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The lockdown measures in response to the SARS-CoV-2 virus outbreak in 2020 have resulted in reductions in emissions of air pollutants and corresponding ambient concentrations. In the Netherlands, the most stringent lockdown measures were in effect from March to May 2020. These measures coincided with a period of unusual meteorological conditions with wind from the north-east and clear-sky conditions, which complicates the quantification of the effect of the lockdown measures on the air quality. Here we quantify the lockdown effects on the concentrations of nitrogen oxides (NOx and NO2), particulate matter (PM10 and PM2.5) and ozone (O3) in the Netherlands, by analyzing observations and simulations with the atmospheric chemistry-transport model EMEP/MSC-W in its EMEP4NL configuration, after eliminating the effects of meteorological conditions during the lockdown. Based on statistical analyses with a Random Forest method, we estimate that the lockdown reduced observed NO2 concentrations by 30% (95% confidence interval 25-35%), 26% (21-32%), and 18% (10-25%) for traffic, urban, and rural background locations, respectively. Slightly smaller reductions of 8-28% are found with the EMEP4NL simulations for urban and regional background locations based on estimates in reductions in economic activity and emissions of traffic and industry in the Netherlands and other European countries. Reductions in observed PM2.5 concentrations of about 20% (10-25%) are found for all locations, which is somewhat larger than the estimates of 5-16% based on the model simulations. A comparison of the calculated NO2 traffic contributions with observations shows a substantial drop of about 35% in traffic contributions during the lockdown period, which is similar to the estimated reductions in mobility data as reported by Apple and Google. Since the largest health effects related to air pollution in the Netherlands are associated with exposure to PM10 and PM2.5, the lockdown measures in spring of 2020 have temporarily improved the air quality in the Netherlands. The concentrations of the most health relevant compounds have only been reduced by about 10-25%.

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BACKGROUND: Elevated temperature and air pollution have been associated with increased mortality. Exposure to heat and air pollution, as well as the density of vulnerable groups varies within cities. The objective was to investigate the extent of neighbourhood differences in mortality risk due to heat and air pollution in a city with a temperate maritime climate. METHODS: A case-crossover design was used to study associations between heat, air pollution and mortality. Different thermal indicators and air pollutants (PM10, NO2, O3) were reconstructed at high spatial resolution to improve exposure classification. Daily exposures were linked to individual mortality cases over a 15year period. RESULTS: Significant interaction between maximum air temperature (Tamax) and PM10 was observed. During "summer smog" days (Tamax>25°C and PM10>50µg/m(3)), the mortality risk at lag 2 was 7% higher compared to the reference (Tamax 15°C and PM10 15µg/m(3)). Persons above age 85 living alone were at highest risk. CONCLUSION: We found significant synergistic effects of high temperatures and air pollution on mortality. Single living elderly were the most vulnerable group. Due to spatial differences in temperature and air pollution, mortality risks varied substantially between neighbourhoods, with a difference up to 7%.

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BACKGROUND/AIMS: Visfatin has been suggested as a marker of visceral adiposity. We hypothesized that visfatin, but not leptin, would be specifically associated with visceral adiposity. We investigated the relation of serum visfatin and leptin with measures of adiposity and body fat distribution in children. METHODS: Serum leptin and visfatin levels were measured in 1,022 12-year-old children participating in the PIAMA birth cohort. BMI, waist, hip and upper arm circumference were available for all children. Multiple linear regression analyses were conducted to study associations between different anthropometric indices and log serum visfatin and leptin levels. RESULTS: All anthropometric indices showed positive and strong dose-response relationships with serum leptin. Visfatin was increased only in children with a high waist-to-hip ratio. The effect size was small compared to those observed for leptin and the association was present in overweight children (n = 133) but not in normal weight children. CONCLUSION: Serum leptin levels strongly increased with increasing adiposity, but were not related to a specific type of fat distribution. In contrast, serum visfatin was associated only with high waist-to-hip ratio in overweight children. Based on our study we would currently not recommend visfatin as a marker of visceral adiposity in the general population of children.

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Health effects have repeatedly been associated with residential levels of air pollution. However, it is difficult to disentangle effects of long-term exposure to locally generated and long-range transported pollutants, as well as to exhaust emissions and wear particles from road traffic. We aimed to investigate effects of exposure to particulate matter fractions on respiratory health in the Swedish adult population, using an integrated assessment of sources at different geographical scales. The study was based on a nationwide environmental health survey performed in 2007, including 25,851 adults aged 18-80 years. Individual exposure to particulate matter at residential addresses was estimated by dispersion modelling of regional, urban and local sources. Associations between different size fractions or source categories and respiratory outcomes were analysed using multiple logistic regression, adjusting for individual and contextual confounding. Exposure to locally generated wear particles showed associations for blocked nose or hay fever, chest tightness or cough, and restricted activity days with odds ratios of 1.5-2 per 10-µg·m(-3) increase. Associations were also seen for locally generated combustion particles, which disappeared following adjustment for exposure to wear particles. In conclusion, our data indicate that long-term exposure to locally generated road wear particles increases the risk of respiratory symptoms in adults.

