Preterm birth in the first pregnancy and risk of neonatal death in the second pregnancy: a propensity score-weighted matching approach.

The study purpose was to assess the relationship between various grades of preterm birth (moderate preterm: 33-36 weeks; severe preterm: 27-32 weeks; extreme preterm: ≤ 26 weeks) in the first pregnancy and neonatal mortality (death within 28 days of birth; early: 0-7 days; late: 8-28 days) in the second pregnancy. Using the Missouri maternally-linked dataset (1989-2005), a population-based, retrospective cohort analysis with propensity score-weighted matching was conducted on mothers with two consecutive singleton live births (n = 310,653 women). Women with a prior preterm birth were more likely to subsequently experience neonatal death. The odds increased in a dose-dependent pattern with ascending severity of the preterm event in the first pregnancy (moderate preterm: AOR = 1.32; 95% CI: 1.10-1.60; severe preterm: AOR = 2.62; 95% CI: 2.01-3.41; extreme preterm: AOR = 5.84; 95% CI: 4.28-7.97; p value for trend < 0.001). However, the pathway for the relationship between prior preterm birth and subsequent neonatal mortality may be the recurrence of preterm birth.

Maternal hepatitis B and hepatitis C infection and neonatal neurological outcomes.

To examine the associations between maternal hepatitis B (HBV) and hepatitis C (HCV) infection status and selected infant neurological outcomes diagnosed at birth, we conducted a population-based, retrospective cohort study on singleton live births in Florida from 1998 to 2009. Primary exposures included maternal HBV and HCV monoinfection. The neurological outcomes included brachial plexus injury, cephalhematoma, foetal distress, feeding difficulties, intraventricular h aemorrhage and neonatal seizures. Multivariable logistic regression models were used to generate odds ratios (OR) and 95% confidence intervals (CI) that were adjusted for socio-demographic characteristics, risky behaviours, pregnancy complications and pre-existing medical conditions, and timing of delivery. The risk of an adverse neurological outcome was higher in infants born to mothers with hepatitis viral infection (7.2% for HCV, 5.0% for HBV), compared with infants of hepatitis virus-free mothers (4.2%). After adjusting for potential confounders, women with HBV were twice as likely to have infants who suffered from brachial plexus injury (OR = 2.04, 95% CI = 1.15-3.60), while those with HCV had an elevated odds of having an infant with feeding difficulties (OR: 1.32, 95% CI = 1.06-1.64) and a borderline increased likelihood for neonatal seizures (OR = 1.74, 95% CI = 0.98-3.10). Additionally, HCV+ mothers had a 22% increased odds of having an infant with some type of adverse neurological outcome (OR: 1.22, 95% CI = 1.03-1.44). Our findings add to current understanding of the association between maternal HBV/HCV infections and infant neurological outcomes. Further research evaluating the role of maternal HBV and HCV infections (including viraemia, treatment) on pregnancy outcomes is warranted.

The association between female genital mutilation and intimate partner violence.

OBJECTIVE: To determine whether female genital mutilation (FGM) is a risk factor for intimate partner violence (IPV) and its subtypes (physical, sexual and emotional). DESIGN: Population-based cross-sectional study. SETTING: The study used the 2006 Demographic and Health Survey (DHS) conducted in Mali. POPULATION: A total of 7875 women aged 15-49 years who responded to the domestic violence and female circumcision modules in the 2006 administration of the DHS in Mali. METHODS: Multivariable logistic regression was used to compute adjusted odds ratios (aOR) and 95% confidence intervals (CI) to measure risk for IPV. MAIN OUTCOME MEASURES: The outcomes of interest were IPV and its subtypes. RESULTS: Women with FGM were at heightened odds of IPV (aOR 2.71, 95% CI 2.17-3.38) and IPV subtypes: physical (aOR 2.85, 95% CI 2.22-3.66), sexual (aOR 3.24, 95% CI 1.80-5.82), and emotional (aOR 2.28, 95% CI 1.68-3.11). The odds of IPV increased with ascending FGM severity (P for trend <0.0001). The most elevated odds were observed among women with severe FGM, who were nearly nine times as likely to experience more than one IPV subtype (aOR 8.81, 95% CI 5.87-13.24). CONCLUSIONS: Study findings underscore the need for multi-tiered strategies, incorporating policy and education, to reduce FGM and IPV, potentially improving the holistic health and wellbeing of Malian women.

