Association between usage of household cooking fuel and congenital birth defects-18 months multi-centric cohort study in Nepal.

BACKGROUND: - An estimated 240,000 newborns die worldwide within 28 days of birth every year due to congenital birth defect. Exposure to poor indoor environment contributes to poor health outcomes. In this research, we aim to evaluate the association between the usage of different type household cooking fuel and congenital birth defects in Nepal, as well as investigate whether air ventilation usage had a modifying effect on the possible association. METHODS: - This is a secondary analysis of multi-centric prospective cohort study evaluating Quality Improvement Project in 12 public referral hospitals of Nepal from 2017 to 2018. The study sample was 66,713 women with a newborn, whose information was available in hospital records and exit interviews. The association between cooking fuel type usage and congenital birth defects was investigated with adjusted multivariable logistic regression. To investigate the air ventilation usage, a stratified multivariable logistic regression analysis was performed. RESULTS: -In the study population (N = 66,713), 60.0% used polluting fuels for cooking and 89.6% did not have proper air ventilation. The prevalence rate of congenital birth defect was higher among the families who used polluting fuels for cooking than those who used cleaner fuels (5.5/1000 vs. 3.5/1000, p < 0.001). Families using polluting fuels had higher odds (aOR 1.49; 95% CI; 1.16, 1.91) of having a child with a congenital birth defect compared to mothers using cleaner fuels adjusted with all available co-variates. Families not using ventilation while cooking had even higher but statistically insignificant odds of having a child with congenital birth defects (aOR 1.34; 95% CI; 0.86, 2.07) adjusted with all other variates. CONCLUSION: - The usage of polluted fuels for cooking has an increased odds of congenital birth defects with no significant association with ventilation. This study adds to the increasing knowledge on the adverse effect of polluting fuels for cooking and the need for action to reduce this exposure.

Exposure to local, source-specific ambient air pollution during pregnancy and autism in children: a cohort study from southern Sweden.

Evidence of air pollution exposure, namely, ambient particulate matter (PM), during pregnancy and an increased risk of autism in children is growing; however, the unique PM sources that contribute to this association are currently unknown. The aim of the present study was to investigate local, source-specific ambient PM exposure during pregnancy and its associations with childhood autism, specifically, and autism spectrum disorders (ASD) as a group. A cohort of 40,245 singleton births from 2000 to 2009 in Scania, Sweden, was combined with data on locally emitted PM with an aerodynamic diameter < 2.5 µm (PM2.5). A flat, two-dimensional dispersion model was used to assess local PM2.5 concentrations (all-source PM2.5, small-scale residential heating- mainly wood burning, tailpipe exhaust, and vehicle wear-and-tear) at the mother's residential address during pregnancy. Associations were analyzed using binary logistic regression. Exposure to local PM2.5 during pregnancy from each of the investigated sources was associated with childhood autism in the fully adjusted models. For ASD, similar, but less pronounced, associations were found. The results add to existing evidence that exposure to air pollution during pregnancy may be associated with an increased risk of childhood autism. Further, these findings suggest that locally produced emissions from both residential wood burning and road traffic-related sources (tailpipe exhaust and vehicle wear-and-tear) contribute to this association.

Health impact assessment of road traffic noise exposure based on different densification scenarios in Malmö, Sweden.

