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Toxics
Special Issues
Exposure to Air Pollution and Respiratory Health Effects
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Exposure to Air Pollution and Respiratory Health Effects

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Air Pollution and Health".

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 7809

Special Issue Editors

Dr. Jianbing Wang

E-Mail Website
Guest Editor
School of Public Health, Zhejiang University, Hangzhou, China
Interests: environmental epidemiology; air pollution; cardiovascular disease; risk factors; cohort study
Special Issues, Collections and Topics in MDPI journals
Dr. Zhenyu Zhang

E-Mail Website
Guest Editor
Department of Global Health, Peking University, Beijing, China
Interests: environmental exposure estimation; air pollution; climate change; cardiovascular diseases; infectious diseases

Special Issue Information

Dear Colleagues,

Air pollutants, including particle pollution, ground-level ozone, carbon monoxide, sulfur oxides, nitrogen oxides, and lead, represent a considerable threat to human health. According to the 2019 Global Burden of Disease Study, exposure to air pollution is the fourth leading risk factor for death worldwide, accounting for 6.67 million deaths in 2019. Recent years have seen global concern regarding the harmful impact of air pollution, with a growing emphasis on respiratory health. Due to direct exposure, the respiratory tract is the main organ affected by air pollution. In fact, these effects can be grouped into short- and long-term effects. Short-term exposure to air pollution is a well-known trigger of respiratory disease exacerbations, including wheezing, coughing and chest tightness, and asthma. The long-term effects are chronic, lasting for years or the patient’s whole life. It can cause chronic laryngitis, chronic lung diseases, and respiratory tract cancers.

The present Special Issue would like to collect original environmental epidemiology studies on air pollution and respiratory health effects, including, but not limited to, ecological studies, case-crossover studies and cohort studies, systematic reviews, and short communications.

Dr. Jianbing Wang
Dr. Zhenyu Zhang
Guest Editors

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Keywords

  • air pollution
  • respiratory disease
  • cohort study
  • ecological study
  • case-crossover study
  • environmental epidemiology

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Published Papers (4 papers)

