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Background: Recent studies suggest that ambient air pollution exposure during pregnancy is associated with stillbirth occurrence. However, the results on the associations between ambient air pollutants and stillbirths are inconsistent and little is known about the gestational timing of sensitive periods for the effects of ambient air pollutants exposure on stillbirth.Objective: This study aimed to examine whether exposure to high levels of ambient air pollutants in a Chinese population is associated with an increased risk of stillbirth, and determine the gestational period when the fetus is most susceptible.Methods: We conducted a population-based cohort study in Wuhan, China, involving 95,354 births between June 10, 2011 and June 9, 2013. The exposure assessments were based on the daily mean concentrations of air pollutants obtained from the exposure monitor nearest to the pregnant women's residence. Logistic regression analyses were performed to determine the associations between stillbirths and exposure to each of the air pollutants at different pregnancy periods with adjustment for confounding factors.Results: Stillbirth increased with a 10 μg/m3 increase in particulate matter 2.5 (PM2.5) in each stage of pregnancy, and a significant association between carbon monoxide (CO) exposure and stillbirth was found during the third trimester (adjusted odds ratio (aOR): 1.01, 95% confidence interval (CI): 1.00-1.01) and in the entire pregnancy (aOR: 1.18, 95% CI: 1.04-1.34). Furthermore, an increased risk of stillbirth in the third trimester was associated with a 10 μg/m3 increase in PM10 (aOR: 1.08, 95% CI: 1.04-1.11), nitrogen dioxide (NO2) (aOR: 1.13, 95% CI: 1.07-1.21) and sulfur dioxide (SO2) (aOR: 1.26, 95% CI: 1.16-1.35). However, no positive association was observed between ozone exposure and stillbirth. In the two-pollutant models, PM2.5 and CO exposures were found to be consistently associated with stillbirth.Conclusions: Our study revealed that exposure to high levels of PM2.5, PM10, SO2, NO2 and CO increases the risk of stillbirth and the most susceptible gestational period to ambient air pollution exposure was in the third trimester. Further toxicological and prospective cohort studies with improved exposure assessments are needed to confirm the causal link between air pollutants and stillbirth. [ABSTRACT FROM AUTHOR]

Background: Existing studies exploring the association between low birth weight (LBW) and maternal fine particulate matter (aerodynamic diameter<2.5μm, PM2.5) exposure have presented equivocal results, and one of the possible reasons for this finding might be due to relatively low maternal exposures. In addition, relatively narrow maternal exposure windows to PM2.5 have not been well established for LBW.Methods: We employed a nested matched case-control design among 43,855 term births in a large maternity and child care hospital in Jinan, China. A total of 369 cases were identified, and four controls per case matched by maternal age were randomly selected among those with normal birth weight (n=1,476) from 2014 to 2016. Ambient air monitoring data on continuous measures of PM2.5, nitrogen dioxide (NO2), and sulfur dioxide (SO2) (24-h average concentrations) from 2013 to 2016 were collected from thirteen local monitoring stations. An inverse distance weighting method based on both home and work addresses was adopted to estimate the individual daily exposures to these air pollutants during pregnancy by weighting the average of the twelve nearest monitoring stations within 30km of each 100m×100m grid cell by an inverse squared distance, and then the average exposure concentrations for gestational months, trimesters and the entire pregnancy were calculated. Adjusted conditional logistic regression models were used to estimate the odds ratios (ORs) per 10μg/m3 increment in PM2.5 and by PM2.5 quartiles during different gestational periods.Results: In this study, the estimated mean values of PM2.5, NO2, and SO2 exposure during the entire pregnancy were 88.0, 54.6, and 63.1μg/m3, respectively. Term low birth weight (TLBW) increased in association with per 10μg/m3 increment in PM2.5 for the 8th month [OR=1.13, 95% confidence interval (CI): 1.04, 1.22], the 9th month (OR=1.06, 95% CI: 0.99, 1.15), the third trimester (OR=1.17, 95% CI: 1.05, 1.29), and the entire pregnancy (OR=1.38, 95% CI: 1.07, 1.77) in models adjusted for one pollutant (PM2.5). In models categorizing the PM2.5 exposure by quartiles, comparing the second, third, and highest with the lowest PM2.5 exposure quartile, the PM2.5 was positively associated with TLBW during the 8th month (OR: 1.77, 95% CI: 1.09, 2.88; OR: 1.77, 95% CI: 1.03, 3.04; OR: 1.92, 95% CI: 1.04, 3.55, respectively) and for the 9th month, only association for exposure in the third versus the lowest quartile was significant (OR: 1.91, 95% CI: 1.02, 3.58).Conclusions: The study provides evidence that exposure to PM2.5 during pregnancy might be associated with the risk of TLBW in the context of very high pollution level of PM2.5, and the 8th and 9th months were identified as potentially relevant exposure windows. [ABSTRACT FROM AUTHOR]

