Exposure to air pollution during preconceptional and prenatal periods and risk of hypertensive disorders of pregnancy: a retrospective cohort study in Seoul, Korea.
ABSTRACT: Previous studies suggested associations between prenatal exposure to air pollution and hypertensive disorders of pregnancy. We explored the associations between ambient concentrations of five major air pollutants during preconceptional and prenatal periods and three hypertensive disorders of pregnancy in Seoul, Korea, using a population-representative cohort.We obtained heath and demographic data of pregnant women residing in Seoul for 2002-2013 from the Korean National Health Insurance Service-National Sample Cohort. For mother's individual exposures to air pollution, we computed concentrations of particulate matter ?10 ?m in diameter (PM10), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) during 1, 3, 6, and 12 months to birth using regulatory monitoring data in Seoul. The associations between air pollution and hypertensive disorders were explored by using logistic regression models after adjusting for individual confounders.Among 18,835 pregnant women in Seoul, 0.6, 0.5, and 0.4% of women developed gestational hypertension, preeclampsia, and preeclampsia requiring magnesium sulfate (Mg-preeclampsia), respectively. Although most odds ratios (ORs) were not statistically significant, we found increasing risk gradients with disease severity depending on the pollutant. There was the association between PM10 during 6 months to birth and gestational hypertension (OR for an interquartile range increase?=?1.68 [95% confidence interval?=?1.09-2.58]). NO2 and ozone during 12 and 1 month, respectively, before birth were associated with Mg-preeclampsia (1.43 [1.01-2.03], 1.53 [1.03-2.27]).We observed positive associations of exposure to some air pollutants before and during pregnancy with hypertensive disorders of pregnancy among the Korean general population. Future studies with refined exposure metrics should confirm our findings.
Project description:Previous studies suggested a possible association between fine particulate matter air pollution (PM2.5) and nitrogen dioxide (NO2) and the development of hypertensive disorders of pregnancy, but effect sizes have been small and methodologic weaknesses preclude firm conclusions.We linked birth certificates in New York City in 2008-2010 to hospital discharge diagnoses and estimated air pollution exposure based on maternal address. The New York City Community Air Survey provided refined estimates of PM2.5 and NO2 at the maternal residence. We estimated the association between exposures to PM2.5 and NO2 in the first and second trimester and risk of gestational hypertension, mild preeclampsia, and severe preeclampsia among 268,601 births.In unadjusted analyses, we found evidence of a positive association between both pollutants and gestational hypertension. However, after adjustment for individual covariates, socioeconomic deprivation, and delivery hospital, we did not find evidence of an association between PM2.5 or NO2 in the first or second trimester and any of the outcomes.Our data did not provide clear evidence of an effect of ambient air pollution on hypertensive disorders of pregnancy. Results need to be interpreted with caution considering the quality of the available exposure and health outcome measures and the uncertain impact of adjusting for hospital. Relative to previous studies, which have tended to identify positive associations with PM2.5 and NO2, our large study size, refined air pollution exposure estimates, hospital-based disease ascertainment, and little risk of confounding by socioeconomic deprivation, does not provide evidence for an association.
Project description:BACKGROUND:Studies on the hypertensive effect of long-term air pollution exposure were inconclusive and showed scarce evidence from rural areas in developing countries. In this context, we examined the associations of air pollution exposure with hypertension and blood pressure, and their effect modifiers in rural Chinese adults. METHODS:We studied 39,259 participants from a cohort established in five rural regions of central China. Individual exposures to PM2.5 and PM10 (particulate matter with an aerodynamic diameter less than or equal to 2.5 ?m and 10 ?m) and nitrogen dioxide (NO2) was evaluated using satellite-based spatiotemporal models. Mixed-effect regression models were applied to examine the associations of long-term exposure to air pollution with hypertension and four blood pressure component measurements, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP). Several potential effect modifiers related to demographic and behavioral factors were also examined. RESULTS:The results showed that for each 1 ?g/m3 increase in PM2.5, PM10 and NO2, the adjusted odds ratio of hypertension was 1.029 (95%CI: 1.001,1.057), 1.015 (95%CI: 1.001, 1.029) and 1.069 (95%CI: 1.038, 1.100), respectively. These three air pollutants were also associated with increased SBP (except for PM10), DBP and MAP. The hypertensive effects of air pollution were more pronounced among males, smokers, drinkers, individuals with a high-fat diet, and those with high-level physical activity. CONCLUSION:Long-term exposure to PM2.5, PM10 and NO2 was associated with increased blood pressure and hypertension in rural Chinese adults, and the associations were modified by several behavioral factors.
