Aldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of cigarette smoke on the Meckel's cartilage of rat fetus : Morphologic, morphometric and stereologic study

The purpose of this study was to investigate the effects of cigarette smoke on the development of the embryo mandible (Meckel's) cartilage in rat fetuses. When inhaled by female Wistar rats between the 9th and the 12th day of pregnancy, cigarette smoke (5 cigarettes a day) caused intrauterine growth retardation, providing smaller fetuses and placentas. In fetuses from the experimental group, the histopathologic examination revealed a poorly developed Meckel' s cartilage with smaller chondroblasts showing a scanty cytoplasm with spherical and paler central nuclei, as well as more abundant cartilage matrix. Morphometric analysis revealed that Meckel's cartilage lacunae were smaller in the fetuses from the experimental group, although not showing any remarkable alteration in shape. The results suggested that inhalation of cigarette smoke by pregnant rats during the organogenic period induced growth retardation and delayed cellular differentiation in rat fetal Meckel's cartilage.

β-carotene attenuates the paradoxical effect of tobacco smoke on the mortality of rats after experimental myocardial infarction

The objective of this study was to investigate the effects of exposure to tobacco smoke (ETS) in rats that were or were not supplemented with dietary β-carotene (BC), on ventricular remodeling and survival after myocardial infarction (Ml). Rats (n = 189) were allocated to 4 groups: the control group, n = 45; group BC administered 500 mg/kg diet, n = 49, BC supplemented rats; group ETS, n - 55, rats exposed to tobacco smoke; and group BC+ETS, n = 40. Wistar rats weighing 10O g were administered one of the treatments until they weighed 200 to 250 g (∼5 wk). The ETS rats were exposed to cigarette smoke for 30 min 4 times/d, in a chamber connected to a smoking device. After reaching a weight of 200-250 g, rats were subjected to experimental MI (coronary artery occlusion) and mortality rates were determined over the next 105 d. In addition, echocardiographic, isolated heart, morphometrical, and biochemical studies were performed. Mortality data were tested using Kaplan-Meyer curves and other data by 2-way ANOVA. Survival rates were greater in the ETS group (58.2%) than in the control (33.3%) (P = 0.001) and BC+ETS rats (30.0%) (P = 0.007). The groups did not differ in the other comparisons. Left ventricular end-diastolic diameter normalized to body weight was greater and maximal systolic pressures were lower in the ETS groups than in non-ETS groups. Previous exposure to tobacco smoke induced a process of cardiac remodeling after MI. There is a paradoxical protector effect with tobacco smoke exposure, characterized by lower mortality, which is offset by BC supplementation. © 2005 American Society for Nutritional Sciences.

Influence of lisinopril on cardiac remodeling induced by tobacco smoke exposure

Background: To investigate the effect of lisinopril on cardiac remodeling induced by smoking. Material/Methods: Rats were allocated into 3 groups: group CON (n=8): control; group CSE (n=8): cigarette smoke exposure; group CSE-LIS (n=8): exposed to tobacco smoke and treated with lisinopril. Results: After 2 months, the tail systolic pressure was lower in CSE-LIS (CON=116 ±27 mm Hg, CSE=126±16, CSE-LIS=89±12; P<.001). CSE animals showed higher left ventricular systolic diameter (CON=8.25±2.16 mm/kg, CSE=11.5±1.3, CSE-LIS=9.27±2.00; P=.009) and myocyte cross-sectional area (CON=245±8 μm2, CSE=260±17, CSE-LIS=238±12; P=.01) than CON and CSE-LIS. The ejection fraction (CON =0.91±0.02, CSE=0.86±0.02, CSE-LIS=0.92±0.03; P=.002) and fractional shortening (CON=55.7±4.41%, CSE=48.7±3.43, CSE-LI=58.2±7.63; P=.006) were lower in CSE group than CON and CSE-LIS. CSE and CSE-LIS animals showed higher collagen amounts (CON=3.49±0.95%, CSE= 5.01±1.58, CSE-LIS=5.27±0.62; P=.009) than CON. CON group showed a higher connexin 43 amount in the intercalated disc (CON=3.70±0.38, CSE=2.13±0.53; CSE-LIS=2.17±0.73; P=.004) than CSE and CSE-LIS. There were no differences in IFN-g or TNF-a cardiac levels among the groups. Conclusions: Lisinopril attenuated both morphologic and functional abnormalities induced by exposure to tobacco smoke. In addition, this effect was associated with diminished blood pressure, but not alterations in connexin 43 distribution, cytokine production or collagen amount. © Med Sci Monit, 2010.

