scholarly journals Epigenetic signatures of starting and stopping smoking

2018 ◽  
Author(s):  
Daniel L McCartney ◽  
Anna J Stevenson ◽  
Robert F Hillary ◽  
Rosie M Walker ◽  
Mairead L Bermingham ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Smoking Cessation ◽  
Cigarette Smoke ◽  
Prolonged Exposure ◽  
Smoking Status ◽  
High Dose ◽  
Former Smokers ◽  
Never Smokers ◽  
Methylation Patterns ◽  
Never Smoker

AbstractBackgroundMultiple studies have made robust associations between differential DNA methylation and exposure to cigarette smoke. But whether a DNA methylation phenotype is established immediately upon exposure, or only after prolonged exposure is less well-established. Here, we assess DNA methylation patterns in current smokers in response to dose and duration of exposure, along with the effects of smoking cessation on DNA methylation in former smokers.MethodsDimensionality reduction was applied to DNA methylation data at 90 previously identified smoking-associated CpG sites for over 4,900 individuals in the Generation Scotland cohort. K-means clustering was performed to identify clusters associated with current and never smoker status based on these methylation patterns. Cluster assignments were assessed with respect to duration of exposure in current smokers (years as a smoker), time since smoking cessation in former smokers (years), and dose (cigarettes per day).ResultsTwo clusters were specified, corresponding to never smokers (97.5% of whom were assigned to Cluster 1) and current smokers (81.1% of whom were assigned to Cluster 2). The exposure time point from which >50% of current smokers were assigned to thesmoker-enrichedcluster varied between 5-9 years in heavier smokers and between 15-19 years in lighter smokers. Low-dose former smokers were more likely to be assigned to thenever smoker-enrichedcluster from the first year following cessation. In contrast, a period of at least two years was required before the majority of former high-dose smokers were assigned to the never smoker-enriched cluster.ConclusionsOur findings suggest that smoking-associated DNA methylation changes are a result of prolonged exposure to cigarette smoke, and can be reversed following cessation. The length of time in which these signatures are established and recovered is dose dependent. Should DNA methylation-based signatures of smoking status be predictive of smoking-related health outcomes, our findings may provide an additional criterion on which to stratify risk.

scholarly journals Maternal exposure to cigarette smoking induces immediate and durable changes in placental DNA methylation affecting enhancer and imprinting control regions

2019 ◽  
Author(s):  
Sophie Rousseaux ◽  
Emie Seyve ◽  
Florent Chuffart ◽  
Ekaterina Bourova-Flin ◽  
Meriem Benmerad ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cigarette Smoking ◽  
Smoking Status ◽  
Gene Clusters ◽  
Tobacco Exposure ◽  
Smoking During Pregnancy ◽  
Former Smokers ◽  
Genomic Regions ◽  
Methylation Patterns ◽  
Control Regions

AbstractObjectiveExposure to cigarette smoking during pregnancy has been robustly associated with cord blood DNA methylation. However, little is known about such effects on the placenta; in particular, whether cigarette smoking before pregnancy could also induce epigenetic alterations in the placenta of former smokers is unknown.Design and resultsPlacental DNA methylation levels were measured in 568 women and compared among non-smokers and women either smoking during their pregnancy or who had ceased smoking before pregnancy. An Epigenome Wide Association Study identified 344 Differentially Methylated Regions (DMRs) significantly associated with maternal smoking status. Among these 344 DMRs, 262 showed “reversible” alterations of DNA methylation, only present in the placenta of current smokers, whereas 44 were also found altered in former smokers, whose placenta had not been exposed directly to cigarette smoking. This observation was further supported by a significant demethylation of LINE-1 sequences in the placentas of both current (−0.43 (−0.83 to −0.02)) and former smokers (−0.55 (−1.02 to −0.08)) compared to nonsmokers. A comparative analysis of the epigenome landscape based on the ENCODE placenta data demonstrated an enrichment of all 344 DMRs in enhancers histone marks. Additionally, smoking-associated DMRs were found near and/or overlapping with 13 imprinting gene clusters encompassing 18 imprinted genes.ConclusionsDNA methylation patterns alterations were found in 344 genomic regions in the placenta of women smoking during their pregnancy, including 44 DMRs and LINE-1 elements, where methylation changes persisted in former smokers, supporting the hypothesis of an “epigenetic memory” of exposure to cigarette smoking before pregnancy. Enhancers regions, including imprinting control regions were also particularly affected by placenta methylation changes associated to smoking, suggesting a biological basis for the sensitivity of these regions to tobacco exposure and mechanisms by which fetal development could be impacted.

