hypertension, pregnancy induced hypertension, eclampsia, renal, cardiac or lungdisease. Hazard rates (risk) of SB were calculated for each week of gestation.

RESULTS: Women R40 y had a significantly increased risk of SB across allgestational ages, which was greatest at R37 weeks (Figure). Women in the 35-39 y group had an increased risk of SB only at R37 weeks, with a relative risk(RR) of 1.25 (95% CI = 1.17, 1.33) compared to women !35 y. The risk ofSB for women R40 y at R37 weeks was approximately 1 in 450 ongoing preg-nancies, RR being 1.83 fold greater (95% CI = 1.61, 2.05) when compared towomen !35 y. 85% of the excess risk of SB for women R40 y at R37 weekswas not directly related to maternal medical disease.

CONCLUSION: In women with nonanomalous singleton stillbirths, a signif-icant proportion of the excess risk for women R40 y at R37 weeks is notassociated with reported maternal medical disease. Antepartum surveillancemay be indicated as there are other factors related to maternal age leading toan increased risk of SB.

647 NF-KB ACTIVATION IN HUMAN JEG3 TROPHOBLAST CELLS AND MURINE PLA-CENTAL FIBROBLASTS AFTER EXPOSURE TO ULTRAFINE PARTICULATE MATTERAMY ROUSE-HO (F)1, JAMES MCGREGOR2, MICHAEL KLEINMAN3, DANING LU4,MELISSA WILSON5, NASSIF KHOURY6, CHARLES SIMMONS6, OZLEM EQUILS4,1Keck School of Medicine at USC, OB/GYN, Los Angeles, California, 2Uni-versity of Southern California, Obstetrics/Gynecology, Los Angeles, Califor-nia, 3University of California, Irvine, Irvine, California, 4Cedars-SinaiMedical Center, Pediatrics, Los Angeles, California, 5University of SouthernCalifornia, Preventive Medicine, Los Angeles, California, 6Cedars-Sinai Med-ical Center, Los Angeles, California

OBJECTIVE: Air pollution is implicated in causing inflammatory-mediatedrespiratory and cardiovascular disease, and may contribute to pregnancydisorders. Inhaling small particles from diesel fuel emissions, among othersources, stimulates local inflammatory responses in the lung and has beenassociated with a systemic proinflammatory state. Particulate matter maycause placental inflammation and increase the risk of preterm birth. Thepurpose of this study is to demonstrate that particulate matter induces NF-kBactivation in human JEG3 trophoblast cells and murine placental fibroblasts.

STUDY DESIGN: JEG3 human trophoblast cells and primary murineplacental fibroblast cells were transfected with NF-kB luciferase and beta-galactosidase expression vectors using Fugene 6 (Boehringer Manheim,Indianapolis, IN) overnight. The cells were then stimulated with commerciallyprepared LPS- free particles measuring 0.1 micron (ultrafine) or measuring0.98 micron (fine) overnight. Control groups were treated with serum-freemedium alone or with lipopolysaccharide (LPS). NF-kB luciferase activity wasassessed by luciferase assay and use of a luminometer. Calorimetric beta-galactosidase assay was performed to correct for transfection efficiency. TheNF-kB activation in the experimental groups was compared to the activity ofthe media-treated or LPS-stimulated cells. Statistical significance was calcu-lated using ANOVA and student t-test.

RESULTS: Data analysis suggested that exposure to particulate matterinduced NF-kB activation in JEG3 trophoblasts after a twenty-four hourstimulation (p=0.02), with a trend toward NF-kB activation in cells exposedto ultrafine particles (0.1 micron) (p=0.14). Data from placental fibroblastssuggest a trend toward activation of NF-kB by ultrafine particles as well(p=0.079). Fine particles (0.98 micron) did not induce NF-kB activation ineither cell type.

CONCLUSION: Ultrafine particles may activate NF-kB in human tropho-blast cells and murine placental fibroblasts, and may contribute to local andsystemic inflammation in pregnancy.

