The influence of external factors on the cardiovascular system. Basic research. Negative effects on the cardiovascular system of other factors

Slide 14

Narcologists

“Don’t drink wine, don’t upset your heart with tobacco - and you will live as long as Titian lived” Academician I.P. Pavlov The influence of alcohol and nicotine on the heart: Tachycardia; -Disturbance of neurohumoral regulation of heart function; Fast fatiguability; Flabbiness of the heart muscle; Heart rhythm disorders; Premature aging of the heart muscle; Increased risk of heart attack; Development of hypertension.

Slide 15

Why is beer harmful?

A large heart mass develops due to the destruction of muscle fibers and their replacement with connective tissue, which cannot contract.

Slide 16

Physiologists

Let's evaluate the state of the cardiovascular system in ourselves. This will require systolic (SBP) and diastolic (DBP) pressure, heart rate (Pulse), height and weight.

Slide 17

Assessment of adaptive potential

AP = 0.0011(PP) + 0.014(SBP) + 0.008(DBP) + 0.009(MT) - 0.009(R) + 0.014(V)-0.27; where AP is the adaptive potential of the circulatory system in points, PR is the pulse rate (bpm); SBP and DBP - systolic and diastolic blood pressure (mm Hg); P - height (cm); BW - body weight (kg); B - age (years).

Slide 18

Based on the values ​​of the adaptation potential, the functional state of the patient is determined: Interpretation of the test: below 2.6 - satisfactory adaptation; 2.6 - 3.9 - tension of adaptation mechanisms; 3.10 - 3.49 - unsatisfactory adaptation; 3.5 and above - failure of adaptation.

Slide 19

Calculation of the Kerdo index

The Kerdo index is an indicator used to assess the activity of the autonomic nervous system. The index is calculated by the formula: Index=100(1-DAD), where: Pulse DAD - diastolic pressure (mm Hg); Pulse - pulse rate (beats per minute). Normal indicator: from – 10 to + 10%

Slide 20

Interpretation of the test: positive value - predominance of sympathetic influences, negative value - predominance of parasympathetic influences. If the value of this index is greater than zero, then we speak of the predominance of sympathetic influences in the activity of the autonomic nervous system; if it is less than zero, then of the predominance of parasympathetic influences; if it is equal to zero, then this indicates functional balance. In a healthy person it is close to zero.

Slide 21

Determination of heart fitness

P2 - P1 T = -------------- * 100% P1 P1 - heart rate in a sitting position P2 - heart rate after 10 squats.

Slide 22

results

T - 30% - heart fitness is good, the heart strengthens its work by increasing the amount of blood released with each contraction. T - 38% - insufficient heart fitness. T - 45% - low fitness, the heart increases its work due to the heart rate.

UDC 574.2:616.1

ECOLOGY AND CARDIOVASCULAR DISEASES

© 2014 E. D. Bazdyrev, O. L. Barbarash

Research Institute of Complex Problems of Cardiovascular Diseases, Siberian Branch of the Russian Academy of Medical Sciences, Kemerovo State Medical Academy, Kemerovo

According to experts from the World Health Organization (WHO), the health status of the population is 49-53% determined by their lifestyle (smoking, drinking alcohol and drugs, diet, working conditions, physical inactivity, material and living conditions, marital status, etc.), by 18-22% - genetic and biological factors, by 17-20% - by the state of the environment (natural and climatic factors, quality of environmental objects) and only by 8-10% - by the level of healthcare development (timeliness and quality of medical care, efficiency preventive measures).

The high rates of urbanization observed in recent years with a reduction in the rural population, a significant increase in mobile sources of pollution (vehicles), non-compliance of treatment facilities at many production enterprises with the requirements of sanitary and hygienic standards, etc. have clearly identified the problem of the influence of ecology on the health of the population.

Clean air is the most important prerequisite for human health and well-being. Air pollution remains a significant threat to human health around the world, despite the introduction of cleaner technologies in industry, energy and transport. Intense air pollution is typical for large cities. The level of most pollutants, and there are hundreds of them in the city, as a rule, exceeds the maximum permissible, and their combined effect is even more significant.

Atmospheric air pollution causes increased mortality and, accordingly, a reduction in life expectancy. Thus, according to the WHO European Bureau, in Europe this risk factor has led to a reduction in life expectancy by 8 months, and in the most contaminated areas - by 13 months. In Russia, the increased level of air pollution leads to an annual additional mortality of up to 40 thousand people.

According to the Federal Information Center of the Social and Hygienic Monitoring Foundation, in Russia in the period from 2006 to 2010 the leading air pollutants exceeding hygienic standards by five or more times were: formaldehyde, 3,4-benz(a)pyrene, ethylbenzene, phenol, nitrogen dioxide, suspended solids, carbon monoxide, sulfur dioxide, lead and its inorganic compounds. Russia ranks 4th in the world in terms of carbon dioxide emissions after the United States, China and the European Union.

Environmental pollution today remains a significant problem throughout the world, causing increased mortality and, in turn, a factor in reducing life expectancy. It is generally accepted that environmental influences, namely airborne pollutants, primarily cause the development of diseases of the respiratory system. However, the impact of various pollutants on the body is not limited only to changes in the bronchopulmonary system. In recent years, studies have appeared that prove the connection between the level and type of air pollution and diseases of the digestive and endocrine systems. In the last decade, convincing data have been obtained on the adverse effects of air pollutants on the cardiovascular system. This review analyzes information both on the connection between various diseases of the cardiovascular system and the effects of air pollutants, and on their possible pathogenetic relationships. Key words: ecology, air pollutants, diseases of the cardiovascular system

In Russia, up to 50 million people live under the influence of harmful substances that exceed hygienic standards by five or more times. Despite the fact that since 2004 there has been a trend towards a reduction in the proportion of atmospheric air samples exceeding hygienic standards of the average for the Russian Federation, this proportion still remains high in the Siberian and Ural Federal Districts.

