Association between long-term exposure to air pollution and mortality in France: A 25-year follow-up study

IntroductionLong-term exposure to air pollution (AP) has been shown to have an impact on mortality in numerous countries, but since 2005 no data exists for France.ObjectivesWe analyzed the association between long-term exposure to air pollution and mortality at the individual level in a large French cohort followed from 1989 to 2013.MethodsThe study sample consisted of 20,327 adults working at the French national electricity and gas company EDF-GDF. Annual exposure to PM₁₀, PM_10–2.5, PM_2.5, NO₂, O₃, SO₂, and benzene was assessed for the place of residence of participants using a chemistry-transport model and taking residential history into account. Hazard ratios were estimated using a Cox proportional-hazards regression model, adjusted for selected individual and contextual risk factors. Hazard ratios were computed for an interquartile range (IQR) increase in air pollutant concentrations.ResultsThe cohort recorded 1967 non-accidental deaths. Long-term exposures to baseline PM_2.5, PM_10-25, NO₂ and benzene were associated with an increase in non-accidental mortality (Hazard Ratio, HR = 1.09; 95% CI: 0.99, 1.20 per 5.9 μg/m³, PM_10-25; HR = 1.09;95% CI: 1.04, 1.15 per 2.2 μg/m³, NO₂: HR = 1.14; 95% CI: 0.99, 1.31 per 19.3 μg/m³ and benzene: HR = 1.10; 95% CI: 1.00, 1.22 per 1.7 μg/m³).The strongest association was found for PM₁₀: HR = 1.14; 95% CI: 1.05, 1.25 per 7.8 μg/m³. PM₁₀, PM_10-25 and SO₂ were associated with non-accidental mortality when using time varying exposure. No significant associations were observed between air pollution and cardiovascular and respiratory mortality.ConclusionLong-term exposure to fine particles, nitrogen dioxide, sulfur dioxide and benzene is associated with an increased risk of non-accidental mortality in France. Our results strengthen existing evidence that outdoor air pollution is a significant environmental risk factor for mortality. Due to the limited sample size and the nature of our study (occupational), further investigations are needed in France with a larger representative population sample.     

Air pollution and diabetes association: Modification by type 2 diabetes genetic risk score

Exposure to ambient air pollution (AP) exposure has been linked to type 2 diabetes (T2D) risk. Evidence on the impact of T2D genetic variants on AP susceptibility is lacking. Compared to single variants, joint genetic variants contribute substantially to disease risk. We investigated the modification of AP and diabetes association by a genetic risk score (GRS) covering 63 T2D genes in 1524 first follow-up participants of the Swiss cohort study on air pollution and lung and heart diseases in adults. Genome-wide data and covariates were available from a nested asthma case-control study design. AP was estimated as 10-year mean residential particulate matter < 10 μm (PM₁₀). We computed count-GRS and weighted-GRS, and applied PM₁₀ interaction terms in mixed logistic regressions, on odds of diabetes. Analyses were stratified by pathways of diabetes pathology and by asthma status. Diabetes prevalence was 4.6% and mean exposure to PM₁₀ was 22 μg/m³. Odds of diabetes increased by 8% (95% confidence interval: 2, 14%) per T2D risk allele and by 35% (− 8, 97%) per 10 μg/m³ exposure to PM₁₀. We observed a positive interaction between PM₁₀ and count-GRS on diabetes [OR_interaction = 1.10 (1.01, 1.20)], associations being strongest among participants at the highest quartile of count-GRS [OR: 1.97 (1.00, 3.87)]. Stronger interactions were observed with variants of the GRS involved in insulin resistance [(OR_interaction = 1.22 (1.00, 1.50)] than with variants related to beta-cell function. Interactions with count-GRS were stronger among asthma cases. We observed similar results with weighted-GRS. Five single variants near GRB14, UBE2E2, PTPRD, VPS26A and KCNQ1 showed nominally significant interactions with PM₁₀ (P < 0.05). Our results suggest that genetic risk for T2D may modify susceptibility to air pollution through alterations in insulin sensitivity. These results need confirmation in diabetes cohort consortia.     