Project description:Background:Air pollution has been associated with hypertension and preterm birth. We examined if prenatal exposure to air pollutants was associated with gestational hypertension and if its association with preterm birth was modified by maternal hypertension. Methods:Data were from birth certificates and hospital discharge records of 252,205 women in San Joaquin Valley of California from 2000-2006. Air quality data were assigned from 24-hour averages of nitrogen dioxide (NO2), particulate matter <10?m (PM10) and <2.5?m (PM2.5), and carbon monoxide (CO) for different averaging periods over pregnancy. We estimated odds of preterm birth and multiplicative interaction between each pollutant and hypertensive disorder. Results:Among normotensive women, odds of preterm birth were slightly higher for higher exposure to all pollutants over the entire pregnancy. Patterns were similar among women with a hypertensive disorder. Among 32-36 week births there was effect modification for exposure to NO2 and CO during the first trimester with higher odds among hypertensive women, and PM2.5 and CO during the last six weeks with higher odds among normotensive women. For 28-31 week births, there was effect modification by hypertensive status for PM10 exposure for entire pregnancy, first, and second trimester with hypertensive women consistently having lower odds of preterm birth than normotensive. Conclusion:There was some evidence of effect modification in the direction counter to our hypothesis for exposure to PM10 and early preterm birth, and CO and PM2.5 at the end of pregnancy, but overall, hypertension did not modify the relationship between pollution and preterm birth.
Project description:BACKGROUND: Exposure to air pollution has been associated with higher C-reactive protein (CRP) levels, suggesting an inflammatory response. Not much is known about this association in pregnancy. OBJECTIVES: We investigated the associations of air pollution exposure during pregnancy with maternal and fetal CRP levels in a population-based cohort study in the Netherlands. METHODS: Particulate matter (PM) with an aerodynamic diameter ? 10 ?m (PM10) and nitrogen dioxide (NO2) levels were estimated at the home address using dispersion modeling for different averaging periods preceding the blood sampling (1 week, 2 weeks, 4 weeks, and total pregnancy). High-sensitivity CRP levels were measured in maternal blood samples in early pregnancy (n = 5,067) and in fetal cord blood samples at birth (n = 4,450). RESULTS: Compared with the lowest quartile, higher PM10 exposure levels for the prior 1 and 2 weeks were associated with elevated maternal CRP levels (> 8 mg/L) in the first trimester [fourth PM10 quartile for the prior week: odds ratio (OR), 1.32; 95% confidence interval (CI): 1.08, 1.61; third PM10 quartile for the prior 2 weeks: OR, 1.28; 95% CI: 1.06, 1.56]; however, no clear dose-response relationships were observed. PM10 and NO2 exposure levels for 1, 2, and 4 weeks preceding delivery were not consistently associated with fetal CRP levels at delivery. Higher long-term PM10 and NO2 exposure levels (total pregnancy) were associated with elevated fetal CRP levels (> 1 mg/L) at delivery (fourth quartile PM10: OR, 2.18; 95% CI: 1.08, 4.38; fourth quartile NO2: OR, 3.42; 95% CI: 1.36, 8.58; p-values for trend < 0.05). CONCLUSIONS: Our results suggest that exposure to air pollution during pregnancy may lead to maternal and fetal inflammatory responses.
Project description:BACKGROUND:Pediatric allergic diseases are a major public health concern, and previous studies have suggested that exposure to traffic-related air pollution (TRAP) exposure is a risk factor. These studies have typically assessed TRAP exposure using traffic measures, such as distance to major roads, or by modeling air pollutant concentrations; however inconsistent associations with pediatric allergic diseases have often been found. Using road proximity and density, we previously found an association between TRAP and atopic eczema among approximately 15,000 children living in Seoul, Korea, heavily populated and highly polluted city in which traffic is a major emission source. We aimed to conduct a parallel analysis using modeled air pollution concentrations and thus examine the consistency of the association. Specifically, we examined the associations of individual-level annual-average concentrations of NO2, PM10, and PM2.5 with symptoms and diagnoses of three pediatric allergic diseases including asthma, allergic rhinitis, and atopic eczema. METHODS:The study population included 14,614 children from the Seoul Atopy Friendly School Project Survey in Seoul, Korea, in 2010. To assess individual exposures to TRAP among these children, we predicted annual-average concentrations of NO2, PM10, and PM2.5 at the children's home addresses in 2010 using universal kriging and land use regression models along with regulatory air quality monitoring data and geographic characteristics. Then, we estimated odds ratios (ORs) of the three allergic diseases for interquartile increases in air pollution concentrations after adjusting for individual risk factors in mixed effects logistic regression. RESULTS:Symptoms and diagnoses of atopic eczema symptoms showed an association with NO2 (OR?=?1.07, 95% confidence interval?=?1.02-1.13; 1.08, 1.03-1.14) and PM10 (1.06, 1.01-1.12; 1.07, 1.01-1.13). ORs of PM2.5 were positive but not statistically significant (1.01, 0.95-1.07; 1.04, 0.98-1.10). No association was found between asthma and allergic rhinitis, although PM2.5 showed a marginal association with allergic rhinitis. CONCLUSIONS:Our consistent findings regarding the association between TRAP and the prevalence of atopic eczema using traffic measures and surrogate air pollutants suggested the effect of TRAP on children's health. Follow-up studies should elucidate the causal link, to support subsequent policy considerations and minimize adverse health effects in children.
