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1.
Medicine (Baltimore) ; 98(28): e16454, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31305478

RESUMO

OBJECTIVE: Tobacco smoke contains carcinogens known to damage somatic and germ cells. In this study, we investigated the effect of tobacco smoking on the risk of childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML). METHODS: Information about tobacco smoking exposures of the mother before, during, and after pregnancy was collected via PubMed, Embase, and Web of Science databases through November 5, 2018. We performed to evaluate the association between smoking exposure and the risk of childhood ALL and AML. Study selection, data abstraction, and quality assessment were performed by 2 independent reviewers. Random effects models were used to obtain summary odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Nineteen case-control studies of childhood leukemia (age < 15 years) conducted in 9 countries from 1974 to 2018. Maternal smoking exposures did not a significant association with childhood ALL (OR = 1.004, 95% CI 0.953-1.058, P = .881) and AML (OR = 0.92, 95% CI 0.815-1.038, P = .177) during exposure time windows. However, there was an association with paternal smoking and ALL (OR = 1.15, 95% CI 1.038-1.275, P = .007). Paternal smoking in AML showed there was no association with smoking exposures and childhood AML (OR = 1.133, 95% CI 0.943-1.362, P = .181). Next, maternal daily cigarettes consumption showed no associations with ALL (OR = 1.08, 95% CI 1.000-1.168, P = .051) during pregnancy. No association with maternal daily smoking and AML (OR = 0.909, 95% CI 0.682-1.211, P = .514). Paternal daily cigarettes consumption was associated with increased risks of childhood ALL (OR = 1.200, 95% CI 1.112-1.302, P = .000). The higher consumption of paternal smoking (more than 10 per day) was significantly related to childhood ALL. Paternal daily smoking consumption also was related to AML (OR = 1.242, 95% CI 1.031-1.496, P = .022). CONCLUSION: Maternal smoking before, during, or after pregnancy was not associated with childhood ALL or AML. However, paternal smoking was related to a significantly elevated risk of childhood ALL during pregnancy, but not for AML. Maternal daily smoking consumption was not associated with ALL or AML during pregnancy. The higher consumption of paternal smoking were, the higher the risk of childhood ALL or AML.


Assuntos
Leucemia Mieloide Aguda/epidemiologia , Leucemia-Linfoma Linfoblástico de Células Precursoras/epidemiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Adolescente , Criança , Feminino , Humanos , Fatores de Risco
2.
BMC Public Health ; 19(1): 690, 2019 Jun 04.
Artigo em Inglês | MEDLINE | ID: mdl-31164109

RESUMO

BACKGROUND: Lung function is lower in people with disadvantaged socio-economic position (SEP) and is associated with hazardous health behaviours and exposures. The associations are likely to be interactive, for example, exposure to socially patterned environmental tobacco smoke (ETS) in childhood is associated with an increased effect of smoking in adulthood. We hypothesise that disadvantaged childhood SEP increases susceptibility to the effects of hazards in adulthood for lung function. We test whether disadvantaged childhood SEP moderates smoking, physical activity, obesity, occupational exposures, ETS and air pollution's associations with lung function. METHODS: Data are from the Nurse Health Assessment (NHA) in waves two and three of the United Kingdom Household Longitudinal Study (UKHLS). Analysis is restricted to English residents aged at least 20 for women and 25 for men, producing a study population of 16,339. Lung function is measured with forced expiratory volume in the first second (FEV1) and standardised to the percentage of expected FEV1 for a healthy non-smoker of equivalent age, gender, height and ethnicity (FEV1%). Using STATA 14, a mixed linear model was fitted with interaction terms between childhood SEP and health behaviours and occupational exposures. Cross level interactions tested whether childhood SEP moderated household ETS and neighbourhood air pollution's associations with FEV1%. RESULTS: SEP, smoking, physical activity, obesity, occupational exposures and air pollution were associated with lung function. Interaction terms indicated a significantly stronger negative association between disadvantaged childhood SEP and currently smoking (coefficient -6.47 %, 95% confidence intervals (CI): 9.51 %, 3.42 %) as well as with formerly smoking and occupational exposures. Significant interactions were not found with physical activity, obesity, ETS and air pollution. CONCLUSION: The findings suggest that disadvantaged SEP in childhood may make people's lung function more susceptible to the negative effects of smoking and occupational exposures in adulthood. This is important as those most likely to encounter these exposures are at greater risk to their effects. Policy to alleviate this inequality requires intervention in health behaviours through public health campaigns and in occupational health via health and safety legislation.


