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Chronic obstructive pulmonary disease (COPD) patients due to biomass exposure (BE-COPD) could be more affected than COPD due to tobacco smoke (TE-COPD) by the coronavirus disease 2019 (COVID-19) pandemic. The aim of this work was to determine the prevalence of COVID-19 in BE-COPD and TE-COPD and if housing conditions, poor attitude, knowledge, and risk perception towards COVID-19, particularly in BE-COPD women, could represent a risk factor for contagion.An 11% prevalence of COVID-19 was found with no significant difference between COPD groups. The BE-COPD group showed poorer socioeconomic status. No significant differences were found to be associated with SARS-CoV-2 infection regarding housing conditions, poor knowledge, attitude, and risk perception towards COVID-19. Living in urban areas and perceiving risk in COVID-19 were significantly associated with increased adherence to sanitary measures and concern of contagion. Around 40% of all patients showed poor risk perception and adherence to sanitary measures towards COVID-19.

Patients with biomass exposure-related COPD (BE-COPD) is a prevalent disease in developing countries and requires a detailed study of its clinical and inflammatory characteristics, specifying interventions that may differ from tobacco exposure-related COPD (TE-COPD). The objective was to describe clinical characteristics, biomarkers of inflammation, T-helper cells, and microbiological agents during a COPD exacerbation in BE-COPD in comparison with TE-COPD.A prospective observational study in patients with moderate or severe exacerbation was recruited either in the emergency room or the COPD clinic. At enrollment, nasopharyngeal swabs and sputum were collected to identify viral and bacterial pathogens. Blood samples were also collected to measure inflammatory biomarkers and T-helper cells levels. Days of hospitalization and mechanical ventilation requirement was evaluated.Clinical characteristics, vaccination history, hospitalization, history of exacerbations, and microbiological pattern between BE-COPD and TE-COPD were similar. The Th2 profile was higher in BE-COPD than in TE-COPD (2.10 [range 1.30-3.30] vs. 1.40 [range 1.20-1.80], p = 0.001). The Th2/Th1 ratio was higher in BE-COPD than TE-COPD (1.22 [range 0.58-2.57 ] vs. 0.71 [range 0.40-1.15], p = 0.004). The need of mechanical ventilation (MV) was higher in TE-COPD than BE-COPD (13% vs. 31.1%, p = 0.01). Nonvaccination history and high CRP levels were significantly associated with hospitalization [OR 1.48 (CI 95% 1.30-4.61, p = 0.005) and OR 1.17 (CI 95% 1.10-1.24, p = 0.001), respectively].Clinical characteristics, inflammatory markers, and microbiological isolates were similar in both groups but BE-COPD show a tendency to present higher inflammatory Th2 cells and low requirement MV compared with TE-COPD.

Background: Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory disease characterized by airflow obstruction, commonly present in smokers and subjects exposed to noxious particles product of biomass-burning smoke (BBS). Several association studies have identified single-nucleotide polymorphisms (SNP) in coding genes related to the heat shock proteins family-genes that codify the heat shock proteins (Hsp). Hsp accomplishes critical roles in regulating immune response, antigen-processing, eliminating protein aggregates and co-activating receptors. The presence of SNPs in these genes can lead to alterations in immune responses. We aimed to evaluate the association of SNPs in the HSP90 gene complex and COPD. Methods: We enrolled 1549 participants, divided into two comparison groups, 919 tobacco-smoking subjects (cases COPD-TS n = 294 and, controls SWOC n = 625) and 630 chronic exposed to BBS (cases COPD-BBS n = 186 and controls BBES n = 444). We genotyped 2 SNPs: the rs13296 in HSP90AB1 and rs2070908 in HSP90B1. Results: Through the dominant model (GC + CC), the rs2070908 is associated with decreased risk (p &lt, 0.01, OR = 0.6) to suffer COPD among chronic exposed BBS subjects. We found an association between rs13296 GG genotype and lower risk (p = 0.01, OR = 0.22) to suffer severe COPD-TS forms in the severity analysis. Conclusions: single-nucleotide variants in the HSP90AB1 and HSP90B1 genes are associated with decreased COPD risk in subjects exposed to BBS and the most severe forms of COPD in tobacco-smoking subjects.

Introduction The efficacy of long-acting bronchodilators for COPD associated with biomass (BE-COPD) has not been properly evaluated. Objective To determine the acute effect of indacaterol (IND) 150 μg q.d and tiotropium (TIO) 18 μg q.d. on lung hyperinflation, walking distance (WD) and dyspnea during the six-minute walking test (6MWT) in moderate BE-COPD at 30, 60 and 240 mins post-drug administration. Design Randomized, controlled, open-level, crossover noninferiority clinical trial. Forty-two women with BE-COPD were randomly assigned to a bronchodilator sequence: IND-TIO or vice versa. Results There were statistically significant changes over time in inspiratory capacity (IC) (p

The tobacco industry promotes electronic nicotine delivery systems (ENDS) and heated tobacco products (HTP) as a safer alternative to conventional cigarettes with misleading marketing sustained by studies with conflict of interest. As a result, these devices sell without regulations and warnings about their adverse effects on health, with a growing user base targeting young people. This systematic review aimed to describe the adverse effects on the respiratory system in consumers of these devices. We conducted a systematic review and bibliometric analysis of 79 studies without conflict of interest evaluating ENDS and HTP effects in the respiratory system in experimental models, retrieved from the PubMed database. We found that the damage produced by using these devices is involved in pathways related to pulmonary diseases, involving mechanisms previously reported in conventional cigarettes as well as new mechanisms particular to these devices, which challenges that the tobacco industry’s claims. The present study provides significant evidence to suggest that these devices are an emerging public health problem and that they should be regulated or avoided.

