The association between ambient air pollution and adverse health effects, such as emergency room visits, hospitalizations, and mortality from respiratory and cardiovascular diseases, has been studied extensively in many countries, including Canada. Recently, studies conducted in China, the Czech Republic, and the United States have related ambient air pollution to adverse pregnancy outcomes. In this study, we examined association between preterm birth, low birth weight, and intrauterine growth retardation (IUGR) among singleton live births and ambient concentrations of sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO), and ozone in Vancouver, Canada, for 1985-1998. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for such effects. Low birth weight was associated with exposure to SO 2 during the first month of pregnancy (OR = 1.11, 95% CI, 1.01-1.22, for a 5.0 ppb increase). Preterm birth was associated with exposure to SO 2 (OR = 1.09, 95% CI, 1.01-1.19, for a 5.0 ppb increase) and to CO (OR = 1.08, 95% CI, 1.01-1.15, for a 1.0 ppm increase) during the last month of pregnancy. IUGR was associated with exposure to SO 2 (OR = 1.07, 95% CI, 1.01-1.13, for a 5.0 ppb increase), to NO 2 (OR = 1.05, 95% CI, 1.01-1.10, for a 10.0 ppb increase), and to CO (OR = 1.06, 95% CI, 1.01-1.10, for a 1.0 ppm increase) during the first month of pregnancy. In conclusion, relatively low concentrations of gaseous air pollutants are associated with adverse effects on birth outcomes in populations experiencing diverse air pollution profiles. Key words: air pollution, intrauterine growth retardation, low birth weight, preterm birth, risk assessment, sulfur dioxide.

This review summarizes the level of epidemiologic evidence for relationships between prenatal and/or early life exposure to environmental chemical contaminants and fetal, child, and adult health. Discussion focuses on fetal loss, intrauterine growth restriction, preterm birth, birth defects, respiratory and other childhood diseases, neuropsychological deficits, premature or delayed sexual maturation, and certain adult cancers linked to fetal or childhood exposures. Environmental exposures considered here include chemical toxicants in air, water, soil/house dust and foods (including human breast milk), and consumer products. Reports reviewed here included original epidemiologic studies (with at least basic descriptions of methods and results), literature reviews, expert group reports, meta-analyses, and pooled analyses. Levels of evidence for causal relationships were categorized as sufficient, limited, or inadequate according to predefined criteria. There was sufficient epidemiological evidence for causal relationships between several adverse pregnancy or child health outcomes and prenatal or childhood exposure to environmental chemical contaminants. These included prenatal high-level methylmercury (CH(3)Hg) exposure (delayed developmental milestones and cognitive, motor, auditory, and visual deficits), high-level prenatal exposure to polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), and related toxicants (neonatal tooth abnormalities, cognitive and motor deficits), maternal active smoking (delayed conception, preterm birth, fetal growth deficit [FGD] and sudden infant death syndrome [SIDS]) and prenatal environmental tobacco smoke (ETS) exposure (preterm birth), low-level childhood lead exposure (cognitive deficits and renal tubular damage), high-level childhood CH(3)Hg exposure (visual deficits), high-level childhood exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (chloracne), childhood ETS exposure (SIDS, new-onset asthma, increased asthma severity, lung and middle ear infections, and adult breast and lung cancer), childhood exposure to biomass smoke (lung infections), and childhood exposure to outdoor air pollutants (increased asthma severity). Evidence for some proven relationships came from investigation of relatively small numbers of children with high-dose prenatal or early childhood exposures, e.g., CH(3)Hg poisoning episodes in Japan and Iraq. In contrast, consensus on a causal relationship between incident asthma and ETS exposure came only recently after many studies and prolonged debate. There were many relationships supported by limited epidemiologic evidence, ranging from several studies with fairly consistent findings and evidence of dose-response relationships to those where 20 or more studies provided inconsistent or otherwise less than convincing evidence of an association. The latter included childhood cancer and parental or childhood exposures to pesticides. In most cases, relationships supported by inadequate epidemiologic evidence reflect scarcity of evidence as...

One important area for focus in obstetrics is prenatal diagnosis of severe CHDs. Such early diagnosis permits optimal care during pregnancy, during delivery, and in the newborn Background-This study quantifies the association between maternal medical conditions/illnesses and congenital heart defects (CHDs) among infants.

