Влияние загрязнения почвы тяжелыми металлами на возникновение заболеваний нервной системы.

Полный текст

1. Introduction

Human economic and industrial activity has led to an ecological crisis, an important manifestation of which is the negative impact on the health of the population [1]. There is an acute environmental and global public health issue in many countries related to the pollution of the ecosystem with toxic metals, according to current data provided by S.A. Bhat et al. [2]. Therefore, anthropogenic changes in the biosphere lead to the primary issue of maintaining health and increasing human life expectancy in today’s realities [3]. Understanding the aetiological causes and patterns of the pathological effects of chemical soil pollution with heavy metals on human health makes it possible to prevent possible negative processes that cause specific syndromes and diseases in the body.

The main anthropogenic pollutants of the environment and soil are heavy metals, poisoning with which ranks third after pesticide and nitrate poisoning, as indicated in the work by X. Shen et al. [4]. Anthropogenic reasons for the accumulation of heavy metals include metallurgical and energy production, transport pollution, corrosion of technical structures, mining, and inefficient waste disposal [5]. Heavy metals enter the environment mainly through dust and its deposits on the soil and leaves, that is, in the form of dry deposits. In Kazakhstan, the Turkestan region, especially the Shymkent region, is considered to be a zone of increased pollution due to active industrial activity, which was studied by A. Baibotaeva et al. [6]. According to current research by K.A. Nurlybaeva et al., the quality of the soil in the Karaganda region is also unsatisfactory in terms of the presence of heavy metals [7].

The presence of heavy metals in the soil has a dual meaning: as trace elements, they are necessary for the course of physiological processes in the biosphere, but at the same time, they are toxic at elevated concentrations, which negatively affects the health of humans and animals [8]. Heavy metal molecules accumulate at all levels of the ecological pyramid, which exacerbates the issue of their influence on the body and the urgency of identifying their aetiological interactions, especially in terms of the ability to accumulate and long-term effects. Despite the natural presence of heavy metals in the earth’s crust and soil, the anthropogenic activity of modern realities, according to Z. Rahman and V.P. Singh, for example, mining, electroplating, smelting, household and allied industries lead to abundant environmental pollution and human exposure to toxic metals [9]. Each of the types of heavy metals has its own characteristics of the effect on the body, but according to the studies of M. Zaynab et al., in conditions of high concentration they have a toxic effect on the gastrointestinal tract, cardiovascular, endocrine, nervous and reproductive systems [10].

Initially, heavy metals, when released from contaminated soil into the human body, accumulate in tissues and organs, and gradually reaching a certain threshold level in the body, they initiate pathological disorders: changes in the activity of enzyme systems, metabolic processes, immunological reactions, disruption of the activity of the main organocomplexes [11]. At the next stage of influence on the body, symptoms of a specific disease appear, unfolding into the clinical picture of the disease. Recent research W. Ahmad et al. revealed that the oxidative breakdown of biological macronutrients is associated with the binding of heavy metals to cellular components in the form of structural proteins, enzymes and nucleic acids, and then with the pathology of their functioning [12].

Chronic exposure to heavy metals shows severe consequences, such as carcinogenic induction of cell metaplasia, negative effects on the cardiovascular, central and peripheral nervous system [13]. Since the nervous system regulates the somatic and vegetative innervation of all internal organs, and is also responsible for the control and conscious functions of the physical and psychoemotional sphere, studying its tendency to the negative chronic influence of the soil is of paramount importance. Violation of the organs and structures of the central nervous system (CNS) leads to a complex disruption of the endocrine, autonomic, metabolic and other areas of the body. Considering the acute environmental problem of soil pollution with heavy metals and their diverse negative impact on human health, the purpose of this work was to conduct a comprehensive analysis of the latest scientific data on the effect of heavy metals on the human nervous system.

