Review articleExposure to traffic-related air pollution and risk of development of childhood asthma: A systematic review and meta-analysis
Introduction
Asthma is a complex and heterogeneous chronic inflammatory disease of the airways (Wenzel, 2012, Xie and Wenzel, 2013). The condition is conservatively estimated to affect 334 million people worldwide (Global Asthma Network, G, 2014). Numerous studies show that the prevalence of childhood asthma has increased dramatically since the 1950s, with some suggestion of plateauing in developed regions (Anandan et al., 2010, Braman, 2006, Pearce et al., 2007, Anderson et al., 2007, Zhang et al., 2013, Huang et al., 2015, Chen et al., 2016). The factors driving these increases are largely unknown, but coinciding changes in environmental exposures are thought to be responsible (Gaffin et al., 2014).
One putative environmental exposure is humans' exposure to ambient air pollution. Although there is sufficient evidence that ambient air pollution can exacerbate pre-existing asthma across a variety of outcomes (Gilmour et al., 2006, Guarnieri and Balmes, 2014, Braback and Forsberg, 2009), the role of air pollution exposure in the initial development of asthma is as yet contested (Eder et al., 2006, Gowers et al., 2012, Gehring et al., 2015a, Deng et al., 2016), partly as a result of the difficulty in conducting adequate epidemiological studies required to address this question.
Earlier reviews have effectively excluded ambient air pollution as a plausible cause of the rise in asthma incidence, with one argument being that the available evidence was inconsistent (Koenig, 1999). Furthermore, previous studies showed that asthma prevalence did not mirror changes in ambient air pollution concentrations, and reductions in levels of ambient sulfur dioxide (SO2) and total suspended particles (TSP), for example, seemed to synchronize with rapid increases of the condition (Eder et al., 2006, Gowers et al., 2012, Heinrich et al., 2002, Anderson, 1997). However, positive associations were subsequently shown between the incidence and prevalence of asthma and wheeze and exposure contrasts at the intra-urban scale, mainly dominated by traffic-related air pollution (TRAP) (Gasana et al., 2012, Anderson et al., 2013, Bowatte et al., 2014, Health Effects Institute, H.E.I, 2010, Favarato et al., 2014). Traffic-related air pollutants are ubiquitous, are of different chemical and physical nature compared to the classical air pollution mix associated with domestic heating and power plant emissions, and thus necessitate specific examination.
Early-life and childhood could represent critical exposure windows for asthma development due to the plasticity and susceptibility of target organs and systems during these developmental periods and the long maturation period of the respiratory, immune and detoxification systems (Schwartz, 2004, Wright and Brunst, 2013, Deng et al., 2015, Bateson and Schwartz, 2007). Moreover, when compared to adults, infants and children exhibit higher ventilation rates (Wright and Brunst, 2013), reduced nasal deposition efficiencies for inhaled particles (Bennett et al., 2007), are more typically mouth-breathers invalidating the nasal filtering and conditioning of the inhaled air in temperature and relative humidity (Bateson and Schwartz, 2007), and tend to be more active outdoors where their exposure to TRAP is generally higher (Braback and Forsberg, 2009, Bateson and Schwartz, 2007).
Section snippets
Objective
In this systematic review and meta-analysis, we provide an up-to-date synthesis of observational epidemiological studies that examined the association between TRAP exposures (exposure) and the subsequent development of asthma (outcome) in children from birth to 18 years of age (participants). We hypothesize that childhood exposure to TRAP increases the risk of subsequent asthma development.
Four meta-analyses were previously published on asthma and TRAP (Gasana et al., 2012, Anderson et al., 2013
Methods
We conducted this systematic review in accordance with established guidance published by the University of York's Centre for Reviews and Dissemination (Akers et al., 2009). We registered the protocol on PROSPERO documenting our methodological approach a priori (Khreis et al., 2016). We completed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist (Stroup et al., 2000), attached in the supplementary material.
Results
Our search yielded 4276 unique articles and from this, 94 records were identified for full-text review (Fig. 2). 41 studies, published between 1999 and September 2016, met our inclusion criteria, 18 of which emerged after year 2014. Table 1 provides a summary of each study. Ages of participants ranged from 1 to 18 years old, except in (Nishimura et al., 2013) where 3% of the participants were 19–21 years old. We included this study as the substantial majority of participants fell within the
Overview, strengths and limitations
In this systematic review and meta-analysis, we synthesized 41 studies, published between 1999 and September 2016, investigating the association between exposure to TRAP and subsequent development of childhood asthma. We conducted overall and age-specific meta-analyses and estimated statistically significant random-effects risk estimates with BC, NO2, PM2.5, and PM10 exposures. Multiple sensitivity analyses supported our findings and conclusions. Across the overall meta-analysis and the
Conclusions and recommendations
Based on this updated evidence base, we believe there is now sufficient evidence to support an association between the exposure to TRAP and the development of childhood asthma. The high degree of consistency in findings and conclusions of the individual studies, the results of the meta-analysis, and considerable support from the existing literature reinforce the hypothesis that childhood exposure to TRAP contributes to their development of asthma. The evidence for BC was less heterogeneous than
Competing financial interests
The authors have nothing to disclose.
Funding
Haneen Khreis is funded by a PhD studentship from Philadelphia University, Jordan. The funding source had no role in this study or the decision to submit it for publication.
Acknowledgments
We thank Michael Brauer, Patrick Ryan, Cole Brokamp, Ulrike Gehring, and Anna Mölter for providing their unpublished risk estimates for continuous exposures and for clarifications when requested.
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