Cigarette smoking is influenced by nicotine&rsquo, s effects on dopaminergic activity, which appear to be moderated by genetic variation, particularly a variable number tandem repeat (VNTR, 48 bp) polymorphism in the third exon of the dopamine receptor gene (DRD4). Smokers with the VNTR &ge, 7 repeats (long, L allele) report markedly increased participation in some smoking behaviors, hence, our aim was to evaluate the association of the L allele in Mexican Mestizo smokers with and without COPD. The DRD4 VNTR 48 bp was genotyped in 492 Mexican Mestizo smokers: 164 COPD patients (&ge, 20 cigarettes per day, cpd), 164 heavy smokers without COPD (HS, &ge, 20 cpd) and 164 light smokers without COPD (LS, 1&ndash, 10 cpd). In the dominant model analysis (SL + LL vs. SS), men in the COPD and HS groups showed a statistical difference compared to LS (p = 0.01, OR = 2.06, CI 95% 1.17&ndash, 3.64 and p = 0.05, OR = 1.88, CI 95% 1.03&ndash, 3.45, respectively). In addition, by clustering smokers &gt, 20 cpd (COPD + HS) and comparing with the LS group, we found an association with increased risk of higher tobacco smoking p = 0.01, OR = 1.99, CI 95% 1.18&ndash, 3.34. In conclusion, the long allele (L) in the VNTR of the DRD4 gene is associated with the risk of presenting higher tobacco smoking in male Mexican Mestizo smokers.

Alejandra Ramírez-Venegas,1 Mónica Velázquez-Uncal,1 Rosaura Pérez-Hernández,2 Nicolás Eduardo Guzmán-Bouilloud,1 Ramcés Falfán-Valencia,3 María Eugenia Mayar-Maya,4 Adrian Aranda-Chávez,1 Raúl H Sansores5 1Tobacco Smoking and COPD Research Department, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico; 2Research Department of Tobacco Smoking, Centro de Investigacion de Salud Poblacional, Instituto Nacional de Salud Pública, Cuernavaca, Mexico; 3HLA Laboratory, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico; 4Medical Attention Department, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico; 5Medica Sur Clinic & Foundation, Mexico City, Mexico Introduction: Biomass smoke exposure (BSE) is a recognized cause of COPD particularly in rural areas. However, little research has been focused on BSE in suburban areas. Objective: The aim of this study was to determine the prevalence of COPD, respiratory symptoms (RS) and BSE in women living in a suburban area of Mexico City exposed to BSE. Methods: A cross-sectional epidemiological survey of a female population aged >35years was performed using a multistage cluster sampling strategy. The participants completed questionnaires on RS and COPD risk factors. The COPD prevalence was based on the postbronchodilator forced expiratory volume in the first second (FEV1)/forced vital capacity (FVC) ratio. Of the 1,333 women who completed the respiratory questionnaires, spirometry data were obtained from 1,190, and 969 of these were scored as A–C. Results: The prevalence of BSE was 47%, and the estimated prevalence of COPD was 2.5% for the total population (n=969) and 3.1% for those with BSE only. The spirometry and oximetry values were significantly lower in women with greater exposure levels. The prevalence of RS (cough, phlegm, wheezing and dyspnea) was significantly higher in the women with BSE compared to those without exposure. We concluded that the association of COPD with biomass exposure is not only a rural phenomenon but also may be observed in the suburban areas of the big cities. Keywords: risk factor, gender, airway obstruction

The aim of this study was to determine differences in executive function between “healthy” patients smokers and nonsmoker’s and also determine the differences in executive functions before and afte...

Tobacco smoking results in a multifactorial disease involving environmental and genetic factors, epigenome-wide association studies (EWAS) show changes in DNA methylation levels due to cigarette consumption, partially reversible upon tobacco smoking cessation. Therefore, methylation levels could predict smoking status. This study aimed to evaluate the DNA methylation level of cg05575921 (AHRR) and cg23771366 (PRSS23) and their correlation with lung function variables, cigarette consumption, and nicotine addiction in the Mexican smoking population. We included 114 non-smokers (NS) and 102 current tobacco smokers (TS), we then further subclassified them as heavy smokers (HS) (n = 53) and light smokers (LS) (n = 49). We used restriction enzymes (MspI/HpaII) and qPCR to determine the DNA methylation level. We observed significant hypomethylation of cg05575921 in smokers compared to NS (p = 0.003), further analysis found a difference between HS and NS (p = 0.02). We did not observe differences between other groups or a positive correlation between methylation levels and age, BMI, cigarette consumption, nicotine addiction, or lung function. In conclusion, the cg05575921 site of AHRR is significantly hypomethylated in Mexican smokers, especially in HS (≥20 cigarettes per day).

This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes CHRNA5 (rs16969968, rs17408276, rs680244) CHRNA3 (rs6495307, rs12914385) NRXN1 (rs10865246, rs1882296, rs985919) and HTR2A (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette smoking at an early age and relapse to smoking cessation treatment Perez-Rubio et al., 2018. These SNPs were selected due to previous associations in other populations, including Mexican Mestizos. Smokers were classified according to the age at onset, cigarettes per day, nicotine dependence, COPD status and therapy received.

