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.     

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.     

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.     

Associations between ultrafine and fine particles and mortality in five central European cities — Results from the UFIREG study

BackgroundEvidence on health effects of ultrafine particles (UFP) is still limited as they are usually not monitored routinely. The few epidemiological studies on UFP and (cause-specific) mortality so far have reported inconsistent results.ObjectivesThe main objective of the UFIREG project was to investigate the short-term associations between UFP and fine particulate matter (PM) < 2.5 μm (PM_2.5) and daily (cause-specific) mortality in five European Cities. We also examined the effects of PM < 10 μm (PM₁₀) and coarse particles (PM_2.5–10).MethodsUFP (20–100 nm), PM and meteorological data were measured in Dresden and Augsburg (Germany), Prague (Czech Republic), Ljubljana (Slovenia) and Chernivtsi (Ukraine). Daily counts of natural and cardio-respiratory mortality were collected for all five cities. Depending on data availability, the following study periods were chosen: Augsburg and Dresden 2011–2012, Ljubljana and Prague 2012–2013, Chernivtsi 2013–March 2014. The associations between air pollutants and health outcomes were assessed using confounder-adjusted Poisson regression models examining single (lag 0–lag 5) and cumulative lags (lag 0–1, lag 2–5, and lag 0–5). City-specific estimates were pooled using meta-analyses methods.ResultsResults indicated a delayed and prolonged association between UFP and respiratory mortality (9.9% [95%-confidence interval: − 6.3%; 28.8%] increase in association with a 6-day average increase of 2750 particles/cm³ (average interquartile range across all cities)). Cardiovascular mortality increased by 3.0% [− 2.7%; 9.1%] and 4.1% [0.4%; 8.0%] in association with a 12.4 μg/m³ and 4.7 μg/m³ increase in the PM_2.5- and PM_2.5–10-averages of lag 2–5.ConclusionsWe observed positive but not statistically significant associations between prolonged exposures to UFP and respiratory mortality, which were independent of particle mass exposures. Further multi-centre studies are needed investigating several years to produce more precise estimates on health effects of UFP.     

Long-term air pollution exposure and diabetes in a population-based Swiss cohort

Air pollution is an important risk factor for global burden of disease. There has been recent interest in its possible role in the etiology of diabetes mellitus. Experimental evidence is suggestive, but epidemiological evidence is limited and mixed. We therefore explored the association between air pollution and prevalent diabetes, in a population-based Swiss cohort.We did cross-sectional analyses of 6392 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults [SAPALDIA], aged between 29 and 73 years. We used estimates of average individual home outdoor PM₁₀ [particulate matter <10 μm in diameter] and NO₂ [nitrogen dioxide] exposure over the 10 years preceding the survey. Their association with diabetes was modeled using mixed logistic regression models, including participants' study area as random effect, with incremental adjustment for confounders.There were 315 cases of diabetes (prevalence: 5.5% [95% confidence interval (CI): 2.8, 7.2%]). Both PM₁₀ and NO₂ were associated with prevalent diabetes with respective odds ratios of 1.40 [95% CI: 1.17, 1.67] and 1.19 [95% CI: 1.03, 1.38] per 10 μg/m³ increase in the average home outdoor level. Associations with PM₁₀ were generally stronger than with NO₂, even in the two-pollutant model. There was some indication that beta blockers mitigated the effect of PM₁₀. The associations remained stable across different sensitivity analyses.Our study adds to the evidence that long term air pollution exposure is associated with diabetes mellitus. PM₁₀ appears to be a useful marker of aspects of air pollution relevant for diabetes. This association can be observed at concentrations below air quality guidelines.     

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.     

Blood pressure changes in association with black carbon exposure in a panel of healthy adults are independent of retinal microcirculation

Exposure to ambient particulate matter and elevated blood pressure are risk factors for cardiovascular morbidity and mortality. Microvascular changes might be an important pathway in explaining the association between air pollution and blood pressure. The objective of the study was to evaluate the role of the retinal microcirculation in the association between black carbon (BC) exposure and blood pressure.We estimated subchronic BC exposure based on 1-week personal measurements (μ-Aethalometer, AethLabs) in 55 healthy nurses. Blood pressure and retinal microvasculature were measured on four different days (range: 2–4) during this week.Subchronic BC exposure averaged (± SD) 1334 ± 631 ng/m³ and ranged from 338 ng/m³ to 3889 ng/m³. An increased exposure of 631 ng/m³ BC was associated with a 2.77 mm Hg (95% CI: 0.39 to 5.15, p = 0.027) increase in systolic blood pressure, a 2.35 mm Hg (95% CI: 0.52 to 4.19, p = 0.016) increase in diastolic blood pressure and with 5.65 μm (95% CI: 1.33 to 9.96, p = 0.014) increase in central retinal venular equivalent. Mediation analysis failed to reveal an effect of retinal microvasculature in the association between blood pressure and subchronic BC exposure.In conclusion, we found a positive association between blood pressure and subchronic black carbon exposure in healthy adults. This finding adds evidence to the association between black carbon exposure and cardiovascular health effects, with elevated blood pressure as a plausible intermediate effector. Our results suggest that the changes in a person's blood pressure as a result of subchronic black carbon exposure operate independently of the retinal microcirculation.     