Air pollution exposure increases the risk of rheumatoid arthritis: A longitudinal and nationwide study

ObjectiveRheumatoid arthritis (RA) has been associated with inhaled pollutants in several studies, and it is a disease of chronic inflammation. The association between air pollution and the risk of RA remains unclear. Therefore, we conducted this nationwide, retrospective, sex-stratification study to evaluate this association.MethodsWe collected data from the Longitudinal Health Insurance Database (LHID), maintained by the Taiwan Bureau of National Health Insurance, and the Taiwan Air Quality-Monitoring Database (TAQMD), released by the Taiwan Environmental Protection Agency. The TAQMD provides the daily concentrations of particulate matter with the aerodynamic diameter < 2.5 μm (PM_2.5) and nitrogen dioxide (NO₂) from 74 ambient air quality-monitoring stations distributed all over Taiwan during 1998–2010. The LHID and TAQMD were linked according to the residential areas of insurants and the areas where the air quality-monitoring stations were located. A residential area was defined according to the location of the clinic and hospital that treated acute upper respiratory tract infections. The yearly average air pollutant concentrations were categorized into 4 levels based on quartiles. We evaluated the risk of RA in residents exposed to 4 levels of PM_2.5 and NO₂ concentrations.ResultsWe detected an increased risk of RA in participants exposed to PM_2.5 and NO₂. Among four quartiles of NO₂ concentration, namely Q1, Q2, Q3, and Q4, the adjusted hazard ratios (aHRs) in Q2, Q3, and Q4 compared with that in Q1 were 1.07 (95% confidence interval [CI] = 0.76–1.50), 1.63 (95% CI = 1.16–2.31),and 1.49 (95% CI = 1.05–2.12), respectively. Regarding the PM_2.5 concentrations, the aHRs after exposure to the Q2, Q3, and Q4 levels were 1.22 (95% CI = 0.85–1.74), 1.15 (95% CI = 0.82–1.62), and 0.79 (95% CI = 0.53–1.16), respectively.ConclusionThe results of this nationwide study suggest an increased risk of RA in residents exposed to NO₂.     

Traffic-related air pollution and hyperactivity/inattention,dyslexia and dyscalculia in adolescents of the German GINIplus and LISAplus birth cohorts

BackgroundFew studies have examined the link between air pollution exposure and behavioural problems and learning disorders during late childhood and adolescence.ObjectivesTo determine whether traffic-related air pollution exposure is associated with hyperactivity/inattention, dyslexia and dyscalculia up to age 15 years using the German GINIplus and LISAplus birth cohorts (recruitment 1995–1999).MethodsHyperactivity/inattention was assessed using the German parent-completed (10 years) and self-completed (15 years) Strengths and Difficulties Questionnaire. Responses were categorized into normal versus borderline/abnormal. Parent-reported dyslexia and dyscalculia (yes/no) at age 10 and 15 years were defined using parent-completed questionnaires. Individual-level annual average estimates of nitrogen dioxide (NO₂), particulate matter (PM)₁₀ mass, PM_2.5 mass and PM_2.5 absorbance concentrations were assigned to each participant's birth, 10 year and 15 year home address. Longitudinal associations between the air pollutants and the neurodevelopmental outcomes were assessed using generalized estimation equations, separately for both study areas, and combined in a random-effects meta-analysis. Odds ratios and 95% confidence intervals are given per interquartile range increase in pollutant concentration.ResultsThe prevalence of abnormal/borderline hyperactivity/inattention scores and parental-reported dyslexia and dyscalculia at 15 years of age was 12.9%, 10.5% and 3.4%, respectively, in the combined population (N = 4745). In the meta- analysis, hyperactivity/inattention was associated with PM_2.5 mass estimated to the 10 and 15 year addresses (1.12 [1.01, 1.23] and 1.11 [1.01, 1.22]) and PM_2.5 absorbance estimated to the 10 and 15 year addresses (1.14 [1.05, 1.25] and 1.13 [1.04, 1.23], respectively).ConclusionsWe report associations suggesting a potential link between air pollution exposure and hyperactivity/inattention scores, although these findings require replication.     

