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Toxics
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Effects of Exposure to Air Pollution on Respiratory Health
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Effects of Exposure to Air Pollution on Respiratory Health

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 25072

Special Issue Editor

Dr. Swapna Upadhyay

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Guest Editor
IMM: Institute of Environmental Medicine, Unit of Integrative Toxicology, Karolinska Institutet, SE-171 77 Stockholm, Sweden
Interests: acute and chronic lung disease (COPD); outdoor (particles and gaseous agents) and indoor (biomass smoke) air pollutants; occupational chemical exposure; e-cigarette exposure; AOP for respiratory disease: advanced in vitro lung mucosa model to human translational approaches
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

The air we breathe has important consequences on our health and development. The respiratory system is a primary target of air pollution-mediated health effects. Ambient air pollution is an established cause of morbidity and mortality—like tobacco smoke. Even more than passive smoking, air pollution is not a lifestyle choice, but ubiquitous involuntary environmental exposure, which can affect the entire population, from womb to death. The enormous burden of disease due to air pollution is increasingly being considered by governments and institutions around the globe as a major public health concern. Respirable particulate matter (PM) has been regarded as a “criteria air pollutant”, along with carbon monoxide, ground level ozone, fine- and ultra-fine particulate matters, diesel/biodiesel particles, metal particles (lead, palladium, etc.), nitrogen dioxide, and sulphur dioxide. Globally, >8 million premature deaths are related to outdoor and indoor air-pollution. Low- and lower-middle income countries (LMICs) bear the maximum brunt of air pollution-related adverse health effects. The source of air pollution in LMICs is two pronged—outdoor and indoor air pollution. Rapid urbanization and industrialization, on the one hand (urban), with a lack of clean energy sources, leading to the use of biomass fuel for cooking and heating purposes (rural), happens simultaneously. A substantial body of epidemiological evidence indicates the association of chronic respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD) to ambient PM exposure. It is estimated that approximately 50% of COPD cases, the fourth leading cause of death globally, can be attributed to non-tobacco-related causes. It is plausible that the mechanism of air pollution-related COPD may be different from tobacco-smoke-mediated COPD. Thus, environmental and occupational causes COPD warrant more attention. Although several works of epidemiological evidence showing the association between exposure to air pollutants and various respiratory impairments do exist. However, details of the molecular mechanism leading to the onset of chronic respiratory (e.g., COPD) diseases remain unclear or under explored.

Therefore, in this Special Issue of Toxics will cover the most recent research on air pollution related respiratory diseases, namely:

  • Respiratory toxicity following exposure to air pollutants.
  • Outdoor and indoor air quality monitoring: special focus on LMIC.
  • Gender perspective air pollution (indoor and outdoor) mediated respiratory adverse outcome pathways.
  • Acute and repeated exposure to ambient gaseous and particulate matters using advanced/physiologically-relevant in vitro models.
  • Air pollutant and molecular pathogenesis for COPD onset: in vivo to human study.

Dr. Swapna Upadhyay
Guest Editor

Manuscript Submission Information

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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. Toxics 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 2600 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

  • air pollutants
  • respiratory diseases
  • indoor and outdoor air pollution
  • respiratory diseases and AOP
  • air pollution and COPD

Published Papers (8 papers)