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Research

9 pages, 212 KiB  
Article
Smoking Exposure and the Risk of Latent Tuberculosis Infection: Results from NHANES 2011–2012
by Xinsong Hu, Jiongya Liu, Yan Shao, Guoli Li, Honghuan Song, Qiao Liu, Cheng Chen and Limei Zhu
Toxics 2024, 12(1), 94; https://doi.org/10.3390/toxics12010094 - 22 Jan 2024
Cited by 4 | Viewed by 2055
Abstract
The association between smoking exposure and latent tuberculosis infection (LTBI) has been investigated in a few studies; however, further investigation is needed. In this study, the 2011–2012 NHANES population was used to evaluate smoking exposure and LTBI risk. A total of 7042 participants [...] Read more.
The association between smoking exposure and latent tuberculosis infection (LTBI) has been investigated in a few studies; however, further investigation is needed. In this study, the 2011–2012 NHANES population was used to evaluate smoking exposure and LTBI risk. A total of 7042 participants with available LTBI results and without active tuberculosis were included for analysis. Smoking was defined as participants who smoked at least 100 cigarettes in their life. Both univariable and multivariable analysis were adopted to evaluate smoking exposure, as well as related factors on the risk of LTBI. LTBI rates among current smokers (12.1%) and former smokers (9.9%) were higher than non-smokers (5.9%). However, current smokers and former smokers were not significantly associated with LTBI risk when compared to non-smokers after adjusting by age and sex in the multivariable analysis. Meanwhile, we found that passive smoking was not associated with LTBI (adjusted odds ratio (AOR), 0.85; 95%CI, 0.66–1.09). In multivariable analysis, current smoking was associated with LTBI (OR, 1.67; 95%CI, 1.28–2.19), while former smokers had an increased OR of LTBI, but the OR did not reach statistical significance (OR, 1.15; 95%CI, 0.90–1.48). Household tuberculosis (TB) contact was also related to LTBI (OR, 1.93; 95%CI, 1.25–2.99). However, BMI and diabetes were not found to be associated with LTBI. Smoking, especially current smoking, was significantly associated with LTBI. LTBI screening should be recommended for active smokers. Former smoking and passive smoking exposure were not found to have a significant relationship with LTBI risk. However, the high LTBI rate among quitters indicated we should pay more attention to former smokers with LTBI. Full article
(This article belongs to the Special Issue Exposure to Air Pollution and Respiratory Health Effects)
12 pages, 964 KiB  
Article
The Combined Effects of Hourly Multi-Pollutant on the Risk of Ambulance Emergency Calls: A Seven-Year Time Series Study
by Hanxu Shi, Qiang Zhou, Hongjuan Zhang, Shengzhi Sun, Junfeng Zhao, Yasha Wang, Jie Huang, Yinzi Jin, Zhijie Zheng, Rengyu Wu and Zhenyu Zhang
Toxics 2023, 11(11), 895; https://doi.org/10.3390/toxics11110895 - 31 Oct 2023
Viewed by 1318
Abstract
Background: Ambulance emergency calls (AECs) are seen as a more suitable metric for syndromic surveillance due to their heightened sensitivity in reflecting the health impacts of air pollutants. Limited evidence has emphasized the combined effect of hourly air pollutants on AECs. This study [...] Read more.
Background: Ambulance emergency calls (AECs) are seen as a more suitable metric for syndromic surveillance due to their heightened sensitivity in reflecting the health impacts of air pollutants. Limited evidence has emphasized the combined effect of hourly air pollutants on AECs. This study aims to investigate the combined effects of multipollutants (i.e., PM2.5, PM10, Ozone, NO2, and SO2) on all-cause and cause-specific AECs by using the quantile g-computation method. Methods: We used ambulance emergency dispatch data, air pollutant data, and meteorological data from between 1 January 2013 and 31 December 2019 in Shenzhen, China, to estimate the associations of hourly multipollutants with AECs. We followed a two-stage analytic protocol, including the distributed lag nonlinear model, to examine the predominant lag for each air pollutant, as well as the quantile g-computation model to determine the associations of air pollutant mixtures with all-cause and cause-specific AECs. Results: A total of 3,022,164 patients were identified during the study period in Shenzhen. We found that each interquartile range increment in the concentrations of PM2.5, PM10, Ozone, NO2, and SO2 in 0–8 h, 0–8 h, 0–48 h, 0–28 h, and 0–24 h was associated with the highest risk of AECs. Each interquartile range increase in the mixture of air pollutants was significantly associated with a 1.67% (95% CI, 0.12–3.12%) increase in the risk of all-cause AECs, a 1.81% (95% CI, 0.25–3.39%) increase in the risk of vascular AECs, a 1.77% (95% CI, 0.44–3.11%) increase in reproductive AECs, and a 2.12% (95% CI, 0.56–3.71%) increase in AECs due to injuries. Conclusions: We found combined effects of pollutant mixtures associated with an increased risk of AECs across various causes. These findings highlight the importance of targeted policies and interventions to reduce air pollution, particularly for PM, Ozone, and NO2 emissions. Full article
(This article belongs to the Special Issue Exposure to Air Pollution and Respiratory Health Effects)
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13 pages, 4111 KiB  