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%.     

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.     

Inflammatory markers in relation to long-term air pollution

Long-term exposure to ambient air pollution can lead to chronic health effects such as cancer, cardiovascular and respiratory disease. Systemic inflammation has been hypothesized as a putative biological mechanism contributing to these adverse health effects. We evaluated the effect of long-term exposure to air pollution on blood markers of systemic inflammation.We measured a panel of 28 inflammatory markers in peripheral blood samples from 587 individuals that were biobanked as part of a prospective study. Participants were from Varese and Turin (Italy) and Umea (Sweden). Long-term air pollution estimates of nitrogen oxides (NO_x) were available from the European Study of Cohorts for Air Pollution Effects (ESCAPE). Linear mixed models adjusted for potential confounders were applied to assess the association between NO_x and the markers of inflammation.Long-term exposure to NO_x was associated with decreased levels of interleukin (IL)-2, IL-8, IL-10 and tumor necrosis factor-α in Italy, but not in Sweden. NO_x exposure levels were considerably lower in Sweden than in Italy (Sweden: median (5th, 95th percentiles) 6.65 μg/m³ (4.8, 19.7); Italy: median (5th, 95th percentiles) 94.2 μg/m³ (7.8, 124.5)). Combining data from Italy and Sweden we only observed a significant association between long-term exposure to NO_x and decreased levels of circulating IL-8.We observed some indication for perturbations in the inflammatory markers due to long-term exposure to NO_x. Effects were stronger in Italy than in Sweden, potentially reflecting the difference in air pollution levels between the two cohorts.     

Associations between short/medium-term variations in black smoke air pollution and mortality in the Glasgow conurbation,UK

ObjectivesTo examine associations between short/medium-term variations in black smoke air pollution and mortality in the population of Glasgow and the adjacent towns of Renfrew and Paisley over a 25-year period at different time lags (0–30 days).MethodsGeneralised linear (Poisson) models were used to investigate the relationship between lagged black smoke concentrations and daily mortality, with allowance for confounding by cold temperature, between 1974 and 1998.ResultsWhen a range of lag periods were investigated significant associations were noted between temperature-adjusted black smoke exposure and all-cause mortality at lag periods of 13–18 and 19–24 days, and respiratory mortality at lag periods of 1–6, 7–12, and 13–18 days. Significant associations between cardiovascular mortality and temperature-adjusted black smoke were not observed. After adjusting for the effects of temperature a 10 μg m^− 3 increase in black smoke concentration on a given day was associated with a 0.9% [95% Confidence Interval (CI): 0.3–1.5%] increase in all cause mortality and a 3.1% [95% CI: 1.4–4.9%] increase in respiratory mortality over the ensuing 30-day period. In contrast for a 10 μg m^− 3 increase in black smoke concentration over 0–3 day lag period, the temperature adjusted exposure mortality associations were substantially lower (0.2% [95% CI: − 0.0–0.4%] and 0.3% [95% CI: − 0.2–0.8%] increases for all-cause and respiratory mortality respectively).ConclusionsThis study has provided evidence of association between black smoke exposure and mortality at longer lag periods than have been investigated in the majority of time series analyses.     

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.     

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.     

Long-term effects of elemental composition of particulate matter on inflammatory blood markers in European cohorts