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Long-term exposure to traffic noise has been suggested to increase the risk of cardiovascular diseases (CVD). However, few studies have been performed in the general population and on railway noise. This study aimed to investigate the cardiovascular effects of living near noisy roads and railways. This cross-sectional study comprised 25,851 men and women, aged 18-80 years, who had resided in Sweden for at least 5 years. All subjects participated in a National Environmental Health Survey, performed in 2007, in which they reported on health, annoyance reactions and environmental factors. Questionnaire data on self-reported doctor's diagnosis of hypertension and/or CVD were used as outcomes. Exposure was assessed as Traffic Load (millions of vehicle kilometres per year) within 500 m around each participant's residential address. For a sub-population (n = 2498), we also assessed road traffic and railway noise in L(den) at the dwelling façade. Multiple logistic regression models were used to assess Prevalence Odds Ratios (POR) and 95% Confidence Intervals (CI). No statistically significant associations were found between Traffic Load and self-reported hypertension or CVD. In the sub-population, there was no association between road traffic noise and the outcomes; however, an increased risk of CVD was suggested among subjects exposed to railway noise ≥50 dB(A); POR 1.55 (95% CI 1.00-2.40). Neither Traffic Load nor road traffic noise was, in this study, associated with self-reported cardiovascular outcomes. However, there was a borderline-significant association between railway noise and CVD. The lack of association for road traffic may be due to methodological limitations.

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BACKGROUND: There is evidence that rapid weight gain during the first year of life is associated with overweight later in life. However, results from studies exploring other critical periods for the development of overweight are inconsistent. OBJECTIVE: The objective was to investigate BMI development to assess at what ages essential differences between normal weight and overweight children occur, and to assess which age intervals the most strongly influence the risk of overweight at 8 years of age. METHODS: Longitudinal weight and height data were collected by annual questionnaires in a population of 3963 children participating in the PIAMA birth cohort study. BMI and BMI standard deviation scores (SDS) were calculated for every year from birth until 8 years of age. BMI, BMI SDS and BMI SDS change in each 1-year-age interval were compared between children with and without overweight at 8 years of age, using t-tests, logistic regression analysis and the analysis of response profiles method. RESULTS: At 8 years of age, 10.5% of the children were overweight. Already at the age of 1 year, these children had a significantly higher mean BMI SDS than normal weight 8-year-olds, (0.53 vs 0.04). In each 1-year-age interval the change in BMI SDS was significantly associated with overweight at 8 years with odds ratios increasing from 1.14 (95% CI 1.04-1.24) per 1 SDS increase at 0-1 year to 2.40 (95% CI 2.09-2.76) at 7-8 years. CONCLUSION: At every age, starting already in the first year of life, a rapid increase in BMI SDS was significantly associated with overweight risk at the age of 8 years. There was no evidence for a specific critical period for the development of overweight. Prevention of overweight should start early in life and be continued with age-specific interventions throughout childhood.

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RATIONALE: Maternal diet during pregnancy has the potential to affect airway development and to promote T-helper-2-cell responses during fetal life. This might increase the risk of developing childhood asthma or allergy. OBJECTIVES: We investigated the influence of maternal food consumption during pregnancy on childhood asthma outcomes from 1 to 8 years of age. METHODS: A birth cohort study consisting of a baseline of 4,146 pregnant women (1,327 atopic and 2,819 nonatopic). These women were asked about their frequency of consumption of fruit, vegetables, fish, egg, milk, milk products, nuts, and nut products during the last month. Their children were followed until 8 years of age. Longitudinal analyses were conducted to assess associations between maternal diet during pregnancy and childhood asthma outcomes over 8 years. MEASUREMENTS AND MAIN RESULTS: Complete data were obtained for 2,832 children. There were no associations between maternal vegetable, fish, egg, milk or milk products, and nut consumption and longitudinal childhood outcomes. Daily consumption of nut products increased the risk of childhood wheeze (odds ratio [OR] daily versus rare consumption, 1.42; 95% confidence interval [95% CI], 1.06-1.89), dyspnea (OR, 1.58; 95% CI, 1.16-2.15), steroid use (OR, 1.62; 95% CI, 1.06-2.46), and asthma symptoms (OR, 1.47; 95% CI, 1.08-1.99). CONCLUSIONS: Results of this study indicate an increased risk of daily versus rare consumption of nut products during pregnancy on childhood asthma outcomes. These findings need to be replicated by other studies before dietary advice can be given to pregnant women.

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