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous entity that may result from different causative agents and risk factors and may follow diverse clinical courses, including COPD secondary to biomass smoke exposure. At present, this phenotype is becoming more important for two reasons: first, because at least almost half of the world's population is exposed to biomass smoke, and second, because the possibility of it being diagnosed is increasing. Biomass smoke exposure COPD affects primarily women and is related with insults to the airways occurred during early life. Although constituents of biomass smoke and tobacco smoke are similar, the physiopathological changes they induce differ depending not only on the chemical composition (related with the type of fuel used) but also on the particle size and the inhalation pattern. Evidence has shown that biomass smoke exposure affects the airway, predominantly the small airways causing anthracofibrosis and peribronchiolar fibrosis changes that will clinically translate into chronic bronchitis symptoms, with a high impact on the quality of life. In this review, we focus especially on the main epidemiological and clinical differences between COPD secondary to biomass exposure and COPD caused by tobacco exposure.

Aim: To identify genetic variants associated with greater tobacco consumption in a Mexican population. Patients & methods: Daily smokers were classified as light smokers (LS; n = 742), heavy smokers (HS; n = 601) and nonsmokers (NS; n = 606). In the first stage, a genotyping microarray that included 347 SNPs in CHRNA2–CHRNA7/CHRNA10, CHRNB2–CHRNB4 and NRXN1 genes and 37 ancestry-informative markers was used to analyze 707 samples (187 HS, 328 LS and 192 NS). In the second stage, 14 SNPs from stage 1 were validated in the remaining samples (HS, LS and NS; n = 414 in each group) using real-time PCR. To predict the role of the associated SNPs, an in silico analysis was performed. Results: Two SNPs in NRXN1 and two in CHRNA5 were associated with cigarette consumption, while rs10865246/C (NRXN1) was associated with high nicotine addiction. The in silico analysis revealed that rs1882296/T had a high level of homology with Hsa-miR-6740-5p, which encodes a putative miRNA that targets glutamate receptor subunits (GRIA2, GRID2) and GABA receptor subunits (GABRG1, GABRA4, GABRB2), while rs1882296/C had a high level of homology with Hsa-miR-6866-5p, which encodes a different miRNA that targets GRID2 and GABRB2. Conclusion: In a Mexican Mestizo population, greater consumption of cigarettes was influenced by polymorphisms in the NRXN1 and CHRNA5 genes. We proposed new hypotheses regarding the putative roles of miRNAs that influence the GABAergic and glutamatergic pathways in smoking addiction.

Chronic obstructive pulmonary disease (COPD) is a complex and multifactorial disease with a strong genetic component. Our objective is to identify the genetic variants associated with COPD risk and its severity in Mexican Mestizo population. We evaluated 1285 single-nucleotide polymorphisms (SNPs) of candidate genes in 299 smokers with COPD (COPD-S) and 531 smokers without COPD (SWOC) using an Illumina GoldenGate genotyping microarray. In addition, 251 ancestry informative markers were included. Allele A of rs2545771 in CYP2F2P is associated with a lower risk of COPD (p = 4.02E-10, odds ratio [OR] = 0.104, confidence interval [CI] 95% 0.05-0.18). When the COPD group was stratified by severity according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD; levels III + IV vs. I + II), 3 SNPs (rs4329505 and rs4845626 in interleukin 6 receptor [IL6R] and rs1422794 in a disintegrin and metalloproteinase domain 19 [ADAM19]) were associated with a lower risk of suffering the most severe stages of the disease. rs2819096 in the surfactant protein D (SFTPD) gene was associated with a higher risk of COPD GOLD III + IV (p = 7.79E-03, OR = 1.80, CI 95% 1.16-2.79). Finally, the haplotype in IL6R was associated with a lower risk of suffering from more severe COPD, whereas the haplotype in ADAM19 was associated with a higher risk (p = 7.40E-03, OR = 2.83, CI 95% 1.20-6.86) of suffering from the severe stages of the disease. Our data suggest that there are alleles and haplotypes in the IL6R, ADAM19, and SFTPD genes associated with different severity stages of COPD; in CYP2F2P, rs25455771 is associated with a lower risk of COPD.

Introduction: the desire to acquire promotional articles from tobacco companies (receptivity) is a risk factor associated with becoming an established smoker. There is a possibility that the perception of sexual content in tobacco advertising (PCS) may be part of that desire and act as an additional risk factor. Objective: the objective of this study was to determine the influence of receptivity and PCS in the smoking process. Method: in 1998, 1186 high school students were surveyed in order to determine their receptivity and PCS. After three years, 303 of them were followed through a telephone interview in order to correlate their current smoking status with the previously recorded antecedent of receptivity and PCS. Results: 62% of the subjects were receptive and 78% perceived some kind of sexual content in the advertising. Both receptivity and PCS were significantly associated with the probability of becoming an Established Smoker (ES) (OR 2.36 [95%CI 2.36-1.18] and OR 2.56 [1.02-6.42] respectively). Discussion and conclusions: receptivity and PCS are independent risk factors than can cause teenagers to become established smokers.----------------------- Introducción: el deseo de adquirir artículos promocionales de las compañías tabacaleras (receptividad) es un factor de riesgo asociado con convertirse en un fumador establecido. Existe la posibilidad de que la percepción de contenido sexual en la publicidad del tabaco (PCS) sea parte de ese deseo y actúe como un factor de riesgo adicional. Objetivo: el objetivo de este estudio fue determinar la influencia de la receptividad y PCS en el proceso de fumar. Método: en 1998, 1186 estudiantes de secundaria fueron encuestados para determinar su receptividad y PCS. Después de tres años, 303 de ellos fueron seguidos a través de una entrevista telefónica con el fin de correlacionar su estado actual de fumador con el antecedente previamente registrado de receptividad y PCS. Resultados: 62% de los sujetos eran receptivos y 78% percibe algún tipo de contenido sexual en la publicidad. Tanto la receptividad como PSC se asociaron significativamente con la probabilidad de convertirse en un fumador establecido (FE) (OR 2,36 [IC 95% 2,36-1,18] y OR 2,56 [1,02-6,42], respectivamente). Discusión y conclusiones: receptividad y PCS son factores de riesgo independientes que pueden ocasionar que los adolescentes se conviertan en fumadores establecidos.

