Post-exposure Period Research Articles

The role of organic matrices in the fate of hydrophobic pesticides: An outdoor stream mesocosm study

To assess potential aquatic pesticide risks, environmental monitoring strategies often focus on water and sediment. However, knowledge gaps with regard to the pollution status of organic matrices important for the structure and functioning of aquatic ecosystems do exist. The present study assessed the dissipation of the triazole fungicide tebuconazole (TEB; KOW = 5.01 × 103) and the pyrethroid insecticide etofenprox (ETO; KOW = 7.94 × 106) as model hydrophobic pesticide compounds among aquatic plants, vertical layers of allochthonous leaf litter, and detritus within flow-through outdoor stream mesocosms. During a 3-h pesticide exposure and a subsequent 24-h post-exposure period, retention was higher for ETO (max concentration: Myriophyllum spicatum > Elodea nuttallii > Ranunculus fluitans > Potamogeton perfoliatus ≫ leaf litter > detritus) and depended amongst other factors on surface area, while in the water compartment the pesticides reached concentration levels < LOQ 2 h after exposure. Desorption was observed for both pesticides in plants, and for TEB in detritus, while in leaves the ETO levels even increased over time, suggesting leaf litter to be a suitable additional sampling matrix for transient hydrophobic pesticide peaks, yet also a potential source of contamination for invertebrate shredders. The upper layer of leaf material contained higher ETO levels than those situated further in the sediment, which implies short-term positive effects for species inhabiting the deeper leaf layers, yet again pinpoints to a potential pesticide exposure pathway via organic matter in aquatic systems.

Health care personnel exposure to a patient with asymptomatic SARS-CoV2 infection during a prolonged surgical intervention

There is ongoing debate regarding the role of aerosols in the transmission of SARS-CoV2 in the health care environment. Here, we report a case in which multiple operating room health care providers were exposed to a patient with asymptomatic SARS-CoV2 infection during a prolonged orthopedic surgical intervention and had no evidence of COVID-19 during the 14-day post-exposure period.

Features of the early diagnosis of respiratory diseases in interns of chemical industries

In the conditions of increasing retirement age and active longevity, it is especially important to maintain health of older workers employed in hazardous industries. Physiological changes occur in the body, including respiratory system, with aging, they are modified under conditions of exposure to chemicals and in the post-exposure period. Incidence rate of temporary disability in the Perm Krai amounted to 45.0 cases per 100 employees. The average regional indicator was exceeded more than twice in chemical enterprises; respiratory diseases predominated in the structure of causes of temporary disability both in the number of cases and the number of days of disability, with an average duration of one case of the disease of 8.3 days. The proportion of diseases caused by industrial aerosols and chemical factors amounted to 25% in 2017 (Russian Federation 2017 - 22.35%), in 2018 - 30%. Share of respiratory diseases in the structure of nosological forms of occupational diseases has increased over the past 10 years, in 2018 it occupied the second place with 25%.

Appearance of Alveolar Macrophage Subpopulations in Correlation With Histopathological Effects in Short-Term Inhalation Studies With Biopersistent (Nano)Materials.

Following inhalation and deposition in the alveolar region at sufficient dose, biopersistent (nano)materials generally provoke pulmonary inflammation. Alveolar macrophages (AMs) are mediators of pulmonary immune responses and were broadly categorized in pro-inflammatory M1 and anti-inflammatory M2 macrophages. This study aimed at identifying AM phenotype as M1 or M2 upon short-term inhalation exposure to different (nano)materials followed by a postexposure period. Phenotyping of AM was retrospectively performed using immunohistochemistry. M1 (CD68+iNOS+) and M2 (CD68+CD206+ and CD68+ArgI+) AMs were characterized in formalin-fixed, paraffin-embedded lung tissue of rats exposed for 6 hours/day for 5 days to air, 100 mg/m3 nano-TiO2, 25 mg/m3 nano-CeO2, 32 mg/m3 multiwalled carbon nanotubes, or 100 mg/m3 micron-sized quartz. During acute inflammation, relative numbers of M1 AMs were markedly increased, whereas relative numbers of M2 were generally decreased compared to control. Following an exposure-free period, changes in iNOS or CD206 expression correlated with persistence, regression, or progression of inflammation, suggesting a role of M1/M2 AMs in the pathogenesis of pulmonary inflammation. However, no clear correlation of AM subpopulations with qualitatively distinct histopathological findings caused by different (nano)materials was found. A more detailed understanding of the processes underlaying these morphological changes is needed to identify biomarkers for different histopathological outcomes.