Project description:Hypertensive disorders of pregnancy (HDP, including gestational hypertension, preeclampsia, and eclampsia) have a substantial public health impact. Maternal exposure to high levels of air pollution may trigger HDP, but this association remains unclear. The objective of our report is to assess and quantify the association between maternal exposures to criteria air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ? 10, 2.5 ?m) on HDP risk. PubMed, EMBASE, MEDLINE, Current Contents, Global Health, and Cochrane were searched (last search: September, 2013). After a detailed screening of 270 studies, 10 studies were extracted. We conducted meta-analyses if a pollutant in a specific exposure window was reported by at least four studies. Using fixed- and random-effects models, odds ratios (ORs) and 95% CIs were calculated for each pollutant with specific increment of concentration. Increases in risks of HDP (OR per 10 ppb = 1.16; 95% CI, 1.03-1.30) and preeclampsia (OR per 10 ppb = 1.10; 95% CI, 1.03-1.17) were observed to be associated with exposure to NO2 during the entire pregnancy, and significant associations between HDP and exposure to CO (OR per 1 ppm = 1.79; 95% CI, 1.31-2.45) and O3 (OR per 10 ppb = 1.09; 95% CI, 1.05-1.13) during the first trimester were also observed. Our review suggests an association between ambient air pollution and HDP risk. Although the ORs were relatively low, the population-attributable fractions were not negligible given the ubiquitous nature of air pollution.
Project description:BACKGROUND: Air pollution exposure during pregnancy might have trimester-specific effects on fetal growth. OBJECTIVE: We prospectively evaluated the associations of maternal air pollution exposure with fetal growth characteristics and adverse birth outcomes in 7,772 subjects in the Netherlands. METHODS: Particulate matter with an aerodynamic diameter < 10 ?m (PM10) and nitrogen dioxide (NO2) levels were estimated using dispersion modeling at the home address. Fetal head circumference, length, and weight were estimated in each trimester by ultrasound. Information on birth outcomes was obtained from medical records. RESULTS: In cross-sectional analyses, NO2 levels were inversely associated with fetal femur length in the second and third trimester, and PM10 and NO2 levels both were associated with smaller fetal head circumference in the third trimester [-0.18 mm, 95% confidence interval (CI): -0.24, -0.12 mm; and -0.12 mm, 95% CI: -0.17, -0.06 mm per 1-?g/m3 increase in PM10 and NO2, respectively]. Average PM10 and NO2 levels during pregnancy were not associated with head circumference and length at birth or neonatally, but were inversely associated with birth weight (-3.6 g, 95% CI: -6.7, -0.4 g; and -3.4 g, 95% CI: -6.2, -0.6 g, respectively). Longitudinal analyses showed similar patterns for head circumference and weight, but no associations with length. The third and fourth quartiles of PM10 exposure were associated with preterm birth [odds ratio (OR) = 1.40, 95% CI: 1.03, 1.89; and OR = 1.32; 95% CI: 0.96, 1.79, relative to the first quartile]. The third quartile of PM10 exposure, but not the fourth, was associated with small size for gestational age at birth (SGA) (OR = 1.38; 95% CI: 1.00, 1.90). No consistent associations were observed for NO2 levels and adverse birth outcomes. CONCLUSIONS: Results suggest that maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth. PM10 exposure was positively associated with preterm birth and SGA.
