The influence of the environment on the human cardiovascular system. Negative factors of influence on the cardiovascular system Research results and their discussion

Date: 01.07.2020

Influence of various factors on the human cardiovascular system

What are the causes of cardiovascular disease? What factors affect the work of the cardiovascular system? How can you strengthen your cardiovascular system?

Ecologists "cardiovascular disasters".

Statistics 1 million 300 thousand people die annually from diseases of the cardiovascular system, and this figure is increasing from year to year. Cardiovascular diseases account for 57% of the total mortality in Russia. About 85% of all diseases of a modern person are associated with adverse environmental conditions arising from his own fault.

Influence of the consequences of human activity on the work 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 production facilities, and people live only in small scientific stations, scientists have discovered toxic (poisonous) substances of modern production facilities. They are brought here by atmospheric streams from other continents.

Influence of human activity on the work 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 in waste, getting into soil, air or water, pass along ecological links from one chain to another, eventually getting into the human body.

90% of CVS defects in children in disadvantaged ecological zones Lack of oxygen in the atmosphere causes hypoxia, heart rate changes Stress, noise, high-speed pace of life deplete the heart muscle Factors that negatively affect the cardiovascular system Environmental pollution with industrial waste leads to developmental pathology cardiovascular system in children Increased background radiation leads to irreversible changes in hematopoietic tissue In areas with polluted air In humans, high blood pressure

Cardiologists Out of 100 thousand people in Russia, 330 men and 154 women die of myocardial infarction every year, 250 men and 230 women die of strokes. The structure of mortality from cardiovascular diseases in Russia

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

Heart disease congenital heart disease rheumatic diseases coronary artery disease hypertension infectious valve lesions primary lesion of the heart muscle

Excess weight contributes to high blood pressure High cholesterol levels lead to loss of vascular elasticity Pathogenic microorganisms cause infectious heart disease 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 drugs poisons the heart muscle , heart failure develops

The chapter examines blood circulation at different levels of physical activity, lack and excess of oxygen, low and high temperatures of the external environment, changes in gravity.

PHYSICAL ACTIVITY

Work can be dynamic, when resistance is overcome at a certain distance, and static - with isometric muscle contraction.

Dynamic work

Physical stress induces immediate reactions in various functional systems, including muscle, cardiovascular, and respiratory. The severity of these reactions is determined by the body's adaptability to physical activity and the severity of the work performed.

Heart rate. By the nature of the change in heart rate, two forms of work can be distinguished: light, non-tiring work - with the achievement of a stationary state - and hard work that causes fatigue (Fig. 6-1).

Even after the end of the work, the heart rate changes depending on the voltage applied. After light work, the heart rate returns to the initial level within 3-5 minutes; after hard work, the recovery period is much longer - with extremely heavy loads, it reaches several hours.

With hard work, the blood flow and metabolism in the working muscle increases more than 20 times. The degree of changes in the indices of cardio- and hemodynamics during muscular activity depends on its power and physical fitness (adaptation) of the body (Table 6-1).

Rice. 6-1.Change in heart rate in persons with average efficiency with light and heavy dynamic work of constant intensity

In persons trained for physical activity, myocardial hypertrophy occurs, the density of capillaries and the contractile characteristics of the myocardium increase.

The heart increases in size due to hypertrophy of cardiomyocytes. The weight of the heart in highly qualified athletes increases to 500 g (Fig. 6-2), the concentration of myoglobin increases in the myocardium, and the heart cavities increase.

The density of capillaries per unit area in a trained heart increases significantly. Coronary blood flow and metabolic processes increase in accordance with the work of the heart.

Myocardial contractility (the maximum rate of increase in pressure and ejection fraction) is markedly increased in athletes due to the positive inotropic action of the sympathetic nerves.

Table 6-1.Changes in physiological indicators during dynamic work of different power in people who do not go in for sports (top line) and in trained athletes (bottom line)

Nature of work	Easy	Average	Submaximal	Maximum
Work power, W		50-100	100-150	150-250
Work power, W	100-150	150-200	200-350	350-500 and>
Heart rate, beats / min	120-140	140-160	160-170	170-190
Heart rate, beats / min	90-120	120-140	140-180	180-210
Systolic blood volume, l / min	80-100	100-120	120-130	130-150
Systolic blood volume, l / min	80-100	100-140	140-170	170-200
Minute blood volume, l / min	10-12	12-15	15-20	20-25
Minute blood volume, l / min	8-10	10-15	15-30	30-40
Average blood pressure, mm Hg	85-95	95-100	100-130	130-150
Average blood pressure, mm Hg	85-95	95-100	100-150	150-170
Oxygen consumption, l / min	1,0-1,5	1,5-2,0	2,0-2,5	2,5-3,0
Oxygen consumption, l / min	0,8-1,0	1,0-2,5	2,5-4,5	4,5-6,5
Blood lactate, mg per 100 ml	20-30	30-40	40-60	60-100
Blood lactate, mg per 100 ml	10-20	20-50	50-150	150-300

With physical exertion, cardiac output increases due to an increase in heart rate and stroke volume, and the changes in these values are purely individual. In healthy young people (with the exception of highly trained athletes), cardiac output rarely exceeds 25 L / min.

Regional blood flow. During physical exertion, the regional blood flow changes significantly (Table 6-2). An increase in blood flow in working muscles is associated not only with an increase in cardiac output and blood pressure, but also with a redistribution of the BCC. With maximum dynamic work, blood flow in the muscles increases by 18-20 times, in the coronary vessels of the heart by 4-5 times, but decreases in the kidneys and abdominal organs.

In athletes, the end-diastolic volume of the heart naturally increases (3-4 times more than the stroke volume). For an ordinary person, this figure is only 2 times higher.

Rice. 6-2.Normal heart and athlete's heart. An increase in the size of the heart is associated with lengthening and thickening of individual myocardial cells. In the heart of an adult, there is approximately one capillary for every muscle cell.

Table 6-2.Cardiac output and organ blood flow in a person at rest and during physical activity of varying intensity

Absorption O 2 , *ml / (min m 2)**
	Rest	Easy	Average	Maximum
	140	400	1200	2000
Region	Blood flow, ml / min
Skeletal muscle	1200	4500	12 500	22 000
Heart				1000
Brain
Celiac	1400	1100
Renal	1100
Leather		1500	1900
Other organs
Cardiac output	5800	9500	17 500	25 000

With muscular activity, the excitability of the myocardium increases, the bioelectric activity of the heart changes, which is accompanied by a shortening of the PQ, QT intervals of the electrocardiogram. The more power of work and the lower the level of physical fitness of the body, the more changes in the electrocardiogram indicators.

With an increase in heart rate up to 200 per minute, the duration of diastole decreases to 0.10-0.11 s, i.e. more than 5 times in relation to this value at rest. In this case, filling of the ventricles occurs within 0.05-0.08 s.

Arterial pressure in humans, during muscular activity, it increases significantly. When running, causing an increase in heart rate up to 170-180 per minute, the following increases:

Systolic pressure on average from 130 to 250 mm Hg;

Average pressure - from 99 to 167 mm Hg;

Diastolic - from 78 to 100 mm Hg

With intense and prolonged muscle activity, the stiffness of the main arteries increases due to the strengthening of the elastic frame and the increase in the tone of smooth muscle fibers. In the arteries of the muscle type, moderate hypertrophy of muscle fibers can be observed.

The pressure in the central veins during muscle activity, as well as the central blood volume, increases. This is due to an increase in venous blood return with an increase in the tone of the vein walls. Working muscles act as an additional pump, which is referred to as a "muscle pump", which provides an increased (adequate) blood flow to the right heart.

The total peripheral vascular resistance during dynamic work can be reduced by 3-4 times compared to the initial, non-working state.

Oxygen consumption increases by an amount that depends on the load and the efficiency of the effort expended.

With light work, a steady state is achieved, when oxygen consumption and its utilization are equivalent, but this occurs only after 3-5 minutes, during which blood flow and metabolism in the muscle adapt to new requirements. Until a steady state is reached, the muscle depends on a small oxygen reserve,

which is provided by O 2 associated with myoglobin, and from the ability to extract oxygen from the blood.

With heavy muscular work, even if it is performed with constant effort, a stationary state does not occur; like heart rate, oxygen consumption is constantly increasing, reaching a maximum.