BackgroundEpidemiological studies have associated long-term exposure to ambient particulate matter with increased mortality from cardiovascular and respiratory disorders. Systemic inflammation is a plausible biological mechanism behind this association. However, it is unclear how the chemical composition of PM affects inflammatory responses.ObjectivesTo investigate the association between long-term exposure to elemental components of PM and the inflammatory blood markers high-sensitivity C-reactive protein (hsCRP) and fibrinogen as part of the European ESCAPE and TRANSPHORM multi-center projects.MethodsIn total, 21,558 hsCRP measurements and 17,428 fibrinogen measurements from cross-sections of five and four cohort studies were available, respectively. Residential long-term concentrations of particulate matter < 10 μm (PM₁₀) and < 2.5 μm (PM_2.5) in diameter and selected elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, zinc) were estimated based on land-use regression models. Associations between components and inflammatory markers were estimated using linear regression models for each cohort separately. Cohort-specific results were combined using random effects meta-analysis. As a sensitivity analysis the models were additionally adjusted for PM mass.ResultsA 5 ng/m³ increase in PM_2.5 copper and a 500 ng/m³ increase in PM₁₀ iron were associated with a 6.3% [0.7; 12.3%] and 3.6% [0.3; 7.1%] increase in hsCRP, respectively. These associations between components and fibrinogen were slightly weaker. A 10 ng/m³ increase in PM_2.5 zinc was associated with a 1.2% [0.1; 2.4%] increase in fibrinogen; confidence intervals widened when additionally adjusting for PM_2.5.ConclusionsLong-term exposure to transition metals within ambient particulate matter, originating from traffic and industry, may be related to chronic systemic inflammation providing a link to long-term health effects of particulate matter.     

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 pollutant exposure and preterm and term small-for-gestational-age births in Detroit,Michigan: Long-term trends and associations

Studies in a number of countries have reported associations between exposure to ambient air pollutants and adverse birth outcomes, including low birth weight, preterm birth (PTB) and, less commonly, small for gestational age (SGA). Despite their growing number, the available studies have significant limitations, e.g., incomplete control of temporal trends in exposure, modest sample sizes, and a lack of information regarding individual risk factors such as smoking. No study has yet examined large numbers of susceptible individuals.We investigated the association between ambient air pollutant concentrations and term SGA and PTB outcomes among 164,905 singleton births in Detroit, Michigan occurring between 1990 and 2001. SO₂, CO, NO₂, O₃ and PM₁₀ exposures were used in single and multiple pollutant logistic regression models to estimate odds ratios (OR) for these outcomes, adjusted for the infant's sex and gestational age, the mother's race, age group, education level, smoking status and prenatal care, birth season, site of residence, and long-term exposure trends.Term SGA was associated with CO levels exceeding 0.75 ppm (OR = 1.14, 95% confidence interval = 1.02–1.27) and NO₂ exceeding 6.8 ppb (1.11, 1.03–1.21) exposures in the first month, and with PM₁₀ exceeding 35 μg/m³ (1.22, 1.03–1.46) and O₃ (1.11, 1.02–1.20) exposure in the third trimester. PTB was associated with SO₂ (1.07, 1.01–1.14) exposure in the last month, and with (hourly) O₃ exceeding 92 ppb (1.08, 1.02–1.14) exposure in the first month.Exposure to several air pollutants at modest concentrations was associated with adverse birth outcomes. This study, which included a large Black population, suggests the importance of the early period of pregnancy for associations between term SGA with CO and NO₂, and between O₃ with PTB; and the late pregnancy period for associations between term SGA and O₃ and PM₁₀, and between SO₂ with PTB. It also highlights the importance of accounting for individual risk factors such as maternal smoking, maternal race, and long-term trends in air pollutant levels and adverse birth outcomes in evaluating relationships between pollutant exposures and adverse birth outcomes.     

Ambient air pollution and children's lung function in China

ObjectiveTo describe the correlations between ambient air pollutants (TSP, SO₂, NO_x) and the level of children's lung function (FVC, FEV₁, MMEF) in China.MethodsWe collected the research articles on ambient air pollution and children's lung function published from 1985 to 2006 and selected 11 articles finally according to the following criteria: (1) Children between the age of 7 and 15 as objects; (2) Local air quality monitoring results were reported; (3) Strict quality control was taken when testing children's lung function; (4) The results were expressed by the average of measured value. Then we analyzed the correlation relationship between the level of ambient air pollutants and children's lung function and compared the effects of ambient air pollutants on children's lung function of boy and girl.ResultsThe selected articles included the results of 7 cities in China. Among them, the results of 6 cities' studies revealed that the levels of children's lung function were significantly lower in the areas with heavy ambient air pollution than those in the areas with light ambient air pollution. According to the articles, the average levels of TSP were at the range of 0.084 mg/m³–0.835 mg/m³, SO₂ were 0.013 mg/m³–0.929 mg/m³, NO_x were 0.044 mg/m³–0.229 mg/m³. Correlation analysis showed significant negative correlation between the levels of TSP and SO₂ and children's FVC and FEV₁, as well as the levels of NO_x and children's MMEF. The correlation coefficient was ? 0.797 (t = ? 4.384, P = 0.001) between TSP and FVC, ? 0.693 (t = ? 4.190, P < 0.001) between Ln (SO₂) and FVC, ? 0.886 (t = ? 5.392, P = 0.001) and ? 0.685 (t = ? 4.101, P = 0.001) between FEV₁ and TSP and Ln (SO₂), and ? 0.973 (t = ? 5.993, P = 0.027) between NO_xNO_x and MMEF, respectively. The results also suggested that the decreases of lung function for girl with the increasing of ambient air pollution were significantly greater for boy.ConclusionThe levels of ambient air TSP and SO₂ correlated with the damage of the big airway function of children, while NO_xNO_x affected the small airway function chiefly. Furthermore, lung function of girl was more susceptible to ambient air pollutants than boy.     