648 AN INVERSE CORRELATION BETWEEN UMBILICAL CORD BLOOD IONIZED MAG-NESIUM (IMG) AND INTERLEUKIN-6 (IL-6) LEVELS COULD NOT BE CONFIRMEDIN THE HUMAN MARK SANTILLAN1, RICHARD E. BESINGER1, JOHNG. GIANOPOULOS1, ROBERT MITTENDORF1, 1Loyola University Medical Center,Department of Obstetrics and Gynecology, Maywood, Illinois

OBJECTIVE: Elevations in fetal cytokines, such as IL-6, are associated withsubsequent neuropathogenesis in children (Am J Obstet Gynecol 2003;188:1438-46). In a murine model, an inverse relationship has been shown betweencytokines and Mg levels (Frontiers in Bioscience 2005;10: 1177-82). Since thepreceding could be relevant to neuroprophylaxis in the human, we wanted tolearn if an inverse relationship exists in our data.

STUDY DESIGN: During the Magnesium and Neurologic Endpoints Trial(MgSO4 was randomized during preterm labor), an Epidemiologic Data Fileof biological data was collected. It included cord blood processed for a) iMg(NIH, Bethesda, AVL 988-4 Analyzer), and b) IL-6 levels (ELISA).

RESULTS: Of 144 enrolled babies, 73 had specimens available for pairedstudy of iMg and IL-6. Fetal blood (taken from the cord just before placentaldelivery) iMg levels ranged from 0.40 to 1.51 mmol/L (median of thoseunexposed to MgSO4, 0.52 mmol/L; Am J Obstet Gynecol 1999;180:S106);IL-6 levels ranged from !10 to 7,780 pg/ml. Using Pearson Correlations,no inverse (negative) relationship was found (Minitab). Overall, the correla-tion was positive (Coefficient, C0.11; P=.34). See Table.

CONCLUSION: Although mild increases in fetal blood iMg levels duringexposure to low dose MgSO4 in preterm labor might provide neuroprotectionvia decreased IL-6 levels, our data are unable to definitively confirm such arelationship.

Sub-group correlations

Fetal iMg (mmol/L) Fetal IL-6 (pg/ml) Correlation coefficients P-value

0.40 to 0.50 !10 to 7,780 C 0.14 .480.50 to 0.60 !10 to 40 � 0.35 .180.60 to 0.70 !10 to 2,976 C 0.25 .340.70 to 0.80 !10 to 2,976 � 0.43 .40O0.80 !10 to 4,630 C 0.02 .94Overall: iMg 0.40 to

1.51 mmol/LOverall: !10 to7,780 pg/ml

C 0.11 .34

SMFM Abstracts S183

646 THE OPTIMAL GESTATIONAL AGE FOR TWIN DELIVERY JULIAN ROBINSON1,BRIAN HEALY2, THOMAS BEATTY3, AMY COHEN4, 1Brigham and Women’s Hospi-tal, Boston, Massachusetts, 2Harvard University, Biostatistics, Boston, Massa-chusetts, 3Newton Wellesley Hospital, Obstetrics and Gynecology, Newton,Massachusetts, 4Harvard University, Information technology, Brookline,Massachusetts

OBJECTIVE: To determine the optimum time for delivery at which there isleast risk of any fetal or any neonatal death for a twin pregnancy.

STUDY DESIGN: The National Center for Health Statistics’ ‘‘MatchedMultiple Birth Data’’ database for 1995 to 2000 was analyzed. Statistics werederived for 636,353 twin fetuses and 315,652 delivered twin pairs. The prospec-tive risk of any fetal death within a twin pregnancy was calculated by gestationalage. The risk of any neonatal death of a liveborn twin sibship was derived bygestational age at delivery. These were compared. The combined risk of any fetaldeath or neonatal death by gestational age at delivery was calculated.

RESULTS: The risk of any neonatal death from a live delivered twin pair isleast at 38 weeks of gestational age. The first significant increase in the prospec-tive risk of any stillbirth from a twin gestation taking into account multiplecomparisons occurs at 34 weeks (p= 0.003) and becomes equal or greater to therisk of neonatal death at 39 weeks. The combined risk of any twin fetal death, ortwin neonatal death once delivered, nadirs at 37 weeks of gestational age.

Perinatal death in twin pregnancy

CONCLUSION: To minimize the risk of any fetal death in a twin pregnancywhile pregnant, or any neonatal death after delivery, consideration should begiven to elective twin delivery at 37 weeks of gestational age.