Since the midtwentieth century, stillbirths (late fetal deaths) and early neonatal deaths have often been combined into a single category of "perinatal" deaths. In the past, such a combination was justified by the fact that asphyxia was a common cause of death during labor (intrapartum stillbirth) and shortly after birth and by geographic and temporal differences in classification of livebirths versus stillbirths. In more recent years, however, the etiologic determinants have diverged sharply, with many fewer early neonatal deaths caused by asphyxia and relatively many more caused by congenital anomalies. Moreover, the increasingly common stratification of pregnancy outcome measures by gestational age or birth weight leads to the use of an inappropriate denominator (total livebirths plus stillbirths within each gestational age or birth weight category) for denoting risk for the stillbirth component, because all unborn fetuses (including the majority of those not born within the specified gestational age or birth weight range) are at risk of being stillborn in that range. The authors suggest that, whenever possible, stillbirths and early neonatal deaths should be reported separately, with gestational age-specific risks of stillbirth based on all fetuses at risk, and that antepartum and intrapartum stillbirths be reported separately.

No abstract

C esarean delivery rates in industrialized countries continue to rise. 1,2 The rates vary widely by country, health care facility and delivering physician, partly because of differing perceptions by health care providers as well as by pregnant women of its benefits and risks. [3][4][5][6][7] The relative safety of cesarean delivery and its perceived advantages relative to vaginal delivery have resulted in a change in the perceived risk-benefit ratio, which has accelerated acceptance. 1,[4][5][6][7][8][9][10][11][12] Indeed, a belief has become widespread that the risks of cesarean delivery for healthy women are so low as to make it a reasonable elective option for childbirth. 1,4,[12][13][14][15][16][17][18][19] Historically, most cesarean deliveries took place because of or in association with obstetrical complications or medical illness. However, rates of elective primary cesarean deliveries with no clear medical or obstetrical indication are rising dramatically. 1,5,6,[15][16][17][18][19][20] There is, therefore, a pressing need to assess the risks of maternal complications and death associated with elective cesarean delivery carried out in healthy women. Allen and colleagues 18 recently used the Nova Scotia Atlee Perinatal Database to compare outcomes of women whose cesarean deliveries were performed at term without labour and those with planned vaginal deliveries, but the relatively small sample size, the rarity of severe morbidity and absence of maternal deaths resulted in an incomplete picture. The main purpose of our study was to compare the risks of low-risk, elective cesarean delivery with those of planned vaginal delivery among healthy women at term. MethodsThe Canadian Institute for Health Information (CIHI) began collecting information on all admissions to Canada's acutecare hospitals in the early 1980s. CIHI's Discharge Abstract Database has been widely used for perinatal surveillance and research. 3,21,22 Data on all deliveries that took place from April 1, 1991 through March 31, 2005 were gathered for study except those occurring in the provinces of Quebec and Manitoba: complete information on these provinces was not contained in the database. The total number of in-hospital deliv-

No abstract

ObjectiveThe association between exposure to ambient particles with a median aerodynamic diameter less than 10/2.5 µm (particulate matter, PM10/2.5) and COPD remains unclear. Our study objective was to examine the association between ambient PM10/2.5 concentrations and lung functions in adults.MethodsA cross-sectional study was conducted in southern China. Seven clusters were randomly selected from four cities across Guangdong province. Residents aged ≥20 years in the participating clusters were randomly recruited; all eligible participants were examined with a standardised questionnaire and spirometry. COPD was defined as a post-bronchodilator FEV1/FVC less than 70%. Atmosphere PM sampling was conducted across the clusters along with our survey.ResultsOf the subjects initially recruited, 84.4% (n=5993) were included for analysis. COPD prevalence and atmosphere PM concentration varied significantly among the seven clusters. COPD prevalence was significantly associated with elevated PM concentration levels: adjusted OR 2.416 (95% CI 1.417 to 4.118) for >35 and ≤75 µg/m3 and 2.530 (1.280 to 5.001) for >75 µg/m3 compared with the level of ≤35 µg/m3 for PM2.5; adjusted OR 2.442 (95% CI 1.449 to 4.117) for >50 and ≤150 µg/m3 compared with the level of ≤50 µg/m3 for PM1. A 10 µg/m3 increase in PM2.5 concentrations was associated with a 26 mL (95% CI −43 to −9) decrease in FEV1, a 28 mL (−49 to −8) decrease in FVC and a 0.09% decrease (−0.170 to −0.010) in FEV1/FVC ratio. The associations of COPD with PM10 were consistent with PM2.5 but slightly weaker.ConclusionsExposure to higher PM concentrations was strongly associated with increased COPD prevalence and declined respiratory function.Trial registration number ChiCTR-OO-14004264; Post-results.