While urbanization provides many opportunities to those arriving in thriving urban areas, a greater number of residents necessitates the expansion of housing and infrastructure. This is often achieved through densification, which can lead to increased noise, particularly through increased road traffic. A key challenge of promoting healthy urban planning is to understand potential health effects, especially on the local level. The aim of the present study is, therefore, to estimate and compare the health impacts of road traffic noise exposure for various urban densification scenarios within a neighborhood (Lorensborg) in Malmö, Sweden. The three scenarios include 1) Present-day, representing the study area as it is presently organized; 2) Planned municipal strategy (the city of Malmö's own densification plans) and 3) Health-centred, which involves major structural alterations and reflects an effort prioritize a health-centred approach. Noise was modelled using the Nordic prediction method for road traffic. Health outcomes included noise annoyance, adverse sleep disturbance, ischemic heart disease (IHD) incidence and mortality. Within all scenarios, a large proportion of the study population was exposed above the WHO's health-based guideline value (Lden 53 dB): >80% for Present-day and Planned municipal strategy scenarios, and almost 50% in the Health-centred scenario. Still, densifying Lorensborg (population ≈9,600) according to the Health-centred scenario could prevent 549 cases of highly annoyed, 193 cases of adverse sleep disturbance, 4.7 new cases of IHD (8.9% of total cases), and 1.5 deaths due to IHD (17.8% of IHD mortality) annually. The results demonstrated that it is possible to considerably lower the health impact with a more health-centred densification strategy. Important co-benefits for public and environmental health include air pollution reduction and green space creation, although their health effects were not quantified in the present study. Urban planning initiatives must be more ambitious in order to create healthy, sustainable cities.

Characterization of fine particulate matter from indoor cooking with solid biomass fuels.

Household burning of solid biomass fuels emits pollution particles that are a huge health risk factor, especially in low-income countries (LICs) such as those in Sub-Saharan Africa. In epidemiological studies, indoor exposure is often more challenging to assess than outdoor exposure. Laboratory studies of solid biomass fuels, performed under real-life conditions, are an important path toward improved exposure assessments. Using on- and offline measurement techniques, particulate matter (PM) from the most commonly used solid biomass fuels (charcoal, wood, dung, and crops residue) was characterized in laboratory settings using a way of burning the fuels and an air exchange rate that is representative of real-world settings in low-income countries. All the fuels generated emissions that resulted in concentrations which by far exceed both the annual and the 24-hour-average WHO guidelines for healthy air. Fuels with lower energy density, such as dung, emitted orders of magnitude more than, for example, charcoal. The vast majority of the emitted particles were smaller than 300 nm, indicating high deposition in the alveoli tract. The chemical composition of the indoor pollution changes over time, with organic particle emissions often peaking early in the stove operation. The chemical composition of the emitted PM is different for different biomass fuels, which is important to consider both in toxicological studies and in source apportionment efforts. For example, dung and wood yield higher organic aerosol emissions, and for dung, nitrogen content in the organic PM fraction is higher than for the other fuels. We show that aerosol mass spectrometry can be used to differentiate stove-related emissions from fuel, accelerant, and incense. We argue that further emission studies, targeting, for example, vehicles relevant for LICs and trash burning, coupled with field observations of chemical composition, would advance our understanding of air pollution in LIC. We believe this to be a necessary step for improved air quality policy.

Estimated public health benefits of a low-emission zone in Malmö, Sweden.

Air pollution is one of the leading causes of morbidity and mortality worldwide. Low-emission zones (LEZ) have been increasingly implemented in cities throughout Europe as a measure to reduce the adverse health effects and premature deaths associated with traffic-related air pollution. In the present study, a health impact analysis was conducted to estimate the effect of a hypothetical LEZ on mortality and morbidity in Malmö, Sweden. Baseline health statistics were gathered from health registers and applied to each resident according to individual-level data on age and/or sex. Concentration-response parameters were derived from current epidemiological literature, specifically meta-analyses. A Gaussian dispersion model (AERMOD) combined with a detailed emission database was used to calculate NO2 emissions from traffic, which could be applied on an individual-level using data on each person's residential coordinates. The adjusted exposure scenario replaced all vehicles on municipal roads having Euro 5 or lower emission standards with Euro 6 equivalents. This LEZ would, on average, decrease NO2 concentrations by 13.4%, preventing an estimated 9-26 deaths in Malmö each year. Additionally, 12 respiratory disease hospitalizations, 8 childhood asthma cases, and 9 cases of hypertensive disorders of pregnancy were estimated to be avoided annually. These results suggest that LEZs can effectively improve air quality, reduce greenhouse gas emissions, and safeguard public health.

