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A special issue of International Journal of Environmental Research and Public Health (ISSN 1660-4601). This special issue belongs to the section "Environmental Health".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 21666

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Special Issue Editors

Prof. Dr. Woo-Jin Kim

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Guest Editor

Department of Internal Medicine, Kangwon National University, Chuncheon 24341, Korea
Interests: environmental lung disease; COPD; air pollution; genomics; epigenomics
Special Issues, Collections and Topics in MDPI journals

Dr. Junghyun Kim

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Guest Editor

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, National Medical Center, Seoul, Korea
Interests: environmental health; air pollution; COPD; pulmonary infectious disease; lung cancer; epidemiology

Special Issue Information

Dear Colleagues,

The respiratory system is susceptible to environmental exposure. The global burden of respiratory diseases due to ambient and household air pollution is substantial. There are also other emerging environmental risk factors for respiratory diseases that are related to public health. Therefore, we need further scientific evidence to make policies for the prevention of environmental lung diseases.

This Special Issue provides an opportunity to publish basic, epidemiological, and clinical research papers on environmental effects on respiratory health and environmental lung diseases. We welcome papers related to evidence of associations and/or mechanisms between environmental factors and respiratory diseases. We are also interested in scientific evidence that could support strategies to prevent environmental lung diseases. All manuscripts will be peer reviewed by experts in this field and would be due by 31 January 2023.

Prof. Dr. Woo-Jin Kim
Dr. Junghyun Kim
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Environmental Research and Public Health is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

environmental lung disease
ambient air pollution
chemical-associated lung disease
COPD
household air pollution
epigenetic alteration
lung function
lung growth

Published Papers (9 papers)

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Research

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14 pages, 5152 KiB

Open AccessArticle

Alveolar Type II Cell Damage and Nrf2-SOD1 Pathway Downregulation Are Involved in PM_2.5-Induced Lung Injury in Rats

by Rui Niu, Jie Cheng, Jian Sun, Fan Li, Huanle Fang, Ronghui Lei, Zhenxing Shen, Hao Hu and Jianjun Li

Int. J. Environ. Res. Public Health 2022, 19(19), 12893; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph191912893 - 08 Oct 2022

Cited by 2 | Viewed by 1597

Abstract

The general toxicity of fine particulate matter (PM_2.5) has been intensively studied, but its pulmonary toxicities are still not fully understood. To investigate the changes of lung tissue after PM_2.5 exposure and identify the potential mechanisms of pulmonary toxicity, PM_2.5 samples were firstly collected and analyzed. Next, different doses of PM_2.5 samples (5 mg/kg, 10 mg/kg, 20 mg/kg) were intratracheally instilled into rats to simulate lung inhalation of polluted air. After instillation for eight weeks, morphological alterations of the lung were examined, and the levels of oxidative stress were detected. The data indicated that the major contributors to PM_2.5 mass were organic carbon, elemental carbon, sulfate, nitrate, and ammonium. Different concentrations of PM_2.5 could trigger oxidative stress through increasing reactive oxygen species (ROS) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, and decreasing expression of antioxidant-related proteins (nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1 (SOD1) and catalase). Histochemical staining and transmission electron microscopy displayed pulmonary inflammation, collagen deposition, mitochondrial swelling, and a decreasing number of multilamellar bodies in alveolar type II cells after PM_2.5 exposure, which was related to PM_2.5-induced oxidative stress. These results provide a basis for a better understanding of pulmonary impairment in response to PM_2.5. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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29 pages, 11099 KiB

Open AccessArticle

Heat Wave and Bushfire Meteorology in New South Wales, Australia: Air Quality and Health Impacts

by Mohammad S. Islam, Tianxin Fang, Callum Oldfield, Puchanee Larpruenrudee, Hamidreza Mortazavy Beni, Md. M. Rahman, Shahid Husain and Yuantong Gu

Int. J. Environ. Res. Public Health 2022, 19(16), 10388; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph191610388 - 20 Aug 2022

