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.     

Air pollution exposure and telomere length in highly exposed subjects in Beijing,China: A repeated-measure study

BackgroundAmbient particulate matter (PM) exposure has been associated with short- and long-term effects on cardiovascular disease (CVD). Telomere length (TL) is a biomarker of CVD risk that is modified by inflammation and oxidative stress, two key pathways for PM effects. Whether PM exposure modifies TL is largely unexplored.ObjectivesTo investigate effects of PM on blood TL in a highly-exposed population.MethodsWe measured blood TL in 120 blood samples from truck drivers and 120 blood samples from office workers in Beijing, China. We measured personal PM_2.5 and Elemental Carbon (EC, a tracer of traffic particles) using light-weight monitors. Ambient PM₁₀ was obtained from local monitoring stations. We used covariate-adjusted regression models to estimate percent changes in TL per an interquartile-range increase in exposure.ResultsCovariate-adjusted TL was higher in drivers (mean = 0.87, 95%CI: 0.74; 1.03) than in office workers (mean = 0.79, 95%CI: 0.67; 0.93; p = 0.001). In all participants combined, TL increased in association with personal PM_2.5 (+ 5.2%, 95%CI: 1.5; 9.1; p = 0.007), personal EC (+ 4.9%, 95%CI: 1.2; 8.8; p = 0.01), and ambient PM₁₀ (+ 7.7%, 95%CI: 3.7; 11.9; p < 0.001) on examination days. In contrast, average ambient PM₁₀ over the 14 days before the examinations was significantly associated with shorter TL (− 9.9%, 95%CI: − 17.6; − 1.5; p = 0.02).ConclusionsShort-term exposure to ambient PM is associated with increased blood TL, consistent with TL roles during acute inflammatory responses. Longer exposures may shorten TL as expected after prolonged pro-oxidant exposures. The observed TL alterations may participate in the biological pathways of short- and long-term PM effects.     

Effect of the shape of the exposure-response function on estimated hospital costs in a study on non-elective pneumonia hospitalizations related to particulate matter

ObjectiveWe used log-linear and log-log exposure-response (E-R) functions to model the association between PM_2.5 exposure and non-elective hospitalizations for pneumonia, and estimated the attributable hospital costs by using the effect estimates obtained from both functions.MethodsWe used hospital discharge data on 3519 non-elective pneumonia admissions from UZ Brussels between 2007 and 2012 and we combined a case-crossover design with distributed lag models. The annual averted pneumonia hospitalization costs for a reduction in PM_2.5 exposure from the mean (21.4 μg/m³) to the WHO guideline for annual mean PM_2.5 (10 μg/m³) were estimated and extrapolated for Belgium.ResultsNon-elective hospitalizations for pneumonia were significantly associated with PM_2.5 exposure in both models. Using a log-linear E-R function, the estimated risk reduction for pneumonia hospitalization associated with a decrease in mean PM_2.5 exposure to 10 μg/m³ was 4.9%. The corresponding estimate for the log-log model was 10.7%. These estimates translate to an annual pneumonia hospital cost saving in Belgium of €15.5 million and almost €34 million for the log-linear and log-log E-R function, respectively.DiscussionAlthough further research is required to assess the shape of the association between PM_2.5 exposure and pneumonia hospitalizations, we demonstrated that estimates for health effects and associated costs heavily depend on the assumed E-R function. These results are important for policy making, as supra-linear E-R associations imply that significant health benefits may still be obtained from additional pollution control measures in areas where PM levels have already been reduced.     

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.     

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.     

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.     

Recent versus chronic exposure to particulate matter air pollution in association with neurobehavioral performance in a panel study of primary schoolchildren

Children's neuropsychological abilities are in a developmental stage. Recent air pollution exposure and neurobehavioral performance are scarcely studied. In a panel study, we repeatedly administered to each child the following neurobehavioral tests: Stroop Test (selective attention) and Continuous Performance Test (sustained attention), Digit Span Forward and Backward Tests (short-term memory), and Digit-Symbol and Pattern Comparison Tests (visual information processing speed). At school, recent inside classroom particulate matter ≤ 2.5 or 10 μm exposure (PM_2.5, PM₁₀) was monitored on each examination day. At the child's residence, recent (same day up to 2 days before) and chronic (365 days before examination) exposures to PM_2.5, PM₁₀ and black carbon (BC) were modeled. Repeated neurobehavioral test performances (n = 894) of the children (n = 310) reflected slower Stroop Test (p = 0.05) and Digit-Symbol Test (p = 0.01) performances with increasing recent inside classroom PM_2.5 exposure. An interquartile range (IQR) increment in recent residential outdoor PM_2.5 exposure was associated with an increase in average latency of 0.087 s (SE: ± 0.034; p = 0.01) in the Pattern Comparison Test. Regarding chronic exposure at residence, an IQR increment of PM_2.5 exposure was associated with slower performances in the Continuous Performance (9.45 ± 3.47 msec; p = 0.007) and Stroop Tests (59.9 ± 26.5 msec; p = 0.02). Similar results were obtained for PM₁₀ exposure. In essence, we showed differential neurobehavioral changes robustly and adversely associated with recent or chronic ambient exposure to PM air pollution at residence, i.e., with recent exposure for visual information processing speed (Pattern Comparison Test) and with chronic exposure for sustained and selective attention.     

