# Air Pollution, Asthma and Diet: From Mechanisms to Prevention Strategies

**Authors:** Pedro Afonso Carvalho, Inês Paciência, André Moreira, Francisca de Castro Mendes

PMC · DOI: 10.3390/nu18040639 · Nutrients · 2026-02-15

## TL;DR

This review explores how air pollution affects asthma and lung function, and how diet and other strategies can help reduce these effects.

## Contribution

The paper provides a comprehensive review of how diet and supplementation may modify the respiratory effects of air pollution.

## Key findings

- Dietary factors like redox buffering and microbiome-immune crosstalk may modulate pollution-related respiratory effects.
- Human evidence on diet's impact remains inconsistent across pollutants and settings.
- Emissions reduction and improved air quality are essential for asthma prevention.

## Abstract

Background/Objectives: Air pollution is a major environmental determinant of asthma morbidity and lung function impairment across the life course. Both outdoor and indoor exposures contribute to asthma development and exacerbations, impaired lung function growth, and accelerated decline, with heightened susceptibility during pregnancy and childhood. In this narrative review, we aimed to: (i) synthesize evidence on outdoor and indoor air pollution in asthma and lung function decline; (ii) describe key modulators of pollution-related risk; (iii) evaluate diet and supplementation as effect modifiers; and (iv) outline strategies and recommendations to mitigate pollution-related asthma burden. Methods: A narrative synthesis was conducted based on a comprehensive PubMed literature search through 2025, integrating evidence from observational and interventional studies evaluating habitual diet and nutritional supplementation as potential modifiers of the respiratory effects of indoor and outdoor air pollution. Results: We synthesized human observational and interventional studies associating outdoor and indoor air pollution with asthma and lung function outcomes, highlighted major susceptibility modulators and mechanistic pathways, and appraised emerging evidence that habitual diet and nutritional supplementation might modify pollutant-related respiratory effects. Mechanistic evidence supported dietary modulation through redox buffering, epithelial-immune pathways, lipid-mediated inflammatory balance, and microbiome-immune crosstalk. However, human evidence remained heterogeneous across pollutants, settings, dietary metrics, and endpoints. Conclusions: Emissions reduction at source remained the cornerstone of prevention. Effective mitigation should be multi-level and equity-focused, combining structural air-quality improvements with pollution-aware asthma care and feasible household practices. Diet should be framed as a supportive, food-first resilience strategy, improving overall diet quality, fat quality, and fiber intake rather than a substitute for emissions reduction or guideline-based asthma management.