 

2. Materials and Methods

In order to analyse modern scientific data on the relationship of soil contamination with heavy metals, as well as their influence on possible complications in the work of organs and structures of the central and peripheral nervous system, a systematic analysis of scientific publications in the fields of ecology, geology, neurology, laboratory diagnostics, epidemiology, internal and social medicine. For the selection of data for the purpose of subsequent analysis and consecration, a number of publications were selected that were published by relevant and reliable periodicals with a high impact factor. The database of processed articles, statistical data, clinical recommendations and literature reviews was based on the principle of using advanced and evidence-based data that reflect the results of long-term studies and observations of various cases from practical medicine: for patients with chronic forms of complications as a result of heavy metal poisoning, with pathologies of the central or peripheral nervous systems due to chronic exposure to heavy metals, and patients with industrial exposure to heavy metals (metal exposure as an occupational hazard). The studies that were used for scientific analysis concerned both representatives of Kazakhstan and European and African countries to compare the actual prevalence of the influence of anthropogenic factors of soil pollution with heavy metals in different ethnic and geographical groups. The latest meta-analyses are also included, which covered large cohorts of patients in the projection from 3 to 5 years of follow-up with different options for complicating the functionality of the nervous system to analyse the features of chronicity or clearance of heavy metal accumulation processes in the body.

To study scientific data, the work includes medical publications for the period from 2019 to 2024 in specialized and relevant publications. Reliable search engines and resources such as Ebsco, Google Scholar, ResearchGate, PubMed, Medscape, and Clarivate were used to find relevant papers. In most cases, material from open databases of relevant scientific data was used. During the work, the identification of the researcher-author of the work was carried out, that is, an authorized entry and search on academic search platforms were used. Identified work with scientific databases allows excluding duplication of the results of the same scientists, related works, outdated data and quickly check the citation and impact factor of the work and the publication itself. In addition to filtering the robot by publication date, a number of keywords were also used during the search. This approach helped to exclude robots that dealt with the influence of other elements of contaminated soil, or other target organs and body systems that are not related to the problem of this work, and also excluded scientific works that dealt with short-term medical observations. In addition to scientific articles, the work includes an analysis of the latest recommendations of the WHO and world associations in the field of prevention of the anthropogenic impact of hazardous elements on the human nervous system, a recommendation regarding the early detection, diagnosis, and prevention of heavy metal accumulation. Part of the work is devoted to the introduction of these recommendations into the practice of screening and epidemiological services in Kazakhstan.

 

3. Results and Discussion

Since various agricultural, household, medical, industrial and technological sectors have led to a wide accumulation of heavy metals in the biosphere, the critical question of their pathological accumulation and impact on the state of various human organ systems arises. It was revealed that the manifestation of high toxicity of heavy metals in the body depends on a number of factors, both on the part of the source of pollution and on the part of the patient’s anamnestic data. [14]. These factors include the chemical composition of the compound, its dose, the duration of exposure, the route of exposure, and the actual amount of accumulated metal. [15]. On the part of the patient, important factors that will determine the severity and sensitivity of pathological manifestations include age, gender, genetic predisposition, state and nutritional value, the work of biorhythms, the presence of toxic working conditions and background diseases. Heavy metals include lead, tin, arsenic, arsenic, cadmium, mercury, which are widely used in daily industrial activities. According to recent studies, cadmium, chromium, lead, and mercury are considered priority metals that are common in contaminated soil and pose a direct threat to the human nervous system due to their proven toxicity [16]. This issue is a public health problem not only in Kazakhstan, but also in other countries of the world with developed industry [6, 7]. The toxicity of these heavy metal compounds is measured by systemic toxicants to determine the degree of impact on the victim and assess possible damage to organ systems.