Assuntos
Envelhecimento/fisiologia , Pulmão/fisiopatologia , Exposição Ocupacional/efeitos adversos , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Fumar/fisiopatologia , Poluição por Fumaça de Tabaco/efeitos adversos , Adolescente , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Criança , Estudos Transversais , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Modelos Lineares , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Testes de Função Respiratória , Fatores Socioeconômicos , Reino Unido , Adulto Jovem
3.
Life Sci ; 232: 116575, 2019 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-31211999

RESUMO

AIMS: Maternal smoking is considered a risk factor for childhood obesity. In a rat model of tobacco exposure during breastfeeding, we previously reported hyperphagia, overweight, increased visceral fat and hyperleptinemia in adult female offspring. Obesity and eating disorders are associated with impairment in the endocannabinoid (EC) and dopaminergic (DA) systems. Considering that women are prone to eating disorders, we hypothesize that adult female Wistar rats that were exposed to cigarette smoke (CS) during the suckling period would develop EC and DA systems deregulation, possibly explaining the eating disorder in this model. MATERIAL AND METHODS: To mimic maternal smoking, from postnatal day 3 to 21, dams and offspring were exposed to a smoking machine, 4×/day/1 h (CS group). Control animals were exposed to ambient air. Offspring were evaluated at 26 weeks of age. KEY FINDINGS: Concerning the EC system, the CS group had increased expression of diacylglycerol lipase (DAGL) in the lateral hypothalamus (LH) and decreased in the liver. In the visceral adipose tissue, the EC receptor (CB1r) was decreased. Regarding the DA system, the CS group showed higher dopamine transporter (DAT) protein expression in the prefrontal cortex (PFC) and lower DA receptor (D2r) in the arcuate nucleus (ARC). We also assessed the hypothalamic leptin signaling, which was shown to be unchanged. CS offspring showed decreased plasma 17ß-estradiol. SIGNIFICANCE: Neonatal CS exposure induces changes in some biomarkers of the EC and DA systems, which can partially explain the hyperphagia observed in female rats.


Assuntos
Neurônios Dopaminérgicos/efeitos dos fármacos , Endocanabinoides/metabolismo , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Animais Recém-Nascidos , Fumar Cigarros , Dopamina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Dopamina/efeitos dos fármacos , Neurônios Dopaminérgicos/fisiologia , Endocanabinoides/fisiologia , Feminino , Região Hipotalâmica Lateral/efeitos dos fármacos , Região Hipotalâmica Lateral/metabolismo , Hipotálamo/metabolismo , Lactação/efeitos dos fármacos , Leptina/metabolismo , Lipase Lipoproteica/efeitos dos fármacos , Exposição Materna/efeitos adversos , Obesidade/etiologia , Obesidade/metabolismo , Ratos , Ratos Wistar , Receptores de Canabinoides/efeitos dos fármacos , Fumar , Tabaco
4.
Eur J Epidemiol ; 34(7): 637-649, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31037572

RESUMO

Ecological observations suggest an inverse relationship between smoking in pregnancy and celiac disease (CD) in offspring. While individual-level analyses have been inconsistent, they have mostly lacked statistical power or refined assessments of exposure. To examine the association between pregnancy-related smoking and CD in the offspring, as well as its consistency across data sets, we analyzed: (1) The Norwegian Mother and Child Cohort (MoBa) of 94,019 children, followed from birth (2000-2009) through 2016, with 1035 developing CD; (2) a subsample from MoBa (381 with CD and 529 controls) with biomarkers; and (3) a register-based cohort of 536,861 Norwegian children, followed from birth (2004-2012) through 2014, with 1919 developing CD. Smoking behaviors were obtained from pregnancy questionnaires and antenatal visits, or, in the MoBa-subsample, defined by measurement of cord blood cotinine. CD and potential confounders were identified through nationwide registers and comprehensive parental questionnaires. Sustained smoking during pregnancy, both self-reported and cotinine-determined, was inversely associated with CD in MoBa (multivariable-adjusted [a] OR = 0.61 [95%CI, 0.46-0.82] and aOR = 0.55 [95%CI, 0.31-0.98], respectively); an inverse association was also found with the intensity of smoking. These findings differed from those of our register-based cohort, which revealed no association with sustained smoking during pregnancy (aOR = 0.97 [95%CI, 0.80-1.18]). In MoBa, neither maternal smoking before or after pregnancy, nor maternal or paternal smoking in only early pregnancy predicted CD. In a carefully followed pregnancy cohort, a more-detailed smoking assessment than oft-used register-based data, revealed that sustained smoking during pregnancy, rather than any smoking exposure, predicts decreased likelihood of childhood-diagnosed CD.


Assuntos
Doença Celíaca/epidemiologia , Cotinina/sangue , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Fumar/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Biomarcadores/sangue , Estudos de Casos e Controles , Doença Celíaca/induzido quimicamente , Feminino , Sangue Fetal , Antígenos HLA , Humanos , Masculino , Pessoa de Meia-Idade , Mães , Noruega/epidemiologia , Gravidez , Sistema de Registros , Fatores de Risco , Autorrelato , Fumar/sangue , Abandono do Hábito de Fumar
5.
Rev Environ Health ; 34(2): 105-124, 2019 Jun 26.
Artigo em Inglês | MEDLINE | ID: mdl-31112510