New experimental model of exposure to environmental tobacco smoke

PURPOSE: To describe a new model to passive smoking for rodents. METHODS: Twenty rats were distributed into two study groups (N=10): control group (CG), that was not exposed to tobacco smoke and used as normal standard for biochemical and histological analysis; Experimental Group (EG), that Animals were exposed to the passive smoking; Euthanasia was performed after 14 days of exposure. The serum level of nicotine and histological analysis were performed. RESULTS: There was a statistical difference on the nicotine serum levels between Experimental and Control group, with level of 286 ±23 nanograma/mL in the EG and undetectable on CG (p<0.01). The histological study suggested the model efficacy producing alveolar destruction and emphysema in the EG compared with the insignificant lesions in the CG's lung. CONCLUSION: The model of exposure to environmental tobacco smoke for rodents induced easily the changes related to secondhand smoke.

A new experimental model of cigarette smoke-induced emphysema in Wistar rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

ENVIRONMENTAL TOBACCO SMOKE INDUCES OXIDATIVE STRESS IN DISTINCT BRAIN REGIONS OF INFANT MICE

Environmental tobacco smoke (ETS) leads to the death of 600,000 nonsmokers annually and is associated with disturbances in antioxidant enzyme capacity in the adult rodent brain. However, little is known regarding the influence of ETS on brain development. The aim of this study was to determine levels of malonaldehyde (MDA) and 3-nitrotyrosine (3-NT), as well as enzymatic antioxidant activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), and superoxide dismutase (SOD), in distinct brain structures. BALB/c mice were exposed to ETS twice daily for 1 h from postnatal day 5 through postnatal day 18. Acute exposure was performed for 1 h on postnatal day 18. Mice were euthanized either immediately (0) or 3 h after the last exposure. Immediately after an acute exposure there were higher GR and GST activities and MDA levels in the hippocampus, higher GPx and SOD activities in the prefrontal cortex, and higher GST activity and MDA levels in the striatum and cerebellum. Three hours later there was an increase in SOD activity and MDA levels in the hippocampus and a decrease in the activity of all enzymes in the prefrontal cortex. Immediately after final repeated exposure there were elevated levels of GST and GR activity and decreased GPx activity in the hippocampus. Moreover, a rise was found in GPx and GST activities in the prefrontal cortex and increased GST and GPx activity in the striatum and cerebellum, respectively. After 3 h the prefrontal cortex showed elevated GR and GST activities, and the striatum displayed enhanced GST activity. Data showed that enzymatic antioxidant system in the central nervous system responds to ETS differently in different regions of the brain and that a form of adaptation occurs after several days of exposure.

Lung morphology and growth of rats exposed to tobacco smoke and alcohol

PURPOSE: Investigate the morphological effects of chronic exposure to tobacco smoke inhalation and alcohol consumption on the lungs and on the growth of rats. METHODS: Sixty male Wistar rats were divided into four groups: control, tobacco, alcohol, tobacco + alcohol, for a period of study 260 days. Morphological analysis was conducted by optical and electron microscopy. Rat growth was investigated by measuring the snout-anus length, body mass index and body weight. RESULTS: The three groups exposed to the drugs presented lower growth and lower weight than the control group. The percentages of alveolitis, bronchiolitis and the mean alveolar diameter were greater, particularly in the groups exposed to tobacco smoke, but were not significantly different from the control group. Electron microscopy revealed more intense apoptotic and degenerative lesions in the smoking group, while degenerative lesions in the lamellar bodies were more intense with the association of both drugs. CONCLUSIONS: This experimental model showed morphological alterations observed by electron microscopy, principally due to tobacco smoke exposure. Alcohol and tobacco hindered the growth of rats, such that tobacco showed a greater effect on body length and alcohol on body weight.