According to S.C. Alvarez et al., heavy metal compounds do not undergo metabolic changes in body tissues, which leads to their direct accumulation in the course of chronic exposure, that is, bioaccumulation as a result of transdermal or parenteral intake into the body due to soil contamination [17]. According to L. Chen et al., the toxicity of heavy metals and their ions is also associated with their solubility in aqueous solutions [18]. Entering the body from contaminated soil with water, heavy metals interact with a number of enzymes circulating in the blood, inhibiting their activity and functioning, which can lead to death. Therefore, even minimal amounts of them can lead to quite severe physiological consequences. In addition to intensive bioaccumulation, heavy metals are characterized by the absence of biodegradation, that is, they cannot be destroyed, neutralized or removed from the body in full [19]. The effect of bioaccumulation of heavy metals in the tissues of the victim is aggravated in cases of ingestion of animal products that have also been exposed to and accumulate heavy metals in contaminated soil. As a result of such a scenario, at the top of the food pyramid, the excess concentration of metals can increase by 100,000 times compared to the concentration of this metal in the soil, leading not only to pathologies of the nervous system, but also to carcinogenesis [20].

 

3.1. Cadmium

Cadmium is used in various types of household batteries, plastic products, industrial pigments, metal structures, and is widely used in electroplating, as referred to by M. Wang et al. [21]. Coal and mineral solutions in soils also contain cadmium. In the latest recommendations of the International Agency for Research on Cancer and the World Health Organization, cadmium compounds are classified as a group of carcinogens of the first degree [22]. Fertilizers are the main source of soil contamination with cadmium: it is introduced into the composition of plants consumed by humans. An additional source of cadmium in the soil is combustion products, especially as a result of large forest fires. The content of cadmium in wood ash varies from 2 to 32 mg per kg; in straw ash – more than 9 mg per kg [23]. Since the ash has mainly alkaline properties, the cadmium present in its composition is insoluble in water and does not penetrate well into plants. But, according to the studies of M. Rizwan et al., cadmium is able to accumulate in the soil, and in the case of fermentation becomes available for absorption by plants [24]. In the human body, cadmium is capable of gradual accumulation. Also, cadmium, together with zinc, often penetrates into seawater through a network of surface and ground soils. Although there are reports of J. Wu et al. on the reduction of cadmium emissions into the soil in various industrialized countries, it is still a source of carcinogenic effects for workers in agriculture and metallurgy, as well as for people living in areas with soil contaminated with cadmium [25].

For a long time, the effect of cadmium on the human body was limited to studies of its accumulation in the nephrons of the kidneys, namely, in the epithelial cells of the proximal tubules and in the bone tissue, which was manifested by pathological changes in the homeostasis of the mineralization of lamellar bone tissue [26]. Modern scientific works carried out on large cohorts of patients show statistically significant effects of cadmium on the nervous tissue in the central and peripheral structures of the nervous system, one of these is the work of R. Zhou et al. [27]. Firstly, these are studies with an evidence-based process of cadmium accumulation in brain tissues, which is also associated with a violation of the blood-brain barrier (BBB) during the bioaccumulation of cadmium compounds in soft tissues. The pathology of the BBB during chronic accumulation of cadmium is pathophysiologically associated with a violation of the oxidative-antioxidant homeostasis of the capillary system of the CNS, which leads to the development of oxidative stress [28]. In contrast to chronic exposure, acute cadmium intoxication shows its maximum concentrations in the structures of the nervous system not surrounded by the BBB, namely the epiphysis and meninges, as referred to by J.J.V. Branca et al. [29]. The degree of BBB resistance to the penetration of cadmium and its compounds also depends on the patient’s medical history, namely his age, comorbidities, and alcohol and smoking abuse [30].

The concentration of cadmium, according to current statistics in residents of developed countries with a developed industrial infrastructure, varies from 0.005 to 7.01 µg/L in blood and from 0.04 to 14 µg/g in urine [31]. The pathophysiology of the neurotoxic effect of cadmium includes the initiation of tissue oxidative stress (with a predominance of oxidants), which affects the activity of enzymes critical for the functioning of neurons and the homeostasis of intercellular interactions inside the brain, affecting the cell cycle and the processes of programmed death of neurons and neuroglia [32, 33]. Cadmium in nervous tissue acts as an initiator of neuronal cell cycle completion by blocking the proliferation of protoplasmic and fibrocytic astrocytes, causing apoptosis and necrosis of multipolar brain neurons, according to J.J. Branca et al. [34]. The effect on the cell cycle is confirmed by altered intracellular levels of calcium ions, increased secretion of reactive oxygen species, increased caspase immunoreactivity, and increased expression of apoptotic factors. Recent studies by Y. Ge et al. show that cadmium is able to disrupt the formation of the neuronal cytoskeleton by inhibiting the expression of proteins for the assembly and organization of cytoplasmic neurofilaments, which are marker organelles for the special purpose of neurons [35].