Cited by 2 | Viewed by 2601

Abstract

The depletion of air quality is a major problem that is faced around the globe. In Australia, the pollutants emitted by bushfires play an important role in making the air polluted. These pollutants in the air result in many adverse impacts on the environment. This paper analysed the air pollution from the bushfires from November 2019 to July 2020 and identified how it affects the human respiratory system. The bush fires burnt over 13 million hectares, destroying over 2400 buildings. While these immediate effects were devastating, the long-term effects were just as devastating, with air pollution causing thousands of people to be admitted to hospitals and emergency departments because of respiratory complications. The pollutant that caused most of the health effects throughout Australia was Particulate Matter (PM) PM_2.5 and PM₁₀. Data collection and analysis were covered in this paper to illustrate where and when PM_2.5 and PM_10, and other pollutants were at their most concerning levels. Susceptible areas were identified by analysing environmental factors such as temperature and wind speed. The study identified how these pollutants in the air vary from region to region in the same time interval. This study also focused on how these pollutant distributions vary according to the temperature, which helps to determine the relationship between the heatwave and air quality. A computational model for PM_2.5 aerosol transport to the realistic airways was also developed to understand the bushfire exhaust aerosol transport and deposition in airways. This study would improve the knowledge of the heat wave and bushfire meteorology and corresponding respiratory health impacts. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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11 pages, 656 KiB

Open AccessArticle

The Role of Polygenic Susceptibility on Air Pollution-Associated Asthma between German and Japanese Elderly Women

by Sara Kress, Akinori Hara, Claudia Wigmann, Takehiro Sato, Keita Suzuki, Kim-Oanh Pham, Qi Zhao, Ashtyn Areal, Atsushi Tajima, Holger Schwender, Hiroyuki Nakamura and Tamara Schikowski

Int. J. Environ. Res. Public Health 2022, 19(16), 9869; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph19169869 - 10 Aug 2022

Viewed by 1614

Abstract

Polygenic susceptibility likely influences individual responses to air pollutants and the risk of asthma. We compared the role of polygenic susceptibility on air pollution-associated asthma between German and Japanese women. We investigated women that were enrolled in the German SALIA cohort (n = 771, mean age = 73 years) and the Japanese Shika cohort (n = 847, mean age = 67 years) with known asthma status. Adjusted logistic regression models were used to assess the associations between (1) particulate matter with a median aerodynamic diameter ≤ 2.5μm (PM_2.5) and nitrogen dioxide (NO₂), (2) polygenic risk scores (PRS), and (3) gene-environment interactions (G × E) with asthma. We found an increased risk of asthma in Japanese women after exposure to low pollutant levels (PM_2.5: median = 12.7µg/m³, p-value < 0.001, NO₂: median = 8.5µg/m³, p-value < 0.001) and in German women protective polygenic effects (p-value = 0.008). While we found no significant G × E effects, the direction in both groups was that the PRS increased the effect of PM_2.5 and decreased the effect of NO₂ on asthma. Our study confirms that exposure to low air pollution levels increases the risk of asthma in Japanese women and indicates polygenic effects in German women; however, there was no evidence of G × E effects. Future genome-wide G × E studies should further explore the role of ethnic-specific polygenic susceptibility to asthma. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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16 pages, 1292 KiB

Open AccessArticle

Hospitalization Costs of Respiratory Diseases Attributable to Temperature in Australia and Projections for Future Costs in the 2030s and 2050s under Climate Change

by Michael Tong, Berhanu Wondmagegn, Jianjun Xiang, Alana Hansen, Keith Dear, Dino Pisaniello, Blesson Varghese, Jianguo Xiao, Le Jian, Benjamin Scalley, Monika Nitschke, John Nairn, Hilary Bambrick, Jonathan Karnon and Peng Bi

Int. J. Environ. Res. Public Health 2022, 19(15), 9706; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph19159706 - 06 Aug 2022

Cited by 7 | Viewed by 2307

Abstract

This study aimed to estimate respiratory disease hospitalization costs attributable to ambient temperatures and to estimate the future hospitalization costs in Australia. The associations between daily hospitalization costs for respiratory diseases and temperatures in Sydney and Perth over the study period of 2010–2016 were analyzed using distributed non-linear lag models. Future hospitalization costs were estimated based on three predicted climate change scenarios-RCP2.6, RCP4.5 and RCP8.5. The estimated respiratory disease hospitalization costs attributable to ambient temperatures increased from 493.2 million Australian dollars (AUD) in the 2010s to more than AUD 700 million in 2050s in Sydney and from AUD 98.0 million to about AUD 150 million in Perth. The current cold attributable fraction in Sydney (23.7%) and Perth (11.2%) is estimated to decline by the middle of this century to (18.1–20.1%) and (5.1–6.6%), respectively, while the heat-attributable fraction for respiratory disease is expected to gradually increase from 2.6% up to 5.5% in Perth. Limitations of this study should be noted, such as lacking information on individual-level exposures, local air pollution levels, and other behavioral risks, which is common in such ecological studies. Nonetheless, this study found both cold and hot temperatures increased the overall hospitalization costs for respiratory diseases, although the attributable fractions varied. The largest contributor was cold temperatures. While respiratory disease hospitalization costs will increase in the future, climate change may result in a decrease in the cold attributable fraction and an increase in the heat attributable fraction, depending on the location. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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14 pages, 3846 KiB