RESUMO

The use of electronic cigarettes (e-cigarettes or "vaping") has seen an unprecedented increase worldwide. Vaping has been promoted as a beneficial smoking cessation tool and an alternative nicotine delivery device that contains no combustion by-products. However, nicotine is highly addictive, and the increased use of nicotine-containing e-cigarettes among teens and individuals who are not in need of smoking cessation may lead to overall greater nicotine dependence in the population. Furthermore, available research indicates that vaping solutions and their emissions may contain much more than just nicotine, including aerosolized flavorings, propylene glycol (PG), and other intentional and unintentional contaminants. These materials could present undefined potential health hazards to both e-cigarette users and bystanders, the full extent of which is not well understood at this time. Whereas e-cigarette usage and exposures may lower some or most of the risks associated with conventional cigarette use, the health effects of nicotine and aerosol exposures from e-cigarettes are not well understood. Research indicates that vaping aerosols are not benign, especially for nearby people in areas with limited ventilation and people with compromised health conditions. In addition, e-juice liquids have already been responsible for an increase in accidental poisonings in children. Because the magnitude of health and safety hazards that vaping may present to nonusers remains unclear, it is prudent to manage and control vaping in indoor locations where smoking is currently restricted. Based on a review of current scientific information, the American Industrial Hygiene Association (AIHA) recommends that e-cigarettes should be considered a source of aerosols, volatile organic compounds (VOCs), and particulates in the indoor environment that have not been thoroughly characterized or evaluated for health risk or safety.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Exposição Ambiental/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Vaping/efeitos adversos , Aerossóis/efeitos adversos , Aerossóis/análise , Poluentes Atmosféricos/análise , Poluição do Ar em Ambientes Fechados/análise , Material Particulado/efeitos adversos , Material Particulado/análise , Medição de Risco , Poluição por Fumaça de Tabaco/análise , Compostos Orgânicos Voláteis/efeitos adversos , Compostos Orgânicos Voláteis/análise
6.
BMC Public Health ; 19(1): 491, 2019 May 02.
Artigo em Inglês | MEDLINE | ID: mdl-31046729

RESUMO

BACKGROUND: Thirdhand smoke (THS) is the persistent residue resulting from secondhand smoke (SHS) that accumulates in dust, objects, and on surfaces in homes where tobacco has been used, and is reemitted into air. Very little is known about the extent to which THS contributes to children's overall tobacco smoke exposure (OTS) levels, defined as their combined THS and SHS exposure. Even less is known about the effect of OTS and THS on children's health. This project will examine how different home smoking behaviors contribute to THS and OTS and if levels of THS are associated with respiratory illnesses in nonsmoking children. METHODS: This project leverages the experimental design from an ongoing pediatric emergency department-based tobacco cessation trial of caregivers who smoke and their children (NIHR01HD083354). At baseline and follow-up, we will collect urine and handwipe samples from children and samples of dust and air from the homes of smokers who smoke indoors, have smoking bans or who have quit smoking. These samples will be analyzed to examine to what extent THS pollution at home contributes to OTS exposure over and above SHS and to what extent THS continues to persist and contribute to OTS in homes of smokers who have quit or have smoking bans. Targeted and nontargeted chemical analyses of home dust samples will explore which types of THS pollutants are present in homes. Electronic medical record review will examine if THS and OTS levels are associated with child respiratory illness. Additionally, a repository of child and environmental samples will be created. DISCUSSION: The results of this study will be crucial to help close gaps in our understanding of the types, quantity, and clinical effects of OTS, THS exposure, and THS pollutants in a unique sample of tobacco smoke-exposed ill children and their homes. The potential impact of these findings is substantial, as currently the level of risk in OTS attributable to THS is unknown. This research has the potential to change how we protect children from OTS, by recognizing that SHS and THS exposure needs to be addressed separately and jointly as sources of pollution and exposure. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02531594 . Date of registration: August 24, 2015.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Saúde da Criança/tendências , Política Antifumo/tendências , Poluição por Fumaça de Tabaco/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar em Ambientes Fechados/análise , Cuidadores , Criança , Pré-Escolar , Poeira/análise , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Projetos de Pesquisa , Poluição por Fumaça de Tabaco/análise
7.
Zhonghua Jie He He Hu Xi Za Zhi ; 42(5): 367-371, 2019 May 12.
Artigo em Chinês | MEDLINE | ID: mdl-31137113