During cadmium-induced oxidative stress, elevated levels of malondialdehyde, nitric oxide, and oxidized glutathione are detected. Another mechanism of the neurotoxic effects of cadmium is explained by the effect of its compounds on the activity of calcium adenosine triphosphatase and calcium magnesium adenosine triphosphatase [36]. The consequences of this deactivation are displayed in a decrease in the level of calcium ions, which takes part in the synaptic communication connection of all types of synapses in the CNS. Thus, the effect of cadmium on the nervous tissue is manifested by various mechanisms that disrupt the cell cycle, intracellular metabolism, which is reflected in premature degenerative processes.

 

3.2. Lead

Diseases associated with the aetiological factor of lead accumulation are called saturnism. A feature of the effect of lead on body tissues is its ability to form colloidal solutions in circulating blood and acidic gastric juice. As U. Zulfiqar et al., lead and plumbum lead compounds, getting into the biofluids of the body, remain and accumulate in it by more than 83% [37]. The use of alcohol, certain pharmacological drugs, a history of past infectious diseases can contribute to its clearance, and lead can again create colloidal solutions. Lead is a highly toxic heavy metal with cumulative properties, affecting mainly the human nervous system, as well as the musculoskeletal and urinary apparatus [38]. In fruits and vegetables contaminated with lead, the metal content can increase more than ten times compared to the natural level of uncontaminated soil. Lead is present in small amounts in almost all plant crops, but its concentration is especially high when these crops are grown on lead-contaminated soils. According to scientific data, high concentrations of lead in cereal grains, legumes, and other food products are highly toxic to humans and also negatively impact field crop yields. Lead itself worsens the physicochemical parameters of the soil and the organization of the microbial environment of the soil [39]. The primary target organs for household exposure or lead poisoning are the organs of the gastrointestinal tract and the nervous system, as A. Apte et al. [40]. From the point of view of the effect on the central nervous system, lead has a pronounced neurotoxicity, which is manifested by a violation of the neurophysiological function and is symptomatically detected in the form of mental disorders and neurocognitive syndromes [39].

It has been proven that children’s bodies are more susceptible to the neurotoxic effects of lead and its compounds than adults. A study by V.I. Naranjo et al. on paediatric patients, showed that children are still exposed to lead, despite the widespread awareness of the community and health systems in different countries and its high toxicity [41]. The authors show that even for children with lead levels in circulating blood below the toxic threshold, specific therapy should be carried out to prevent the development of negative consequences for the CNS. The N-methyl-D-aspartate receptor is involved in the maturation of brain neurocytes and the plasticity of their work, which occurs in human prenatal development during the first three months of embryonic development. Lead inhibits this receptor and leads to the interruption of long-term potentiation of learned skills and memory abilities. Also, lead is able to penetrate the BBB of the brain, inhibiting the activity of endotheliocytes in the BBB system. The histocytological effects of lead disrupt the normal processes of development of the nervous system, both in the prenatal period of development and in childhood. These disorders include disruption of signalling growth and differentiation factors during proliferation and differentiation of CNS multipolar neurons, impaired formation of synaptic connections mediated by reduced production of sialic acid by neurocytes; violations of the chronological sequence of differentiation of glial cells. Pharmacological effects of lead poisoning are manifested in the form of lead replacement for calcium and the initiation of disturbances in cascades involving calmodulin [42]. Lead also blocks the secretion of neurotransmitters from the presynaptic membrane into the synaptic cleft, disrupting the GABAergic, dopaminergic, and cholinergic systems of the CNS. Inside the cytoplasm, lead blocks the excretion of calcium ions both from the cytoplasmic contents of the cell and directly from mitochondria, which leads to the accumulation of reactive oxygen species, activation of mitochondrial lysis and, accordingly, the initiation of programmed processes of apoptosis or necrosis.