Prenatal Exposure to Locally Emitted Air Pollutants Is Associated with Birth Weight: An Administrative Cohort Study from Southern Sweden.

While prenatal exposure to ambient air pollution has been shown to be associated with reduced birth weight, there is substantial heterogeneity across studies, and few epidemiological studies have utilized source-specific exposure data. The aim of the present study was, therefore, to investigate the associations between local, source-specific exposure to fine particulate matter (PM2.5) during pregnancy and birth weight. An administrative cohort comprising 40,245 singleton births from 2000 to 2009 in Scania, Sweden, was combined with data on relevant covariates. Investigated sources of PM2.5 included all local sources together as well as tailpipe exhaust, vehicle wear-and-tear, and small-scale residential heating separately. The relationships between these exposures, represented as interquartile range (IQR) increases, and birth weight (continuous) and low birth weight (LBW; <2500 g) were analyzed in crude and adjusted models. Each local PM2.5 source investigated was associated with reduced birth weight; average decreases varied by source (12−34 g). Only small-scale residential heating was clearly associated with LBW (adjusted odds ratio: 1.14 (95% confidence interval: 1.04−1.26) per IQR increase). These results add to existing evidence that prenatal exposure to ambient air pollution disrupts fetal growth and suggest that PM2.5 from both vehicles and small-scale residential heating may reduce birth weight.

Ambient and indoor air pollution exposure and adverse birth outcomes in Adama, Ethiopia.

Air pollution poses a threat to human health, with pregnant women and their developing fetuses being particularly vulnerable. A high dual burden of ambient and indoor air pollution exposure has been identified in Ethiopia, but studies investigating their effects on adverse birth outcomes are currently lacking. This study explores the association between ambient air pollution (NOX and NO2) and indoor air pollution (cooking fuel type) and fetal and neonatal death in Adama, Ethiopia. A prospective cohort of mothers and their babies was used, into which pregnant women were recruited at their first antenatal visit (n = 2085) from November 2015 to February 2018. Previously developed land-use regression models were utilized to assess ambient concentrations of NOX and NO2 at the residential address, whereas data on cooking fuel type was derived from questionnaires. Birth outcome data was obtained from self-reported questionnaire responses during the participant's postnatal visit or by phone if an in-person meeting was not possible. Binary logistic regression was employed to assess associations within the final study population (n = 1616) using both univariate and multivariate models; the latter of which adjusted for age, education, parity, and HIV status. Odds ratios (OR) and their corresponding 95% confidence intervals (CI) were reported. Within the cohort, 69 instances of fetal death (n = 16 miscarriages; n = 53 stillbirths) and 16 cases of neonatal death were identified. The findings suggest a tendency towards an association between ambient NOX and NO2 exposure during pregnancy and an increased risk of fetal death overall as well as stillbirth, specifically. However, statistical significance was not observed. Results for indoor air pollution and neonatal death were inconclusive. As limited evidence on the effects of exposure to ambient air pollution on adverse birth outcomes exists in Sub-Saharan Africa and Ethiopia, additional studies with larger study populations should be conducted.

Influence of Socio-Economic Factors and Region of Birth on the Risk of Preeclampsia in Sweden.

