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Contents lists available at ScienceDirect

Paediatric Respiratory Reviews

Review

Urban Air Pollution and Respiratory Infections Rossa Brugha, Jonathan Grigg * Centre for Paediatrics, Blizard Institute, Queen Mary, University of London

EDUCATIONAL AIMS Following this review, readers may:  Understand the composition of particulate air pollution  Recognise the worldwide impact of polluted air, both outdoor and indoor  Consider how to identify vulnerable children in their care

A R T I C L E I N F O

S U M M A R Y

Keywords: Air pollution Particulate matter Diesel exhaust particles Infection

Public awareness of the impact of air quality on health is increasing worldwide. Indoor and outdoor air pollutants impair children’s growing lungs, and increase the risk of respiratory infections. In many cities, children face indoor air pollution from fuels used for cooking and heating, as well as outdoor pollution from vehicle exhausts. Research identifies at-risk groups and seeks to establish biological plausibility for the associations already observed; and looks towards identifying the harmful pollutants that are responsible for respiratory morbidity and mortality. These findings may then serve to influence public debate and future policy at national and international level to improve air quality in cities, and improve children’s health. ß 2014 Elsevier Ltd. All rights reserved.

AIR POLLUTION The worldwide urban population, now over 3.5 billion, is projected to rise to 6.5 billion by 2050 [1]. Particulate matter (PM) air pollution in urban areas is a major public health concern. Burning solid fuels indoors for heating, light and cooking, and burning liquid fuels outdoors to power vehicle engines, results in a complex mix of gases and particulate matter (PM). The most convincing evidence for adverse health effects exists for PM. In Europe, 80% of the population live in areas where PM levels exceed World Health Organisation (WHO) air quality guidelines, and the life expectancy of Europeans is decreased, on average, by almost 9 months due to PM. Worldwide, it is estimated that the fraction of outdoor PM below 2.5 micrometers in diameter (PM2.5) accounted for 3.1 million deaths in 2010 [2]. These effects manifest as cardiorespiratory diseases (myocardial infarctions, stroke, COPD, lung cancer) [2] exacerbations of asthma [3,4] and cystic fibrosis [5], and respiratory infections in children [4]. In resource poor

* Corresponding author. Tel.: +44 207 882 2615. E-mail address: [email protected] (J. Grigg).

settings, approximately 3 billion people depend on burning solid fuels (coal or biomass fuels; wood, animal dung, crop wastes) for heating and cooking. PM generated from indoor solid fuel combustion exposes individuals who spend long periods of time near stoves (predominantly women and young children) to 100fold levels in excess of those considered acceptable. As a direct result, indoor air pollution is responsible for 2.7% of the global burden of disease [6,7] and contributes to 2 million deaths per year – exceeding the annual mortality attributed to malaria [8]. 85% of future global population growth is predicted to occur in cities in the developing world [1], and in the absence of major policy shifts towards cleaner environments, the majority of children in the first half of this century are likely to grow up exposed to unsafe air both at home and outdoors. This review will focus on one component of the adverse effects of PM - respiratory infection - and will consider both the effects of fossil fuel and biomass-derived PM.

COMPOSITION OF PARTICULATE MATTER Atmospheric particles are visible to the naked eye at a lower limit of approximately 100 mm, around the diameter of particles of

http://dx.doi.org/10.1016/j.prrv.2014.03.001 1526-0542/ß 2014 Elsevier Ltd. All rights reserved.

Please cite this article in press as: Brugha R, Grigg J. Urban Air Pollution and Respiratory Infections. Paediatr. Respir. Rev. (2014), http:// dx.doi.org/10.1016/j.prrv.2014.03.001

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‘‘heavy dust’’ that are released during construction or demolition on building sites. Below this size, pollen, mould spores and fly ash (ash from coal combustion, usually in coal fired power stations) lie in the 10 - 100 mm range. Some fly ash particles are greater than 100 mm in diameter, which is why ash can be seen when released from chimneys, but the majority lies in the range invisible to the eye. Bacteria and the majority of particulates from traffic fumes lie in the 1 to 10 mm range, as does ‘‘soot’’ (incompletely combusted black carbon). Although not covered in this review, the majority of smoke from cigarettes lies in the 0.01 to 1 mm range, well below the particle sizes visible to our eyes [9]. Particulate matter is a term that encompasses solid and aerosolised liquid particles suspended in the air. These particles are described by size distribution in microns. PM10 is particulate matter with a particle diameter of up to 10 mm, PM2.5 has a diameter of up to 2.5 mm, and PM45.9 microg/m3) subsequently experienced more episodes of recurrent bronchitis and pneumonia with respect to those in the lower tertiles over the 7 year follow-up. The mechanism for this association is unknown, however one explanation may be that children with lower birth weight may have under-developed lungs with a concomitant increase in risk to infection. Postnatal lung growth is a crucial developmental stage where initial insults may result in life-long effects on lung function [21]. Comparing high and low pollution districts in the Czech Republic, Hertz-Picciotto and colleagues followed a birth cohort of 1,130 children through the first 4.5 years of life [22]. They found that a 25 microg/m3 increase in 30-day average PM2.5 resulted in a 30% increased risk of ‘‘bronchitis’’, but no increase in croup, in children below 2 years (RR 1.30, 95% CI 1.08-1.58). A similar effect was seen with PAHs. The latest meta-analysis of 10 European birth cohorts from the ESCAPE project [23] used land use regression models to predict exposure to PM in 16,059 children across Sweden, Italy, Germany, the Netherlands, Spain and the UK. Pollutant exposures were then matched to physician diagnosed pneumonia, as well as otitis media and croup at various time points (depending on the cohort) up to 3 years. PM10 and traffic exposure were significantly associated with an increased risk of pneumonia (adjusted OR; PM10 1.76, 95% CI 1.00 to 3.90, p=0.051, NO2 1.30, 95% CI 1.02 to 1.65, p = 0.024). It is notable that in this study, measured PM2.5 was not associated with an increased risk (adjusted OR 2.58, 95% CI (0.91, 7.27). Pre- and post-natal pollution exposures are likely to be highly correlated, and this approach is not able to identify the crucial time point, either pre- or post-natal, at which interventions might be best targeted, but this large meta-analysis provides robust evidence to infer that chronic exposure to traffic derived air pollution is associated with an increased risk of respiratory infection in childhood.

