Prenatal exposures to persistent and non-persistent organic compounds and effects on immune system development.
Immune system development, particularly in the prenatal period, has far-reaching consequences for health during early childhood, as well as throughout life. Environmental disturbance of the complex balances of Th1 and Th2 response mechanisms can alter that normal development. Dysregulation of this process or an aberrant trajectory or timing of events can result in atopy, asthma, a compromised ability to ward off infection, or other auto-immune disease. A wide range of chemical, physical and biological agents appear to be capable of disrupting immune development. This MiniReview briefly reviews developmental milestones of the immune system in the prenatal period and early life, and then presents examples of environmentally induced alterations in immune markers. The first example involves a birth cohort study linked to an extensive programme of air pollution monitoring; the analysis shows prenatal ambient polycyclic aromatic hydrocarbons (PAH) and fine particle (PM2.5) exposures to be associated with altered lymphocyte immunophenotypic distributions in cord blood and possible changes in cord serum immunoglobulin E levels. The second example is a study of prenatal-polychlorinated biphenyl (PCB) exposures and the foetal development of the thymus, the organ responsible for lymphocyte maturation. Mothers with higher serum concentrations of PCBs gave birth to neonates having smaller indices of thymus size. Finally, this report underscores the tight connection between development of the immune system and that of the central nervous system, and the plausibility that disruption of critical events in immune development may play a role in neurobehavioural disorders.
Hertz-Picciotto
Irva
I
Center for Children's Environmental Health and Department of Public Health Sciences, University of California, Davis, CA 95616, USA. ihp@ucdavis.edu
Park
Hye-Youn
HY
Dostal
Miroslav
M
Kocan
Anton
A
Trnovec
Tomas
T
Sram
Radim
R
D000397:Air Pollution / Q000009:adverse effects; D000818:Animals; D001321:Autistic Disorder / Q000209:etiology; D004785:Environmental Pollutants / Q000633:toxicity*; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000209:etiology; D007107:Immune System / Q000187:drug effects* / Q000196:embryology; D018811:Maternal Exposure; D008431:Maternal-Fetal Exchange; D011078:Polychlorinated Biphenyls / Q000633:toxicity; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
D004785:Environmental Pollutants; D011084:Polycyclic Aromatic Hydrocarbons; D011078:Polychlorinated Biphenyls