👤 Wojciech Piekoszewski

Smoking cigarettes and alcohol addiction are serious problems in health hazard and life of society. Tobacco smoke leads to many kinds of cancer formation and scientific research indicates, that heart-vascular disease and lung cancer are the most common diseases caused by tobacco smoke. While talking about ethanol, it is responsible for liver, pancreas, mucous membrane damage and leads to central and circular nervous disorder. Scientific research indicates, that many smokers drink alcohol and vice versa. Unfortunately in that case the risk of many diseases increases. Both of these stimulants leads to enlarged production of reactive oxygen species, which is connected with unbalance between pro and antioxidant processes in human organism. Free radicals in normal conditions plays positive role but with tobacco smoke and alcohol connection may lead to serious changes in human organism. They damage organs, it comes to protein structure, nucleic acid and fat violation, which in consequence leads to immunity decrease and many pathological changes. Reactive oxygen species also plays role in pathogenesis of many diseases: diabetes mellitus, atherosclerosis and Down syndrome. ROS may also increase the risk of pancreas, lung, larynx and urinary bladder cancer formation. Human organism defends oneself from harmful influence of reactive oxygen species owing to enzymatic and non-enzymatic systems presence-Non-enzymatic antioxidants: glutathione, carotene, bilirubin, tocopherol, uric acid and ions metals temporary complex belong to non-enzymatic systems. To enzymatic ones belong: catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase. The aim of the study was tobacco smoke and ethyl alcohol influence evaluation in rats addicted to these substances on activity of chosen enzymes responsible for organism defense against toxic compounds action. To this study 63 white, Wistar tribe rats at the age of 3,5 months were used - males addicted to ethyl alcohol. They were divided into 3 groups, each consist of 21 rats. Animals of Group I were exposed on harmful tobacco smoke influence. Group II constitute animals, which were given by stomach probe 10% alcohol dilution once at a dose of 2 g/kg weight. The next Group - III, in which animals at first were exposed on tobacco smoke influence. When exposition was over, animals were given by stomach probe 10% alcohol dilution once at a dose of 2 g/kg weight. Depending on the type of marker and studied organ, changes in the levels of selected enzymes, responsible for defending organism against reactive forms of oxygen has been shown. Both tobacco smoke and ethyl alcohol resulted in a change of glutathione levels in the serum and tissues of animals. Tobacco smoke has the biggest influence on protein nitrozylation in the brain and ethyl alcohol had influence on glutathione level in serum, kidney, brain and superoxide dismutase activity in the brain. Application of many oxidative stress markers allows for evaluation of its differential influence on various organs. Show less

Usually, alcohol addicted persons smokes cigarettes. In the study, the effect of combined exposure to alcohol and tobacco smoke in alcohol addicted rats on liver peroxidation was evaluated. Alcohol abuse and its presence in blood did not influence the cotinine level, what indicates the lack of the importance of this factor in nicotine metabolism. Similarly, enzymatic markers of liver damage (AspAT, AIAT, ALP) did not change, what showed lack of hepatotoxic effect studied compounds in applied model of alcohol addiction and tobacco smoke exposure. Combined exposure to alcohol and tobacco smoke increases the level of lipid peroxidation in brain, liver and lungs however decreases in serum. In kidneys the results are not unambiguous. Show less

The aim of this work was the assessment of the clinical condition, birth weight, frequency of premature birth and incidence of intrauterine growth restriction (IUGR) of the newborns whose mothers were active and passive smokers. This was a prospective study conducted in a group of 147 newborns born during the years 2003-2004 in the Princess Anna Mazowiecka Hospital, Warsaw, and hospitalized in the Neonatal and Intensive Care Department of Warsaw Medical University. Based on a questionnaire identifying the exposure to tobacco smoke and cotinine concentration in the mother's urine, the newborns were assigned to three groups: the newborns whose mothers were active smokers, the newborns whose mothers were passive smokers and the newborns of non-smoking mothers. There were no statistically significant differences in the Apgar score assessment at the 1st and 5th minute between the three groups of the newborns. Acid-base balance parameters (pH, BE) were also similar. The birth weight of the newborns of mothers who were active smokers was 325g lower than the birth weight of the newborns of non-smoking mothers. This difference was statistically significant p = 0.033. Maternal smoking in pregnancy was associated with an increased risk of deficit in birth weight 2.6 (1.0-6.9, CI 95%). In the group of the newborns whose mothers were active smokers, the incidence of lower birth weight (< 2500g) was also statistically significantly higher p = 0.01. There were no statistically significant differences in the incidence of premature birth and intrauterine growth restriction (IUGR). Show less

The aim in this survey was analysis of contribution of exposure to tobacco smoke and selected socioeconomic factors in occurrence of low birth weight. The research was done on the group of 1528 pregnant women. Smoking habit was declared by 18.2% of women and passive exposure to tobacco smoke was stated by 31% of respondents. Significant association between active and passive smoking and socioeconomic status of respondents was observed. Cigarette smoking during pregnancy was the main cause of lower birth weight of newborns. The newborns of actively smoking mothers were lighter of about 332 g according to those ones of mothers who did not smoke and were not exposed to passive smoking, and were lighter than newborns of mothers who were not exposed to passive smoking of about 342 g. Show less

Among other toxic compounds, tobacco smoke contains also heavy metals, for example lead. Lead can cross the placenta barrier and have negative influences on fetus development. In the study compared urine lead concentration of pregnancy women exposed to tobacco smoke (active smokers and exposed to environmental tobacco smoke--ETS) with unexposed. There was find that mean urine lead concentrations in groups of pregnant women exposed and unexposed to tobacco smoke was no different (F2,189=0.2 p>0.8). However it was found that in urine of women exposed to tobacco smoke the concentration of lead increase with increase the concentration of cotinine (r2=0.14, t106=4.2, p<<0.0001). Show less

The exposition to tobacco smoke is overall: in home, work and public places. For the examination of the presence and concentration of environmental tobacco smoke (ETS) in indoor environments the nicotine and respirable suspended particulates (RSP) are determined. A variety of biomarkers (nicotine, cotinine, thiocyanate, carboxyhemoglobin, protein and DNA adducts) are propose for measurement of exposure to tobacco smoke. The most popular is measurement of cotinine concentration in body fluids (blood, urine, saliva). Plasma cotinine concentration correlated to numbers of cigarettes smoked and to various biological effects of cigarette smoking and exposure to ETS. Other biomarkers as carboxyhemoglobin, thiocyanate, and amines and polycyclic aromatic hydrocarbons adduct can be also use. Show less