The contributions to long-term health-relevant particulate matter at the UK EMEP supersites between 2010 and 2013: Quantifying the mitigation challenge

Human health burdens associated with long-term exposure to particulate matter (PM) are substantial. The metrics currently recommended by the World Health Organization for quantification of long-term health-relevant PM are the annual average PM₁₀ and PM_2.5 mass concentrations, with no low concentration threshold. However, within an annual average, there is substantial variation in the composition of PM associated with different sources. To inform effective mitigation strategies, therefore, it is necessary to quantify the conditions that contribute to annual average PM₁₀ and PM_2.5 (rather than just short-term episodic concentrations). PM₁₀, PM_2.5, and speciated water-soluble inorganic, carbonaceous, heavy metal and polycyclic aromatic hydrocarbon components are concurrently measured at the two UK European Monitoring and Evaluation Programme (EMEP) ‘supersites’ at Harwell (SE England) and Auchencorth Moss (SE Scotland). In this work, statistical analyses of these measurements are integrated with air-mass back trajectory data to characterise the ‘chemical climate’ associated with the long-term health-relevant PM metrics at these sites. Specifically, the contributions from different PM concentrations, months, components and geographic regions are detailed. The analyses at these sites provide policy-relevant conclusions on mitigation of (i) long-term health-relevant PM in the spatial domain for which these sites are representative, and (ii) the contribution of regional background PM to long-term health-relevant PM.At Harwell the mean (± 1 sd) 2010–2013 annual average concentrations were PM₁₀ = 16.4 ± 1.4 μg m^− 3 and PM_2.5 = 11.9 ± 1.1 μg m^− 3 and at Auchencorth PM₁₀ = 7.4 ± 0.4 μg m^− 3 and PM_2.5 = 4.1 ± 0.2 μg m^− 3. The chemical climate state at each site showed that frequent, moderate hourly PM₁₀ and PM_2.5 concentrations (defined as approximately 5–15 μg m^− 3 for PM₁₀ and PM_2.5 at Harwell and 5–10 μg m^− 3 for PM₁₀ at Auchencorth) determined the magnitude of annual average PM₁₀ and PM_2.5 to a greater extent than the relatively infrequent high, episodic PM₁₀ and PM_2.5 concentrations. These moderate PM₁₀ and PM_2.5 concentrations were derived across the range of chemical components, seasons and air-mass pathways, in contrast to the highest PM concentrations which tended to associate with specific conditions. For example, the largest contribution to moderate PM₁₀ and PM_2.5 concentrations – the secondary inorganic aerosol components, specifically NO₃⁻ – were accumulated during the arrival of trajectories traversing the spectrum of marine, UK, and continental Europe areas. Mitigation of the long-term health-relevant PM impact in the regions characterised by these two sites requires multilateral action, across species (and hence source sectors), both nationally and internationally; there is no dominant determinant of the long-term PM metrics to target.     

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.     

Personal exposure to fine particulate matter and blood pressure: A role of angiotensin converting enzyme and its DNA methylation

BackgroundThe underlying intermediate mechanisms about the association between fine particulate matter (PM_2.5) air pollution and blood pressure (BP) were unclear. Few epidemiological studies have explored the potential mediation effects of angiotensin-converting enzyme (ACE) and its DNA methylation.MethodsWe designed a longitudinal panel study with 4 follow-ups among 36 healthy college students in Shanghai, China from December 17, 2014 to July 11, 2015. We measured personal real-time exposure to PM_2.5, serum ACE level, and blood methylation of ACE gene and the repetitive elements. We applied linear mixed-effects models to examine the effects of PM_2.5 on ACE protein, DNA methylation and BP markers. Furthermore, we conducted mediation analyses to evaluate the potential pathways.ResultsAn interquartile range increase (26.78 μg/m³) in 24-h average exposure to PM_2.5 was significantly associated with 1.12 decreases in ACE average methylation (%5mC), 13.27% increase in ACE protein, and increments of 1.13 mmHg in systolic BP, 0.66 mmHg in diastolic BP and 0.82 mmHg in mean arterial pressure. ACE hypomethylation mediated 11.78% (P = 0.03) of the elevated ACE protein by PM_2.5. Increased ACE protein accounted for 3.90 ~ 13.44% (P = 0.35 ~ 0.68) of the elevated BP by PM_2.5. Repetitive-element methylation was also decreased but did not significantly mediate the association between PM_2.5 and BP.ConclusionsThis investigation provided strong evidence that short-term exposure to PM_2.5 was significantly associated with BP, ACE protein and ACE methylation. Our findings highlighted a possible involvement of ACE and ACE methylation in the effects of PM_2.5 on elevating BP.     