Oxygen debt. With the start of work, the need for energy increases instantly, but it takes some time for blood flow and aerobic metabolism to adjust; thus, oxygen debt arises:

With light work, the amount of oxygen debt remains constant after reaching a steady state;

With hard work, it grows until the very end of the work;

At the end of work, especially in the first minutes, the rate of oxygen consumption remains above the resting level - the oxygen debt is “paid off”.

A measure of physical stress. As the intensity of the dynamic work increases, the heart rate increases, and the rate of oxygen consumption increases; the greater the load on the body, the greater this increase in comparison with the level at rest. Thus, heart rate and oxygen consumption serve as a measure of physical stress.

Ultimately, the adaptation of the body to the action of high physical activity leads to an increase in the power and functional reserves of the cardiovascular system, since it is this system that limits the duration and intensity of the dynamic load.

HYPODYNAMY

The release of a person from physical labor leads to physical de-training of the body, in particular, to a change in blood circulation. In such a situation, one would expect an increase in efficiency and a decrease in the intensity of the functions of the cardiovascular system. However, this does not happen - the economy, power and efficiency of blood circulation are reduced.

In the systemic circulation, a decrease in systolic, mean and pulse blood pressure is more often observed. In the pulmonary circulation, when hypokinesia is combined with a decrease in the hydrostatic blood pressure (bed rest, weightless

bridge) increases blood flow to the lungs, increases the pressure in the pulmonary artery.

At rest during hypokinesia:

Heart rate increases naturally;

Cardiac output and BCC decrease;

With prolonged bed rest, the size of the heart, the volume of its cavities, as well as the mass of the myocardium, noticeably decrease.

The transition from hypokinesia to a regimen of normal activity causes:

Pronounced increase in heart rate;

Increase in minute volume of blood flow - IOC;

Decrease in total peripheral resistance.

With the transition to intense muscular work, the functional reserves of the cardiovascular system decrease:

In response to muscular load, even of weak intensity, the heart rate rises rapidly;

Shifts in blood circulation are achieved due to the inclusion of less economical components;

At the same time, the IOC grows mainly due to an increase in heart rate.

In conditions of hypokinesia, the phase structure of the cardiac cycle changes:

The phase of blood expulsion and mechanical systole is reduced;

The duration of the phase of tension, isometric contraction and relaxation of the myocardium increases;

The initial rate of increase in intraventricular pressure decreases.

Myocardial hypodynamia. All of the above testifies to the development of the phase syndrome of "hypodynamia" of the myocardium. This syndrome, as a rule, is observed in a healthy person against the background of a reduced return of blood to the heart during light physical exertion.

ECG changes.With hypokinesia, electrocardiogram indices change, which are expressed in positional changes, relative slowdown of conduction, decrease in P and T waves, change in the ratio of T values in different leads, periodic displacement of the S-T segment, and change in the repolarization process. Hypokinesic changes in the electrocardiogram, regardless of the picture and severity, are always reversible.

Changes in the vascular system. With hypokinesia, a stable adaptation of the vascular system and regional blood flow to these conditions develops (Table 6-3).

Table 6-3.The main indicators of the cardiovascular system in humans under hypokinesia

Changes in the regulation of blood circulation. With hypokinesia, signs of the predominance of sympathetic influences over parasympathetic influences change the system of regulation of heart activity:

The high activity of the hormonal link of the sympathoadrenal system indicates the high stress potential of hypokinesia;

Increased excretion of catecholamines in the urine and their low content in tissues is realized by a violation of hormonal regulation of the activity of cell membranes, in particular, cardiomyocytes.

Thus, the decrease in the functional capabilities of the cardiovascular system during hypokinesia is determined by the duration of the latter and the degree of restriction of mobility.

BLOOD CIRCULATION IN OXYGEN INSUFFICIENCY

With increasing altitude, atmospheric pressure decreases and the partial pressure of oxygen (PO 2) decreases in proportion to the decrease in atmospheric pressure. The reaction of the body (primarily of the respiratory, circulatory and blood organs) to oxygen deficiency depends on its severity and duration.

For short-term reactions in high-altitude conditions, only a few hours are required, for initial adaptation - several days or even months, and the stage of stable adaptation of migrants takes years. The most effective adaptive reactions are manifested in the indigenous population of high mountainous regions due to long-term natural adaptation.

Initial adaptation period

The movement of a person (migration) from a flat area to the mountains is accompanied by a pronounced change in the hemodynamics of the large and small circle of blood circulation.

Tachycardia develops and the minute volume of blood flow (MCV) increases. Heart rate at an altitude of 6000 m for new arrivals in resting conditions reaches 120 per minute. Physical activity causes more pronounced tachycardia and an increase in IOC than at sea level.

The stroke volume changes insignificantly (both an increase and a decrease can be observed), but the linear blood flow velocity increases.

Systemic blood pressure in the first days of stay at altitudes slightly increases. The rise in systolic blood pressure is mainly caused by an increase in the IOC, and diastolic blood pressure is caused by an increase in peripheral vascular resistance.

BCC increases due to the mobilization of blood from the depot.

Excitation of the sympathetic nervous system is realized not only by tachycardia, but also by paradoxical dilatation of the veins of the systemic circulation, which leads to a decrease in venous pressure at altitudes of 3200 and 3600 m.

There is a redistribution of regional blood flow.

The blood supply to the brain increases due to the reduction of blood flow in the vessels of the skin, skeletal muscles and the digestive tract. The brain is one of the first to react

for oxygen deficiency. This is due to the special sensitivity of the cerebral cortex to hypoxia due to the use of a significant amount of O 2 for metabolic needs (a brain weighing 1400 g consumes about 20% of the oxygen consumed by the body).

In the first days of high-altitude adaptation, blood flow in the myocardium decreases.

The volume of blood in the lungs increases markedly. Primary high-altitude arterial hypertension- an increase in blood pressure in the vessels of the lungs. At the heart of the disease is an increase in the tone of small arteries and arterioles in response to hypoxia, usually pulmonary hypertension begins to develop at an altitude of 1600-2000 m above sea level, its value is directly proportional to the height and persists during the entire period of stay in the mountains.

An increase in pulmonary blood pressure during ascent to an altitude occurs immediately, reaching its maximum in a day. On the 10th and 30th days, pulmonary blood pressure gradually decreases, but does not reach the initial level.

The physiological role of pulmonary hypertension is to increase the volumetric perfusion of the pulmonary capillaries due to the inclusion of structural and functional reserves of the respiratory organs in gas exchange.

Inhalation of pure oxygen or a gas mixture enriched with oxygen at high altitude leads to a decrease in blood pressure in the pulmonary circulation.

Pulmonary hypertension in combination with an increase in IOC and central blood volume impose increased demands on the right ventricle of the heart. At high altitudes, when adaptive reactions are disrupted, altitude sickness or acute pulmonary edema can develop.

Altitude thresholds of effects

The effect of oxygen deficiency, depending on the altitude and the degree of extremeness of the terrain, can be divided into four zones (Fig. 6-3), delimited from each other by effective thresholds (Ruf S., Strughold H., 1957).

Neutral zone. Up to an altitude of 2000 m, the ability for physical and mental activity suffers little or no change.

Full compensation zone. At altitudes between 2000 and 4000 m, even at rest, the heart rate, cardiac output and rate of return increase. The increase in these indicators during operation at such heights occurs at a greater

degree than at sea level, so that both physical and mental performance are significantly reduced.

Incomplete compensation zone (danger zone). At altitudes from 4000 to 7000 m, an unadapted person develops various disorders. Upon reaching the threshold of violations (safety limit) at an altitude of 4000 m, physical performance decreases significantly, as well as the ability to react and make decisions. Muscle twitching occurs, blood pressure decreases, consciousness gradually clouded. These changes are reversible.

Rice. 6-3.Influence of oxygen deficiency during ascent to altitude: the numbers on the left are the partial pressure of O 2 in the alveolar air at the corresponding altitude; the numbers on the right - the oxygen content in gas mixtures, which gives the same effect at sea level

Critical zone. Starting from 7000 m and above, in the alveolar air it becomes below the critical threshold - 30-35 mm Hg. (4.0-4.7 kPa). Potentially lethal disorders of the central nervous system occur, accompanied by unconsciousness and seizures. These disturbances can be reversible with a rapid increase in the inhaled air. In the critical zone, the duration of oxygen deprivation is of decisive importance. If hypoxia continues for too long,

there are violations in the regulatory links of the central nervous system and death occurs.