Today it is generally accepted that the influence of the environment, namely the pollution of the atmospheric pool with airborne pollutants, is the cause of the development of predominantly diseases of the respiratory system, since most of all pollutants enter the body mainly through the respiratory system. It has been proven that the impact of air pollutants on the respiratory system is manifested by suppression of the local defense system, a damaging effect on the respiratory epithelium with the formation of acute and chronic inflammation. It is known that ozone, sulfur dioxide, and nitrogen oxides cause bronchoconstriction, bronchial hyperreactivity due to the release of neuropeptides from C-fibers and the development of neurogenic inflammation. It has been established that average and maximum concentrations of nitrogen dioxide and maximum concentrations of sulfur dioxide contribute to the development of bronchial asthma.

However, the impact of various pollutants on the body is not limited only to changes in the bronchopulmonary system. Thus, according to a study conducted in Ufa, as a result of an eight-year observation (2000-2008), it was shown that in the adult population there is a significant correlation between the level of atmospheric air pollution with formaldehyde and diseases of the endocrine system, the content of gasoline in the atmospheric air and general morbidity, including diseases of the digestive system.

In the last decade, convincing data have emerged on the adverse effects of air pollutants on the cardiovascular system (CVS). The first reports of the connection between chemical pollutants and one of the significant risk factors for cardiovascular diseases (CVD) - atherogenic dyslipidemias - were published back in the 80s of the last century. The reason for the search for associations was an even earlier study that demonstrated an almost 2-fold increase in mortality from coronary heart disease (CHD) in men with more than 10 years of work experience exposed to carbon disulfide at work.

B. M. Stolbunov and co-authors found that among people living near chemical plants, the level of morbidity in the circulatory system was 2-4 times higher. A number of studies have examined the impact of chemical pollutants on the likelihood of not only

chronic, but also acute forms of IHD. Thus, A. Sergeev and co-authors analyzed the incidence of myocardial infarction (MI) in persons living near sources of organic pollutants, where the incidence of hospitalization was 20% higher than the incidence of hospitalization in persons not exposed to organic pollutants. Another study found that the highest degree of “chemical contamination” of the body with toxic elements was observed in patients with MI who worked for more than 10 years in contact with industrial xenobiotics.

When conducting five-year medical and environmental monitoring in the Khanty-Mansi Autonomous Okrug, a connection was shown between the frequency of CVD spread and the level of air pollutants. Thus, the researchers drew a parallel between the frequency of hospitalizations for angina pectoris and the increase in the level of average monthly concentrations of carbon monoxide and phenol. In addition, increased atmospheric phenol and formaldehyde levels were associated with increased hospitalizations for MI and hypertension. Along with this, the minimum frequency of decompensation of chronic coronary insufficiency corresponded to a decrease in the concentration of nitrogen dioxide in the atmospheric air and the minimum average monthly concentrations of carbon monoxide and phenol.

Published in 2012, the results of studies conducted by A. R. Hampel et al. and R. Devlin et al. showed the acute effect of ozone on impaired myocardial repolarization according to ECG data. A study in London illustrated that increases in atmospheric pollutants, particularly those with a sulfite component, in patients with implantable cardioverter defibrillators resulted in an increase in the incidence of ventricular premature beats, flutter, and atrial fibrillation.

Undoubtedly, one of the most informative and objective criteria characterizing the health status of the population is the mortality rate. Its value largely characterizes the sanitary and epidemiological well-being of the entire population. Thus, according to the American Heart Association, an increase in the level of dust particles with a size of less than 2.5 microns for several hours a week can cause death in patients with CVD, as well as a reason for hospitalization for rapid MI and decompensated heart failure. Similar data obtained in a study conducted in California and in a twelve-year observation in China showed that long-term exposure to dust particles and nitric oxide was not only a risk of developing coronary heart disease and stroke, but also a predictor of cardiovascular and cerebrovascular mortality.

A striking example of the connection between mortality from CVD and the level of air pollutants was the result of an analysis of the structure of mortality in the Moscow population during the anomalous summer of 2011. The increase in the concentration of pollutants in the city's atmosphere had two peaks - on July 29 and August 7, 2011, reaching 160 mg/m3 and 800 mg/m3, respectively. At the same time, suspended particles with a diameter of more than 10 microns predominated in the air. The concentration of particles with a diameter of 2.0-2.5 microns was particularly high on June 29. When comparing the dynamics of mortality with indicators of air pollution, there was a complete coincidence of peaks in the number of deaths with an increase in the concentration of particles with a diameter of 10 microns.

Along with the negative effects of various pollutants, there are publications about their positive effects on the CVS. For example, the level of carbon monoxide in high concentrations has a cardiotoxic effect - due to increasing the level of carboxyhemoglobin, but in small doses it is cardioprotective against heart failure.

Due to the paucity of studies on the possible mechanisms of the negative effects of environmental pollution on CVS, it is difficult to draw a convincing conclusion. However, according to available publications, this interaction may be due to the development and progression of subclinical atherosclerosis, coagulopathy with a tendency to thrombus formation, as well as oxidative stress and inflammation.