Pregnancy in the workplace.

BACKGROUND: Women constitute a large percentage of the workforce in industrialized countries. As a result, addressing pregnancy-related health issues in the workplace is important in order to formulate appropriate strategies to promote and protect maternal and infant health. AIMS: To explore issues affecting pregnant women in the workplace. METHODS: A systematic literature review was conducted using Boolean combinations of the terms 'pregnant women', 'workplace' and 'employment' for publications from January 1990 to November 2010. Studies that explicitly explored pregnancy in the workplace within the UK, USA, Canada or the European Union were included. RESULTS: Pregnancy discrimination was found to be prevalent and represented a large portion of claims brought against employers by women. The relationship between environmental risks and exposures at work with foetal outcomes was inconclusive. In general, standard working conditions presented little hazard to infant health; however, pregnancy could significantly impact a mother's psychosocial well-being in the workplace. CONCLUSIONS: Core recommendations to improve maternal and infant health outcomes and improve workplace conditions for women include: (i) shifting organizational culture to support women in pregnancy; (ii) conducting early screening of occupational risk during the preconception period and (iii) monitoring manual labour conditions, including workplace environment and job duties.

Does maternal obesity cause preeclampsia? A systematic review of the evidence.

AIM: The aim of this paper was to assess whether maternal obesity causes preeclampsia. METHODS: A systematic literature review of the previous two decades (1992-2011) was conducted. The exposure was maternal obesity while the outcome of interest was preeclampsia. RESULTS: Our review revealed consistent findings showing strong association between obesity and preeclampsia. Multiple biomarkers that potentially explain the mechanistic pathway in this relationship were identified, including leptin and adiponectin, matrix metalloproteinase (MMP), C-reactive protein (CRP), and sex hormone-binding globulin (SHBG). A causative biologic linkage remains, however, elusive. CONCLUSION: Epidemiologic evidence exists linking maternal obesity and preeclampsia. However, the exact causal pathway remains poorly defined. Given the minimal understanding of the nature of this relationship, research studies that utilize prospective designs and expand on the previous examination of biomarkers are recommended to determine potential causative pathways.

Infant mortality and subsequent risk of stillbirth: a retrospective cohort study.

OBJECTIVE: To examine the association between infant mortality in a first pregnancy and risk for stillbirth in a second pregnancy. DESIGN: Population-based, retrospective cohort study. SETTING: Maternally linked cohort data files for the state of Missouri. POPULATION: Women who had two singleton pregnancies in Missouri during the period 1989-2005 (n = 320 350). METHODS: Women whose first pregnancy resulted in infant death were compared with those whose infant from the first pregnancy survived the first year of life. The Kaplan-Meier product limit estimator was employed to compare probabilities for stillbirth in the second pregnancy between both groups of women. Adjusted hazard ratios (AHRs) and 95% confidence intervals (95% CIs) were generated to assess the association between infant mortality in the first pregnancy and stillbirth in the second pregnancy. MAIN OUTCOME MEASURES: Exposure was defined as infant mortality in the first pregnancy, and the outcome was defined as stillbirth in the second pregnancy. RESULTS: Women with prior infant deaths were about three times as likely to experience stillbirth in their subsequent pregnancy (AHR 2.91; 95% CI 2.02-4.18). White women with a previous infant death were nearly twice as likely to experience a subsequent stillbirth, compared with white women with a surviving infant (AHR 1.96; 95% CI 1.13-3.39). Black women with a previous infant death were more than four times as likely to experience subsequent stillbirth, compared with black women with a surviving infant (AHR 4.28; 95% CI 2.61-6.99). CONCLUSIONS: Previous infant mortality results in an elevated risk for subsequent stillbirth, with the most profound increase observed among black women. Interconception care should consider prior childbearing experiences to avert subsequent fetal loss.