Mode of silver clearance following 28-day inhalation exposure to silver nanoparticles determined from lung burden assessment including post-exposure observation periods.

Recently revised OECD inhalation toxicity testing guidelines require measurements of lung burden immediately after and for periods following exposure for nanomaterials. Lung burden is a function of pulmonary deposition and retention of nanoparticles. Using lung burden studies as per OECD guidelines, it may be possible to assess clearance mechanisms of nanoparticles. In this study, male rats were exposed to silver nanoparticle (AgNP) aerosols (18.1-19.6nm) generated from a spark generator. Exposure groups consisted of (1) control (fresh air), (2) low (31.2 ± 8.5µg/m3), (3) moderate (81.8 ± 11.4µg/m3), and (4) high concentrations (115.6 ± 30.5µg/m3). Rats were exposed for 6-h/day, 5-days/week for 4weeks (28-days) based on the revised OECD test guideline 412. Bronchoalveolar lavage (BAL) fluids were collected on post-exposure observation (PEO)-1 and PEO-7days and analyzed for inflammatory cells and inflammatory biomarkers. The lung burdens of Ag from AgNPs were measured on PEO-1, PEO-7, and PEO-28days to obtain quantitative mass concentrations per lung. Differential counting of blood cells and inflammatory biomarkers in BAL fluid and histopathological evaluation of lung tissue indicated that exposure to the high concentrations of AgNP aerosol induced inflammation at PEO-1, slowly resolved at PEO-7 and completely resolved at PEO-28days. Lung burden measurement suggested that Ag from AgNPs was cleared through two different modes; fast and slow clearance. The fast clearance component was concentration-dependent with half-times ranging from two to four days and clearance rates of 0.35-0.17/day-1 from low to high concentrations. The slow clearance had half-times of 100, 57, and 76days and clearance rates of 0.009, 0.012, and 0.007/day-1 for the high, moderate and low concentration exposure. The exact mechanism of clearance is not known currently. The fast clearance component which was concentration-dependent could be dependent on the dissolution of AgNPs and the slow clearance would be due to slow clearance of the low dissolution AgNPs secondary particles originating from silver ions reacting with biogenic anions. These secondary AgNPs might be cleared by mechanisms other than dissolution such as mucociliary escalation, translocation to the lymphatic system or other organs.

In Vitro Acaricidal Activity of Selected Medicinal Plants Traditionally Used against Ticks in Eastern Ethiopia.

A study was carried out to evaluate the acaricidal activities of crude methanolic extract of leaves of six medicinal plants, namely, Vernonia amygdalina, Calpurnia aurea, Schinus molle, Ricinus communis, Croton macrostachyus, and Nicotiana tabacum, against Rhipicephalus (Boophilus) decoloratus and Rhipicephalus pulchellus using an in vitro adult immersion test. Five graded concentrations of the crude extracts, 6.25, 12.5, 25, 50, and 100 mg/ml, were tested at different time intervals, and temporal changes in tick viability were recorded for 24 hours. Diazinon (0.1%) and distilled water were used as positive and negative controls, respectively. Standard procedures were applied to screen the phytochemical constituents of the tested plant parts. Phytochemical screening showed the presence of a condensed amount of tannins in all extracts. Starting from 30 min post exposure, the 100 mg/ml concentration of C. aurea and R. communis extracts has caused significantly higher mortality (P < 0.05) compared to the diazinon. A significant increase in tick mortality started 2 hr post exposure with diazinon and 50 and 100 mg/ml concentrations of S. molle. Vernonia amygdalina extract and diazinon showed a significant increase in tick mortality 3 hr post exposure with 100 mg/ml concentration. Similarly, a significant increase in tick mortality started 2 hr post exposure with diazinon and 100 mg/ml concentrations of C. macrostachyus and N. tabacum. At 24 hr post exposure, diazinon and 50 and 100 mg/ml concentrations of all the extracts have caused significantly higher tick mortality than the rest of the concentrations (P < 0.05). Higher concentrations of all the extracts had showed a comparable and strong acaricidal effect on Rhipicephalus (Boophilus) decoloratus and Rhipicephalus pulchellus having no significant difference with that of the positive control (P > 0.05) at 24 hr post exposure period. Tick killing activity of all evaluated plant extracts increases with increasing exposure time and concentration as well. Thus, all the tested plants could be used against Rhipicephalus (Boophilus) decoloratus and Rhipicephalus pulchellus as a potential alternative to substitute commercially available drugs. We recommend further study on fractionating each component separately and validating the materials.

