<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medlit</journal-id><journal-title-group><journal-title xml:lang="ru">Гигиена и санитария</journal-title><trans-title-group xml:lang="en"><trans-title>Hygiene and Sanitation</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0016-9900</issn><issn pub-type="epub">2412-0650</issn><publisher><publisher-name>Federal Scientific Center of Hygiene named after F.F. Erisman</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.47470/0016-9900-2025-104-11-1549-1553</article-id><article-id custom-type="edn" pub-id-type="custom">hskznr</article-id><article-id custom-type="elpub" pub-id-type="custom">medlit-5308</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ПРОФИЛАКТИЧЕСКАЯ ТОКСИКОЛОГИЯ И ГИГИЕНИЧЕСКОЕ НОРМИРОВАНИЕ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>PREVENTIVE TOXICOLOGY AND HYGIENIC STANDARTIZATION</subject></subj-group></article-categories><title-group><article-title>Исследование цитотоксичности экстракта торфяного дыма на культуре клеток 3T3-SV40</article-title><trans-title-group xml:lang="en"><trans-title>Evaluation of cytotoxicity of peat smoke extract on 3T3-SV40 cell culture</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9406-5424</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Абрамова</surname><given-names>Вера Александровна</given-names></name><name name-style="western" xml:lang="en"><surname>Abramova</surname><given-names>Vera A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Канд. фарм. наук, ст. науч. сотр. лаб. биомоделирования и трансляционной медицины ФГБНУ ВСИМЭИ, 665827, Ангарск, Россия</p><p>e-mail: tyutrina.v.a@yandex.ru</p></bio><bio xml:lang="en"><p>PhD (Pharmacology), senior researcher, Laboratory of biomodelling and translational medicine, East-Siberian Institute of Medical and Ecological Research, Angarsk, 665827, Russian Federation</p><p>e-mail: tyutrina.v.a@yandex.ru</p></bio><email xlink:type="simple">tyutrina.v.a@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8165-8052</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Вокина</surname><given-names>Вера Александровна</given-names></name><name name-style="western" xml:lang="en"><surname>Vokina</surname><given-names>Vera A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Канд. биол. наук, ст. науч. сотр. лаб. биомоделирования и трансляционной медицины ФГБНУ ВСИМЭИ, 665827, Ангарск, Россия</p><p>e-mail: vokina.vera@gmail.com</p></bio><bio xml:lang="en"><p>PhD (Biology), senior researcher, Laboratory of biomodelling and translational medicine, East-Siberian Institute of Medical and Ecological Research, Angarsk, 665827, Russian Federation</p><p>e-mail: vokina.vera@gmail.com</p></bio><email xlink:type="simple">vokina.vera@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1052-4601</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Соседова</surname><given-names>Лариса Михайловна</given-names></name><name name-style="western" xml:lang="en"><surname>Sosedova</surname><given-names>Larisa M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Доктор мед. наук, профессор, зав. лаб. биомоделирования и трансляционной медицины ФГБНУ ВСИМЭИ, 665827, Ангарск, Россия</p><p>e-mail: sosedlar@mail.ru</p></bio><bio xml:lang="en"><p>DSc (Medicine), professor, head, Laboratory of biomodelling and translational medicine, East-Siberian Institute of Medical and Ecological Research, Angarsk, 665827, Russian Federation</p><p>e-mail: sosedlar@mail.ru</p></bio><email xlink:type="simple">sosedlar@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Восточно-Сибирский институт медико-экологических исследований»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>East-Siberian Institute of Medical and Ecological Research</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>20</day><month>12</month><year>2025</year></pub-date><volume>104</volume><issue>11</issue><fpage>1549</fpage><lpage>1553</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Абрамова В.А., Вокина В.А., Соседова Л.М., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Абрамова В.А., Вокина В.А., Соседова Л.М.</copyright-holder><copyright-holder xml:lang="en">Abramova V.A., Vokina V.A., Sosedova L.M.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.rjhas.ru/jour/article/view/5308">https://www.rjhas.ru/jour/article/view/5308</self-uri><abstract><sec><title>Введение</title><p>Введение. В последние десятилетия природные пожары происходят чаще и с большей интенсивностью, однако механизмы цитотоксического действия дыма на клеточном уровне изучены недостаточно. Определение цитотоксичности экстракта торфяного дыма (ЭТД) на фибробластах служит адекватной моделью для изучения острых и хронических эффектов его воздействия.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. Оценка цитотоксичности торфяного дыма проведена в серии экспериментов in vitro с использованием ЭТД в восьми разведениях (содержание компонентов дыма 12,5; 25; 37,5; 50; 62,5; 75; 87,5 и 100%) на эмбриональных мышиных фибробластах 3T3-SV40. Цитотоксическое действие оценивали после 24-часовой инкубации по концентрации лактатдегидрогеназы (ЛДГ) в культуральной среде и с помощью метилтетразолиевого теста (МТТ), представлена морфологическая оценка клеток.</p></sec><sec><title>Результаты</title><p>Результаты. Установлено, что ЭТД приводит в первую очередь к снижению метаболической активности фибробластов, о чём свидетельствует более низкая средняя ингибирующая концентрация (IC50) (53,6%), рассчитанная по МТТ-тесту. При оценке цитотоксического эффекта ЭТД в ЛДГ-тесте наблюдалось резкое снижение жизнеспособности клеток при концентрации более 62,5%, величина IC50 в данном тесте составила 57,7%. Воздействие ЭТД в концентрациях 37,5% и более приводит к морфологическим изменениям: нарушается целостность монослоя, появляются фибробласты с признаками дистрофии, зернистостью цитоплазмы, а также отдельные фра гментированные фибробласты, определяются зоны деструкции и лизиса клеток.</p></sec><sec><title>Ограничения исследования</title><p>Ограничения исследования. Исследование ограничено изучением цитотоксичности ЭТД на культуре клеток 3T3-SV40 с помощью морфологической оценки, МТТ-теста и определения концентрации ЛДГ.</p></sec><sec><title>Заключение</title><p>Заключение. Дана оценка воздействия торфяного дыма на фибробласты in vitro, что позволило установить первичную токсикологическую характеристику ЭТД.</p><p>Соблюдение этических стандартов. Исследование одобрено локальным этическим комитетом ФГБНУ ВСИМЭИ (протокол № 7 от 15.12.2023 г.), проведено в соответствии с Европейской конвенцией о защите позвоночных животных, используемых для экспериментов или в иных научных целях (ETS N 123), директивой Европейского парламента и Совета Европейского союза 2010/63/EC от 22.09.2010 г. о защите животных, использующихся для научных целей.</p></sec><sec><title>Участие авторов</title><p>Участие авторов: Абрамова В.А. – концепция и дизайн исследования, сбор и обработка данных, статистическая обработка, написание текста, редактирование; Вокина В.А. – концепция и дизайн исследования, сбор и обработка данных, статистическая обработка, написание текста; Соседова Л.М. – концепция и дизайн исследования, редактирование. Все соавторы – утверждение окончательного варианта статьи, ответственность за целостность всех её частей.</p></sec><sec><title>Конфликт интересов</title><p>Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов в связи с публикацией данной статьи.</p></sec><sec><title>Финансирование</title><p>Финансирование. Работа выполнена по плану НИР в рамках государственного задания.</p></sec><sec><title>Поступила</title><p>Поступила: 20.07.2025 / Поступила после доработки: 03.10.2025 / Принята к печати: 15.10.2025 / Опубликована: 19.12.2025</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. In recent decades, wildfires have become more frequent and intense in many fire-prone areas. However, the mechanisms of smoke cytotoxicity at the cellular level are poorly understood. The study of peat smoke extract (PSE) cytotoxicity in fibroblasts is an important model for studying the acute and chronic effects of smoke exposure.