Abstract P132: Time Since Smoking Cessation and Pulse Wave Velocity: The Atherosclerosis Risk in Communities (ARIC) Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Ricky L Camplain ◽  
Michelle L Snyder ◽  
Priya Palta ◽  
Hanyu Ni ◽  
Kenneth R Butler ◽  
...  
Keyword(s):  
Older Adults ◽  
Smoking Cessation ◽  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Smoking Status ◽  
Former Smokers ◽  
Never Smokers ◽  
Aric Study

Cigarette smoking is a preventable cause of cardiovascular disease and is associated with arterial stiffening among young adults. While smoking cessation lowers the risk of cardiovascular morbidity and mortality, evidence for a relationship between time since smoking cessation and arterial stiffness is limited in older adults. We assessed the association of smoking status and time since smoking cessation with arterial stiffness, measured by carotid-femoral (cfPWV) and brachial-ankle (baPWV) pulse wave velocity, conditional on intensity and duration of exposure to smoking (pack-years). Analyses included 1,996 men and 2,767 women aged 67 to 90 years examined in the ARIC study in 2011-2013. Smoking status was ascertained at all five ARIC examinations and during annual telephone interviews. Information on age at initiation of smoking, smoking intensity and duration were also collected. Pack-years were calculated as the product of the average number of cigarettes smoked per day and years smoked divided by 20. Two measures of baPWV and cfPWV were obtained then averaged. Multivariable linear regression was used to estimate the association between smoking status and time since smoking cessation with PWV by gender, adjusted for age, hypertension, body mass index (BMI), and heart rate. Estimates of the association between smoking cessation and PWV were further adjusted for pack-years. Among women, former smokers and current smokers had a lower baPWV when compared to never smokers [β = -40.9 (95% confidence interval (CI): -64.2, -17.6) and β = -119.7 (95%CI: -168.7, -70.7), respectively]. Similar patterns were observed for cfPWV; however, the relationship was only significant among former smokers [β = -25.3 (95%CI: -48.0, -2.5)]. Association of smoking status and PWV was not significant in men. Among men who were former smokers there was a negative and significant association between smoking cessation and cfPWV [β = -1.4 (-2.7, -0.4)]; however, this same relationship was not observed for baPWV. BMI modified the association between smoking cessation and PWV in women. Time since smoking cessation was positively associated with PWV in women with a BMI <25 kg/m 2 [baPWV: β = 3.8 (95%CI: 1.2, 6.5); cfPWV: β = 2.5 (0.3, 4.7)], but not in women with a BMI ≥25 kg/m 2 . In these cross-sectional analyses, ever smokers had lower PWV compared to never smokers among older women, but not among older men. Greater time since smoking cessation was positively associated with arterial stiffness among normal or underweight women, but not among women who were overweight or obese, or among men. Accounting for cumulative exposure to smoking over the life course, gender-specific and arterial segment-specific patterns were observed in the association between time since smoking cessation and arterial stiffness measured in community-dwelling older adults, as well as a modification of these associations by excess weight among women.

scholarly journals Effect of Smoking Cessation On Tooth Loss: A Systematic Review With Meta-Analysis

2019 ◽  
Author(s):  
Maria Luisa Silveira Souto ◽  
Emanuel Silva Rovai ◽  
Cristina Cunha Villar ◽  
Mariana Minatel Braga ◽  
Claudio Mendes Pannuti
Keyword(s):  
Smoking Cessation ◽  
Tooth Loss ◽  
Positive Impact ◽  
Smoking Status ◽  
Meta Analysis ◽  
Cross Sectional ◽  
Increased Risk ◽  
Former Smokers ◽  
Meta Regression ◽  
Never Smokers