Super-obesity and risk for early and late pre-eclampsia.

OBJECTIVE: To examine the association between obesity subtypes and risk of early and late pre-eclampsia. DESIGN: Population-based retrospective study. SETTING: State of Missouri maternally linked birth cohort files. POPULATION: All singleton live births in the state of Missouri from 1989 to 2005. METHODS: The body mass index (BMI) was used to classify women as normal weight (BMI = 18.5-24.9 kg/m(2)), class I obesity (BMI = 30-34.9 kg/m(2)), class II obesity (BMI = 35-39.9 kg/m(2)), class III obesity (BMI = 40-49.9 kg/m(2)) or super-obesity (BMI > or = 50 kg/m(2)). Adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between obesity and the risk of pre-eclampsia were obtained from logistic regression models with adjustment for intracluster correlation. RESULTS: The rate of pre-eclampsia increased with increasing BMI, with super-obese women having the highest incidence (13.4%). Compared with normal weight women, obese women (BMI > or = 30 kg/m(2)) had a higher risk for pre-eclampsia (OR = 2.59, 95% CI = 2.87-3.01). This risk remained approximately the same for late-onset pre-eclampsia (pre-eclampsia occurring at 34 weeks or more of gestation) and was slightly reduced for early-onset pre-eclampsia (pre-eclampsia occurring at 34 weeks or less of gestation). Within each BMI category, the risk of pre-eclampsia increased with the rate of weight gain. Compared with normal weight mothers with moderate weight gain, super-obese women with a high rate of weight gain had the greatest risk for pre-eclampsia (OR = 7.52, 95% CI = 2.70-21.0). CONCLUSION: BMI and rate of weight gain are synergistic risk factors that amplify the burden of pre-eclampsia among super-obese women.

Effect of thymidine on uptake, DNA alkylation, and DNA repair in L1210 cells treated with 1,3-bis(2-chloroethyl)-1-nitrosourea or 3'-[3-(2-chloroethyl)-3-nitrosoureido]-3'-deoxythymidine.

In order to define the mechanism for the enhancement by thymidine (dThd) of the antitumor activity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and 3'-[3-(2-chloroethyl)-3-nitrosoureido]-3'-deoxythymidine (3'-CTNU) in mice, we have investigated the effect(s) of dThd on the uptake of nitrosourea by L1210 cells in culture, DNA alkylation, and repair of the alkyl lesion. Using a rapid centrifugation technique through silicone:paraffin oil, we observe a 1.3- and 1.5-fold increase in the uptake of radioactivity from 0.1 mM [chloroethyl-14C]BCNU in the presence of a 5- and 25-fold excess of dThd, respectively. Similarly, an enhancement of DNA alkylation was observed upon treatment of L1210 cells for up to 3 h with 0.1 mM [chloroethyl-14C]BCNU from 70 pmol 14C/mg DNA in control to 85, 95, and 120 pmol 14C/mg DNA with equimolar 5- and 25-fold excess dThd, respectively. No effect of dThd on the uptake of 0.1 mM [chloroethyl-14C]-3'-CTNU was observed, although a small increase in DNA alkylation at 3 h was evident. DNA repair, as measured by the amount of radioactivity remaining associated with the DNA after an initial 2-h treatment with labeled BCNU was largely unaffected by dThd. Although dThd appears to enhance the cellular uptake of BCNU and the alkylation of DNA by both BCNU and 3'-CTNU, dealkylative repair proceeds unhindered in the presence of dThd.

Inhibition of poly(adenosine diphosphate-ribose) polymerase by thymidine and thymidine analogues in L1210 cells and its relationship to the potentiation of the antitumor activity of 1,3-bis(2-chloroethyl)-1-nitrosourea but not of 3'-[3-(2-chloroethyl)-3-nitrosoureido]-3'-deoxythymidine.

