Overweight, air and noise pollution: Universal risk factors for pediatric pre-hypertension

Roya Kelishadi1, Parinaz Poursafa, Kasra Keramatian

  • 1Professor, Department of Paediatrics, Child Health Promotion Research Center, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Insights

Pediatric pre-hypertension (pre-HTN) is influenced by gene-environment interactions and escalating environmental factors like pollution and obesity. Early prevention targeting modifiable risks from prenatal stages is crucial for long-term health.

Area of Science:

  • Pediatric Cardiology
  • Environmental Health
  • Public Health

Background:

  • Pediatric pre-hypertension (pre-HTN) presents a complex, multifactorial etiology.
  • While often secondary, a significant portion of pediatric pre-HTN is essential, involving gene-gene and gene-environment interactions.
  • Escalating prevalence is anticipated due to strong links with environmental factors like air/noise pollution, passive smoking, and obesity.

Purpose of the Study:

  • To review the diagnosis, prevalence, and etiology of pediatric pre-hypertension.
  • To highlight the impact of environmental factors and obesity on pediatric blood pressure.
  • To outline practical measures for the prevention and control of pediatric pre-HTN.

Main Methods:

  • Literature review focusing on pediatric pre-hypertension etiology and risk factors.
  • Analysis of biological pathways linking environmental exposures to blood pressure elevation.
  • Examination of the role of obesity and associated metabolic changes in pediatric pre-HTN development.

Main Results:

  • Exposure to ambient particulate matter can acutely increase blood pressure via autonomic imbalance, oxidative stress, and inflammation.
  • Maternal and parental smoking are associated with increased systolic blood pressure in infants and young children.
  • Noise exposure is linked to elevated blood pressure and pre-HTN states in preschoolers.
  • Excess weight contributes to adipose tissue dysfunction, vascular inflammation, oxidative stress, and activation of the renin-angiotensin-aldosterone system, leading to pre-HTN.

Conclusions:

  • Environmental factors (pollution, smoking, noise) and obesity are significant contributors to pediatric pre-hypertension.
  • Interventions targeting modifiable risk factors from the prenatal period onwards are essential for primordial and primary prevention.
  • Early management of pediatric pre-HTN can mitigate the long-term risk of chronic non-communicable diseases.

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