Long stay in the highlands

With a long stay of a person in high altitude conditions at altitudes up to 5000 m, further adaptive changes in the cardiovascular system occur.

Heart rate, stroke volume and MVV stabilize and decrease to the initial values and even lower.

Severe hypertrophy of the right heart develops.

The density of blood capillaries in all organs and tissues increases.

BCC remains increased by 25-45% due to an increase in plasma volume and erythrocyte mass. In high-altitude conditions, erythropoiesis increases, therefore, the concentration of hemoglobin and the number of erythrocytes increase.

Natural adaptation of the highlanders

The dynamics of the main hemodynamic parameters among the aborigines of the highlands (highlanders) at an altitude of up to 5000 m remains the same as among the inhabitants of the lowlands at sea level. The main difference between “natural” and “acquired” adaptation to high-altitude hypoxia is the degree of tissue vascularization, microcirculation and tissue respiration. For permanent residents of the highlands, these parameters are more pronounced. Despite the reduced regional blood flow in the brain and heart in the aborigines of the highlands, the minute oxygen consumption by these organs remains the same as in the inhabitants of the plains at sea level.

BLOOD CIRCULATION WITH EXCESS OF OXYGEN

Long-term exposure to hyperoxia leads to the development of toxic effects of oxygen and a decrease in the reliability of the adaptive reactions of the cardiovascular system. Excess oxygen in tissues also leads to increased lipid peroxidation (LPO) and depletion of endogenous antioxidant reserves (in particular, fat-soluble vitamins) and the antioxidant enzymatic system. In this regard, the processes of catabolism and deenergization of cells are enhanced.

The heart rate decreases, the development of arrhythmias is possible.

With short-term hyperoxia (1-3 kg X sec / cm -2), the electrocardiographic characteristics do not go beyond the physiological norm, but after many hours of exposure to hyperoxia, the P wave disappears in some subjects, which indicates the appearance of an atrioventricular rhythm.

Blood flow in the brain, heart, liver and other organs and tissues is reduced by 12-20%. In the lungs, blood flow can decrease, increase and return to its original level.

Systemic blood pressure changes slightly. Diastolic blood pressure usually rises. Cardiac output is significantly reduced and total peripheral resistance is increased. The blood flow rate and BCC during breathing with a hyperoxic mixture are significantly reduced.

The pressure in the right ventricle of the heart and pulmonary artery with hyperoxia often decreases.

Bradycardia with hyperoxia is mainly due to increased vagal influences on the heart, as well as the direct action of oxygen on the myocardium.

The density of the functioning capillaries in the tissues decreases.

The vasoconstriction during hyperoxia is determined either by the direct action of oxygen on vascular smooth muscles, or indirectly through a change in the concentration of vasoactive substances.

Thus, if the human body responds to acute and chronic hypoxia with a complex and rather effective complex of adaptive reactions that form the mechanisms of long-term adaptation, then the body does not have effective means of protection for the action of acute and chronic hyperoxia.

CIRCULATION AT LOW EXTERNAL TEMPERATURES

There are at least four external factors that have a serious impact on human blood circulation in the Far North:

Sharp seasonal, inter- and intraday changes in atmospheric pressure;

Cold exposure;

A sharp change in photoperiodicity (polar day and polar night);

Fluctuations of the Earth's magnetic field.

The complex of climatic and ecological factors of high latitudes makes strict demands on the cardiovascular system. Adaptation to high latitude conditions is divided into three stages:

Adaptive voltage (up to 3-6 months);

Stabilization of functions (up to 3 years);

Adaptability (up to 3-15 years old).

Primary northern arterial pulmonary hypertension - the most characteristic adaptive reaction. An increase in blood pressure in the pulmonary circulation occurs at sea level under conditions of normal barometric pressure and O 2 content in the air. At the heart of such hypertension is the increased resistance of small arteries and arterioles of the lungs. Northern pulmonary hypertension is widespread among the newcomers and the indigenous population of the circumpolar regions and occurs in adaptive and maladaptive forms.

The adaptive form is asymptomatic, equalizes ventilation-perfusion relations and optimizes the oxygen regime of the body. The systolic pressure in the pulmonary artery with hypertension rises to 40 mm Hg, the total pulmonary resistance increases slightly.

Maladaptive form. Latent respiratory failure - "polar shortness of breath" develops, working capacity decreases. The systolic pressure in the pulmonary artery reaches 65 mm Hg, and the total pulmonary resistance exceeds 200 dynes. Xsek X cm -5. In this case, the trunk of the pulmonary artery expands, pronounced hypertrophy of the right ventricle of the heart develops, and simultaneously the stroke and minute volumes of the heart decrease.

BLOOD CIRCULATION UNDER EXPOSURE TO HIGH TEMPERATURES

Distinguish between adaptation in arid and humid zones.

Human adaptation in arid zones

Arid zones are characterized by high temperatures and low relative humidity. The temperature conditions in these zones during the hot season and during the daytime are such that the heat input into the body through insolation and contact with hot air can exceed the heat production in the body at rest by 10 times. Similar heat stress in the absence of

efficient heat transfer mechanisms quickly leads to overheating of the body.

The thermal states of the body under conditions of high external temperatures are classified as normothermia, compensated hyperthermia and uncompensated hyperthermia.

Hyperthermia- the borderline state of the organism, from which a transition to normothermia or death (heat death) is possible. The critical body temperature at which heat death occurs in humans corresponds to + 42-43? C.

The effect of high air temperature on a person who is not adapted to heat causes the following changes.

Expansion of peripheral vessels is the main reaction to heat in arid zones. Expansion of blood vessels, in turn, should be accompanied by an increase in the BCC; if this does not happen, then a drop in systemic blood pressure occurs.

The volume of circulating blood (BCC) in the first stages of heat exposure increases. With hyperthermia (due to evaporative heat transfer), the BCC decreases, which entails a decrease in central venous pressure.

Total peripheral vascular resistance. Initially (first phase), even with a slight increase in body temperature, systolic and diastolic blood pressure decreases. The main reason for the decrease in diastolic pressure is a decrease in the total peripheral vascular resistance. During heat stress, when the body temperature rises to + 38 ° C, the total peripheral vascular resistance decreases by 40-55%. This is due to dilatation of peripheral vessels, primarily the skin. A further increase in body temperature (second phase), on the contrary, may be accompanied by an increase in the total peripheral vascular resistance and diastolic pressure with a pronounced decrease in systolic pressure.

Heart rate (HR) increases, especially in less trained and poorly adapted people. In a person at rest at a high external temperature, the increase in the number of heart contractions can reach 50-80%. In well-adapted people, heat does not cause heart rate to rise until the heat stress becomes too severe.

Central venous pressure increases with increasing body temperature, but heat exposure can also cause the opposite effect - a transient decrease in the central blood volume and a persistent decrease in pressure in the right atrium. The variability of indicators of central venous pressure is due to the difference in the activity of the heart and BCC.

The minute volume of blood circulation (MVC) increases. The stroke volume of the heart remains normal or decreases slightly, which is observed more often. The work of the right and left ventricles of the heart when exposed to high external temperatures (especially with hyperthermia) increases significantly.

A high external temperature, which practically excludes all heat transfer pathways in humans, except for the evaporation of sweat, requires a significant increase in cutaneous blood flow. The growth of blood flow in the skin is provided mainly by an increase in the IOC and, to a lesser extent, by its regional redistribution: under heat load at rest in a person, blood flow in the celiac region, kidneys and skeletal muscles decreases, which "frees" up to 1 L of blood / min; the rest of the increased cutaneous blood flow (up to 6-7 liters of blood / min) is provided by cardiac output.

Intense sweating ultimately leads to dehydration of the body, thickening of the blood and a decrease in the BCC. This puts additional stress on the heart.

Adaptation of migrants in arid zones. Newly arrived migrants in arid zones of Central Asia, when doing hard physical work, have hyperthermia 3-4 times more often than indigenous people. By the end of the first month of staying in these conditions, the indicators of heat exchange and hemodynamics in migrants improve and approach those of local residents. By the end of the summer season, there is a relative stabilization of the functions of the cardiovascular system. Starting from the second year, the hemodynamic parameters of the migrants hardly differ from those of local residents.

Aboriginal arid zones. The aborigines of arid zones show seasonal fluctuations in hemodynamic parameters, but to a lesser extent than among migrants. The skin of the indigenous people is abundantly vascularized, has developed venous plexuses, in which blood moves 5-20 times slower than in the great veins.

