34 Placental-Fetal Distribution of Carbon Particles in a Pregnant Rabbit Model After Repeated Exposure to Diluted Diesel Engine Exhaust

• Published in: Annals of work exposures and health Vol. 67; no. Supplement_1; p. i48
• Main Authors: Bongaerts, Eva, Nawrot, Tim, Wang, Congrong, Chavatte-Palmer, Pascale, Ameloot, Marcel, Bové, Hannelore, Roeffaers, Maarten, Couturier-Tarrade, Anne, Cassee, Flemming
• Format: Journal Article
• Language: English
• Published: 10-05-2023
• ISSN: 2398-7308; 2398-7316
• DOI: 10.1093/annweh/wxac087.117

Airborne pollution particles have been shown to translocate from the mother’s lung to the fetal circulation but their placental-fetal distribution and internal tissue load remain poorly explored. Here, we investigated the placental-fetal distribution of diesel engine exhaust particles during gestation under controlled exposure conditions using a pregnant rabbit model. Pregnant dams were exposed by nose-only inhalation to either clean air (controls) or diluted and filtered diesel engine exhaust (1 mg/m3) for 2h/day, 5 days/week, from gestational day (GD) 3 to GD27. At GD28, placental and fetal tissues (i.e., heart, kidney, liver, lung and gonads) were collected for biometry and to study the accumulation of carbon particles (CPs) using white light generation by carbon particles under femtosecond pulsed laser illumination. CPs were detected in the placenta, fetal heart, kidney, liver, lung and gonads in significantly higher amounts compared with controls. By using multiple factor analysis, we were able to discriminate the diesel engine-exposed pregnant rabbits from the control group taking all variables related to fetoplacental biometry and CP load into consideration. Although our findings did not reveal a sex effect, a potential interaction effect might be present between exposure and fetal sex. The results confirm the translocation of maternally inhaled CPs from diesel engine exhaust to the placenta and the ability to reach fetal organs during late-stage pregnancy. The differential particle load in the fetal organs may contribute to the disruption of blood flow in the placenta with possible effects on fetoplacental biometry and placental function.