Progression of chronic wasting disease in white-tailed deer analyzed by serial biopsy RT-QuIC and immunohistochemistry.

Chronic wasting disease (CWD) continues to spread or be recognized in the United States, Canada, and Europe. CWD is diagnosed by demonstration of the causative misfolded prion protein (PrPCWD) in either brain or lymphoid tissue using immunodetection methods, with immunohistochemistry (IHC) recognized as the gold standard. In recent years, in vitro amplification assays have been developed that can detect CWD prion seeding activity in tissues, excreta, and body fluids of affected cervids. These methods potentially offer earlier and more facile detection of CWD, both pre- and post-mortem. Here we provide a longitudinal profile of CWD infection progression, as assessed by both real-time quaking-induced conversion (RT-QuIC) and IHC on serial biopsies of mucosal lymphoid tissues of white-tailed deer orally exposed to low doses of CWD prions. We report that detection of CWD infection by RT-QuIC preceded that by IHC in both tonsil and recto-anal lymphoid tissue (RAMALT) in 14 of 19 deer (74%). Of the 322 biopsy samples collected in post-exposure longitudinal monitoring, positive RT-QuIC results were obtained for 146 samples, 91 of which (62%) were concurrently also IHC-positive. The lower frequency of IHC positivity was manifest most in the earlier post-exposure periods and in biopsies in which lymphoid follicles were not detected. For all deer in which RT-QuIC seeding activity was detected in a tonsil or RAMALT biopsy, PrPCWD was subsequently or concurrently detected by IHC. Overall, this study (a) provides a longitudinal profile of CWD infection in deer after low yet infectious oral prion exposure; (b) illustrates the value of RT-QuIC for sensitive detection of CWD; and (c) demonstrates an ultimate high degree of correlation between RT-QuIC and IHC positivity as CWD infection progresses.

Studies of interrelations between neurotrophic antibodies and individual neurophysiological indices in patients with professional chronic mercury intoxication at the post-exposure period

Studies of interrelations between neurotrophic antibodies and individual neurophysiological indices in patients with professional chronic mercury intoxication at the post-exposure period

Springing Bottles Enrichment Toy Effect on Behaviors and Cortisol Level of Kenneled Dogs (Canis lupus familiaris)

Environmental enrichment used in captive animals with goals of increasing the activity, behavioral diversity, utilization of the environment and reducing abnormal behaviors. The present study was designed to determine the springing feeding bottles toy ameliorative effect on behaviors and cortisol level of kenneled Caucasian dogs. Sixteen healthy kenneled Caucasian shepherd dogs were utilized. The experimental procedure consisted of four phases: 1) habituation period, 2) baseline period (pre-enrichment phase), 3) treatment period (enrichment phase)– and 4) post-exposure period (post-enrichment phase). Each phase last for 3 days during which dogs were video recorded for state and event behaviors except the first one. Hair was collected during the three phases (pre, during and post enrichment) for cortisol analysis. The provision of the feeding enrichment shorter the lying time and stereotypies frequencies, while increased the activity level. These behaviors persisted after withdrawal of enrichment with improvement in feeding time. Hair cortisol levels also was lower during and after enrichment with a marked reduction after withdrawal. Therefore, it appears that the provision of feeding enrichment toy could improve the behavioral repertoire and decrease cortisol level in kennelled dogs, and thus enhance its welfare.

