# Breastfeeding Duration and Airway Inflammation in Children With Asthma Living in a Polluted Megacity

**Authors:** Víctor González‐Uribe, Zaira Selene Mojica‐González, Jimena Prieto‐Gómez, Ricardo Martinez‐Tenopala, Tamara Hernández‐Hernández, María Julia Rendón‐Salazar, Luis Ángel Hernández‐Zárate

PMC · DOI: 10.1111/crj.70172 · 2026-02-15

## TL;DR

Breastfeeding for at least six months may help reduce asthma-related inflammation in children living in polluted cities.

## Contribution

This study shows that prolonged breastfeeding can mitigate the negative effects of urban air pollution on asthma control and airway inflammation in children.

## Key findings

- Breastfeeding for six months or more was linked to better asthma control and lower FeNO levels in children.
- High pollution levels were associated with worse asthma control and higher FeNO.
- Breastfeeding duration modified the impact of pollution on respiratory outcomes.

## Abstract

Children with asthma living in highly polluted megacities are at increased risk of poor asthma control and airway inflammation. Breastfeeding has immunomodulatory effects, but its potential to buffer pollution‐related inflammation remains understudied.

To evaluate whether breastfeeding duration is associated with asthma control and airway eosinophilic inflammation (FeNO), and whether it modifies the impact of urban air pollution in children with asthma living in Mexico City.

We conducted a multicenter retrospective study (2022–2025) including children aged 6–17 years with physician‐diagnosed asthma. Asthma control (ACT), airway inflammation (FeNO, NIOX VERO), breastfeeding duration (0–12 months), and borough‐level pollution categories (high/medium/low) were evaluated. Multivariable logistic and linear regression models assessed associations and breastfeeding × pollution interactions.

A total of 162 children were included (mean age 10.8 years; 51.2% female). Breastfeeding ≥ 6 months was associated with better asthma control (ACT ≥ 20: OR 2.1; 95% CI 1.3–3.5) and significantly lower FeNO (β −0.24; p < 0.01). High‐pollution residence was linked to lower ACT scores and higher FeNO (both p < 0.01). A significant interaction indicated that breastfeeding ≥ 6 months attenuated the detrimental effect of pollution on airway inflammation and asthma control (p for interaction < 0.05).

Prolonged breastfeeding was independently associated with improved asthma control and reduced airway eosinophilic inflammation, partially mitigating the respiratory burden of chronic pollution exposure.

Breastfeeding may serve as an accessible, low‐cost protective strategy for children with asthma living in polluted urban environments, supporting its integration into respiratory health policies and early‐life preventive care.

Children with asthma exposed to high levels of urban pollution show increased airway inflammation.This study identifies breastfeeding ≥ 6 months as a protective factor that attenuates pollution‐related increases in FeNO and improves asthma control.These findings support implementing breastfeeding promotion as part of integrated pediatric asthma care in megacities.

Children with asthma exposed to high levels of urban pollution show increased airway inflammation.

This study identifies breastfeeding ≥ 6 months as a protective factor that attenuates pollution‐related increases in FeNO and improves asthma control.

These findings support implementing breastfeeding promotion as part of integrated pediatric asthma care in megacities.

Prolonged breastfeeding (≥ 6 months) was associated with better asthma control and lower airway inflammation (FeNO) in children living in polluted areas of Mexico City. These findings suggest that breastfeeding provides a protective effect against the respiratory consequences of urban air pollution in pediatric asthma.

## Linked entities

- **Diseases:** asthma (MONDO:0004979)

## Full-text entities

- **Diseases:** FeNO (MESH:D054144), allergic multimorbidity (MESH:D004342), lung function (MESH:D055370), Asthma (MESH:D001249), lung disease (MESH:D008171), immunodeficiency (MESH:D007153), Airway Inflammation (MESH:D007249)
- **Chemicals:** reactive oxygen species (MESH:D017382), nitric oxide (MESH:D009569), NO2 (MESH:D009585), oligosaccharides (MESH:D009844), polyunsaturated fatty acids (MESH:D005231), LABA (-), O3 (MESH:D010126)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12907516/full.md

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Source: https://tomesphere.com/paper/PMC12907516