According to a number of experimental studies, the pathological connection between lipophilic xenobiotics and ischemic heart disease is realized through the initiation of lipid metabolism disorders with the development of persistent hypercholesterolemia and hypertriglyceridemia, which underlie arterial atherosclerosis. Thus, a study in Belgium showed that in non-smoking patients with diabetes, each doubling of the distance of residence from major highways was associated with a decrease in low-density lipoprotein levels.

According to other studies, xenobiotics themselves are capable of directly damaging the vascular wall with the development of a generalized immunoinflammatory reaction, triggering the proliferation of smooth muscle cells, muscular-elastic hyperplasia of the intima and fibrous plaque mainly in small and medium-sized vessels. These changes in blood vessels are called arteriosclerosis, emphasizing that the root cause of the disorders is sclerosis, and not the accumulation of lipids.

In addition, a number of xenobiotics cause lability of vascular tone and initiate thrombus formation. Scientists from Denmark came to a similar conclusion, showing that increasing levels of suspended particles in the atmosphere are associated with an increased risk of blood clots.

As another pathogenetic mechanism underlying the development of CVD, the processes of free radical oxidation in areas of environmental distress are being actively studied. The development of oxidative stress is a natural response of the body to the effects of xenobiotics, regardless of their nature. It has been proven that peroxidation products are responsible for initiating damage to the genome of vascular endothelial cells, which underlies the development of the cardiovascular continuum.

A study conducted in Los Angeles and Germany showed that long-term exposure to dust particles is associated with thickening of the intima/media complex as a sign of the development of subclinical atherosclerosis and increased blood pressure levels.

Currently, there are publications indicating a connection between genetic predisposition, inflammation, on the one hand, and cardiovascular risk, on the other. Thus, high polymorphism of glutathione S-transferases, which accumulate when exposed to pollutants or smoking, increases the risk of a decrease in lung function throughout life, the development of dyspnea and inflammation. Developed pulmonary oxidative stress and inflammation induce the development of systemic inflammation, which, in turn, increases cardiovascular risk.

Thus, it is possible that one of the possible pathogenetic links in the influence of environmental pollution on the formation of CVD is the activation of inflammation. This fact is also interesting because in recent years, new data have emerged on the connection between laboratory markers of inflammation and an unfavorable prognosis in both healthy individuals and patients with CVD.

It is now generally accepted that the main cause of most types of respiratory pathology is inflammation. In recent years, data have been obtained indicating that an increase in the blood level of a number of nonspecific inflammatory markers is associated with an increased risk of developing coronary artery disease, and in the case of an existing disease, with an unfavorable prognosis.

The fact of inflammation plays a major role in the development of atherosclerosis as one of the leading causes of the development of ischemic heart disease. MI has been found to be more common among people with high levels of various inflammatory proteins in the blood plasma, and decreased lung function is associated with increased levels of fibrinogen, C-reactive protein (CRP) and white blood cells.

Both in pulmonary pathology (chronic obstructive pulmonary disease has been well studied in this regard) and in many CVDs (coronary artery disease, myocardial infarction, atherosclerosis), an increase in the level of CRP is observed,

interleukins-1p, 6, 8, as well as tumor necrosis factor alpha, and proinflammatory cytokines increase the expression of metalloproteinases.

Thus, according to the presented analysis of publications on the problem of the influence of environmental pollution on the occurrence and development of cardiovascular pathology, their connection has been confirmed, but its mechanisms have not been fully studied, which should be the subject of further research.

Bibliography

1. Artamonova G.V., Shapovalova E.B., Maksimov S.A., Skripchenko A.E., Ogarkov M.Yu. Environment as a risk factor for the development of coronary heart disease in an urbanized region with a developed chemical industry // Cardiology . 2012. No. 10. P. 86-90.

2. Askarova Z. F., Askarov R. A., Chuenkova G. A., Baykina I. M. Assessment of the influence of polluted atmospheric air on the morbidity of the population in an industrial city with developed petrochemistry // Health of the Russian Federation. 2012. No. 3. P. 44-47.

3. Boev V. M., Krasikov S. I., Leizerman V. G., Bugrova O. V., Sharapova N. V., Svistunova N. V. The influence of oxidative stress on the prevalence of hypercholesterolemia in an industrial city // Hygiene and sanitation. 2007. No. 1. P. 21-25.

4. Zayratiants O.V., Chernyaev A.L., Polyanko N.I., Osadchaya V.V., Trusov A.E. Structure of mortality of the Moscow population from diseases of the circulatory and respiratory organs during the abnormal summer of 2010 // Pulmonology . 2011. No. 4. P. 29-33.

5. Zemlyanskaya O. A., Panchenko E. P., Samko A. N., Dobrovolsky A. B., Levitsky I. V., Masenko V. P., Tita-eva E. V. Matrix metalloproteinases, C- reactive protein and markers of thrombopenia in patients with stable angina and restenosis after percutaneous coronary interventions // Cardiology. 2004. No. 11. P. 4-12.

6. Zerbino D. D., Solomenchuk T. N. Atherosclerosis - a specific pathology of the arteries or a “unified” group definition? Search for the causes of arteriosclerosis: an ecological concept // Pathology Archives. 2006. T. 68, No. 4. P. 49-53.

7. Zerbino D. D., Solomenchuk T. N. Content of a number of chemical elements in the hair of patients who have had myocardial infarction and healthy people // Occupational Medicine and Industrial Ecology. 2007. No. 2. P. 17-21.