The mucous membrane of the upper respiratory tract is also abundantly vascularized.

Human adaptation in humid zones

Human adaptation in humid zones (tropics), where - apart from elevated temperatures - high relative air humidity, proceeds similarly to arid zones. The tropics are characterized by a significant tension in the water and electrolyte balance. For permanent residents of the humid tropics, the difference between the temperatures of the "core" and "shell" of the body, hands and feet is greater than that of migrants from Europe, which contributes to better removal of heat from the body. In addition, the aborigines of the humid tropics have more perfect mechanisms for generating heat with sweat than those of visitors. In response to temperatures above + 27 ° C, aboriginal people start sweating faster and more intensely than migrants from other climatic and geographical regions. For example, the amount of sweat evaporated from the surface of the body among the Australian aborigines is twice that of the Europeans under identical conditions.

BLOOD CIRCULATION WITH ALTERED GRAVITATION

The gravitational factor has a constant effect on blood circulation, especially in low pressure areas, forming the hydrostatic component of blood pressure. Due to the low pressure in the pulmonary circulation, the blood flow in the lungs largely depends on the hydrostatic pressure, i.e. the gravitational effect of blood.

The model of the gravitational distribution of pulmonary blood flow is shown in Fig. 6-4. In an adult, in an upright position, the tops of the lungs are located about 15 cm above the base of the pulmonary artery, so the hydrostatic pressure in the upper parts of the lungs is approximately equal to the arterial pressure. In this regard, the capillaries of these sections are perfused insignificantly or not at all. In the lower parts of the lungs, on the contrary, the hydrostatic pressure is added to the arterial pressure, which leads to additional stretching of the vessels and their plethora.

These features of the hemodynamics of the small circle are accompanied by a significant uneven blood flow in various parts of the lungs. This unevenness significantly depends on the position of the body and is reflected in the indicators of regional saturation.

Rice. 6-4.A model linking the uneven distribution of pulmonary blood flow in an upright position of the human body with the magnitude of the pressure acting on the capillaries: in zone 1 (apex), the alveolar pressure (P A) exceeds the pressure in the arterioles (P a), and the blood flow is limited. In zone 2, where P a> P A, the blood flow is greater than in zone 1. In zone 3, the blood flow is increased and is determined by the difference in pressure in arterioles (P a) and pressure in venules (Py). In the center of the lung diagram are the pulmonary capillaries; vertical tubes on the sides of the lung - pressure gauges

blood oxygen. However, despite these features, in a healthy person, the saturation of the blood of the pulmonary veins with oxygen is 96-98%.

With the development of aviation, rocketry and manned space travel, changes in systemic hemodynamics under conditions of gravitational overloads and weightlessness acquire great importance. Changes in hemodynamics are determined by the type of gravitational loads: longitudinal (positive and negative) and transverse.

QUESTIONS FOR SELF-CONTROL

1. What types of work can be distinguished by heart rate changes?

2. What changes in the myocardium and regional blood circulation are observed during physical exertion?

3. What mechanisms are used to regulate blood circulation during physical exertion?

4. How does oxygen consumption change during physical activity?

5. What changes occur in the circulatory system during hypokinesia?

6. Name the types of hypoxia depending on the duration of action.

7. What changes in the circulatory system are observed during adaptation to high mountains?

The paper presents research materials to study the influence of environmental factors of the urban environment on the incidence of diseases of the circulatory system in the adult population of Kirov. The method of identifying the main components was used to determine 3 factors that explain 86% of the total variance of the variables. Among the factors identified, the main load (45% of the variance) falls on the factor of chemical pollution of atmospheric air and soil, which has a strong effect on both the general level of prevalence of diseases of the circulatory system (r = 0.84), and the levels of prevalence of certain nosological forms (diseases, characterized by high blood pressure - r = 0.91, cerebrovascular disease - r = 0.87, coronary heart disease - r = 0.73). Factors characterizing the quality of tap water (29% of dispersion), acoustic and electromagnetic loads (12% of dispersion) affect the average strength on the overall prevalence of circulatory system diseases (r = 0.51 and r = 0.56, respectively) and on the prevalence rates individual nosological forms (r = 0.52 - 0.65). With a detailed description of the multicomponent chemical pollution of atmospheric air in the studied urban area, the leading role in the formation of diseases of the circulatory system of the factor of technogenic chemical load associated with suspended solids, sulfur and nitrogen oxides (r = 0.70 - 0.78) was established.

urban environment

chemical pollution of atmospheric air and soil

drinking water quality

street noise

electromagnetic fields

adult population

incidence of diseases of the circulatory system

factor analysis

1. Vladimirov Yu.A. Free radicals and antioxidants / Yu.A. Vladimirov // Bulletin of the Russian Academy of Medical Sciences. - 1998. - No. 7. - P. 43–51.

2. Kushakovsky M.S. Metabolic heart disease. - SPb: Folio. –2000. - 127 p.

3. Lankin V.Z. Free radical processes in diseases of the cardiovascular system / V.Z. Lankin, A.K. Tihaze, Yu.N. Belenkov // Cardiology. - 2000. - No. 7. - P. 48–61.

4. Petrov S.B. Investigation of the biological action of fly ash in the composition of a dust and gas mixture / S.B. Petrov, B.A. Petrov, P.I. Tsapok, T.I. Sheshunova // Human Ecology. - 2009. - No. 12. - P. 13-16.

5. Petrov S.B. Medico-ecological aspects of the protection of atmospheric air in the areas of location of combined heat and power plants (monograph). - Kirov, 2010 .-- 222 p.

6. Petrov B.A. Research on the assessment of the influence of ecological factors of the urban environment on the health of the population / B.A. Petrov, I.S. Sennikov // Fundamental Research. - 2014. - No. 7. - Part 2. - P. 349–352.

7. Khalafyan A.A. Modern statistical methods of medical research / A.A. Khalafyan // Rostov-on-Don, 2008 .-- 320 p.

Diseases of the circulatory system (CVD) are one of the main medical and social problems in urbanized areas due to high morbidity, disability and mortality. Given the multifactorial nature of the formation and development of diseases of the circulatory system, an important aspect of risk assessment is to determine the structure of determinant factors, including environmental ones.

The purpose of this study was the study of the influence of ecological factors of the urban environment (chemical pollution of atmospheric air and soil, quality of drinking water, street noise, electromagnetic fields) on the incidence of diseases of the circulatory system in the adult population of Kirov.

The objectives of the study included hygienic zoning of the urban area according to the levels of intensity of environmental factors, statistical analysis with the establishment of cause-and-effect relationships in the system "environmental factors - the adult population - diseases of the circulatory system."

Materials and research methods

For the regionalization of the urban area according to the level of environmental factors impact, the calculation of such integral indicators as the coefficient of complex air pollution (K '), the coefficient of total chemical water pollution (Kvoda), the coefficient of total chemical soil pollution (Zс) was carried out. The criteria for assessing the acoustic mode were the multiplicity of excess of the actual noise levels from the value of the maximum permissible level (L Aeq), the electromagnetic load - the multiplicity of excess of the standard values of the field strength for the electric component (V / m) and the energy flux density (μW / cm2).

The morbidity of the adult population of BSC was studied by analyzing the data on the registration of all cases of seeking medical care in city health care institutions (f. No. 12). The collection of information was carried out in polyclinics serving the population of districts, ranked according to the levels of intensity of environmental factors.

To characterize the influence of environmental factors of the urban environment on the incidence of the population of BSC, factor analysis was applied by the method of isolating the main components, by "varimax" rotation with Kaiser normalization. The assessment of the strength, direction and statistical significance of the relationships between the studied indicators was carried out by the method of correlation analysis according to Pearson. Statistical processing of the research results was carried out using SPSS for Windows, version 18.

Research results and their discussion

As can be seen from those given in table. 1 of the data, when characterizing the ecological factors of the urban area by the method of isolating the main components, 3 factors were identified that explain 86% of the total variance of the variables - 45%, 29% and 12%, respectively.

The main load for factor No. 1 falls on the level of chemical pollution of atmospheric air and soil. These indicators are closely related to each other and can be presented as one factor characterizing the level of technogenic load of a chemical nature. This factor accounts for the largest percentage of variance (45%), and it strongly affects the level of prevalence of diseases of the circulatory system.