The mortality effect of ship-related fine particulate matter in the Sydney greater metropolitan region of NSW,Australia

This study investigates the mortality effect of primary and secondary PM_2.5 related to ship exhaust in the Sydney greater metropolitan region of Australia. A detailed inventory of ship exhaust emissions was used to model a) the 2010/11 concentration of ship-related PM_2.5 across the region, and b) the reduction in PM_2.5 concentration that would occur if ships used distillate fuel with a 0.1% sulfur content at berth or within 300 km of Sydney. The annual loss of life attributable to 2010/11 levels of ship-related PM_2.5 and the improvement in survival associated with use of low-sulfur fuel were estimated from the modelled concentrations.In 2010/11, approximately 1.9% of the region-wide annual average population weighted-mean concentration of all natural and human-made PM_2.5 was attributable to ship exhaust, and up to 9.4% at suburbs close to ports. An estimated 220 years of life were lost by people who died in 2010/11 as a result of ship exhaust-related exposure (95% CI_β: 140–290, where CI_β is the uncertainty in the concentration-response coefficient only). Use of 0.1% sulfur fuel at berth would reduce the population weighted-mean concentration of PM_2.5 related to ship exhaust by 25% and result in a gain of 390 life-years over a twenty year period (95% CI_β: 260–520). Use of 0.1% sulfur fuel within 300 km of Sydney would reduce the concentration by 56% and result in a gain of 920 life-years over twenty years (95% CI_β: 600–1200).Ship exhaust is an important source of human exposure to PM_2.5 in the Sydney greater metropolitan region. This assessment supports intervention to reduce ship emissions in the GMR. Local strategies to limit the sulfur content of fuel would reduce exposure and will become increasingly beneficial as the shipping industry expands. A requirement for use of 0.1% sulfur fuel by ships within 300 km of Sydney would provide more than twice the mortality benefit of a requirement for ships to use 0.1% sulfur fuel at berth.     

Associations among plasma metabolite levels and short-term exposure to PM2.5 and ozone in a cardiac catheterization cohort

RationaleExposure to ambient particulate matter (PM) and ozone has been associated with cardiovascular disease (CVD). However, the mechanisms linking PM and ozone exposure to CVD remain poorly understood.ObjectiveThis study explored associations between short-term exposures to PM with a diameter < 2.5 μm (PM_2.5) and ozone with plasma metabolite concentrations.Methods and resultsWe used cross-sectional data from a cardiac catheterization cohort at Duke University, North Carolina (NC), USA, accumulated between 2001 and 2007. Amino acids, acylcarnitines, ketones and total non-esterified fatty acid plasma concentrations were determined in fasting samples. Daily concentrations of PM_2.5 and ozone were obtained from a Bayesian space-time hierarchical model, matched to each patient's residential address. Ten metabolites were selected for the analysis based on quality criteria and cluster analysis. Associations between metabolites and PM_2.5 or ozone were analyzed using linear regression models adjusting for long-term trend and seasonality, calendar effects, meteorological parameters, and participant characteristics.We found delayed associations between PM_2.5 or ozone and changes in metabolite levels of the glycine-ornithine-arginine metabolic axis and incomplete fatty acid oxidation associated with mitochondrial dysfunction. The strongest association was seen for an increase of 8.1 μg/m³ in PM_2.5 with a lag of one day and decreased mean glycine concentrations (− 2.5% [95% confidence interval: − 3.8%; − 1.2%]).ConclusionsShort-term exposures to ambient PM_2.5 and ozone is associated with changes in plasma concentrations of metabolites in a cohort of cardiac catheterization patients. Our findings might help to understand the link between air pollution and cardiovascular disease.     

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.     

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.     

Prenatal particulate air pollution and neurodevelopment in urban children: Examining sensitive windows and sex-specific associations