Objectives Tobacco smoking is a complex and multifactorial disease involving both environmental and genetic factors. In the Mexican mestizo population, single-nucleotide polymorphisms (SNPs) associated with cigarette smoking and a greater degree of nicotine addiction have been identified; however, no possible roles have been explored in regard to the age of onset of smoking or in the success of quitting. Methods In this study, 151 Mexican mestizo, who smoke cigarettes, were included. They were grouped according to the age at which they started smoking: those who started smoking before 18 years of age (early smokers, ES) and those who started smoking ≥18 years of age (late smokers, LS). In addition, relapse in smoking was evaluated at the first month after the end of treatment. Genetic association was evaluated characterizing 10 SNPs in 4 genes (CHRNA5, CHRNA3, NRXN1, and HTR2A). Results According to the dominant model of genetic inheritance, rs6313 (CT+TT) of the HTR2A gene was associated (p = 0.0201) with cigarette consumption at early ages (OR = 2.68, CI = 1.18–6.07). When the risk of relapse was analyzed one month after the end of treatment, regardless of the age of onset, the T allele (rs6313) of HTR2A appeared to be a risk factor for relapse (OR = 2.92, 95% CI = 1.06–8.11); the T allele was found more frequently in those who relapsed (50.0%) compared with people who maintained abstinence (25.4%) (p = 0.0332). Conclusions Our findings suggest that in Mexican mestizos who smoke cigarettes, the presence of the T allele in rs6313 of the HTR2A gene increases the risk for the early onset of cigarette smoking as well as the risk for relapsing one month after completing smoking cessation treatment.

Background Between 2011 and 2016, Global Bridges (GB) in Latin America successfully trained health care providers (HCP) in declarative and procedural knowledge and confidence in competencies (Moore `s level 3A, B and 4). However, a study that explored patients´ reported HCP performance failed to show effect. Methods Cross-sectional study among all trainees between 2011 and 2016. The survey was electronically conducted (Survey Monkey) with 26 questions that explored demography, confidence in skills and practices in smoking cessation. A sample size of 400 individuals was required. Inclusion criteria were: attended at least one day session and a valid email. A mathematical model of impact estimation was developed (subrogate of level 5 of Moore). Abstinence rates for brief advice and intensive intervention of were appraised from Cochrane Review. Results Of 1915 trainees with valid e-mail, 402 surveys were obtained in 2 recruitment rounds. The response rate was different for the two periods 2011-2014 (17%) and 2014-2016 (56%). Countries (Argentina 28%, Uruguay 20% and Mexico 17%) and occupation (physicians 61% and psychologists 18%) were unevenly represented. Among the responses, female gender prevailed (64.7%). 79.4% stated GB training was extremely/very useful and more than 80% expressed to be very confident/ confident to provide SC support. Respondents declared to assist 2.1 smokers per day (CI 1.6-2.6), and to offer brief advice and intensive advice, with or without drugs, in 80% and 69% of cases respectively. The model estimated that 1,564 trainees would have achieved 12,012 quitters with brief advice and 38,788 quitters due to intensive intervention in the following year after training, in the worst case scenario (lower CI). Conclusions GB´s SC program in Latin America exhibited to maintain trainees´ confidence in competences in the medium term and to return at least 50,800 quitters in the following year of the educational intervention.

Background: Quitting smoking is key for patients with Chronic Obstructive Pulmonary Disease (COPD). Standard recommendations for quitting smoking are implemented for COPD as well. Varenicline Tartrate (VT) is the most effective drug to help quit smoking, but few studies have analysed its effectiveness. Aim of the study: To determine the Abstinence Rate (AR) at 12 months, in COPD and non-COPD smokers. Methods: Observational study in 31 COPD (post bronchodilator-BD FEV1/FVC

Aim: To evaluate association of single nucleotide polymorphisms (SNPs) in the MMP1, MMP2, MMP9 and MMP12 genes and serum MMP-2 and MMP-9 levels in smoking chronic obstructive pulmonary disease (COPD) patients. Materials & methods: Genotyping using real-time PCR in 330 smokers with COPD (COPD), 658 smokers without COPD (SNC) and 150 nonsmokers (NCNS), the analysis of samples used was χ2 test. Using ELISA, the proteins were evaluated. Multiple comparisons were made by ANOVA. Results: rs243864 (OR: 7.44; 95% CI: 3.62–15.26) and rs11646643 (OR: 1.58; 95% CI: 1.07–2.34) of the MMP-2 gene and rs3918253 (OR: 1.72; 95% CI: 1.08–2.71) of the MMP-9 gene, were associated with the risk of COPD. Serum MMP-2 level in the COPD group was lower compared with SNC (p < 0.05). Serum MMP-9 level was elevated in the COPD group compared with SNC (p < 0.05). Conclusion: Polymorphisms in MMP2 and MMP9 but not in MMP1 and MMP12 are associated with the risk of COPD in the Mexican mestizo population.