For factor 2, the main load falls on the level of chemical pollution of water, which makes it possible to represent it as a factor characterizing the quality of tap drinking water. This factor has a relatively low percentage of dispersion (29%) and has an average effect on the level of prevalence of diseases of the circulatory system.

Factor No. 3, which characterizes the level of technogenic load of physical nature (noise, EMF), accounts for the lowest percentage of dispersion (12%), and it has an average effect on the level of prevalence of diseases of the circulatory system.

Table 2 shows the characteristics of the relationship between factors and the incidence rate of diseases of the circulatory system for individual nosological forms.

Table 1

Factor loads on the selected components

Components

	% variance 45	% variance 29	% variance 12
General level of BSK
Ambient air quality
Technogenic soil pollution
Drinking water quality
Street noise
Electromagnetic fields

table 2

Influence of the selected factors on the prevalence of diseases of the circulatory system for individual nosological forms

< 0,05.

Table 3

The influence of chemical factor groups on the prevalence of diseases of the circulatory system

Note. * - the level of significance of the correlation coefficient p< 0,05.

As can be seen from this table, there is a statistically significant, direct correlation between the selected factors on the prevalence of all presented nosological forms of BSK, except for chronic rheumatic heart diseases. The greatest influence on the prevalence of BSC is exerted by factor No. 1, which has a strong correlation with diseases characterized by high blood pressure, cerebrovascular diseases, and an association of moderate strength with coronary heart disease.

The levels of statistical significance of the correlation coefficients indicate the combined influence of the selected factors on the formation of diseases of the circulatory system among the adult urban population.

Thus, the results of factor analysis indicate the dominant influence of the factor of anthropogenic chemical load on the formation of BSC.

With a detailed description of the multicomponent airborne industrial pollution of the urban area under study, the method of isolating the main components identified 3 factors that explain 81% of the total variance of the variables - 55%, 17% and 9%, respectively. With factor No. 1, the concentration in the atmospheric air of suspended solids, sulfur and nitrogen oxides has the greatest correlation, with factor No. 2 - the concentration of aromatic hydrocarbons, with factor No. 3 - the concentration of phenol.

Table 3 shows the characteristics of the relationships between the identified chemical factor groups and the incidence rates of CDS for individual nosological forms.

As can be seen from this table, the leading role in the formation of BSC belongs to factor No. 1 (strong, direct correlation) associated with suspended solids, sulfur and nitrogen oxides. With regard to diseases characterized by high blood pressure, there is a combined effect of factors No. 1 and No. 2, however, with factor No. 2, there is a relationship of average strength. Probably, one of the reasons for the dominant influence of these factors is the pronounced ability of suspended solids to adsorb toxic gaseous compounds with the formation of dust and gas compositions.

The role of dust and gas compositions in the development of pathological processes is confirmed by the results of our experimental studies. Thus, the biological effect of the main air pollutant in the study area of fly ash from solid fuel combined heat and power plants in the composition of a dust-gas mixture with prolonged chronic exposure in low doses is characterized, along with a resorptive-toxic effect, an intensive generation and accumulation of reactive oxygen species, an increase in the content of lipoperoxides, a decrease in antioxidant activity. systems and the formation of immunopathological processes. Pathomorphological changes in the heart of experimental animals poisoned with a dust-gas mixture were manifested by the development of inflammatory processes and dystrophic changes in the myocardium. The mechanisms of these pathological processes are associated, first of all, with the influence of an excess amount of free radicals on the development of inflammatory processes in the myocardium, mitochondrial hypoxia and an increase in energy deficit in cardiomyocytes, which leads to dystrophic changes in the myocardium. Lipid peroxidation products can change the barrier properties of cell membranes, cause vasoconstriction of arterioles and an increase in total peripheral resistance.

Reviewers:

Nemtsov BF, Doctor of Medical Sciences, Professor, Head of the Department of Hospital Therapy of the Kirov State Medical Academy, Kirov;

Spitsin A.P., Doctor of Medical Sciences, Professor, Head of the Department of Pathological Physiology of the Kirov State Medical Academy, Kirov.

Bibliographic reference

Petrov S.B., Sennikov I.S., Petrov B.A. THE INFLUENCE OF ECOLOGICAL FACTORS OF THE URBAN ENVIRONMENT ON THE INCIDENCE OF DISEASES OF THE BLOOD CIRCULATION SYSTEM // Fundamental research. - 2015. - No. 1-5. - S. 1025-1028;
URL: http://fundamental-research.ru/ru/article/view?id=37509 (date accessed: 10/01/2020). We bring to your attention the journals published by the "Academy of Natural Sciences"

UDC 574.2: 616.1

ECOLOGY AND CARDIOVASCULAR DISEASES

E. D. Bazdyrev and O. L. Barbarash

Research Institute of Complex Issues 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, alcohol and drug use, diet, working conditions, physical inactivity, material and living conditions, marital status, etc.), by 18-22% - by genetic and biological factors, by 17-20% - by the state of the environment (natural and climatic factors, the quality of environmental objects) and only by 8-10% - by the level of health care development (timeliness and quality of medical care, efficiency preventive measures).

The high rates of urbanization observed in recent years with a decrease in the rural population, a significant increase in mobile sources of pollution (vehicles), the inadequacy of treatment facilities at many industrial enterprises with the requirements of sanitary and hygienic standards, etc., clearly identified the problem of the impact of ecology on the health of the population.

Clean air is essential for human health and well-being. Air pollution continues to be 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 polluting agents, and there are hundreds of them in the city, as a rule, exceeds the maximum permissible level, and their combined effect turns out to be even more significant.

Air pollution is the cause of increased mortality and, consequently, a reduction in life expectancy. Thus, according to the WHO European Office, 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 Foundation for Social and Hygienic Monitoring, in Russia in the period from 2006 to 2010, the leading air pollutants exceeding hygiene 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, is the cause of increased mortality and, in turn, a factor in reducing life expectancy. It is generally accepted that the influence of the environment, namely the pollution of the atmospheric basin by air pollutants, is the main cause of the development of diseases of the respiratory system. However, the impact on the body of various pollutants is not limited to changes in the bronchopulmonary system. In recent years, studies have appeared that prove the relationship 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 relationship of various diseases of the cardiovascular system with exposure to 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 tendency towards a reduction in the share of atmospheric air samples exceeding the hygienic standards of the average for the Russian Federation, this share 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 basin by air pollutants, is the cause of the development of mainly diseases of the respiratory system, since most of all pollutants enter the body mainly through the respiratory system. It has been proven that the effect of air pollutants on the respiratory organs 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, nitrogen oxides cause bronchoconstriction, hyperreactivity of the bronchi due to the release of neuropeptides from C-fibers and the development of neurogenic inflammation. It has been established that the average and maximum concentrations of nitrogen dioxide and the maximum concentration of sulfur dioxide contribute to the development of bronchial asthma.

However, the impact on the body of various pollutants is not limited 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 the adult population has a significant correlation between the level of atmospheric air pollution with formaldehyde and diseases of the endocrine system, the content of gasoline in the air and the general morbidity. including diseases of the digestive system.

In the last decade, there have been convincing data on the adverse effects of air pollutants on the cardiovascular system (CVS). The first reports on the relationship of chemical pollutants with one of the significant risk factors for cardiovascular diseases (CVD) - atherogenic dyslipidemias - were published in the 1980s. The reason for the search for associations was an even earlier study that showed an almost 2-fold increase in mortality from coronary heart disease (IHD) in men with more than 10 years of experience exposed to carbon disulfide at work.

BM Stolbunov and co-authors found that in persons living near chemical enterprises, the incidence rate of the circulatory system was 2-4 times higher. A number of studies have examined the effect of chemical pollutants on the likelihood of not only

chronic, but also acute forms of ischemic heart disease. Thus, A. Sergeev et al. 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 frequency of hospitalizations of persons not exposed to organic pollutants. In another study, it was found that the highest degree of "chemical contamination" of the body with toxic elements was observed in patients with MI who had worked for more than 10 years in contact with industrial xenobiotics.

During a five-year medical and environmental monitoring in the Khanty-Mansiysk Autonomous Okrug, a relationship was shown between the frequency of CVD spread and the level of air pollutants. So, the researchers drew a parallel between the frequency of hospitalizations for angina pectoris and an increase in the average monthly concentration of carbon monoxide and phenol. In addition, increased levels of phenol and formaldehyde in the atmosphere 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, the minimum monthly mean concentrations of carbon monoxide and phenol.

