Air pollution and children with cystic fibrosis

  • Research type

    Research Study

  • Full title

    Reducing the effects of air pollution on children with cystic fibrosis

  • IRAS ID

    215879

  • Contact name

    Jonathan Grigg

  • Contact email

    j.grigg@qmul.ac.uk

  • Sponsor organisation

    Director of Research Services and Business Development

  • Duration of Study in the UK

    3 years, 0 months, 0 days

  • Research summary

    Summary of Research
    Cystic Fibrosis (CF) is a condition where recurrent lung infections cause progressive lung damage. Children with CF are adversely affected by air pollution soot particles (e.g. from traffic). This study aims to address the vulnerability of CF children to air pollution. Firstly, their personal exposure will be assessed by using air pollution monitors, which will both be carried by participants/parents, and placed at their homes, over the course of 2 weeks. Secondly, by sampling cells called macrophages (cells that normally remove inhaled unwanted material) from their breathing tube (airway), we will find out whether removal of inhaled soot by these cells is impaired in CF. We expect to find lower amounts of soot in cells from CF children compared with healthy children.

    Prostaglandin E2 (PGE2) is a substance produced in the lungs, it is known to be associated with impaired uptake of soot particles within the breathing tube. We will compare levels of PGE2 in the breathing tube in CF and healthy children. We then aim to co-design with parents and children tips on their own exposure reduction, such as avoiding hot spots.

    Summary of Results
    This project demonstrated that children with cystic fibrosis (CF), despite being exposure to comparable level of air pollutants to their healthy counterparts, they have impaired airway macrophages (immune cells) function against inhaled air pollutants - they are less able to engulf and remove inhaled pollutants. This is in part due to their underlying condition of CF, which predispose to them to having ongoing inflammation in the airway/lungs, inflammation increase the presence of a substance of prostaglandin E2 (PGE2), this is found to have inhibitory effect on the the immune cells. Application of prostaglandin E2 inhibitors in a laboratory setting, reversed this phenomenon, to further support the theory.

  • REC name

    East Midlands - Nottingham 1 Research Ethics Committee

  • REC reference

    17/EM/0023

  • Date of REC Opinion

    24 Jan 2017

  • REC opinion

    Further Information Favourable Opinion