Streptococcus pneumoniae is responsible for several clinical syndromes, such as community-acquired pneumonia, sinusitis, otitis media, and others. The most severe clinical entity caused by this bacterium is undoubtedly invasive pneumococcal disease. Certain factors are known to increase the risk of presenting invasive pneumococcal disease, the most important being smoking and underlying concomitant diseases. This article comprises a consensus document on antipneumococcal vaccination in smokers, drawn up by a Smoking Expert Group from the Spanish Society of Pulmonology and Thoracic Surgery and the Latin American Chest Association.

Streptococcus pneumoniae is responsible for several clinical syndromes, such as community-acquired pneumonia, sinusitis, otitis media, and others. The most severe clinical entity caused by this bacteria is undoubtedly invasive pneumococcal disease. Certain factors are known to increase the risk of presenting invasive pneumococcal disease, the most important being smoking habit and underlying concomitant diseases. This article comprises a consensus document on antipneumococcal vaccination in smokers, drawn up by a Smoking Expert Group from the Spanish Society of Pulmonology and Thoracic Surgery and the Latin American Chest Association.

Juan Manuel Reséndiz-Hernández,1,2 Raúl H Sansores,3 Rafael de Jesús Hernández-Zenteno,3 Gilberto Vargas-Alarcón,4 Laura Colín-Barenque,5 Mónica Velázquez-Uncal,3 Angel Camarena,1 Alejandra Ramírez-Venegas,3 Ramcés Falfán-Valencia1 1Laboratory HLA, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico; 2Graduate Program in Biological Sciences, Universidad Nacional Autónoma de México, Mexico City, Mexico; 3Research Department in smoking and COPD, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico; 4Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico; 5Department of Neuroscience, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla de Baz, Mexico State, Mexico Abstract: Chronic obstructive pulmonary disease (COPD) is an inflammatory disease that arises in response to noxious particles or gases. Associations of genetic polymorphisms in TNF have been reported in Asians and Caucasians, but not in Mestizo populations. A case-control study was conducted in two stages: in the first stage, patients with COPD (COPD group, n=165) and smokers without disease (SNC group, n=165) were included and the TNF promoter sequence was determined using direct sequencing. In the second stage, the identified polymorphisms were validated by real-time polymerase chain reaction (PCR) in COPD (n=260) and SNC (n=506). In the first stage, 11 different sets of “contig” alignments were determined, of which contig 10 was found to be associated with susceptibility (P=5.0E-04, OR [odds ratio] =3.64) and contig 1 with Global Initiative for COPD (GOLD) greater grade (P=1.0E-02, OR =3.82). The single nucleotide polymorphisms found in this region were individually identified; the GA genotypes of rs1800629 (P=0.038, OR =2.07), rs56036015 (P=0.0082, OR =3.18), and rs361525 (P=1.0E-02, OR =4.220) were higher in the COPD group vs the SNC group; after second-stage validation, rs1800629 (P=6.00E-03, OR =2.26) and rs56036015 (P=1.10E-03, OR =2.54) are maintained. There are genetic variants in the TNF promoter associated with increased risk of COPD secondary to smoking and with a higher GOLD grade in the Mexican Mestizo population. Keywords: lung, cigarette smoking, SNP, GOLD, Mexican population

Introduction Chronic obstructive pulmonary disease (COPD) is characterized by restricted airflow. The best-documented genetic factor is alpha-1 antitrypsin (AAT). AAT is encoded by the SERPINA1 gene. The PiZ (rs28929474) and PiS (rs17580) variants are believed to cause severe AAT deficiency and are linked to a high risk of developing COPD. This study sought to identify whether genetic polymorphisms rs28929474 and rs17580 are associated with COPD susceptibility and lung function values in a Mexican mestizo population. Methods In this study, 558 smokers were included, of whom 279 had COPD and 279 did not (smokers without COPD – SWC). The PiS and PiZ variants were genotyped by allelic discrimination. Independent populations and lung function values were compared using the Kruskal–Wallis test. A bivariate logistic regression analysis was also conducted. Results Stage I and IV COPD patients showed significant differences in the frequencies of both heterozygous genotypes compared to SWC. For PiS, individuals with the heterozygous genotype AT demonstrated a decreased FEV1/FVC ratio compared to subjects with the homozygous genotype AA (P=.037). A significant association was found between the FEV1/FVC ratio and genotype AA for PiS (OR = 0.982, β coefficient = −0.019, 95% CI = 0.966–0.997). Conclusions COPD-causing AAT deficiency risk alleles exist at a very low frequency among Mexican mestizo population. Although they are not directly linked in our study population with disease susceptibility, these risk alleles are associated with poorer lung function measurements. It is important to characterize how often these genetic risk variants occur in other Latin American populations.

