Residential PM2 Research Articles

The effect of portable HEPA filter air cleaners on indoor PM2.5 concentrations and second hand tobacco smoke exposure among pregnant women in Ulaanbaatar, Mongolia: The UGAAR randomized controlled trial

BackgroundPortable HEPA filter air cleaners can reduce indoor fine particulate matter (PM2.5), but their use has not been adequately evaluated in high pollution settings. We assessed air cleaner effectiveness in reducing indoor residential PM2.5 and second hand smoke (SHS) exposures among non-smoking pregnant women in Ulaanbaatar, Mongolia. MethodsWe randomized 540 participants to an intervention group receiving 1 or 2 HEPA filter air cleaners or a control group receiving no air cleaners. We followed 259 intervention and 253 control participants to the end of pregnancy. We measured one-week indoor residential PM2.5 concentrations in early (~11weeks gestation) and late (~31weeks gestation) pregnancy and collected outdoor PM2.5 data from centrally-located government monitors. We assessed blood cadmium in late pregnancy. Hair nicotine was quantified in a subset (n=125) to evaluate blood cadmium as a biomarker of SHS exposure. We evaluated air cleaner effectiveness using mixed effects and multiple linear regression models and used stratified models and interaction terms to evaluate potential modifiers of effectiveness. ResultsThe overall geometric mean (GM) one-week outdoor PM2.5 concentration was 47.9μg/m3 (95% CI: 44.6, 51.6μg/m3), with highest concentrations in winter (118.0μg/m3; 110.4, 126.2μg/m3). One-week indoor and outdoor PM2.5 concentrations were correlated (r=0.69). Indoor PM2.5 concentrations were 29% (21, 37%) lower in intervention versus control apartments, with GMs of 17.3μg/m3 (15.8, 18.8μg/m3) and 24.5μg/m3 (22.2, 27.0μg/m3), respectively. Air cleaner effectiveness was greater when air cleaners were first deployed (40%; 31, 48%) than after approximately five months of use (15%; 0, 27%). Blood cadmium concentrations were 14% (4, 23%) lower among intervention participants, likely due to reduced SHS exposure. ConclusionsPortable HEPA filter air cleaners can lower indoor PM2.5 concentrations and SHS exposures in highly polluted settings.

Prenatal Air Pollution and Newborns' Predisposition to Accelerated Biological Aging

Telomere length is a marker of biological aging that may provide a cellular memory of exposures to oxidative stress and inflammation. Telomere length at birth has been related to life expectancy. An association between prenatal air pollution exposure and telomere length at birth could provide new insights in the environmental influence on molecular longevity. To assess the association of prenatal exposure to particulate matter (PM) with newborn telomere length as reflected by cord blood and placental telomere length. In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 2014, all with a singleton full-term birth (≥37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere lengths were included, resulting in a final study sample size of 641. Maternal residential PM2.5 (particles with an aerodynamic diameter ≤2.5 μm) exposure during pregnancy. In the newborns, cord blood and placental tissue relative telomere length were measured. Maternal residential PM2.5 exposure during pregnancy was estimated using a high-resolution spatial-temporal interpolation method. In distributed lag models, both cord blood and placental telomere length were associated with average weekly exposures to PM2.5 during pregnancy, allowing the identification of critical sensitive exposure windows. In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, -14.1% to -3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, -19.3% to -6.7%) shorter placental telomere length. These associations were controlled for date of delivery, gestational age, maternal body mass index, maternal age, paternal age, newborn sex, newborn ethnicity, season of delivery, parity, maternal smoking status, maternal educational level, pregnancy complications, and ambient temperature. Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere length. The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length during life. Therefore, improvements in air quality may promote molecular longevity from birth onward.