8. Karpin V. A. Medical and environmental monitoring of diseases of the cardiovascular system in the urbanized North // Cardiology. 2003. No. 1. P. 51-54.

9. Koroleva O. S., Zateyshchikov D. A. Biomarkers in cardiology: registration of intravascular inflammation // Farmateka. 2007. No. 8/9. pp. 30-36.

10. Kudrin A.V., Gromova O.A. Microelements in neurology. M.: GEOTAR-Media, 2006. 304 p.

11. Nekrasov A. A. Immunoinflammatory mechanisms in cardiac remodeling in patients with chronic obstructive pulmonary disease // Journal of Heart Failure. 2011. T. 12, No. 1. P. 42-46.

12. Onishchenko G. G. On the sanitary and epidemiological state of the environment // Hygiene and Sanitation. 2013. No. 2. P. 4-10.

13. Assessment of the influence of environmental factors on the health of the population of the Kemerovo region: information and analytical review. Kemerovo: Kuzbassvuzizdat, 2011. 215 p.

14. Pulmonology [Set]: national manual with annex on CD / ed. A. G. Chu-chalina. M.: GEOTAR-Media, 2009. 957 p.

15. Revich B. A., Maleev V. V. Climate change and health of the Russian population: Analysis of the situation. M.: LENAD, 201 1. 208 p.

16. Tedder Yu. R., Gudkov A. B. From environmental hygiene to medical ecology // Human Ecology. 2002. No. 4. P. 15-17.

17. Ungureanu T. N., Lazareva N. K., Gudkov A. B., Buzinov R. V. Assessment of the tension of the medical and environmental situation in industrial cities of the Arkhangelsk region // Human Ecology. 2006. No. 2. P. 7-10.

18. Ungureanu T. N., Novikov S. M., Buzinov R. V., Gudkov A. B. Risk to public health from chemicals polluting the atmospheric air in a city with a developed pulp and paper industry // Hygiene and Sanitation . 2010. No. 4. pp. 21-24.

19. Khripach L.V., Revazova Yu.A., Rakhmanin Yu.A. The role of free radical oxidation in genome damage by environmental factors // Bulletin of the Russian Academy of Medical Sciences. 2004. No. 3. P. 16-18.

20. Shoikhet Ya. N., Korenovsky Yu. V., Motin A. V., Lepilov N. V. The role of matrix metalloproteinases in inflammatory lung diseases // Problems of clinical medicine. 2008. No. 3. P. 99-102.

21. Anderson H. R., Armstrong B., Hajat S., Harrison R., Monk V., Poloniecki J., Timmis A., Wilkinson P. Air pollution and activation of implantable cardioverter defibrillators in London // Epidemiology. 2010. Vol. 21. R. 405-413.

22. Baker E. L. Jr., Landrigan P. J., Glueck C. J., Zack M. M. Jr., Liddle J. A., Burse V. W., Housworth W. J., Needham L. L. Metabolic consequences of exposure to polychlorinated biphenyls (PCB) in sewage sludge // Am. J. Epidemiol. 1980. Vol. 112. R. 553-563.

23. Bauer M., Moebus S., Mohlenkamp S., Dragano N., Nonnemacher M., Fuchsluger M., Kessler C., Jakobs H., Memmesheimer M., Erbel R., Jockel K. H., Hoffmann B. Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study // J. Am. Coll. Cardiol. 2010. Vol. 56. R. 1803-1808.

24. Brook R. D., Rajagopalan S., Pope C. A. 3rd., Brook J. R., Bhatnagar A., ​​Diez-Roux A. V., Holguin F., Hong Y., Luepker R. V., Mittleman M. A., Peters A., Siscovick D., Smith S. C. Jr., Whitsel L., Kaufman J. D. American Heart Association Council on Epidemiology and Prevention. Council on the Kidney in Cardiovascular Diseases, end Council on Nutrition. Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association // Circulation. 2010. Vol. 121. R. 2331-2378.

25. Devlin R. B., Duncan K. E., Jardim M., Schmitt M. T., Rappold A. G., Diaz-Sanchez D. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects // Circulation. 2012. Vol. 126. R. 104-111.

26. Engstrom G., Lind P., Hedblad B., Wollmer P., Stavenow L., Janzon L., Lindgarde F. Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins // Circulation. 2002. Vol. 106. R. 2555-2660.

27. Engstrom G., Lind P., Hedblad B., Stavenow L., Janzon L., Lindgarde F. Effects of cholesterol and inflammation-sensitive plasma proteins on the incidence of myocardial infarction and stroke in men // Circulation. 2002. Vol. 105. P. 2632-2637.

28. Lind P. M, Orberg J, Edlund U. B, Sjoblom L., Lind L. The dioxin-like pollutant PCB 126 (3,3",4,4",5-p

entachlorobiphenyl) affects risk factors for cardiovascular disease in female rats // Toxicol. Lett. 2004. Vol. 150. P. 293-299.

29. Franchini M., Mannucci P. M. Thrombogenicity and cardiovascular effects of ambient air pollution // Blood. 2011. Vol. 118. P. 2405-2412.

30. Fuks K., Moebus S., Hertel S., Viehmann A., Nonnemacher M., Dragano N., Mohlenkamp S., Jakobs H., Kessler C, ErbelR., Hoffmann B. Long-term urban particulate air pollution , traffic noise, and arterial blood pressure // Environ. Health Perspective. 2011. Vol. 119. P. 1706-1711.

