Exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence: a population-based birth cohort study

Gehring, Ulrike; Wijga, Alet H.; Hoek, Gerard; Bellander, Tom; Berdel, Dietrich; Brüske, Irene; Fuertes, Elaine; Gruzieva, Olena; Heinrich, Joachim; Hoffmann, Barbara; Jongste, Johan C. de; Klümper, Claudia; Koppelman, Gerard H.; Korek, Michal; Krämer, Ursula; Maier, Dieter; Melén, Erik; Pershagen, Göran; Postma, Dirkje S.; Standl, Marie; Berg, Andrea von; Antó, Josep M.; Bousquet, Jean; Keil, Thomas; Smit, Henriëtte A.; Brunekreef, Bert

doi:10.1016/s2213-2600(15)00426-9

Cited by 213 publications

(141 citation statements)

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“…Heredity is a wellknown risk factor, exemplified by strong associations between chromosome 17q21 variants and childhood asthma (2), but genetic factors cannot solely explain its increasing prevalence in the past few decades. Exposure to traffic-related air pollution in early childhood (often indicated by the level of nitrogen dioxide [NO 2 ]) has been associated with asthma exacerbations (3) and reduced lung function in children (4-7), but its association with initial asthma development has been less consistent (8)(9)(10)(11).…”

Section: At a Glance Commentarymentioning

confidence: 99%

Genome-Wide Interaction Analysis of Air Pollution Exposure and Childhood Asthma with Functional Follow-up

Gref¹,

Merid²,

Gruzieva³

et al. 2017

Am J Respir Crit Care Med

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107

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Section: At a Glance Commentarymentioning

confidence: 99%

Genome-Wide Interaction Analysis of Air Pollution Exposure and Childhood Asthma with Functional Follow-up

Gref¹,

Merid²,

Gruzieva³

et al. 2017

Am J Respir Crit Care Med

Self Cite

107

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“…Exposure to elevated levels of airborne particulate matter (PM) pollution has been associated with adverse health outcomes such as asthma and chronic obstructive pulmonary disease (COPD) [1, 2]. Interestingly, several epidemiological studies have also recognized an association between exposure to elevated levels of PM and respiratory tract viral infections in infants and young children [3–5].…”

Section: Introductionmentioning

confidence: 99%

Regulatory T cells and IL10 suppress pulmonary host defense during early-life exposure to radical containing combustion derived ultrafine particulate matter

et al. 2017

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BackgroundExposure to elevated levels of particulate matter (PM) is associated with increased risk of morbidity and mortality due to respiratory tract viral infections in infants. Recent identification of environmentally persistent free radicals (EPFRs) in the PM from a variety of combustion sources suggests its role in the enhancement of disease severity of lower respiratory tract infections (LRTI). Our previous studies demonstrated that acute exposure to EPFRs induces pulmonary immunosuppression allowing for enhanced influenza disease severity. Here, we determine the mechanism of EPFR-induced immunosuppression and its impact on the immune response towards influenza infection.MethodsNeonatal mice (3 days old) were acutely exposed to DCB (combustion derived PM with chemisorbed EPFR) for seven consecutive days. Four days post-exposure (dpe), mice were infected with influenza virus. Pulmonary T cell phenotypes including regulatory T cells (Tregs) were analyzed by flow cytometry. The role of IL10 in EPFR-induced exacerbation of influenza disease severity was determined by administering recombinant IL10 (rIL10) to wild type mice or by using IL10 deficient (IL10−/−) neonatal mice. Mice were assessed for morbidity by measuring percent weight change and pulmonary viral load.ResultsNeonatal mice exposed to EPFRs had a significant increase in pulmonary Tregs and the immunosuppressive cytokine IL10 following influenza infection, which coincided with decreased protective T cell responses to influenza infection at 6 dpi. Depletion of Tregs in EPFR-exposed neonatal mice resulted in increased protective, adaptive T cell responses, whereas adoptive transfer of Tregs from EPFR-exposed neonates to air-exposed neonatal mice suppressed adaptive T cell responses towards influenza infection. Further, treatment with rIL10 could recapitulate EPFR-induced exacerbation of morbidity and pulmonary viral load compared to air exposed and influenza infected mice, whereas, EPFR-exposed IL10−/− neonates exhibited significant reductions in morbidity, pulmonary viral load and adaptive T cell responses following influenza infection.ConclusionsNeonatal exposure to EPFRs induced Tregs and IL10 resulting in suppressed adaptive T cell responses and enhanced influenza disease severity in neonatal mice. Depletion of Tregs increased adaptive T cell responses and deficiency of IL10 reduced morbidity and conferred enhanced protection against influenza virus.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-016-0487-4) contains supplementary material, which is available to authorized users.