Seasonal trends of indoor fine particulate matter and its determinants in urban residences in Nanjing, China

Most people spend more than 80% of their time indoors; thus, indoor air pollution has a significant influence on an individual's exposure to air pollution. In this study, PM2.5 concentrations in both indoor and outdoor air were simultaneously measured in urban residences in Nanjing, China. The measurements were carried out using MicroPEM personal exposure monitors during summer, winter and transition seasons from March 2016 to February 2017. Information on building characteristics, occupants' activities and socioeconomic status (SES) variables was obtained through questionnaires during the sampling period. Significant seasonal variations in indoor and outdoor PM2.5 levels were observed in this study, with the highest PM2.5 concentration in winter and the lowest in summer. The correlation between indoor and outdoor PM2.5 concentrations in transition seasons was higher than that in winter and summer. Linear regression models were fitted to log-transformed indoor PM2.5 concentrations to determine potential influencing factors. Outdoor PM2.5 was found to be the major source of residential indoor PM2.5 pollution. The household activity of cooking was an indoor determinant of PM2.5 concentrations in homes with open-plan kitchens or when the kitchen door was open during cooking. More frequent building ventilation could increase indoor exposure to outdoor PM2.5 in transition seasons and winter or when the outdoor air quality is poor. SES variables such as dwelling ownership and household income were associated with indoor PM2.5 concentrations.

Maternal residential air pollution and placental imprinted gene expression

BackgroundMaternal exposure to air pollution is associated with reduced fetal growth, but its relationship with expression of placental imprinted genes (important regulators of fetal growth) has not yet been studied. ObjectivesTo examine relationships between maternal residential air pollution and expression of placental imprinted genes in the Rhode Island Child Health Study (RICHS). MethodsWomen-infant pairs were enrolled following delivery between 2009 and 2013. We geocoded maternal residential addresses at delivery, estimated daily levels of fine particulate matter (PM2.5; n=355) and black carbon (BC; n=336) using spatial-temporal models, and estimated residential distance to nearest major roadway (n=355). Using linear regression models we investigated the associations between each exposure metric and expression of nine candidate genes previously associated with infant birthweight in RICHS, with secondary analyses of a panel of 108 imprinted genes expressed in the placenta. We also explored effect measure modification by infant sex. ResultsPM2.5 and BC were associated with altered expression for seven and one candidate genes, respectively, previously linked with birthweight in this cohort. Adjusting for multiple comparisons, we found that PM2.5 and BC were associated with changes in expression of 41 and 12 of 108 placental imprinted genes, respectively. Infant sex modified the association between PM2.5 and expression of CHD7 and between proximity to major roadways and expression of ZDBF2. ConclusionsWe found that maternal exposure to residential PM2.5 and BC was associated with changes in placental imprinted gene expression, which suggests a plausible line of investigation of how air pollution affects fetal growth and development.

An Exposure-Mortality Relationship for Residential Indoor PM2.5 Exposure from Outdoor Sources

A large proportion of particulate air pollution exposure in urban areas occurs due to the penetration of outdoor pollution into the residential indoor environment. Theoretical considerations suggest that quantifying health effects due to changes to indoor particulate concentrations derived from outdoor sources requires the adjustment of exposure-response coefficients based on epidemiological studies of outdoor air. Using the PM2.5-mortality coefficient from the American Cancer Society (ACS) cohort study as an example, we developed a theoretical model to quantify the relationship between the published coefficient and one based on personal exposure, and explored how this adjusted coefficient might be applied to changes in indoor PM2.5 from outdoor sources. Using a probabilistic approach, our estimated average mortality coefficient for personal PM2.5 exposure is 30–50% greater than the ACS coefficient. However, since the indoor PM2.5 of outdoor origin accounts for only a proportion of the overall exposure, the average net adjustment required for indoor exposure is very modest. The results suggest that it is generally appropriate to apply unadjusted exposure-response functions derived from cohort studies to assess the health impact of changes in indoor particle concentrations from outdoor sources. However, it may be important to re-scale the coefficients for assessing exposures of population groups who spend a greater proportion of their time at home.

Fine particulate matter exposure and incidence of stroke: A cohort study in Hong Kong.