OBJECTIVES: To investigate the association between socio-economic factors and the risk of preeclampsia in Sweden, specifically investigating if this relationship is confounded by maternal region of birth. STUDY DESIGN: All singleton births between 1999 and 2009 in an ethnically diverse area in southern Sweden, totaling 46,618 pregnancies, were included in this study. The data on maternal pregnancy outcomes were retrieved from a regional birth register and socio-economic variables from Statistics Sweden. The risk ratios for preeclampsia were calculated for educational level and household disposable income, adjusting for maternal region of birth, maternal age, body mass index, parity, and smoking. RESULTS: Low income levels were associated with a higher risk for preeclampsia, adjusted risk ratio (aRR) = 1.25 (95% confidence interval [CI]: 0.99, 1.59) and aRR = 1.36 (95% CI: 1.10, 1.68) for the two lowest quintiles, respectively, compared to the highest. There was an educational gradient in preeclampsia risk, although not all categories reached statistical significance: aRR = 1.16, (95% CI: 0.89-1.50) for low educational attainment and aRR = 1.23 (95% CI: 1.08, 1.41) for intermediate educational attainment compared to women with highest education. The socio-economic gradient remained after adjusting for region of birth. There was a lower risk for preeclampsia for women born in Asia, aRR = 0.60 (95% CI: 0.47, 0.75), regardless of socio-economic position. CONCLUSION: An increased risk for preeclampsia was seen for women with measures of lower socio-economic position, even in a universal, government-funded healthcare setting. The relationship was not explained by region of birth, indicating that the excess risk is not due to ethnically differential genetic pre-disposition but rather due to modifiable factors.

Early Pregnancy Exposure to Ambient Air Pollution among Late-Onset Preeclamptic Cases Is Associated with Placental DNA Hypomethylation of Specific Genes and Slower Placental Maturation.

Exposure to ambient air pollution during pregnancy has been associated with an increased risk of preeclampsia (PE). Some suggested mechanisms behind this association are changes in placental DNA methylation and gene expression. The objective of this study was to identify how early pregnancy exposure to ambient nitrogen oxides (NOx) among PE cases and normotensive controls influence DNA methylation (EPIC array) and gene expression (RNA-seq). The study included placentas from 111 women (29 PE cases/82 controls) in Scania, Sweden. First-trimester NOx exposure was assessed at the participants' residence using a dispersion model and categorized via median split into high or low NOx. Placental gestational epigenetic age was derived from the DNA methylation data. We identified six differentially methylated positions (DMPs, q < 0.05) comparing controls with low NOx vs. cases with high NOx and 14 DMPs comparing cases and controls with high NOx. Placentas with female fetuses showed more DMPs (N = 309) than male-derived placentas (N = 1). Placentas from PE cases with high NOx demonstrated gestational age deceleration compared to controls with low NOx (p = 0.034). No differentially expressed genes (DEGs, q < 0.05) were found. In conclusion, early pregnancy exposure to NOx affected placental DNA methylation in PE, resulting in placental immaturity and showing sexual dimorphism.

Indoor Air Pollution Exposure of Women in Adama, Ethiopia, and Assessment of Disease Burden Attributable to Risk Factor.

INTRODUCTION AND AIM: Air pollution, a major environmental threat to human health, contributes to the premature deaths of millions of people worldwide. Cooking with solid fuels, such as charcoal and wood, in low- and middle-income countries generates very high emissions of particulate matter within and near the household as a result of their inefficient combustion. Women are especially exposed, as they often perform the cooking. The purpose of this study was to assess the burden of disease attributable to household air pollution exposure from cooking among women in Adama, Ethiopia. METHODS: AirQ+ software (WHO Regional Office for Europe, Copenhagen, Denmark) was used to assess the health impact of household air pollution by estimating the burden of disease (BoD) including Acute Lower Respiratory Infections (ALRI), Chronic Obstructive Pulmonary Disease (COPD), Ischemic Heart Disease (IHD), lung cancer, and stroke, among a cohort of women in Adama. Household air pollution exposure estimated by cooking fuel type was assessed through questionnaires. RESULTS: Three-quarters (75%) of Adama's population used solid fuel for cooking; with this, the household air pollution attributable mortality was estimated to be 50% (95% CI: 38-58%) due to ALRI, 50% (95% CI: 35-61%) due to COPD, 50% (95% CI: 27-58%) due to lung cancer, (95% CI: 23-48%) due to IHD, and (95% CI: 23-51%) due to stroke. The corresponding disability-adjusted life years (DALYs) per 100,000 women ranged between 6000 and 9000 per disease. CONCLUSIONS: This health impact assessment illustrates that household air pollution due to solid fuel use among women in Adama leads to premature death and a substantial quantity of DALYs. Therefore, decreasing or eliminating solid fuel use for cooking purposes could prevent deaths and improve quality of life.

