Introduction. Influence of incidental nanoparticles of industrial aerosols on occupational lung diseases development is not studied enough. As nanoparticles has properties to induce inflammation and fibrosis, it is hypothesized that they affect occupational chronic obstructive pulmonary disease (COPD) phenotype. The aim was to establish monocyte subsets, airway inflammation, clinical and functional features in occupational COPD due to aerosols containing nanoparticles exposure. Materials and methods. Study design was a single center prospective cohort observational. Subjects with occupational COPD (GOLD 2011-2021 criteria) exposed to aerosols containing nanoparticles (n=50) enrolled. Comparison group - COPD in tobacco smokers (n=50), control group - healthy people (n=50). Groups were matched by demographics and COPD duration. Nanoparticles at workplaces air were measured by inductively coupled plasma atomic emission spectrometry and by scanning electron microscopy. Of participants 26 were exposed to maximal concentrations of metal nanoparticles and 24 - of silica nanoparticles. Spirography, body pletysmography, lung diffusing capacity (DLco/Va), Doppler-ehocardiography, induced sputum cytology, COPD exacerbations assessment were done. Monocyte subsets were determined by flow cytometry. Linear regression model was used to explore relationships. Results. COPD due to aerosols containing metal nanoparticles was characterized by most severe airflow limitation, lung hyperinflation, pulmonary hypertension, most prominent decrease in DLco/Va, frequent and severe COPD exacerbations, eosinophilic inflammation. The largest proportion of «classical» CD14+CD16- monocytes subset, 96,4% (90,3%; 97,2%), high level of CCR5 expression were seen in this group. The features of COPD due to aerosols containing silica nanoparticles were substantial decrease in DLco/Va, the least airflow limitation, mild lung hyperinflation, rare COPD exacerbations, paucigranulocytic inflammation. The largest proportion of «non-classical» CD14DimCD16+ monocytes with high level of CCR2 expression revealed. Mass concentration of metal nanoparticles was associated with «classical» monocytes, (B=1,5), silica nanoparticles - with «non-classical» monocytes (B=1,4). On their turn, «classical» monocytes were associated with DLco (B=-1,6), functional residual volume (B=1,2), mean pulmonary artery pressure (B=-1,4), eosinophilic inflammation. «Non-classical» monocytes were associated with DLco (B=-1,5) and paucigranulocytic inflammation (B=1,2), p<0,015. Conclusions. Exposure of incidental nanoparticles was associated with circulated monocyte subsets, airway inflammation and occupaitonal CODP phenotype.

Aim. To establish symptoms, lung function and to evaluate subsequent exacerbations of chronic obstructive pulmonary disease (COPD) during a year after virus-induced COPD exacerbations. Materials and methods. Patients hospitalized with viral (n=60), bacterial (n=60) and viral-bacterial (n=60) COPD exacerbations were enrolled to single-center prospective observational study. COPD was diagnosed according spirography criteria. Viral infection was established in bronchoalveolar lavage fluid or sputum by real-time reverse transcription-polymerase chain reaction for RNA of influenza A and B virus, rhinovirus, respiratory syncytial virus and SARS-CoV-2. Symptoms, lung function, COPD exacerbations were assessed. Patients were investigated at the hospitalization onset and then 4 and 52 weeks following the discharge from the hospital. Results. After 52 weeks in viral and viral-bacterial COPD exacerbations groups the rate of forced expiratory volume in one second (FEV1) decline were maximal 71 (68; 73) ml/year and 69 (67; 72) ml/year versus 59 (55; 62) ml/year after bacterial exacerbations. Low levels of diffusion lung capacity for carbon monoxide (DLco/Va) 52.5% (45.1%; 55.8%), 50.2% (44.9%; 56.0%) and 75.3% (72.2%; 80.1%) respectively, of 6-minute walk distance; p0.001 in relation to bacterial exacerbations. In Cox proportional hazards regression analyses viral and viral-bacterial exacerbations were associated with increased risk of subsequent COPD exacerbations by 2.4 times independent of exacerbations rate before index event and FEV1. In linear regression models the relationships between airflow limitation and respiratory syncytial virus, rhinovirus and influenza virus infection, between low DLco/Va and rhinovirus, influenza virus and SARS-CoV-2 infection. Conclusion. COPD after virus-induced exacerbations were characterized by progression of airflow limitation, low DLco/Va, low 6-minute walking test distance, subsequent COPD exacerbations risk.