31. GoldD. R., Metteman M. A. New insights into pollution and the cardiovascular system 2010 to 2012 // Circulation. 2013. Vol. 127. P. 1903-1913.

32. HampelR., Breitner S., Zareba W., Kraus U., Pitz M., Geruschkat U., Belcredi P., Peters A., Schneider A. Immediate ozone affects on heart rate and repolarization parameters in potentially susceptible individuals / /Occup. Environ. Med. 2012. Vol. 69. P. 428-436.

33. Hennig B., Meerarani P., Slim R., Toborek M., Daugherty A., Silverstone A. E., Robertson L. W. Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence // Toxicol. Appl. Pharmacol. 2002. Vol. 181. P. 174-183.

34. Jacobs L., Emmerechts J., Hoylaerts M. F., Mathieu C., Hoet P. H., Nemery B., Nawrot T. S. Traffic air pollution and oxidized LDL // PLoS ONE. 2011. N 6. P. 16200.

35. Kunzli N., Perez L., von Klot S., Baldassarre D., Bauer M., Basagana X., Breton C., Dratva J., Elosua R., de Faire U., Fuks K., de Groot E., Marrugat J., Penell J., Seissler J., Peters A., Hoffmann B. Investigation of air pollution and atherosclerosis in humans: concepts and outlook // Prog. Cardiovasc. Dis. 2011. Vol. 53. P. 334-343.

36. Lehnert B. E., Iyer R. Exposure to low-level chemicals and ionizing radiation: reactive oxygen species and cellular pathways // Human and Experimental Toxicology. 2002. Vol. 21. P. 65-69.

37. Lipsett M. J., Ostro B. D., Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith D. F., Garcia C., Chang E. T., Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort // Am. J. Respira. Care Med. 2011. Vol. 184. P. 828-835.

38. Matsusue K., Ishii Y., Ariyoshi N., Oguri K. A. Highly toxic PCB produces unusual changes in the fatty acid composition of rat liver // Toxicol. Lett. 1997. Vol. 91. P. 99-104.

39. Mendall M. A., Strachan D. P., Butland B. K, Ballam L., Morris J., Sweetnam P. M., Elwood P. C. C-reactive protein: relation to total mortality, cardiovascular mortality and cardiovascular risk factors in men // Eur. Heart J. 2000. Vol. 21. P. 1584-1590.

40. Schiller C. M., Adcock C. M., Moore R. A., Walden R. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and fasting on body weight and lipid parameters in rats // Toxicol. Appl. Pharmacol. 1985. Vol. 81. P. 356-361.

41. Sergeev A. V., Carpenter D. O. Hospitalization rates for coronary heart disease in relation to residence near areas contaminated with persistent organic pollutants and other pollutants // Environ. Health Perspective. 2005. Vol. 113. P. 756-761.

42. Taylor A. E. Cardiovascular Effects of Environmental Chemicals Otolaryngology - Head and Neck // Surgery. 1996. Vol. 114. P. 209-211.

43. Tiller J. R., Schilling R. S. F., Morris J. N. Occupational

Toxic Factor in Mortality from Coronary Heart Disease // Br. Med. J. 1968. No. 4. P. 407-41 1.

44. Zhang P., Dong G., Sun B., Zhang L., Chen X., Ma N, Yu F, Guo H, Huang H, Lee Y. L, Tang N, Chen J. Long-term exposure to ambient air pollution and mortality due to cardiorespiratory disease and cerebrovascular disease in Shenyang China // PLoS ONE. 2011. N 6. P. 20827.

1. Artamonova G. V., Shapovalova Je. B., Maksimov S. A., Skripchenko A. E., Ogarkov M. Ju. The Environment as a Risk Factor of Coronary Heart Disease in an Urbanized Region With Developed Chemical Industry. Cardiology. 2012, 10, pp. 86-90.

2. Askarova Z. F., Askarov R. A., Chuenkova G. A., Bajkina I. M. Evaluation of the influence of polluted ambient air on morbidity in an industrial town with developed petrochemical industry. Zdravoohranenije Rossiiskoy Federatsii. 2012, 3, pp. 44-47.

3. Boev V. M., Krasikov S. I., Lejzerman V. G., Bugrova O. V., Sharapova N. V., Svistunova N. V. Impact of oxidative stress on the prevalence of hypercholesterolemia under the conditions of an industrial town. Hygiene and sanitary. 2007, 1, pp. 21-25.

4. Zajrat "janc O. V., Chernjaev A. L., Poljanko N. I., Osadchaja V. V., Trusov A. E. Structure of mortality from cardiovascular and respiratory diseases during abnormal weather in summer, 2010, in Moscow. Pul"monologija. 2011, 4, pp. 29-33.

5. Zemljanskaja O. A., Panchenko E. P., Samko A. N., Dobrovol'skij A. B., Levickij I. V., Masenko V. P., Titaeva E. V. Matrix Metalloproteinases, C-Reactive Protein, and Markers of Thrombinemia in Patients With Stable Angina and Restenoses After Percutaneous Coronary Interventions. Kardiologija. 2004, 1 1, pp. 4-12.

6. Zerbino D. D., Solomenchuk T. N. Is atherosclerosis a specific arterial lesion or a “unified” group definition? Search for the causes of arteriosclerosis: an ecologic concept. Arhiv Pathologii. 2006, 68 (4), pp. 4953.

7. Zerbino D. D., Solomenchuk T. N. Some chemical elements content of hair in post-infarction patients and healthy people. Meditsina truda ipromyshlennaya ekologija. 2007, 2, pp. 1721.