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“…The air EQI score accounted for effects from the six criteria air pollutants including PM, SO 2 , NO 2 , and CO. Future studies will examine the individual criteria air pollutants in relation to pediatric MS and assess whether fine particulate matter (PM 2.5 compared to larger sized particulate matter, PM 10 ) impacts these relationships. Air pollution is also a known risk factor for other conditions such as asthma, stroke, and cardiovascular disease (Mölter et al, 2015; Gehring et al, 2015; Yorifuji et al, 2014; Zhang et al, 2011; Franklin et al, 2015; Short term exposure to air pollution and stroke, 2016; Maheswaran, 2016). Poor air quality has negative effects on the central nervous system and has been associated with cognitive delays in children (Kristiansson et al, 2015; Guxens et al, 2012; Block and Calderón-garcidueñas, 2010).…”

Section: Discussionmentioning

confidence: 99%

Examining the contributions of environmental quality to pediatric multiple sclerosis

Lavery

Waldman

Casper

et al. 2017

Multiple Sclerosis and Related Disorders

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Background Multiple sclerosis (MS) is a presumed autoimmune disease caused by genetic and environmental factors. It is hypothesized that environmental exposures (such as air and water quality) trigger the innate immune response thereby activating a pro-inflammatory cascade. Objective To examine potential environmental factors in pediatric MS using geographic information systems (GIS). Methods Pediatric MS cases and healthy controls were identified as part of an ongoing multicenter case-control study. Subjects’ geographic locations were mapped by county centroid to compare to an Environmental Quality Index (EQI). The EQI examines 5 individual environmental components (air, land, water, social, built factors). A composite EQI score and individual scores were compared between cases and controls, stratified by median proximity to enrollment centers (residence < 20 or ≥20 miles from the recruiting center), using logistic regression. Results Of the 287 MS cases and 445 controls, 46% and 49% respectively live in areas where the total EQI is the highest (worst environmental quality). Total EQI was not significantly associated with the odds for MS (p = 0.90 < 20 miles from center; p = 0.43 ≥ 20 miles); however, worsening air quality significantly impacted the odds for MS in those living near a referral center (OR = 2.83; 95%CI 1.5, 5.4) and those who reside ≥20 miles from a referral center (OR = 1.61; 95%CI 1.2, 2.3). Conclusion Among environmental factors, air quality may contribute to the odds of developing MS in a pediatric population. Future studies will examine specific air constituents and other location-based air exposures and explore potential mechanisms for immune activation by these exposures.

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Exposure to air pollution and development of asthma and rhinoconjunctivitis throughout childhood and adolescence: a population-based birth cohort study

Abstract: Word count abstract: 246 Word count introduction-conclusions: 3,1943 Abstract Background: The role of air pollution exposure in the development of childhood and

Cited by 213 publications

References 35 publications

Genome-Wide Interaction Analysis of Air Pollution Exposure and Childhood Asthma with Functional Follow-up

Genome-Wide Interaction Analysis of Air Pollution Exposure and Childhood Asthma with Functional Follow-up

Regulatory T cells and IL10 suppress pulmonary host defense during early-life exposure to radical containing combustion derived ultrafine particulate matter

Examining the contributions of environmental quality to pediatric multiple sclerosis

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