Published in 2012, the results of studies carried out by A. R. Hampel et al and R. Devlin et al. Showed an acute effect of ozone on impaired myocardial repolarization according to ECG data. A study in London illustrated that an increase in the amount of pollutants in the atmosphere, especially with a sulfite component in patients with an implanted cardioverter-defibrillator, led to an increase in the number 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 be the cause of death in patients with CVD, as well as the cause of hospitalization for frolicking MI and decompensation of heart failure. Similar data obtained in a study conducted in California and in a twelve-year follow-up in China showed that prolonged exposure to dust particles, nitric oxide was not only a risk of coronary heart disease, stroke, but also a predictor of cardiovascular and cerebrovascular mortality.

A striking example of the relationship between CVD mortality and the level of air pollutants was the result of an analysis of the mortality structure of the Moscow population during the abnormal 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 mgk / m3 and 800 mgk / m3, respectively. At the same time, suspended particles with a diameter of more than 10 microns prevailed in the air. The concentration of particles with a diameter of 2.0-2.5 microns was especially high on June 29. When comparing the dynamics of mortality with indicators of air pollution, there was a complete coincidence of the peaks in the number of deaths with an increase in the concentration of particles with a diameter of 10 microns.

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

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

According to a number of experimental studies, the pathological relationship 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 atherosclerosis of the arteries. For example, a study in Belgium showed that in nonsmoking patients with diabetes, every 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 immune-inflammatory reaction that triggers the proliferation of smooth muscle cells, muscular-elastic hyperplasia of the intima and fibrous plaque, mainly in small and medium-sized vessels. These vascular changes are called arteriosclerosis, emphasizing that the root cause of the disorders is sclerosis, and not lipid accumulation.

In addition, a number of xenobiotics cause lability of the vascular tone and initiate thrombosis. A similar conclusion was reached by scientists from Denmark, who showed that an increase in the level of suspended particles in the atmosphere is 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 ecological disadvantage 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 the products of peroxidation are responsible for the initiation of damage to the genome of vascular endothelial cells, which underlies the development of the cardiovascular continuum.

A study in Los Angeles and Germany has shown that prolonged exposure to dust particles is associated with thickening of the intima / media complex as a sign of subclinical atherosclerosis and increased blood pressure.

Currently, there are publications indicating a link between genetic predisposition, inflammation, on the one hand, and cardiovascular risk, on the other. Thus, a high polymorphism of glutathione S-transferases, which accumulate when exposed to pollutants or smoking, increases the risk of a decrease in lung function during life, the development of dyspnea and inflammation. Developed pulmonary oxidative stress and inflammation induce 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 there have been new data on the relationship of laboratory markers of inflammation with an unfavorable prognosis both in healthy individuals and in patients with CVD.

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

The fact of inflammation is assigned the main role in the development of atherosclerosis as one of the leading causes of the development of ischemic heart disease. It was found that MI is 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 leukocytes.

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

interleukins-1p, 6, 8, as well as tumor necrosis factor alpha, and pro-inflammatory 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. S. 86-90.

2. Askarova ZF, Askarov RA, Chuenkova GA, Bai-kina IM Assessment of the influence of polluted atmospheric air on the incidence of the population in an industrial city with developed petrochemistry // Healthcare of the Russian Federation. 2012. No. 3. S. 44-47.

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

4. Zayratyants O. V., Chernyaev A. L., Polyanko N. I., Osadchaya V. V., Trusov A. E. The structure of mortality of the Moscow population from circulatory and respiratory diseases during the abnormal summer of 2010 // Pulmonology ... 2011. No. 4. S. 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, S- reactive protein and markers of thrombopenia in patients with stable angina pectoris and restenosis after percutaneous coronary interventions // Cardiology. 2004. No. 11. S. 4-12.

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

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

8. Karpin VA Medical and ecological monitoring of diseases of the cardiovascular system in the urbanized North // Cardiology. 2003. No. 1. S. 51-54.

9. Koroleva OS, Zateishchikov DA Biomarkers in cardiology: registration of intravascular inflammation // Farmateka. 2007. No. 8/9. S. 30-36.

10. Kudrin AV, Gromova OA Trace elements in neurology. M.: GEOTAR-Media, 2006.304 p.

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

12. Onishchenko GG About the sanitary and epidemiological state of the environment // Hygiene and sanitation. 2013. No. 2. S. 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 [Kit]: a national guide with an appendix on CD / ed. A.G. Chu-chalina. M.: GEOTAR-Media, 2009.957 p.

15. Revich BA, Maleev VV Climate change and health of the population of Russia: Analysis of the situation. M.: LENAD, 201 1.208 p.

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

17. Unguryanu TN, Lazareva NK, Gudkov AB, Bu-zinov RV Assessment of the tension of the medical and ecological situation in the industrial cities of the Arkhangelsk region // Human Ecology. 2006. No. 2. S. 7-10.

18. Unguryanu T.N., Novikov S.M., Buzinov R.V., Gudkov A. B. Risk for public health from chemicals that pollute the atmospheric air in a city with a developed pulp and paper industry // Hygiene and sanitation ... 2010. No. 4. S. 21-24.

19. Khripach LV, Revazova Yu. A., Rakhmanin Yu. A. Role of free radical oxidation in genome damage by environmental factors // Bulletin of the Russian Academy of Medical Sciences. 2004. No. 3. S. 16-18.

20. Shoikhet Ya. N., Korenovskiy Yu. V., Motin AV, Lepilov NV The role of matrix metalloproteinases in inflammatory lung diseases // Problems of clinical medicine. 2008. No. 3. S. 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. P. 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. P. 553-563.

23. Bauer M., Moebus S., Mohlenkamp S., Dragano N., Nonnemacher M., Fuchsluger M., Kessler C., Jakobs H., Memmesheimer M., Erbel R., Jockel KH, 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. P. 1803-1808.

24. Brook RD, Rajagopalan S., Pope CA 3rd., Brook JR, Bhatnagar A., Diez-Roux AV, Holguin F., Hong Y., Luepker RV, Mittleman MA, Peters A., Siscovick D., Smith SC Jr., Whitsel L., Kaufman JD 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. P. 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. P. 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. P. 2555-2660.

27. Engstrom G., Lind P., Hedblad B., Stavenow L., Janzon L., Lindgarde F. Effects of cholesterol and inflammation-sensitive plasma proteins on 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, Erbel R., Hoffmann B. Long-term urban particulate air pollution , traffic noise, and arterial blood pressure // Environ. Health Perspect. 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. 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 repolarisation 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 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 MJ, Ostro BD, Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith DF, Garcia C., Chang ET, Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort // Am. J. Respir. 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 Perspect. 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 Urbanized Region With Developed Chemical Industry. Kardiologija. 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. Gigiena i sanitarija. 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 OA, Panchenko EP, Samko AN, Dobrovol "skij AB, Levickij IV, Masenko VP, Titaeva EV Matrix Metalloproteinases, C-Reactive Protein, and Markers of Thrombinemia in Patients With Stable Angina and Restenoses After Percutaneous Coronary Interventions. Kardi 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 conception. Arhiv Patologii. 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. Kardiologija. 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. Gigiena i sanitarija. 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 environment 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. Gigiena i sanitarija. 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 klinicheskoy meditsiny. 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.

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.

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

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

28. Lind PM, Orberg J., Edlund UB, 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 Perspect. 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.

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.

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 MJ, Ostro BD, Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith DF, Garcia C., Chang ET, Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort. Am. J. Respir. 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 Perspect. 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 YL, 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 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 relation between levels and types of atmospheric air pollution and diseases of the digestive and endocrine systems. Earnest data about 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 of the Department of Multifocal Atherosclerosis of the Federal State Budgetary Institution "Research Institute for Complex Issues 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 health care of the Russian Federation

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

2.2.5. Influence of environmental factors on the prevalence of some diseases

A large number of scientific studies are devoted to the study of the relationship between environmental factors and various types of diseases, a huge number of articles and monographs have been published. We will try to give a very short analysis of only the main lines of research on this problem.

When analyzing the causal relationships between health indicators and the state of the environment, researchers, first of all, pay attention to the dependences of health indicators on the state of individual components of the environment: air, water, soil, food, etc. 2.13 provides an indicative list of environmental factors and their influence on the development of various pathologies.