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Research

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16 pages, 3617 KiB  
Article
Establishment of Repeated In Vitro Exposure System for Evaluating Pulmonary Toxicity of Representative Criteria Air Pollutants Using Advanced Bronchial Mucosa Models
by Swapna Upadhyay, Ashesh Chakraborty, Tania A. Thimraj, Marialuisa Baldi, Anna Steneholm, Koustav Ganguly, Per Gerde, Lena Ernstgård and Lena Palmberg
Toxics 2022, 10(6), 277; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics10060277 - 24 May 2022
Cited by 3 | Viewed by 2113
Abstract
There is mounting evidence that shows the association between chronic exposure to air pollutants (particulate matter and gaseous) and onset of various respiratory impairments. However, the corresponding toxicological mechanisms of mixed exposure are poorly understood. Therefore, in this study, we aimed to establish [...] Read more.
There is mounting evidence that shows the association between chronic exposure to air pollutants (particulate matter and gaseous) and onset of various respiratory impairments. However, the corresponding toxicological mechanisms of mixed exposure are poorly understood. Therefore, in this study, we aimed to establish a repeated exposure setting for evaluating the pulmonary toxicological effects of diesel exhaust particles (DEP), nitrogen dioxide (NO2), and sulfur dioxide (SO2) as representative criterial air pollutants. Single, combined (DEP with NO2 and SO2), and repeated exposures were performed using physiologically relevant human bronchial mucosa models developed at the air–liquid interface (bro-ALI). The bro-ALI models were generated using human primary bronchial epithelial cells (3–4 donors; 2 replicates per donor). The exposure regime included the following: 1. DEP (12.5 µg/cm2; 3 min/day, 3 days); 2. low gaseous (NO2: 0.1 ppm + SO2: 0.2 ppm); (30 min/day, 3 days); 3. high gaseous (NO2: 0.2 ppm + SO2: 0.4 ppm) (30 min/day, 3 days); and 4. single combined (DEP + low gaseous for 1 day). The markers for pro-inflammatory (IL8, IL6, NFKB, TNF), oxidative stress (HMOX1, GSTA1, SOD3,) and tissue injury/repair (MMP9, TIMP1) responses were assessed at transcriptional and/ or secreted protein levels following exposure. The corresponding sham-exposed samples under identical conditions served as the control. A non-parametric statistical analysis was performed and p < 0.05 was considered as significant. Repeated exposure to DEP and single combined (DEP + low gaseous) exposure showed significant alteration in the pro-inflammatory, oxidative stress and tissue injury responses compared to repeated exposures to gaseous air pollutants. The study demonstrates that it is feasible to predict the long-term effects of air pollutants using the above explained exposure system. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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9 pages, 1155 KiB  
Article
Modulation by Ozone of Glucocorticoid-Regulating Factors in the Lungs in Relation to Stress Axis Reactivity
by Jith Thomas and Errol M. Thomson
Toxics 2021, 9(11), 290; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9110290 - 03 Nov 2021
Cited by 1 | Viewed by 1400
Abstract
Exposure to air pollutants increases levels of circulating glucocorticoid stress hormones that exert profound effects relevant to health and disease. However, the nature and magnitude of tissue-level effects are modulated by factors that regulate local glucocorticoid activity; accordingly, inter-individual differences could contribute to [...] Read more.
Exposure to air pollutants increases levels of circulating glucocorticoid stress hormones that exert profound effects relevant to health and disease. However, the nature and magnitude of tissue-level effects are modulated by factors that regulate local glucocorticoid activity; accordingly, inter-individual differences could contribute to susceptibility. In the present study, we characterized effects of ozone (O3) inhalation on glucocorticoid-regulating factors in the lungs of rat strains with contrasting hypothalamic–pituitary–adrenal stress axis responses. Hyper-responsive Fischer (F344) and less responsive Lewis (LEW) rats were exposed to air or 0.8 ppm O3 for 4 h by nose-only inhalation. Levels of the high-specificity and -affinity corticosteroid-binding globulin protein increased in the lungs of both strains proportional to the rise in corticosterone levels following O3 exposure. Ozone reduced the ratio of 11β-hydroxysteroid dehydrogenase type 1 (HSDB1)/HSDB2 mRNA in the lungs of F344 but not LEW, indicating strain-specific transcriptional regulation of the major glucocorticoid metabolism factors that control tissue-level action. Intercellular adhesion molecule (ICAM)-1 and total elastase activity were increased by O3 in both strains, consistent with extravasation and tissue remodeling processes following injury. However, mRNA levels of inflammatory markers were significantly higher in the lungs of O3-exposed LEW compared to F344. The data show that strain differences in the glucocorticoid response to O3 are accompanied by corresponding changes in regulatory factors, and that these effects are collectively associated with a differential inflammatory response to O3. Innate differences in glucocorticoid regulatory factors may modulate the pulmonary effects of inhaled pollutants, thereby contributing to differential susceptibility. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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15 pages, 2104 KiB  
Article
Circulating Secretoglobin Family 1A Member 1 (SCGB1A1) Levels as a Marker of Biomass Smoke Induced Chronic Obstructive Pulmonary Disease
by Vivek Vardhan Veerapaneni, Swapna Upadhyay, Tania A. Thimraj, Jayaraj Biligere Siddaiah, Chaya Sindaghatta Krishnarao, Komarla Sundararaja Lokesh, Rajesh Thimmulappa, Lena Palmberg, Koustav Ganguly and Mahesh Padukudru Anand
Toxics 2021, 9(9), 208; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9090208 - 31 Aug 2021
Cited by 3 | Viewed by 2282
Abstract
Secretoglobin family 1A member 1 (SCGB1A1) alternatively known as club cell protein 16 is a protective pneumo-protein. Decreased serum levels of SCGB1A1 have been associated with tobacco smoke induced chronic obstructive pulmonary disease (TS-COPD). Exposure to biomass smoke (BMS) is an important COPD [...] Read more.
