Abnormal Development - Air Pollution

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Particulate matter comparative size
Metal contamination.jpg

Air pollution has recently been identified through statistical studies to be involved with abnormal development (See also smoking). With industrialisation and vehicle produced air pollution, it can consist of particulate matter, heavy metals and a range of chemicals.

Vehicle traffic air pollution can consist of several different components including: (elemental carbon, nitrogen dioxide, and ultrafine particle matter (10-700 nm).

In addition to their direct toxic effects, the potential reduction in fetal growth and long-term effects should also be considered. Much of the basic research relies on studies in various animal models of development and we should also consider the ongoing development of new industrial products in the environment with unknown or untested effects upon development.

Environmental Links: Introduction | low folic acid | iodine deficiency | Nutrition | Drugs | Australian Drug Categories | USA Drug Categories | thalidomide | herbal drugs | Illegal Drugs | smoking | Fetal Alcohol Syndrome | TORCH | viral infection | bacterial infection | fungal infection | zoonotic infection | toxoplasmosis | Malaria | maternal diabetes | maternal hypertension | maternal hyperthermia | Maternal Inflammation | Maternal Obesity | hypoxia | biological toxins | chemicals | heavy metals | air pollution | radiation | Prenatal Diagnosis | Neonatal Diagnosis | International Classification of Diseases | Fetal Origins Hypothesis

Some Recent Findings

Yinchuan, China
Yinchuan, Ningxia, China
  • Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health[1] "Prenatal air pollution exposure has been linked to many adverse health conditions in the offspring. However, little is known about the mechanisms underlying these associations. Epigenetics may be one plausible biologic link. Here, we sought to identify site-specific and global DNA methylation (DNAm) changes, in developmentally relevant tissues, associated with prenatal exposure to nitrogen dioxide (NO2) and ozone (O3). Additionally, we assessed whether sex-specific changes in methylation exist and whether DNAm changes are consistently observed across tissues. RESULTS: We identified global and locus-specific changes in DNA methylation related to prenatal exposure to NO2 and O3 in 2 developmentally relevant tissues. Neonates with increased prenatal O3 exposure had lower aggregate levels of DNAm at CpGs located in open sea and shelf regions of the genome. We identified 6 DMRs associated with prenatal NO2 exposure, including 3 sex-specific. An additional 3 sex-specific DMRs were associated with prenatal O3 exposure levels. DMRs initially detected in cord blood samples (n = 4) showed consistent exposure-related changes in DNAm in placenta. However, the DMRs initially detected in placenta (n = 5) did not show DNAm differences in cord blood and, thus, they appear to be tissue-specific. CONCLUSIONS: We observed global, locus, and sex-specific methylation changes associated with prenatal NO2 and O3 exposures. Our findings support DNAm is a biologic target of prenatal air pollutant exposures and highlight epigenetic involvement in sex-specific differential susceptibility to environmental exposure effects in 2 developmentally relevant tissues." epigenetics
  • The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study[2] "Few studies from western countries have linked prenatal exposure to ambient particulate matter <2.5 μm (PM2.5) with increased risk of congenital anomalies. However, the results are mixed. Particularly, evidence is limited for Chinese pregnant women. METHODS: In this retrospective cohort study, we matched the data of all pregnant women laboured in public hospitals during 2015-2016 in Yinchuan, a capital city of northwest China and the data of daily average PM2.5, nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone (O3) concentrations of the nearest monitor station. We calculated a time-dependent exposure over the entire pregnancy for each woman. We used a time varying Cox proportional hazards model to explore the association between PM2.5 exposure and the risk of congenital anomalies, after adjusting for individual confounders and other pollutants. RESULTS: A total of 39,386 singleton live births were included in the study, and 530 (1.35%) were with congenital anomalies. An increase of 10 μg/m3 in PM2.5 exposure over the entire pregnancy was significantly associated with increased risk of congenital anomalies, with hazard ratio (HR) of 1.35 [95% confidence interval (95%CI): 1.16, 1.58]. For subtype analyses, PM2.5 exposure exhibited a significant association with cardiac anomalies and other unclassifiable anomalies, with HRs of 1.60 (95%CI: 1.24, 2.08) and 1.42 (95%CI: 1.07, 1.89), respectively. The impacts of PM2.5 exposure on orofacial anomalies and musculoskeletal anomalies were not significant. CONCLUSION: Our results indicate high concentration of PM2.5 could increase the risk of congenital anomalies among Chinese, especially for cardiac anomalies. Self-protective measures involving reducing PM2.5 pollution exposure during pregnancy as well as environmental policies aiming to restrict PM2.5 emission could be helpful to reduce the burden of cognitional anomalies."
  • Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children[3] "Air pollution exposure during fetal life has been related to impaired child neurodevelopment, but it is unclear if brain structural alterations underlie this association. The authors assessed whether air pollution exposure during fetal life alters brain morphology and whether these alterations mediate the association between air pollution exposure during fetal life and cognitive function in school-age children. We used data from a population-based birth cohort set up in Rotterdam, The Netherlands (2002-2006). Residential levels of air pollution during the entire fetal period were calculated using land-use regression models. Structural neuroimaging and cognitive function were performed at 6 to 10 years of age (n = 783). Mean fine particle levels were 20.2 μg/m3 (range, 16.8-28.1 μg/m3). CONCLUSIONS: Exposure to fine particles during fetal life was related to child brain structural alterations of the cerebral cortex, and these alterations partially mediated the association between exposure to fine particles during fetal life and impaired child inhibitory control. Such cognitive impairment at early ages could have significant long-term consequences."
  • Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study[4] "Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development. METHODS AND FINDINGS: We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). CONCLUSIONS: Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development."
More recent papers  
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Search term: Air Pollution Teratology