Abstract Background: Smoking is a major risk factor for periodontitis and tooth loss. Smoking cessation has a positive impact in periodontal treatment. However, so far, no systematic reviewhas evaluatedthe effect of smoking cessation on tooth loss. Therefore, this review aimed to evaluate if smoking cessation reduces the risk of tooth loss. Methods: Observational (cross-sectional and longitudinal) studiesthat investigated the association between smoking cessation and tooth loss were included. MEDLINE, EMBASE and LILACS databases were searched for articles published up to November 2018. Pooled results for subgroups of current and former smokers were compared in meta-analysis. Meta-regression was used to test the influence of smoking status on estimates and explore the heterogeneity. Results: Of 230 potentially relevant publications, 21 studies were included in the qualitative review and 12 in the quantitative analysis. Meta-analysis of cross-sectional studies did not show any differences between former and current smokers in the chance of losing 1 or more teeth (OR = 1.00; 95% CI = 0.80 to 1.24, I 2 = 80%), losing more than 8 teeth (OR = 1.02; 95% CI = 0.78 to 1.32, I 2 = 0%) or being edentulous (OR = 1.37; 95% CI = 0.94 to 1.99, I 2 = 98%). Meta-analysis from longitudinal studies showed that, when compared to never smokers, former smokers presented no increased risk of tooth loss (RR = 1.15; 95% CI = 0.98 to 1.35, I 2 = 76%), while current smokers presented an increased risk of tooth loss (RR = 2.60; 95% CI = 2.29 to 2.96, I 2 = 61%). Meta-regression showed that, among former smokers, the time of cessation was the variable that better explained heterogeneity (approximately 60%). Conclusions: Risk for tooth loss in former smokers is comparable to that of never smokers. Moreover, former smokers have a reduced risk of tooth loss, when compared to current smokers.

scholarly journals Self-reported and cotinine-verified smoking and increased risk of incident hearing loss

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Woncheol Lee ◽  
Yoosoo Chang ◽  
Hocheol Shin ◽  
Seungho Ryu
Keyword(s):  
Smoking Status ◽  
Objective Measure ◽  
Self Report ◽  
Urinary Cotinine ◽  
Increased Risk ◽  
Former Smokers ◽  
Never Smokers ◽  
Time Varying Covariates ◽  
New Onset

AbstractWe examined the associations of smoking status and urinary cotinine levels, an objective measure of smoking, with the development of new-onset HL. This cohort study was performed in 293,991 Korean adults free of HL who underwent a comprehensive screening examination and were followed for up to 8.8 years. HL was defined as a pure-tone average of thresholds at 0.5, 1.0, and 2.0 kHz ≥ 25 dB in both ears. During a median follow-up of 4.9 years, 2286 participants developed new-onset bilateral HL. Self-reported smoking status was associated with an increased risk of new-onset bilateral HL. Multivariable-adjusted HRs (95% CIs) for incident HL comparing former smokers and current smokers to never-smokers were 1.14 (1.004–1.30) and 1.40 (1.21–1.61), respectively. Number of cigarettes, pack-years, and urinary cotinine levels were consistently associated with incident HL. These associations were similarly observed when introducing changes in smoking status, urinary cotinine, and other confounders during follow-up as time-varying covariates. In this large cohort of young and middle-aged men and women, smoking status based on both self-report and urinary cotinine level were independently associated with an increased incidence of bilateral HL. Our findings indicate smoking is an independent risk factor for HL.

scholarly journals Multigenerational and transgenerational impact of paternal bisphenol A exposure on male fertility in a mouse model

2020 ◽  
Vol 35 (8) ◽  
pp. 1740-1752 ◽  
Author(s):  
Md Saidur Rahman ◽  
Won-Ki Pang ◽  
Do-Yeal Ryu ◽  
Yoo-Jin Park ◽  
Myung-Geol Pang
Keyword(s):  
Dna Methylation ◽  
Bisphenol A ◽  
Large Scale ◽  
Corn Oil ◽  
Sperm Count ◽  
Future Generations ◽  
High Dose ◽  
Male Mice ◽  
Paternal Exposure ◽  
Methylation Patterns

