Indirect Methods to Determine the Risk of Damage to the Health of Firefighters and Children Due to Exposure to Smoke Emission from Burning Wood/Coal in a Controlled Environment.

People are constantly exposed to particulate matter and chemicals released during fires. However, there are still few studies on gas and particulate emissions related to exposure to burning firewood and charcoal during forest fires, making it difficult to understand the effects on the health of the population. The objective of this study was to quantify the metal(loid)s present in the smoke from wood and charcoal fires through the deposition of metals in beef topside and pork loin, considering the routes of skin exposure, inhalation, and ingestion, contributing to the understanding of metals in the increase of the risks of cancer and mortality associated with firefighting and children. The concentrations of metals [aluminum (Al), chromium (Cr), copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), molybdenum (Mo), vanadium (V), zinc (Zn)] and metalloids arsenic (As) were determined by inductively coupled plasma-mass spectrometry (ICP OES) after microwave digestion. Moreover, we assessed the associated risk regarding the elemental intake of these elements through the smoke, using the hazard quotient (HQ), hazard index (HI), Total Hazard Index (HIt), and carcinogenic risk (CR). All samples had results for HQ and HIt < 1, indicating a non-potential health risk. However, the carcinogenic risks posed by As and Cr via the three exposure pathways (except for inhalation exposure to children and adults, and by Cr via ingestion and inhalation for children and adults) exceeded the standard threshold. In conclusion, continuous exposure of firefighters or children to smoke from fires containing high concentrations of heavy metals such as As and Cr can be harmful to health. The study used animal tissues; thus, new methods must be developed to quantify the concentration of heavy metals deposited in human tissue when humans are exposed to smoke from fires.

Prevalence of Chronic Bronchitis and Respiratory Health Profile of a Population Exposed to Wood Smoke in Nicaragua.

BACKGROUND: Household air pollution (HAP) is one of the most important environmental risk factors worldwide associated with chronic respiratory diseases. OBJECTIVES: The present study focused on respiratory health in a population with high wood smoke exposure in Nicaragua. METHODS: We employed a cross-sectional study with 213 participants. Data on the prevalence of chronic bronchitis (chronic bronchitis), chronic obstructive pulmonary disease (COPD) and asthma, including respiratory scores and pulmonary function tests, were documented. The role of risk factors for chronic bronchitis was analyzed. RESULTS: We found a high prevalence of chronic airway diseases in the population exposed to wood smoke. A higher prevalence of chronic bronchitis was found in persons serving as primary cooks in households. Further confounding factors for chronic bronchitis included age, a prior diagnosis of asthma, inhalational allergies and lower socioeconomic status. Respiratory scores were elevated in individuals with chronic bronchitis. CONCLUSIONS: This is one of the first studies in a wood smoke-exposed population in Nicaragua showing a high prevalence of chronic bronchitis and COPD with an emphasis on the analysis of personal and environmental risk factors. Further studies are needed to address which combination of interventions is most efficient for ameliorating respiratory health hazards. PARTICIPANT CONSENT: Obtained. ETHICS APPROVAL: The study protocol was approved by the Ethics Committee of the University of Luebeck, Germany (reference number 12-214), and by the Ethics Committee of the Department of Medical Sciences at National Autonomous University of Nicaragua, Managua, Nicaragua. COMPETING INTERESTS: The authors declare no competing financial interests.

miR-34a in serum is involved in mild-to-moderate COPD in women exposed to biomass smoke.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I-II). METHODS: In the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS. RESULTS: miR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS. CONCLUSIONS: This is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases.

Comparative study on the effects of cigarette smoke exposure, ethanol consumption and association: Behavioral parameters, apoptosis, glial fibrillary acid protein and S100ß immunoreactivity in different regions of the rat hippocampus.

