Elsevier

Environment International

Volume 100, March 2017, Pages 1-31
Environment International

Review article
Exposure to traffic-related air pollution and risk of development of childhood asthma: A systematic review and meta-analysis

https://doi.org/10.1016/j.envint.2016.11.012Get rights and content

Highlights

  • Whether children's exposure to traffic-related air pollution contributes to their development of asthma is an unresolved question.

  • We conducted a systematic review and a meta-analysis of observational studies published until 8 September 2016 investigating this question.

  • Forty-one studies met our eligibility criteria and there was an epidemic growth in publications after 2014.

  • Overall, there was notable variability in asthma definitions, TRAP exposure assessment and confounder adjustment.

  • The meta-analysis showed positive and statistically significant associations between asthma onset and the exposure to BC, NO2, PM2.5 and PM10, with the least heterogeneity detected in the BC and PM analyses and the most detected in the NO2 and NOx analyses.

Abstract

Background and objective

The question of whether children's exposure to traffic-related air pollution (TRAP) contributes to their development of asthma is unresolved. We conducted a systematic review and performed meta-analyses to analyze the association between TRAP and asthma development in childhood.

Data sources

We systematically reviewed epidemiological studies published until 8 September 2016 and available in the Embase, Ovid MEDLINE (R), and Transport databases.

Study eligibility criteria, participants, and interventions

We included studies that examined the association between children's exposure to TRAP metrics and their risk of ‘asthma’ incidence or lifetime prevalence, from birth to age 18 years old.

Study appraisal and synthesis methods

We extracted key characteristics of each included study using a predefined data items template and these were tabulated. We used the Critical Appraisal Skills Programme checklists to assess the validity of each included study. Where four or more independent risk estimates were available for a continuous pollutant exposure, we conducted overall and age-specific meta-analyses, and four sensitivity analyses for each summary meta-analytic exposure-outcome association.

Results

Forty-one studies met our eligibility criteria. There was notable variability in asthma definitions, TRAP exposure assessment methods and confounder adjustment. The overall random-effects risk estimates (95% CI) were 1.08 (1.03, 1.14) per 0.5 × 10 5 m 1 black carbon (BC), 1.05 (1.02, 1.07) per 4 μg/m3 nitrogen dioxide (NO2), 1.48 (0.89, 2.45) per 30 μg/m3 nitrogen oxides (NOx), 1.03 (1.01, 1.05) per 1 μg/m3 Particulate Matter < 2.5 μm in diameter (PM2.5), and 1.05 (1.02, 1.08) per 2 μg/m3 Particulate Matter < 10 μm in diameter (PM10). Sensitivity analyses supported these findings. Across the main analysis and age-specific analysis, the least heterogeneity was seen for the BC estimates, some heterogeneity for the PM2.5 and PM10 estimates and the most heterogeneity for the NO2 and NOx estimates.

Limitations, conclusions and implication of key findings

The overall risk estimates from the meta-analyses showed statistically significant associations for BC, NO2, PM2.5, PM10 exposures and risk of asthma development. Our findings support the hypothesis that childhood exposure to TRAP contributes to their development of asthma. Future meta-analyses would benefit from greater standardization of study methods including exposure assessment harmonization, outcome harmonization, confounders' harmonization and the inclusion of all important confounders in individual studies.

Systematic review registration number

PROSPERO 2014: CRD42014015448.

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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