The neurological effects of air pollution in children
Open accessAbstract
Environmental exposures in utero and during early life may permanently change the body’s structure, physiology and metabolism, and lead to diseases in adult life [1]. Infants are particularly vulnerable because of their rapid growth and cell differentiation, immaturity of metabolic pathways and development of vital organ systems. The central nervous system has unprotected barriers and a broad time window of conformation, leading to a long period of vulnerability in the developmental process and to susceptibility to any environmental insult [2]. Research conducted among a limited series of pollutants (including lead, mercury and polycyclic aromatic hydrocarbons (PAH)) shows that early-life exposure to chemicals at current environmental levels can be neurotoxic years or even decades after exposure [3]. Traffic-related air pollution, basically urban outdoor pollution, is a global public health problem [4]. Cardiorespiratory effects and mechanisms have been fully investigated [5]. In contrast, little is known regarding neurological effects, with only some preliminary evidence. In rats, ultrafine carbon particles have been found in the olfactory bulb and the cerebrum and cerebellum after inhalation exposure [6]; this finding has been reproduced more recently with manganese particles directly translocated to the olfactory nerve from the nose to the brain [7]. In one study, dogs living in a highly polluted region in Mexico City (Mexico) had an increase in brain inflammation compared with animals living in a less polluted area [8]. The brain tissue of animals from Mexico City had higher levels of nuclear factor-kB activation and nitric oxide production, as well as the principal pro-inflammatory cytokines interleukin (IL)-1 and tumour necrosis factor (TNF)-a, compared with the animals from the nonpolluted area [9]. In a study on human autopsies in Mexico City, exposure to severe air pollution has been associated with increased levels of cyclooxygenase (COX)-2 and accumulation of the 42-amino-acid form of b-amyloid, a cause of neuronal dysfunction [10].
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Some air pollutants induce oxidative stress and cause a systemic inflammatory reaction, a proposed mechanism whereby air pollutant exposures may perturb neurodevelopment.
“Some air pollutants are known to induce oxidative stress and cause a systemic inflammatory reaction, a proposed mechanism whereby air pollutant exposures may perturb neurodevelopment.66–68”
From Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence (2014) · cites this paper as [68]
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- Authors
- Sunyer, J.
- Affiliations
- Universitat Pompeu Fabra (ES)
- Corresponding author
- Sunyer, J.
- ORCID
- Sunyer, J.
- Venue
- European Respiratory Journal
- Publisher
- European Respiratory Society (ERS)
- Published
- 2008-08-29
- Volume
- 32
- Issue
- 3
- Pages
- 535-537
- ISSN
- 0903-1936 (ISSN-L)
- 1399-3003
- OpenAlex
- W2097819953
- Cited by
- 80
- References
- 29
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 4 · 2023: 7 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 6 · 2018: 3 · 2017: 9 · 2016: 1 · 2015: 5 · 2014: 3 · 2013: 1 · 2012: 1
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Respiratory Journal (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Social Sciences › Sociology and Political Science › Environmental Justice and Health Disparities
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Keywords
- air pollution, neurotoxicity, children, early life exposure, traffic-related air pollution, ultrafine carbon particles, neuroinflammation, inflammatory cytokines, amyloid accumulation, brain development, Mexico City
- MeSH terms
- Air Pollution, Vehicle Emissions, Brain, Child, Child, Preschool, Female, Humans, Infant, Nervous System Diseases, Pregnancy, Prenatal Exposure Delayed Effects, Oxidative Stress, Particulate Matter
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