Background: Particulate matter (PM) from traffic and other sources has been associated with adverse health effects. One unifying theory is that PM, whatever its source, acts on the human body via its capacity to cause damaging oxidation reactions related to its content of pro-oxidants components. Few epidemiological studies have investigated particle oxidative potential (OP) and health. We conducted a time series analysis to assess associations between daily particle OP measures and numbers of deaths and hospital admissions for cardiovascular and respiratory diseases.Methods: During 2011 and 2012 particles with an aerodynamic diameter less than 2.5 and 10μm (PM2.5 and PM10 respectively) were collected daily on Partisol filters located at an urban background monitoring station in Central London. Particulate OP was assessed based on the capacity of the particles to oxidize ascorbate (OP(AA)) and glutathione (OP(GSH)) from a simple chemical model reflecting the antioxidant composition of human respiratory tract lining fluid. Particulate OP, expressed as % loss of antioxidant per μg of PM, was then multiplied by the daily concentrations of PM to derive the daily OP of PM mass concentrations (% loss per m(3)). Daily numbers of deaths and age- and cause-specific hospital admissions in London were obtained from national registries. Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death or admission associated with an interquartile increment in particle OP.Results: We found little evidence for adverse associations between OP(AA) and OP(GSH) and mortality. Associations with cardiovascular admissions were generally positive in younger adults and negative in older adults with confidence intervals including 0%. For respiratory admissions there was a trend, from positive to negative associations, with increasing age although confidence intervals generally included 0%.Conclusions: Our study, the first to analyse daily particle OP measures and mortality and admissions in a large population over two years, found little evidence to support the hypothesis that short-term exposure to particle OP is associated with adverse health effects. Further studies with improved exposure assessment and longer time series are required to confirm or reject the role of particle OP in triggering exacerbations of disease. [ABSTRACT FROM AUTHOR]

Ambient air particulate matter (PM) represents a class of heterogeneous substances that form one component of air pollution. Oxidative stress has been implicated as an important action mechanism for PM on the human organism. Oxidative damage induced by reactive oxygen species (ROS) may affect any cellular macromolecule. The aim of our study was to investigate the impact of air pollution on oxidative DNA damage [8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG)] and lipid peroxidation [15-F2t-isoprostane (15-F2t-IsoP)] in the urine and blood from mothers and newborns from two localities with different levels of air pollution: Ceske Budejovice (CB), a locality with a clean air, and Karvina, a locality with high air pollution. The samples from normal deliveries (38-41 week+) of nonsmoking mothers and their newborns were collected in the summer and winter seasons. Higher PM2.5 concentrations were found in Karvina than in CB in the summer 2013 (mean±SD: 20.41±6.28 vs. 9.45±3.62μg/m(3), P<0.001), and in the winter 2014 (mean±SD: 53.67±19.76 vs. 27.96±12.34μg/m(3), P<0.001). We observed significant differences in 15-F2t-IsoP levels between the summer and winter seasons in Karvina for newborns (mean±SD: 64.24±26.75 vs. 104.26±38.18pg/ml plasma, respectively) (P<0.001). Levels of 8-oxodG differed only in the winter season between localities, they were significantly higher (P<0.001) in newborns from Karvina in comparison with CB (mean±SD: 5.70±2.94 vs. 4.23±1.51 nmol/mmol creatinine, respectively). The results of multivariate regression analysis in newborns from Karvina showed PM2.5 concentrations to be a significant predictor for 8-oxodG excretion, PM2.5 and B[a]P (benzo[a]pyrene) concentrations to be a significant predictor for 15-F2t-IsoP levels. The results of multivariate regression analysis in mothers showed PM2.5 concentrations to be a significant predictor of 8-oxodG levels. [ABSTRACT FROM AUTHOR]

Background: Long-term exposure to fine particulate matter (PM2.5) may lead to increased blood pressure (BP). The role of industry- and traffic-specific PM2.5 remains unclear.Objective: We investigated the associations of residential long-term source-specific PM2.5 exposure with arterial BP and incident hypertension in the population-based Heinz Nixdorf Recall cohort study.Methods: We defined hypertension as systolic BP≥140mmHg, or diastolic BP≥90mmHg, or current use of BP lowering medication. Long-term concentrations of PM2.5 from all local sources (PM2.5ALL), local industry (PM2.5IND) and traffic (PM2.5TRA) were modeled with a dispersion and chemistry transport model (EURAD-CTM) with a 1km(2) resolution. We performed a cross-sectional analysis with BP and prevalent hypertension at baseline, using linear and logistic regression, respectively, and a longitudinal analysis with incident hypertension at 5-year follow-up, using Poisson regression with robust variance estimation. We adjusted for age, sex, body mass index, lifestyle, education, and major road proximity. Change in BP (mmHg), odds ratio (OR) and relative risk (RR) for hypertension were calculated per 1μg/m(3) of exposure concentration.Results: PM2.5ALL was highly correlated with PM2.5IND (Spearman's ρ=0.92) and moderately with PM2.5TRA (ρ=0.42). In adjusted cross-sectional analysis with 4539 participants, we found positive associations of PM2.5ALL with systolic (0.42 [95%-CI: 0.03, 0.80]) and diastolic (0.25 [0.04, 0.46]) BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.67]) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.73]). We found crude positive association of PM2.5TRA with prevalence (OR 1.41 [1.10, 1.80]) and incidence of hypertension (RR 1.38 [1.03, 1.85]), attenuating after adjustment (OR 1.19 [0.90, 1.58] and RR 1.28 [0.94, 1.72]). We found no association of PM2.5ALL and PM2.5IND with hypertension.Conclusions: Long-term exposures to all-source and industry-specific PM2.5 were positively related to BP. We could not separate the effects of industry-specific PM2.5 from all-source PM2.5. Estimates with traffic-specific PM2.5 were generally higher but inconclusive. [ABSTRACT FROM AUTHOR]