We aimed to assess the association of long-term residential exposure to fine particulate matter (PM) with aerodynamic diameter less than 2.5 μm (PM2.5) with the incidence of stroke and its major subtypes. We ascertained the first occurrence of emergency hospital admission for stroke in a Hong Kong Chinese cohort of 66,820 older people (65+ years) who enrolled during 1998-2001 (baseline) and were followed up to December 31, 2010. High-resolution (1 × 1 km) yearly mean concentrations of PM2.5 were predicted from local monitoring data and US National Aeronautics and Space Administration satellite data using linear regression. Baseline residential PM2.5 exposure was used as a proxy for long-term exposure. We used Cox proportional hazards to evaluate the risk of incident stroke associated with PM2.5 exposure adjusted for potential confounders, including individual and neighborhood factors. Over a mean follow-up of 9.4 years, we ascertained 6,733 cases of incident stroke, of which 3,526 (52.4%) were ischemic and 1,175 (17.5%) were hemorrhagic. The hazard ratio for every 10 μg/m3 higher PM2.5 concentration was statistically significant at 1.21 (95% confidence interval [CI] 1.04-1.41) for ischemic and non-statistically significant at 0.90 (95% CI 0.70-1.17) for hemorrhagic stroke in fully adjusted model 3. The estimates for ischemic stroke were higher in older participants (>70 years), less educated participants, and in men for current smokers. Long-term PM2.5 exposure was associated with higher risk of incident ischemic stroke, but the association with incident hemorrhagic stroke was less clear.

Daytime profile of residential PM2.5 concentrations in a ger, a traditional residence in Mongolia

Daytime profile of residential PM2.5 concentrations in a ger, a traditional residence in Mongolia

Investigation and modeling of the residential infiltration of fine particulate matter in Beijing, China

ABSTRACTThe objective of this study was to estimate the residential infiltration factor (Finf) of fine particulate matter (PM2.5) and to develop models to predict PM2.5 Finf in Beijing. Eighty-eight paired indoor–outdoor PM2.5 samples were collected by Teflon filters for seven consecutive days during both non-heating and heating seasons (from a total of 55 families between August, 2013 and February, 2014). The mass concentrations of PM2.5 were measured by gravimetric method, and elemental concentrations of sulfur in filter deposits were determined by energy-dispersive x-ray fluorescence (ED-XRF) spectrometry. PM2.5 Finf was estimated as the indoor/outdoor sulfur ratio. Multiple linear regression was used to construct Finf predicting models. The residential PM2.5 Finf in non-heating season (0.70 ± 0.21, median = 0.78, n = 43) was significantly greater than in heating season (0.54 ± 0.18, median = 0.52, n = 45, p < 0.001). Outdoor temperature, window width, frequency of window opening, and air conditioner use were the most important predictors during non-heating season, which could explain 57% variations across residences, while the outdoor temperature was the only predictor identified in heating season, which could explain 18% variations across residences. The substantial variations of PM2.5 Finf between seasons and among residences found in this study highlight the importance of incorporating Finf into exposure assessment in epidemiological studies of air pollution and human health in Beijing. The Finf predicting models developed in this study hold promise for incorporating PM2.5 Finf into large epidemiology studies, thereby reducing exposure misclassification.Implications: Failure to consider the differences between indoor and outdoor PM2.5 may contribute to exposure misclassification in epidemiological studies estimating exposure from a central site measurement. This study was conducted in Beijing to investigate residential PM2.5 infiltration factor and to develop a localized predictive model in both nonheating and heating seasons. High variations of PM2.5 infiltration factor between the two seasons and across homes within each season were found, highlighting the importance of including infiltration factor in the assessment of exposure to PM2.5 of outdoor origin in epidemiological studies. Localized predictive models for PM2.5 infiltration factor were also developed.

Residential Building PM2 .5 Pollution Control f rom a n Ergonomic a nd Energy Conservation Prospective

Residential Building PM2 .5 Pollution Control f rom a n Ergonomic a nd Energy Conservation Prospective

Residential home heating: The potential for air source heat pump technologies as an alternative to solid and liquid fuels