The coadministration of thymidine (dThd) with either 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or 3'-[3-(2-chloroethyl)-3-nitrosoureido]-3'-deoxythymidine (3'-CTNU) to L1210-bearing mice significantly enhanced the antitumor activity of both nitrosoureas (T-S. Lin and W. H. Prusoff, Cancer Res., 47:394-397, 1987, and T-S. Lin, P.H. Fischer, J. C. Marsh, and W. H. Prusoff, Cancer Res., 42:1624-1629, 1982). As a possible mechanism for this observed enhancement, we have investigated the role of dThd as an inhibitor of poly(ADP-ribose) polymerase (ADPRP), an enzyme which is activated in response to DNA damage. Exposure of L1210 cells in culture to 50 microM BCNU resulted in a greater than 10-fold increase in ADPRP activity within 3-4 h. The polymerase activity increased with increasing BCNU concentration after a 4-h exposure, reaching apparent saturation at 50 microM BCNU. However, this activation was abolished by 2 mM dThd. Median inhibition of the ADPRP activity elicited by 30 and 75 microM BCNU occurred at 38 and 135 microM dThd, respectively. When BCNU was replaced by 3'-CTNU, no activation of ADPRP was observed, even at or above concentration of 3'-CTNU previously shown to cause DNA damage. 3'-Amino-3'-deoxythymidine, the principal hydrolysis product of 3'-CTNU, was found to be an inhibitor of BCNU-stimulated ADPRP activity with potency similar to dThd. Furthermore, intact 3'-CTNU was found to inhibit BCNU-stimulated ADPRP activity. Although 3'-CTNU should be capable of activating ADPRP by causing DNA damage, our results suggest that no net activation is observed due to inhibition by the various thymidine species present. Thus, inhibition of ADPRP by dThd following DNA damage by BCNU is consistent with the potentiation of antitumor activity previously reported. However, the observed potentiation of 3'-CTNU activity by dThd does not appear to result from such a mechanism.

Synthesis and antiviral activity of several 2,5'-anhydro analogues of 3'-azido-3'-deoxythymidine, 3'-azido-2',3'-dideoxyuridine, 3'-azido-2',3'-dideoxy-5-halouridines, and 3'-deoxythymidine against human immunodeficiency virus and Rauscher-murine leukemia virus.

Several 2,5'-anhydro analogues of 3'-azido-3'-deoxythymidine (AZT), 3'-azido-2'3'-dideoxyuridine (AZU), 3'-azido-2'3'-dideoxy-5-bromouridine, 3'-azido-2',3'-dideoxy-5-iodouridine, and 3'-deoxythymidine and the 3'-azido derivative of 5-methyl-2'-deoxyisocytidine have been synthesized for evaluation as potential anti-HIV (human immunodeficiency virus) agents. These 2,5'-anhydro derivatives, compounds 13-17, demonstrated significant anti-HIV-1 activity with IC50 values of 0.56, 4.95, 26.5, 27.1, and 48 microM, respectively. Compared to that of the parent compounds AZT and AZU, the respective 2,5'-anhydro analogues, compounds 13 and 14, were somewhat less active. Whereas AZT was cytotoxic with a TCID50 of 29 microM, the toxicity of the 2,5'-anhydro derivative of AZT, compound 13, was reduced considerably to a TCID50 value of greater than 100 microM. The 2,5'-anhydro analogue of 5-methyl-2'-deoxyisocytidine also demonstrated anti-HIV-1 activity with an IC50 value of 12 microM. These compounds were also evaluated against Rauscher-Murine leukemia virus (R-MuLV) in cell culture. Among them, AZT, 3'-azido-2',3'-dideoxy-5-iodouridine, 3'-azido-2',3'-dideoxy-5-bromouridine, and 2,5'-anhydro-3'-azido-3'-deoxythymidine (13) were found to be most active, with IC50 values of 0.023, 0.21, 0.23, and 0.27 microM, respectively.

1-(2,3-Dideoxy-beta-D-glycero-pent-2-enofuranosyl)thymine. A highly potent and selective anti-HIV agent.

