Exposure to toxic environments across the life course: consequences for development, DNA methylation and ageing

Zhijun Zeng

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    Early life exposure to cigarette smoke interferes with lung development and is in children associated with an increased risk of getting lung infections and asthma. In adult life, smoking is one of the exogenous stimuli that is linked with accelerated ageing of the lung and the development of chronic obstructive pulmonary disease (COPD). Similarly, in China, prenatal and childhood exposure to e-waste originated pollutants is associated with adverse birth outcomes, abnormal development and growth impairment. E-waste pollutants arise when in a primitive and unsafe manner electronics are recycled. This results in the contamination of the environment (air, soil and water) with a mixture of chemicals that are well known for their adverse health effects, such as lead, cadmium, manganese and carcinogenic polycyclic aromatic hydrocarbons (PAHs). Pregnant women and young children that live in areas where electronics recycling takes place have a high risk of getting health problems.
    Risk factors for a particular disease can be hereditary and are then fixed in our genetic material, our DNA. In addition, environmental exposures during life induce changes in the use of the DNA. These are so-called epigenetic changes. Epigenetic mechanisms such as DNA methylation can be persistent and underlying chronic diseases and ageing.

    UMCG researcher Zhijun Zeng investigated the effect of (early life) smoke exposure on development and ageing in a mouse model of (maternal) smoking which was linked to Igf1 promoter methylation across 3 developmental stages, in liver and lung. The insulin-like growth factor (IGF) pathway has a pivotal role in (fetal) growth, development, and ageing. Prenatal smoke exposure induced differential Igf1 methylation in mouse offspring, which was persistent across the fetal stage to adulthood, and which was organ- and sex-specific. In addition, in offspring mice exposed to cigarette smoke for 12 weeks, the added effect of prenatal smoke exposure on smoke-induced lung ageing was only modest. The in China conducted study on prenatal exposure to e-waste-originated heavy metals showed an association with epigenome-wide differential methylation of 79 genes related to development and cell death. Childhood exposure to atmospheric e-waste was negatively associated with growth and linked with reduced plasma IGF1 levels.
    Originele taal-2English
    KwalificatieDoctor of Philosophy
    Toekennende instantie
    • Rijksuniversiteit Groningen
    Begeleider(s)/adviseur
    • Hylkema, Machteld, Supervisor
    • Xu, Xijin, Supervisor, Externe Persoon
    • Brandsma, Corry-Anke, Co-supervisor
    Datum van toekenning27-mei-2020
    Plaats van publicatie[Groningen]
    Gedrukte ISBN's978-94-034-2739-3
    Elektronische ISBN's978-94-034-2740-9
    DOI's
    StatusPublished - 2020

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