Secretoglobin family 1A member 1 (SCGB1A1) alternatively known as club cell protein 16 is a protective pneumo-protein. Decreased serum levels of SCGB1A1 have been associated with tobacco smoke induced chronic obstructive pulmonary disease (TS-COPD). Exposure to biomass smoke (BMS) is an important COPD risk factor among women in low and lower-middle income countries. Therefore, in a cross-sectional study (n = 50/group; total 200 subjects) we assessed serum SCGB1A1 levels in BMS-COPD subjects (11 male, 39 female) compared to TS-COPD (all male) along with TS-CONTROL (asymptomatic smokers, all male) and healthy controls (29 male, 21 female) in an Indian population. Normal and chronic bronchitis like bronchial mucosa models developed at the air–liquid interface using human primary bronchial epithelial cells (3 donors, and three replicates per donor) were exposed to cigarette smoke condensate (CSC; 0.25, 0.5, and 1%) to assess SCGB1A1 transcript expression and protein secretion. Significantly (p < 0.0001) decreased serum SCGB1A1 concentrations (median, interquartile range, ng/mL) were detected in both BMS-COPD (1.6; 1.3–2.4) and TS-COPD (1.8; 1.4–2.5) subjects compared to TS-CONTROL (3.3; 2.9–3.5) and healthy controls (5.1; 4.5–7.2). The levels of SCGB1A1 were positively correlated (r = 0.7–0.8; p < 0.0001) with forced expiratory volume in 1 s, forced vital capacity, their ratios, and exercise capacity. The findings are also consistent within the BMS-COPD sub-group as well. Significantly (p < 0.03) decreased SCGB1A1 concentrations were detected with severity of COPD, dyspnea, quality of life, and mortality indicators. In vitro studies demonstrated significantly (p < 0.05) decreased SCGB1A1 transcript and/or protein levels following CSC exposure. Circulating SCGB1A1 levels may therefore also be considered as a potent marker of BMS-COPD and warrant studies in larger independent cohorts. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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17 pages, 1255 KiB  
Article
Impact of a Large Fire and Subsequent Pollution Control Failure at a Coke Works on Acute Asthma Exacerbations in Nearby Adult Residents
by Tricia L. Morphew, Arvind Venkat, John Graham, Matthew Mehalik, Norman Anderson and Deborah Gentile
Toxics 2021, 9(7), 147; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9070147 - 25 Jun 2021
Viewed by 2499
Abstract
Clairton, Pennsylvania, is home to the largest coke works facility in the United States (US). On 24 December 2018, a large fire occurred at this facility and damaged pollution control equipment. Although repairs were not completed for several months, production continued at pre-fire [...] Read more.
Clairton, Pennsylvania, is home to the largest coke works facility in the United States (US). On 24 December 2018, a large fire occurred at this facility and damaged pollution control equipment. Although repairs were not completed for several months, production continued at pre-fire capacity and daily emissions increased by 24 to 35 times, with multiple exceedances of monitored levels of outdoor air pollution (OAP). The aim of this study was to objectively evaluate the impact of this industrial incident and resultant OAP exceedances on asthma morbidity. We assessed pre-fire and post-fire rate ratios (RR) of outpatient and emergency department (ED) visits for asthma exacerbations among nearby adult residents. Pre-fire versus post-fire RRs increased for both visit types: RR = 1.82 (95% CI: 1.30, 2.53; p < 0.001) and 1.84 (95% CI: 1.05, 3.22; p = 0.032) for outpatient and ED visits, respectively. Additionally, total visit rates increased on days with OAP exceedances: RR = 2.47 (95% CI: 1.52, 4.01; p < 0.0001), 1.58 (95% CI: 1.00, 2.48; p = 0.048) and 1.79 (95% CI: 1.27, 2.54; p = 0.001) for PM2.5, SO2, and H2S exceedance days, respectively. These results show a near doubling of acute visits for asthma exacerbations in nearby adult residents during this industrial incident and underscore the need for prompt remediation and public notification of OAP exceedances to prevent adverse health impacts. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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14 pages, 2760 KiB  
Article
Inflammatory Biomarkers Interleukin 1 Beta (IL-1β) and Tumour Necrosis Factor Alpha (TNF-α) Are Differentially Elevated in Tobacco Smoke Associated COPD and Biomass Smoke Associated COPD
by Bellipady Shyam Prasad Shetty, Sindaghatta Krishnarao Chaya, Sravan Kumar V, Maheswarappa Mahendra, Biligere Siddaiah Jayaraj, Komarla Sundararaja Lokesh, Koustav Ganguly and Padukudru Anand Mahesh
Toxics 2021, 9(4), 72; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9040072 - 01 Apr 2021
Cited by 17 | Viewed by 2568
Abstract
Chronic obstructive pulmonary disease (COPD), the leading cause of mortality and morbidity worldwide, is characterized by abnormal activation of inflammatory cells. The increased pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), further amplify the inflammation. We evaluated [...] Read more.
Chronic obstructive pulmonary disease (COPD), the leading cause of mortality and morbidity worldwide, is characterized by abnormal activation of inflammatory cells. The increased pro-inflammatory cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), further amplify the inflammation. We evaluated the dose response relationship of IL-1β and TNF-α levels and severity of airflow limitation, and differential responses in IL-1β and TNF-α between biomass COPD (BMS-COPD) and tobacco smoke COPD (TS-COPD) using a case control design in 160 subjects. Patients with COPD had higher serum levels of both IL-1β and TNF-α compared to healthy controls. A large difference in TNF-α was observed between TS-COPD and BMS-COPD, where TS-COPD patients had much higher levels. Serum IL-1β levels were higher in BMS-COPD. Levels of IL-1β correlated better with severity of airflow limitation than TNF-α levels. Both TNF-α and IL-1β levels had a negative linear relationship with Forced Expiratory Volume in 1st second (FEV1) and six-minute walk distance. The correlations were stronger with FEV1 than six-minute walk distance. The correlations of TNF-α and IL-1β with St George Respiratory Questionnaire (SGRQ) scores and body mass index (BMI) were not significant. In conclusion, the levels of pro-inflammatory cytokines TNF-α and IL-1β are differently elevated in TS-COPD and BMS-COPD, respectively. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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Review