</p></sec><sec><title>Materials and methods</title><p>Materials and methods. The cytotoxicity of peat smoke was assessed in a series of in vitro experiments using PSE in 8 dilutions (12.5, 25, 37.5, 50, 62.5, 75, 87.5 and 100%) on 3T3-SV forty mouse embryonic fibroblasts. The cytotoxic effect was assessed after 24-hour incubation by determining the concentration of lactate dehydrogenase (LDH) in the culture medium and performing the MTT test; a morphological assessment of the cells was given.</p></sec><sec><title>Results</title><p>Results. The results of the study indicate that PSE primarily leads to a decrease in the metabolic activity in fibroblasts, as evidenced by a lower value of the mean inhibitory concentration (IC50) (53.6%) calculated by the MTT test. When assessing the cytotoxic effect of PSE in the LDH test, a sharp decrease in cell viability was observed at its concentration above 62.5%, the IC50 value in this test was 57.7%.</p></sec><sec><title>Limitations</title><p>Limitations. The study is limited to the investigation of the cytotoxicity of PSE on the 3T3-SV 40 cell culture using morphological assessment, MTT test and determination of LDH concentration.</p></sec><sec><title>Conclusion</title><p>Conclusion. As a result of the conducted studies, an assessment of the impact of peat smoke on fibroblasts in vitro was carried out, with the help of which a primary toxicological characteristic of PSE was given.</p><p>Compliance with ethical standards. The study was approved by the local ethics committee of the East-Siberian Institute of Medical and Ecological Research (Protocol No.7 of 12/15/2023), conducted in accordance with the European Convention for the Protection of Vertebrate Animals Used for Experiments or for Other Scientific Purposes (ETS N 123), Directive 2010/63/EC of the European Parliament and the Council of 09/22/2010 on the protection of animals used for scientific purposes.</p></sec><sec><title>Contribution</title><p>Contribution: Abramova V.A. – concept and design of research, data collection and processing, statistical data processing, text writing, editing; Vokina V.A. – concept and design of research, data collection and processing, statistical data processing, text writing; Sosedova L.M. – concept and design of research, editing. All authors are responsible for the integrity of all parts of the manuscript and approval of the manuscript final version.</p></sec><sec><title>Conflict of interest</title><p>Conflict of interest. The authors declare no conflict of interest.</p></sec><sec><title>Funding</title><p>Funding. The work was carried out according to the research plan within the framework of the state task.</p></sec><sec><title>Received</title><p>Received: July 20, 2025 / Revised: October 3, 2025 / Accepted: October 15, 2025 / Published: December 19, 2025</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>торфяной дым</kwd><kwd>цитотоксичность</kwd><kwd>культура клеток</kwd><kwd>МТТ-тест</kwd><kwd>определение ЛДГ</kwd></kwd-group><kwd-group xml:lang="en"><kwd>peat smoke</kwd><kwd>cytotoxicity</kwd><kwd>cell culture</kwd><kwd>MTT Assay</kwd><kwd>LDH Assay</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Martin W.K., Schladweiler M.C., Oshiro W., Smoot J., Fisher A., Williams W., et al. Wildfire-related smoke inhalation worsens cardiovascular risk in sleep disrupted rats. Front. Environ. Health. 2023; (2): 1166918. https://doi.org/10.3389/fenvh.2023.1166918</mixed-citation><mixed-citation xml:lang="en">Martin W.K., Schladweiler M.C., Oshiro W., Smoot J., Fisher A., Williams W., et al. Wildfire-related smoke inhalation worsens cardiovascular risk in sleep disrupted rats. Front. Environ. Health. 2023; (2): 1166918. https://doi.org/10.3389/fenvh.2023.1166918</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">David P., Dunsford D., Lu J., Moochhala S. Animal models of smoke inhalation induced injuries. Front. Biosci. (Landmark Ed). 