Abstract STUDY QUESTION How does paternal exposure to bisphenol A (BPA) affect the fertility of male offspring in mice in future generations? SUMMARY ANSWER Paternal exposure to BPA adversely affects spermatogenesis, several important sperm functions and DNA methylation patterns in spermatozoa, which have both multigenerational (in F0 and F1) and partial transgenerational (mainly noticed in F2, but F3) impacts on the fertility of the offspring. WHAT IS KNOWN ALREADY BPA, a synthetic endocrine disruptor, is used extensively to manufacture polycarbonate plastics and epoxy resins. Growing evidence suggests that exposure to BPA during the developmental stages results in atypical reproductive phenotypes that could persist for generations to come. STUDY DESIGN, SIZE, DURATION CD-1 male mice (F0) were treated with BPA (5 or 50 mg/kg body weight per day (bw/day)) or ethinylestradiol (EE) (0.4 μg/kg bw/day) for 6 weeks. Control mice were treated with vehicle (corn oil) only. The treated male mice were bred with untreated female mice to produce first filial generation (F1 offspring). The F2 and F3 offspring were produced similarly, without further exposure to BPA. PARTICIPANTS/MATERIALS, SETTING, METHODS Histological changes in the testis along with functional, biochemical and epigenetic (DNA methylation) properties of spermatozoa were investigated. Subsequently, each parameter of the F0–F3 generations was compared between BPA-treated mice and control mice. MAIN RESULTS AND THE ROLE OF CHANCE Paternal BPA exposure disrupted spermatogenesis by decreasing the size and number of testicular seminiferous epithelial cells, which eventually led to a decline in the total sperm count of F0–F2 offspring (P &lt; 0.05). We further showed that a high BPA dose decreased sperm motility in F0–F2 males by mediating the overproduction of reactive oxygen species (F0–F1) and decreasing intracellular ATP (F0–F2) in spermatozoa (P &lt; 0.05). These changes in spermatozoa were associated with altered global DNA methylation patterns in the spermatozoa of F0–F3 males (P &lt; 0.05). Furthermore, we noticed that BPA compromised sperm fertility in mice from the F0–F2 (in the both dose groups) and F3 generations (in the high-dose group only). The overall reproductive toxicity of BPA was equivalent to or higher (high dose) than that of the tested dose of EE. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION Further research is required to determine the variables (e.g. lowest BPA dose) that are capable of producing changes in sperm function and fertility in future generations. WIDER IMPLICATIONS OF THE FINDINGS These results may shed light on how occupational exposure to BPA can affect offspring fertility in humans. STUDY FUNDING/COMPETING INTEREST(S) This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (Grant No. NRF-2018R1A6A1A03025159). M.S.R. was supported by Korea Research Fellowship Program through the NRF funded by the Ministry of Science and ICT (Grant No. 2017H1D3A1A02013844). There are no competing interests.

scholarly journals Smoking cessation is associated with lower disease activity and predicts cardiovascular risk reduction in rheumatoid arthritis patients

Rheumatology ◽  
2019 ◽  
Vol 59 (8) ◽  
pp. 1997-2004 ◽  
Author(s):  
Ida K Roelsgaard ◽  
Eirik Ikdahl ◽  
Silvia Rollefstad ◽  
Grunde Wibetoe ◽  
Bente A Esbensen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Smoking Cessation ◽  
Risk Factor ◽  
Disease Activity ◽  
Smoking Status ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Never Smokers ◽  
Event Rates ◽  
Lower Disease Activity