 

3.3. Mercury

Mercury is present in almost all human foods and ranges from <1 to 50 µg per kg of body weight, and may be higher in marine products [43]. This metal is present in soil and water contaminated with heavy metals, and can be converted to methylmercury by microorganisms. Methylmercury and mercuric chloride are evidence-based highly carcinogenic factors, as H. Kim et al. [44]. Mercury is easily absorbed by enterocytes when mercury-contaminated food is consumed, and almost 100% of ingested mercury is deposited and not excreted from the cells after ingestion. The nervous system is sensitive to all types of mercury, because it has a high neurotoxicity. Consumed mercury first forms complexes with sulfhydryl groups of blood plasma proteins and tissues, and then it can be transported through cell plasma membranes to target organs. More than 12% of the mass of mercury that has entered the body settles in the brain tissues, less – in the hepatocytes of the liver and epithelial cells of the nephrons of the kidneys. The classic symptoms of organic mercury poisoning according to L. Yang et al. include depressive disorder, headache, limb tremors, memory problems; disorders of the gastrointestinal tract (diarrhoea, nausea), the appearance of a skin rash, weakness, and high blood pressure [43]. Anthropogenic activities directly or indirectly pollute the soil with three types of mercury: elemental, inorganic and organic [45].

Methylmercury is extremely toxic to most tissues of the body and easily penetrates three-dimensional cell membranes, which has been proven by many studies, including the work of L.C. Abbott and F. Nigussie [46]. Mercury toxicity at the biochemical level is manifested by blocking the work of sulfhydryl-containing enzymes of cellular metabolism, increased circulation of reactive oxygen species, oxidative stress, and disruption of the intracellular functioning of calcium ions. The latter is similar to the action of lead inside the cells of target organs. Since intracellular calcium ions perform many important functions for both synapse transmission and neuronal function, disturbance of intracellular calcium levels has been shown to be the main mechanism explaining mercury neurotoxicity. These changes include inhibition by cells of the ability to use calcium from intracellular stores, a violation of the physical properties of calcium to penetrate through specific transmembrane channels of the plasma membrane, and a change in the processes of protein phosphorylation. Oxidative stress due to mercury poisoning can affect the viability of nervous system cells directly or indirectly through disturbances in intracellular calcium homeostasis.

Due to the high similarity of methylmercury to thiol groups in body cells, methylmercury intoxication during prenatal differentiation of neuroblasts during late neurulation leads to aberrant migration of stem cells and disorganization of the emerging brain neocortex. According to the scientific theory published in the work of S. Yawei et al. [47] and S.T. Zulaikhah et al. [48], but which has not been studied in humans, methylmercury disrupts the genetic sequences that control the normal process of neurulation in the first trimester of pregnancy, altering cellular signalling factors for neuroblastic migration, leading to dysplasia and abnormal cortical cytoarchitectonics and myeloarchitectonics. Among these signalling pathways, the Notch receptor is distinguished, which is sensitive to the effects of mercury even at threshold concentrations, which has been proven in experimental animals [49]. The work of J.G. Dórea shows that the neurotoxicity of methylmercury is associated with blocking the polymerization of cytoplasmic microtubules, which in turn inhibits cell migration and their cell cycle with division, since the formation of the mitotic spindle division is impossible [50].

