title: Maternal and childhood asthma: risk factors, interactions, and ramifications.
abstract: Asthma is emerging as a premier example of a health risk that can largely be molded by the status of the mother and the environmental conditions encountered during sensitive windows of prenatal and early childhood development. While genetic background, allergic status of parents, and predisposition for atopy and inflammation play a role, early-life environmental conditions can completely alter the course of immune and respiratory system development. Environmentally induced alterations that (1) maintain the Th2 bias seen during gestation, (2) block the maturation of innate immune cells and (3) create inflammatory dysfunction in the infant provide the foundation for childhood asthma. No single risk factor can fully explain the increased prevalence of asthma in recent decades but it is assumed that the rapid increase is due to environmental and/or epigenetic changes. Well-established and suspected environmental risk factors cover all categories of early life interactions from diet, exposure to environmental contaminants and drugs, maternal and neonatal infections, hygiene, timing of vaccinations and even the mode of birth delivery. Because asthma is connected to the risk of several comorbid chronic conditions, the benefit of asthma risk reduction and prevention is greater than initially may be apparent. This review discusses strategies to optimize preventative and therapeutic options across life stages.
authors.affiliation: Department of Microbiology and Immunology, College of Veterinary Medicine, C5-135 VMC, Cornell University, North Tower Rd., Ithaca, NY 14853, USA. rrd1@cornell.ed
authors.forename: Rodney R
authors.initials: RR
authors.lastname: Dietert
mesh_terms: D001249:Asthma / Q000196:embryology / Q000453:epidemiology / Q000209:etiology* / Q000235:genetics; D002648:Child; D002657:Child Development / Q000502:physiology; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D006801:Humans; D007107:Immune System / Q000254:growth & development / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000453:epidemiology / Q000209:etiology*; D015995:Prevalence; D012307:Risk Factors