As you can see, air pollution is considered one of the main causes of diseases of the circulatory system, congenital anomalies and pathologies of pregnancy, neoplasms of the mouth, nasopharynx, upper respiratory tract, trachea, bronchi, lungs and other respiratory organs, neoplasms of the genitourinary system.

Among the causes of these diseases, air pollution is in the first place. Air pollution ranks second, third and fourth among the causes of other diseases.

Table 2.13

Indicative list of environmental factors in connection with their

possible impact on prevalence

some classes and groups of diseases

	Pathology
	Diseases of the circulatory system	1. Air pollution with sulfur oxides, carbon monoxide, nitrogen oxides, phenol, benzene, ammonia, sulfur compounds, hydrogen sulfide, ethylene, propylene, butylene, fatty acids, mercury, etc. 3. Housing conditions 4. Electromagnetic fields 5. Composition of drinking water: nitrates, chlorides, nitrites, water hardness 6. Biogeochemical features of the area: lack or excess of calcium, magnesium, vanadium, cadmium, zinc, lithium, chromium, manganese, cobalt, barium, copper, strontium, iron in the environment 7. Environmental pollution with pesticides and pesticides 8. Natural and climatic conditions: speed of weather change, humidity, barometric pressure, insolation level, wind strength and direction
	Diseases of the skin and subcutaneous tissue	1. Insolation level 3. Air pollution
	Diseases of the nervous system and sense organs. Mental disorders	1. Natural and climatic conditions: the speed of weather change, humidity, barometric pressure, temperature factor 2. Biogeochemical features: high mineralization of soil and water 3. Housing conditions 4. Air pollution with sulfur oxides, carbon monoxide, nitrogen oxides, chromium, hydrogen sulfide, silicon dioxide, formaldehyde, mercury, etc. 6. Electromagnetic fields 7. Organochlorine, organophosphorus and other pesticides
	Respiratory diseases	1. Natural and climatic conditions: the speed of changing weather, humidity 2. Housing conditions 3. Air pollution: dust, sulfur oxides, nitrogen oxides, carbon monoxide, sulfur dioxide, phenol, ammonia, hydrocarbon, silicon dioxide, chlorine, acrolein, photooxidants, mercury, etc. 4. Organochlorine, organophosphorus and other pesticides
	Diseases of the digestive system	1. Environmental pollution with pesticides and pesticides 2. Lack or excess of trace elements in the external environment 3. Housing conditions 4. Pollution of atmospheric air with carbon disulfide, hydrogen sulfide, dust, nitrogen oxides, chlorine, phenol, silicon dioxide, fluorine, etc. 6. Composition of drinking water, water hardness

Continuation of table. 2.13

	Diseases of the blood and blood-forming organs	1. Biogeochemical features: lack or excess of chromium, cobalt, rare earth metals in the environment 2. Air pollution with sulfur oxides, carbon monoxide, nitrogen oxides, hydrocarbons, hydrazoic acid, ethylene, propylene, amylene, hydrogen sulfide, etc. 3. Electromagnetic fields 4. Nitrite and nitrate in drinking water 5. Environmental pollution with pesticides and pesticides.
	Congenital anomalies	4. Electromagnetic fields
	Endocrine system diseases, eating disorders, metabolic disorders	1. Insolation level 2. Excess or deficiency of lead, iodine, boron, calcium, vanadium, bromine, chromium, manganese, cobalt, zinc, lithium, copper, barium, strontium, iron, urochrome, molybdenum in the external environment 3. Air pollution 5. Electromagnetic fields 6. Hardness of drinking water
	Diseases of the genitourinary organs	1. Lack or excess of zinc, lead, iodine, calcium, manganese, cobalt, copper, iron in the environment 2. Pollution of atmospheric air with carbon disulfide, carbon dioxide, hydrocarbon, hydrogen sulfide, ethylene, sulfur oxide, butylene, amylene, carbon monoxide 3. Hardness of drinking water
	Including: pathology of pregnancy	1. Air pollution 2. Electromagnetic fields 3. Environmental pollution with pesticides and pesticides 4. Lack or excess of trace elements in the external environment
	Neoplasms of the mouth, nasopharynx, upper respiratory tract, trachea, bronchi, lungs and other respiratory organs	1. Air pollution 2. Humidity, insolation level, temperature factor, number of days with dry winds and dust storms, barometric pressure

Continuation of table. 2.13

Neoplasms of the esophagus, stomach and other digestive organs

1. Environmental pollution with pesticides and pesticides

2. Air pollution with carcinogenic substances, acrolein and other photooxidants (nitrogen oxides, ozone, surfactants, formaldehyde, free radicals, organic peroxides, fine aerosols).

3. Biogeochemical features of the area: lack or excess of magnesium, manganese, cobalt, zinc, rare earth metals, copper, high soil mineralization

4. Composition of drinking water: chlorides, sulfates. Hardness of water

Neoplasms of the genitourinary organs

1. Pollution of atmospheric air with carbon disulfide, carbon dioxide, hydrocarbon, hydrogen sulfide, ethylene, butylene, amylene, sulfur oxides, carbon monoxide

2. Pollution of the environment with pesticides

3. Lack or excess of magnesium, manganese, zinc, cobalt, molybdenum, copper in the environment

4. Chlorides in drinking water

The second in the degree of influence on the incidence due to environmental reasons in most cases can be considered a lack or excess of microelements in the external environment. For neoplasms of the esophagus, stomach and other digestive organs, this is manifested in the biogeochemical features of the area: lack or excess of magnesium, manganese, cobalt, zinc, rare earth metals, copper, high soil mineralization. For diseases of the endocrine system, eating disorders, metabolic disorders - this is an excess or lack of lead, iodine, boron, calcium, vanadium, bromine, chromium, manganese, cobalt, zinc, lithium, copper, barium, strontium, iron, urochrome, molybdenum in external environment, etc.

Table data. 2.13 show that cancer-causing chemicals, dust, and mineral fibers tend to act selectively to target specific organs. Most cancers caused by chemicals, dust, and mineral fibers are apparently related to occupational activities. However, as shown by risk studies, the population living in areas affected by hazardous chemical industries (for example, in the city of Chapayevsk) is also exposed. Increased levels of cancer have been identified in these areas. Arsenic and its compounds, as well as dioxins, affect the entire population due to their high prevalence. Household habits and food products naturally affect the entire population.

The work of many Russian and foreign scientists is devoted to the study of the possibility of the intake of toxic substances simultaneously in several ways and their complex effect on the health of the population (Avaliani S.L., 1995; Vinokur I.L., Gildenskiold R.S., Ershova T.N., etc. ., 1996; Gildenskiold R.S., Korolev A.A., Suvorov G.A. et al., 1996; Kasyanenko A.A., Zhuravleva E.A., Platonov A.G. et al., 2001; Ott WR, 1985).

One of the most dangerous chemical compounds are persistent organic pollutants (POPs), which enter the environment during the production of chlorine-containing substances, incineration of household and medical waste, and the use of pesticides. These substances include eight pesticides (DDT, aldrin, dieldrin, endrin, heptachlor, chlordane, toxaphene, mirex), polychlorinated biphenyls (PCBs) dioxins, furans, hexachlorobenzene (Revich BA, 2001). These substances pose a danger to human health, regardless of the ways in which they enter the body. Table 2.14 shows the characteristics of the effects of the listed eight pesticides and polychlorinated biphenyls.

As you can see, these substances also affect reproductive functions, and are the cause of cancer, lead to disorders of the nervous and immune systems and other equally dangerous effects.