International commitments on greenhouse gases, renewables and air quality warrant consideration of alternative residential heating technologies. The residential sector in Ireland accounts for approximately 25% of primary energy demand with roughly half of primary home heating fuelled by oil and 11% by solid fuels. Displacing oil and solid fuel usage with air source heat pump (ASHP) technology could offer household cost savings, reductions in emissions, and reduced health impacts. An economic analysis estimates that 60% of homes using oil, have the potential to deliver savings in the region of €600 per annum when considering both running and annualised capital costs. Scenario analysis estimates that a grant of €2400 could increase the potential market uptake of oil users by up to 17% points, whilst a higher oil price, similar to 2013, could further increase uptake from heating oil users by 24% points. Under a combined oil-price and grant scenario, CO2 emissions reduce by over 4 million tonnes per annum and residential PM2.5 and NOX emissions from oil and peat reduce close to zero. Corresponding health and environmental benefits are estimated in the region of €100m per annum. Sensitivity analyses are presented assessing the impact of alternate discount rates and technology performance. This research confirms the potential for ASHP technology and identifies and informs policy design considerations with regard to oil price trends, access to capital, targeting of grants, and addressing transactions costs.

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 10μm exposure (PM2.5, PM10) was monitored on each examination day. At the child's residence, recent (same day up to 2days before) and chronic (365days before examination) exposures to PM2.5, 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 PM2.5 exposure. An interquartile range (IQR) increment in recent residential outdoor PM2.5 exposure was associated with an increase in average latency of 0.087s (SE: ±0.034; p=0.01) in the Pattern Comparison Test. Regarding chronic exposure at residence, an IQR increment of PM2.5 exposure was associated with slower performances in the Continuous Performance (9.45±3.47msec; p=0.007) and Stroop Tests (59.9±26.5msec; 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.

Carbon load in airway macrophages, a biomarker for traffic related air pollution. Repeated measurements over one year.

Introduction Carbon load in airway macrophages (AM) has been proposed as a biomarker of past long-term individual exposure to traffic-derived particulate matter (PM) air pollution. However, the repeatability of this measurement has not been formally assessed. This work was designed to study the kinetics of AM carbon over one year follow-up. Methods In 14 healthy non-smokers (aged 28 ± 5.7 years), having resided in Belgium for at least one year, we performed sputum induction to retrieve AM every 6 weeks and up to 8 times. Spirometry and blood and urine samples were also obtained. Carbon load was quantified by assessing the median area (µm2) occupied by black inclusions in 25 AM, using light microscopy and ImageJ. Average residential PM2.5 values were estimated for lags of 1 week, 1 month, 3 months, 6 months, and one year, based on interpolated levels of PM2.5 for each home address. The association of the median carbon content with previous PM2.5 levels and country of origin was calculated using mixed regression models. Results AM carbon was measured in 105 samples (94%). The mean (±SD) carbon content for 8 successive measurements amounted to 0.32 (±0.24), 0.29 (±0.25), 0.30 (±0.23), 0.26 (±0.19), 0.39 (±0.24), 0.37 (±0.22), 0.38 (±0.32), and 0.32 (±0.24) µm2. Daily PM2.5 values ranged from 2.8 to 70.8 µg/m3, with the highest median levels observed over one year lag (13 µg/m3; IQR=0.4). The individual median AM carbon was not associated with residential PM2.5. However, the median carbon load in the immigrants (n=7) was 0.26 µm2 higher (95% CI: 0.06-0.46) than in the locals (n=7). Conclusions Measurements of carbon load in AM proved to be stable over one year regardless of variations in air pollution. The unexpectedly large difference of carbon load between immigrants and locals suggests that AM carbon load reflects an exposure window even longer than one year.

Long-Term Exposure to Ambient Particulate Matter and Incident Stroke: Results from the Women’s Health Initiative