Older Papers  
These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.

See also the Discussion Page for other references listed by year and References on this current page.

Particulate Matter

Fine ambient particulate matter consists of small particles of 2.5  μm or less in size. While ultrafine particle matter occurs in the range of 10-700 nm.


Flow limitation during tidal expiration in early life significantly associated with the development of physician-diagnosed asthma by the age of 2 years. Infants with abnormal lung function soon after birth may have a genetic predisposition to asthma or other airway abnormalities that predict the risk of subsequent lower respiratory tract illness. Asthma phenotypes have a number of different classifications; allergic asthma, intrinsic or nonallergic asthma, infectious asthma, and aspirin-exacerbated asthma, and environmental exposures (occupational agents, smoking, air pollution, cold dry air).[5]

A recent Dutch PIAMA birth cohort study has shown that air pollution exposure is associated with a lower lung function in schoolchildren.[6]


  1. Ladd-Acosta C, Feinberg JI, Brown SC, Lurmann FW, Croen LA, Hertz-Picciotto I, Newschaffer CJ, Feinberg AP, Fallin MD & Volk HE. (2019). Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health. Environ Int , 126, 363-376. PMID: 30826615 DOI.
  2. Liu C, Li Q, Yan L, Wang H, Yu J, Tang J, Yao H, Li S, Zhang Y & Guo Y. (2019). The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study. Environ Int , 122, 316-321. PMID: 30455103 DOI.
  3. Guxens M, Lubczyńska MJ, Muetzel RL, Dalmau-Bueno A, Jaddoe VWV, Hoek G, van der Lugt A, Verhulst FC, White T, Brunekreef B, Tiemeier H & El Marroun H. (2018). Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children. Biol. Psychiatry , 84, 295-303. PMID: 29530279 DOI.
  4. Sunyer J, Esnaola M, Alvarez-Pedrerol M, Forns J, Rivas I, López-Vicente M, Suades-González E, Foraster M, Garcia-Esteban R, Basagaña X, Viana M, Cirach M, Moreno T, Alastuey A, Sebastian-Galles N, Nieuwenhuijsen M & Querol X. (2015). Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study. PLoS Med. , 12, e1001792. PMID: 25734425 DOI.
  5. Hekking PP & Bel EH. (2014). Developing and emerging clinical asthma phenotypes. J Allergy Clin Immunol Pract , 2, 671-80; quiz 681. PMID: 25439356 DOI.
  6. Finke I, de Jongste JC, Smit HA, Wijga AH, Koppelman GH, Vonk J, Brunekreef B & Gehring U. (2018). Air pollution and airway resistance at age 8 years - the PIAMA birth cohort study. Environ Health , 17, 61. PMID: 30016982 DOI.



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Cite this page: Hill, M.A. (2019, December 8) Embryology Abnormal Development - Air Pollution. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Air_Pollution

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