Please cite this article in press as: Brugha R, Grigg J. Urban Air Pollution and Respiratory Infections. Paediatr. Respir. Rev. (2014), http:// dx.doi.org/10.1016/j.prrv.2014.03.001

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The data from the ESCAPE cohorts considers long-term air pollution exposure, but air pollution is not homogenous in time or place. Another approach to assessing the impact of PM is to link daily changes in air quality to health outcomes. Levels of PM vary widely in cities, from street to street, hour by hour and from day to day, depending on local pollution sources (mainly traffic flows) and the prevalent wind and weather conditions. As the air quality fluctuates it is possible to indirectly measure health effects by looking at Emergency Department (ED) visits. Peel and colleagues studied 4 million ED attendances across 31 hospitals in Atlanta, GA and compared respiratory attendances to 5 pollutants [26]. They showed that a 2 microg/m3 increase in organic carbon in the PM 2.5 range was associated in a 3% increase in cases of pneumonia across all ages. Although randomised trials of childhood exposure to traffic derived PM are not possible, occasionally for political reasons a population may experience a sudden change in air quality. The best known example is during the Beijing Olympics in 2008, where measurements of exhaled nitric oxide in children reduced as the air quality improved in the short term due to government enforced restrictions on traffic [27] but no data has been reported on respiratory infections. In 2002, following an outcry about air quality in Beirut, the Lebanon banned all diesel vehicles from the city. Data on respiratory admissions in children under 17 comparing the winters pre- and post the ban shows a decrease in the incidence of pneumonia and upper respiratory tract infections, but only when the year immediately after the ban came in is considered [28]. In the second year the effect disappears; although this may be due to how strictly the ban was enforced after two years. Finally, clean coal legislation in Ireland in 1990 resulted in a –155% (–191 to –116) decrease in respiratory deaths [29], and although this data is for all respiratory causes and across all ages, it serves to indicate that removing the source pollutant (Dublin saw a 36% fall in levels of black smoke) has a subsequent beneficial effect on mortality. Summarising these studies, we can conclude that traffic derived PM is strongly associated with an increased risk of respiratory infections in early childhood, and that data exists to suggest that cleaner air may rapidly decrease these risks. INDOOR PM AND RESPIRATORY INFECTIONS Studies in the mid 1980s suggested for the first time that indoor biomass smoke is associated with an increased risk of pneumonia in children [30]. Large quantities of PM are generated indoors by burning either wood, dung or crop wastes (generating biomass smoke) or by burning coal on open fires, and the greater the exposure, the greater the disease burden [31]. Externally vented stoves, and burning fuels at higher temperatures (decreasing incomplete combustion) are technological approaches to decreasing the burden of indoor PM [32,33]. In 2011, the RESPIRE trial reported the results of a cluster-randomised trial of woodstoves with chimneys in rural Guatemala [34]. Over 500 households were randomised, with children below 18 months (before they started to walk greater distances and could affect their exposure levels) assessed for episodes of pneumonia. The cook stoves reduced exposure (measured by carbon monoxide levels as a surrogate for particles) by 50%. Overall the trial result was negative (rate ratio 078; 059–106, p = 0095) for the primary outcome of cases of pneumonia, although the secondary outcome for severe pneumonia was a significant reduction. Possible explanations are i) the trial was underpowered (effect size 22%, trial powered to 25%), and ii) children in houses with cook stoves did not necessarily have lower PM exposures than those with traditional open fires. When PM exposures were subsequently assessed, a 50% reduction in exposure was associated with a significant decrease in physician-diagnosed

pneumonia (RR 082; 070–098). These results, and others [35], are an indication that clean cook stoves (new models can decrease particles by up to 90%) have the potential to make a significant impact on under 5s morbidity and mortality worldwide, and followup studies are ongoing [36]. The WHO estimate that 900000 children under 5 die per year from pneumonia resulting from air pollution; and cook stove interventions may be the most beneficial public health initiative for children worldwide. VULNERABILITY FACTORS Urban children from poorer families are more likely to live in areas with high housing density, high levels of traffic, and more likely to be closer to polluting industries [37]. Using methodology linking hospital admissions to air quality data, Yap and colleagues looking at data from California demonstrated that children living in certain areas with lower socioeconomic status (SES) are more likely to experience adverse respiratory outcomes, including acute respiratory infection and pneumonia, than children in areas with higher incomes for the same changes in PM2.5; although this outcome was not consistent across all the areas studied [38]. In the developing world, a respective cohort analysis of children in Ecuador aged between 18-42 months (in socioeconomically similar areas with differing levels of PM2.5) showed that children who were anaemic (Hb

Urban air pollution and respiratory infections.

Public awareness of the impact of air quality on health is increasing worldwide. Indoor and outdoor air pollutants impair children's growing lungs, an...
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