Exposure to long-term air pollution and road traffic noise in relation to cholesterol: A cross-sectional study

BackgroundExposure to traffic noise and air pollution have both been associated with cardiovascular disease, though the mechanisms behind are not yet clear.ObjectivesWe aimed to investigate whether the two exposures were associated with levels of cholesterol in a cross-sectional design.MethodsIn 1993–1997, 39,863 participants aged 50–64 year and living in the Greater Copenhagen area were enrolled in a population-based cohort study. For each participant, non-fasting total cholesterol was determined in whole blood samples on the day of enrolment. Residential addresses 5-years preceding enrolment were identified in a national register and road traffic noise (L_den) were modeled for all addresses. For air pollution, nitrogen dioxide (NO₂) was modeled at all addresses using a dispersion model and PM_2.5 was modeled at all enrolment addresses using a land-use regression model. Analyses were done using linear regression with adjustment for potential confounders as well as mutual adjustment for the three exposures.ResultsBaseline residential exposure to the interquartile range of road traffic noise, NO₂ and PM_2.5 was associated with a 0.58 mg/dl (95% confidence interval: − 0.09; 1.25), a 0.68 mg/dl (0.22; 1.16) and a 0.78 mg/dl (0.22; 1.34) higher level of total cholesterol in single pollutant models, respectively. In two pollutant models with adjustment for noise in air pollution models and vice versa, the association between air pollution and cholesterol remained for both air pollution variables (NO₂: 0.72 (0.11; 1.34); PM_2.5: 0.70 (0.12; 1.28) mg/dl), whereas there was no association for noise (− 0.08 mg/dl). In three-pollutant models (NO₂, PM_2.5 and road traffic noise), estimates for NO₂ and PM_2.5 were slightly diminished (NO₂: 0.58 (− 0.05; 1.22); PM_2.5: 0.57 (− 0.02; 1.17) mg/dl).ConclusionsAir pollution and possibly also road traffic noise may be associated with slightly higher levels of cholesterol, though associations for the two exposures were difficult to separate.     

Seasonal variation in outdoor,indoor, and personal air pollution exposures of women using wood stoves in the Tibetan Plateau: Baseline assessment for an energy intervention study

Cooking and heating with coal and biomass is the main source of household air pollution in China and a leading contributor to disease burden. As part of a baseline assessment for a household energy intervention program, we enrolled 205 adult women cooking with biomass fuels in Sichuan, China and measured their 48-h personal exposure to fine particulate matter (PM_2.5) and carbon monoxide (CO) in winter and summer. We also measured the indoor 48-h PM_2.5 concentrations in their homes and conducted outdoor PM_2.5 measurements during 101 (74) days in summer (winter). Indoor concentrations of CO and nitrogen oxides (NO, NO₂) were measured over 48-h in a subset of ~ 80 homes. Women's geometric mean 48-h exposure to PM_2.5 was 80 μg/m³ (95% CI: 74, 87) in summer and twice as high in winter (169 μg/m³ (95% CI: 150, 190), with similar seasonal trends for indoor PM_2.5 concentrations (winter: 252 μg/m³; 95% CI: 215, 295; summer: 101 μg/m³; 95% CI: 91, 112). We found a moderately strong relationship between indoor PM_2.5 and CO (r = 0.60, 95% CI: 0.46, 0.72), and a weak correlation between personal PM_2.5 and CO (r = 0.41, 95% CI: − 0.02, 0.71). NO₂/NO ratios were higher in summer (range: 0.01 to 0.68) than in winter (range: 0 to 0.11), suggesting outdoor formation of NO₂ via reaction of NO with ozone is a more important source of NO₂ than biomass combustion indoors. The predictors of women's personal exposure to PM_2.5 differed by season. In winter, our results show that primary heating with a low-polluting fuel (i.e., electric stove or wood-charcoal) and more frequent kitchen ventilation could reduce personal PM_2.5 exposures. In summer, primary use of a gaseous fuel or electricity for cooking and reducing exposure to outdoor PM_2.5 would likely have the greatest impacts on personal PM_2.5 exposure.     