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27 pages, 3528 KiB  
Review
Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution
by Myles X. Hodge, Andres R. Henriquez and Urmila P. Kodavanti
Toxics 2021, 9(6), 132; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9060132 - 04 Jun 2021
Cited by 7 | Viewed by 6025
Abstract
Adrenergic receptors (ARs) and glucocorticoid receptors (GRs) are activated by circulating catecholamines and glucocorticoids, respectively. These receptors regulate the homeostasis of physiological processes with specificity via multiple receptor subtypes, wide tissue-specific distribution, and interactions with other receptors and signaling processes. Based on their [...] Read more.
Adrenergic receptors (ARs) and glucocorticoid receptors (GRs) are activated by circulating catecholamines and glucocorticoids, respectively. These receptors regulate the homeostasis of physiological processes with specificity via multiple receptor subtypes, wide tissue-specific distribution, and interactions with other receptors and signaling processes. Based on their physiological roles, ARs and GRs are widely manipulated therapeutically for chronic diseases. Although these receptors play key roles in inflammatory and cellular homeostatic processes, little research has addressed their involvement in the health effects of air pollution. We have recently demonstrated that ozone, a prototypic air pollutant, mediates pulmonary and systemic effects through the activation of these receptors. A single exposure to ozone induces the sympathetic–adrenal–medullary and hypothalamic–pituitary–adrenal axes, resulting in the release of epinephrine and corticosterone into the circulation. These hormones act as ligands for ARs and GRs. The roles of beta AR (βARs) and GRs in ozone-induced pulmonary injury and inflammation were confirmed in a number of studies using interventional approaches. Accordingly, the activation status of ARs and GRs is critical in mediating the health effects of inhaled irritants. In this paper, we review the cellular distribution and functions of ARs and GRs, their lung-specific localization, and their involvement in ozone-induced health effects, in order to capture attention for future research. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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Other