ACETYL RADICAL IN TOBACCO SMOKE: DETECTION, QUANTIFICATION AND SIMULATION

Free radicals are present in cigarette smoke and can have a negative effect on human health by attacking lipids, nucleic acids, proteins and other biologically important species. However, because of the complexity of the tobacco smoke system and the dynamic nature of radicals, little is known about the identity of the radicals, and debate continues on the mechanisms by which those radicals are produced. In this study, acetyl radicals were trapped from the gas phase using 3-amino-2, 2, 5, 5- tetramethyl-proxyl (3AP) on solid support to form stable 3AP adducts for later analysis by high performance liquid chromatography (HPLC), mass spectrometry/tandem mass spectrometry (MS-MS/MS) and liquid chromatography- mass spectrometry (LC-MS). Simulations of acetyl radical generation were performed using Matlab and the Master Chemical Mechanism (MCM) programs. A range of 10- 150 nmol/cigarette of acetyl radical was measured from gas phase tobacco smoke of both commerial and research cigarettes under several different smoking conditions. More radicals were detected from the puff smoking method compared to continuous flow sampling. Approximately twice as many acetyl radicals were trapped when a GF/F particle filter was placed before the trapping zone. Computational simulations show that NO/NO2 reacts with isoprene, initiating chain reactions to produce a hydroxyl radical, which abstracts hydrogen from acetaldehyde to generate acetyl radical. With initial concentrations of NO, acetaldehyde, and isoprene in a real-world cigarette smoke scenario, these mechanisms can account for the full amount of acetyl radical detected experimentally. This study contributes to the overall understanding of the free radical generation in gas phase cigarette smoke.

Smoke free restaurant ordinance, compliance with the regulation to reduce exposure to environmental tobacco smoke while dining at local restaurants in San Antonio, Texas

This study is a secondary analysis of a survey developed by Dr. Jimmy Perkins and administered by San Antonio/Bexar County Metropolitan Health District. The survey was developed subsequent to the implementation of the city smoking ordinance effective January 1, 2004. The survey had a multi-purpose plan to establish the number of restaurants having smoke free status prior to and following the ordinance, determine compliance as it relates to a necessary smoking section and proper signage, and expose the rationale for restaurants to become smoke free. The data resulting from the survey was presented to the San Antonio/Bexar County Metropolitan Health District. The summary presented the types of establishments surveyed, smoking status of the establishment, reasons for the establishment becoming smoke free, compliance with smoking sections, compliance with signage requirements, awareness of ordinance, and chain status of the establishment. ^ The results of this study display the relationships among the variables previously mentioned. The following relationships have been examined and the outcomes have determined whether each is significant. After careful analysis, knowledge translates into compliance with signage regulations, which then translate into ordinance compliance. Size does matter as it relates to an establishment's number of employees and seating capacity. The smaller the establishment the more likely the establishment is to have become smoke free before the ordinance went into effect. Restaurants, rather than fast food establishments most commonly cited their reason for becoming smoke free was to comply with the ordinance and only ten percent of restaurants gave policy as the main reason for becoming smoke free. ^ This study is important for public health because the negative health effects of environmental tobacco smoke (ETS) are still an overwhelming problem in the United States (3). ETS is a Known Human Group A Carcinogen (5). The Environmental Protection Agency (EPA) has estimated that around 3,000 non-smoking Americans die every year from lung cancer caused by ETS (6). This information illustrates the importance of providing smoke free establishments, especially to non-smoking patrons. ^

Environmental tobacco smoke exposure, respiratory and cardiovascular health in restaurant and bar workers in Mexico

