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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.

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Immunosenescence are alterations on immune system that occurs throughout an individual life. The main characteristic of this process is replicative senescence, evaluated by telomere shortening. Several factors implicate on telomere shortening, such as smoking. In this study, we evaluated the influence of smoking and Chronic Obstructive Pulmonary Disease (COPD) on cytokines, telomere length and telomerase activity. Blood samples were collected from subjects aged over 60 years old: Healthy (never smokers), Smokers (smoking for over 30 years) and COPDs (ex-smokers for ≥15 years). A young group was included as control. PBMCs were cultured for assessment of telomerase activity using RT-PCR, and cytokines secretion flow cytometry. CD4+ and CD8+ purified lymphocytes were used to assess telomere length using FlowFISH. We observed that COPD patients have accelerated telomere shortening. Paradoxically, smokers without lung damage showed preserved telomere length, suggesting that tobacco smoking may affect regulatory mechanisms, such as telomerase. Telomerase activity showed diminished activity in COPDs, while Smokers showed increased activity compared to COPDs and Healthy groups. Extracellular environment reflected this unbalance, indicated by an anti-inflammatory profile in Smokers, while COPDs showed an inflammatory prone profile. Further studies focusing on telomeric maintenance may unveil mechanisms that are associated with cancer under long-term smoking.

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BACKGROUND: Barriers to early childhood development (ECD) are a global concern. Limited research exists on prenatal smoking and ECD in vulnerable populations, especially as it relates to school readiness (SR). AIMS: To examine how maternal cigarette use during pregnancy is associated with SR in a sample of Brazilian preschool-age children. STUDY DESIGN: We used the Brazilian Preschool Mental Health Study, a cross-sectional, epidemiological study of preschool-age children in Embu das Artes, São Paulo. SR was assessed using the Engle Scale of Child Development (ESCD). We restricted analyses to biological mothers, who represented 81.9% (n = 591) of the total 722 with ESCD data. Logistic regression models, adjusting for birth and child characteristics (year of preschool, sex, race, history of head trauma, coma, convulsions or epilepsy), sociodemographic factors and school environment, were used to estimate odds ratios and 95% confidence intervals. RESULTS: Prenatal smoking was negatively associated with SR. Children of mothers who smoked during pregnancy were more likely to be in the lowest ESCD quartile (aOR = 1.26, 95%CI: [1.02-1.55]) compared to those of non-smoking mothers, and each cigarette resulted in additional risk (aOR = 1.03, 95%CI:[1.01-1.05]). Children of heavy smokers had worse ESCD scores compared to children of non-smokers (aOR = 1.69, 95%CI:[1.18-2.44]), as well as when compared to children of moderate and non-smokers combined (aOR = 1.77, 95%CI:[1.22-2.57]). This relationship was not seen when comparing children of moderate smokers to children of non-smokers. Inferences were robust when examining very heavy smoking. CONCLUSION: Maternal tobacco use during pregnancy may affect child SR. Additional studies in other populations are needed to corroborate these results.

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Telomere length and mitochondrial DNA content are considered biomarkers of cellular aging, oxidative stress, and inflammation, but there is almost no information on their association with tobacco smoke exposure in fetal and early life. The aim of this study was to assess whether prenatal and childhood tobacco exposure were associated with leukocyte telomere length (LTL) and mitochondrial DNA (mtDNA) content in children. As part of a multi-centre European birth cohort study HELIX (Human Early-Life Exposome) (n = 1396) we assessed maternal smoking status during pregnancy through questionnaires, and through urinary cotinine levels that were then used to classify women as not exposed to smoking (<10 µg/L), exposed to secondhand smoke (SHS) (10-50 µg/L) and active smokers (>50 µg/L). When the children were around 8 years of age (range: 5.4-12.0 years), childhood SHS tobacco smoke exposure was assessed through an extensive questionnaire and through measurements of urinary cotinine (<3.03 µg/L non-detected, >3.03 µg/L detected). Leukocyte mtDNA content and LTL were measured in the children at 8 years employing real time polymerase chain reaction (qPCR). Effect estimates were calculated using multivariate linear regression models for prenatal and childhood exposures adjusted for potential confounders. Maternal cotinine levels indicative of SHS exposure during pregnancy were associated with a decrease of 3.90% in LTL in children (95% CI: -6.68, -0.91), compared with non-smoking, whereas the association for maternal cotinine levels indicative of active smoking did not reach statistical significance (-3.24%; 95% CI: -6.59, 0.21). Childhood SHS tobacco exposure was not associated with LTL in children. Global SHS exposure during childhood was associated with an increase of 3.51% (95% CI: 0.78, 6.27) in mtDNA content. Our findings suggest that tobacco smoke exposure during pregnancy, even at SHS levels, may accelerate telomere shortening in children and thus induce biological aging from an early age.