Introduction: Long-term exposure to ambient air pollution has been associated with risk of cerebrovascular events. However, cerebrovascular disease manifests in acute events with heterogeneous etiopathologies, not all of which are necessarily related to air pollution. Methods: We used Cox models to evaluate the association between long-term residential exposure to fine (PM2.5) and respirable (PM10) particulate matter and subtypes of incident cerebrovascular events among 146,802 post-menopausal women participating in the US Women’s Health Initiative (WHI) and free of cardiovascular disease at enrollment in 1993-1998. We estimated residential annual average PM2.5 and PM10 using national geostatistical models. All analyses were adjusted for age, race, smoking, BMI, high cholesterol, family history of stroke, alcohol consumption, physical activity, markers of individual and neighborhood socioeconomic status, study component, and WHI study region at enrollment. Results: Over a median follow-up time of 14.0 years, there were 4,089 hospitalized strokes (2,854 for ischemic stroke, 643 for hemorrhagic stroke) and 928 cerebrovascular deaths. Annual average PM2.5 levels at enrollment ranged from 3.0 to 23.7 μg/m3 with a mean ± SD of 14.1 ± 2.7 μg/m3. An interquartile range shift in PM2.5 (3.5 μg/m3) was associated with a hazard ratio (HR) of hospitalized stroke of 1.07 (95% CI: 1.03, 1.12). The data suggest a more pronounced association for hospitalized ischemic stroke (HR: 1.08; 95% CI: 1.03-1.13) than for hospitalized hemorrhagic stroke (HR: 1.03; 0.92-1.14) or cerebrovascular death (HR: 1.05; 95% CI: 0.97, 1.14). PM10 was not associated with any outcome. Conclusions: In this cohort of US post-menopausal women, long-term residential PM2.5 was associated with rates of hospitalized ischemic stroke. These results suggest that the association between particulate matter and cerebrovascular events may differ by both particulate matter size fraction and stroke etiology.

Eco-toxicological bioassay of atmospheric fine particulate matter (PM2.5) with Photobacterium Phosphoreum T3

A bioluminescent bacterium, Photobacterium phosphoreum T3 (PPT3), was used as a bio-indicator for the atmospheric fine particulate matter (PM2.5) to determine the eco-toxicity of PM2.5. The PM2.5 contains toxic chemicals, which reduce light output. The PM2.5 samples were collected in the period from March 2014 to January 2015 in Nanjing and analyzed for the chemical composition versus their eco-toxicity. The eco-toxicological responses of each toxicant were detected in PM2.5 samples with PPT3. The dose-response curves obtained were verified using the Weibull fitting function. According to the measured EC50 values (EC50, the concentration of a toxicant that inhibits 50% of the bioluminescence), the toxicity sequence was: B[a]P>hexa-PCB>tetra-PCB>tri-PCB>Pb2+>DEHP>Cu2+>DBP>BDE209>Zn2+>DMP>DEP, where B[a]P is benzo(a)pyrene, PCB is polychlorinated biphenyl, DEHP is diethylhexyl phthalate, DBP is dibutyl phthalate, BDE209 is decabromodiphenyl ether, DMP is dimethyl phthalate, and DEP is diethyl phthalate. All the PM2.5 samples analyzed proved to be weak toxic for PPT3. The toxicity of PM2.5 was assessed by the dose-addition of organic species and heavy metallic elements existing in PM2.5 with PPT3. The bioluminescence test showed that the metals and organics detected in PM2.5 promoted PM2.5 toxicity. The total detectable organics (denoted by ΣOrs) exhibited slightly higher toxicity than the total metals (denoted by ΣMs). In contrast, the sum of water-soluble ions (denoted by ΣIons) was beneficial to PPT3. The PM2.5 toxicity increased as the PM2.5 trapped more organics or metallic elements from the industrial or densely populated urban areas, where the PM2.5 had a high inhibition rate of bioluminescence for PPT3 in contrast to the residential PM2.5 samples, where the minimum inhibition rate was observed. The toxicity of PM2.5 samples varied with the mass concentrations, chemical constituents, and sampling locations. The chemicals in PM2.5, especially organic species and metallic elements, affected its eco-toxicity. These data provided good understanding of the atmospheric PM2.5 pollution in the large portion of the East China.

Association of long-term exposure to local industry- and traffic-specific particulate matter with arterial blood pressure and incident hypertension.