Respiratory medication sales and urban air pollution in Brussels (2005 to 2011)

BackgroundWe investigated the associations between daily sales of respiratory medication and air pollutants in the Brussels-Capital Region between 2005 and 2011.MethodsWe used over-dispersed Poisson Generalized Linear Models to regress daily individual reimbursement data of prescribed asthma and COPD medication from the social security database against each subject's residential exposure to outdoor particulate matter (PM₁₀) or NO₂ estimated, by interpolation from monitoring stations. We calculated cumulative risk ratios (RR) and their 95% confidence intervals (CI) for interquartile ranges (IQR) of exposure for different windows of past exposure for the entire population and for seven age groups.ResultsMedian daily concentrations of PM₁₀ and NO₂ were 25 μg/m³ (IQR = 17.1) and 38 μg/m³ (IQR = 20.5), respectively. PM₁₀ was associated with daily medication sales among individuals aged 13 to 64 y. For NO₂, significant associations were observed among all age groups except > 84 y. The highest RR were observed for NO₂, among adolescents, including three weeks lags (RR = 1.187 95%CI: 1.097–1.285).ConclusionThe associations found between temporal changes in exposure to air pollutants and daily sales of respiratory medication in Brussels indicate that urban air pollution contributes to asthma and COPD morbidity in the general population.     

Chronic disease prevalence in women and air pollution — A 30-year longitudinal cohort study

BackgroundAir pollution, such as fine particulate matter (PM_2.5), can increase risk of adverse health events among people with heart disease, diabetes, asthma and chronic obstructive pulmonary disease (COPD) by aggravating these conditions. Identifying the influence of PM_2.5 on prevalence of these conditions may help target interventions to reduce disease morbidity among high-risk populations.ObjectivesThe objective of this study is to measure the association of exposure of PM_2.5 with prevalence risk of various chronic diseases among a longitudinal cohort of women.MethodsWomen from Ontario who enrolled in the Canadian National Breast Screening Study (CNBSS) from 1980 to 1985 (n = 29,549) were linked to provincial health administrative data from April 1, 1992 to March 31, 2013 to determine the prevalence of major chronic disease and conditions (heart disease, diabetes, asthma, COPD, acute myocardial infarction, angina, stroke and cancers). Exposure to PM_2.5 was measured using satellite data collected from January 1, 1998 to December 31, 2006 and assigned to resident postal-code at time of entry into study. Poisson regression models were used to describe the relationship between exposure to ambient PM_2.5 and chronic disease prevalence. Prevalence rate ratios (PRs) were estimated while adjusting for potential confounders: baseline age, smoking, BMI, marital status, education and occupation. Separate models were run for each chronic disease and condition.ResultsCongestive heart failure (PR = 1.31, 95% CI: 1.13, 1.51), diabetes (PR = 1.28, 95% CI: 1.16, 1.41), ischemic heart disease (PR = 1.22, 95% CI: 1.14, 1.30), and stroke (PR = 1.21, 95% CI: 1.09, 1.35) showed over a 20% increase in PRs per 10 μg/m³ increase in PM_2.5 after adjusting for risk factors. Risks were elevated in smokers and those with BMI greater than 30.ConclusionsThis study estimated significant elevated prevalent rate ratios per unit increase in PM_2.5 in nine of the ten chronic diseases studied.     

A method to derive the relationship between the annual and short-term air quality limits—Analysis using the WHO Air Quality Guidelines for health protection

The World Health Organization (WHO) Air Quality Guidelines (AQG) were launched in 2006, but gaps remain in evidence on health impacts and relationships between short-term and annual AQG needed for health protection. We tested whether relationships between WHO short-term and annual AQG for particulates (PM₁₀ and PM_2.5) and nitrogen dioxide (NO₂) are concordant worldwide and derived the annual limits for sulfur dioxide (SO₂) and ozone (O₃) based on the short-term AQG. We obtained air pollutant data over seven years (2004–2010) in seven cities from Asia-Pacific, North America and Europe. Based on probability distribution concept using maximum as the short-term limit and arithmetic mean as the annual limit, we developed a new method to derive limit value one from another in each paired limits for each pollutant with capability to account for allowable exceedances. We averaged the limit derived each year for each city, then used meta-analysis to pool the limit values in all cities. Pooled mean short-term limit for NO₂ (140.5 μg/m³ [130.6–150.4]) was significantly lower than the WHO AQG of 200 μg/m³ while for PM₁₀ (46.4 μg/m³ [95CI:42.1–50.7]) and PM_2.5 (28.6 μg/m³ [24.5–32.6]) were not significantly different from the WHO AQG of 50 and 25 μg/m³ respectively. Pooled mean annual limits for SO₂ and O₃ were 4.6 μg/m³ [3.7–5.5] and 27.0 μg/m³ [21.7–32.2] respectively. Results were robust in various sensitivity analyses. The distribution relationships between the current WHO short-term and annual AQG are supported by empirical data from seven cities for PM₁₀ and PM_2.5, but not for NO₂. The short-term AQG for NO₂ should be lowered for concordance with the selected annual AQG for health protection.     