Resumen Introduccion La enfermedad pulmonar obstructiva cronica (EPOC) se caracteriza por dificultad para respirar. El factor genetico mejor documentado es la deficiencia de alfa-1 antitripsina (A1AT). La A1AT esta codificada por el gen SERPINA1. Se considera que las variantes PiZ (rs28929474) y PiS (rs17580) causan una deficiencia grave de A1AT y que estan relacionadas con un alto riesgo de desarrollar EPOC. En este estudio se busca identificar si los polimorfismos geneticos rs28929474 y rs17580 conllevan a la predisposicion a la EPOC y su relacion con los valores de funcion pulmonar en la poblacion mestiza mexicana. Metodos Para el estudio actual se incluyeron 558 fumadores, de los cuales 279 padecian EPOC y 279 no (fumadores sin EPOC [FSE]). Se genotiparon las variantes PiS y PiZ por discriminacion alelica. Se evaluo la comparacion entre poblaciones independientes y los valores de funcion pulmonar mediante la prueba de Kruskal-Wallis. Ademas, se realizo un analisis de regresion logistica bivariada. Resultados Los pacientes con EPOC en estadio i y iv presentaron diferencias significativas en cuanto a las frecuencias de ambos genotipos heterocigotocigotos en comparacion con los FSE. Para PiS, los sujetos con el genotipo heterocigotocigoto AT presentaron una reduccion del cociente FEV1/FVC en comparacion con los sujetos con el genotipo homocigoto AA (p = 0,037). Se detecto una relacion significativa entre el valor FEV1/FVC y el genotipo AA para PiS (OR = 0,982; coeficiente = –0,019; IC 95% = 0,966-0,997). Conclusiones Los alelos con riesgo de deficiencia de A1AT que causan EPOC son poco frecuentes entre la poblacion mestiza mexicana. Aunque en nuestra poblacion de estudio no tienen relacion directa con la predisposicion genetica a la enfermedad, estos alelos de riesgo se asocian a peores niveles de funcion pulmonar. Es importante describir con que frecuencia aparecen estas variantes geneticas de riesgo en otras poblaciones latinoamericanas.

This article contains data on the single nucleotide polymorphisms (SNPs) rs1137115, rs1801272 and rs28399433 rs4105144 in CYP2A6 associated to smoking related variables in Mexican Mestizo smokers (Pérez-Rubio et al., 2017) [1]. These SNPs were selected due to previous associations with other populations. Mexican Mestizo smokers were classified according their smoking pattern. A genetic association test was performed. Keywords: CYP2A6, Smoking, Nicotine addiction

The ALAT and SEPAR Treatment and Control of Smoking Groups have collaborated in the preparation of this document which attempts to answer, by way of PICO methodology, different questions on health interventions for helping COPD patients to stop smoking. The main recommendations are: (i) moderate-quality evidence and strong recommendation for performing spirometry in COPD patients and in smokers with a high risk of developing the disease, as a motivational tool (particularly for showing evidence of lung age), a diagnostic tool, and for active case-finding; (ii) high-quality evidence and strong recommendation for using intensive dedicated behavioral counselling and drug treatment for helping COPD patients to stop smoking; (iii) high-quality evidence and strong recommendation for initiating interventions for helping COPD patients to stop smoking during hospitalization with improvement when the intervention is prolonged after discharge, and (iv) high-quality evidence and strong recommendation for funding treatment of smoking in COPD patients, in view of the impact on health and health economics. © 2017 SEPAR

Background Genes encoding the receptors involved in the dopaminergic and serotonergic pathways are potential candidates in the mechanisms of nicotine addiction. Aims To identify genetic variants in the promoter regions and exons of the DRD4 and HTR2A genes associated with tobacco smoking and the degree of nicotine addiction in Mexican mestizos. Methods The study included 438 non-smokers (NS) and 1,157 current smokers, ranked based on their consumption of cigarettes per day (cpd): 574 heavy smokers (HS, >20 cpd) and 583 light smokers (LS, 1–10 cpd). Genotyping was performed for 4 and 8 single nucleotide polymorphisms (SNPs) in the DRD4 and HTR2A genes, respectively. Results The C allele of rs1800955 in DRD4 was found to be associated with cigarette smoking in the HS vs. NS and LS vs. NS comparisons (p = 2.34E-03 and p = 1.13E-03, respectively); the association was maintained in the homozygous CC genotype (p = 5.00E-04 and p = 2.00E-04, respectively). The T allele of rs6313 in HTR2A was significantly associated with cigarette smoking and a greater degree of nicotine addiction (p = 4.77E-03, OR = 1.55); the association was maintained in the homozygous genotype (TT) (p = 4.90E-03, OR = 1.96). The A allele of rs6313 was associated with cigarette smoking in the HS vs. NS comparison (p = 1.53E-02, OR = 1.36); the risk was nearly doubled in the homozygous AA genotype (p = 1.30E-03, OR = 1.83) compared with the heterozygous GA genotype (OR = 1.38). Conclusions Among Mexican mestizos, the C allele of rs1800955 in the DRD4 gene and the A allele of rs6311 in the HTR2A gene are associated with cigarette smoking, whereas the T allele of rs6313 in HTR2A is associated with cigarette smoking and the degree of nicotine addiction.