Project description:Air pollution exposure during pregnancy might affect placental growth and function, perhaps leading to pregnancy complications.We prospectively evaluated the associations of maternal air pollution exposure with markers of placental growth and function among 7,801 pregnant women in the Netherlands.We estimated levels of particulate matter ? 10 µm in aerodynamic diameter (PM10) and nitrogen dioxide (NO2) at the home address for different periods during pregnancy using dispersion modeling techniques. Pro- and anti-angiogenic factors [placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1), respectively] were measured in first- and second-trimester maternal blood and in fetal cord blood samples at delivery. Pulsatility index of the uterine and umbilical arteries was measured by Doppler ultrasound in second and third trimester, and notching was assessed in third trimester. Placenta weight and birth weight were obtained from medical records.Higher PM10 and NO2 exposure levels were associated with lower second-trimester maternal sFlt-1 and PlGF levels. PM10 and NO2 exposures averaged over total pregnancy were associated with higher sFlt-1 and lower PlGF levels in fetal cord blood, consistent with an anti-angiogenic state. PM10 and NO2 exposures were not consistently associated with second- or third-trimester placental resistance indices. NO2 exposure was associated with third-trimester notching (odds ratio 1.33; 95% CI: 0.99, 1.78 per 10-µg/m3 increase in the prior 2 months). PM10 and NO2 exposures were associated with lower placenta weight (-11.8 g; 95% CI: -20.9, -2.7, and -10.7 g; 95% CI: -19.0, -2.4, respectively, per 10-µg/m3 increase in the prior 2 months), but not with placenta to birth weight ratio.Our results suggest that maternal air pollution exposure may influence markers of placental growth and function. Future studies are needed to confirm these findings and explore the maternal and fetal consequences.
Project description:Congenital heart defects are the most prevalent type of birth defects. The association of air pollution with congenital heart defects is not well understood. We investigated a cohort of 8,969 singleton live births in Lanzhou, China during 2010-2012. Using inverse distance weighting, maternal exposures to particulate matter with diameter ?10?m (PM10), nitrogen dioxide (NO2), and sulfur dioxide (SO2) were estimated as a combination of monitoring station levels for the time spent at home and the work location. We used logistic regression to estimate the associations, adjusting for maternal age, education, income, BMI, disease, folic acid intake and therapeutic drug use, and smoking; season of conception; fuels for cooking; and temperature. We found significant positive associations of Patent Ductus Arteriosus (PDA) with PM10 during the 1st trimester, 2nd trimester and the entire pregnancy (OR 1st trimester=3.96, 95% Confidence Interval (CI): 1.36, 11.53; OR 2nd trimester=3.59, 95% Confidence Interval (CI): 1.57, 8.22; OR entire pregnancy=2.09, 95% CI: 1.21, 3.62, per interquartile range (IQR) increment for PM10 (IQR=71.2, 61.6, and 27.4 ?g/m3 respectively)), and associations with NO2 during 2nd trimester and entire pregnancy (OR 2nd trimester= 1.92, 95% CI: 1.11, 3.34; OR entire pregnancy=2.32, 95% Cl: 1.14, 4.71, per IQR increment for NO2 (IQR=13.4 and 10.9 ?g/m3 respectively)). The associations for congenital malformations of the great arteries and pooled cases showed consistent patterns. We also found positive associations for congenital malformations of cardiac septa with PM10 exposures in the 2nd trimester and the entire pregnancy, and SO2 exposures in the entire pregnancy. Results indicate a health burden from maternal exposures to air pollution, with increased risk of congenital heart defects.
Project description:Chronic air pollution exposure increases risk for hypertensive disorders of pregnancy, but the effect of acute air pollution exposure on blood pressure during pregnancy is less well known.We studied 151,276 singleton term deliveries from the Consortium on Safe Labor (2002-2008) with clinical blood pressure measured at admission to labor/delivery and diagnoses of hypertensive disorders collected from electronic medical records and hospital discharge summaries. Air pollution exposures were estimated for the admission hour and the 4 hours preceding admission using a modified version of the Community Multiscale Air Quality models and observed air monitoring data. Blood pressure was categorized as normal; high normal; and mild, moderate, or severe hypertension based on pregnancy cut points. Adjusted ordinal logistic regression estimated the odds of women having a higher admission blood pressure category as a function of air pollutant, hypertensive disorders, and their interaction effect.Odds of high blood pressure at admission to labor/delivery were increased in normotensive women after exposure to nitrogen oxides (by 0.2%/5 units), sulfur dioxide (by 0.3%/1 unit), carbon monoxide and several air toxics (by 3%-4%/high exposure). The effects were often similar or stronger among women with gestational hypertension and preeclampsia. Exposure to particulate matter <10 ?m increased odds of high blood pressure in women with preeclampsia by 3%/5 units.Air pollution can influence admission blood pressure in term deliveries and may increase likelihood of preeclampsia screening at delivery admission.