Associations of gestational and early life exposures to ambient air pollution with childhood respiratory diseases in Shanghai,China: A retrospective cohort study

BackgroundAssociations of ambient air pollutants with respiratory health are inconsistent.ObjectivesWe analyzed the associations of gestational and early life exposures to air pollutants with doctor-diagnosed asthma, allergic rhinitis, and pneumonia in children.MethodsWe selected 3358 preschool children who did not alter residences after birth from a cross-sectional study in 2011–2012 in Shanghai, China. Parents reported children's respiratory health history, home environment, and family lifestyle behaviors. We collected daily concentrations of sulphur dioxide (SO₂), nitrogen dioxide (NO₂), and particulate matter with an aerodynamic diameter ≤ 10 μm (PM₁₀) during the child's total lifetime (2006–2012) for each district where the children lived. We analyzed the associations using logistic regression models.ResultsAfter adjusting for covariates and the other studied pollutants, we found that exposure to NO₂ (increment of 20 μg/m³) during the first year of life was significantly associated with asthma [odds ratio (OR) = 1.77; 95% confidence interval (CI): 1.29–2.43] and allergic rhinitis (OR = 1.67; 95% CI: 1.07–2.61). Exposure to NO₂ during gestation, the first two and three years, and over total lifetimewas all consistently associated with increased odds of allergic rhinitis. Quartiles of NO₂ concentration during different exposure periods showed a slight dose–response relationship with the studied diseases. These diseases had significant associations with pollutant mixtures that included NO₂, but had no significant association with exposures to SO₂ and PM₁₀ individually or in mixtures.ConclusionsGestational and early life exposures to ambient NO₂ are risk factors for childhood respiratory diseases.     

High resolution exposure modelling of heat and air pollution and the impact on mortality

BackgroundElevated 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.MethodsA 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 15 year period.ResultsSignificant interaction between maximum air temperature (Ta_max) and PM₁₀ was observed. During “summer smog” days (Ta_max > 25 °C and PM₁₀ > 50 μg/m³), the mortality risk at lag 2 was 7% higher compared to the reference (Ta_max 15 °C and PM₁₀ 15 μg/m³). Persons above age 85 living alone were at highest risk.ConclusionWe 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%.     

Associations between maternal exposure to air pollution and traffic noise and newborn's size at birth: A cohort study

BackgroundMaternal exposure to air pollution and traffic noise has been suggested to impair fetal growth, but studies have reported inconsistent findings.ObjectiveTo investigate associations between residential air pollution and traffic noise during pregnancy and newborn's size at birth.MethodsFrom a national birth cohort we identified 75,166 live-born singletons born at term with information on the children's size at birth. Residential address history from conception until birth was collected and air pollution (NO₂ and NO_x) and road traffic noise was modeled at all addresses. Associations between exposures and indicators of newborn's size at birth: birth weight, placental weight and head and abdominal circumference were analyzed by linear and logistic regression, and adjusted for potential confounders.ResultsIn mutually adjusted models we found a 10 μg/m³ higher time-weighted mean exposure to NO₂ during pregnancy to be associated with a 0.35 mm smaller head circumference (95% confidence interval (CI): 95% CI: − 0.57; − 0.12); a 0.50 mm smaller abdominal circumference (95% CI: − 0.80; − 0.20) and a 5.02 g higher placental weight (95% CI: 2.93; 7.11). No associations were found between air pollution and birth weight. Exposure to residential road traffic noise was weakly associated with reduced head circumference, whereas none of the other newborn's size indicators were associated with noise, neither before nor after adjustment for air pollution.ConclusionsThis study indicates that air pollution may result in a small reduction in offspring's birth head and abdominal circumference, but not birth weight, whereas traffic noise seems not to affect newborn's size at birth.     

