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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 (PM 2.5 ). A flat, two-dimensional dispersion model was used to assess local PM 2.5 concentrations (all-source PM 2.5 , 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 PM 2.5 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., (© 2023. The Author(s).)

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 (PM 2.5 ), 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 PM 2.5 experienced by the study population was 11.88 µg/m 3 . The PM 2.5 exposure was estimated to cause 9-11% of cases of LBW and 6% of deaths from natural causes. Locally produced PM 2.5 alone contributed to 2-9% of the cases of diseases and disorders investigated. Reducing concentrations to a maximum of 10 µg/m 3 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.

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 (PM 2.5 and PM 10 ), and NO X 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/m 3 increase in locally emitted PM 2.5 was 2.74 (95% CI: 1.68, 4.47) in the entire pregnancy. Similar patterns were observed for each 5 µg/m 3 increment in locally emitted PM 10 . 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.

Air pollution is responsible for one in eight premature deaths worldwide, and thereby a major threat to human health. Health impact assessments of hypothetic changes in air pollution concentrations can be used as a mean of assessing the health impacts of policy, plans and projects, and support decision-makers in choices to prevent disease. The aim of this study was to estimate health impacts attributable to a hypothetical decrease in air pollution concentrations in the city of Malmö in Southern Sweden corresponding to a policy on-road transportations without tail-pipe emissions in the municipality. We used air pollution data modelled for each of the 326,092 inhabitants in Malmö by a Gaussian dispersion model combined with an emission database with >40,000 sources. The dispersion model calculates Nitrogen Oxides (NO x ) (later transformed into Nitrogen Dioxide (NO 2 )) and particulate matter with an aerodynamic diameter < 2.5 μg/m 3 (PM 2.5 ) with high spatial and temporal resolution (85 m and 1 h, respectively). The average individual reduction was 5.1 (ranging from 0.6 to 11.8) μg/m 3 in NO 2, which would prevent 55 (2% of all deaths) to 93 (4%) deaths annually, depending on dose-response function used. Furthermore, we estimate that the NO 2 reduction would result in 21 (6%) fewer cases of incident asthma in children, 95 (10%) fewer children with bronchitis every year, 30 (1%) fewer hospital admissions for respiratory disease, 87(4%) fewer dementia cases, and 11(11%) fewer cases of preeclampsia every year. The average reduction in PM 2.5 of 0.6 (ranging from 0.1 till 1.7) μg/m 3 would mean that 2729 (0.3%) work days would not be lost due to sick-days and that there would be 16,472 fewer restricted activity days (0.3%) that year had all on-road transportations been without tail-pipe emissions. Even though the estimates are sensitive to the dose-response functions used and to exposure misclassification errors, even the most conservative estimate of the number of prevented deaths is 7 times larger than the annual traffic fatalities in Malmö, indicating a substantial possibility to reduce the health burden attributed to tail-pipe emissions in the study area., (Copyright © 2018. Published by Elsevier Ltd.)

Purpose: Both road traffic noise and air pollution have been linked to cardiovascular disease. However, there are few prospective epidemiological studies available where both road traffic noise and air pollution have been analyzed simultaneously. The aim of this study was to investigate the relation between road traffic noise, air pollution and incident myocardial infarction in both current (1-year average) and medium-term (3-year average) perspective., Methods: This study was based on a stratified random sample of persons aged 18-80 years who answered a public health survey in Skåne, Sweden, in 2000 (n = 13,512). The same individuals received a repeated survey in 2005 and 2010. Diagnoses of myocardial infarction (MI) were obtained from medical records for both inpatient and outpatient specialized care. The endpoint was first MI during 2000-2010. Participants with prior myocardial infarction were excluded at baseline. Yearly average levels of noise (L DEN) and air pollution (NO x ) were estimated using geographic information system for residential address every year until censoring., Results: The mean exposure levels for road traffic noise and air pollution in 2005 were L DEN 51 dB(A) and NO x 11 µg/m(3), respectively. After adjustment for individual confounders (age, sex, body mass index, smoking, education, alcohol consumption, civil status, year, country of birth and physical activity), a 10-dB(A) increase in current noise exposure did not increase the incidence rate ratio (IRR) for MI, 0.99 (95 % CI 0.86-1.14). Neither did a 10-μg/m(3) increase in current NO x increase the risk of MI, 1.02 (95 % CI 0.86-1.21). The IRR for MI associated with combined exposure to road traffic noise >55 dB(A) and NO x >20 µg/m(3) was 1.21 (95 % CI 0.90-1.64) compared to <55 dB(A) and <20 µg/m(3)., Conclusions: This study did not provide evidence for an increased risk of MI due to exposure to road traffic noise or air pollution at moderate average exposure levels.

Background: Genetic and non-genetic factors probably act together to initiate and accelerate development of type 1 diabetes [T1D]. One suggested risk factor contributing to development of T1D is air pollution., Objective: The aim of the study was to investigate whether maternal exposure during pregnancy to air pollution, measured as nitrogen oxides [NOx] and ozone, in a low-dose exposure area was associated with the child developing T1D., Method: In Scania (Skåne), the most southern county in Sweden, 84,039 infants were born during the period 1999-2005. By the end of April 2013, 324 of those children had been diagnosed with T1D. For each of those T1D children three control children were randomly selected and matched for HLA genotype and birth year. Individually modelled exposure data at residence during pregnancy were assessed for nitrogen oxides [NOx], traffic density and ozone., Results: Ozone as well as NOx exposures were associated with T1D. When the highest exposure group was compared to the lowest group an odds ratios of 1.62 (95% confidence interval [CI] 0.99-2.65) was observed for ozone in the second trimester and 1.58 (95% CI 1.06-2.35) for NOx in the third trimester., Conclusion: This study indicates that living in an area with elevated levels of air pollution during pregnancy may be a risk factor for offspring T1D., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: The knowledge about air pollution effects on birth weight, prematurity, and small for gestational age (SGA) in low-exposure areas is insufficient., Objectives: The aim of this birth cohort study was to investigate whether low-level exposure to air pollution was associated with prematurity and fetal growth and whether there are sex-specific effects., Method: We combined high-quality registry information on 81,110 births with individually modeled exposure data at residence for nitrogen oxides (NO(x)) and proximity to roads with differing traffic density. The data were analyzed by logistic and linear regression with and without potential confounders., Results: We observed an increased risk for babies being SGA when we compared highest and lowest NO(x) quartiles, adjusting for maternal age, smoking, sex, and year of birth. After additional adjustment for maternal country of origin and parity (which were highly intercorrelated), the increase was no longer statistically significant. However, in subgroup analyses when we compared highest and lowest NO(x) quartiles we still observed an increased risk for SGA for girls [odds ratio (OR)=1.12; 95% confidence interval (CI), 1.01-1.24); we also observed increased risk among mothers who had not changed residency during pregnancy (OR=1.09; 95% CI, 1.01-1.18). The confounders with the greatest impact on SGA were parity and country of origin. Concerning prematurity, the prevalence was lower in the three higher NO(x) exposure quartiles compared with the lowest category., Conclusion: For future studies on air pollution effects on birth outcomes, careful control of confounding is crucial.