In chronic obstructive pulmonary disease (COPD) are two clinical phenotypes, emphysema and chronic bronchitis. Phenotypes share clinical symptoms such as dyspnea and bronchial obstruction to air fl ow and an increase of innate immune cells (macrophages and neu-trophils), the release of multiple in fl ammatory mediators (chemokines, cytokines, and growth factors), oxidative stress, increased extracellular matrix metalloproteinases (MMPs) in the airways and lung. Disease progression is associated with the presence of chronic in fl ammation and increased proteolytic activity of enzymes such as MMPs resulting in the degradation of elastin and collagen fi bers in the walls of the alveoli and the lung’s extracellular matrix. Of particular interest for this review was to describe the role of MMPs, their participati on in the development of COPD, both in the extracellular matrix destruction and abnormal lung remodeling damaged. Also mentioned genetic association studies of polymorphisms in MMPs type SNP in Caucasian populations such as the development and progression of COPD, and the importance of carrying out studies in Mexican mestizo population. The role of MMPs has also been known through animal models and knockout mic e MMPs exposed to cigarette smoke. All these studies implicate MMPs as key mediators in the pathogenesis of COPD. Finally, the study o f MMPs base allow for future therapies, potential therapeutic targets and disease treatments.

RESUMEN. Existen diversos padecimientos y factores que pueden tener un impacto sobre el funcionamiento cerebral debido a los cambios fi siologicos en estructuras cerebrales. En la practica clinica, las enfermedades respiratorias, incluyendo el tabaquismo y la enfermedad pulmonar obstructiva cronica (EPOC) no siempre son abordadas desde el angulo neuropsicologico. Aunadas a otras comorbilidades y a diferentes niveles, el tabaquismo y la EPOC propician una serie de alteraciones fi siologicas causando, a su vez, cambios neuropsicologicos que impactan sobre la calidad de vida y el funcionamiento de los pacientes. Esta revision resume aspectos criticos relacionados con el fun- cionamiento cognitivo y las enfermedades respiratorias. Palabras clave: Adiccion, EPOC, hipoxia, neuropsicologia, tabaquismo. ABSTRACT. There are several conditions and factors that may have an impact on brain functioning due to physiological changes in brain structures. In clinical practice, respiratory disease, including smoking and chronic obstructive pulmonary disease (COPD) are not always ap- proached from a neuropsychological angle. With other comorbidities and at different levels, smoking and COPD foster a series of physiological and neuropsychological changes that have an impact on quality of life and functioning of patients. This review summarizes critical aspects of cognitive functioning and respiratory diseases.

We hypothesised that biomass smoke exposure is associated with an airway-predominant chronic obstructive pulmonary disease (COPD) phenotype, while tobacco-related COPD is associated with an emphysema-predominant phenotype. In this cross-sectional study, female never-smokers with COPD and biomass exposure (n=21) and female ex-cigarette smokers with COPD without biomass exposure (n=22) completed computed tomography (CT) at inspiration and expiration, pulmonary function, blood gas, exercise tolerance, and quality of life measures. Two radiologists scored the extent of emphysema and air trapping on CT. Quantitative emphysema severity and distribution and airway wall thickness were calculated using specialised software. Women in the tobacco group had significantly more emphysema than the biomass group (radiologist score 2.3 versus 0.7, p=0.001; emphysema on CT 27% versus 19%, p=0.046; and a larger size of emphysematous spaces, p=0.006). Women in the biomass group had significantly more air trapping than the tobacco group (radiologist score 2.6 and 1.5, respectively; p=0.02) and also scored lower on the symptom, activities and confidence domains of the quality of life assessment and had lower oxygen saturation at rest and during exercise (p

Introduction: Use of varenicline for as long as necessary to achieve abstinence has not been studied. The aim of this study was to test whether smokers with mild-to-moderate chronic obstructive pulmonary disease (COPD) are able to quit if they use varenicline for a sufficient length of time. Methods: A total of 30 heavy smokers with COPD took varenicline for sufficiently long enough for smoking cessation. Smokers were allowed to smoke without a fixed quit date. The main endpoints were the time of voluntary abstinence (VA) and the continuous abstinence rate (CAR) at 12 and 18 months. Results: Of 28 subjects, eight subjects continued to smoke and 20 subjects stopped smoking, demonstrating a CAR up to 18 months (71%). Median time of treatment was 6 (range 3–24) and 2 (range 1–8) months for abstainers and non-abstainers, respectively, and the median time of VA for abstainers was 4 (range 1–21) months. Conclusions: Use of varenicline for more than the traditional 12 recommended weeks may be a good strategy to increase the cessation rate in heavy smokers with mild COPD.

For very severe COPD patients with frequent exacerbations, non-invasive positive pressure ventilation (NIPPV) may an alternative to reduce exacerbations. Objective: To evaluate the impact of the high-intensity non-invasive positive pressure ventilation (HI-NIPPV) in patients with stable normocapnic very severe COPD (Forced Expiratory Volume in the first second (FEV 1 ) lower than 30%p) on the frequency of exacerbations. Methods: A randomized, double blind, clinical trial study. Fifty eligible patients were randomized to receive HI-NIPPV (nspiratory positive pressure of 22 cm H2O or higher) or the sham intervention (S-NIV) during one year. The inclusion criteria were the presence of FEV 1 Results: No differences were found at baseline between groups in number of exacerbation, FEV 1 , dyspnea, exercise capacity, gas exchange, and quality of life. The compliance to the NIPPV was in average 10 hours/day and 26 ± 4cmH2O was the IPAP used in the HI-NIPPV group. The overall reduction in the rate of exacerbations mostly explained by mild and moderate exacerbations was observed in the HI-NIPPV treatment group (reduction by 55%) compared with the S-NIV [0.38 (0.24-0.51) versus 0.22 (0.15-0.29), p =0.012]. The 20% reduction in the rate of severe exacerbations with HI-NIPPV group treatment compared with the S-NIV was not significantly different. Only Dyspnea and PaCO2, showed significant improvement with the HI-NIPPV in comparison with the S-NIV. Conclusions: HI-NIPPV may be a useful additional intervention to prevent mild and moderate exacerbations in patients with severe airflow limitation.

