Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Introduction. Growing prevalence of allergic rhinitis (AR) and significant socioeconomic losses related to implementing medical and prevention activities indicate the necessity to examine what role exogenous factors play in the disease onset and development. The aim of this study was to establish pathogenetic peculiarities of AR onset and development in schoolchildren under combined exposure to various environmental risk factors. Materials and methods. We analyzed results of clinical and laboratory examinations of schoolchildren’s health and data obtained by questioning and taken from diaries of daily rations provided at school for four hundred thirty nine AR children. They attended either an ordinary secondary school or a school with profound studies of some subjects. Influence of risk factors on clinical and laboratory indicators was evaluated by using one-factor logistic regression models that described “adverse exposure – likelihood of a response (effect)” relationships. Leading risk factors and pathogenetic peculiarities of AR onset and development were identified based on analyzing established cause-effect relations “risk factor – laboratory indicator – likelihood of diagnosing AR». Results. More significant violations of hygienic standards were established in schools with profound studies of some subjects; we identified improper management of educational activities, non-rational diets, and too intensive use of electronic devices. Likelihood of AR is 4.2 times higher for schoolchildren in such schools than for their counterparts from ordinary schools (OR=4.2) under combined exposure to adverse factors related to the educational process, diets, the environment (blood contamination with nickel, chromium, manganese, zinc, benzene, and toluene) and low physical activity. We established cause-effect relations between the disease development and the examined factors as well as their contributions to likelihood of risk-associated AR (12–60 %). We identified adverse laboratory effects in AR children who attended schools with profound studies of some subjects and established their association with affecting environmental factors. Pathogenetic peculiarities of the disease onset and development were posited based on modelling associations between laboratory indicators of disrupted homeostasis and AR development. Limitations. The examination was performed with 439 schoolchildren participating in it. Participants were not divided into sex-specific groups when describing peculiarities of allergic rhinitis development. Conclusion. The established key pathogenetic components in development of risk-associated AR are relevant targets for hygienic activities as regards the educational process and quality of the environment
Introduction. Growing prevalence of allergic rhinitis (AR) and significant socioeconomic losses related to implementing medical and prevention activities indicate the necessity to examine what role exogenous factors play in the disease onset and development. The aim of this study was to establish pathogenetic peculiarities of AR onset and development in schoolchildren under combined exposure to various environmental risk factors. Materials and methods. We analyzed results of clinical and laboratory examinations of schoolchildren’s health and data obtained by questioning and taken from diaries of daily rations provided at school for four hundred thirty nine AR children. They attended either an ordinary secondary school or a school with profound studies of some subjects. Influence of risk factors on clinical and laboratory indicators was evaluated by using one-factor logistic regression models that described “adverse exposure – likelihood of a response (effect)” relationships. Leading risk factors and pathogenetic peculiarities of AR onset and development were identified based on analyzing established cause-effect relations “risk factor – laboratory indicator – likelihood of diagnosing AR». Results. More significant violations of hygienic standards were established in schools with profound studies of some subjects; we identified improper management of educational activities, non-rational diets, and too intensive use of electronic devices. Likelihood of AR is 4.2 times higher for schoolchildren in such schools than for their counterparts from ordinary schools (OR=4.2) under combined exposure to adverse factors related to the educational process, diets, the environment (blood contamination with nickel, chromium, manganese, zinc, benzene, and toluene) and low physical activity. We established cause-effect relations between the disease development and the examined factors as well as their contributions to likelihood of risk-associated AR (12–60 %). We identified adverse laboratory effects in AR children who attended schools with profound studies of some subjects and established their association with affecting environmental factors. Pathogenetic peculiarities of the disease onset and development were posited based on modelling associations between laboratory indicators of disrupted homeostasis and AR development. Limitations. The examination was performed with 439 schoolchildren participating in it. Participants were not divided into sex-specific groups when describing peculiarities of allergic rhinitis development. Conclusion. The established key pathogenetic components in development of risk-associated AR are relevant targets for hygienic activities as regards the educational process and quality of the environment