RESUMO

Objective: To compare chronic obstructive pulmonary disease (COPD) mouse models established by two different methods-cigarette smoke (CS) exposure alone and CS exposure combined with airway instillation of bacterial LPS. Methods: Male C57 mice were randomly divided into control group(CTL group), CS exposure group (CS group) and intra-tracheal LPS instillation combined with CS exposure group (LPS+CS group) according to the random number table, with 8 rats in each group. After the models were established, we measured the lung function and collected the bronchoalveolar lavage fluid (BALF) to detect the number of inflammatory cells and the expression of mucin and inflammatory mediators. HE and PAS staining were performed to observe the pathological changes in airway and lung tissue and to detect the goblet cells in airway, respectively. Results: Total lung capacity (TLC), functional residual capacity (FRC) and airway resistance (RI) of the CS and LPS+CS groups were higher than those of the CTL group, while the FEV(50)/FVC of these 2 groups was lower (P<0.05). Moreover, both RI and FEV(50)/FVC in the LPS+CS group were higher compared with the CS group (P<0.05). HE staining of lung tissue showed that the average alveolar intercept and thickness of small airway wall in the CS and LPS+CS groups were higher compared to the CTL group. In addition, the average alveolar intercept in the LPS+CS group was lower than that in the CS group [(47.86±2.82) µm and (61.94±7.68) µm respectively, P<0.05], but the area of bronchial inflammation of LPS+CS group was higher. The number of total white blood cells, neutrophils, lymphocytes, macrophages and the level of interleukin-6 (IL-6) in BALF of CS and LPS+CS groups were higher than those of CTL group (all P<0.05). Furthermore, the number of neutrophils and IL-6 level in BALF of LPS+CS group were higher in comparison with CS group, while the number of macrophages in BALF of LPS+CS group was lower (P<0.05). PAS staining of lung tissue indicated that the number of goblet cells in large airways of CS and LPS+CS groups increased more significantly compared to the CTL group, and the number of goblet cells in the LPS+CS group was higher than that in the CS group [(0.16±0.02) and (0.09±0.02) respectively, P<0.05]. The expression levels of Muc5ac and Muc5b in BALF of LPS+CS and CS groups were also higher than those of CTL group (P<0.05), and the level of Muc5ac in BALF of LPS+CS group was higher compared with CS group[(2.69±0.72) and (2.19±0.29) respectively, P<0.05]. Conclusions: Combined exposure of LPS and CS for establishing a COPD mouse model could better simulate the pathological characteristics of human COPD during the acute exacerbation period. The COPD mouse model established by CS exposure alone was able to better imitate the basic features of human COPD in the stable period. Researchers could choose a more appropriate modeling method according to different purposes.


Assuntos
Brônquios/metabolismo , Lipopolissacarídeos/efeitos adversos , Pulmão/fisiologia , Doença Pulmonar Obstrutiva Crônica/metabolismo , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Líquido da Lavagem Broncoalveolar , Masculino , Camundongos , Doença Pulmonar Obstrutiva Crônica/etiologia , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
8.
Adv Exp Med Biol ; 1176: 63-69, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31016633

RESUMO

Chronic exposure to cigarette smoke (CS) causes structural and functional changes in the respiratory tract. It is a major risk factor for cardiovascular and systemic pulmonary diseases. The aim of this study was to investigate the effect of acute CS exposure (2 h) on oxidative stress, heat shock protein 70 (HSP70) expression, autophagy (LC3 expression), and oxidative stress (DCF fluorescence) in human alveolar epithelial cell line A549. Cell culture medium was conditioned with CS using commercial cigarettes, and A549 cells were grown in modified media for 2 h. In some experiments, A549 cells were pretreated with 100 µM of L-buthionine-sulfoximine (BSO) for 24 h to induce glutathione (GSH) depletion. In the cells grown in CS-conditioned medium, GSH was depleted by more than 30%, and reactive oxygen species were increased. Moreover, there was a considerable overexpression of HSP70 and a substantial accumulation of LC3. Similar changes were found when the cells were pretreated with BSO. We conclude that the short-term exposure of epithelial cells to CS increases oxidative stress that entails enhanced autophagy activity.


Assuntos
Células Epiteliais Alveolares , Autofagia , Estresse Oxidativo , Poluição por Fumaça de Tabaco/efeitos adversos , Células A549 , Células Epiteliais Alveolares/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Fumar Cigarros/efeitos adversos , Humanos , Estresse Oxidativo/efeitos dos fármacos
9.
BMC Neurosci ; 20(1): 15, 2019 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-30947684

RESUMO

BACKGROUND: Smoking (TS) and recently e-cigarettes (EC) vaping, have been associated with vascular endothelial dysfunction primarily relevant to oxidative stress, exposure to nicotine, and smoking-induced inflammation. It is accepted that both EC and TS enhance glucose intolerance and the risk of developing type-2 diabetes mellitus which is also one of the causes of blood-brain barrier (BBB) damage and the higher risk of cerebrovascular diseases. Recent studies have shown how Metformin, the first common antidiabetic drug, can protect the BBB integrity through enhancement of nuclear factor erythroid 2-related factor (Nrf2) activity. Herein, we investigated the role of rosiglitazone (RSG; family of thiazolidinedione class used oral anti-diabetic drug) in TS/EC-induced BBB impairment. RESULTS: Although the exact mechanism of RSG is not fully understood, previous studies have revealed that RSG can promote counteractive protective mechanisms primarily associated with the enhancement of Nrf2 activity through activation of the peroxisome proliferator-activated receptor gamma. In line with these findings, our results show an increased expression of PPARy by RSG, enhancement of Nrf2 activity and BBB protection against TS/EC exposure including reduced inflammation, oxidative stress, tight junction downregulation and loss of BBB integrity. CONCLUSIONS: RSG could be considered as a promising therapeutic potential to prevent TS/EC induced cerebrovascular dysfunction and possibly other xenobiotic substances which may impact the BBB via oxidative stress-mediated effects. However, additional in vivo studies and clinical setting will be needed to validate our results and assess the full extent of RSG protective effects.


Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Permeabilidade Capilar/efeitos dos fármacos , Sistemas Eletrônicos de Liberação de Nicotina , Fármacos Neuroprotetores/farmacologia , Rosiglitazona/farmacologia , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Barreira Hematoencefálica/metabolismo , Barreira Hematoencefálica/patologia , Permeabilidade Capilar/fisiologia , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Relação Dose-Resposta a Droga , Células Endoteliais/efeitos dos fármacos , Células Endoteliais/metabolismo , Células Endoteliais/patologia , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Inflamação/patologia , Camundongos Endogâmicos C57BL , Microvasos/efeitos dos fármacos , Microvasos/metabolismo , Microvasos/patologia , NAD(P)H Desidrogenase (Quinona)/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , PPAR gama/metabolismo , Dados Preliminares , Espécies Reativas de Oxigênio/metabolismo
10.
Artigo em Inglês | MEDLINE | ID: mdl-31010129

RESUMO

Secondhand smoke (SHS), a common environmental exposure factor, has become a serious public health problem. Metabolic syndrome is another worldwide clinical challenge. Our study tried to determine the age differences in the relationship between SHS and the risk of metabolic syndrome. Studies were searched in PubMed and Web of Science from 11 November to 30 November 2018. Eighteen studies were finally included based on inclusion and exclusion criteria. The relationship between SHS and the risk indicators of metabolic syndrome was analyzed. The weighted mean difference (WMD) of fasting plasma glucose (FPG), insulin, body mass index (BMI), and waist circumference (WC), and the standard mean difference (SMD) of total cholesterol, triglycerides, and low- and high-density lipoprotein-cholesterol (LDL-C, HDL-C) were calculated in a meta-analysis. SHS was positively associated with the level of insulin and WC. According to the subgroup analysis based on age difference, SHS was positively associated with FPG in the upper age group, and positively associated with LDL-C and negatively associated with HDL-C in the lower age group. BMI showed a more obvious positive correlation in the adults group than in the children and the teenagers group. In conclusion, the association of metabolic syndrome with SHS varies with age. When exposed to SHS, older people may be more susceptible to glucose metabolic disorder, but younger people may be more susceptible to lipid metabolic disorder.


Assuntos
Envelhecimento/metabolismo , Síndrome Metabólica/epidemiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Adolescente , Adulto , Fatores Etários , Glicemia/análise , Índice de Massa Corporal , Criança , HDL-Colesterol/sangue , Humanos , Insulina/sangue , Resistência à Insulina , Metabolismo dos Lipídeos , Síndrome Metabólica/sangue , Síndrome Metabólica/etiologia , Obesidade/sangue , Obesidade Abdominal/etiologia , Fatores de Risco , Triglicerídeos/sangue , Circunferência da Cintura
11.
Psychiatr Danub ; 31(Suppl 1): 39-43, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30946716

RESUMO

Tobacco consumption is one of the most common preventable cause of premature deaths worldwide. Persisting effects of exposure to tobacco smoke on children and adolescents are apparent during pregnancy and in early infancy, passive exposure to environmental tobacco smoke in home and elsewhere, and active smoking during adolescence. While, lung development in these stages of growth is not complete, tobacco smoke puts children and adolescents in danger of severe respiratory diseases and may interfere with the growth of their lungs. Active tobacco consumption by adolescents may have immediate adverse health outcomes such as addiction, impaired lung growth or reduced lung function. Much of the current evidence comes from longitudinal and cross-sectional longitudinal observational studies and propose that the strongest associations with smoke exposure are in the pregnancy and early childhood. The association of nicotine with respiratory system among children and adolescents is less clearly understood and the evidence primarily comes from in vitro and animal studies.


Assuntos
Nível de Saúde , Efeitos Tardios da Exposição Pré-Natal , Poluição por Fumaça de Tabaco , Adolescente , Animais , Criança , Pré-Escolar , Estudos Transversais , Exposição Ambiental , Feminino , Humanos , Gravidez , Fumar , Tabaco , Poluição por Fumaça de Tabaco/efeitos adversos
12.
Eur Arch Otorhinolaryngol ; 276(6): 1713-1719, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30980189

RESUMO

PURPOSE: Laryngeal pathologies due to cigarette smoking vary among individuals, whereas some smokers remain disease free. These differences can be explained by multiple factors among individuals. In this context, an animal study was designed to determine if there is any protective effect of aerobic exercise against the detrimental effects of cigarette smoke on laryngeal tissues. METHODS: A total of 24 male Wistar albino rats were divided into three groups of eight animals each: control (no smoke exposure), smoking (smoke exposure), and exercise (smoke exposure and exercise) groups. Histopathological (light and electron microscopy) and immunohistochemical (GSTA1, CYP1A1, CYP2E1) evaluations of the vocal folds were performed at the end of experimental period. RESULTS: Exercise group revealed statistically significant decrease in edema (p = 0.03) and inflammatory cell infiltration (p = 0.02) compared to smoking group. In electron microscopic evaluation; cytoplasmic vacuoles were also present in exercise group, but were smaller than smoking group. Edema and swollen mitochondria were also less prominent in exercise group. Condensed chromatin material in the periphery of nucleus was observed only in few cells in exercise group, and observed in more cells in smoking group. GSTA1 expression was higher (p = 0.047) and CYP1A1 expression was lower (p = 0.01) in exercise group than smoking group. CONCLUSIONS: Our results indicate that aerobic exercise has a protective role on the larynx against the damaging effect of cigarette smoke. Smokers who exercise regularly may be at a lower risk of cigarette smoke-related laryngeal diseases, as compared with those who do not exercise.