Women are both more susceptible and more vulnerable than men when it comes to COPDhttp://ow.ly/UhMQ3

SummaryBackgroundChronic obstructive pulmonary disease (COPD) is a progressive disorder characterized by an inflammatory response to cigarette smoke. A disorder in immune regulation contributing to the pathogenesis of COPD has been suggested, however, little is known about the involvement of CD4 + T cells. To determine the distribution of different CD4+ T cell subsets in patients with COPD, current smokers without COPD (CS) and healthy subjects (HS), and its correlation with pulmonary function.MethodsTh1, Th2, Th17 and Treg, subsets, were quantified by flow cytometry in peripheral blood (PB) of 39 patients with COPD, 14 CS and 15 HS. Correlations were assessed with Spearman’s rank test. The association between Th17 and lung function was evaluated with a multivariate logistic regression analysis.ResultsAn increase of Th17 cells (median 9.7% range 0.8–22.5%) was observed in patients with COPD compared with CS (median 2.8% range 0.8–10.6) and HS (median 0.6% range 0.4–1%, p

Tobacco smoking is the primary risk factor for chronic obstructive pulmonary disease (COPD). However, recent epidemiological studies have established domestic exposure to wood smoke and other biomass fuels as additional important risk factors, characteristic in developing countries. Oxidative stress is one of the mechanisms concerned with pathogenesis of COPD. However, the molecular mechanisms involved in the onset and progress of COPD associated with biomass and specifically that derived from wood smoke exposure remain unknown. We analyzed the relationship between forced expiratory volume in first second (FEV(1)) with plasma malondialdehyde (MDA) concentration and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase (GST) in COPD patients associated with wood smoke (WSG; n = 30), tobacco smoking (TSG; n = 30), and healthy control subjects (HCG; n = 30). Differences between FEV(1) from WSG and TSG (58 +/- 22% and 51 +/- 24%, respectively) with HCG (100 +/- 6%) were observed (P < 0.01). Plasma MDA concentration was higher in both WSG and TSG (1.87 +/- 0.81 and 1.68 +/- 0.82 nmol/mL, respectively) compared with HCG (0.42 +/- 0.17 nmol/mL; P < 0.01). SOD activity showed a significant increase in both WSG and TSG (0.36 +/- 0.12 and 0.37 +/- 0.13 U/mL) compared with HCG (0.19 +/- 0.04 U/mL; P < 0.01). No differences were shown regarding GPx, GR, and GST activities between COPD and control groups. Inverse correlations were founded between MDA and SOD with FEV(1) in both COPD patients and control subjects (P < 0.001). These results indicate a role for oxidative stress in COPD associated with wood smoke similar to that observed with tobacco smoking in subjects who ceased at least 10 years previous to this study.

Objective. Although prevalence of tobacco smoking is different in the Latin American regions, the consequences on health are similar. Material and Methods. Therefore, guidelines on treatment are needed and ideally speaking must be useful in the different countries. In order to make quick recommendations useful in the region we made a search in PubMed from the last 5 years with the titles “Smoking cessation guidelines” and “Smoking cessation treatment meta-analysis” to know the content of different guidelines and with the titles of “Nicotine replacement therapy”, “Nicotine chewing gum”, “Nicotine patches”, “Nicotine inhaler”, “Bupropion therapy”, “Varenicline therapy” and “Individual and grupal behavioural counselling for smoking cessation” to determine the efficacy of each intervention. Results and conclusion. Our recommendation based on the availability of pharmacotherapy and human resources is that medical advice and behavioural grupal counseling must be primary interventions either adding, or not, first line drugs for smoking cessation

Raúl H Sansores, Mónica Velázquez-Uncal, Oliver Pérez-Bautista, Jaime Villalba-Caloca, Ramcés Falfán-Valencia, Alejandra Ramírez-VenegasTobacco Smoking and COPD Research Department, National Institute of Respiratory Diseases, Ismael Cosio Villegas, Mexico City, MexicoBackground: Physicians do not routinely recommend smokers to undergo spirometry unless they are symptomatic.Objective: To test the hypothesis that there are a significant number of asymptomatic smokers with chronic obstructive pulmonary disease (COPD), we estimated the prevalence of COPD in a group of asymptomatic smokers.Methods: Two thousand nine hundred and sixty-one smokers with a cumulative consumption history of at least 10 pack-years, either smokers with symptoms or smokers without symptoms (WOS) were invited to perform a spirometry and complete a symptom questionnaire.Results: Six hundred and thirty-seven (21.5%) smokers had no symptoms, whereas 2,324 (78.5%) had at least one symptom. The prevalence of COPD in subjects WOS was 1.5% when considering the whole group of smokers (45/2,961) and 7% when considering only the group WOS (45/637). From 329 smokers with COPD, 13.7% were WOS. Subjects WOS were younger, had better lung function and lower cumulative consumption of cigarettes, estimated as both cigarettes per day and pack-years. According to severity of airflow limitation, 69% vs 87% of subjects were classified as Global Initiative for Chronic Obstructive Lung Disease stagesI–II in the WOS and smokers with symptoms groups, respectively (P