Long-term exposure to fine particulate matter (PM2.5) may lead to increased blood pressure (BP). The role of industry- and traffic-specific PM2.5 remains unclear. We investigated the associations of residential long-term source-specific PM2.5 exposure with arterial BP and incident hypertension in the population-based Heinz Nixdorf Recall cohort study. We defined hypertension as systolic BP≥140mmHg, or diastolic BP≥90mmHg, or current use of BP lowering medication. Long-term concentrations of PM2.5 from all local sources (PM2.5ALL), local industry (PM2.5IND) and traffic (PM2.5TRA) were modeled with a dispersion and chemistry transport model (EURAD-CTM) with a 1km(2) resolution. We performed a cross-sectional analysis with BP and prevalent hypertension at baseline, using linear and logistic regression, respectively, and a longitudinal analysis with incident hypertension at 5-year follow-up, using Poisson regression with robust variance estimation. We adjusted for age, sex, body mass index, lifestyle, education, and major road proximity. Change in BP (mmHg), odds ratio (OR) and relative risk (RR) for hypertension were calculated per 1μg/m(3) of exposure concentration. PM2.5ALL was highly correlated with PM2.5IND (Spearman's ρ=0.92) and moderately with PM2.5TRA (ρ=0.42). In adjusted cross-sectional analysis with 4539 participants, we found positive associations of PM2.5ALL with systolic (0.42 [95%-CI: 0.03, 0.80]) and diastolic (0.25 [0.04, 0.46]) BP. Higher, but less precise estimates were found for PM2.5IND (systolic: 0.55 [-0.05, 1.14]; diastolic: 0.35 [0.03, 0.67]) and PM2.5TRA (systolic: 0.88 [-1.55, 3.31]; diastolic: 0.41 [-0.91, 1.73]). We found crude positive association of PM2.5TRA with prevalence (OR 1.41 [1.10, 1.80]) and incidence of hypertension (RR 1.38 [1.03, 1.85]), attenuating after adjustment (OR 1.19 [0.90, 1.58] and RR 1.28 [0.94, 1.72]). We found no association of PM2.5ALL and PM2.5IND with hypertension. Long-term exposures to all-source and industry-specific PM2.5 were positively related to BP. We could not separate the effects of industry-specific PM2.5 from all-source PM2.5. Estimates with traffic-specific PM2.5 were generally higher but inconclusive.

Air pollution exposure and gestational diabetes mellitus among pregnant women in Massachusetts: a cohort study.

BackgroundRodent and human studies suggest an association between air pollution exposure and type 2 diabetes mellitus, but the extent to which air pollution is associated with gestational diabetes mellitus (GDM) is less clear.MethodsWe used the Massachusetts Registry of Vital Records to study primiparous women pregnant from 2003-2008 without pre-existing diabetes. We used satellite-based spatiotemporal models to estimate first and second trimester residential particulate (PM2.5) exposure and geographic information systems to estimate neighborhood traffic density. We obtained GDM status from birth records. We performed logistic regression analyses adjusted for sociodemographics on the full cohort and after stratification by maternal age and smoking habits.ResultsOf 159,373 women, 5,381 (3.4 %) developed GDM. Residential PM2.5 exposure ranged 1.3–19.3 μg/m3 over the second trimester. None of the exposures were associated with GDM in the full cohort [e.g. OR 0.99 (95 % CI: 0.95, 1.03) for each interquartile range (IQR) increment in second trimester PM2.5]. There were also no consistent associations after stratification by smoking habits. When the cohort was stratified by maternal age, women less than 20 years had 1.36 higher odds of GDM (95 % CI: 1.08, 1.70) for each IQR increment in second trimester PM2.5 exposure.ConclusionsAlthough we found no evidence of an association between air pollution exposure and GDM among all women in our study, greater exposure to PM2.5 during the second trimester was associated with GDM in the youngest age stratum.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0121-4) contains supplementary material, which is available to authorized users.

Prenatal and early life exposure to traffic pollution and cardiometabolic health in childhood.

Prenatal exposure to traffic pollution has been associated with faster infant weight gain, but implications for cardiometabolic health in later childhood are unknown. Among 1418 children in Project Viva, a Boston-area pre-birth cohort, we assessed anthropometric and biochemical parameters of cardiometabolic health in early (median age 3.3 years) and mid- (median age 7.7 years) childhood. We used spatiotemporal models to estimate prenatal and early life residential PM2.5 and black carbon exposure as well as traffic density and roadway proximity. We performed linear regression analyses adjusted for sociodemographics. Children whose mothers lived close to a major roadway at the time of delivery had higher markers of adverse cardiometabolic risk in early and mid-childhood. For example, total fat mass was 2.1 kg (95%CI: 0.8, 3.5) higher in mid-childhood for children of mothers who lived <50 m vs. ≥200 m from a major roadway. Black carbon exposure and traffic density were generally not associated with cardiometabolic parameters, and PM2.5 exposure during the year prior was paradoxically associated with improved cardiometabolic profile. Infants whose mothers lived close to a major roadway at the time of delivery may be at later risk for adverse cardiometabolic health.