Evaluation of acute toxicity and copper accumulation in organs of Wistar rats, 14 days after oral exposure to copper oxide (II) nano- and microparticles

Copper oxide (II) nanoparticles (CuO-NPs) have been increasingly used in products of human interest, such as coating for food packaging and wood protection. The main objective of this study was to evaluate in vivo acute toxicity of CuO-NPs after oral exposure and compare it with CuO microparticles (CuO-MPs). Female rats were orally exposed, through gavage procedure, to the analyzed materials. After 14 days of observation, hematological, biochemical, histopathological, and copper organ accumulation analyses were performed. CuO-NPs (25.17 ± 8 nm) and CuO-MPs (1.092 ± 0.52 μm) were characterized and compared regarding their acute oral toxicity. Animals treated with CuO-NPs at the dose of 2000 mg kg−1 presented changes in feces and copper hepatic accumulation. Histopathological exam of livers demonstrated hepatocyte binucleation and megalocytosis. None of the animals tested with CuO-MPs showed any alterations. Oral exposure to CuO-NPs, at the dosage of 2000 mg kg−1, may cause mild transitory liver damage, mainly resolved during a 14-day post-exposure period. Also, the nanoparticulated material showed to be more toxic than the microparticulated one.

Evaluation of protective effect of Thiocetam drug by morphological changes in the heart and vessels after administration of lead nanoparticles of various sizes (experimental study)

Introduction of nanotechnologies to the modern industry gave rise to new challenges. The issue of development and implementation of recommendations regarding the prevention of potential negative impact of lead nanoparticles on population health is of particular importance. The locally manufactured drug Thiocetam which possesses nootropic, antiischemic, antioxidative and membrane stabilizing properties has drawn our attention. The research aimed at studying the protective effect of Thiocetam in Wistar rats with simulated subchronic toxic effect of lead compounds of various sizes (by morphological changes in the heart and vessels). The experiments were conducted on Wistar rats (mean body weight of 160-180 g). Colloidal solutions of lead sulphide obtained by chemical synthesis with the use of sodium polyphosphate stabilizer, (PbS) with the mean size of 26-34 nm (1-PbS) and 50-80 nm (2-PbS), and lead nitrate Pb(NO3)2 (3-Pb) in the ionic form were used in simulating the toxic effect, while normal saline solution was administered to the control group. The studied substances were injected (intraperitoneally daily 5 times a week) in a dose of 0.94 mg/kg (in lead equivalent). The toxic effects were evaluated after 60 injections (three months) and one month after the discontinuation of exposure with and without Thiocetam. The drug Thiocetam in the dose of 250 mg/kg had been administered to rats intragastrically on an empty stomach daily for one month. Histological slides of the rats’ myocardium and aortal wall were studied and morphometric analysis and statistical processing performed. In the postexposure recovery period (PEP) period a lower degree of interstitial swelling and myocardial blood vessel filling was observed, which was considered to be a regression of damage. After the administration of Thiocetam a pronounced transverse striation of cardiomyocytes, the density of collagen fibers around cardiomyocytes and microvessels were revealed, which indicated the protective effect of pharmacological correction. However, leukocyte infiltration was also found in the myocardial or aortic microvessels in the experimental groups. Aortic morphometric data revealed no differences between the PbS NPs groups and Pb(NO3)2, although the aortic wall morphology was quite preserved. The use of Thiocetam prevented dystrophic changes in the atrial epicardium and the aortic adventitia, which indicate cytoprotective and connective tissue effects. In the postexposure period without pharmacological correction a tendency to spontaneous recovery of morphological changes of the heart and aortic walls under the influence of PbS NPs and lead nitrate was observed. However, morphometric parameters demonstrate the absence of complete recovery be it with or without Thiocetam.

Evaluation of the dose-response and fate in the lung and pleura of chrysotile-containing brake dust compared to TiO2, chrysotile, crocidolite or amosite asbestos in a 90-day quantitative inhalation toxicology study – Interim results Part 2: Histopathological examination, Confocal microscopy and collagen quantification of the lung and pleural cavity

The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos.In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group.Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1–3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis.The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces.The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.