Article
Long-Term Exposure to PM2.5 and Mortality: A Cohort Study in China
by Jingjing Hu, Luhua Yu, Zongming Yang, Jie Qiu, Jing Li, Peng Shen, Hongbo Lin, Liming Shui, Mengling Tang, Mingjuan Jin, Kun Chen and Jianbing Wang
Toxics 2023, 11(9), 727; https://doi.org/10.3390/toxics11090727 - 24 Aug 2023
Cited by 2 | Viewed by 1620
Abstract
We investigated the association of long-term exposure to atmospheric PM2.5 with non-accidental and cause-specific mortality in Yinzhou, China. From July 2015 to January 2018, a total of 29,564 individuals aged ≥ 40 years in Yinzhou were recruited for a prospective cohort study. [...] Read more.
We investigated the association of long-term exposure to atmospheric PM2.5 with non-accidental and cause-specific mortality in Yinzhou, China. From July 2015 to January 2018, a total of 29,564 individuals aged ≥ 40 years in Yinzhou were recruited for a prospective cohort study. We used the Cox proportional-hazards model to analyze the relationship of the 2-year average concentration of PM2.5 prior to the baseline with non-accidental and cause-specific mortality. The median PM2.5 concentration was 36.51 μg/m3 (range: 25.57–45.40 μg/m3). In model 4, the hazard ratios per 10 μg/m3 increment in PM2.5 were 1.25 (95%CI: 1.04–1.50) for non-accidental mortality and 1.38 (95%CI:1.02–1.86) for cardiovascular disease mortality. We observed no associations between PM2.5 and deaths from respiratory disease or cancer. In the subgroup analysis, interactions were observed between PM2.5 and age, as well as preventive measures on hazy days. The observed association between long-term exposure to atmospheric PM2.5 at a relatively moderate concentration and the risk of non-accidental and cardiovascular disease mortality among middle-aged and elderly Chinese adults could provide evidence for government decision-makers to revise environmental policies towards a more stringent standard. Full article
(This article belongs to the Special Issue Exposure to Air Pollution and Respiratory Health Effects)
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17 pages, 3793 KiB  
Article
Comparable Response Following Exposure to Biodiesel and Diesel Exhaust Particles in Advanced Multicellular Human Lung Models
by Mizanur Rahman, Swapna Upadhyay, Koustav Ganguly, Micol Introna, Jie Ji, Christoffer Boman, Ala Muala, Anders Blomberg, Thomas Sandström and Lena Palmberg
Toxics 2023, 11(6), 532; https://doi.org/10.3390/toxics11060532 - 14 Jun 2023
Cited by 4 | Viewed by 2096
Abstract
Biodiesel is considered to be a sustainable alternative for fossil fuels such as petroleum-based diesel. However, we still lack knowledge about the impact of biodiesel emissions on humans, as airways and lungs are the primary target organs of inhaled toxicants. This study investigated [...] Read more.
Biodiesel is considered to be a sustainable alternative for fossil fuels such as petroleum-based diesel. However, we still lack knowledge about the impact of biodiesel emissions on humans, as airways and lungs are the primary target organs of inhaled toxicants. This study investigated the effect of exhaust particles from well-characterized rapeseed methyl ester (RME) biodiesel exhaust particles (BDEP) and petro-diesel exhaust particles (DEP) on primary bronchial epithelial cells (PBEC) and macrophages (MQ). The advanced multicellular physiologically relevant bronchial mucosa models were developed using human primary bronchial epithelial cells (PBEC) cultured at air–liquid interface (ALI) in the presence or absence of THP-1 cell-derived macrophages (MQ). The experimental set-up used for BDEP and DEP exposures (18 µg/cm2 and 36 µg/cm2) as well as the corresponding control exposures were PBEC-ALI, MQ-ALI, and PBEC co-cultured with MQ (PBEC-ALI/MQ). Following exposure to both BDEP and DEP, reactive oxygen species as well as the stress protein heat shock protein 60 were upregulated in PBEC-ALI and MQ-ALI. Expression of both pro-inflammatory (M1: CD86) and repair (M2: CD206) macrophage polarization markers was increased in MQ-ALI after both BDEP and DEP exposures. Phagocytosis activity of MQ and the phagocytosis receptors CD35 and CD64 were downregulated, whereas CD36 was upregulated in MQ-ALI. Increased transcript and secreted protein levels of CXCL8, as well as IL-6 and TNF-α, were detected following both BDEP and DEP exposure at both doses in PBEC-ALI. Furthermore, the cyclooxygenase-2 (COX-2) pathway, COX-2-mediated histone phosphorylation and DNA damage were all increased in PBEC-ALI following exposure to both doses of BDEP and DEP. Valdecoxib, a COX-2 inhibitor, reduced the level of prostaglandin E2, histone phosphorylation, and DNA damage in PBEC-ALI following exposure to both concentrations of BDEP and DEP. Using physiologically relevant multicellular human lung mucosa models with human primary bronchial epithelial cells and macrophages, we found BDEP and DEP to induce comparable levels of oxidative stress, inflammatory response, and impairment of phagocytosis. The use of a renewable carbon-neutral biodiesel fuel does not appear to be more favorable than conventional petroleum-based alternative, as regards of its potential for adverse health effects. Full article
(This article belongs to the Special Issue Exposure to Air Pollution and Respiratory Health Effects)
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