Fine particulate air pollution and systemic autoimmune rheumatic disease in two Canadian provinces

ObjectiveTo estimate the degree to which fine particulate (PM2.5) air pollution is associated with systemic autoimmune rheumatic diseases (SARDs). MethodsWe used population-based administrative data from Alberta (1993–2007) and Quebec (1989–2011). SARD algorithms included ≥2 physician billing codes, or ≥1 rheumatology billing code, or ≥1 hospitalization diagnostic code (for systemic lupus, Sjogren's Syndrome, scleroderma, polymyositis, dermatomyositis, or undifferentiated connective tissue disease). Bayesian hierarchical latent class regression models estimated the probability that any given resident was a SARD case, based on the algorithms. Mean 2001–2006 residential ambient PM2.5 levels were assigned using satellite-derived data for dissemination area regions in Alberta and CLSC regions in Quebec. The sum of individual level probabilities provided the estimated total cases per region in each province, according to age, sex, urban-versus-rural residence, income, and PM2.5 levels. In Alberta, we ran separate models for First-Nations (FN) and non-First Nations subgroups. Bayesian logistic regression modeling generated odds ratio (OR) estimates for being a SARD case, accounting concurrently for demographics, as well as an interaction term between age and sex. ResultsOur data suggested that the probability of being a SARD case was higher among females versus males and for residents aged >45 versus younger, with the highest ORs for older females. Independently, the odds of being a SARDs case increased with PM2.5 levels in both provinces. ConclusionOur data suggest that PM2.5 exposure may be associated with an increased risk of SARDs.

Exposure to sub-chronic and long-term particulate air pollution and heart rate variability in an elderly cohort: the Normative Aging Study.

BackgroundShort-term particulate air pollution exposure is associated with reduced heart rate variability (HRV), a risk factor for cardiovascular morbidity and mortality, in many studies. Associations with sub-chronic or long-term exposures, however, have been sparsely investigated. We evaluated the effect of fine particulate matter (PM2.5) and black carbon (BC) exposures on HRV in an elderly cohort: the Normative Aging Study.MethodsWe measured power in high frequency (HF) and low frequency (LF), standard deviation of normal-to-normal intervals (SDNN), and the LF:HF ratio among participants from the Greater Boston area. Residential BC exposures for 540 men (1161 study visits, 2000–2011) were estimated using a spatio-temporal land use regression model, and residential PM2.5 exposures for 475 men (992 visits, 2003–2011) were modeled using a hybrid satellite based and land-use model. We evaluated associations between moving averages of sub-chronic (3–84 day) and long-term (1 year) pollutant exposure estimates and HRV parameters using linear mixed models.ResultsOne-standard deviation increases in sub-chronic, but not long-term, BC were associated with reduced HF, LF, and SDNN and an increased LF:HF ratio (e.g., 28 day BC: −2.3 % HF [95 % CI:−4.6, −0.02]). Sub-chronic and long-term PM2.5 showed evidence of relations to an increased LF and LF:HF ratio (e.g., 1 year PM: 21.0 % LF:HF [8.6, 34.8]), but not to HF or SDNN, though the effect estimates were very imprecise and mostly spanned the null.ConclusionsWe observed some evidence of a relation between longer-term BC and PM2.5 exposures and changes in HRV in an elderly cohort. While previous studies focused on short-term air pollution exposures, our results suggest that longer-term exposures may influence cardiac autonomic function.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-015-0074-z) contains supplementary material, which is available to authorized users.

Air pollution: 6.6million premature deaths in 2050!

Air pollution: 6.6million premature deaths in 2050!