Abstract Objectives Smoking is a major risk factor for the development of both cardiovascular disease (CVD) and RA and may cause attenuated responses to anti-rheumatic treatments. Our aim was to compare disease activity, CVD risk factors and CVD event rates across smoking status in RA patients. Methods Disease characteristics, CVD risk factors and relevant medications were recorded in RA patients without prior CVD from 10 countries (Norway, UK, Netherlands, USA, Sweden, Greece, South Africa, Spain, Canada and Mexico). Information on CVD events was collected. Adjusted analysis of variance, logistic regression and Cox models were applied to compare RA disease activity (DAS28), CVD risk factors and event rates across categories of smoking status. Results Of the 3311 RA patients (1012 former, 887 current and 1412 never smokers), 235 experienced CVD events during a median follow-up of 3.5 years (interquartile range 2.5–6.1). At enrolment, current smokers were more likely to have moderate or high disease activity compared with former and never smokers (P &lt; 0.001 for both). There was a gradient of worsening CVD risk factor profiles (lipoproteins and blood pressure) from never to former to current smokers. Furthermore, former and never smokers had significantly lower CVD event rates compared with current smokers [hazard ratio 0.70 (95% CI 0.51, 0.95), P = 0.02 and 0.48 (0.34, 0.69), P &lt; 0.001, respectively]. The CVD event rates for former and never smokers were comparable. Conclusion Smoking cessation in patients with RA was associated with lower disease activity and improved lipid profiles and was a predictor of reduced rates of CVD events.

The Association Between Smoking Cessation Period and Metabolic Syndrome in Korean Men

2018 ◽  
Vol 30 (5) ◽  
pp. 415-424 ◽  
Author(s):  
Hwang Sik Shin ◽  
Jung Eun Oh ◽  
Yong Jin Cho
Keyword(s):  
Physical Activity ◽  
Metabolic Syndrome ◽  
Smoking Cessation ◽  
Odds Ratio ◽  
Health And Nutrition ◽  
Quit Smoking ◽  
Education Levels ◽  
History Of ◽  
Former Smokers ◽  
Never Smokers

The association between smoking cessation period and metabolic syndrome (MS) is currently unknown. We studied 6032 men aged >19 years who participated in the Korean National Health and Nutrition Examination Surveys between 2010 and 2012. The risk of MS according to the amount of smoking and duration of smoking cessation was examined, and adjusted for age, amount of alcohol consumed, physical activity, body mass index, income, and education levels. Compared with never-smokers, there was a significant increase in the risk of MS among current smokers >10 pack-years and former smokers with a history of pack-years >30. The odds ratio for MS increased with smoking amount in both current and former smokers. But the risk of MS in former smokers was no longer significant after 20 years of smoking cessation adjusted for past smoking amount. Thus, to prevent MS, current smokers should quit smoking early and former smokers should continue quitting.

scholarly journals Tobacco smoking among nursing students in Saudi Arabia: A descriptive correlational study

2017 ◽  
Vol 7 (10) ◽  
pp. 98
Author(s):  
Ahmad H. Abu Raddaha ◽  
Amirat A. Al-Sabeely ◽  
Heba M. Mohamed ◽  
Eid H. Aldossary
Keyword(s):  
Smoking Cessation ◽  
Saudi Arabia ◽  
Nursing Students ◽  
Tobacco Smoking ◽  
Future Research ◽  
Formal Training ◽  
Attitudes And Beliefs ◽  
Former Smokers ◽  
Never Smokers ◽  
Training Modules

Background and objectives: Tobacco smoking is a global epidemic and health threat that continues to increase. Nursing students primarily develop their professional roles toward smoking cessation during their academic nursing education.  We assessed prevalence and behavioral patterns of tobacco smoking among nursing students. Along with nature of education received on tobacco smoking cessation, we sought to explore their knowledge, attitudes and beliefs toward tobacco smoking.Methods: Using convenience sampling, a descriptive correlational research design was used. Subjects were undergraduate students from a public university located in Alriyadh, the capital of Saudi Arabia. A standardized self-administered questionnaire, the Global Health Professional Student Survey, was utilized.Results: Eighty-four percent reported not smoking tobacco throughout their lifetime (i.e., never smokers), while the remaining were former smokers. Although 11.7% indicated that they had received formal training on tobacco-smoking cessation, more former smokers reported receiving such formal training than never smokers (25% vs. 9.3%, χ2 = 4.04, df = 1, p = .04). Students who were in third year of program, who thought that a smoker who quits smoking tobacco products would avoid/decrease serious health problems, and who stated that tobacco smoking never been allowed inside their living homes while children were present were more likely be never smokers.Conclusions: Adding training modules on smoking cessation to undergraduate nursing program curricula is highly suggested. Considering our unique findings on the effect of smoking status on the attitudes and beliefs toward smoking among nursing students when planning and implementing training modules seems beneficial. Future research is recommended to explore the lived experiences and consequences of smoking behavior among former smokers group.