## Linked entities

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

## Full-text entities

- **Genes:** FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, MUC5AC (mucin 5AC, oligomeric mucus/gel-forming) [NCBI Gene 4586] {aka MUC5, TBM, leB, mucin}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, GSTT1 (glutathione S-transferase theta 1) [NCBI Gene 2952], GSTM1 (glutathione S-transferase mu 1) [NCBI Gene 2944] {aka GST1, GSTM1-1, GSTM1a-1a, GSTM1b-1b, GTH4, GTM1}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, G6PD (glucose-6-phosphate dehydrogenase) [NCBI Gene 2539] {aka CNSHA1, G6PD1}, CXCR6 (C-X-C motif chemokine receptor 6) [NCBI Gene 10663] {aka BONZO, CD186, CDw186, STRL33, TYMSTR}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, FFAR3 (free fatty acid receptor 3) [NCBI Gene 2865] {aka FFA3R, GPR41}, TRAP [NCBI Gene 100187907], FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2353] {aka AP-1, C-FOS, p55}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}, GPR166P (G protein-coupled receptor 166, pseudogene) [NCBI Gene 442206] {aka GPCR, PGR9}, HDAC9 (histone deacetylase 9) [NCBI Gene 9734] {aka HD7, HD7b, HD9, HDAC, HDAC7B, HDAC9B}, FFAR2 (free fatty acid receptor 2) [NCBI Gene 2867] {aka FFA2R, GPR43}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}
- **Diseases:** wheeze (MESH:D012135), hypoxic (MESH:D002534), Obesity (MESH:D009765), respiratory (MESH:D012131), overweight (MESH:D050177), allergic (MESH:D004342), airway disease (MESH:D029424), HDM (MESH:D000092542), function (MESH:D003291), bronchospasm (MESH:D001986), immune dysregulation (OMIM:614878), airway injury (MESH:D000402), Metabolic Dysfunction (MESH:D008659), fungal (MESH:D009181), impaired immune tolerance (MESH:D018149), chronic diseases (MESH:D002908), hypoxia (MESH:D000860), impaired lung function (MESH:D003072), epithelial injury (MESH:D009375), loss in FEV1 (MESH:D016388), respiratory symptoms (MESH:D012818), acute respiratory infections (MESH:D012141), dietary inadequacy (MESH:D000740), injury (MESH:D014947), Airway inflammation (MESH:D007249), neutrophilia (MESH:C563010), impaired lung function growth (MESH:D006130), mitochondrial injury (MESH:D028361), eosinophilic (MESH:D017681), like (MESH:C537419), flu-like (MESH:D007251), eczema (MESH:D004485), asthmatic (MESH:D013224), adverse lung function (MESH:D008171), bronchitis (MESH:D001991), Asthma (MESH:D001249), eosinophilia (MESH:D004802), tachypnea (MESH:D059246), decreased lung function (MESH:D055370), cough (MESH:D003371), toxicity (MESH:D064420)
- **Chemicals:** carotenoids (MESH:D002338), glutathione (MESH:D005978), omega-6 PUFA (MESH:D043371), styrene (MESH:D020058), CO2 (MESH:D002245), gases (MESH:D005740), crotonaldehyde (MESH:C012796), E (MESH:D004540), water (MESH:D014867), polyphenols (MESH:D059808), benzene (MESH:D001554), nitrogen oxides (MESH:D009589), alpha-tocopherol (MESH:D024502), 2-butoxyethanol (MESH:C017096), butylated hydroxytoluene (MESH:D002084), LPS (MESH:D008070), DE (MESH:D004054), lipid (MESH:D008055), arachidonic-acid (MESH:D016718), beta-carotene (MESH:D019207), isothiocyanates (MESH:D017879), FO (MESH:D005395), vitamin C (MESH:D001205), N-Acetylcysteine (MESH:D000111), PM (MESH:D011399), SCFA (MESH:D005232), PAHs (MESH:D011084), o-xylene (MESH:C026114), BS (MESH:D001895), SABA (MESH:C046122), calcium (MESH:D002118), ROS (MESH:D017382), FA (MESH:D005492), glucose (MESH:D005947), formaldehyde (MESH:D005557), volatile organic compound (MESH:D055549), SO2 (MESH:D013458), nitric oxide (MESH:D009569), Vitamin D (MESH:D014807), BSE (-), O3 (MESH:D010126), Fat (MESH:D005223), organophosphates (MESH:D010755), ethylbenzene (MESH:C004912), eicosanoids (MESH:D015777), OO (MESH:D000069463), hexane (MESH:D006586), fiber (MESH:D004043), PUFA (MESH:D005231), albuterol (MESH:D000420), gamma-Tocopherol (MESH:D024504), Vitamin E (MESH:D014810), Vitamin D3 (MESH:D002762), toluene (MESH:D014050), NO2 (MESH:D009585), cyclohexanone (MESH:C036468), CO (MESH:D002248), Thiol (MESH:D013438), C (MESH:D002244), nicotine (MESH:D009538)
- **Species:** Brassica oleracea var. italica (asparagus broccoli, varietas) [taxon 36774], Cladosporium (genus) [taxon 5498], Alternaria sect. Alternaria (section) [taxon 2499237], Nicotiana tabacum (American tobacco, species) [taxon 4097], Medicago sativa (alfalfa, species) [taxon 3879], Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

145 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942803/full.md

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Source: https://tomesphere.com/paper/PMC12942803