 

3.4. Chromium

Chromium occurs in the biosphere in various oxidation states, but it is trivalent and hexavalent chromium that is toxic to the human body, as M. Pavesi and J.C. Moreira point out [51]. Chromium pollution occurs during the combustion of oil and coal, pigment oxidizers, household fertilizers, chromium steel, and drilling of oil wells. The effect of chromium on the human body depends on the volume of the dose, the route of exposure and the duration of contact. Chromium compounds can act directly at the site of contact (this is especially true for the skin) or can be transported and accumulated in other tissues. Hexavalent chromium is today a global environmental pathogen that increases the risk of carcinogenesis and pathologies of the nervous system due to neurotoxicity [52]. Some scientific works have shown a violation of the olfactory function during industrial, chronic exposure to chromium; the risk of developing motor neuron disease in complex poisoning with heavy metals, including chromium, leading to death; the development of schizophrenia, especially those with a psychiatric history, as referred to by J. Ma et al. [53]. The authors point out that high levels of chromium in the initial stages of schizophrenia may exacerbate serotonin synthesis, contributing to disease burden [54].

Trivalent chromium circulates in soil organic matter and in the form of oxides, hydroxides and sulphates, according to the work of T. Pavesi and J.C. Moreira [51]. As indicated by H. Hossini et al. chromium workers, as a social group at high risk of complications due to chromium exposure, in studies show symptoms of regular headaches, systemic dizziness and weakness, no information was found on neurological effects [55]. There is evidence of acute neurological complications in people with acute chromium poisoning after ingestion of more than 8 mg of the metal in the form of potassium dichromate. Complications included cerebral oedema and necrotic lesions, which resulted in death. Thus, contaminated soil poses a number of threats to human health, based on the spectrum of heavy metals, which exceed the threshold norms. Given the wide range of routes of heavy metals from contaminated soil into the human body and the increasing number of industrial and agricultural sources of soil contamination with metals, this problem remains relevant for the health care system of the developed countries of the world. A summary of the main features of heavy metals that have been discussed above are presented in tabl. 1 for the purpose of basic diagnostic differentiation of their effects on the human nervous system.

Table 1. Differentiated comparison of the main manifestations of soil heavy metals on the human nervous system

 

Characteristics of manifestation	Cadmium	Lead	Mercury	Chromium
Influence on the development of the nervous system prenatally	Possible	Proven	Proven	Possible
Impact on the children’s body	Possible	Proven	Proven	Possible
Breach of the blood-brain barrier	Present	Present	Present	Not typical
Psychiatric disorders in metal poisoning	Present	Present	Not typical	Not typical
Disruption of synaptic transmission	Not typical	Characteristically	Characteristically	Characteristically
Neurological symptoms	Present	Present	Present	Present

 

Source: compiled by the authors.

 

Despite some common features in the pathophysiological effects of heavy metals on the human nervous system, in particular the development of oxidative stress in the hemocirculation system and neuroglia, disruption of calcium-dependent mechanisms in intracellular metabolism, and blocking of synaptic transmission in the system of multipolar CNS neurons, there are also specific features of a particular soil heavy metal type, given its valency and the compounds it forms. Further research on this issue should include the study of specific regions with soil contaminated with heavy metals, the identification of patient groups vulnerable to metal intoxication, and the diagnosis of background conditions that can cause complicated course options.

 

