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Establishing the exposure–outcome relation between airborne particulate matter and children’s health
  1. Renyi Zhang1,
  2. Natalie M Johnson2,
  3. Yixin Li3
  1. 1Atmospheric Sciences and Chemistry, Texas A&M University, College Station, Texas, USA
  2. 2Department of Environmental and Occupational Health/School of Public Health, Texas A&M University, College Station, Texas, USA
  3. 3Chemistry, Texas A&M University, College Station, Texas, USA
  1. Correspondence to Dr Renyi Zhang, Atmospheric Sciences & Chemistry, Texas A&M University, College Station, Texas, USA; renyi-zhang{at}tamu.edu

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With increasing urbanisation, industrialisation and economic growth worldwide, air pollution has emerged as one of the greatest global public health epidemics in the 21st century. The impacts of air pollution on human health are enormous. Globally, nine in ten people breathe air containing high levels of pollutants, and one in nine of the deaths are caused by exposure to air pollution, reaching an annual premature mortality of over seven million.1 Air pollutants comprise a complex mixture of gases and particulate matter (PM), which are directly emitted from natural and anthropogenic sources or are formed in air via a multitude of chemical processes.2 In particular, fine PM (diameter smaller than 2.5 µm or PM2.5) has been unequivocally linked to various adverse human health effects, ranging from aggravated allergies to the development of chronic diseases, to premature death.3 Exposure of vulnerable individuals to air pollution is especially worrisome, such as pregnant women and children.4 5 The morbidity and mortality associated with air pollution for children are relevant to both prenatal and postnatal exposures. For example, epidemiological and animal model studies have revealed that maternal exposure to fine PM results in adverse birth outcomes and postnatal health conditions.5 Specifically, animal model experiments employing ultrafine particles (diameter smaller than 0.1 µm or UFP) have shown that prenatal exposure predisposes offspring to long-term metabolic syndrome and pulmonary immunosuppression, with profound implications for respiratory infection risks.6 7

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Footnotes

  • Contributors RZ conceived and designed the work and drafted the manuscript. All authors critically revised the manuscript for content, approved the final version to be published, and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

  • Funding RZ acknowledged the Robert A Welch Foundation (A-1417). NMJ was funded by the National Institute of Environmental Health Sciences (R01ES02886). YL was supported by a Dissertation Fellowship at Texas A&M University.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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