Effect of marijuana smoking on lung function change in older ever tobacco smokers.
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ABSTRACT:
SUBMITTER: Barjaktarevic I
PROVIDER: S-EPMC9945875 | biostudies-literature | 2022 Sep
REPOSITORIES: biostudies-literature
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Effect of marijuana smoking on lung function change in older ever tobacco smokers.
Barjaktarevic Igor I Cooper Christopher B CB Shing Tracie T Buhr Russell G RG Hoffman Eric A EA Woodruff Prescott G PG Drummond M Bradley MB Kanner Richard E RE Han MeiLan K MK Hansel Nadia N NN Bowler Russell P RP Kinney Gregory L GL Jacobson Sean S Morris Madeline A MA Martinez Fernando J FJ Ohar Jill J Couper David D Tashkin Donald P DP
The European respiratory journal 20220922 3
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| S-EPMC8215593 | biostudies-literature
Project description:BackgroundSusceptibility to future smoking among youth never smokers has not changed in the past 20 years, although experimental cigarette smoking has decreased. We assessed how smoking susceptibility and tobacco industry-related marketing influenced smoking initiation.MethodsFour waves (2013-2018) of the Population Assessment of Tobacco and Health Study data were analyzed among youth aged 12 to 17 years at wave 1 who completed wave 4. Susceptibility was assessed by 4 items (openness to curiosity, try soon, try in the next year, and if your best friend offered) and categorized into 4 levels (0 = definitely no to all; 1 = yes to 1; 2 = yes to 2; and 3 + 4 = yes to 3 or 4 susceptibility items). Multivariable logistic regression evaluated how susceptibility levels, electronic cigarette use, and tobacco-related media activity predicted future experimental (≥1 puff), current (past 30 days), or established (≥100 cigarettes) smoking.ResultsAmong 8899 never smokers at wave 1, 16.4% became experimental smokers, 7.6% current smokers, and 1.8% established smokers at wave 4. Black and Latino/a youth were less likely to experiment. Youth who endorsed 3 or 4 susceptibility items at wave 1 were more likely to be experimental (adjusted odds ratio [aOR] = 6.0; confidence interval [CI] = 4.8-7.4), current (aOR = 4.2; CI = 3.2-5.4), or established (aOR = 4.4; CI = 2.4-7.9) smokers at wave 4. Exposure to tobacco marketing, using tobacco-related apps, seeing social media content posted about tobacco, and ever use of electronic cigarettes also predicted experimental smoking.ConclusionsSmoking susceptibility and exposure to tobacco industry-related marketing were predictive of cigarette smoking. Clinicians should consider screening adolescents for smoking susceptibility and tobacco-related media exposure.
| S-EPMC8331193 | biostudies-literature
Project description:BackgroundVariation in ADAM33 has been shown to be important in the development of asthma and altered lung function. This relationship however, has not been investigated in the population susceptible to COPD; long term tobacco smokers. We evaluated the association between polymorphisms in ADAM33 gene with COPD and lung function in long term tobacco smokers.MethodsCaucasian subjects, at least 50 year old, who smoked >or= 20 pack-years (n = 880) were genotyped for 25 single nucleotide polymorphisms (SNPs) in ADAM33. COPD was defined as an FEV1/FVC ratio < 70% and percent-predicted (pp)FEV1 < 75% (n = 287). The control group had an FEV1/FVC ratio >or= 70% and ppFEV(1) >or= 80% (n = 311) despite >or= 20 pack years of smoking. Logistic and linear regressions were used for the analysis. Age, sex, and smoking status were considered as potential confounders.ResultsFive SNPs in ADAM33 were associated with COPD (Q-1, intronic: p < 0.003; S1, Ile --> Val: p < 0.003; S2, Gly --> Gly: p < 0.04; V-1 intronic: p < 0.002; V4, in 3' untranslated region: p < 0.007). Q-1, S1 and V-1 were also associated with ppFEV1, FEV1/FVC ratio and ppFEF25-75 (p values 0.001 - 0.02). S2 was associated with FEV1/FVC ratio (p < 0.05). The association between S1 and residual volume revealed a trend toward significance (p value < 0.07). Linkage disequilibrium and haplotype analyses suggested that S1 had the strongest degree of association with COPD and pulmonary function abnormalities.ConclusionFive SNPs in ADAM33 were associated with COPD and lung function in long-term smokers. Functional studies will be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD.
