Association between gaseous air pollutants and biomarkers of systemic inflammation: A systematic review and meta-analysis

Xu, Zhouyang; Wang, Wanzhou; Liu, Qisijing; Li, Zichuan; Lei, Lei; Ren, Lihua; Deng, Furong; Guo, Xinbiao; Wu, Shaowei

doi:10.1016/j.envpol.2021.118336

Cited by 64 publications

(40 citation statements)

References 79 publications

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“…For example, fine (PM 2.5 ) and ultrafine (PM 0.1 ) PM, due to their small size and large reactive surface area, can penetrate deeply into the lungs, reaching the alveoli and potentially translocating in the bloodstream, which may cause both local (lung) and systemic (blood, cardiovascular system) inflammation, as well the onset of cardio-pulmonary impairments [34][35][36]. Furthermore, these air pollutants (PM) have been accompanied by an increase in the levels of other pollutants, such as nitrogen oxide, sulfur dioxide, volatile organic compounds (VOCs), dioxins, and polycyclic aromatic hydrocarbons (PAHs), which are all considered as air pollutants that are harmful to humans [17,36,37]. However, only few epidemiological, in vivo and/or in vitro studies are available that show the combined effect of PM and gaseous components of air pollutants on the exacerbation of respiratory diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence from epidemiological and in vivo studies suggests that both long-term and shortterm exposure to gaseous air pollutants can induce oxidative damage in cells and lining fluids of the airways, resulting in subsequent inflammatory responses in the respiratory system [15,16]. Furthermore, chronic exposure to those pollutants has also been linked to enhanced sensitization and inflammatory responses within and beyond the lungs [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Establishment of Repeated In Vitro Exposure System for Evaluating Pulmonary Toxicity of Representative Criteria Air Pollutants Using Advanced Bronchial Mucosa Models

Upadhyay

Chakraborty

Thimraj

et al. 2022

Toxics

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Establishment of Repeated In Vitro Exposure System for Evaluating Pulmonary Toxicity of Representative Criteria Air Pollutants Using Advanced Bronchial Mucosa Models

Upadhyay

Chakraborty

Thimraj

et al. 2022

Toxics

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“…Although the exact biologic mechanisms remain to be elucidated, the association between air pollution and pregnancy loss is biologically plausible. Exposures to fine particles can induce the release of systemic oxidative stress [61] and inflammation markers [62,63], which are capable of compromising placental-fetal exchange and disrupt the normal oxygen and nutrients delivery into fetal circulation [64]. Oxidative stress and inflammatory markers can also cross the maternal-fetal blood barrier to perturb fetal development [64,65].…”

Section: Biologic Mechanismsmentioning

confidence: 99%

Outdoor Air Pollution and Pregnancy Loss: a Review of Recent Literature

Ghimire

Martinez

2022

Curr Epidemiol Rep

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Purpose of Review This review summarizes recent literature about the impacts of outdoor air pollution on pregnancy loss (spontaneous abortion/miscarriage and stillbirth), identifies challenges and opportunities, and provides recommendations for actions. Recent Findings Both short- and long-term exposures to ubiquitous air pollutants, including fine particulate matter < 2.5 and < 10 μm, may increase pregnancy loss risk. Windows of susceptibility include the entire gestational period, especially early pregnancy, and the week before event. Vulnerable subpopulations were not consistently explored, but some evidence suggests that pregnant parents from more disadvantaged populations may be more impacted even at the same exposure level. Summary Given environmental conditions conductive to high air pollution exposures become more prevalent as the climate shifts, air pollution’s impacts on pregnancy is expected to become a growing public health concern. While awaiting larger preconception studies to further understand causal impacts, multi-disciplinary efforts to minimize exposures among pregnant women are warranted.

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“…Raised ozone levels due to higher temperatures and air pollutants from burning fossil fuels also increase cardiorespiratory mortality and morbidity, possibly by increasing cholesterol levels and systemic inflammation. 8 9 Rising incidence of kidney disease and mental illness associated with exposure to urban heat are other devastating effects. 2 4 5 Additionally, increasing urban heat is expected to reduce labour productivity and outdoor working capacity, particularly in the tropics and subtropics.…”

Section: Health Consequences Of Heat Exposurementioning

confidence: 99%