Air pollution and childhood bronchitis: Interaction with xenobiotic, immune regulatory and DNA repair genes

Ghosh, Rakesh; Rössner, Pavel; Hoňková, K.; Dostál, Miroslav; Šrám, Radìm J.; Hertz‐Picciotto, Irva

doi:10.1016/j.envint.2015.10.002

Cited by 35 publications

(16 citation statements)

References 43 publications

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“…First, a hypothesis forwarded in the environmental justice literature is that poorer air quality is linked to increases in respiratory illnesses, which results in school absenteeism, and diminished academic performance (Pastor et al 2002, 2004, 2006; Lucier et al, 2011). In support of this hypothesis are those studies linking exposure to air pollution to increases in respiratory infections and asthma (Belleudi et al 2010; Grineski et al 2010; Peden 2015; Ghosh et al, 2016) and those associating exposure to air pollution with increased absenteeism (Currie 2009; Gilliland et al 2001). However, the link between asthma and poorer school performance is tenuous.…”

Section: Discussionmentioning

confidence: 94%

School-based exposure to hazardous air pollutants and grade point average: A multi-level study

Grineski

Clark-Reyna

Collins

2016

Environmental Research

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The problem of environmental health hazards around schools is serious but it has been neglected by researchers and analysts. This is concerning because children are highly susceptible to the effects of chemical hazards. Some ecological studies have demonstrated that higher school-level pollution is associated with lower aggregate school-level standardized test scores at school, likely related to increased respiratory illnesses and/or impaired cognitive development. However, an important question remains unexamined: How do school-level exposures impact individual children’s academic performance? To address this, we obtained socio-demographic and grades data from the parents of 1,888 fourth and fifth grade children in the El Paso (Texas, USA) Independent School District in 2012. El Paso is located on the US-side of the Mexican border and has a majority Mexican-origin population. School-based hazardous air pollution (HAP) exposure was calculated using census block-level US Environmental Protection Agency National Air Toxics Assessment risk estimates for respiratory and diesel particulate matter (PM). School-level demographics were obtained from the school district. Multi-level models adjusting for individual-level covariates (e.g., age, sex, race/ethnicity, English proficiency, and economic deprivation) and school-level covariates (e.g., percent of students economically disadvantaged and student-teacher ratio) showed that higher school-level HAPs were associated with lower individual-level grade point averages. An interquartile range increase in school-level HAP exposure was associated with an adjusted 0.11 to 0.40 point decrease in individual students’ grade point averages (GPAs), depending on HAP type and emission source. Respiratory risk from HAPs had a larger effect on GPA than did diesel PM risk. Non-road mobile and total respiratory risk had the largest effects on children’s GPA of all HAP variables studied and only mother’s level of education had a larger effect than those two variables on children’s GPA. The five school-level demographic indicators were only weakly associated with GPA. The study findings indicate the need for regulations on school siting and adjacent land uses to protect children’s environmental health.

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Section: Discussionmentioning

confidence: 94%

School-based exposure to hazardous air pollutants and grade point average: A multi-level study

Grineski

Clark-Reyna

Collins

2016

Environmental Research

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“…Another study suggested that organic compounds in PM2.5 are able to aggravate the infection of upper and lower respiratory tract infections in children (112). It has also been indicated that the DNA repair gene xeroderma pigmentosum complementation group C may serve an essential function in the pathogenesis of PM2.5-induced bronchitis (113). To the best of our knowledge, the effect of PM2.5 in respiratory infection has not been demonstrated.…”

Section: Pm25-induced Pathogenesis In Respiratory Infectionmentioning

confidence: 97%

Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

2018

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Previous research has identified that air pollution is associated with various respiratory diseases, but few studies have investigated the function served by particulate matter 2.5 (PM2.5) in these diseases. PM2.5 is known to cause epigenetic and microenvironmental alterations in lung cancer, including tumor-associated signaling pathway activation mediated by microRNA dysregulation, DNA methylation, and increased levels of cytokines and inflammatory cells. Autophagy and apoptosis of tumor cells may also be detected in lung cancer associated with PM2.5 exposure. A number of mechanisms are involved in triggering and aggravating asthma and COPD, including PM2.5-induced cytokine release and oxidative stress. The present review is an overview of the underlying molecular mechanisms of PM2.5-induced pathogenesis in lung cancer and chronic airway inflammatory diseases.

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“…The inflammatory reaction is associated with an imbalance of Th cell (CD4 + T cell) subpopulations, which include Th1, Th2, Th17 and Treg cells. Th cells have a regulatory role in inducing the inflammatory response or suppressing immune responses (16,17).…”

Section: Discussionmentioning

confidence: 99%

Changes of Treg and Th17 cells as well as cytokines in children with acute bronchitis

Xue

Chen

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate changes of T-regulatory (Treg) and T-helper (Th)17 cells as well as cytokines in peripheral blood of children with acute bronchitis, and to explore the roles of these cells in the pathogenesis of acute bronchitis. A total of 126 children who had presented at Renji Hospital (Shanghai, China) with acute bronchitis were selected as the observation group and 30 healthy children were selected as the control group. Th17/Tregs in the peripheral blood of the children of the observation group and the control group was detected by flow cytometry. The levels of cytokines interleukin (IL)-17, IL-22, IL-10 and transforming growth factor (TGF)-β in peripheral blood serum were detected by ELISA. Compared with those in the control group, Treg cells, the Treg/Th17 ratio as well as serum IL-10 and TGF-β levels were significantly decreased in the observation group (P<0.05), while Th17 cells as well as serum levels of IL-17 and IL-22 were significantly increased (P<0.05). In conclusion, Treg/Th17 and the expression of associated cytokines lost their balance in children with acute bronchitis, suggesting that Treg and Th17 cells as well as their cytokines may be involved in the pathogenesis of acute bronchitis. It may be of certain guiding significance to detect Treg/Th17 and levels of serum cytokines in peripheral blood for clinical treatment.

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Air pollution and childhood bronchitis: Interaction with xenobiotic, immune regulatory and DNA repair genes

Cited by 35 publications

References 43 publications

School-based exposure to hazardous air pollutants and grade point average: A multi-level study

School-based exposure to hazardous air pollutants and grade point average: A multi-level study

Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases (Review)

Changes of Treg and Th17 cells as well as cytokines in children with acute bronchitis

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