| S-EPMC2664793 | biostudies-literature
Project description:BackgroundThe incidence and mortality rates of smoking-associated lung cancer are high among Chinese immigrant smokers. Coming from a country with different smoking policies, culture, and economic background than the U.S., Chinese smokers may change their smoking behaviors after immigrating to the U.S.ObjectivesThis study aims to explore the trajectory of smoking behavior change among Chinese immigrant smokers migrating to the U.S.MethodsThis qualitative study was guided by the Grounded theory. Semi-structured intensive individual interviews were conducted among 10 eligible participants. A purposive theoretical sampling method was used to recruit participants through a website. Individual interviews were conducted online, via telephone, or in-person in Mandarin. Data were transcribed verbatim in Mandarin, translated into English, and triangulated with follow-up interviews and dialogues among authors to enhance trustworthiness and consistency of the study. Process coding and content analysis were used to analyze data.ResultsA total of 10 participants, 7 males and 3 females, were interviewed. Results showed the trajectory of smoking behavior change among Chinese immigrant smokers went through three phases: 1) Beginning to smoke, which included learning to smoke from others, trying to smoke and learning to smoke, and hiding their smoking behaviors from others; 2) maintaining smoking, which included setting boundary around smoking, smoking as a facilitator or barrier to social interaction, feeling pressures related to smoking behavior, and making others happy: Collective smoking and controlling smoking desire; and 3) changing smoking behaviors, which included experiencing life events that were triggers to changing smoking behavior, boredom as a reason for relapses, personal will as a key to quitting smoking, and quitting smoking for a loved one. Although some differences existed between male and female Chinese immigrant smokers' smoking behaviors, their trajectories of smoking behavior change were generally similar.DiscussionFindings from this study can help health care providers to extend their understanding toward smoking behavior change among Chinese immigrant smokers across different socio-cultural contexts.
| S-EPMC7853480 | biostudies-literature
Project description:BackgroundTobacco use is one of the main risk factors for Lung Cancer (LC) development. However, about 10-20% of those diagnosed with the disease are never-smokers. For Non-Small Cell Lung Cancer (NSCLC) there are clear differences in both the clinical presentation and the tumor genomic profiles between smokers and never-smokers. For example, the Lung Adenocarcinoma (LUAD) histological subtype in never-smokers is predominately found in young women of European, North American, and Asian descent. While the clinical presentation and tumor genomic profiles of smokers have been widely examined, never-smokers are usually underrepresented, especially those of a Latin American (LA) background. In this work, we characterize, for the first time, the difference in the genomic profiles between smokers and never-smokers LC patients from Chile.MethodsWe conduct a comparison by smoking status in the frequencies of genomic alterations (GAs) including somatic mutations and structural variants (fusions) in a total of 10 clinically relevant genes, including the eight most common actionable genes for LC (EGFR, KRAS, ALK, MET, BRAF, RET, ERBB2, and ROS1) and two established driver genes for malignancies other than LC (PIK3CA and MAP2K1). Study participants were grouped as either smokers (current and former, n = 473) or never-smokers (n = 200) according to self-report tobacco use at enrollment.ResultsOur findings indicate a higher overall GA frequency for never-smokers compared to smokers (58 vs. 45.7, p-value < 0.01) with the genes EGFR, KRAS, and PIK3CA displaying the highest prevalence while ERBB2, RET, and ROS1 the lowest. Never-smokers present higher frequencies in seven out of the 10 genes; however, smokers harbor a more complex genomic profile. The clearest differences between groups are seen for EGFR (15.6 vs. 21.5, p-value: < 0.01), PIK3CA (6.8 vs 9.5) and ALK (3.2 vs 7.5) in favor of never-smokers, and KRAS (16.3 vs. 11.5) and MAP2K1 (6.6 vs. 3.5) in favor of smokers. Alterations in these genes are comprised almost exclusively by somatic mutations in EGFR and mainly by fusions in ALK, and only by mutations in PIK3CA, KRAS and MAP2K1.ConclusionsWe found clear differences in the genomic landscape by smoking status in LUAD patients from Chile, with potential implications for clinical management in these limited-resource settings.