The nucleoside analogue 1-(2,3-dideoxy-beta-D-glycero-pent-2-enofuranosyl)thymine (d4T, 1) was prepared by ring opening of the 3',5'-anhydro compound 5. This method has been refined such that it can be used to prepare d4T on a large scale. The triphosphate of d4T was also synthesized from 1 in order to examine the mode of action. The in vitro inhibitory activity of d4T was found to be comparable to that of AZT in HIV-infected CEM cells. The triphosphate of d4T (8) and that of AZT inhibited the HIV reverse transcriptase with poly(rA):oligo(dT) as the template:primer with Ki values of 0.032 and 0.007 microM, respectively. The in vitro toxicity of d4T against normal human hematopoietic progenitor cells (CFU-GM) was measured in comparison to AZT. While d4T reduces colony-forming units by 50% at a concentration of 100 microM, it takes only 1 microM AZT to have a similar toxic effect. With erythrocyte burst forming units (BFU-E) the in vitro toxicities for d4T and AZT have comparable ID50 values of 10 and 6.7 microM, respectively.

Non-steroidal anti-inflammatory drugs and tumor progression: inhibition of fibroblast hyaluronic acid production by indomethacin and mefenamic acid.

The antitumor effects of non-steroidal anti-inflammatory drugs (NSAIDs) have been documented in a variety of both clinical and experimental settings, although the mechanisms responsible remain unclear. In the present study, we show that the NSAIDs indomethacin and mefenamic acid inhibit the calf serum-stimulated production of hyaluronic acid (HA) in murine Swiss 3T3 fibroblasts, at concentrations where DNA synthesis is unaffected. HA is an extracellular matrix glycosaminoglycan associated with cell migration and tumor invasion. Our data suggest that one mechanism whereby NSAIDs inhibit tumor progression may be to inhibit the synthesis of HA by host fibroblasts, and that the eicosenoid pathway may represent an important control point in the growth-factor-mediated production of HA in fibroblasts. Thus the use of an agent which inhibits HA synthesis may be a novel approach to alter the invasive and metastatic properties of tumor cells in a non-cytotoxic fashion.

Effect of 3'-deoxythymidin-2'-ene (d4T) on nucleoside metabolism in H9 cells.

The effect of 3'-deoxythymidin-2'-ene (d4T) on the metabolism of exogenously supplied radiolabeled nucleosides was investigated. Following a 24-hr exposure to 250 microM d4T, we observed no significant effect on the incorporation of [3H]thymidine or [3H]deoxycytidine into DNA. In contrast, the amounts of [3H]uridine, [3H]deoxyuridine, and [3H]cytidine were significantly lower than those incorporated by control cultures. d4T had no significant effect on the incorporation of [3H]uridine or [3H]cytidine into RNA, or the incorporation of 3H-labeled amino acids into protein. In d4T-treated cells the relative proportions of [3H]dTMP, [3H]dTDP, and [3H]dTTP formed did not change but their absolute concentrations were increased. d4T significantly reduced the level of [3H]dUMP, and a parallel decrease in [3H]dTMP derived from [3H]dUMP was also evident. d4T increased the amounts of labeled deoxycytidine metabolites formed, with increased dCMP levels the most prominent. In a cell-free extract, [3H]d4T was phosphorylated at a rate of 1.6 pmol/30 min. Increasing concentrations of both thymidine and deoxyuridine inhibited the phosphorylation of [3H]d4T with IC50 values of 5.7 and 35 microM respectively. d4T was found to be a weak substrate for purified H9 cytosolic thymidine kinase (Km = 138 microM) and a weak competitive inhibitor of thymidine and deoxyuridine phosphorylation by this enzyme (Ki = 1.37 and 0.33 mM respectively).

Cyclopentenyl uracil: an effective inhibitor of uridine salvage in vivo.