Assuntos
Fumar Cigarros/efeitos adversos , Condicionamento Físico Animal , Poluição por Fumaça de Tabaco/efeitos adversos , Prega Vocal/patologia , Animais , Citocromo P-450 CYP1A1/metabolismo , Glutationa Transferase/metabolismo , Isoenzimas/metabolismo , Masculino , Ratos , Ratos Wistar , Prega Vocal/metabolismo
13.
BMC Cancer ; 19(1): 348, 2019 Apr 11.
Artigo em Inglês | MEDLINE | ID: mdl-30975121

RESUMO

BACKGROUND: Extrahepatic cholangiocarcinoma (ECC) has become one of the most rapidly increasing malignancies in China during recent decades. The relationship between tobacco exposure and ECC epidemics is unclear; this study aimed to explore this relationship. METHODS: We included 55,806 participants aged 30 years or older from the National Mortality and Smoking Survey of China. Smoking in participants and spouses was defined as 1 cigarette or more per day for up to 1 year. Spouses' smoking was taken as a measure of exposure to passive smoking. Smoking information in 1980 was ascertained and outcomes were defined as ECC mortality during 1986-1988. RESULTS: We found that either passive or active smoking increased the risk of death from ECC by 20% (risk ratio [RR], 1.20; 95% confidence interval [CI], 0.99-1.47), compared with no exposure to any tobacco. This risk was a notable 98% (RR, 1.98; 95% CI, 1.49-2.64) for individuals exposed to passive plus active smoking. These findings were highly consistent among men and women. Pathology-based analyses showed dose-response relationships of ECC with pack-years for all types of smoking exposure (Ps for trend < 0.05); the RR reached 2.75 (95% CI, 1.20-6.30) in individuals exposed to combined smoking with the highest exposure dose. The findings were similar for non-pathology-based analysis. CONCLUSIONS: This study indicates that tobacco exposure increases ECC risk. Given the dramatic increase of exposure to secondhand smoke and patients with ECC, an inadequate provision of smoke-free environments could be contributing to ECC epidemics and could further challenge public health and medical services, based on the current disease spectrum.


Assuntos
Neoplasias dos Ductos Biliares/mortalidade , Causas de Morte , Colangiocarcinoma/mortalidade , Poluição por Fumaça de Tabaco/efeitos adversos , Fumar Tabaco/efeitos adversos , Adulto , Idoso , Neoplasias dos Ductos Biliares/etiologia , Neoplasias dos Ductos Biliares/patologia , Neoplasias dos Ductos Biliares/prevenção & controle , Ductos Biliares Extra-Hepáticos/patologia , Estudos de Casos e Controles , China/epidemiologia , Colangiocarcinoma/etiologia , Colangiocarcinoma/patologia , Colangiocarcinoma/prevenção & controle , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Poluição por Fumaça de Tabaco/estatística & dados numéricos , Fumar Tabaco/epidemiologia
14.
Monaldi Arch Chest Dis ; 89(1)2019 Mar 20.
Artigo em Inglês | MEDLINE | ID: mdl-30968672

RESUMO

The spectrum of eosinophilic lung diseases comprises a diverse group of pulmonary disorders associated with tissue or peripheral eosinophilia. [Acute eosinophilic pneumonia (AEP)] is an uncommon eosinophilic lung disease that can be idiopathic, but identifiable causes include medications, inhalational exposures and infections. Most cases in the literature are associated with first-time cigarette smoking or resuming smoking. Herein, we present a case of AEP in an elderly man triggered by exposure to secondhand tobacco smoke, in whom a transbronchial biopsy was diagnostic. The patient recovered fully with glucocorticoid therapy without recurrence after avoiding further secondhand smoke.


Assuntos
Glucocorticoides/uso terapêutico , Eosinofilia Pulmonar/etiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Doença Aguda , Idoso , Biópsia , Humanos , Masculino , Eosinofilia Pulmonar/diagnóstico , Eosinofilia Pulmonar/tratamento farmacológico , Resultado do Tratamento
15.
BMC Public Health ; 19(1): 406, 2019 Apr 15.
Artigo em Inglês | MEDLINE | ID: mdl-30987624

RESUMO

BACKGROUND: This study explored the role of outdoor air pollution [nitrogen dioxide (NO2) and sulphur dioxide (SO2)] and indoor air quality (measured with damp or condensation and secondhand smoke exposures) at age 9 months in emotional, conduct and hyperactivity problems at age 3 years. METHOD: Data from 11,625 Millennium Cohort Study children living in England and Wales were modelled using multilevel regression. RESULTS: After adjusting for a host of confounders, having a damp or condensation problem at home was related to both emotional and conduct problems. Secondhand smoke exposure was associated with all three problem types. Associations with outdoor air pollution were less consistent. CONCLUSIONS: Exposures to damp or condensation and secondhand smoke in the home are likely to be risk factors for child emotional and behavioural problems. Parents should continue to be educated about the dangers of exposing their children to poor air quality at home.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Poluição do Ar/efeitos adversos , Transtornos do Comportamento Infantil/etiologia , Criança , Comportamento Infantil , Bem-Estar da Criança/estatística & dados numéricos , Pré-Escolar , Estudos de Coortes , Inglaterra , Feminino , Humanos , Lactente , Masculino , Dióxido de Nitrogênio/efeitos adversos , Fatores de Risco , Dióxido de Enxofre/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , País de Gales
16.
Life Sci ; 227: 58-63, 2019 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-31009626