8. Karpin V. A. Medico-Ecological Monitoring of Cardiovascular Diseases in the Urbanized North. Cardiology. 2003, 1, pp. 51-54.

9. Koroleva O. S., Zatejshhikov D. A. Biomarkers in Cardiology: registration of intravascular inflammation. Farmateka. 2007, 8/9, pp. 30-36.

10. Kudrin A. V., Gromova O. A. Mikrojelementy v nevrologii. Moscow, GEOTAR-Media Publ., 2006, 304 p.

11. Nekrasov A. A. Immunoinflammatory mechanisms in heart remodeling in patients with chronic obstructive pulmonary disease. Zhurnal Serdechnaja nedostatochnost". 2011, 12 (1), pp. 42-46.

12. Onishhenko G. G. On Sanitary and Epidemiological State of the Environment. Hygiene and sanitary. 2013, 2, pp. 4-10.

13. Ocenka vlijanija faktorov sredy obitanija na zdorov"e naselenija Kemerovskoj oblasti: informacionno-analiticheskij obzor. Kemerovo, Kuzbassvuzizdat, 2011, 215 p.

14. Pul"monologija. Nacional"noe rukovodstvo s prilozheniem na kompakt-diske. Ed. A. G. Chuchalin. Moscow, GEOTAR-Media Publ., 2009, 957 p.

15. Revich B. A., Maleev V. V. Izmenenie klimata i zdorov"ja naselenija Rossii. Analiz situacii. Moscow, LENAD Publ., 201 1, 208 p.

16. Tedder Ju. R., Gudkov A. B. From the environmental hygiene to medical ecology Ekologiya cheloveka. 2002, 4, pp.15-17.

17. Ungurjanu T. N., Lazareva N. K., Gudkov A. B., Buzinov R. V. Evaluation of medical-ecological situation tension in industrial cities of Arkhangelsk region. Ekologiya cheloveka. 2006, 2, pp.7-10.

18. Ungurjanu T. N., Novikov S. M., Buzinov R. V., Gudkov A. B. Human health risk of chemical air pollutants in a developed pulp and paper industry town. Hygiene and sanitary. 2010, 4, pp. 21-24.

19. Hripach L. V., Revazova Ju. A., Rahmanin Ju. A. Active oxygen forms and genome damage by environmental factors. Vestnik RAMN. 2004, 3, pp. 16-18.

20. Shojhet Ja. N., Korenovskij Ju. V., Motin A. V., Lepilov N. V. Role of matrix metalloproteinase in inflammatory diseases of the lungs. Problemy clinical medicine. 2008, 3, pp. 99-102.

21. Anderson H. R., Armstrong B., Hajat S., Harrison R., Monk V, Poloniecki J., Timmis A., Wilkinson P. Air pollution and activation of implantable cardioverter defibrillators in London. Epidemiology. 2010, 21, pp. 405-413.

22. Baker E. L. Jr., Landrigan P. J., Glueck C. J., Zack M. M. Jr., Liddle J. A., Burse V. W., Housworth W. J., Needham L. L. Metabolic consequences of exposure to polychlorinated biphenyls (PCB) in sewage sludge. Am. J. Epidemiol. 1980, 1 12, pp. 553-563.

23. Bauer M., Moebus S., Mohlenkamp S., Dragano N., Nonnemacher M., Fuchsluger M., Kessler C., Jakobs H., Memmesheimer M., Erbel R., Jockel K. H., Hoffmann B. Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study. J. Am. Coll. Cardiol. 2010, 56, pp. 1803-1808.

24. Brook R. D., Rajagopalan S., Pope C. A. 3rd., Brook J. R., Bhatnagar A., ​​Diez-Roux A. V., Holguin F., Hong Y., Luepker R. V., Mittleman M. A., Peters A., Siscovick D., Smith S. C. Jr., Whitsel L., Kaufman J. D. American Heart Association Council on Epidemiology and Prevention. Council on the Kidney in Cardiovascular Diseases, end Council on Nutrition. Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. Circulation. 2010, 121, pp. 2331-2378.

25. Devlin R. B., Duncan K. E., Jardim M., Schmitt M. T., Rappold A. G., Diaz-Sanchez D. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects. Circulation. 2012, 126, pp. 104-111.

26. Engstrom G., Lind P., Hedblad B., Wollmer P., Stavenow L., Janzon L., Lindgarde F. Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins. Circulation. 2002, 106, pp. 2555-2660.

27. Engstrom G., Lind P., Hedblad B., Stavenow L.,

Janzon L., Lindgarde F. Effects of cholesterol and inflammation-sensitive plasma proteins on the incidence of myocardial infarction and stroke in men. Circulation. 2002, 105, pp. 2632-2637.

28. Lind P. M., Orberg J., Edlund U. B., Sjoblom L., Lind L. The dioxin-like pollutant PCB 126 (3,3",4,4",5-p entachlorobiphenyl) affects risk factors for cardiovascular disease in female rats. Toxicol. Lett. 2004, 150, pp. 293-299.

29. Franchini M., Mannucci P. M. Thrombogenicity and cardiovascular effects of ambient air pollution. Blood. 2011, 118, pp. 2405-2412.

30. Fuks K., Moebus S., Hertel S., Viehmann A., Nonnemacher M., Dragano N., Mohlenkamp S., Jakobs H., Kessler C., Erbel R., Hoffmann B. Long-term urban particulate air pollution, traffic noise, and arterial blood pressure. Environ. Health Perspective. 2011, 119, pp. 1706-1711.