Improvement in Pediatric Cardiac Surgical Outcomes Through Interhospital Collaboration

BackgroundPatients undergoing complex pediatric cardiac surgery remain at considerable risk of mortality and morbidity, and variation in outcomes exists across hospitals. The Pediatric Cardiac Critical Care Consortium (PC4) was formed to improve the quality of care for these patients through transparent data sharing and collaborative learning between participants. ObjectivesThe purpose of this study was to determine whether outcomes improved over time within PC4. MethodsThe study analyzed 19,600 hospitalizations (18 hospitals) in the PC4 clinical registry that included cardiovascular surgery from August 2014 to June 2018. The primary exposure was 2 years of PC4 participation; this provided adequate time for hospitals to accrue data and engage in collaborative learning. Aggregate case mix–adjusted outcomes were compared between the first 2 years of participation (baseline) and all months post-exposure. We also evaluated outcomes from the same era in a cohort of similar, non-PC4 hospitals. ResultsDuring the baseline period, there was no evidence of improvement. We observed significant improvement in the post-exposure period versus baseline for post-operative intensive care unit mortality (2.1% vs. 2.7%; 22% relative reduction [RR]; p = 0.001), in-hospital mortality (2.5% vs. 3.3%; 24% RR; p = 0.001), major complications (10.1% vs. 11.5%; 12% RR; p < 0.001), intensive care unit length of stay (7.3 days vs. 7.7 days; 5% RR; p < 0.001), and duration of ventilation (61.3 h vs. 70.6 h; 13% RR; p = 0.01). Non-PC4 hospitals showed no significant improvement in mortality, complications, or hospital length of stay. ConclusionsThis analysis demonstrates improving cardiac surgical outcomes at children’s hospitals participating in PC4. This change appears unrelated to secular improvement trends, and likely reflects PC4’s commitment to transparency and collaboration.

Risk of Venous Thromboembolism After Carbon Monoxide Poisoning: A Nationwide Population-Based Study

Few studies have investigated the association between carbon monoxide (CO) poisoning and risk of venous thromboembolism. We aim to identify the risk of pulmonary embolism and deep venous thrombosis after CO poisoning. We conducted a nationwide cohort-crossover study using administrative claims data in Korea. We compared the risk of venous thromboembolism (pulmonary embolism or deep venous thrombosis) in the cohort period after CO poisoning to that of the same period 1 year later (crossover period), using conditional logistic regression analysis. We included 22,699 patients with a diagnosis of CO poisoning during the study period between 2004 and 2015. The risk of venous thromboembolism was significantly elevated during days 0 to 90 after CO poisoning (odds ratio 3.96; 95% confidence interval 2.50 to 6.25). However, this risk was not significantly elevated during subsequent postexposure periods through 360 days. During days 0 to 30 after CO poisoning, the risks of pulmonary embolism (odds ratio 22.00; 95% confidence interval 5.33 to 90.75) and deep venous thrombosis (odds ratio 10.33; 95% confidence interval 3.16 to 33.80) were significantly elevated. We found that the risk of venous thromboembolism persisted for up to 90 days after CO poisoning. The risk was increased 22-fold for pulmonary embolism and 10-fold for deep venous thrombosis, especially in the first month after CO poisoning. Patients should be monitored for venous thromboembolism risk after CO poisoning.

Electrocardiography Abnormalities in Macaques after Infection with Encephalitic Alphaviruses.

Eastern (EEEV) and Venezuelan (VEEV) equine encephalitis viruses (EEVs) are related, (+) ssRNA arboviruses that can cause severe, sometimes fatal, encephalitis in humans. EEVs are highly infectious when aerosolized, raising concerns for potential use as biological weapons. No licensed medical countermeasures exist; given the severity/rarity of natural EEV infections, efficacy studies require animal models. Cynomolgus macaques exposed to EEV aerosols develop fever, encephalitis, and other clinical signs similar to humans. Fever is nonspecific for encephalitis in macaques. Electrocardiography (ECG) metrics may predict onset, severity, or outcome of EEV-attributable disease. Macaques were implanted with thermometry/ECG radiotransmitters and exposed to aerosolized EEV. Data was collected continuously, and repeated-measures ANOVA and frequency-spectrum analyses identified differences between courses of illness and between pre-exposure and post-exposure states. EEEV-infected macaques manifested widened QRS-intervals in severely ill subjects post-exposure. Moreover, QT-intervals and RR-intervals decreased during the febrile period. VEEV-infected macaques suffered decreased QT-intervals and RR-intervals with fever onset. Frequency-spectrum analyses revealed differences in the fundamental frequencies of multiple metrics in the post-exposure and febrile periods compared to baseline and confirmed circadian dysfunction. Heart rate variability (HRV) analyses revealed diminished variability post-exposure. These analyses support using ECG data alongside fever and clinical laboratory findings for evaluating medical countermeasure efficacy.