Measurement and health risk assessment of PM2.5, flame retardants,carbonyls and black carbon in indoor and outdoor air in kindergartens in Hong Kong

Indoor air pollution is closely related to children's health. Polybrominated diphenyl ethers (PBDEs) and dechlorane plus (DP) transmitted through indoor PM_2.5 and dust, along with carbonyl compounds and black carbon (BC) aerosol were analysed in five Hong Kong kindergartens. The results showed that 60% of the median PM_2.5 levels (1.3 × 10¹ to 2.9 × 10¹ μg/m³ for indoor; 9.5 to 8.8 × 10¹ μg/m³ for outdoor) in the five kindergartens were higher than the guidelines set by the World Health Organization (2.5 × 10¹ μg/m³). Indoor PM_2.5 mass concentrations were correlated with outdoor PM_2.5 in four of the kindergartens. The PBDEs (0.10–0.64 ng/m³ in PM_2.5; 0.30–2.0 × 10² ng/g in dust) and DP (0.05–0.10 ng/m³ in PM_2.5; 1.3–8.7 ng/g in dust) were detected in 100% of the PM_2.5 and dust samples. Fire retardant levels in the air were not correlated with the levels of dust in this study. The median BC concentrations varied by > 7-fold from 8.8 × 10² ng/m^− 3 to 6.7 × 10³ ng/m^− 3 and cooking events might have caused BC concentrations to rise both indoors and outdoors. The total concentrations of 16 carbonyls ranged from 4.7 × 10¹ μg/m³ to 9.3 × 10¹ μg/m³ indoors and from 1.9 × 10¹ μg/m³ to 4.3 × 10¹ μg/m³ outdoors, whilst formaldehyde was the most abundant air carbonyl. Indoor carbonyl concentrations were correlated with outdoor carbonyls in three kindergartens. The health risk assessment showed that hazard indexes (HIs) HIs of non-cancer risks from PBDEs and DPs were all lower than 0.08, whilst non-cancer HIs of carbonyl compounds ranged from 0.77 to 1.85 indoors and from 0.50 to 0.97 outdoors. The human intake of PBDEs and DP through inhalation of PM_2.5 accounted for 78% to 92% of the total intake. The cancer hazard quotients (HQs) of formaldehyde ranged from 4.5E − 05 to 2.1E − 04 indoors and from 1.9E − 05 to 6.2E − 05 outdoors. In general, the indoor air pollution in the five Hong Kong kindergartens might present adverse effects to children, although different schools showed distinct pollution levels, so indoor air quality might be improved through artificial measures. The data will be useful to developing a feasible management protocol for indoor environments.     

Back-extrapolated and year-specific NO2 land use regression models for Great Britain - Do they yield different exposure assessment?

Robust methods to estimate historic population air pollution exposures are important tools for epidemiological studies evaluating long-term health effects. We developed land use regression (LUR) models for NO₂ exposure in Great Britain for 1991 and explored whether the choice of year-specific or back-extrapolated LUR yields 1) similar LUR variables and model performance, and 2) similar national and regional address-level and small-area concentrations. We constructed two LUR models for 1991using NO₂ concentrations from the diffusion tube monitoring network, one using 75% of all available measurement sites (that over-represent industrial areas), and the other using 75% of a subset of sites proportionate to population by region to study the effects of monitoring site selection bias. We compared, using the remaining (hold-out) 25% of monitoring sites, the performance of the two 1991 models with back-extrapolation of a previously published 2009 model, developed using NO₂ concentrations from automatic chemiluminescence monitoring sites and predictor variables from 2006/2007. The 2009 model was back-extrapolated to 1991 using the same predictors (1990 & 1995) used to develop 1991 models. The 1991 models included industrial land use variables, not present for 2009. The hold-out performance of 1991 models (mean-squared-error-based-R²: 0.62–0.64) was up to 8% higher and ~ 1 μg/m³ lower in root mean squared error than the back-extrapolated 2009 model, with best performance from the subset of sites representing population exposures. Year-specific and back-extrapolated exposures for residential addresses (n = 1.338,399) and small areas (n = 10.518) were very highly linearly correlated for Great Britain (r > 0.83). This study suggests that year-specific model for 1991 and back-extrapolation of the 2009 LUR yield similar exposure assessment.