Communicating air pollution-related health risks to the public: An application of the Air Quality Health Index in Shanghai,China

The Air Quality Health Index (AQHI) was originally developed in Canada. However, little is known about its validity in communicating morbidity risks. We aimed to establish the AQHI in Shanghai, China, and to compare the associations of AQHI and existing Air Pollution Index (API) with daily mortality and morbidity. We constructed the AQHI as the sum of excess total mortality associated with individual air pollutants, and then adjusted it to an arbitrary scale (0–10), according to a time-series analysis of air pollution and mortality in Shanghai from 2001 to 2008. We examined the associations of AQHI with daily mortality and morbidity, and compared these associations with API from 2005 to 2008. The coefficients of short-term associations of total mortality with particulate matter with an aerodynamic diameter less than 10 μm (PM₁₀), PM_2.5 and nitrogen dioxide (NO₂) were used in the establishment of AQHI. During 2005–2008, the AQHI showed linear non-threshold positive associations with daily mortality and morbidity. A unit increase of the PM₁₀-AQHI was associated with a 0.90% [95% (confidence interval, CI), 0.43 to 1.37], 1.04% (95%CI, 0.04 to 2.04), 1.62% (95%CI, 0.39 to 2.85) and 0.51% (95%CI, 0.09 to 0.93) increase of current-day total mortality, hospital admissions, outpatient visits and emergency room visits, respectively. The PM_2.5-AQHI showed quite similar effect estimates with the PM₁₀-AQHI. In contrast, the associations for API were much weaker and generally statistically insignificant. The AQHI, compared with the existing API, provided a more effective tool to communicate the air pollution-related health risks to the public.     

Air pollution,ethnicity and telomere length in east London schoolchildren: An observational study

BackgroundShort telomeres are associated with chronic disease and early mortality. Recent studies in adults suggest an association between telomere length and exposure to particulate matter, and that ethnicity may modify the relationship. However associations in children are unknown.ObjectivesWe examined associations between air pollution and telomere length in an ethnically diverse group of children exposed to high levels of traffic derived pollutants, particularly diesel exhaust, and to environmental tobacco smoke.MethodsOral DNA from 333 children (8–9 years) participating in a study on air quality and respiratory health in 23 inner city London schools was analysed for relative telomere length using monochrome multiplex qPCR. Annual, weekly and daily exposures to nitrogen oxides and particulate matter were obtained from urban dispersion models (2008–10) and tobacco smoke by urinary cotinine. Ethnicity was assessed by self-report and continental ancestry by analysis of 28 random genomic markers. We used linear mixed effects models to examine associations with telomere length.ResultsTelomere length increased with increasing annual exposure to NO_x (model coefficient 0.003, [0.001, 0.005], p < 0.001), NO₂ (0.009 [0.004, 0.015], p < 0.001), PM_2.5 (0.041, [0.020, 0.063], p < 0.001) and PM₁₀ (0.096, [0.044, 0.149], p < 0.001). There was no association with environmental tobacco smoke. Telomere length was increased in children reporting black ethnicity (22% [95% CI 10%, 36%], p < 0.001)ConclusionsPollution exposure is associated with longer telomeres in children and genetic ancestry is an important determinant of telomere length. Further studies should investigate both short and long-term associations between pollutant exposure and telomeres in childhood and assess underlying mechanisms.     

Estimation of exposure to atmospheric pollutants during pregnancy integrating space–time activity and indoor air levels: Does it make a difference?

