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Effect of maternal exposure to ozone on reproductive outcome and immune, inflammatory, and allergic responses in the offspring
Citation:
Sharkhuu, T., D. L. DOERFLER, C. B. COPELAND, R. W. LUEBKE, AND M. I. GILMOUR. Effect of maternal exposure to ozone on reproductive outcome and immune, inflammatory, and allergic responses in the offspring. JOURNAL OF IMMUNOTOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, 8(2):183-194, (2011).
Impact/Purpose:
There is growing concern that exposure to air pollutants during pregnancy affects health outcomes in the offspring due to alterations in the development of immune and other homeostatic processes.
Description:
There is growing concern that exposure to air pollutants during pregnancy affects health outcomes in the offspring due to alterations in the development of immune and other homeostatic processes. To assess the risks of maternal inhalation exposure to ozone (O3), timed pregnant BALB/c mice were exposed to different concentrations of O3 (0, 0.4, 0.8, and 1.2ppm) for 4 h/day for 10 days during gestation (GD9-GD18), and pulmonary inflammation and immune responses were assessed in the offspring at 6 weeks of age. Maternal 03 exposure reduced the number of productive dams by 25% at the highest 03 concentration (1.2ppm) and decreased the rate of weight gain in the offspring. Delayed-type hypersensitivity responsesto bovine serum albumin were suppressed in the female offspring by maternal exposure to the two highest concentrations of O3, whereas humoral immune responses to sheep red blood cells were not altered in either sex. Maternal exposure to 1.2ppm 03 increased lactate dehydrogenase (LDH) 88 31 activity in bronchoalveolar lavage fluid (BALF) of the offspring but did not affect the number of inflammatory cells 89 or levels of total protein, IFN-y, IL-17, and IL-4 cytokines in BALF, or CD4+, CD8+, CD25+, and TCRB+CD1d+ T-cells in the spleen. Offspring born from air-exposed dams sensitized early in life (postnatal day [PND] 3) to ovalbumin (OVA) antigen and then challenged as adults developed eosinophilia, elevated levels of LDH activity and total protein in BALF, and increased pulmonary responsiveness to methacholine, compared with animals sensitized at PND42. Maternal 03 exposure in the 1.2ppm 03 groupd ecreased BALF eosinophilia and serum OVA-specific IgE in the female offspring sensitized early in life but did not affect development of allergic airway inflammation sensitized late in life. In summary, maternal exposure to 03 affected reproductive outcome and produced modest decreases in immune function and indicators of allergic lung disease in surviving offspring.