Association of Prenatal Ambient Air Pollution Exposure With Placental Mitochondrial DNA Copy Number, Telomere Length and Preeclampsia.

Background: Studies have shown that ambient air pollution is linked to preeclampsia (PE), possibly via generation of oxidative stress in the placenta. Telomere length and mitochondrial DNA copy number (mtDNAcn) are sensitive to oxidative stress damage. Objective: To study the association between prenatal exposure to ambient nitrogen oxides (NOx, a marker for traffic-related air pollution), and PE, as well as potential mediation effects by placental telomere length and mtDNAcn. Methods: This is a cross-sectional study of 42 preeclamptic and 95 arbitrarily selected normotensive pregnant women with gestational ambient NOx exposure assessment in southern Scania, Sweden. Hourly concentrations of NOx were estimated at the residential addresses by a Gaussian-plume dispersion model with 100 × 100 m spatial resolutions and aggregated into trimester-specific mean concentrations. Placental relative mtDNAcn and telomere length were measured using qPCR. Linear and logistic regression models were used to investigate associations, adjusted for perinatal and seasonal characteristics. Results: Exposure was categorized into low and high exposures by median cut-offs during first [11.9 µg/m3; interquartile range (IQR) 7.9, 17.9], second (11.6 µg/m3; IQR: 7.1, 21.1), third trimesters (11.9 µg/m3; IQR: 7.7, 19.5) and entire pregnancy (12.0 µg/m3; IQR: 7.6, 20.1). Increased risk of PE was found for high prenatal NOx exposure during the first trimester (OR 4.0; 95% CI: 1.4, 11.1; p = 0.008), and entire pregnancy (OR 3.7; 95% CI: 1.3, 10.4; p = 0.012). High exposed group during the first trimester had lower placental relative mtDNAcn compared with low exposed group (-0.20; 95% CI: -0.36, -0.04; p = 0.01). Changes in relative mtDNAcn did not mediate the association between prenatal NOx exposure and PE. No statistically significant association was found between placental relative telomere length, prenatal NOx exposure and PE. Conclusion: In this region with relatively low levels of air pollution, ambient NOx exposure during the first trimester was associated with reduced placental relative mtDNAcn and an increased risk of PE. However, we did not find any evidence that mtDNAcn or TL mediated the association between air pollution and PE. Future research should further investigate the role of mtDNAcn for pregnancy complications in relation to exposure to ambient air pollution during pregnancy.

Air Quality in Africa: Public Health Implications.

This review highlights the importance of air quality in the African urban development process. We address connections between air pollution and (a) rapid urbanization, (b) social problems, (c) health impacts, (d) climate change, (e) policies, and (f) new innovations. We acknowledge that air pollution levels in Africa can be extremely high and a serious health threat. The toxic content of the pollution could relate to region-specific sources such as low standards for vehicles and fuels, cooking with solid fuels, and burning household waste. We implore the pursuit of interdisciplinary research to create new approaches with relevant stakeholders. Moreover, successful air pollution research must regard conflicts, tensions, and synergies inherent to development processes in African municipalities, regions, and countries. This includes global relationships regarding climate change, trade, urban planning, and transportation. Incorporating aspects of local political situations (e.g., democracy) can also enhance greater political accountability and awareness about air pollution.

Health Impacts from Ambient Particle Exposure in Southern Sweden.