2009; 14(12): 4618–30. https://doi.org/10.2741/3554</mixed-citation><mixed-citation xml:lang="en">David P., Dunsford D., Lu J., Moochhala S. Animal models of smoke inhalation induced injuries. Front. Biosci. (Landmark Ed). 2009; 14(12): 4618–30. https://doi.org/10.2741/3554</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Migliaccio C.T., Mauderly J.L. Biomass smoke exposures: toxicology and animal study design. Inhal. Toxicol. 2010; 22(2): 104–7. https://doi.org/10.3109/08958370903008870</mixed-citation><mixed-citation xml:lang="en">Migliaccio C.T., Mauderly J.L. Biomass smoke exposures: toxicology and animal study design. Inhal. Toxicol. 2010; 22(2): 104–7. https://doi.org/10.3109/08958370903008870</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Krewski D., Acosta D. Jr., Andersen M., Anderson H., Bailar J.C. 3rd, Boekelheide K., et al. Toxicity testing in the 21st century: a vision and a strategy. J. Toxicol. Environ. Health B Crit. Rev. 2010; 13(2–4): 51–138. https://doi.org/10.1080/10937404.2010.483176</mixed-citation><mixed-citation xml:lang="en">Krewski D., Acosta D. Jr., Andersen M., Anderson H., Bailar J.C. 3rd, Boekelheide K., et al. Toxicity testing in the 21st century: a vision and a strategy. J. Toxicol. Environ. Health B Crit. Rev. 2010; 13(2–4): 51–138. https://doi.org/10.1080/10937404.2010.483176</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Ashrin A., Anna E., Peyret E., Barbier G., Floreani M., Pointart C., et al. Evaluation of the toxicity of combustion smokes at the air-liquid interface: a comparison between two lung cell models and two exposure methods. Arch. Toxicol. 2025; 99(4): 1471–84. https://doi.org/10.1007/s00204-025-03964-x</mixed-citation><mixed-citation xml:lang="en">Ashrin A., Anna E., Peyret E., Barbier G., Floreani M., Pointart C., et al. Evaluation of the toxicity of combustion smokes at the air-liquid interface: a comparison between two lung cell models and two exposure methods. Arch. Toxicol. 2025; 99(4): 1471–84. https://doi.org/10.1007/s00204-025-03964-x</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Ihantola T., Di Bucchianico S., Happo M., Ihalainen M., Uski O., Bauer S., et al. Influence of wood species on toxicity of log-wood stove combustion aerosols: a parallel animal and air-liquid interface cell exposure study on spruce and pine smoke. Part Fibre Toxicol. 2020; 17(1): 27. https://doi.org/10.1186/s12989-020-00355-1</mixed-citation><mixed-citation xml:lang="en">Ihantola T., Di Bucchianico S., Happo M., Ihalainen M., Uski O., Bauer S., et al. Influence of wood species on toxicity of log-wood stove combustion aerosols: a parallel animal and air-liquid interface cell exposure study on spruce and pine smoke. Part Fibre Toxicol. 2020; 17(1): 27. https://doi.org/10.1186/s12989-020-00355-1</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Marchetti S., Bengalli R., Floris P., Colombo A., Mantecca P. Combustion-derived particles from biomass sources differently promote epithelial-to-mesenchymal transition on A549 cells. Arch. Toxicol. 2021; 95(4): 1379–90. https://doi.org/10.1007/s00204-021-02983-8</mixed-citation><mixed-citation xml:lang="en">Marchetti S., Bengalli R., Floris P., Colombo A., Mantecca P. Combustion-derived particles from biomass sources differently promote epithelial-to-mesenchymal transition on A549 cells. Arch. Toxicol. 2021; 95(4): 1379–90. https://doi.org/10.1007/s00204-021-02983-8</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">La Rocca G., Anzalone R., Magno F., Farina F., Cappello F., Zummo G. Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A) activity in human lung fibroblasts. Respir. Res. 2007; 8(1): 23. https://doi.org/10.1186/1465-9921-8-23</mixed-citation><mixed-citation xml:lang="en">La Rocca G., Anzalone R., Magno F., Farina F., Cappello F., Zummo G. Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A) activity in human lung fibroblasts. Respir. Res. 2007; 8(1): 23. https://doi.org/10.1186/1465-9921-8-23</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Wong L.S., Green H.M., Feugate J.E., Yadav M., Nothnagel E.A., Martins-Green M. Effects of «second-hand» smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodeling. BMC Cell Biol. 2004; 5(1): 13. https://doi.org/10.1186/1471-2121-5-13</mixed-citation><mixed-citation xml:lang="en">Wong L.S., Green H.M., Feugate J.E., Yadav M., Nothnagel E.A., Martins-Green M. Effects of «second-hand» smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodeling. BMC Cell Biol. 2004; 5(1): 13. https://doi.org/10.1186/1471-2121-5-13</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Вокина В.А., Андреева Е.С., Новиков М.А., Соседова Л.М. Устройство для моделирования интоксикации у мелких лабораторных животных продуктами горения биомассы. Патент РФ № 213283; 2022. https://elibrary.ru/rvksgf</mixed-citation><mixed-citation xml:lang="en">Vokina V.A., Andreeva E.S., Novikov M.A., Sosedova L.M. Device for modeling intoxication in small laboratory animals with biomass combustion products. Patent RF №213283; 2022. (in Russian)</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Лемешевская Е.П., Куренкова Г.В., Жукова Е.В. Профессиональный риск здоровью работников промышленных предприятий. Иркутск; 2016. https://elibrary.ru/ikagty</mixed-citation><mixed-citation xml:lang="en">Lemeshevskaya E.P., Kurenkova G.V., Zhukova E.V. Occupational Health Risks to Workers in Industrial Enterprises [Professional’nyi risk zdorov’yu rabotnikov promyshlennykh predpriyatii]. Irkutsk; 2016. https://elibrary.ru/ikagty (in Russian)</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Kunitomo M., Yamaguchi Y., Kagota S., Yoshikawa N., Nakamura K., Shinozuka K. Biochemical evidence of atherosclerosis progression mediated by increased oxidative stress in apolipoprotein E-deficient spontaneously hyperlipidemic mice exposed to chronic cigarette smoke. J. Pharmacol. Sci. 2009; 110(3): 354–61. https://doi.org/10.1254/jphs.09100fp</mixed-citation><mixed-citation xml:lang="en">Kunitomo M., Yamaguchi Y., Kagota S., Yoshikawa N., Nakamura K., Shinozuka K. Biochemical evidence of atherosclerosis progression mediated by increased oxidative stress in apolipoprotein E-deficient spontaneously hyperlipidemic mice exposed to chronic cigarette smoke. J. Pharmacol. Sci. 2009; 110(3): 354–61. https://doi.org/10.1254/jphs.09100fp</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Yamaguchi Y., Nasu F., Harada A., Kunitomo M. Oxidants in the gas phase of cigarette smoke pass through the lung alveolar wall and raise systemic oxidative stress. J. Pharmacol. Sci. 2007; 103(3): 275–82. https://doi.org/10.1254/jphs.fp0061055</mixed-citation><mixed-citation xml:lang="en">Yamaguchi Y., Nasu F., Harada A., Kunitomo M. Oxidants in the gas phase of cigarette smoke pass through the lung alveolar wall and raise systemic oxidative stress. J. Pharmacol. Sci. 2007; 103(3): 275–82. https://doi.org/10.1254/jphs.fp0061055</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Asano H., Horinouchi T., Mai Y., Sawada O., Fujii S., Nishiya T., et al. Nicotine- and tar-free cigarette smoke induces cell damage through reactive oxygen species newly generated by PKC-dependent activation of NADPH oxidase. J. Pharmacol. Sci. 2012; 118(2): 275–87. https://doi.org/10.1254/jphs.11166fp</mixed-citation><mixed-citation xml:lang="en">Asano H., Horinouchi T., Mai Y., Sawada O., Fujii S., Nishiya T., et al. Nicotine- and tar-free cigarette smoke induces cell damage through reactive oxygen species newly generated by PKC-dependent activation of NADPH oxidase. J. Pharmacol. Sci. 2012; 118(2): 275–87. https://doi.org/10.1254/jphs.11166fp</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Mai Y., Higashi T., Terada K., Hatate C., Nepal P., Horiguchi M., et al. Nicotine- and tar-free cigarette smoke extract induces cell injury via intracellular Ca2+-dependent subtype-specific protein kinase C activation. J. Pharmacol. Sci. 2012; 120(4): 310–4. https://doi.org/10.1254/jphs.12219sc</mixed-citation><mixed-citation xml:lang="en">Mai Y., Higashi T., Terada K., Hatate C., Nepal P., Horiguchi M., et al. Nicotine- and tar-free cigarette smoke extract induces cell injury via intracellular Ca2+-dependent subtype-specific protein kinase C activation. J. Pharmacol. Sci. 2012; 120(4): 310–4. https://doi.org/10.1254/jphs.12219sc</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Corsini E., Budello S., Marabini L., Galbiati V., Piazzalunga A., Barbieri P., et al. Comparison of wood smoke PM2.5 obtained from the combustion of FIR and beech pellets on inflammation and DNA damage in A549 and THP-1 human cell lines. Arch. Toxicol. 