31. Gold D. R., Metteman M. A. New insights into pollution and the cardiovascular system 2010 to 2012. Circulation. 2013, 127, pp. 1903-1913.

32. Hampel R., Breitner S., Zareba W., Kraus U., Pitz M., Geruschkat U., Belcredi P., Peters A., Schneider A. Immediate ozone affects on heart rate and repolarization parameters in potentially susceptible individuals . Occup. Environ. Med. 2012, 69, pp. 428-436.

33. Hennig B., Meerarani P., Slim R., Toborek M., Daugherty A., Silverstone A. E., Robertson L. W. Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence. Toxicol. Appl. Pharmacol. 2002, 181, pp. 174-183.

34. Jacobs L., Emmerechts J., Hoylaerts M. F., Mathieu C., Hoet P. H., Nemery B., Nawrot T. S. Traffic air pollution and oxidized LDL. PLoS ONE. 2011, 6, p. 16200.

35. Kunzli N., Perez L., von Klot S., Baldassarre D., Bauer M., Basagana X., Breton C., Dratva J., Elosua R., de Faire U., Fuks K., de Groot E., Marrugat J., Penell J., Seissler J., Peters A., Hoffmann B. Investigation of air pollution and atherosclerosis in humans: concepts and outlook. Prog. Cardiovasc. Dis. 201 1, 53, pp. 334-343.

36. Lehnert B. E., Iyer R. Exposure to low-level chemicals and ionizing radiation: reactive oxygen species and cellular pathways. Human and Experimental Toxicology. 2002, 21, pp. 65-69.

37. Lipsett M. J., Ostro B. D., Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith D. F., Garcia C., Chang E. T., Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort. Am. J. Respira. Care Med. 201 1, 184, pp. 828-835.

38. Matsusue K., Ishii Y., Ariyoshi N., Oguri K. A. Highly toxic PCB produces unusual changes in the fatty acid composition of rat liver. Toxicol. Lett. 1997, 91, pp. 99-104.

39. Mendall M. A., Strachan D. P., Butland B. K., Ballam L., Morris J., Sweetnam P. M., Elwood P. C. C-reactive protein: relation to total mortality, cardiovascular mortality and cardiovascular risk factors in men. Eur. Heart J. 2000, 21, pp. 1584-1590.

40. Schiller C. M., Adcock C. M., Moore R. A., Walden R. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and fasting on body weight and lipid parameters in rats. Toxicol. Appl. Pharmacol. 1985, 81, pp. 356-361.

41. Sergeev A. V., Carpenter D. O. Hospitalization rates for coronary heart disease in relation to residence near areas contaminated with persistent organic pollutants and other pollutants. Environ. Health Perspective. 2005, 113, pp. 756-761.

42. Taylor A. E. Cardiovascular Effects of Environmental Chemicals Otolaryngology - Head and Neck. Surgery. 1996, 114, pp. 209-211.

43. Tiller J. R., Schilling R. S. F., Morris J. N. Occupational Toxic Factor in Mortality from Coronary Heart Disease. Br. Med. J. 1968, 4, pp. 407-41 1.

44. Zhang P., Dong G., Sun B., Zhang L., Chen X., Ma N., Yu F., Guo H., Huang H., Lee Y. L., Tang N., Chen J. Long- term exposure to ambient air pollution and mortality due to cardiorespiratory disease and cerebrovascular disease in Shenyang China. PLoS ONE. 2011, 6, p. 20827.

ECOLOGY AND CARDIOVASCULAR DISEASES

E. D. Bazdyrev, O. L. Barbarash

Research Institute for Complex Issues of Cardiovascular Diseases Siberian Branch RAMS, Kemerovo Kemerovo State Medical Academy, Kemerovo, Russia

Currently around the world, environmental pollution remains a significant problem causing increased mortality rates and a factor of reduced life expectancy. Admittedly, influence of the environment that is pollution of the atmosphere with air pollutants, results in preferential development of the respiratory system diseases. However, effects of different pollutants on human bodies are not limited only to bronchopulmonary

changes. Recently, a number of studies were conducted and proved a relationship between levels and types of atmospheric air pollution and diseases of the digestive and endocrine systems. Earnest data about the harmful effects of air pollutants on the cardiovascular system was obtained in the recent decade. In the review, there has been analyzed information both about the relation between different cardiovascular diseases and the aeropollutants" effects and their possible pathogenetic interrelations.

Keywords: ecology, air pollutants, cardiovascular diseases Contact information:

Bazdyrev Evgeniy Dmitrievich - Candidate of Medical Sciences, senior researcher in the department of multifocal atherosclerosis of the Federal State Budgetary Institution "Research Institute of Complex Problems of Cardiovascular Diseases" of the Siberian Branch of the Russian Academy of Medical Sciences, assistant of the department of faculty therapy, occupational diseases and endocrinology of the Kemerovo State Medical Academy of the Ministry healthcare of the Russian Federation

Address: 650002, Kemerovo, Sosnovy Boulevard, 6 E-mail: [email protected]

Statistics 1 million 300 thousand people die annually from diseases of the cardiovascular system, and this figure increases from year to year. Among the total mortality in Russia, cardiovascular diseases account for 57%. About 85% of all diseases of modern man are associated with unfavorable environmental conditions arising through his own fault

The influence of the consequences of human activity on the functioning of the cardiovascular system It is impossible to find a place on the globe where pollutants are not present in one concentration or another. Even in the ice of Antarctica, where there are no industrial productions and people live only at small research stations, scientists have discovered toxic (poisonous) substances from modern industries. They are brought here by atmospheric currents from other continents.