A health impact assessment (HIA) is an important tool for making informed decisions regarding the design and evaluation of environmental interventions. In this study, we performed a quantitative HIA for the population of Scania (1,247,993), the southernmost county in Sweden, in 2016. The impact of annual mean concentrations of particulate matter with an aerodynamic diameter <2.5 µm (PM2.5), modeled at their home residences for the year 2011, on mortality, asthma, dementia, autism spectrum disorders, preeclampsia and low birth weight (LBW) was explored. Concentration-response (C-R) functions were taken from epidemiological studies reporting meta-analyses when available, and otherwise from single epidemiological studies. The average level of PM2.5 experienced by the study population was 11.88 µg/m3. The PM2.5 exposure was estimated to cause 9-11% of cases of LBW and 6% of deaths from natural causes. Locally produced PM2.5 alone contributed to 2-9% of the cases of diseases and disorders investigated. Reducing concentrations to a maximum of 10 µg/m3 would, according to our estimations, reduce mortality by 3% and reduce cases of LBW by 2%. Further analyses of separate emission sources' distinct effects were also presented. Reduction of air pollution levels in the study area would, as expected, have a substantial effect on both mortality and adverse health outcomes. Reductions should be aimed for by local authorities and on national and even international levels.

Through Internet and Friends: Translation of Air Pollution Research in Malmö Municipality, Sweden.

Air pollution is estimated to cause more than 7000 deaths annually in Sweden alone. To reduce the impact of air pollution and to plan and build sustainable cities, it is vital that research is translated into efficient decisions and practice. However, how do civil servants in a municipality access research results? How do they normally find relevant information, and what obstacles are there to accessing and applying research results? As part of the collaborative and transdisciplinary research project Air Pollution Research in Local Environmental Planning (ARIEL), these questions were explored through interviews and seminars with civil servants within the Malmö Municipality Environmental Office. We found that the civil servants generally have proficiency in processing research results, but often do not use such results as part of their everyday decision making and practices. Instead, the data and measurements used are mostly produced case-by-case within the municipal sector itself. Information about best practices is also collected via a number of knowledge access practices, involving the Internet or social networks within other municipalities. Lack of time, paywalls, and the insufficient applicability of research hinder the dissemination of up-to-date results. This slows down the process whereby research, funded by tax-money, can be put to best practice in the effort to create healthy and sustainable cities.

Exposure to wood smoke particles leads to inflammation, disrupted proliferation and damage to cellular structures in a human first trimester trophoblast cell line.

The ongoing transition to renewable fuel sources has led to increased use of wood and other biomass fuels. The physiochemical characteristics of biomass combustion derived aerosols depends on appliances, fuel and operation procedures, and particles generated during incomplete combustion are linked to toxicity. Frequent indoor wood burning is related to severe health problems such as negative effects on airways and inflammation, as well as chronic hypoxia and pathological changes in placentas, adverse pregnancy outcome, preterm delivery and increased risk of preeclampsia. The presence of combustion-derived black carbon particles at both the maternal and fetal side of placentas suggests that particles can reach the fetus. Air pollution particles have also been shown to inhibit trophoblast migration and invasion, which are vital functions for the development of the placenta during the first trimester. In this study we exposed a placental first trimester trophoblast cell line to wood smoke particles emitted under Nominal Burn rate (NB) or High Burn rate (HB). The particles were visible inside exposed cells and localized to the mitochondria, causing ultrastructural changes in mitochondria and endoplasmic reticulum. Exposed cells showed decreased secretion of the pregnancy marker human chorionic gonadotropin, increased secretion of IL-6, disrupted membrane integrity, disrupted proliferation and contained specific polycyclic aromatic hydrocarbons (PAHs) from the particles. Taken together, these results suggest that wood smoke particles can enter trophoblasts and have detrimental effects early in pregnancy by disrupting critical trophoblast functions needed for normal placenta development and function. This could contribute to the underlying mechanisms leading to pregnancy complications such as miscarriage, premature birth, preeclampsia and/or fetal growth restriction. This study support the general recommendation that more efficient combustion technologies and burning practices should be adopted to reduce some of the toxicity generated during wood burning.