2013; 87(12): 2187–99. https://doi.org/10.1007/s00204-013-1071-z</mixed-citation><mixed-citation xml:lang="en">Corsini E., Budello S., Marabini L., Galbiati V., Piazzalunga A., Barbieri P., et al. Comparison of wood smoke PM2.5 obtained from the combustion of FIR and beech pellets on inflammation and DNA damage in A549 and THP-1 human cell lines. Arch. Toxicol. 2013; 87(12): 2187–99. https://doi.org/10.1007/s00204-013-1071-z</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Hansson A., Rankin G., Uski O., Friberg M., Pourazar J., Lindgren R., et al. Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans. Part Fibre Toxicol. 2023; 20(1): 30. https://doi.org/10.1186/s12989-023-00541-x</mixed-citation><mixed-citation xml:lang="en">Hansson A., Rankin G., Uski O., Friberg M., Pourazar J., Lindgren R., et al. Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans. Part Fibre Toxicol. 2023; 20(1): 30. https://doi.org/10.1186/s12989-023-00541-x</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Bølling A.K., Totlandsdal A.I., Sallsten G., Braun A., Westerholm R., Bergvall C., et al. Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines. Part Fibre Toxicol. 2012; 9(1): 45. https://doi.org/10.1186/1743-8977-9-45</mixed-citation><mixed-citation xml:lang="en">Bølling A.K., Totlandsdal A.I., Sallsten G., Braun A., Westerholm R., Bergvall C., et al. Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines. Part Fibre Toxicol. 2012; 9(1): 45. https://doi.org/10.1186/1743-8977-9-45</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Kasurinen S., Jalava P.I., Happo M.S., Sippula O., Uski O., Koponen H., et al. Particulate emissions from the combustion of birch, beech, and spruce logs cause different cytotoxic responses in A549 cells. Environ. Toxicol. 2017; 32(5): 1487–99. https://doi.org/10.1002/tox.22369</mixed-citation><mixed-citation xml:lang="en">Kasurinen S., Jalava P.I., Happo M.S., Sippula O., Uski O., Koponen H., et al. Particulate emissions from the combustion of birch, beech, and spruce logs cause different cytotoxic responses in A549 cells. Environ. Toxicol. 2017; 32(5): 1487–99. https://doi.org/10.1002/tox.22369</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Lee T.S., Liu Y.J., Tang G.J., Yien H.W., Wu Y.L., Kou Y.R. Wood smoke extract promotes both apoptosis and proliferation in rat alveolar epithelial type II cells: the role of oxidative stress and heme oxygenase-1. Crit. Care Med. 2008; 36(9): 2597–606. https://doi.org/10.1097/CCM.0b013e318184979c</mixed-citation><mixed-citation xml:lang="en">Lee T.S., Liu Y.J., Tang G.J., Yien H.W., Wu Y.L., Kou Y.R. Wood smoke extract promotes both apoptosis and proliferation in rat alveolar epithelial type II cells: the role of oxidative stress and heme oxygenase-1. Crit. Care Med. 2008; 36(9): 2597–606. https://doi.org/10.1097/CCM.0b013e318184979c</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Krimmer D., Ichimaru Y., Burgess J., Black J., Oliver B. Exposure to biomass smoke extract enhances fibronectin release from fibroblasts. PLoS One. 2013; 8(12): e83938. https://doi.org/10.1371/journal.pone.0083938</mixed-citation><mixed-citation xml:lang="en">Krimmer D., Ichimaru Y., Burgess J., Black J., Oliver B. Exposure to biomass smoke extract enhances fibronectin release from fibroblasts. PLoS One. 2013; 8(12): e83938. https://doi.org/10.1371/journal.pone.0083938</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