Environmental tobacco smoke (ETS) is a well established health hazard, being causally associated to lung cancer and cardiovascular disease. ETS regulations have been developed worldwide to reduce or eliminate exposure in most public places. Restaurants and bars constitute an exception. Restaurants and bar workers experience the highest ETS exposure levels across several occupations, with correspondingly increased health risks. In Mexico, previous exposure assessment in restaurants and bars showed concentrations in bars and restaurants to be the highest across different public and workplaces. Recently, Mexico developed at the federal level the General Law for Tobacco Control restricting indoors smoking to separated areas. AT the local level Mexico City developed the Law for the Protection of Non-smokers Health, completely banning smoking in restaurants and bars. Studies to assess ETS exposure in restaurants and bars, along with potential health effects were required to evaluate the impact of these legislative changes and to set a baseline measurement for future evaluations.^ A large cross-sectional study conducted in restaurants and bars from four Mexican cities was conducted from July to October 2008, to evaluate the following aims: Aim 1) Explore the potential impact of the Mexico City ban on ETS concentrations through comparison of Mexico City with other cities. Aim 2). Explore the association between ETS exposure, respiratory function indicators and respiratory symptoms. Aim 3). Explore the association between ETS exposure and blood pressure and heart rate.^ Three cities with no smoking ban were selected: Colima (11.5% smoking prevalence), Cuernavaca (21.5% smoking prevalence) and Toluca (27.8% smoking prevalence). Mexico City (27.9% smoking prevalence), the only city with a ban at the time of the study, was also selected. Restaurants and bars were randomly selected from municipal records. A goal of 26 restaurants and 26 bars per city was set, 50% of them under 100 m2. Each establishment was visited during the highest occupancy shift, and managers and workers answered to a questionnaire. Vapor-phase nicotine was measured using passive monitors, that were activated at the beginning and deactivated at the end of the shift. Also, workers participated at the beginning and end of the shift in a short physical evaluation, comprising the measurement of Forced Expiratory Volume in the first second (FEV1) and Peak Expiratory Flow (PEF), as well as blood pressure and heart rate.^ A total of 371 establishments were invited, 219 agreed to participate for a 60.1% participation rate. In them, 828 workers were invited, 633 agreed to participate for a 76% participation rate. Mexico City had at least 4 times less nicotine compared to any of the other cities. Differences between Mexico City and other cities were not explained by establishment characteristics, such as ventilation or air extraction. However, differences between cities disappeared when ban mechanisms, such as policy towards costumer's smoking, were considered in the models. An association between ETS exposure and respiratory symptoms (cough OR=1.27, 95%CI=1.04, 1.55) and respiratory illness (asthma OR=1.97, 95%CI=1.20, 3.24; respiratory illness OR=1.79, 95%CI=1.10, 2.94) was observed. No association between ETS and phlegm, wheezing or respiratory infections was observed. No association between ETS and any of the spirometric indicators was observed. An association between ETS exposure and increased systolic and diastolic blood pressure at the end of the shift was observed among non-smokers (systolic blood pressure beta=1.51, 95%CI=0.44, 2.58; diastolic blood pressure beta=1.50, 95%CI=0.72, 2.28). The opposite effect was observed in heavy smokers, were increased ETS exposure was associated with lower blood pressure at the end of the shift (systolic blood pressure beta=1.90, 95%CI=-3.57, -0.23; diastolic blood pressure beta=-1.46, 95%CI=-2.72, -0.02). No association in light smokers was observed. No association for heart rate was observed. ^ Results from this dissertation suggest Mexico City's smoking ban has had a larger impact on ETS exposure. Ventilation or air extraction, mechanisms of ETS control suggested frequently by tobacco companies to avoid smoking bans were not associated with ETS exposure. This dissertation suggests ETS exposure could be linked to changes in blood pressure and to increased respiratory symptoms. Evidence derived from this dissertation points to the potential negative health effects of ETS exposure in restaurants and bars, and provides support for the development of total smoking bans in this economic sector. ^