Fact caused the deaths, the findings would seem to be inconsistent with the work of Clarke et al. 1999 ; and Kodavanti et al. 2000 ; , who used larger CAP exposures, but in those studies, bronchitis was produced by lesser concentrations of SO2. Conceivably, susceptibility to death depends on the severity of bronchitis, on the particular composition of CAP, or on some stresses associated with CAP exposure, but not control exposure, in certain experimental settings. Mortality aside, there are indications in these studies that some CAP effects are larger in bronchitic rats than healthy animals, but dose-response is lacking and effects may be transient. CAP studies of animal models of cardiopulmonary disease Epidemiologic studies suggest that exposure to ambient particulate increases deaths from cardiopulmonary diseases. It is hypothesized that people with preexisting cardiopulmonary conditions are particularly susceptible to exposure. Work by Gordon et al. 1998 and 2000 ; and Godleski et al. 2000 ; has investigated effects of CAP exposure on animals rats, guinea pigs, and dogs ; with natural or induced heart disease. The findings of Gordon et al. 1998 ; are difficult to interpret, as the methods are insufficiently detailed and no data are presented. It appears that rats were injected with monocrotaline to induce pulmonary hypertension, a model for cor pulmonale.10 Treated and untreated animals were then exposed to CAP for three hours, at concentrations ranging at least from 110 to 360 : g m3. CAP exposures concentrations not specified ; induced increases in circulating neutrophils and decreases in lymphocytes three but not 24 hours after exposure in both treated and untreated rats; whether changes were larger in monocrotaline-treated animals is not discussed. No signs of lung injury or inflammation were seen during necropsy. Cell counts, protein, and LDH were increased in BAL fluid of monocrotaline-treated rats at 360 : g m3 but not at lower concentrations, and never in untreated animals. Heart rate was increased for several hours, to a similar degree, after CAP exposure in animals both treated and not treated with monocrotaline. This increase in heart rate was more persistent after repeated CAP exposures. Monocrotaline-treated rats were also exposed to CAP in the investigation of Gordon et al. 2000 ; . Unfortunately, healthy rats were not always exposed to the same CAP atmospheres as monocrotaline-treated rats, so whether CAP responses differ according to pulmonary disease status is sometimes unclear. In treated rats, a single exposure to 400 : g m3 CAP, but not 217 : g m3, caused a statistically significant increase in cell count, protein content, and LDH activity in BAL fluid, compared to values in air-exposed treated rats; but the highest CAP exposure used for healthy animals in this part of the investigation was 184 : g m3. In monocrotaline-treated rats, exposure to at least 217 : g m3 CAP, but not 157 : g m3, caused a statistically significant increase in the percentage of neutrophils and decrease in the percentage of lymphocytes in blood. Similar changes occurred in healthy animals at lower CAP exposures, but not at concentrations of 212 to 350 : g m3. These hematologic changes were present three hours after, but not 24 hours after, the single six-hour CAP exposures. In monocrotaline-treated rats exposed to 400 : g m3 CAP, but not 127 : g m3, heart rate was statistically significantly increased during the first postexposure hour. In normal rats, exposure to CAP of 132 : g m3 more caused an increase in heart rate over various post-exposure intervals. CAP exposure of 219 : g m3 produced no observable histologic alterations in lungs of healthy or monocrotaline-treated rats, and exposure to 181 : g m3 produced no spirometric changes. Overall, there is little evidence in this study that CAP exposure had a more detrimental effect on monocrotaline-exposed rats than healthy rats. Cor pulmonale is an enlargement of the right ventricle that occurs because of pulmonary hypertension from lung disorders commonly chronic bronchitis or emphysema!

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Table 7 Types of Reproductive and Developmental Risk Factors. 35.

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Table 4. Maternal and neonatal outcomes. Variables Chorioamnionitis Postpartum metritis Neonatal birth weight g ; 1-min Apgar score less than 7 5-min Apgar score less than 7 Admission to NICU Neonatal stay d ; Dinoprostone n 75 12 16% ; 5 6.6% ; 3195451 8 0 7 EASI n 76 10 13.1% ; 4 5.2% ; 3276529 10 1 value N.S N.S N.S N.S N.S N.S N.S.