BackgroundBrain growth and structural organization occurs in stages beginning prenatally. Toxicants may impact neurodevelopment differently dependent upon exposure timing and fetal sex.ObjectivesWe implemented innovative methodology to identify sensitive windows for the associations between prenatal particulate matter with diameter ≤ 2.5 μm (PM_2.5) and children's neurodevelopment.MethodsWe assessed 267 full-term urban children's prenatal daily PM_2.5 exposure using a validated satellite-based spatio-temporally resolved prediction model. Outcomes included IQ (WISC-IV), attention (omission errors [OEs], commission errors [CEs], hit reaction time [HRT], and HRT standard error [HRT-SE] on the Conners' CPT-II), and memory (general memory [GM] index and its components — verbal [VEM] and visual [VIM] memory, and attention-concentration [AC] indices on the WRAML-2) assessed at age 6.5 ± 0.98 years. To identify the role of exposure timing, we used distributed lag models to examine associations between weekly prenatal PM_2.5 exposure and neurodevelopment. Sex-specific associations were also examined.ResultsMothers were primarily minorities (60% Hispanic, 25% black); 69% had ≤ 12 years of education. Adjusting for maternal age, education, race, and smoking, we found associations between higher PM_2.5 levels at 31–38 weeks with lower IQ, at 20–26 weeks gestation with increased OEs, at 32–36 weeks with slower HRT, and at 22–40 weeks with increased HRT-SE among boys, while significant associations were found in memory domains in girls (higher PM_2.5 exposure at 18–26 weeks with reduced VIM, at 12–20 weeks with reduced GM).ConclusionsIncreased PM_2.5 exposure in specific prenatal windows may be associated with poorer function across memory and attention domains with variable associations based on sex. Refined determination of time window- and sex-specific associations may enhance insight into underlying mechanisms and identification of vulnerable subgroups.     

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.     

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.     

Status and characteristics of ambient PM2.5 pollution in global megacities

Ambient PM_2.5 pollution is a substantial threat to public health in global megacities. This paper reviews the PM_2.5 pollution of 45 global megacities in 2013, based on mass concentration from official monitoring networks and composition data reported in the literature. The results showed that the five most polluted megacities were Delhi, Cairo, Xi'an, Tianjin and Chengdu, all of which had an annual average concentration of PM_2.5 greater than 89 μg/m³. The five cleanest megacities were Miami, Toronto, New York, Madrid and Philadelphia, the annual averages of which were less than 10 μg/m³. Spatial distribution indicated that the highly polluted megacities are concentrated in east-central China and the Indo-Gangetic Plain. Organic matter and SNA (sum of sulfate, nitrate and ammonium) contributed 30% and 36%, respectively, of the average PM_2.5 mass for all megacities. Notable seasonal variation of PM_2.5 polluted days was observed, especially for the polluted megacities of China and India, resulting in frequent heavy pollution episodes occurring during more polluted seasons such as winter. Marked differences in PM_2.5 pollution between developing and developed megacities require more effort on local emissions reduction as well as global cooperation to address the PM_2.5 pollution of those megacities mainly in Asia.     

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.     

Racial isolation and exposure to airborne particulate matter and ozone in understudied US populations: Environmental justice applications of downscaled numerical model output

BackgroundResearchers and policymakers are increasingly focused on combined exposures to social and environmental stressors, especially given how often these stressors tend to co-locate. Such exposures are equally relevant in urban and rural areas and may accrue disproportionately to particular communities or specific subpopulations.ObjectivesTo estimate relationships between racial isolation (RI), a measure of the extent to which minority racial/ethnic group members are exposed to only one another, and long-term particulate matter with an aerodynamic diameter of < 2.5 μ (PM_2.5) and ozone (O₃) levels in urban and nonurban areas of the eastern two-thirds of the US.MethodsLong-term (5 year average) census tract-level PM_2.5 and O₃ concentrations were calculated using output from a downscaler model (2002–2006). The downscaler uses a linear regression with additive and multiplicative bias coefficients to relate ambient monitoring data with gridded output from the Community Multi-scale Air Quality (CMAQ) model. A local, spatial measure of RI was calculated at the tract level, and tracts were classified by urbanicity, RI, and geographic region. We examined differences in estimated pollutant exposures by RI, urbanicity, and demographic subgroup (e.g., race/ethnicity, education, socioeconomic status, age), and used linear models to estimate associations between RI and air pollution levels in urban, suburban, and rural tracts.ResultsHigh RI tracts (≥ 80th percentile) had higher average PM_2.5 levels in each category of urbanicity compared to low RI tracts (< 20th percentile), with the exception of the rural West. Patterns in O₃ levels by urbanicity and RI differed by region. Linear models indicated that PM_2.5 concentrations were significantly and positively associated with RI. The largest association between PM_2.5 and RI was observed in the rural Midwest, where a one quintile increase in RI was associated with a 0.90 μg/m³ (95% confidence interval: 0.83, 0.99 μg/m³) increase in PM_2.5 concentration. Associations between O₃ and RI in the Northeast, Midwest and West were positive and highest in suburban and rural tracts, even after controlling for potential confounders such as percentage in poverty.ConclusionRI is associated with higher 5 year estimated PM_2.5 concentrations in urban, suburban, and rural census tracts, adding to evidence that segregation is broadly associated with disparate air pollution exposures. Disproportionate burdens to adverse exposures such as air pollution may be a pathway to racial/ethnic disparities in health.