Table 2.14

Health effects of POPs (short list): empirical findings

(Revich B.A., 2001)

Substances	Impact
	Reproductive damage in wildlife, especially egg shell thinning in birds
	DDE, a metabolite of DCT, may be associated with breast cancer (M.S, Wolff, P.G. Toniolo, 1995), but the results are ambiguous (N. Krieger et al., 1994; D.J. Hunter et al., 1997)
	High doses lead to disorders of the nervous system (convulsions, tremors, muscle weakness) (R. Carson, 1962)
Aldrin, Deel Drin, Endrin	These substances have a similar effect, but endrin is the most toxic of them.
	Associated with suppression of the immune system (T. Colborn, C. Clement, 1992)
	Nervous system disorders (convulsions), effects on liver function at high exposure levels (R. Carson, 1962)
Aldrin, Deel Drin, Endrin	Dieldrin - effects on reproductive function and behavior (S. Wiktelius, C.A. Edwards, 1997)
	Possible human carcinogen; in high concentrations, probably contributes to the occurrence of breast tumors (K. Nomata et al., 1996)
Heptachlor	Effects on progesterone and estrogen levels in laboratory rats (J.A. Oduma et al., 1995)
Heptachlor	Disorders of the nervous system and liver function (EPA, 1990)
Hexachloroben- ash (HCB)
	Affects DNA in human liver cells (R. Canonero et al., 1997)
	Changes in the function of white blood cells during industrial exposure (M.L. Queirox et al., 1997)
	Changes in steroid formation (W.G. Foster et al., 1995)
	High exposure levels have been associated with porphyrinuria. metabolic liver disease (I.M. Rietjens et al., 1997)
	Thyroid enlargement, scarring and arthritis occur in the offspring of accidentally exposed women (T. Colborn, C. Clement, 1992)
	Probable human carcinogen
	Causes suppression of the immune system (T. Colborn, C. Clement, 1992)
	Shows fetal toxicity in rats, including cataract formation (WHO, Environmental Health Criteria 44: Mirex, 1984)
	Liver hypertrophy due to long-term low dose exposure in rats (WHO, 1984)

Continuation of table 2.14

Polychlorinated dibenzo p- dioxins - PCDDs and polychlorinated dibenzofurans - PCDF	Toxic effects on development, endocrine, immune system; human reproductive function
	2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDC) is a human carcinogen (IARC, 1997)
	Developmental and immune system toxicity in animals, especially rodents (A. Schecter, 1994)
	Changes in hormone levels - estrogen, progesterone, testosterone and thyroid - in some individuals; decrease in serum testosterone levels in exposed people (A. Schecter, 1994)
	Interferes with the action of estrogen in some individuals; decrease in fertility, brood size and uterine weight in mice, rats, primates (A. Schecter, 1994)
	Chloracne as a response to a high dose due to cutaneous or systemic exposure (A. Schecter, 1994)
	Acneform rash due to skin contact (N.A. Tilson et al., 1990)
	Estrogenic effects on wildlife (J.M. Bergeron et al., 1994)
Toxaphene	Potentially human carcinogen, causing reproductive and developmental disorders in mammals
Toxaphene	Shows estrogenic activity (S.F. Arnold et al., 1997)
Polychlorinated biphenyls - PCBs	Impact on the fetus, which results in changes in the nervous system and development of the child, a decrease in his psychomotor functions, short-term memory and cognitive functions, long-term effects on intelligence (N.A. Tilson et al. 1990; Jacobson et al., 1990; JL Jacobson, SW Jacobson, 1996)

In the XX century, for the first time, environmental diseases arose, i.e., diseases, the occurrence of which is associated only with the effect of specific chemicals (Table 2.15). Among them, the most famous and well-studied diseases associated with exposure to mercury - Minamata disease; cadmium - Itai-Itai disease; arsenic - "black foot"; polychlorinated biphenyls - Yu-Sho and Yu-Cheng (Revich B.A., 2001).

Table 2.15

Pollutants and Environmental Diseases of the Population

Contaminants	Environmental diseases
Arsenic in food and water	Skin cancer - the province of Cordoba (Argentina), "black foot" - the island of Taiwan. Chile
Methylmercury in water, fish	Minamata disease. 1956, Niigata, 1968 -Japan
Methylmercury in food	Deaths - 495 people, poisoning - 6,500 people - Iraq, 1961
Cadmium in water and rice	Itai-Itai Disease - Japan, 1946
Rice contamination with PCB oil	Yu-Sho disease - Japan, 1968; Yu-Cheng disease - Taiwan Island, 1978-1979

When studying cancers of the population associated with exposure to various chemicals, it is useful to know which substances are recognized as responsible for the disease of certain organs (Table 2.16).

Table 2.16

Proven carcinogens to humans (IARC group 1)

(V. Khudoley, 1999;Revich B.A., 2001)

	Factor name		Target Organs		Population group
1. Chemical compounds
	4-Aminobiphenyl		Bladder
	Benzidine		Bladder
			Hematopoietic system
	Beryllium and its compounds
	Bis (chloromethyl) ether and technical chloromethyl ether
	Vinyl chloride		Liver, blood vessels (brain, lungs, lymphatic system)
	Mustard gas (sulfur mustard gas)		Pharynx, larynx, lungs
	Cadmium and its compounds		Lungs, prostate gland
	Coal pitches		Skin, lungs, bladder (larynx, oral cavity)
	Coal tar		Skin, lungs (bladder)
	Mineral oils (unrefined)		Skin (lungs, bladder)
	Arsenic and its compounds		Lungs, skin		General population groups
	2-Naphthylamine		Bladder (lungs)
	Nickel and its compounds		Nasal cavity, lungs
	Shale oils		Skin (gastrointestinal tract)
	Dioxins		Lungs (subcutaneous tissue, lymphatic system)		Workers, general population groups
	Chromium hexavalent		Lungs (nasal cavity)
	Ethylene oxide		Hematopoietic and lymphatic systems
2. Household habits
		Alcoholic drinks		Pharynx, esophagus, liver, larynx, oral cavity (mammary gland)		General population groups
		Chewing betel nut with tobacco		Oral cavity, pharynx, esophagus		General population groups
		Tobacco (smoking, tobacco smoke)		Lungs, bladder, esophagus, larynx, pancreas		General population groups
		Tobacco products, smokeless		Oral cavity, pharynx, esophagus		General population groups
3. Dust and mineral fibers
			Lungs, pleura, peritoneum (gastrointestinal tract, larynx)
	Wood dust		Nasal cavity and paranasal sinuses
	Crystalline silicon
			Skin, lungs

			Pleura, peritoneum

Continuation of table 2.16

A number of pollutants and ionizing radiation have a negative impact on reproductive health - see table. 2.17 - (Revich B.A., 2001).

Table 2.17

Contaminants and Reproductive Health Disorders

(Priority Health Conditions, 1993;T... Aldrich, J. Griffith, 1993)

Substance	Violations
Ionizing radiation	Infertility, microcephaly, chromosomal abnormalities, cancer in children
	Menstrual irregularities, spontaneous abortion, blindness, deafness, mental retardation
	Infertility, spontaneous abortion, congenital malformations, low birth weight, sperm disorders
	Low birth weight
Manganese	Infertility
	Spontaneous abortion, weight loss in newborns, congenital malformations
Polyaromatic hydrocarbons (PAHs)	Decreased fertility
Dibromochloropropane	Infertility, sperm changes
	Spontaneous abortion, low birth weight, congenital malformations, infertility
1,2-dibromo-3-chloro-propane	Semen disorders, sterility
	Congenital malformations (eyes, ears, mouth), disorders of the central nervous system, perinatal mortality

Dichlorethylene	Congenital malformations (heart)
Dieldrin	Spontaneous abortion, premature birth
Hexachlorocyclohexane	Hormonal disorders, spontaneous abortion, premature birth
	Spontaneous abortion, low birth weight, menstrual irregularities, ovarian atrophy
Carbon disulfide	Menstrual irregularities, spermatogenesis disorders
Organic solvents	Congenital malformations, cancer in children
Anesthetics	Infertility, spontaneous abortion, low birth weight, tumors in the embryo

Since 1995, Russia has begun to implement a methodology for assessing the health risks of the population caused by environmental pollution, developed by the United States Environmental Protection Agency (USA EPA). In a number of cities (Perm, Volgograd, Voronezh, Novgorod Veliky, Volgograd, Novokuznetsk, Krasnouralsk, Angarsk, Nizhniy Tagil), with the support of the Agency for International Development and the US Environmental Protection Agency, projects were carried out to assess and manage the public health risk caused by pollution air and drinking water (Risk Management, 1999; Risk Methodology, 1997). The great merit in carrying out these studies, organizing work and introducing scientific results belongs to the outstanding Russian scientists G.G. Onishchenko, S.L. Avaliani, K.A. Bushtueva, Yu.A. Rachmanin, S.M. Novikov, A.V. Kiselev and others.

Test questions and tasks

1. Analyze and characterize environmental factors for various diseases (see table. 2.13).

2. What diseases are caused by exposure to persistent organic pollutants?

3. List the most famous diseases that appeared in the twentieth century, the impact of which substances were they caused and in what way were they manifested?

4. What substances are classified as proven carcinogens and diseases of which human organs do they cause?

5. What substances cause reproductive health problems?

6. Analyze and characterize the influence of environmental factors on various types of pathologies in accordance with table 2.14.