Prenatal exposure to PCBs is related to asthma in female adult offspring
Karmaus, W., Osuch, J., Zhang, J., Mikucki, D., & Haan, P. (2008). Prenatal exposure to PCBs is related to asthma in female adult offspring. In ISEE 20th Annual Conference, Pasadena, California, October 12-16, 2008, , p. S128. .
Objectives: In 2001, we reported that asthma in schoolchildren was associated with their serum concentration of dichlorodiphenyl ethylene (DDE). These findings were corroborated by Spanish studies and motivated us to test whether prenatal exposure to organochlorines such as DDE and polychlorinated biphenyls (PCB) are also associated with asthma in adults.
Methods and Procedures: We have established a two-generation cohort of female fish-eaters in Michigan including the mother and at least one daughter. The mothers participated between 1973 and 1991 in a minimum one of three consecutive surveys with serum measurements of DDE and total sum of PCBs. Based on linear regression, DDE and PCB levels were extrapolated to the time of the pregnancy of the respective offspring. Health information on their daughters was collected through telephone interviews in 2001/02 and repeated in 2006/07. Using repeated measurement analyses nested for mothers, we analyzed the association between prenatal DDE and PCBs and asthma in offspring (odds ratios). Statistically, we controlled for age, maternal history of asthma/wheezing (collected in 1989/91), and breastfeeding (gathered from the mother and the offspring). Prenatal DDE and PCB levels were grouped into quartiles.
Results: Of mothers with organochlorines levels, 151 female offspring participated in 2001/02 and 129 in 2006/07; 104 participated in both investigations. The offspring were between 18 and 58 years old. Doctor's diagnosed asthma was reported by 17.2% in 2001/02 and 10.1% in 2006/07. There was moderate agreement between asthma reported in 2001/02 and 2006/07 (kappa = 0.59). Compared to the lowest quartile, prenatal PCB levels >5 mg/L (highest quartile) were related to a 10.4-fold increased odds of adult offspring asthma (P = 0.001). Prenatal DDE did not show any association with asthma. Since prenatal DDE and PCB levels were correlated, we ran the analyses again, excluding DDE. In this case, the highest PCB quartile showed a 5.58 fold increased odds for asthma in adult offspring.
Conclusion: Our results provide further evidence that prenatal exposure to endocrine disrupting chemicals may be associated with an increased risk of asthma. Since our results are based on the total sum of PCBs, further investigations are needed to determine which PCB congener may be associated with asthma.