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Ambient pollen and air quality on children’s lung function: is there a synergy?
  1. Yutong Cai1,2
  1. 1 Nuffield Department of Women's & Reproductive Health, University of Oxford, Oxford, UK
  2. 2 Deep Medicine programme, Oxford Martin School, University of Oxford, Oxford, UK
  1. Correspondence to Dr Yutong Cai, Nuffield Department of Women's and Reproductive Health, Women's Centre (Level 3), John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, UK; yutong.cai{at}wrh.ox.ac.uk

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Children are particularly vulnerable to airborne pollutants due to their immature lungs and immune system. Many studies have reported deleterious effects of exposure to ambient air pollution, in acute or chronic timeframe, on respiratory health in children.1 Airborne pollen are microscopic grains that are released from trees, grasses and weeds. Ample epidemiological evidence has suggested associations between high airborne pollen count and emergency hospital visits for allergies and asthma exacerbation in children.2

The interplay between air pollutants and pollen is well described in many experimental studies. Particulate matter and gaseous pollutants (eg, nitrogen dioxide (NO2), ozone (O3)) can increase allergen absorption into the lungs by binding to pollen grains, facilitate faster release of allergens, and/or modulate pollen allergenic potency.3 In epidemiological studies, while it is clear that both ambient air pollution and pollen have independent associations with poor respiratory health, their interactive effects are less certain.3 4 These mixed results, in fact, reflect the complexity in concentration, toxicity/allergenicity and seasonality of both air pollutants and pollen in diverse geographical settings. To date, most studies in this field were of time-series or case-crossover design, and focused primarily on asthma and respiratory symptoms.

To address this knowledge gap, in this issue of Thorax, Amazouz et al investigated whether recent exposure to both air pollution and pollen could affect levels of spirometric lung function and fractional exhaled nitric oxide (FeNO) among 1063 eight-year-old children from the population-based Pollution and Asthma Risk: an Infant Study cohort.5 Daily air quality index for PM10 (particulate matter with a diameter less than 10 µm), NO2 and O3 for the Greater Paris region were collected for 4 days preceding the lung function measurement. Similarly, daily pollen data for the 4-day period were collected from a single aerobiological monitoring station in central Paris. For the first time, a daily allergenic risk index, combining both pollen grain count and allergenicity, was computed for nine taxa. A daily total pollen count was also calculated. Using these 13 exposure variables, an unsupervised cluster analysis was performed to assign children to four clusters with distinct exposure profiles. The authors went on to analyse the associations between these exposure clusters and lung function, and additionally to investigate the joint impacts on lung function from exposures to high grass pollen (ie, >10 grains/m3) and poor air quality (ie, daily air quality index ≥6 on a scale from 1 to 10, based on the daily average concentrations of PM10, NO2, O3 and sulphur dioxide).

Comparing children in the low exposure cluster, children with moderate exposure to grass pollen and low level air pollution exposure (ie, grass pollen cluster) in the 4 days prior to lung function testing had significantly lower forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) levels by 40 and 57 mL, respectively. Children with high PM10 exposure but low pollen exposure (ie, PM10 cluster) had higher levels of FeNO, a biomarker of airway inflammation. These associations tended to be stronger among asthmatic children but not pollen-sensitised children. It is important to mention that numbers of asthmatic children in both grass pollen and PM10 clusters are relatively small and hence the observed effect estimates are subject to a larger degree of uncertainty. The joint analysis showed that children (5% of total 973) with simultaneous exposures to high grass pollen and poor air quality had lower FEV1 and FVC levels by 70 and 92 mL, respectively, as compared with children (51% of total 973) with low exposure to both grass pollen and air pollution.

While the study by Amazouz et al is an important addition to the current knowledge, several issues merit further discussion. First and foremost, it is still uncertain whether there is a synergistic effect between ambient pollen and air pollution on children’s lung function levels. Data from the joint analysis seem to suggest a multiplicative interaction; however, a formal test of interaction is unlikely to reach conventional levels of significance given the inadequate statistical power in this relatively small cohort. In addition, as only air quality index, rather than individual air pollutants, was used in this joint analysis, it is unclear which air pollutant (PM, NO2 or O3) is more likely to interact with grass pollen on lung function. In general, current evidence3 4 is inconsistent with regard to pollen–air pollutant interactions on respiratory outcomes. Second, unlike air pollution monitoring, pollen monitoring is still insufficient in many cities and countries. The majority of existing studies, including that by Amazouz et al, relied on only one monitoring station to assign daily average pollen count for the entire study area. It remains crucial to capture greater spatial variations of different pollen taxa, in particular, when considering the interactive effects with air pollution on health outcomes. Given that pollen count is not an ideal proxy to represent allergen exposure, future studies on respiratory and other health outcomes are recommended to measure amount of airborne allergenic load (ie, pollen allergenicity) in each type of pollen. Pollen allergenicity could vary by different grains, throughout the season under different meteorological conditions, and across locations, posing significant challenges in its assessment. New methods developed in the field of molecular aerobiology,6 together with continuous enhancement of the monitoring network and novel deployment of portable pollen monitors,7 hold great promise to enable a more accurate assessment and improve our understanding in the health impacts at both population and individual level. It should be noted that the method leading to the calculation of a daily allergenic risk index was not explicitly described by Amazouz et al and the associated health risk with this index cannot be assessed due to the statistical design. Third, all current studies only investigated potentially transient health effects of both pollen and air pollution exposures. Large cohort studies of long-term exposures at an individual level on longitudinal changes in health outcomes are needed to address this knowledge gap.

Human-caused climate change has been shown to lengthen the pollen seasons (+20 days) as well as to increase pollen concentrations (+21%) significantly across North American continent over the last three decades.8 Climate-driven trends in pollen, air pollutants and temperature are likely to further exacerbate respiratory health in coming decades if global actions are not taken firmly. Health impacts of these climate-driven trends may be collectively larger than previously estimated risk of each individual exposure if future evidence did support synergistic effects among these exposures. Locally, in the wake of the COVID-19 pandemic, many cities are now considering greening projects that aim to provide an oasis to their residents as well as to mitigate harmful urban pollution. In order to safeguard public health, a delicate balance should be supported by scientific evidence in planning urban green spaces, with careful considerations on pollen allergenicity in different plant species, as well as air pollution and traffic noise mitigation.9

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Footnotes

  • Twitter @samuelyutongcai

  • Contributors YC personally wrote the editorial.

  • Funding This article was completed with support from the PEAK Urban programme, funded by UK Research and Innovation’s Global Challenge Research Fund (grant number: ES/P011055/1).

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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