Exposure to cigarette smoke and ethanol are proposed to trigger neurotoxicity, apoptosis, and to impair neuronal signaling. However, it is little known how the combination of both might trigger astrogliosis and the morphological changes capable of affecting a differential susceptibility of hippocampal regions to these licit drugs. The present study investigated the chronic effects of exposure to cigarette smoke and/or ethanol on behavioral parameters, apoptosis, and alteration in immunoreactivity of glial fibrillary acid protein (GFAP) and S100ß in the CA1, CA3, and dentate gyrus (DG) of the rat hippocampus. Adult male Wistar rats (n = 32) were divided into four groups: vehicle (VE, glucose 3% in water, 10 mL/kg), cigarette smoke (TOB, total 12 cigarettes per day), ethanol (ethanol, 2 g/kg), and cigarette smoke plus ethanol (TOB plus ethanol, total 12 cigarettes per day plus ethanol 2 g/kg) for 54 days. The groups were submitted to tail-flick, open-field, and inhibitory avoidance tasks. The results showed that ethanol per se worsened the short-term memory. The association between TOB and ethanol increased the immunoreactivity of cleaved caspase-3 in the CA3 and DG regions. The TOB plus ethanol group showed a lower immunoreactivity to GFAP in all regions of the hippocampus. In addition, ethanol and TOB per se also reduced the immunoreactivity for GFAP in the DG. Ethanol increased S100ß immunoreactivity only in the DG. In conclusion, this study showed that only ethanol worsened short-term memory, and the DG became more susceptible to changes in the markers investigated. This evidence suggests that DG is more sensitive to neurotoxicity induced by cigarette smoke and ethanol.

Women with COPD by biomass show different serum profile of adipokines, incretins, and peptide hormones than smokers.

BACKGROUND: The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS. METHODS: Clinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls. Data were compared with one-way ANOVA and Tukey's post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn's post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women. RESULTS: FEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure. CONCLUSIONS: women with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.

Secondhand tobacco smoke exposure and pulmonary function: a cross-sectional study among non-smoking employees of bar and restaurants in Santiago, Chile.

INTRODUCTION: The workplace remains a significant source of secondhand smoke (SHS) exposure. This pollutant is known to be associated with respiratory and cardiovascular problems, but its effects on specific pulmonary function parameters remain largely unexplored. The objectives of this study were to measure SHS exposure among non-smoking employees of bar and restaurants in Santiago, Chile and to evaluate the effects of such exposure on pulmonary function. METHODS: Cross-sectional design. The study sample included non-smoking workers from 57 restaurants and bars in Santiago, Chile. The outcome variable was pulmonary function and the exposure variables were urine cotinine concentration, a biomarker for current SHS exposure, and years of SHS exposure in the workplace as proxy of chronic exposure. Personal and occupational variables were also recorded. Data analysis was performed using linear regression models adjusted by confounders. RESULTS: The median age of the workers was 35 years and the median employment duration at the analysed venues was 1 year. Workers in smoking facilities reported greater SHS exposure (36 hours per week) than workers in smoke-free locations (4 hours per week). Urine cotinine levels were inversely correlated with forced vital capacity, but the finding was not statistically significant (ß=-0.0002; 95% CI -0.007 to 0.006). Years of exposure to SHS showed to be significantly associated with forced expiratory flow25/75 (ß=-0.006; 95% CI -0.010 to -0.0004). CONCLUSION: These findings suggest that cumulative exposure to SHS at work may contribute to deterioration of pulmonary function in non-smoking employees.

Secondhand Smoke Exposure and Preclinical Markers of Cardiovascular Risk in Toddlers.

OBJECTIVE: To investigate relationships between secondhand smoke exposure in young children and several preclinical markers of cardiovascular risk that have been established as relevant to adult populations. STUDY DESIGN: There were 139 children, 2-5 years of age, enrolled in a cross-sectional study. Secondhand smoke exposure was objectively determined by hair nicotine level; a comprehensive panel of clinical markers (morning blood pressure, fasting glucose and insulin, lipid profiles, inflammation) and research markers (markers of oxidation, endothelial stress, and endothelial repair) of cardiovascular risk status were assessed. Univariate and multivariate linear regression were used to evaluate relationships between secondhand smoke exposure and cardiovascular risk markers. RESULTS: Hair nicotine levels were correlated directly with blood pressure and serum C-reactive protein, and inversely correlated with serum high-density lipoprotein cholesterol and endothelial cell progenitor cell prevalence. In multivariate analyses, these relationships remained when controlled for age, sex, body mass index z-score, maternal education, and method of payment. Additionally, in multivariate analyses, hair nicotine level was significantly negatively correlated with total antioxidant capacity. CONCLUSIONS: These results support the view that secondhand smoke exposure in the very young has a detectable relationship with several markers of cardiovascular risk, long before the emergence of clinical disease. Further studies to define mechanisms and strategies to prevent and mitigate these risks early in life are warranted.

Brief Counseling on Secondhand Smoke Exposure in Pregnant Women in Argentina and Uruguay.