RESUMO

AIMS: The prevalence of waterpipe tobacco smoking is increasing among breastfeeding women. Herein, the effect of maternal waterpipe tobacco smoke (WTS) exposure during lactation on learning and memory of adult offspring rats was examined. MAIN METHODS: Lactating rats received either fresh air or mainstream WTS (1 h twice daily) from day 4 to day 21. Learning and memory was examined by the radial arm water maze and the levels of brain derived neurotrophic factor (BDNF) and oxidative stress biomarkers superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase and thiobarbituric acid reactive substances (TBARS) were assessed in the hippocampus of adult male offspring rats. KEY FINDINGS: Maternal exposure to WTS during lactation impaired the long-term memory and reduced levels of BDNF (P < 0.05) in hippocampus in adult male offspring rats. The activity of SOD, GPx and catalase were reduced (P < 0.05) while level of TBARS was increased (P < 0.05). SIGNIFICANCE: Maternal WTS exposure during lactation impaired the long-term memory of adult male offspring that was associated with low levels of BDNF and altered oxidative stress balance. Therefore, careful measures should be taken to enhance waterpipe smoking cessation during breastfeeding.


Assuntos
Aprendizagem/efeitos dos fármacos , Memória/efeitos dos fármacos , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Biomarcadores/metabolismo , Fator Neurotrófico Derivado do Encéfalo/análise , Catalase/análise , Feminino , Glutationa Peroxidase/análise , Hipocampo/metabolismo , Lactação , Masculino , Exposição Materna/efeitos adversos , Transtornos da Memória/metabolismo , Memória de Longo Prazo/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Ratos , Superóxido Dismutase/análise , Tabaco para Cachimbos de Água , Fumar Cachimbo de Água/efeitos adversos
17.
Biomed Res Int ; 2019: 5829676, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31016192

RESUMO

Tobacco smoking is established as a cofactor of human papillomavirus (HPV) for cervical cancer risk. However, the role of secondhand smoking in cervical carcinogenesis is controversial. We aimed to assess the association between secondhand smoking and high risk- (HR-) HPV persistence, a pivotal event in development of cervical cancer. In total, 9,846 women who underwent health-screening examinations from 2002 to 2011 at the National Cancer Center, Korea, were included. Secondhand smoking was defined as being exposed to secondhand smoke at home or in the workplace. Multivariate logistic regression analysis was used to estimate the odds ratios (OR) and 95% confidence intervals (CIs) for risks of HR-HPV infection at baseline (N, 9,846, negative vs. positive), 1-year persistence (n, 1,237, 1-year negative vs. 1-year persistence), and 2-year persistence (n, 481, 2-year negative vs. 2-year persistence). Active smoking, secondhand smoking, and secondhand smoking in nonactive smokers had no association with these risks. Among alcohol drinkers, secondhand smoking in nonactive smokers had higher risks of HR-HPV infection at baseline (OR = 1.25, 95% CI = 1.05-1.48, p for multiplicative interaction = 0.003), 1-year persistence (1.75, 1.14-2.68, 0.004), and 2-year persistence (2.96, 1.42-6.15, 0.006), when compared to HR-HPV negative, 1-year negative, and 2-year negative categories, respectively. However, among nonalcohol drinkers, there was no association between smoking or secondhand smoking status and these risks. These findings suggest that women exposed to secondhand smoking at home or in the workplace might be at high risk of HR-HPV persistence when it is combined with alcohol drinking, even though neither active smoking nor secondhand smoking independently affects the risk.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Infecções por Papillomavirus/etiologia , Fumar/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Colo do Útero/fisiopatologia , Colo do Útero/virologia , Feminino , Humanos , Programas de Rastreamento/métodos , Pessoa de Meia-Idade , Papillomaviridae/patogenicidade , Infecções por Papillomavirus/virologia , República da Coreia , Fatores de Risco , Neoplasias do Colo do Útero/etiologia , Neoplasias do Colo do Útero/fisiopatologia , Neoplasias do Colo do Útero/virologia
18.
Asian Pac J Cancer Prev ; 20(3): 971-976, 2019 Mar 26.
Artigo em Inglês | MEDLINE | ID: mdl-30912422

