Collaborative efforts add critical information to understanding effects of BPA

BPA (bisphenol A), is used in the manufacturing of various plastics and food packaging, consumer products, some paper receipts, and medical devices. It is controversial because it exerts weak, but detectable, hormone-like properties which can mimic estrogen and may lead to far-ranging negative health effects including increased cardiovascular disease and diabetes in adults, increased cancer rates, including breast cancer, neurological difficulties, and hormonal and reproductive issues in both sexes and at all stages of life.

Recent results from research at the California National Primate Research Center (CNPRC) have shown that fetal BPA
exposure during a critical window of susceptibility in the third trimester, at levels similar to those measured in human blood, caused an increase in mucin genes and mucous cell maturation in the lungs (Environmental Health Perspectives, National Institutes of Health).

This is of environmental health importance because increases in airway mucins are hallmarks of a number of childhood lung diseases that may be impacted by BPA exposure. Overly abundant secretion and storage of mucous can cause airway obstruction as found in a number of lung diseases including asthma and bronchitis.

CNPRC scientists Drs. Laura S. Van Winkle, Respiratory Diseases Unit, and Catherine A. VandeVoort, Reproductive Sciences and Regenerative Medicine Unit, along with co-authors Drs. Shannon R. Murphy and Miriam V. Boetticher (UC Davis Center for Health and the Environment), conducted this collaborative study to investigate the effects of BPA on fetal development.

Their data indicate that exposure to environmentally relevant levels of BPA during fetal lung development can alter expression of secretory genes (Muc5B, Clara cell secretory protein (CCSP)) and proteins (Muc5B mucins and CCSP) in the conducting airways. They also found that this increase is most pronounced in the bronchi (proximal conducting airways).

In companion studies conducted at the CNPRC, it has been shown that exposure of pregnant monkeys to BPA disrupts development of fetal ovaries, potentially causing birth defects and reproductive problems that would not emerge for a generation (Link); and that BPA also affects several developmental parameters of the mammary gland of rhesus monkeys, including some that are relevant to breast cancer risk in humans (Link).

The study of BPA in a primate model is critical because the rhesus monkey has estrogen levels as well as reproductive and developmental processes that are similar to humans.

Dr. Van Winkle is a faculty member of the Department of Anatomy, Physiology and Cell Biology at the UC Davis School of Veterinary Medicine, and the UC Davis Center for Health and the Environment, as well as an Affiliate Scientist at the CNPRC .

Dr. VandeVoort is a faculty member of the Department of Obstetrics and Gynecology, UC Davis School of Medicine, in addition to being a Core Scientist at the CNPRC.

This research was funded by the National Institutes of Health.