| S-EPMC11297669 | biostudies-literature
Project description:BackgroundProlonged past exposure to secondhand tobacco smoke (SHS) in never-smokers is associated with abnormal lung function and reduced diffusing capacity suggestive of an associated lung tissue injury and damage. The mechanisms by which past SHS exposure may contribute to lung tissue damage are unknown. Elastin is a major constituent of extracellular matrix in lung parenchyma.ObjectiveTo determine whether past exposure to SHS is associated with ongoing lung tissue damage as indicated by elevated elastin degradation products that are linked to lung function.MethodsWe measured the plasma levels of elastin degradation markers (EDM) from 193 never-smoking flight attendants with a history of remote SHS exposure in aircraft cabins and 103 nonsmoking flight attendants or sea-level control participants without such history of cabin SHS exposure and examined those levels versus their lung function with adjustment for covariates. The cabin SHS exposure was estimated based on airline employment history and years of the smoking ban enactment.ResultsThe median [interquartile range] plasma EDM level for all participants was 0.30 [0.24-0.36] ng/mL with a total range of 0.16-0.65 ng/mL. Plasma EDM levels were elevated in those with a history of exposure to cabin SHS compared to those not exposed (0.33±0.08 versus 0.26±0.06 ng/mL; age- and sex-adjusted P<0.001). In those with a history of cabin SHS exposure, higher EDM levels were associated with a lower diffusing capacity (parameter estimate [PE] 95% [confidence interval(CI)]=4.2 [0.4-8.0] %predicted decrease per 0.1 ng/mL increase in EDM; P=0.030). Furthermore, EDM levels were inversely associated with forced expiratory volume in 1 second (FEV1), FEV1 to forced vital capacity (FVC) ratio , and forced expiratory flow rate between 25% and 75% ( FEF25%-75%) (PE [95%CI]=5.8 [2.1-9.4], 4.0 [2.2-5.7], and 12.5 [5.8-19.2] %predicted decrease per 0.1 ng/mL increase in EDM, respectively; P<0.001). Plasma EDM mediated a substantial fraction of the association of SHS with FEV1, FVC, and FEF25%-75% (P<0.05).ConclusionsLong after past exposure to SHS, there is ongoing elastin degradation beyond what is expected from the aging process, which likely contributes to lower lung function and a reduced pulmonary capillary bed as seen in chronic obstructive pulmonary disease (COPD).
| S-EPMC9448014 | biostudies-literature
Project description:Background: Marijuana is often smoked via a filterless cigarette and contains similar chemical makeup as smoked tobacco. There are few publications describing usage patterns and respiratory risks in older adults or in those with chronic obstructive pulmonary disease (COPD). Methods: A cross-sectional analysis of current and former tobacco smokers from the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) study assessed associations between marijuana use and pulmonary outcomes. Marijuana use was defined as never, former (use over 30 days ago), or current (use within 30 days). Respiratory health was assessed using quantitative high-resolution computed tomography (HRCT) scans, pulmonary function tests and questionnaire responses about respiratory symptoms. Results: Of the total 2304 participants, 1130 (49%) never, 982 (43%) former, and 192 (8%) current marijuana users were included. Neither current nor former marijuana use was associated with increased odds of wheeze (odds ratio [OR] 0.87, OR 0.97), cough (OR 1.22; OR 0.93) or chronic bronchitis (OR 0.87; OR 1.00) when compared to never users. Current and former marijuana users had lower quantitative emphysema (P=0.004, P=0.03), higher percent predicted forced expiratory volume in 1 second (FEV1%) (P<0.001, P<0.001), and percent predicted forced vital capacity (FVC%) (p<0.001, P<0.001). Current marijuana users exhibited higher total tissue volume (P=0.003) while former users had higher air trapping (P<0.001) when compared to never marijuana users. Conclusions: Marijuana use was found to have little to no association with poor pulmonary health in older current and former tobacco smokers after adjusting for covariates. Higher forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) was observed among current marijuana users. However, higher joint years was associated with more chronic bronchitis symptoms (e.g., wheeze), and this study cannot determine if long-term heavy marijuana smoking in the absence of tobacco smoking is associated with lung symptoms, airflow obstruction, or emphysema, particularly in those who have never smoked tobacco cigarettes.
