a completed clinical trial (n = 474). Menthol cigarette use was based on self-report. NMR was defined dichotomously (0 = fast, 1 = slow) to distinguish between fast (≥0.47) versus slow NMR. Using logistic regression analysis, we tested whether cigarette type moderated the association between NMR and bioverified 7-day point prevalence abstinence at Week 8. Covariates include nicotine dependence, age, race, and gender. Three hundred two participants reported smoking menthol cigarettes, of which 234 (77%) were classified as slow NMR. Among the 172 nonmenthol smokers, 136 were classified as slow NMR (79%). Contrary to our expectations, the NMR ×Cigarette Type interaction effect on abstinence was not significant (odds ratio [OR] = 0.91, p = .86). Excluding the interaction variable, fast NMR was associated with decreased likelihood of abstinence (OR = 0.55, p = .03), but menthol cigarette use was not (OR = 1.15, p = .56). Further exploration of risk factors among menthol cigarette smokers, especially among racially diverse and light smokers, could clarify the association between menthol cigarette use and poorer smoking outcomes. (PsycINFO Database Record

Testing Familial Transmission of Smoking With Two Different Research Designs.

Classical twin studies show that smoking is heritable. To determine if shared family environment plays a role in addition to genetic factors, and if they interact (G×E), we use a children-of-twins design. In a second sample, we measure genetic influence with polygenic risk scores (PRS) and environmental influence with a question on exposure to smoking during childhood. Data on smoking initiation were available for 723 children of 712 twins from the Netherlands Twin Register (64.9% female, median birth year 1985). Children were grouped in ascending order of risk, based on smoking status and zygosity of their twin-parent and his/her co-twin: never smoking twin-parent with a never smoking co-twin; never smoking twin-parent with a smoking dizygotic co-twin; never smoking twin-parent with a smoking monozygotic co-twin; and smoking twin-parent with a smoking or never smoking co-twin. For 4072 participants from the Netherlands Twin Register (67.3% female, median birth year 1973), PRS for smoking were computed and smoking initiation, smoking heaviness, and exposure to smoking during childhood were available. Patterns of smoking initiation in the four group children-of-twins design suggested shared familial influences in addition to genetic factors. PRS for ever smoking were associated with smoking initiation in all individuals. PRS for smoking heaviness were associated with smoking heaviness in individuals exposed to smoking during childhood, but not in non-exposed individuals. Shared family environment influences smoking, over and above genetic factors. Genetic risk of smoking heaviness was only important for individuals exposed to smoking during childhood, versus those not exposed (G×E). This study adds to the very few existing children-of-twins (CoT) studies on smoking and combines a CoT design with a second research design that utilizes polygenic risk scores and data on exposure to smoking during childhood. The results show that shared family environment affects smoking behavior over and above genetic factors. There was also evidence for gene-environment interaction (G×E) such that genetic risk of heavy versus light smoking was only important for individuals who were also exposed to (second-hand) smoking during childhood. Together, these findings give additional incentive to recommending parents not to expose their children to cigarette smoking.

Influence of cigarette smoking on osteonecrosis of the femoral head (ONFH): a systematic review and meta-analysis.

Current studies demonstrate controversy regarding the relationship between cigarette smoking and osteonecrosis of the femoral head (ONFH). We conducted a meta-analysis to evaluate the association between smoking and ONFH. Relevant articles published before September 2016 were identified by a systematic search of EMBASE and MEDLINE via Ovid. Summary odds ratios (OR) were calculated using random effects models, and study quality was assessed using a modified Newcastle-Ottawa scale. 102 citations were screened and 7 case-control studies were identified and included in the review. When compared with nonsmokers, current smokers had a higher risk of developing ONFH (OR 2.53; 95% confidence interval [CI] 1.68-3.79), as did former smokers (OR 1.82; 95% CI, 1.10-3.00). Within the group of current smokers, those classified as heavy smokers (with a daily number >20 cigarettes/day) demonstrated higher risks of ONFH (OR 2.03; 95% CI, 1.29-3.19), and light smokers classified as smoking <20 cigarettes/day, also demonstrated a higher risk of ONFH when compared with nonsmokers (OR 1.73; 95% CI, 1.06-2.83). When smoking was classified by pack-years, heavy smokers (>20 pack-years) were at a higher risk of ONFH (OR 2.26; 95% CI, 1.24-4.13), but no significant difference in risk was identified in light smokers (<20 pack-years) (OR 1.81; 95% CI, 0.88-3.71) when compared with nonsmokers. Our meta-analysis showed that current smokers were at a higher risk of ONFH, this high risk can also be found in former smokers. And heavy cigarette smoking showed a higher risk of ONFH than light smoking.

Progression to established patterns of cigarette smoking among young adults

BackgroundAs tobacco control policies have been implemented across the U.S. over the past decade, patterns of smoking cigarettes have significantly changed, particularly among young adults. For many users, the typical daily use pattern of smoking several packs of cigarettes per day has been supplanted by a variety of use patterns, often referred to as light, intermittent, and occasional smoking. MethodsThe aim of this study was to examine progression to established smoking patterns among a nationally representative, longitudinal sample of young adults (n=9791). Using repeated measures latent class techniques (RMLCA), we modeled the distribution of cigarette smoking intensity over time and latent class categories. ResultsFindings demonstrate that young adults fall into three discrete classes that reflect probabilities for never to low use, daily use, and variable cigarette use for progression to established use of cigarettes: 79.3% fall into the class of “never or ever users” of cigarettes (no current use of cigarettes), 11.3% fall into the class of “rapid escalators” or daily users of cigarettes, and 9.4% fall into the “dabbler” class. Smoking patterns were found to be stable by the age of 21. ConclusionsIntervening prior to age 21 has the potential to disrupt progression to established smoking and reduce the long-term health consequences of smoking in this age group.

The association between cigarette smoking, virologic suppression, and CD4+ lymphocyte count in HIV-Infected Russian women

ABSTRACTCigarette smoking among people living with HIV/AIDS is associated with significant morbidity and mortality, but findings regarding the association between cigarette smoking and HIV viral load and CD4+ lymphocyte counts have been inconsistent. This study characterized the prevalence of cigarette smoking among HIV-infected Russian women and examined the association between smoking frequency and quantity and HIV viral load and CD4+ lymphocyte counts. HIV-infected Russian women (N = 250; M age = 30.0) in St. Petersburg, Russia, completed an audio computer-assisted self-interview survey assessing cigarette use, antiretroviral medication adherence, and provided blood samples assayed for HIV viral load and CD4+ lymphocyte counts. The majority (60.4%) reported cigarette smoking in the past month; 49.0% of recent smokers were classified as moderate or heavy smokers, defined as smoking ≥10 cigarettes daily. Viral load status did not differ between infrequent smokers and regular smokers. However, moderate/heavy smokers (relative to light smokers) were more likely to have a detectable viral load (AOR = 2.3, 95% CI: 1.1, 5.1). There were no significant differences in CD4+ lymphocyte counts by smoking frequency or quantity of cigarettes smoked. Results highlight the need for additional research to examine the association between cigarette smoking and virologic suppression and markers of HIV disease progression. Adverse health consequences of cigarette smoking coupled with a potential link between heavy smoking and poor virologic suppression highlight the need for assessment of cigarette use and provision of evidence-based smoking-cessation interventions within HIV medical care.