Argentina and Uruguay have a high prevalence of smoking during pregnancy, as well as of secondhand smoke (SHS) exposure. In this secondary analysis of a trial to implement brief smoking cessation counseling during antenatal care in Argentina and Uruguay, we aim to evaluate the effects of the intervention on the rates of self-reported SHS exposure at home and at work, and on attitudes recalled by non-smoker women enrolled in the intervention group compared with the control group. We randomly assigned (1:1) 20 antenatal care clusters in Argentina and Uruguay to receive a multifaceted intervention to implement brief smoking cessation counseling, which also included questions and counseling regarding SHS exposure, or to receive the standard of care. There was not a statistically significant difference between groups of the intervention's effect (reduction of exposure to SHS) on any of the three exposure outcome measures (exposure at home, work or other indoor areas) or on the attitudes of women regarding exposure (avoiding breathing SHS and having rooms where smoking is forbidden). This analysis shows that we should not expect reductions in SHS exposure with this modest intervention alone. To achieve such reductions, strategies engaging partners and other household members may be more effective.

Pulmonary effects of active smoking and secondhand smoke exposure among adolescent students in Juárez, Mexico.

BACKGROUND: Youth smoking trends among Latin American countries, including Mexico, are on the rise. Notably, although the high prevalence of smoking in teens has been well documented in the literature, few studies have evaluated the impact of smoking and secondhand smoke (SHS) exposure on their respiratory system. OBJECTIVE: To investigate the effects of smoking and SHS exposure on the respiratory health and lung function among eighth-grade students in Juárez, Mexico. METHODS: A cross-sectional study was undertaken on a sample of convenience. The study outcomes centered on evaluating 300 students' lung function by spirometry (forced expiratory volume in 1 second [FEV1], forced expiratory volume in 1 second/forced vital capacity ratio [FEV1/FVC], and forced mid-expiratory flow rate [FEF25%-75%]) and their respiratory health (smoking behavior and SHS exposure) by their self-reported responses to a standardized respiratory questionnaire. The study outcomes were compared among three distinct groups: 1) nonsmokers/nonexposed to SHS; 2) nonsmokers/exposed to SHS; and 3) smokers. RESULTS: The majority of the study participants were 14 years old (85%), females (54%), who attended eighth grade in a public school setting (56%). Approximately, half reported being of low socioeconomic status (49%) and nonsmokers/exposed to SHS (49%). The lung function parameters of smokers were found to be lower (FEV1 =62.88±10.25; FEV1/FVC =83.50±14.15; and FEF25%-75% =66.35±12.55) than those recorded for the nonsmokers/exposed to SHS (FEV1 =69.41±11.35; FEV1/FVC =88.75±15.75; and FEF25%-75% =78.90±14.65) and significantly reduced when compared to the nonsmokers/nonexposed to SHS (FEV1 =79.14±13.61; FEV1/FVC =94.88±21.88; and FEF25%-75% =87.36±17.02) (P<0.001). Similarly, respiratory complaints were more prevalent among smokers and those exposed to SHS when compared to nonsmokers/nonexposed to SHS. CONCLUSION: Our findings suggest that initiation of cigarette smoking and, to a lesser extent, exposure to SHS in adolescence leads to increased respiratory symptoms and reduction of pulmonary function test values. Public health initiatives that aim to prevent smoking initiation, assist in cessation, and lessen SHS exposure of adolescents need to be school-based and employed as early as middle school.

Clinical Decision Support Tool for Parental Tobacco Treatment in Hospitalized Children.

OBJECTIVES: To create and evaluate the feasibility, acceptability, and usability of a clinical decision support (CDS) tool within the electronic health record (EHR) to help pediatricians provide smoking cessation counseling and treatment to parents of hospitalized children exposed to secondhand smoke (SHS). METHODS: Mixed method study of first-year pediatric residents on one inpatient unit. Residents received training in smoking cessation counseling, nicotine replacement therapy (NRT) prescribing, and use of a CDS tool to aid in this process. The tool, which alerted when a patient was identified as exposed to SHS based on the history taken on admission or during a prior encounter, had the following capabilities: adding SHS exposure to the patient's problem list; referral to Free Quitline through discharge instructions; and linking to a printable NRT prescription form. We measured feasibility by EHR utilization data. We measured acceptability and usability of the tool by administering questionnaires to residents. RESULTS: From June-August 2015, the alert triggered for 106 patients, and the tool was used for 52 (49%) patients. 41 (39%) patients had SHS exposure added to the problem list, 34 (32%) parents were referred to the Quitline through discharge instructions, and 15 (14%) parents were prescribed NRT. 10 out of 15 (67%) eligible pediatricians used the tool. All clinicians surveyed (9 out of 10) found the tool acceptable and rated its usability good to excellent (average System Usability Scale score was 85 out of 100, 95% CI, 76-93). CONCLUSIONS: A non-interruptive CDS tool to help residents provide smoking cessation counseling in the hospital was feasible, acceptable, and usable. Future work will investigate impacts on patient outcomes.