| S-EPMC5870739 | biostudies-literature
Project description:SignificanceIncreased rates of smoking cessation will be essential to maximize the population benefit of low-dose CT screening for lung cancer. The NCI's Smoking Cessation at Lung Examination (SCALE) Collaboration includes eight randomized trials, each assessing evidence-based interventions among smokers undergoing lung cancer screening (LCS). We examined predictors of trial enrollment to improve future outreach efforts for cessation interventions offered to older smokers in this and other clinical settings.MethodsWe included the six SCALE trials that randomized individual participants. We assessed demographics, intervention modalities, LCS site and trial administration characteristics, and reasons for declining.ResultsOf 6285 trial- and LCS-eligible individuals, 3897 (62%) declined and 2388 (38%) enrolled. In multivariable logistic regression analyses, Blacks had higher enrollment rates (OR 1.5, 95% CI 1.2,1.8) compared to Whites. Compared to "NRT Only" trials, those approached for "NRT + prescription medication" trials had higher odds of enrollment (OR 6.1, 95% CI 4.7,7.9). Regarding enrollment methods, trials using "Phone + In Person" methods had higher odds of enrollment (OR 1.6, 95% CI 1.2,1.9) compared to trials using "Phone Only" methods. Some of the reasons for declining enrollment included "too busy" (36.6%), "not ready to quit" (8.2%), "not interested in research" (7.7%), and "not interested in the intervention offered" (6.2%).ConclusionEnrolling smokers in cessation interventions in the LCS setting is a major priority that requires multiple enrollment and intervention modalities. Barriers to enrollment provide insights that can be addressed and applied to future cessation interventions to improve implementation in LCS and other clinical settings with older smokers.ImplicationsWe explored enrollment rates and reasons for declining across six smoking cessation trials in the lung cancer screening setting. Offering multiple accrual methods and pharmacotherapy options predicted increased enrollment across trials. Enrollment rates were also greater among Blacks compared to Whites. The findings offer practical information for the implementation of cessation trials and interventions in the lung cancer screening context and other clinical settings, regarding intervention modalities that may be most appealing to older, long-term smokers.
| S-EPMC8570664 | biostudies-literature
Project description:BACKGROUND:Heroin smokers have high rates of COPD, respiratory morbidity, hospital admission, and mortality. We assessed the natural history of symptoms and lung function in this population over time. METHODS:A cohort of heroin smokers with COPD was followed for 18 to 24 months. At baseline and follow-up, respiratory symptoms were measured by the Medical Research Council Dyspnea Scale (MRC) and the COPD Assessment Tool (CAT), and postbronchodilator spirometry was performed. Frequency of health-care-seeking episodes was extracted from routine health records. Parametric, nonparametric, and linear regression models were used to analyze the change in symptoms and lung function over time. RESULTS:Of 372 participants originally recruited, 161 were assessed at follow-up (mean age, 51.0 ± 5.3 years; 74 women [46%]) and 106 participants completed postbronchodilator spirometry. All participants were current or previous heroin smokers, and 122 (75.8%) had smoked crack. Symptoms increased over time (MRC score increased by 0.48 points per year, P < .001; CAT score increased by 1.60 points per year, P < .001). FEV1 declined annually by 90 ± 190 mL (P < .001). This deterioration was not associated with change in tobacco or heroin smoking status or use of inhaled medications. CONCLUSIONS:Heroin smokers experience a high and increasing burden of chronic respiratory symptoms and a decline in FEV1 that exceeds the normal age-related decline observed among tobacco smokers with COPD and healthy nonsmokers. Targeted COPD diagnostic and treatment services hosted within opiate substitution services could benefit this vulnerable, relatively inaccessible, and underserved group of people.
| S-EPMC7078587 | biostudies-literature
Project description:Background/aimsGenome wide and candidate gene association studies have identified polymorphisms associated with the risk of lung cancer in never-smokers. This study was conducted to evaluate the association between 11 polymorphisms identified in female never smokers and the lung cancer risk in male smokers.MethodsThis study included 714 lung cancer patients and 626 healthy controls. The polymorphisms were genotyped using SEQUENOM MassARRAY iPLEX assay or Taq-Man assay.ResultsTwo polymorphisms were associated with the risk of lung cancer in male smokers, as in female never smokers. Male smokers carrying the rs4975616 variant allele had a significantly decreased risk of lung cancer (in a codominant model: odds ratio, 0.77; 95% confidence interval, 0.61 to 0.96; p = 0.02). The rs9387478 polymorphism also reduced lung cancer risk in male smokers (in a codominant model: odds ratio, 0.85; 95% confidence interval, 0.73 to 0.997; p = 0.046). In a stratified analysis, the association between these polymorphisms and the risk of lung cancer was predominant in lighter smokers and for cases of adenocarcinoma.ConclusionThese results suggest that a subset of polymorphisms known to be associated with the risk of lung cancer in female never smokers is also associated with the risk of lung cancer in male smokers.
| S-EPMC7373985 | biostudies-literature