The significant prevalence of industrial aerosols with unintentional nanoparticles and the increasing use of engineering nanoparticles in modern production determine the relevance of research on the patterns of interaction with the human bronchopulmonary system. Unintentional nanoparticles are formed during various production processes: melting and welding of metals, combustion, crushing, grinding of minerals, plasma processing of materials. Engineering nanoparticles are released into the air of the work area during their production or use in any technological processes. The respiratory system, as a barrier organ, is most vulnerable to the effects of adverse environmental factors. At the same time, nanoparticles are the least studied component of industrial aerosols. In order to systematize data on the role of nanoparticles in the development of occupational bronchopulmonary pathology, the authors conducted a literature review. The size determines the features of the physical, chemical and biological properties of nanoparticles. They have high values of the ratio of surface area to volume, total surface area, which leads to an increase in reactogenicity and penetrating power. The pathogenic properties of nanoparticles depend on the chemical composition, shape, curvature of the surface, structure, charge, mass concentration, total surface area of the particles, and exposure time. The multidimensionality of hygienic characteristics determines the complexity of hygienic rationing and monitoring of nanoparticles. To date, safe exposure levels have not been established. When interacting with cells of the respiratory tract, nanoparticles induce the following cellular and molecular mechanisms: oxidative stress, inflammation, violation of the epithelial barrier, autophagy and dysfunction of lysosomes, stress of the endoplasmic reticulum, apoptosis, senescence, fibrosis, endothelial dysfunction, DNA damage. This leads to the development of interstitial pneumonitis, pulmonary fibrosis and obstructive disorders, and an increase in the activity of allergic inflammation. All these mechanisms are present in the pathogenesis of occupational lung diseases. Under the influence of nanoparticles of various chemical compositions, separate phenotypes of occupational chronic obstructive pulmonary disease are formed. There is a lack of epidemiological studies of the possible etiological role of nanoparticles. Nanoparticles of industrial aerosols are a significant factor in the development of occupational diseases of the bronchopulmonary system and have a significant impact on the formation of phenotypes.

Introduction. Cardiovascular diseases (СVD) rank first in terms of morbidity and mortality not only in the Russian Federation but throughout the world. Since the end of 2019 a pandemic of Severe Acute Respiratory Syndrome (SARS) or new coronavirus infection (NCI) has spread throughout the world, which contributed to the development and course of CVD. Therefore, genetic markers began to be considered as factors potentially influencing CVD, its development and severity. Objective: To evaluate the association of the nucleotide sequence variant rs12329760 of the TMPRSS2 gene with acute coronary syndrome in patients who have had a new coronavirus infection.Material and methods. The study included 100 patients (women – 50, men – 50) with ACS and previous NCI, who were selected on the basis of a positive PCR test for the presence of SARS-CoV-2 in the anamnesis, hospitalized at the regional vascular center No. 7 of the City Clinical Hospital No. 2 of the city of Novosibirsk. Women age was 59.5 ± 7.2 years, men age was 53.5 ± 9.3 years. The diagnosis of ACS was established according to a set of criteria proposed and established by the Russian Society of Cardiology and in accordance with the updated clinical recommendations of the Ministry of Health of the Russian Federation of 2020. Patients underwent clinical and instrumental examination, coronary angiography with possible stenting, as provided for in the standards of medical care and clinical guidelines. The nucleotide sequence variant rs12329760 of the TMPSS2 gene was determined in patients using PCR with further analysis of restriction fragment length polymorphism. The comparison group consisted of 200 patients with ACS without previous NCI (no positive PCR test, no positive antibodies).Results. Carriage of CC, СТ, TT, genotype variants of the nucleotide sequence rs12329760 of the TMPSS2 gene are not associated with an increased risk of developing ACS in patients with previous NCI. When comparing the frequencies of the rs12329760 genotypes of the TMPSS2 gene in groups with ACS with NCI and ACS without NCI, no statistically significant differences were obtained. In the group with ACS with NCI, carriage of the homozygous genotype was more common (p = 0.011).Conclusions. Variants of the nucleotide sequence rs12329760 of the TMPSS2 gene are not associated with ACS with previous NCI.

Aim. To assess the rs2285666 nucleotide sequence of the angiotensin-converting enzyme 2 (ACE2) gene and its association with acute coronary syndrome (ACS) in patients after coronavirus disease 2019 (COVID-19).Material and methods. The study included 100 patients after COVID-19, including 50 men and 50 women, hospitalized with a diagnosis of ACS. The diagnosis of COVID-19 in all 100 patients was confirmed by a positive polymerase chain reaction (PCR) smear. All patients underwent percutaneous transluminal coronary angioplasty with stenting, standard clinical and paraclinical examination, and genetic testing of the rs2285666 ACE2 gene by PCR followed by restriction fragment length polymorphism analysis. The comparison group consisted of 200 patients with ACS after COVID-19, confirmed by a PCR smear or antibody titer.Results. Statistically significant differences were obtained for the AA genotype, carriage of which among male patients with ACS after COVID-19 was 2,5 times less common than in men in the control group (OR =0,391, 95% CI: 0,167-0,917; p=0,028). On the other hand, carriage of the rs2285666 GA genotype of the ACE2 gene is not associated with an increased risk of ACS in women after COVID-19. There were no significant differences in genotype frequencies in the group of women and in the general group (without division by sex).Conclusion. The data obtained may indicate a protective role of the rs2285666 AA genotype of the ACE2 gene for males regarding ACS development after COVID-19. These results are the first steps towards building a prognostic model to estimate the ACS risk in patients after COVID-19, which will reduce morbidity and mortality for this group of patients.