Gene-expression profiles in lung adenocarcinomas related to chronic wood smoke or tobacco exposure.

BACKGROUND: Tobacco-smoke is the major etiological factor related to lung cancer. However, other important factor is chronic wood smoke exposure (WSE). Approximately 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular characteristics compared to tobacco related lung cancer, including differences in mutational profiles. There are several molecular alterations identified in WSE associated lung cancer, however most studies have focused on the analysis of changes in several pathogenesis related proteins. METHODS: Our group evaluated gene expression profiles of primary lung adenocarcinoma, from patients with history of WSE or tobacco exposure. Differential expression between these two groups were studied through gene expression microarrays. RESULTS: Results of the gene expression profiling revealed 57 statistically significant genes (p < 0.01). The associated biological functional pathways included: lipid metabolism, biochemistry of small molecules, molecular transport, cell morphology, function and maintenance. A highlight of our analysis is that three of the main functional networks represent 37 differentially expressed genes out of the 57 found. These hubs are related with ubiquitin C, GABA(A) receptor-associated like protein; and the PI3K/AKT and MEK/ERK signaling pathways. CONCLUSION: Our results reflect the intrinsic biology that sustains the development of adenocarcinoma related to WSE and show that there is a different gene expression profile of WSE associated lung adenocarcinoma compared to tobacco exposure, suggesting that they arise through different carcinogenic mechanisms, which may explain the clinical and mutation profile divergences between both lung adenocarcinomas.

[Malignant mesothelioma risk factors: experience in the General Hospital of Mexico]. / Mesotelioma maligno: factores de riesgo, experiencia en el Hospital General de México.

BACKGROUND: Malignant mesothelioma is a neoplasm of bad prognosis, it is linked with asbestos contact, but there are cases without this antecedent. OBJECTIVE: To investigate the relationship of asbestos exposition and other factors with malignant mesothelioma. METHODS: Retrospective analysis of histologic confirmed cases of malignant mesothelioma, neoplasic familiar history, tobacco smoking, exposure to wood smoke and to asbestos, were annotated in a paired case/control study 1: 1-3 with logistic regression model to identify risk factors for OR. RESULTS: 61 cases of malignant mesothelioma were confirmed by histopathologic study, 41 male and 20 female. Mean age was 56 years ± 13 years; 56 cases (91.8%) correspond to epithelial malignant mesothelioma, three sarcomatous (4.9%) one desmoplastic and one biphasic. One in eight (13.1%) had exposure to asbestos. Model of logistic regression with four variables: history of familiar cancer, tobacco smoking, wood smoke and asbestos exposition, the the last one with an OR= 3.083 and p > 0.05. No other variables found to be a risk factor for malignant mesothelioma. CONCLUSIONS: Exposure to asbestos is a risk factor for malignant mesothelioma, which is confirmed in this study, however it is important to extend the investigation of other possible causal factors of this disease.

Antecedentes: el mesotelioma maligno es un tumor de mal pronóstico relacionado con el contacto con asbesto; sin embargo, existen numerosos casos sin este antecedente. Objetivo: describir la relación entre la exposición al asbesto y otros factores con el mesotelioma maligno. Material y métodos: estudio retrospectivo de casos y controles pareado 1: 1-3 por edad y sexo de pacientes con diagnóstico de mesotelioma maligno. Se registraron: la exposición al asbesto, tabaco, humo de leña y antecedentes familiares de cáncer. Se empleó regresión logística para razones de momios (ORs). Resultados: se estudiaron 61 casos con mesotelioma maligno, 41 hombres y 20 mujeres. La edad promedio fue 56 ± 13 años; 56 casos fueron mesotelioma maligno epitelial (91.8%), tres sarcomatosos (4.9%), uno desmoplásico y uno bifásico. Sólo en 8 (13.1%) se identificó exposición al asbesto. En el modelo de regresión logística el asbesto tuvo una razón de momios de 3.083 p > 0.05. Ninguna otra variable resultó ser un factor de riesgo para mesotelioma maligno. Conclusiones: la exposición al asbesto es un factor de riesgo para mesotelioma maligno, lo que se confirma en este estudio; sin embargo, es importante ampliar la investigación de otros posibles factores causales de esta enfermedad.