Studies of air pollution effects during pregnancy generally only consider exposure in the outdoor air at the home address. We aimed to compare exposure models differing in their ability to account for the spatial resolution of pollutants, space–time activity and indoor air pollution levels. We recruited 40 pregnant women in the Grenoble urban area, France, who carried a Global Positioning System (GPS) during up to 3 weeks; in a subgroup, indoor measurements of fine particles (PM_2.5) were conducted at home (n = 9) and personal exposure to nitrogen dioxide (NO₂) was assessed using passive air samplers (n = 10). Outdoor concentrations of NO₂, and PM_2.5 were estimated from a dispersion model with a fine spatial resolution. Women spent on average 16 h per day at home. Considering only outdoor levels, for estimates at the home address, the correlation between the estimate using the nearest background air monitoring station and the estimate from the dispersion model was high (r = 0.93) for PM_2.5 and moderate (r = 0.67) for NO₂. The model incorporating clean GPS data was less correlated with the estimate relying on raw GPS data (r = 0.77) than the model ignoring space–time activity (r = 0.93). PM_2.5 outdoor levels were not to moderately correlated with estimates from the model incorporating indoor measurements and space–time activity (r = − 0.10 to 0.47), while NO₂ personal levels were not correlated with outdoor levels (r = − 0.42 to 0.03). In this urban area, accounting for space–time activity little influenced exposure estimates; in a subgroup of subjects (n = 9), incorporating indoor pollution levels seemed to strongly modify them.     

Exposure to fine particle matter,nitrogen dioxide and benzene during pregnancy and cognitive and psychomotor developments in children at 15 months of age

BackgroundPrenatal exposure to air pollutants has recently been identified as a potential risk factor for neuropsychological impairment.ObjectivesTo assess whether prenatal exposure to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) and benzene were associated with impaired development in infants during their second year of life.MethodsRegression analyses, based on 438 mother–child pairs, were performed to estimate the association between mother exposure to air pollutants during pregnancy and neurodevelopment of the child. The average exposure to PM_2.5, NO₂ and benzene over the whole pregnancy was calculated for each woman. During the second year of life, infant neuropsychological development was assessed using the Bayley Scales of Infant Development. Regression analyses were performed to estimate the association between exposure and outcomes, accounting for potential confounders.ResultsWe estimated that a 1 μg/m³ increase during pregnancy in the average levels of PM_2.5 was associated with a − 1.14 point decrease in motor score (90% CI: − 1.75; − 0.53) and that a 1 μg/m³ increase of NO₂ exposure was associated with a − 0.29 point decrease in mental score (90% CI: − 0.47; − 0.11). Benzene did not show any significant association with development. Considering women living closer (≤ 100 m) to metal processing activities, we found that motor scores decreased by − 3.20 (90% CI: − 5.18; − 1.21) for PM_2.5 and − 0.51 (− 0.89; − 0.13) for NO₂, while mental score decreased by − 2.71 (90% CI: − 4.69; − 0.74) for PM_2.5, and − 0.41 (9% CI: − 0.76; − 0.06) for NO₂.ConclusionsOur findings suggest that prenatal residential exposure to PM_2.5 and NO₂ adversely affects infant motor and cognitive developments. This negative effect could be higher in the proximity of metal processing plants.     

Health effects of ambient air pollution: Do different methods for estimating exposure lead to different results?

BackgroundSpatially resolved exposure models are increasingly used in epidemiology. We previously reported that, although exhibiting a moderate correlation, pregnancy nitrogen dioxide (NO₂) levels estimated by the nearest air quality monitoring station (AQMS) model and a geostatistical model, showed similar associations with infant birth weight.ObjectivesWe extended this study by comparing a total of four exposure models, including two highly spatially resolved models: a land-use regression (LUR) model and a dispersion model. Comparisons were made in terms of predicted NO₂ and particle (aerodynamic diameter < 10 μm, PM₁₀) exposure and adjusted association with birth weight.MethodsThe four exposure models were implemented in two French metropolitan areas where 1026 pregnant women were followed as part of the EDEN mother–child cohort.ResultsCorrelations between model predictions were high (≥ 0.70), except for NO₂ between the AQMS and both the LUR (r = 0.54) and dispersion models (r = 0.63). Spatial variations as estimated by the AQMS model were greater for NO₂ (95%) than for PM₁₀ (22%). The direction of effect estimates of NO₂ on birth weight varied according to the exposure model, while PM₁₀ effect estimates were more consistent across exposure models.ConclusionsFor PM₁₀, highly spatially resolved exposure model agreed with the poor spatial resolution AQMS model in terms of estimated pollutant levels and health effects. For more spatially heterogeneous pollutants like NO₂, although predicted levels from spatially resolved models (all but AQMS) agreed with each other, our results suggest that some may disagree with each other as well as with the AQMS regarding the direction of the estimated health effects.     