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15 pages, 3051 KiB  
Systematic Review
Effect of Indoor Air Pollution on Chronic Obstructive Pulmonary Disease (COPD) Deaths in Southern Asia—A Systematic Review and Meta-Analysis
by Bellipady Shyam Prasad Shetty, George D’Souza and Mahesh Padukudru Anand
Toxics 2021, 9(4), 85; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics9040085 - 16 Apr 2021
Cited by 13 | Viewed by 3943
Abstract
Background: About half of the population in developing countries are exposed to indoor pollution such as combustion fuels at present. Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality globally and the primary cause of COPD in women is [...] Read more.
Background: About half of the population in developing countries are exposed to indoor pollution such as combustion fuels at present. Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality globally and the primary cause of COPD in women is indoor air pollution exposure, while tobacco smoking is the leading cause in men. The aim of this systematic review and meta-analysis is to evaluate the correlation between the indoor air pollution and deaths related to COPD and COPD prevalence in South Asia. Methods: A systematic search on studies with sufficient statistical power has been conducted from 1985 until 30 June 2020, in English electronic databases following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines in MEDLINE and PubMed databases with the terms Chronic Obstructive Pulmonary disease COPD or Chronic Bronchitis or Emphysema or COPD Deaths or Chronic Obstructive Lung Disease or Airflow Obstruction or Chronic Airflow Obstruction or Airflow Obstruction, Chronic or Bronchitis, Chronic and Mortality or Death or Deceased was conducted. Studies were eligible if they were Prospective controlled or non-controlled trials conducted in Southern Asia/ Asia and Retrospective studies conducted in Southern Asia/ Asia. Results: The results have concluded that long term exposure to indoor pollution had a significant effect on COPD deaths as well as its symptoms. Odd’s ratio was in a range of 1.05 (Randomized controlled trials) to 7.87 (Cross sectional studies) for all the studies mentioned. Meta-analysis observed a significantly higher Odds Ratio of 2.13 for COPD mortality and 2.08 for COPD prevalence on exposure to indoor air pollution. Conclusion: Exposure to solid fuel smoke is consistently and significantly correlated with COPD mortality and COPD prevalence in South Asian countries, in spite of heterogeneity observed in the studies included. For performing domestic tasks, initiatives are to be taken to reduce dependency on solid fuel by using cleaner alternatives or comparatively cleaner technology. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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17 pages, 1803 KiB  
Conference Report
Clinical, Epidemiological and Experimental Approaches to Assess Adverse Health Outcomes of Indoor Biomass Smoke Exposure: Conclusions from An Indo-Swedish Workshop in Mysuru, January 2020
by Mahesh Padukudru Anand, Kjell Larsson, Gunnar Johanson, Harish C. Phuleria, P. Veeranna Ravindra, Lena Ernstgård, Ulaganathan Mabalirajan, Murali Krishna, Lena Palmberg, Krystal J. Godri Pollitt, Swapna Upadhyay and Koustav Ganguly
Toxics 2020, 8(3), 68; https://0-doi-org.brum.beds.ac.uk/10.3390/toxics8030068 - 05 Sep 2020
Cited by 2 | Viewed by 3153
Abstract
This report summarizes the outcome of a workshop held in Mysuru, India in January 2020 addressing the adverse health effects of exposure to biomass smoke (BMS). The aim of the workshop was to identify uncertainties and gaps in knowledge and possible methods to [...] Read more.
This report summarizes the outcome of a workshop held in Mysuru, India in January 2020 addressing the adverse health effects of exposure to biomass smoke (BMS). The aim of the workshop was to identify uncertainties and gaps in knowledge and possible methods to address them in the Mysuru study on Determinants of Health in Rural Adults (MUDHRA) cohort. Specific aims were to discuss the possibility to improve and introduce new screening methods for exposure and effect, logistic limitations and other potential obstacles, and plausible strategies to overcome these in future studies. Field visits were included in the workshop prior to discussing these issues. The workshop concluded that multi-disciplinary approaches to perform: (a) indoor and personalized exposure assessment; (b) clinical and epidemiological field studies among children, adolescents, and adults; (c) controlled exposure experiments using physiologically relevant in vitro and in vivo models to understand molecular patho-mechanisms are warranted to dissect BMS-induced adverse health effects. It was perceived that assessment of dietary exposure (like phytochemical index) may serve as an important indicator for understanding potential protective mechanisms. Well trained field teams and close collaboration with the participating hospital were identified as the key requirements to successfully carry out the study objectives. Full article
(This article belongs to the Special Issue Effects of Exposure to Air Pollution on Respiratory Health)
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