Introduction. The immune system plays the key role in the formation of adaptive responses and is the most sensitive to environmental exposures. An immune response under exposure to viruses or other factors is induced by toll-like receptors stimulating production of pro-inflammatory cytokines. Simultaneous exposure to exogenous chemical pollutants in ambient air modifies the adaptation process. Materials and methods. An in vitro experiment was accomplished on samples of peripheral blood. The study focused on a mixed population of immune-competent cells (n=64 samples). Effects produced by exogenous factors (benz(a)pyrene, SARS-CoV-2) and managing elements (interleukin-1β, cortisol) were considered influencing factors. All the lymphocyte cultures were incubated for 72 hours; after that, the quantitative content of cytokines in the samples was determined by the ELISA tests. Results. The inhibition of cytokines was experimentally demonstrated when the SARS-CoV-2 vaccine antigen was introduced into cell culture in combination with cortisol and an immunomodulator (IL-6, IL-10), and a significant decrease in the level of INF-gamma in samples with the addition of IL-1β was also noted. Benz(a)pyrene exerted a catalytic effect on the cytokine-producing function of immunocompetent cells with an increase in the production of IL-6 and IFN-gamma relative to spontaneous production. Suppression of cytokines (IL-6, IFN-gamma, and IL-10) was observed in samples containing vaccine antigens SARS-CoV-2, compared with the spontaneous level, which suggests the formation of possible mechanisms of post-vaccination complications. Limitations. The study has no limitations associated with the use of the selected methods or characteristics of the research objects. Conclusions. Experimental modelling in vitro made it possible to estimate the additive effects of the mixed action of benz(a)pyrene and SARS-CoV-2 (vaccine antigen) on protein molecules and hyperproduction of inflammatory modulators was evaluated. The study aimed to facilitate investigation of the examined mechanism and development of relevant programs for preventing risks of negative effects produced on health by chemical and biological factors.
Introduction. The study of genetically determined cell death features in children under the conditions of aerogenic exposure to benzo(a)pyrene is relevant in the identification of immunological and genetic markers of technogenic chemical factor exposure. Materials and methods. Five hundred sixty nine preschool children were examined. Observation group included 384 children living under the conditions of aerogenic exposure to benzo(a)pyrene. Comparison group consisted of 185 children living in a relatively clean area. Determination of the content of benzo(a)pyrene in atmospheric air and in blood was carried out by HPLC. Determination of Annexin-FITC+7AAD–, Annexin-FITC+7AAD+, Bax, Bcl-2, CD95+-, p53, TNFR was made by flow cytofluorometry. The study of FAS (rs1159120) and TP53 (rs1042522) gene polymorphism was performed by real-time PCR. Results. The aerogenic benzo(a)pyrene exposure (7.4 MPCad) at a dose of 0.000163 mg/(kg · day) causes an increase in the level of contamination in children blood relative to the comparison group and the reference level (p<0.05). Changes in the immune profile of the examined contingent (increased content of apoptosis markers – Annexin-FITC+7AAD–-cells, CD3+CD95+-lymphocytes, p53, TNFR against the background of compensatory anti-apoptotic protein Bcl-2 hyperproduction) are associated with the C-allele (OR=1.38; 95% CI: 1.02–1.88, p<0.05); and CC-genotype (OR=2.53; 95% CI: 1.72–3.72, p<0.05) of FAS gene (rs1159120), and the C-allele (OR=1.96; 95% CI: 1.53–2.53, p<0.05) and CC-genotype (OR=2.53; 95% CI: 1.72–3.72, p<0.05) of t TP53 gene (rs1042522). Limitations. There are no restrictions on conducting research related to the possibility of using the selected methods and the characteristics of the objects of research. Conclusion. Changes in the immune profile associated with blood contamination with benzo(a)pyrene (excess of AnnexinV-FITC+7AAD– and CD3+CD95+-lymphocytes, p53, TNFR, Bcl-2 cells) are associated with the C-allele (OR=1.38; 95% CI: 1.02–1.88, p<0.05); and CC-genotype (OR=2.53; 95% CI: 1.72–3.72, p<0.05) of FAS gene (rs1159120), and C-allele (OR=1.96; 95% CI: 1.53–2.53, p<0.05) and CC-genotype (OR=2.53; 95% CI: 1.72–3.72, p<0.05) of t TP53 gene (rs1042522) form the risks of programmed cell death violations in children living under the conditions of aerogenic exposure to benzo(a)pyrene, when it is entered the body at a dose of more than 0.000163 mg/(kg · day).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.