Urban PM2.5 Induces Cellular Toxicity, Hormone Dysregulation, Oxidative Damage, Inflammation, and Mitochondrial Interference in the HRT8 Trophoblast Cell Line.

Objective: Epidemiological studies have found air pollution to be a driver of adverse pregnancy outcomes, including gestational diabetes, low term birth weight and preeclampsia. It is unknown what biological mechanisms are involved in this process. A first trimester trophoblast cell line (HTR-8/SVneo) was exposed to various concentrations of PM2.5 (PM2.5) in order to elucidate the effect of urban particulate matter (PM) of size <2.5 µm on placental function. Methods: PM2.5 were collected at a site representative of urban traffic and dispersed in cell media by indirect and direct sonication. The HTR-8 cells were grown under standard conditions. Cellular uptake was studied after 24 and 48 h of exposure by transmission electron microscopy (TEM). The secretion of human chorionic gonadotropin (hCG), progesterone, and Interleukin-6 (IL-6) was measured by ELISA. Changes in membrane integrity and H2O2 production were analyzed using the CellToxTM Green Cytotoxicity and ROSGloTM assays. Protease activity was evaluated by MitoToxTM assay. Mitochondrial function was assessed through high resolution respirometry in an Oroboros O2k-FluoRespirometer, and mitochondrial content was quantified by citrate synthase activity. Results: TEM analysis depicted PM2.5 cellular uptake and localization of the PM2.5 to the mitochondria after 24 h. The cells showed aggregated cytoskeleton and generalized necrotic appearance, such as chromatin condensation, organelle swelling and signs of lost membrane integrity. The mitochondria displayed vacuolization and disruption of cristae morphology. At 48 h exposure, a significant drop in hCG secretion and a significant increase in progesterone secretion and IL-6 production occurred. At 48 h exposure, a five-fold increase in protease activity and a significant alteration of H2O2 production was observed. The HTR-8 cells exhibited evidence of increased cytotoxicity with increasing exposure time and dose of PM2.5. No significant difference in mitochondrial respiration or mitochondrial mass could be demonstrated. Conclusion: Following exposure to air pollution, intracellular accumulation of PM may contribute to the placental dysfunction associated with pregnancy outcomes, such as preeclampsia and intrauterine growth restriction, through their direct and indirect effects on trophoblast protein secretion, hormone regulation, inflammatory response, and mitochondrial interference.

Maternal Exposure to Ambient Air Pollution and Risk of Preeclampsia: A Population-Based Cohort Study in Scania, Sweden.

The aim of this study was to investigate the risk of developing preeclampsia (PE) associated with gestational exposure to ambient air pollutants in southern Sweden, a low-exposure area. We used a cohort of 43,688 singleton pregnancies and monthly mean exposure levels of black carbon (BC), local and total particulate matter (PM2.5 and PM10), and NOX at the maternal residential address estimated by Gaussian dispersion modeling from 2000 to 2009. Analyses were conducted using binary logistic regression. A subtype analysis for small-for-gestational age (SGA) was performed. All analyses were adjusted for obstetrical risk factors and socioeconomic predictors. There were 1286 (2.9%) PE cases in the analysis. An adjusted odds ratio (AOR) of 1.35 with a 95% confidence interval (CI) of 1.11-1.63 was found when comparing the lowest quartile of BC exposure to the highest quartile in the third trimester The AOR for PE associated with each 5 µg/m3 increase in locally emitted PM2.5 was 2.74 (95% CI: 1.68, 4.47) in the entire pregnancy. Similar patterns were observed for each 5 µg/m3 increment in locally emitted PM10. In pregnancies complicated by PE with SGA, the corresponding AOR for linear increases in BC was 3.48 (95% CI: 1.67, 7.27). In this low-level setting, maternal exposure to ambient air pollution during gestation was associated with the risk of developing PE. The associations seemed more pronounced in pregnancies with SGA complications, a finding that should be investigated further.