4. Conclusions

Detailed studies of the chain of influence, pathogenetic cascades of involvement of heavy metals in the development of pathologies of the nervous system are important for the development of appropriate preventive and protective measures for their chronic effects on the human body. Early exposure to toxic metal compounds can have negative neurological consequences for the development of the fetus and children. The pathological effect of cadmium on the nervous system is carried out through the initiation of oxidative stress with subsequent accumulation in structures that do not have a blood-brain barrier (pineal gland, brain membranes). In acute cadmium intoxication, the blood-brain barrier is permeable to cadmium compounds, which allows it to accumulate in the neuroglia of the brain. Currently, the understanding of the high neurotoxicity of mercury is explained by its effect on cell cycle disruption (including mitosis), blocking the expression of neural differentiation genes, inhibition of cell signalling pathways during neurulation, impaired protein phosphorylation and calcium ion homeostasis, and impaired neuroblast migration prenatally. Chromium enters the air, water and soil as a result of biological processes and anthropological activities. Humans can be pathologically exposed to chromium from contaminated soil through food, drink, and skin contact with solutions or solids, or chromium compounds. Chromium exhibits pronounced carcinogenic effects under chronic exposure, including chromosomal aberrations and mutagenic effects due to the breakdown of the genetic material of target cells. The pathophysiological effects of heavy metals on the cells and neuroglia of the human nervous system have common properties, which include the development of oxidative stress in the hemocirculation system and neurocytes, the blocking of calcium-dependent mechanisms in intracellular metabolism, and the disruption of synaptic transmission in the system of multipolar neurons. However, each of them has specific features that help to conduct a differentiated diagnosis. Primary prevention and identification of high-risk social groups are reasonable and cost-effective measures to combat the problem of the impact of soil contaminated with heavy metals on critical organs and structures of the nervous system at the public health level.

ADDITIONAL INFORMATION

Funding source. This research was funded by the Science Committee of the Ministry of Science and Higher Education of the Republic of Kazakhstan (Grant No. AP19677517).

Competing interests. The authors declare that they have no competing interests.

Author contribution. All authors confirm that their authorship meets the international ICMJE criteria (all authors have made a significant contribution to the development of the concept, research and preparation of the article, read and approved the final version before publication). G. Batyrova —literature review, collection and analysis of literary sources, writing the text and editing the article; G. Umarova  — literature review, collection and analysis of literary sources, preparation and writing of the text of the article; S. Urazayeva—collection and analysis of literary sources, preparation and writing of the text of the article; A. Issaldinova  — literature review, collection and analysis of literary sources, writing the text and editing the article; U.  Sarsembin, G. Taskozhina, Zh. Issanguzhina, Ye. Umarov — literature review, collection and analysis of literary sources, writing the text and editing the article.

Об авторах

Гульнара Арыстангалиевна Батырова

Западно-Казахстанский медицинский университет имени Марата Оспанова

Автор, ответственный за переписку.
Email: batyrovagulnara77@gmail.com
ORCID iD: 0000-0001-7970-4059
SPIN-код: 8584-5024

PhD, руководитель кафедры клинической лабораторной  диагностики

Казахстан, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан;

Гульмира Умарова

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: uga_80@mail.ru
ORCID iD: 0000-0001-7637-113X
SPIN-код: 9146-3959

PhD, Доцент кафедры Доказательной медицины и научного менеджмента

Россия, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан

Салтанат Уразаева

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: s.urazaeva@mail.ru
ORCID iD: 0000-0002-4773-0807

Candidate of medical sciences,

Head of Department of epidemiology

Казахстан, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан

Умбетали Cарсембин

Актюбинский региональный университет имени К. Жубанова

Email: umbetali_s.k@mail.ru
ORCID iD: 0000-0002-0796-3737

PhD, Senior lecturer. Department of Ecology

Казахстан, 030000, 34, пр. А.Молдагуловой, г.Актобе, Казахстан

Асель Исалдинова

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: aselisaldinova@gmail.com
ORCID iD: 0000-0003-4843-5823

Master of  "Medical and Preventive Care"

Казахстан, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан

Гулайм Таскожина

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: g.taskozhina@zkmu.kz
ORCID iD: 0000-0003-3922-0054

PhD student

Казахстан, West Kazakhstan Marat Ospanov Medical University

Жамиля Исангужина

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: gamilia0452@gmail.com
ORCID iD: 0000-0002-7557-8486

Кандидат медицинских наук, доцент кафедры Детские болезни №2

Казахстан, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан

Ескендир Умаров

Западно-Казахстанский медицинский университет имени Марата Оспанова

Email: eskendir.um@gmail.com
ORCID iD: 0000-0002-5661-4023

магистр естественных наук

Казахстан, 030019 ул.Маресьева, дом 68, г.Актобе, Казахстан

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