Open AccessArticle

Analysis of Infection Transmission Routes through Exhaled Breath and Cough Particle Dispersion in a General Hospital

by Minji Jung, Woong June Chung, Minki Sung, Seongmin Jo and Jinkwan Hong

Int. J. Environ. Res. Public Health 2022, 19(5), 2512; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph19052512 - 22 Feb 2022

Cited by 7 | Viewed by 1463

Abstract

Identifying infection transmission routes in hospitals may prevent the spread of respiratory viruses and mass infections. Most previous related research focused on the air movement of passive tracers, which typically represent breathing. In this study, particle evaporation and dispersions with various particle sizes were applied to evaluate particle movement because of breathing and coughing using computational fluid dynamics (CFD) simulations. Pyeongtaek St. Mary Hospital, where a Middle East respiratory syndrome (MERS) index patient infected several patients on the same floor, was used for a case study. We compared the dispersion characteristics of various particle sizes and validated results by comparing infection rates in different ward. Results indicated that droplets spread across the corridor and dispersed to wards that were more than 17 m apart from the index patient by natural ventilation. Droplets from exhaled breath under steady-state simulation showed a wider range of dispersion than cough droplets under transient simulation, but cough droplet dispersion was more consistent with the actual infection rate in each ward. Cough droplets sized under 75 µm evaporated to 26% of the initial size and started to disperse into the corridor within one minute; in nine minutes, droplets dispersed throughout every ward. This study may increase awareness on the dispersion characteristics of infectious particles. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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20 pages, 2324 KiB

Open AccessArticle

The Sulfotransferase SULT1C2 Is Epigenetically Activated and Transcriptionally Induced by Tobacco Exposure and Is Associated with Patient Outcome in Lung Adenocarcinoma

by Candace Johnson, Daniel J. Mullen, Suhaida A. Selamat, Mihaela Campan, Ite A. Offringa and Crystal N. Marconett

Int. J. Environ. Res. Public Health 2022, 19(1), 416; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph19010416 - 31 Dec 2021

Cited by 3 | Viewed by 1735

Abstract

Lung cancer is the leading cause of cancer-related death. Tobacco exposure is associated with 80–90% of lung cancer cases. The SULT1C2 sulfotransferase modifies xenobiotic compounds to enhance secretion but can also render these compounds carcinogenic. To determine if SULT1C2 contributes to tobacco-related carcinogenesis in the lung, we analyzed the expression and epigenetic state of SULT1C2 in human lung adenocarcinoma (LUAD) samples and in LUAD cell lines exposed to cigarette smoke condensate (CSC). SULT1C2 expression was significantly positively correlated to overall LUAD patient survival in smokers, was elevated in LUAD tumors compared to adjacent non-tumor lung, and was significantly correlated with levels of patient exposure to tobacco smoke. SULT1C2 promoter DNA methylation was inversely correlated with expression in LUAD, and hypomethylation of the SULT1C2 promoter was observed in Asian patients, as compared to Caucasians. In vitro analysis of LUAD cell lines indicates that CSC stimulates expression of SULT1C2 in a dose-dependent and cell-line-specific manner. In vitro methylation of the SULT1C2 promoter significantly decreased transcriptional activity of a reporter plasmid, and SULT1C2 expression was activated by the DNA demethylating agent 5-Aza-2′-deoxycytidine in a cell line in which the SULT1C2 promoter was hypermethylated. An aryl hydrocarbon receptor (AHR) binding site was detected spanning critical methylation sites upstream of SULT1C2. CSC exposure significantly increased AHR binding to this predicted binding site in the SULT1C2 promoter in multiple lung cell lines. Our data suggest that CSC exposure leads to activation of the AHR transcription factor, increased binding to the SULT1C2 promoter, and upregulation of SULT1C2 expression and that this process is inhibited by DNA methylation at the SULT1C2 locus. Additionally, our results suggest that the level of SULT1C2 promoter methylation and gene expression in normal lung varies depending on the race of the patient, which could in part reflect the molecular mechanisms of racial disparities seen in lung cellular responses to cigarette smoke exposure. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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Review

