Prevalence, attitude, knowledge, and risk perception towards COVID-19 in COPD patients associated to biomass exposure.

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.

Protective Role of Genetic Variants in HSP90 Genes-Complex in COPD Secondary to Biomass-Burning Smoke Exposure and Non-Severe COPD Forms in Tobacco Smoking Subjects.

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 < 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.

SMALLa AIRWAY DISEASE IN COPD ASSOCIATED TO BIOMASS EXPOSURE.

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.

Varenicline for long term smoking cessation in patients with COPD.

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 <0.70) and in 63 non-COPD smokers, were invited to receive treatment with Varenicline Tartrate (VT). Fourteen subjects with COPD and 46 non-COPD subjects received additionally Cognitive-Behavioral Therapy (CBT). Abstinence rate (AR) was validated by exhaled carbon monoxide CO (COe), in addition to a phone or face-to-face interview. Motivation score was measured with a visual analogue scale (MS). RESULTS: Differences between COPD and non-COPD, mean FEV1/FVC ratio 0.52 ±â€¯0.10 vs. 0.90 ±â€¯0.15, age 60 ±â€¯10 vs. 47 ±â€¯10 years, smoking pack-years 37 ±â€¯3.5 vs. 22 ±â€¯12, and COe 16 ±â€¯11 vs. 12 ±â€¯9 ppm were statistically significant (p < 0.05); for MS the score was 93 ±â€¯11 vs. 93 ±â€¯11 and for attempts to quit (AQ) 2 ±â€¯2 vs. 2 ±â€¯3 were not. AR was not significantly different at 12 months (61.2 vs. 42.8% p = 0.072). Motivation was the only significant one-year AR predictor. CONCLUSIONS: COPD smokers had a similar response (higher tendency) to VT regardless of the presence of airflow obstruction and stronger nicotine addiction.

Genetic Variants in IL6R and ADAM19 are Associated with COPD Severity in a Mexican Mestizo Population.

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.

FEV1 decline in patients with chronic obstructive pulmonary disease associated with biomass exposure.

RATIONALE: Biomass exposure is an important risk factor for chronic obstructive pulmonary disease (COPD). However, the time-course behavior of FEV1 in subjects exposed to biomass is unknown. OBJECTIVES: We undertook this study to determine the FEV1 rate decline in subjects exposed to biomass. METHODS: Pulmonary function was assessed every year in a Mexican cohort of patients with COPD associated with biomass or tobacco during a 15-year follow-up period. MEASUREMENTS AND MAIN RESULTS: The mean rate of decline was significantly lower for the biomass exposure COPD group (BE-COPD) than for the tobacco smoke COPD group (TS-COPD) (23 vs. 42 ml, respectively; P < 0.01). Of the TS-COPD group, 11% were rapid decliners, whereas only one rapid decliner was found in the BE-COPD group; 69 and 21% of smokers versus 17 and 83% of the BE-COPD group were slow decliners and sustainers, respectively. A higher FEV1 both as % predicted and milliliters was a predictive factor for decline for BE-COPD and TS-COPD, whereas reversibility to bronchodilator was a predictive factor for both groups when adjusted by FEV1% predicted and only for the TS-COPD group when adjusted by milliliters. CONCLUSIONS: In the biomass exposure COPD group the rate of FEV1 decline is slower and shows a more homogeneous rate of decline over time in comparison with smokers. The rapid rate of FEV1 decline is a rare feature of biomass-induced airflow limitation.

COPD phenotypes in biomass smoke- versus tobacco smoke-exposed Mexican women.

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<0.05). Biomass smoke exposure is associated with less emphysema but more air trapping than tobacco smoke exposure, suggesting an airway-predominant phenotype.

FEV1 inversely correlates with metalloproteinases 1, 7, 9 and CRP in COPD by biomass smoke exposure.

BACKGROUND: Matrix metalloproteinases (MMPs) and C-reactive protein (CRP) are involved in chronic obstructive pulmonary disease (COPD) pathogenesis. The aim of the present work was to determine plasma concentrations of MMPs and CRP in COPD associated to biomass combustion exposure (BE) and tobacco smoking (TS). METHODS: Pulmonary function tests, plasma levels of MMP-1, MMP-7, MMP-9, MMP-9/TIMP-1 and CRP were measured in COPD associated to BE (n = 40) and TS (n =40) patients, and healthy non-smoking (NS) healthy women (controls, n = 40). RESULTS: Plasma levels of MMP-1, MMP-7, MMP-9, and MMP-9/TIMP-1 and CRP were higher in BE and TS than in the NS healthy women (p <0.01). An inverse correlation between MMP-1, MMP-7, MMP-9, MMP-9/TIMP-1 and CRP plasma concentrations and FEV1 was observed. CONCLUSIONS: Increase of MMPs and CRP plasma concentrations in BE suggests a systemic inflammatory phenomenon similar to that observed in COPD associated to tobacco smoking, which may also play a role in COPD pathogenesis.

Characterization of the lung microbiome and inflammatory cytokine levels in women exposed to environmental risk factors: A pilot study.

