Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases

Early development appears to be a time of increased sensitivity to xenobiotics and risk of adverse immune outcomes that are likely to persist into later life

2014 Study Abstract

Developmental immunotoxicity (DIT) is a term given to encompass the environmentally induced disruption of normal immune development resulting in adverse outcomes. A myriad of chemical, physical, and psychological factors can all contribute to DIT. As a core component of the developmental origins of adult disease, DIT is interlinked with three important concepts surrounding health risks across a lifetime:

  1. the Barker Hypothesis, which connects prenatal development to later-life diseases,
  2. the hygiene hypothesis, which connects newborns and infants to risk of later-life diseases
  3. and fetal programming and epigenetic alterations, which may exert effects both in later life and across future generations.

While human immunological studies on diethylstilbestrol (DES) are limited compared with other health-related studies, there are reports suggesting that prenatally-exposed offspring are at a higher risk of immune-based disease.

Overall DES daughters exposed in utero self-reported an increased risk of all immune-based diseases (infections, allergies, and autoimmune conditions). Within specific categories, the women experienced more infectious diseases than non-DES exposed daughters.

In a separate study, Strohsnitter et al. examined the incidence of selected autoimmune conditions among DES daughters. They found no overall increase in disease associations for rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), optic neuritis (ON), or idiopathic thrombocytopenic purpura (ITP). However, there was a significant increase in the onset of rheumatoid arthritis by 45 years of age in the DES-exposed versus nonexposed groups.

  • Read and download the full study (free access) Developmental Immunotoxicity, Perinatal Programming, and Noncommunicable Diseases: Focus on Human Studies, on the NCBI, PubMed, Advances in Medicine
    Volume 2014, Article ID 867805, PMC4590951, 2014 Jan 23.
  • Image credit Daniel Liporace.

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