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INTRODUCTION: The role of environmental and behavioral exposures on childhood leukemia etiology is poorly understood. We examined the association of maternal and paternal tobacco smoking at different time points with the risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) in Costa Rican children. MATERIALS AND METHODS: We conducted a population-based case-control study on childhood leukemia in Costa Rica. Cases (n ALL = 252; n AML = 40) were diagnosed between 1995 and 2000 (aged <15 years at diagnosis) and identified from the Costa Rican Cancer Registry and the National Children's Hospital. A total of 578 frequency-matched population controls were sampled from the National Birth Registry. Parental tobacco smoking was assessed via face-to-face interviews. We used logistic regression models to examine the association of paternal and maternal tobacco smoking before conception, during pregnancy, and after birth with childhood ALL and AML risk, adjusted for child sex, birth year, maternal/paternal age, and parental education. RESULTS: Paternal smoking before conception, during pregnancy, and after birth was associated with an increased risk of childhood AML (Odds Ratio (OR): 2.51, 95% CI: 1.21-5.17; OR: 3.21, 95% CI: 1.56-6.60; and OR: 2.83, 95% CI: 1.36-5.90, respectively). Maternal smoking during pregnancy was also associated with a modest, but imprecise increase in AML risk. We observed null associations of maternal and paternal smoking with ALL in the offspring. CONCLUSION: Our results suggest an association between parental smoking and risk of AML, but not ALL, in Costa Rican children. These findings add to the established evidence of numerous health risks associated with smoking and highlight the potential harm of smoking during sensitive windows of the development of fetus and child.

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Cytochrome P450 2A6 (CYP2A6) catalyzes nicotine metabolism and contributes to the metabolism of the tobacco-specific lung carcinogen, NNK. Genetic variation in CYP2A6 may affect smoking behavior and contribute to lung cancer risk. A nested case-control study of 325 lung cancer cases and 356 controls was conducted within a prospective cohort of 18,244 Chinese men in Shanghai, China. Quantified were 4 allelic variants of CYP2A6 [*1(+51A), *4, *7, and *9] and urinary total nicotine, total cotinine, total trans-3'-hydroxycotinine (3HC) and total NNAL (an NNK metabolite). Calculated were total nicotine equivalents (TNE), the sum of total nicotine, total cotinine and total 3HC and the total 3HC:total cotinine ratio as a measure of CYP2A6 activity. The nicotine metabolizer status (normal, intermediate, slow and poor) was determined by CYP2A6 genotypes. The smoking-adjusted odds ratios (95% confidence intervals) of lung cancer for the highest vs lowest quartile of total nicotine, total cotinine, total 3HC, TNE and total NNAL were 3.03 (1.80-5.10), 4.70 (2.61-8.46), 4.26 (2.37-7.68), 4.71 (2.61-8.52), and 3.15 (1.86-5.33) (all Ptrend < 0.001), respectively. Among controls CYP2A6 poor metabolizers had a 78% lower total 3HC:total cotinine ratio and 72% higher total nicotine (Ptrend ≤ 0.002). Poor metabolizers had an odds ratio of 0.64 (95% confidence interval = 0.43-0.97) for lung cancer, which was statistically nonsignificant (odds ratio = 0.74, 95% confidence interval = 0.48-1.15) after adjustment for urinary TNE and smoking intensity and duration. The lower lung cancer risk observed in CYP2A6 poor metabolizers is partially explained by the strong influence of CYP2A6 genetic polymorphisms on nicotine uptake and metabolism.

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Objetivo. Analizar la probabilidad de abuso de sustancias en relación con la edad de inicio del consumo de tabaco. Material y métodos. Los datos provienen de la Encuesta Nacional de Adicciones (1998) realizada en población urbana. Resultados. La edad de mayor riesgo para experimentar con sustancias es entre los 15 y los 19 años. Solamente en 5.6 por ciento de los usuarios de drogas y 13 por ciento de los que han consumido alcohol, el uso del tabaco no ocurrió primero. La probabilidad de beber en forma consuetudinaria y de presentar dependencia es mayor cuando la edad de inicio es temprana y disminuye en la medida en que se retrasa la edad de inicio. La experimentación con drogas, el continuar usándolas y el poliuso son más frecuentes entre quienes se iniciaron antes de los 15 años. Conclusiones. El inicio temprano en el consumo de tabaco incrementa la probabilidad de uso y abuso de sustancias.

Objective. To assess the likelihood of substance abuse predicted by age of first exposure to tobacco. Material and Methods. Data from the 1998 National Household Survey on Addictions in urban areas were analyzed. Results. The age period of greater likelihood of drug experimentation is between 15 and 19 years; only 5.6 percent of drug users and 13 percent of alcohol beverage drinkers reported having experimented with drugs before trying tobacco. The probability of heavy drinking and dependence was higher at early ages of first exposure to tobacco and decreased with increasing age. Experimentation with drugs, continued use, and multiple drug use, are more frequent among smokers who started before 15 years of age. Conclusions. Early tobacco use increases the likelihood of substance abuse.

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