Short-term PM2.5 exposure induces sustained pulmonary fibrosis development during post-exposure period in rats

Up to now, while some toxicological studies have identified pulmonary fibrosis immediately induced by long-term PM2.5 exposure, there has been no evidence indicating, whether short-term exposure can lead to post-exposure development of pulmonary fibrosis. Here, we treated rats with PM2.5 for 1 month (10 times), followed by normal feeding for 18 months. 18F-FDG intake, which is linked with the initiation and development of pulmonary fibrosis in living bodies, was found to gradually increase in lung following exposure through micro PET/CT imaging. Histolopathological examination revealed continuous deterioration of pulmonary injury post-exposure. Collagen deposition and hydroxyproline content continued to increase all along in the post-exposure duration, indicating pulmonary fibrosis development. Chronic and persistent induction of pulmonary inflammatory gene expression (Tnf, Il1b, Il6, Ccl2, and Icam1), epithelial mesenchymal transition (EMT, reduction of E-cadherin and elevation of fibronectin) and RelA/p65 upregulation, as well as serum inflammatory cytokine production, were also found in PM2.5-treated rats. Pulmonary oxidative stress, manifested by increase of MDA and decrease of GSH and SOD, was induced during exposure but disappeared in later post-exposure duration. These results suggested that short-term PM2.5 exposure could lead to sustained post-exposure pulmonary fibrosis development, which was mediated by oxidative-stress-initiated NF-κB/inflammation/EMT pathway.

The evaluation of immunoregulatory markers in the course of neurointoxication by mercury over the post-exposure period

There was executed the examination of patients with occupational chronic mercury intoxication in the post-exposure period after the exposure to metallic mercury vapor. 47 persons with an established diagnosis of chronic mercury intoxication (HMI) passed the laboratory and immunological examination in the period of exposure to metallic mercury vapor in a production environment. The average age of men accounted for 49.2±1.2 years. The experience of work in hazardous working conditions amounted of 21.65±1.61 years (1 observation). All these same cases were observed in the institute clinic again after 5 years (2 observation) and 10 years (3 observation). A control group of healthy men consisted of 47 cases included persons of representative both age and general work experience, without a professional route of contact with hazardous substances. The level of such cytokines as IL-1β, IL-2, IL-4, IL-6, TNF-a, INF-y and neurotropic IgG class antibodies directed to proteins of the nervous tissue (NF-200, GFAP, MBP, B-dependent Ca-channel, Glu-R, DA-R, R-GABA, Ser-R, R-Chol, DNA, B2GP) in serum were determined by enzyme linked immunosorbent assay. There was established the gain in the imbalance of inflammatory mediators and production ofneural antibodies in dynamics after the termination of the production in conditions of metallic mercury vapors. Revealed features of the regulatory relationship between the level of cytokines and the severity of the autoimmune process were shown to contribute to the maintenance and progression of neurodegenerative processes. There was recommended the identification of immunoregulatory markers (IL-1β, IL-4, TNF-a, NF-AT to 200, GFAP, S-100) as an additional criteria for the diagnosis of health disorders in operating and monitoring the course of the progredient professional mercury intoxication.

PHENOTYPIC COMPOSITION OF PERIPHERAL BLOOD LYMPHOCYTES AND THEIR COOPERATION IN PATIENTS WITH CHRONIC MERCURY INTOXICATION IN A POST-CONTACT PERIOD