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12 pages, 393 KiB

Open AccessReview

The Impact of Ambient Environmental and Occupational Pollution on Respiratory Diseases

by Chinatsu Nishida and Kazuhiro Yatera

Int. J. Environ. Res. Public Health 2022, 19(5), 2788; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph19052788 - 27 Feb 2022

Cited by 20 | Viewed by 4773

Abstract

Ambient pollutants and occupational pollutants may cause and exacerbate various lung and respiratory diseases. This review describes lung and respiratory diseases in relation to ambient pollutants, particularly particulate matter (PM_2.5), and occupational air pollutants, excluding communicable diseases and indoor pollutants, including tobacco smoke exposure. PM_2.5 produced by combustion is an important ambient pollutant. PM_2.5 can cause asthma attacks and exacerbations of chronic obstructive pulmonary disease in the short term. Further, it not only carries a risk of lung cancer and death, but also hinders the development of lung function in children in the long term. It has recently been suggested that air pollution, such as PM_2.5, is a risk factor for severe coronavirus disease (COVID-19). Asbestos, which causes asbestosis, lung cancer, and malignant mesothelioma, and crystalline silica, which cause silicosis, are well-known traditional occupational pollutants leading to pneumoconiosis. While work-related asthma (WRA) is the most common occupational lung disease in recent years, many different agents cause WRA, including natural and synthetic chemicals and irritant gases. Primary preventive interventions that increase awareness of pollutants and reduce the development and exacerbation of diseases caused by air pollutants are paramount to addressing ambient and occupational pollution. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

19 pages, 373 KiB

Open AccessReview

Is Isocyanate Exposure and Occupational Asthma Still a Major Occupational Health Concern? Systematic Literature Review

by Elie Coureau, Luc Fontana, Céline Lamouroux, Carole Pélissier and Barbara Charbotel

Int. J. Environ. Res. Public Health 2021, 18(24), 13181; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph182413181 - 14 Dec 2021

Cited by 7 | Viewed by 2965

Abstract

Isocyanate, whose disease-inducing mechanism is poorly understood, with poor prognosis, is widely used. Asthma is the most frequent manifestation of prolonged exposure. We assessed the evolution of the incidence of isocyanate-induced occupational asthma over time. PubMed and Cochrane databases were systematically searched for studies published since 1990 that assessed the relationship between occupational exposure to isocyanates and asthma. We identified 39 studies: five retrospective cohort studies, seven prospective cohort studies, three of which were inception cohorts), seven observational cross-sectional studies, five literature reviews, two case series, and 13 registry studies. The incidence of occupational asthma secondary to isocyanate exposure has decreased from more than 5% in the early 1990s to 0.9% in 2017 in the United States. Despite the wide use of optimal collective and individual protection measures, the risk of occupational asthma has stabilized. Occupational asthma risk can be assessed with good sensitivity using self-questionnaires and pulmonary function tests. Occupational avoidance should be implemented as soon as possible after the first symptoms appear because the prognosis becomes increasingly poor with the persistence of exposure. It is now necessary to study specifically cutaneous sensitization to isocyanates and to define what protective equipment is effective against this mode of exposure. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

Other

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9 pages, 900 KiB

Open AccessOpinion

A Review of the Role of Pollen in COVID-19 Infection

by Nur Sabrina Idrose, Jingwen Zhang, Caroline J. Lodge, Bircan Erbas, Jo A. Douglass, Dinh S. Bui and Shyamali C. Dharmage

Int. J. Environ. Res. Public Health 2023, 20(10), 5805; https://0-doi-org.brum.beds.ac.uk/10.3390/ijerph20105805 - 12 May 2023

Cited by 1 | Viewed by 1366

Abstract

There is current interest in the role of ambient pollen in the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2 or COVID-19) infection risk. The aim of this review is to summarise studies published up until January 2023 investigating the relationship between airborne pollen and the risk of COVID-19 infection. We found conflicting evidence, with some studies showing that pollen may increase the risk of COVID-19 infection by acting as a carrier, while others showed that pollen may reduce the risk by acting as an inhibiting factor. A few studies reported no evidence of an association between pollen and the risk of infection. A major limiting factor of this research is not being able to determine whether pollen contributed to the susceptibility to infection or just the expression of symptoms. Hence, more research is needed to better understand this highly complex relationship. Future investigations should consider individual and sociodemographic factors as potential effect modifiers when investigating these associations. This knowledge will help to identify targeted interventions. Full article

(This article belongs to the Special Issue Environment and Respiratory Health)

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