INTRODUCTION: Lung microbiome dysbiosis affects the immune system balance and promotes lung inflammation. We aimed to characterize and compare the lung bacteriome composition and the cytokine profile in women with normal lung function exposed to risk factors for chronic lung diseases (tobacco smoking and biomass-burning smoke exposure). METHODS: We included women with biomass-burning smoke exposure (BE, n = 11) and current smokers women (TS, n = 10). The bacteriome composition was performed in induced sputum, sequencing the 16 rRNA gene. Cytokine levels were measured using enzyme-linked immunosorbent assay multiplex assay in the supernatant of induced sputum. For quantitative variables, we used medians and minimum and maxim values. For the amplicon sequence variants (ASV) differential abundance testing between groups. RESULTS: At the taxa level, the phylum Proteobacteria was found in a higher proportion in the TS group concerning BE (p = .045); however, after the false discovery rate adjustment, this difference was not retained (p = .288). We found a higher concentration of IL-1ß in the TS group than in the BE group (248.6 vs. 177.9 pg/mL, p = .010). Women with high biomass-burning smoke exposure in an hour per day had a positive correlation with the abundance of Bacteroidota (ρ = 0.71, p = .014) and Fusobacteriota (ρ = 0.73, p = .011). FEV1/FVC had a positive correlation with an abundance of Bacteroidota, Proteobacteria, and Fusobacteria (ρ = 0.74, p = .009, ρ = 0.85, p = .001, and ρ = 0.83, p = .001, respectively). In tobacco smoking, women had a positive correlation (ρ = 0.77, p = .009) between cigarettes per day and Firmicutes' abundance. CONCLUSION: Compared to biomass-burning smoke-exposed women, current smokers have poor lung function and high levels of IL-1ß in sputum. Women with biomass-burning smoke exposure present an increased abundance of Bacteroidota and Fusobacteriota.

Air quality in Mexico City during the COVID-19 lockdown possibly decreased COPD exacerbations.

The reduction of air pollution during the #COVID19 lockdown in Mexico City possibly reduced the exacerbation rate in #COPD patients due to biomass and tobacco despite that the self-isolation was not as strict as expected. https://bit.ly/3Iyv98t.

Clinical and microbiological characteristics and inflammatory profile during an exacerbation of COPD due to biomass exposure. A comparison with COPD due to tobacco exposure.

BACKGROUND: 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. METHODS: 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. RESULTS: 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]. CONCLUSIONS: 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.

The "Slow Horse Racing Effect" on Lung Function in Adult Life in Chronic Obstructive Pulmonary Disease Associated to Biomass Exposure.

Although different trajectories in lung function decline have been identified in patients with COPD associated to tobacco exposure (TE-COPD), genetic, environmental, and infectious factors affecting lung function throughout life have not been fully elucidated in patients with COPD associated to biomass (BE-COPD). In this review, we present current epidemiological findings and notable advances in the natural history of lung decline in BE-COPD, as well as conditions modeling the FEV1 trajectory, such as health insults, during the first years of childhood. Evidence shows that women exposed to biomass smoke reach adult life with a lower FEV1 than expected. However, in contrast to the "horse racing effect" predicting an excessive lung-function decline in forthcoming years, as observed in smokers, this decline is slower in non-smokers, and no rapid decliners are observed. Accordingly, BE-COPD might be considered another phenotype of COPD based on assessments of lung function decline. Likewise, other functional and clinical aspects described in this review suggest that this condition might be similar to TE-COPD. More research is needed to fully characterize this subgroup of variants of COPD.

Lung Damage Caused by Heated Tobacco Products and Electronic Nicotine Delivery Systems: A Systematic Review.

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.

Hypomethylation of AHRR (cg05575921) Is Related to Smoking Status in the Mexican Mestizo Population.

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).

Malondialdehyde and superoxide dismutase correlate with FEV(1) in patients with COPD associated with wood smoke exposure and tobacco smoking.

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.

[Proposal of Latin-American guidelines for smoking cessation]. / Guías de atención médica para dejar de fumar. Una propuesta para Latinoamérica.

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 group 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 group counseling must be primary interventions either adding, or not, first line drugs for smoking cessation.

[Anxiety and depression in Mexican smokers, and their relationship with the severity of addiction]. / Ansiedad y depresión en fumadores mexicanos y su relación con el grado de adicción.

OBJECTIVE: To determine the relationship between the degree of addiction (DA) and pattern of tobacco consumption (PTC) with anxiety and depression in smokers who want to quit smoking. MATERIAL AND METHODS: At admission to a smoking cessation program 495 smokers were surveyed to determine anxiety (IDARE Test), depression (Beck Inventory Test), DA (Fagerström Test) and PTC (pack-years). RESULTS: DA ≥ 6 points was associated with high anxiety levels RM=1.94, (IC95%1.02-3.72), p<0.04]; and with symptoms of severe depression; [RM=2.24, (IC95%1.00-4.99), p<0.04)]. The PCT equal or greater than 21 pack-year, was associated with moderate anxiety; [RM=3.19 (IC95%1.94-5.25), p<.00]; high anxiety; [RM=3.36 (IC95% 1.66-6-80), p<.00]; with moderate depressive symptoms; [RM=3.14, (IC95% 1.75-5-62), p<.00] and severe depressive symptoms; [RM=9.85, (IC95% 3.30-29.37), p<.00)]. CONCLUSION: A significant association exists in smokers having high GA and PCT, with moderate and high anxiety and depressive symptoms that should be considered during interventions to quit.