The influence of human activity on the functioning of the cardiovascular system Human economic activity is the main source of pollution of the biosphere. Gaseous, liquid and solid industrial wastes enter the natural environment. Various chemicals contained in waste, entering the soil, air or water, pass through ecological links from one chain to another, ultimately ending up in the human body.

90% of cardiovascular defects in children in disadvantaged ecological zones Lack of oxygen in the atmosphere causes hypoxia, the heart rate changes Stress, noise, and fast pace of life deplete the heart muscle Factors that negatively affect the cardiovascular system Environmental pollution from industrial wastes lead to developmental pathologies cardiovascular system in children Increased background radiation leads to irreversible changes in hematopoietic tissue In areas with polluted air People have high blood pressure

The main risk factors leading to the development of cardiovascular diseases: high blood pressure; age: men over 40 years old, women over 50 years old; psycho-emotional stress; cardiovascular diseases in close relatives; diabetes; obesity; total cholesterol more than 5.5 mmol/l; smoking.

Excess weight contributes to high blood pressure High cholesterol levels lead to loss of elasticity of blood vessels Pathogenic microorganisms cause infectious heart diseases A sedentary lifestyle leads to flabbiness of all body systems Heredity increases the likelihood of developing diseases Factors that negatively affect the cardiovascular system Frequent use of medications poisons the heart muscle , heart failure develops

Narcologists “Don’t drink wine, don’t upset your heart with tobacco - and you will live as long as Titian lived” Academician I.P. Pavlov The influence of alcohol and nicotine on the heart: -Tachycardia; --Disturbance of neurohumoral regulation of heart function; -Fast fatiguability; - Flabbiness of the heart muscle; - Heart rhythm disorders; - Premature aging of the heart muscle; -Increased risk of heart attack; - Development of hypertension.

Assessment of adaptive potential AP = (PR) (SBP) (DBP) (MT) (P) (V)-0.27; where AP is the adaptive potential of the circulatory system in points, PR is the pulse rate (bpm); SBP and DBP - systolic and diastolic blood pressure (mm Hg); P - height (cm); BW - body weight (kg); B - age (years).

Based on the values ​​of the adaptation potential, the patient’s functional state is determined: Interpretation of the test: below satisfactory adaptation; tension of adaptation mechanisms; unsatisfactory adaptation; 3.5 and higher - adaptation failure.

Calculation of the Kerdo index Kerdo index is an indicator used to assess the activity of the autonomic nervous system. The index is calculated using the formula: autonomic nervous system Index=100 (1-DAD), where: Pulse DAD diastolic pressure (mm Hg); mm Hg. Art. Pulse pulse rate (beats per minute).pulse Normal indicator: from – 10 to + 10%

Interpretation of the test: positive value - predominance of sympathetic influences, negative value - predominance of parasympathetic influences. If the value of this index is greater than zero, then we speak of the predominance of sympathetic influences in the activity of the autonomic nervous system; if it is less than zero, then of the predominance of parasympathetic influences; if it is equal to zero, then this indicates functional balance. In a healthy person it is close to zero.

Results T - 30% - heart fitness is good, the heart strengthens its work by increasing the amount of blood released with each contraction. T - 38% - insufficient heart fitness. T - 45% - low fitness, the heart increases its work due to the heart rate.

“Structure and work of the heart” - Humoral regulation of the heart The activity of the heart is regulated by chemicals. Veins are vessels that carry blood to the heart. The total length of capillaries in humans is about 100 thousand km. Automaticity of the heart. What is a heart? "Structure and work of the heart." Cardiac cycle - 0.8 s Atrial contraction - 0.1 s Ventricular contraction - 0.3 s Relaxation of the ventricles and atria - 0.4 s.

“Work of the heart” - 0.3. Atria - ventricles. Blood from the ventricles enters the pulmonary artery and aorta. Blood from the veins enters the atrium and partially flows into the ventricles. 4. The valves are closed, the lunates are open. What is a heart? The structure and work of the heart. Label the parts of the heart with numbers on the diagram.

“Cardiovascular system” - Provides blood flow through blood vessels. Human cardiovascular system. The mass of the heart is approximately 220-300 g. The duration of the recovery period (in seconds). According to my research, the process of heart rate restoration is the smallest in children involved in sports. The shape is determined by age, gender, physique, health, and other factors.

“Structure of the heart” - Find the vessels flowing into the right and left halves of the heart. Cardiac muscle. Right ventricle. The structure of the heart of fish. Aristotle. Locate the flapper valves in the pictures. What is the heart covered with? The structure of the heart of reptiles. The structure of the heart of amphibians. Pulmonary artery. Left ventricle. Identify the right and left sides of the heart.

“The Human Heart” - Study questions: What is the structure of the heart? The heart was and remains an organ that indicates the entire state of a person. Didactic goals of the project: What happens to the heart during various physical activities? Completed by: Mamontova Larisa Aleksandrovna. What is a cardiac cycle? Methodological tasks: What are cardiac phases?

“Cardiac system” - The influence of smoking: vasospasm, impaired blood supply to organs, gangrene of the legs, etc. Main diseases of the cardiovascular system. Quitting smoking and alcohol abuse. Rational and balanced nutrition. Physical inactivity is insufficient physical activity. Hygiene of the cardiovascular system.

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