Cyclopentenyl uracil, a non-cytotoxic inhibitor of uridine kinase, was found to effectively block the salvage of circulating uridine by host and tumor tissues in the intact mouse. Dose-response characteristics of the inhibition were determined. Large doses (1 g/kg) of cyclopentenyl uracil were required, and the effect of a single dose fell rapidly over a 24-hr period. A sustained inhibition of uridine salvage of > 64-79% could be maintained by multiple doses of 1 g/kg given on an every 8-hr schedule. Mice given cyclopentenyl uracil (1 g/kg) every 8 hr for 5 days continued to gain weight and showed no signs of toxicity; however, the combination of cyclopentenyl uracil with a non-toxic dose of N-(phosphonacetyl)-L-aspartic acid (PALA; 200 mg/kg daily for 5 days) was lethal to mice, indicating that circulating uridine modifies the toxicity of agents that act on enzymes of the de novo pyrimidine pathway. Although the duration of action and potency of cyclopentenyl uracil are not ideal, this is the first demonstration of an effective inhibition of uridine salvage in the intact mouse with a non-cytotoxic agent. This makes possible the evaluation of concurrent inhibition of de novo and salvage routes to pyrimidine nucleotides as an approach to chemotherapy.

Metabolism and mode of selective inhibition of human immunodeficiency virus replication by 3'-azido-2',3'-dideoxy-5-iodouridine and 3'-azido-2',3'-dideoxy-5-bromouridine.

3'-Azido-2',3'-dideoxy-5-iodouridine (AzIdUrd) and 3'-azido-2',3'-dideoxy-5-bromouridine (AzBdUrd), previously shown to be potent and selective inhibitors of human immunodeficiency virus replication in vitro were minimally toxic to the uninfected human lymphoid cell line H9 (IC50 = 197 and 590 microM, respectively). Both compounds strongly inhibited the incorporation of [3H]thymidine but not [3H]deoxyadenosine into DNA, and we observed no significant inhibition of [3H]uridine incorporation into RNA or [3H]amino acid incorporation into protein. Exposure of H9 cells to AzIdUrd or AzBdUrd (100 microM, 24 hr) and pulse-labeling with [3H]thymidine resulted in approximately 80% reduction in levels of tritiated dTMP, dTDP, and dTTP relative to control. [125I]AzIdUrd was phosphorylated rapidly in H9 cells with the monophosphate accounting for over 90% of total soluble radioactivity. A relatively low but stable level of AzIdUTP was maintained over a 12-hr period. [125I]AzIdUrd was phosphorylated by a cell free extract of H9 cells at a rate approximately three times that of thymidine and its phosphorylation was inhibited by excess thymidine. AzIdUrd was found to be a competitive inhibitor of cytosolic thymidine kinase with a Ki of 2.63 microM and AzIdUMP a weak competitive inhibitor of thymidylate kinase with a Ki of 55.3 microM. Both AzIdUTP and AzBdUTP were potent competitive inhibitors of HIV-1 reverse transcriptase (Ki = 0.028 and 0.043 microM, respectively) and relatively poor inhibitors of H9 cell DNA polymerase alpha (Ki = 42.0 and 42.7 microM, respectively). Thus, the high therapeutic index of these compounds is due to the sensitivity of the viral reverse transcriptase, coupled with the relative insensitivity of the host cell DNA polymerase alpha.

Inhibition of fibroblast hyaluronic acid production by suramin.

Hyaluronic acid (HA) is an extracellular matrix glycosaminoglycan localized in the stroma of solid tumors, where it facilitates cell movement and thus tumor invasion and metastasis. This localization of HA is due to its synthesis by stromal fibroblasts in response to paracrine factors produced by the tumor. Such tumor-stromal interactions have been shown to be crucial to the development and progression of prostate cancer. Suramin is an effective antitumor agent in hormone-refractory prostate cancer, but its mechanism(s) of action is not well understood. However, the properties of suramin as an agent which disrupts growth factor action, and the importance of tumor-stroma interactions in prostate tumor development and in HA synthesis led us to study the effect of suramin on HA synthesis. Suramin inhibited HA synthesis by calf serum-stimulated Swiss 3T3 fibroblasts at clinically relevant concentrations (IC50 = 183 micrograms/mL). Increasing the serum concentration from 10 to 20% did not change the IC50 for HA synthesis, but increased the IC50 for [3H]thymidine incorporation from 206 to 342 micrograms/mL, indicating that the antiproliferative effect of suramin can be dissociated from its effect on HA synthesis. Suramin did not alter the cellular concentrations of the two precursors for HA synthesis (UDP-glucuronic acid and UDP-N-acetylglucosamine) at early time points and did not inhibit the HA synthetase activity of isolated membranes at concentrations up to 800 micrograms/mL.(ABSTRACT TRUNCATED AT 250 WORDS)

All-cause infant mortality and the risk for subsequent preterm birth.