Exposure to emissions from municipal solid waste incinerators and miscarriages: A multisite study of the MONITER Project

BackgroundMiscarriages are an important indicator of reproductive health but only few studies have analyzed their association with exposure to emissions from municipal solid waste incinerators.This study analyzed the occurrence of miscarriages in women aged 15–49 years residing near seven incinerators of the Emilia-Romagna Region (Northern Italy) in the period 2002–2006.MethodsWe considered all pregnancies occurring in women residing during the first trimester of pregnancy within a 4 km radius of each incinerator. Addresses were geocoded and exposures were characterized by a dispersion model (ADMS Urban model) producing pollution maps for incinerators based on PM₁₀ stack measurements and for other pollution sources based on NO_x ground measurements. Information on pregnancies and their outcomes was obtained from the Hospital Discharge Database. Simplified True Abortion Risks (STAR) × 100 estimated pregnancies were calculated. We ran logistic regressions adjusting for maternal characteristics, exposure to other sources of pollution, and sites, considering the whole population and stratifying by miscarriage history.ResultsThe study analyzed 11,875 pregnancies with 1375 miscarriages. After adjusting for confounders, an increase of PM₁₀ due to incinerator emissions was associated with an increased risk of miscarriage (test for trend, p = 0.042). The odds ratio for the highest quartile of exposed versus not exposed women was 1.29, 95% CI 0.97–1.72. The effect was present only for women without previous miscarriages (highest quartile of exposed versus not exposed women 1.44, 95% CI 1.06–1.96; test for trend, p = 0.009).ConclusionExposure to incinerator emissions is associated with an increased risk of miscarriage. This result should be interpreted with those of a previous study on reproductive health conducted in the same area that observed an association between incinerator exposure and preterm births.     

Modeling indoor air pollution of outdoor origin in homes of SAPALDIA subjects in Switzerland

Given the shrinking spatial contrasts in outdoor air pollution in Switzerland and the trends toward tightly insulated buildings, the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) needs to understand to what extent outdoor air pollution remains a determinant for residential indoor exposure. The objectives of this paper are to identify determining factors for indoor air pollution concentrations of particulate matter (PM), ultrafine particles in the size range from 15 to 300 nm, black smoke measured as light absorbance of PM (PM_absorbance) and nitrogen dioxide (NO₂) and to develop predictive indoor models for SAPALDIA. Multivariable regression models were developed based on indoor and outdoor measurements among homes of selected SAPALDIA participants in three urban (Basel, Geneva, Lugano) and one rural region (Wald ZH) in Switzerland, various home characteristics and reported indoor sources such as cooking. Outdoor levels of air pollutants were important predictors for indoor air pollutants, except for the coarse particle fraction. The fractions of outdoor concentrations infiltrating indoors were between 30% and 66%, the highest one was observed for PM_absorbance. A modifying effect of open windows was found for NO₂ and the ultrafine particle number concentration. Cooking was associated with increased particle and NO₂ levels. This study shows that outdoor air pollution remains an important determinant of residential indoor air pollution in Switzerland.     

Air pollution and hospitalization for acute complications of diabetes in Chile

Exposure to air pollution has been shown to cause insulin resistance in mice. To determine the relevance to humans, we tested the association between daily air pollution concentrations and daily hospitalization for acute serious complications of diabetes, coma and ketoacidosis, in Santiago between 2001 and 2008, using generalized linear models with natural splines to control for long term trends.For an interquartile range (IQR) increase in air pollutant, the relative risks (95% CI) of hospitalization for diabetes were: 1.15 (1.10, 1.20) for carbon monoxide (IQR = 1.00); 1.07 (0.98, 1.16) for ozone (IQR = 63.50); 1.14 (1.06, 1.22) for sulfur dioxide (IQR = 5.88); 1.12(1.05, 1.20) for nitrogen dioxide (IQR = 27.94); 1.11 (1.07, 1.15) for particulate matter ≤ 10 μm diameter(IQR = 34.00); and 1.11 (1.06, 1.16) for fine particulate matter ≤ 2.5 μm diameter (IQR = 18.50). Results were similar when stratified by age, sex and season. Air pollution appears to increase the risk of acute complications of diabetes requiring hospitalization, suggesting that improvements in air quality may reduce morbidity from diabetes.