RESUMO

Background: Secondhand smoke has been a big problem for human being worldwide as it is well-established risk factors for cancers. ASEAN (Association of Southeast Asian Nations) bear high burden of cancers since the high prevalence of secondhand smoke. The objective of this study is to estimate the burden of cancer attributable to secondhand smoking in ASEAN. Methods: This research was using descriptive epidemiological incidence and prevalence-based research design, with cancers incidence and mortality data gained from GLOBOCAN 2012. Secondhand smoke attributable fractions (SAFs) of six cancers (lung, bladder, colorectal, stomach, pancreas and larynx) were estimated and burden of cancers caused by secondhand smoking in ASEAN were calculated in term of incidence and mortality. Results: Secondhand smoking estimated for 453,562 cancer cases and 323,284 of total cancer mortality in 2012. The number of incidence and death of lung cancer attributable to secondhand smoking show the highest number compared with other type of cancers. Furthermore, we found that the number of cancer cases and cancer deaths attributable to secondhand smoking varied by each countries due to differences in size of population, various background risk of the cancer, and prevalence of secondhand smoking in each country. Conclusion: Secondhand smoking has been a risk factor for about two-fifth of cancer incidence and mortality in ASEAN. Therefore, ASEAN member countries are strongly encouraged to put in place stronger tobacco control policies and to strengthen the existing tobacco control measure in order to decrease the number of secondhand smokers and more effectively control cancers.


Assuntos
Neoplasias/epidemiologia , Neoplasias/mortalidade , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Ásia Sudeste/epidemiologia , Feminino , Seguimentos , Humanos , Incidência , Masculino , Neoplasias/etiologia , Prognóstico , Fatores de Risco , Taxa de Sobrevida
19.
Clin Epigenetics ; 11(1): 46, 2019 03 12.
Artigo em Inglês | MEDLINE | ID: mdl-30867047

RESUMO

BACKGROUND: Both SOX2 promoter methylation and air pollution have been associated with lung cancer risk. However, little has been done to assess SOX2 promoter methylation in individuals living in air pollution areas. The aim of this study was to investigate SOX2 promoter methylation in non-smoking Taiwanese adults living in areas with different levels of air pollution especially particulate matter with diameter < 2.5 µm (PM2.5). METHODS: A total of 1142 individuals aged 30-70 years were recruited. Data on SOX2 methylation, residence, age, and exposure to second-hand smoke (SHS) among others were extracted from the Taiwan Biobank dataset (2008-2015). After excluding former and current smokers, alongside those with incomplete information, a total of 461 non-smokers comprising 176 men and 285 women were included in the study. Participants' residences were grouped under northern and central/southern areas because air pollution (PM2.5) is lower in northern compared to central and southern areas. RESULTS: The methylation levels in men (0.16310 ± 0.01230) and women (0.15740 ± 0.01240) were significantly different (P < .0001). In both sexes, the SOX2 promoter region was shown to be significantly hypermethylated in central and southern areas compared with the northern areas. The regression coefficient (ß) was 0.00331 (P = 0.0257) in men and 0.00514 (P < .0001) in women. CONCLUSION: SOX2 was significantly hypermethylated in both men and women residing in central and southern areas. The consistency in the results for both sexes shows that SOX2 promoter methylation could serve as a potential biomarker for industrial air pollution exposure. Moreover, it might reflect predisposition to cancer. Hence, healthy non-smokers at precancerous stages who have not been clinically diagnosed could be identified.


Assuntos
Metilação de DNA , Fatores de Transcrição SOXB1/genética , Poluição por Fumaça de Tabaco/análise , Adulto , Idoso , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Metilação de DNA/efeitos dos fármacos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Regiões Promotoras Genéticas/efeitos dos fármacos , Análise de Regressão , Taiwan , Poluição por Fumaça de Tabaco/efeitos adversos
20.
Pediatrics ; 143(4)2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30858346

RESUMO

OBJECTIVES: To determine how smoke-free and vape-free home and car policies differ for parents who are dual users of cigarettes and electronic cigarettes (e-cigarettes), who only smoke cigarettes, or who only use e-cigarettes. To identify factors associated with not having smoke-free or vape-free policies and how often smoke-free advice is offered at pediatric offices. METHODS: Secondary analysis of 2017 parental interview data collected after their children's visit in 5 control practices participating in the Clinical Effort Against Secondhand Smoke Exposure trial. RESULTS: Most dual users had smoke-free home policies, yet fewer had a vape-free home policies (63.8% vs 26.3%; P < .01). Dual users were less likely than cigarette users to have smoke-free car (P < .01), vape-free home (P < .001), or vape-free car (P < .001) policies. Inside cars, dual users were more likely than cigarette users to report smoking (P < .001), e-cigarette use (P < .001), and e-cigarette use with children present (P < .001). Parental characteristics associated with not having smoke-free or vape-free home and car policies include smoking ≥10 cigarettes per day, using e-cigarettes, and having a youngest child >10 years old. Smoke-free home and car advice was infrequently delivered. CONCLUSIONS: Parents may perceive e-cigarette aerosol as safe for children. Dual users more often had smoke-free policies than vape-free policies for the home. Dual users were less likely than cigarette-only smokers to report various child-protective measures inside homes and cars. These findings reveal important opportunities for intervention with parents about smoking and vaping in homes and cars.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina/estatística & dados numéricos , Pais , Política Antifumo , Fumar/epidemiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Automóveis , Criança , Pré-Escolar , Feminino , Humanos , Incidência , Entrevistas como Assunto , Modelos Logísticos , Masculino , Análise Multivariada , Medição de Risco , Prevenção do Hábito de Fumar , Estados Unidos
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