AIM: The aim of this paper was to assess the association between all-cause infant mortality (death<365 days) in the first pregnancy and the risk of preterm birth (<37 weeks of gestation) in the second pregnancy. METHODS: Using the Missouri maternally linked dataset from 1989 to 2005 (N.=639134 singleton live births), we conducted a population-based retrospective cohort analysis with women who had two singleton births between 1989 and 2005. We employed Cox Proportional Hazards Regression to generate adjusted hazard ratios (AHR) and 95% confidence intervals (CI) to approximate relative risks. RESULTS: Prior infant mortality was associated with an increased risk for preterm birth in the second pregnancy (AHR=1.96, 95% CI=1.80-2.13). For black women, the risk of preterm birth following infant mortality was more than three-fold (AHR=3.37, 95% CI=2.92-3.89), while the risk for white women was twice as high (AHR=2.04, 95% CI=1.86-2.26) (referent=white women without infant death in the first pregnancy). CONCLUSION: Women with a history of infant mortality are at risk for preterm birth in subsequent pregnancies. This risk was significantly elevated for black women. These findings provide further evidence that previous childbearing experiences play a critical role in the occurrence of adverse feto-infant outcomes.

Applicability of a multiresidue method and high performance liquid chromatography for determining quinomethionate in apples and oranges.

The AOAC multiresidue method for nonpolar pesticide residues in nonfatty foods has been coupled with a high performance liquid chromatographic (HPLC)-fluorometric system for determining quinomethionate residues on apples and oranges. Quinomethionate is extracted with acetonitrile, and coextractives are removed with liquid-liquid partitioning and Florisil adsorbent using the AOAC multipesticide residue method for nonfatty foods. The quinomethionate fraction is then chromatographed on an HPLC octyl-bonded column and detected in-line with a fluorescence detector using 362 nm excitation and 395 nm emission. Recovery studies were conducted with apples fortified with quinomethionate at 0.05 ppm and oranges at 0.05 and 0.5 ppm. The recoveries averaged 100% (range 92-108) at the 0.05 ppm fortification level and 102% (range 93-110) at the 0.5 ppm level.

Applicability of a carbamate insecticide multiresidue method for determining additional types of pesticides in fruits and vegetables.

Several fruits and vegetables were fortified at a low (0.02-0.5 ppm) and at a high (0.1-5 ppm) level with pesticides and with a synergist, and recoveries were determined. Analyses were performed by using 3 steps of a multiresidue method for determining N-methylcarbamates in crops: methanol extraction followed by removal of plant co-extractives by solvent partitioning and chromatography with a charcoal-silanized Celite column. Eleven compounds were determined by using a high performance liquid chromatograph equipped with a reverse phase column and a fluorescence detector. Twelve additional compounds were determined by using a gas-liquid chromatograph equipped with a nonpolar packed column and an electron capture or flame photometric detector. Recoveries of 10 pesticides (azinphos ethyl, azinphos methyl, azinphos methyl oxygen analog, carbaryl, carbofuran, naphthalene acetamide, naphthalene acetic acid methyl ester, napropamide, phosalone, and phosalone oxygen analog) and the synergist piperonyl butoxide, which were determined by high performance liquid chromatography, averaged 100% (range 86-117) at the low fortification level and 102% (range 93-115) at the high fortification level. Quantitative recovery of naphthalene acetamide through the method required that an additional portion of eluting solution be passed through the charcoal column. Recoveries of 7 additional pesticides (dimethoate, malathion, methyl parathion, mevinphos, parathion, phorate oxygen analog, and pronamide), which were determined by gas-liquid chromatography (GLC), averaged 108% (range 100-120) at the low fortification level and 107% (range 99-122) at the high fortification level. DDT, diazinon, dieldrin, phorate, and pirimiphos ethyl, which were determined by GLC, were not quantitatively recovered.