Introduction. Based on the current understanding of the progression of professional chronic mercury intoxication, it is extremely important to study the regulatory activity of immunocompetent cells after the cessation contact with mercury to develop effective therapeutic measures. The purpose of the study was to study the population and subpopulation spectrum of peripheral blood lymphocytes and their cooperation in patients with chronic mercury intoxication in a distant postexposure period. Material and methods. Phenotyping of lymphocytes in the blood of the subjects was carried out by the method of indirect immunofluorescence using monoclonal antibodies to the molecules CD3+, CD4+, CD8+, CD9+, CD16+, CD20+, CD21+, CD23+, CD25+, CD95+. Results. In patients with chronic mercury intoxication in the long-term postexposure period, there were revealed features of the immune system functioning, indicating hyperactivation of both T- and B-components of the immune system. An increase in the total population of T-lymphocytes was established due to an increase in cells with receptors CD4+ (T-lymphocyte-helper cells) and CD16+ (killer cells), as well as an increase in the number of mature B-lymphocytes (CD20+) and pre-B-immature-lymphocytes (CD9+). Changes in the system of lymphocyte apoptosis, characterized by an increase in the number of cells expressing receptors for readiness for Fas-dependent apoptosis (CD95+), have been recorded. The established relationships between populations and subpopulations of lymphocytes indicate their importance in the implementation of the immune response, high activity and contingency between the components of the immune system in persons with chronic mercury intoxication after the termination of contact with the toxicant. Conclusion. The results obtained are the basis for long-term monitoring of the health status and improvement of the tactics of treating patients with neurointoxication with mercury in the postexposure period.

MARKERS OF VASCULAR TONE AND INFLAMMATION IN PERSONS EXPOSED TO MERCURY

Introduction. Endothelial dysfunction (ED) is an important link in the development of cardiovascular disease. There is evidence that exposure to mercury and its compounds can be a risk factor for the development of ED. The aim - the study of endothelial dysfunction markers involved in the regulation of vascular tone, inflammation, and vascular endothelial damage in patients with cardiovascular disease, the exposed and unexposed mercury. Material and Methods. In persons exposed due to their occupational activities with metallic mercury, who had been working for over five years, people with newly diagnosed chronic mercury intoxication and patients with chronic mercury intoxication in the long post-exposure period, and the persons are not exposed mercury a cross-sectional survey was conducted using biochemical methods Results. In examinees there have been revealed changes in the content of biochemical indices of ED - reducing nitrogen oxide, an elevated level of endothelin-1, angiotensin II, histamine, hsCRP, homocysteine. There has been established a breach in the content of ED markers that are pathogenic factors in the development of ED and, as a consequence, the development of cardiovascular disease in chronic mercury exposure. Conclusion. In persons exposed to mercury there were the most pronounced changes in the regulation of vascular tone, which may be one of the factors in the development of vascular disease. At the same time the importance of inflammation indices and vascular endothelial damage plays a secondary role.

ALTERATION OF BRAIN TISSUE, LIVER, AND KIDNEY IN THE POST-CONTACT PERIOD IN WHITE RATS EXPOSED TO VIBRATION

Introduction. Experimental studies in animals have shown ultrastructural changes in hepatic sinusoidal endothelial cells, tissue hypoxia of the kidneys, changes in the activity of oxidative processes and antioxidant enzymes, the formation of bioenergetic hypoxia, cell response in the form of infiltration of both lymphoid and macrophage cells to develop due to exposure to vibration. However, there is almost no data about the status of animals’ organs in the post-contact period. Material and methods. The study was carried out in white male rats weighing 220-240 g, were exposed to 40 Hz vibration for 60 days 5 times a week for 4 hours a day. Histological and morphometric analysis was used to assess the sensorimotor cortex tissue and hepatorenal system. Results. A decrease in the total number of brain neurons, astraglial cells in rats in 30, 60 and 120 days of the post-exposure period was found. There was hyperemia in the portal and Central veins, an increase in the number of Kupffer cells in the liver tissue at the 30th, 60th, 120th day after the exposure. Decrease in the area of the Shumlyansky-Bowman capsule was recorded in the experimental rats’ kidney tissue 30 days after the end of vibration exposure; though there were no differences in the number of renal bodies in the tissue of white rats of the experimental and control groups at 60th and 120th day after the end of exposure to vibration. Conclusion. Morphological changes in the tissues of white rats exposed to prolonged vibration presented in the form of a decrease in the total number of neurons and astroglia cells in the brain tissue, a pronounced macrophage response in the liver tissue have been preserved in the post-contact period following the exposure to vibration.