scholarly journals Effect of smoking cessation on tooth loss: a systematic review with meta-analysis

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Maria Luisa Silveira Souto ◽  
Emanuel Silva Rovai ◽  
Cristina Cunha Villar ◽  
Mariana Minatel Braga ◽  
Cláudio Mendes Pannuti
Keyword(s):  
Systematic Review ◽  
Smoking Cessation ◽  
Longitudinal Studies ◽  
Tooth Loss ◽  
Meta Analysis ◽  
Cross Sectional ◽  
Increased Risk ◽  
Former Smokers ◽  
Meta Regression ◽  
Never Smokers

Abstract Background Smoking is a major risk factor for periodontitis and tooth loss. Smoking cessation has a positive impact in periodontal treatment. However, so far, no systematic review has evaluated the effect of smoking cessation on tooth loss. Therefore, this review aimed to evaluate if smoking cessation reduces the risk of tooth loss. Methods Observational (cross-sectional and longitudinal) studies that investigated the association between smoking cessation and tooth loss were included. MEDLINE, EMBASE and LILACS databases were searched for articles published up to November 2018. Pooled results for subgroups of current and former smokers were compared in meta-analysis. Meta-regression was used to test the influence of smoking status on estimates and explore the heterogeneity. Results Of 230 potentially relevant publications, 21 studies were included in the qualitative review and 12 in the quantitative analysis. Meta-analysis of cross-sectional studies did not show any differences between former and current smokers in the chance of losing 1 or more teeth (OR = 1.00; 95% CI = 0.80 to 1.24, I2 = 80%), losing more than 8 teeth (OR = 1.02; 95% CI = 0.78 to 1.32, I2 = 0%) or being edentulous (OR = 1.37; 95% CI = 0.94 to 1.99, I2 = 98%). Meta-analysis from longitudinal studies showed that, when compared to never smokers, former smokers presented no increased risk of tooth loss (RR = 1.15; 95% CI = 0.98 to 1.35, I2 = 76%), while current smokers presented an increased risk of tooth loss (RR = 2.60; 95% CI = 2.29 to 2.96, I2 = 61%). Meta-regression showed that, among former smokers, the time of cessation was the variable that better explained heterogeneity (approximately 60%). Conclusions Risk for tooth loss in former smokers is comparable to that of never smokers. Moreover, former smokers have a reduced risk of tooth loss, when compared to current smokers.

scholarly journals Longitudinal decline in lung function: a community-based cohort study in Korea

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Ah Young Leem ◽  
Boram Park ◽  
Young Sam Kim ◽  
Joon Chang ◽  
Sungho Won ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Lung Function ◽  
Mixed Model ◽  
Smoking Status ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Lung Function Decline ◽  
Rate Of Decline ◽  
Never Smokers ◽  
Over Time

Abstract Progressive decline in lung function is the hallmark of chronic obstructive pulmonary disease (COPD). We aimed to assess the rate of decline in forced expiratory volume in 1 second (FEV1) in patients from a community cohort database in Korea. 5,865 subjects aged 40–69 years from the Ansung-Ansan cohort database I–III (2001–2006) were included in this study. We assessed the annual rate of decline in FEV1 over time in relation to smoking status, patient sex, and presence or absence of pre-bronchodilator airflow limitation using a generalized additive mixed model. The mean follow-up duration was 3.8 years. The annual mean decline in FEV1 in the entire cohort was significantly more rapid for men than women (31.3 mL vs 27.0 mL, P = 0.003). Among men without pre-bronchodilator airflow limitation, annual mean declines in FEV1 were 31.5, 35.5, and 40.1 mL for never smokers, former smokers (P = 0.09 vs. never smokers), and current smokers (P < 0.001 vs. never smokers), respectively; and 23.4, 19.7, and 33.9 mL, respectively, for men with pre-bronchodilator airflow limitation. Thus, among Korean males, smoking accelerates lung function decline over time whereas smoking cessation slows the rate of FEV1 decline regardless of pre-bronchodilator airflow limitation. This underscores the importance of smoking cessation in Koreans.

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