Particulate Matter Air Pollution Exposure Research Articles

Ambient particulate matter air pollution exposure and ovarian cancer incidence in the USA: An ecological study.

To investigate associations between air particulate matter of ≤2.5 μm in diameter (PM2.5 ) and ovarian cancer. County-level ecological study. Surveillance, epidemiology, and end results from a collection of state-level cancer registries across 744 counties. Data from the Environmental Protection Agency's network for PM2.5 monitoring was used to calculate trailing 5- and 10-year PM2.5 county-level values. County-level data on demographic characteristics were obtained from the American Community Survey. A total of 98 751 patients with histologically confirmed ovarian cancer as a primary malignancy from 2000 to 2016. Generalised linear regression models were developed to estimate the association between PM2.5 and PM10 levels, over 5- and 10-year periods of exposure, and ovarian cancer risk, after accounting for county-level covariates. Risk ratios for associations between ovarian cancer (both overall and specifically epithelial ovarian cancer) and PM2.5 levels. For the 744 counties included, the average PM2.5 level from 1990 through 2018 was 11.75 μg/m3 (SD = 3.7) and the average PM10 level was 22.7 μg/m3 (SD = 5.7). After adjusting for county-level covariates, the overall annualised ovarian cancer incidence was significantly associated with increases in 5-year PM2.5 (RR = 1.11 per 10 units (μg/m3 ) increase, 95% CI 1.06-1.16). Similarly, when the analysis was limited to epithelial cell tumours and adjusted for county-level covariates there was a significant association with trailing 5-year PM2.5 exposure models (RR = 1.12 per 10 units increase, 95% CI 1.08-1.17). Likewise, 10-year PM2.5 exposure was associated with ovarian cancer overall and with epithelial ovarian cancer. Higher county-level ambient PM2.5 levels are associated with 5- and 10-year incidences of ovarian cancer, as measurable in an ecological study.

Socioeconomic and racial disparities in source-apportioned PM2.5 levels across urban areas in the contiguous US, 2010

Fine particulate matter (PM2.5) air pollution exposure is associated with short and long-term health effects. Several studies found differences in PM2.5 exposure associated with neighborhood racial and socioeconomic composition. However, most focused on total PM2.5 mass rather than its chemical components and their sources. In this study, we describe the ZIP code characteristics that drive the disparities in exposure to PM2.5 chemical components attributed to source categories both nationally and regionally. We obtained annual mean predictions of PM2.5 and fourteen of its chemical components from spatiotemporal models and socioeconomic and racial predictor variables from the 2010 US Census, and the American Community Survey 5-year estimates. We used non-negative matrix factorization to attribute the chemical components to five source categories. We fit generalized nonlinear models to assess the associations between the neighborhood predictors and each PM2.5 source category in urban areas in the United States in 2010 (n = 25,790 zip codes). We observed higher PM2.5 levels in ZIP codes with higher proportions of Black individuals and lower socioeconomic status. Racial exposure disparities were mainly attributed to Heavy Fuel, Oil and Industrial, Metal Processing Industry and Agricultural, and Motor Vehicle sources. Economic disparities were mainly attributed to Soil and Crustal Dust, Heavy Fuel Oil and Industrial, Metal Processing Industry and Agricultural, and Motor Vehicle sources. Upon further analysis through stratifying by regions within the United States, we found that the associations between ZIP code characteristics and source-attributed PM2.5 levels were generally greater in Western states. In conclusion, racial, socioeconomic, and geographic inequalities in exposure to PM2.5 and its components are driven by systematic differences in component sources that can inform air quality improvement strategies.

Fine particulate matter (PM2.5)-induced pulmonary oxidative stress contributes to increases in glucose intolerance and insulin resistance in a mouse model of circadian dyssynchrony

Results of human and animal studies independently suggest that either ambient fine particulate matter (PM2.5) air pollution exposure or a disturbed circadian rhythm (circadian dyssynchrony) are important contributing factors to the rapidly evolving type-2-diabetes (T2D) epidemic. The objective of this study is to investigate whether circadian dyssynchrony increases the susceptibility to PM2.5 and how PM2.5 affects metabolic health in circadian dyssynchrony. We examined systemic and organ-specific changes in glucose homeostasis and insulin sensitivity in mice maintained on a regular (12/12 h light/dark) or disrupted (18/6 h light/dark, light-induced circadian dyssynchrony, LICD) light cycle exposed to air or concentrated PM2.5 (CAP, 6 h/day, 30 days). Exposures during Zeitgeber ZT3–9 or ZT11–17 (Zeitgeber in circadian time, ZT0 = begin of light cycle) tested for time-of-day PM2.5 sensitivity (chronotoxicity). Mice transgenic for lung-specific overexpression of extracellular superoxide dismutase (ecSOD-Tg) were used to assess the contribution of CAP-induced pulmonary oxidative stress. Both, CAP exposure from ZT3–9 or ZT11–17, decreased glucose tolerance and insulin sensitivity in male mice with LICD, but not in female mice or in mice kept on a regular light cycle. Although changes in glucose homeostasis in CAP-exposed male mice with LICD were not associated with obesity, they were accompanied by white adipose tissue (WAT) inflammation, impaired insulin signaling in skeletal muscle and liver, and systemic and pulmonary oxidative stress. Preventing CAP-induced oxidative stress in the lungs mitigated the CAP-induced decrease in glucose tolerance and insulin sensitivity in LICD. Our results demonstrate that circadian dyssynchrony is a novel susceptibility state for PM2.5 and suggest that PM2.5 by inducing pulmonary oxidative stress increases glucose intolerance and insulin resistance in circadian dyssynchrony.

Fine Particulate Matter (PM2.5)-Induced Pulmonary Oxidative Stress Contributes to Changes in the Plasma Lipidome and Liver Transcriptome in Mice.

Fine particulate matter (PM2.5) air pollution exposure increases the cardiovascular disease risk. Although the specific mechanisms remain elusive, it is thought that PM2.5-induced oxidative stress and endothelial dysfunction contribute to this pathogenesis. Our previous findings indicate that PM2.5 impairs vascular health via a circulating factor and that plasma lipid changes contribute to the observed vascular effects. In the current study, we extend on these findings by further characterizing PM2.5-induced changes in circulating lipids and examining whether the observed changes were accompanied by related alterations in the liver transcriptome. To address the role of pulmonary oxidative stress, we exposed wild-type (WT) mice and mice that overexpress extracellular superoxide dismutase (ecSOD-Tg) in the lungs to concentrated ambient PM2.5 (CAP, 9 days). We found that CAP decreased circulating complex lipids and increased free fatty acids and acylcarnitines in WT, but not ecSOD-Tg mice. These plasma lipid changes were accompanied by transcriptional changes in genes that regulate lipid metabolism (e.g., upregulation of lipid biosynthesis, downregulation of mitochondrial/peroxisomal FA metabolism) in the liver. The CAP-induced changes in lipid homeostasis and liver transcriptome were accompanied by pulmonary but not hepatic oxidative stress and were largely absent in ecSOD-Tg mice. Our results suggest that PM2.5 impacts hepatic lipid metabolism; however, it remains unclear whether the transcriptional changes in the liver contribute to PM2.5-induced changes in plasma lipids. Regardless, PM2.5-induced changes in the plasma lipidome and hepatic transcriptome are, at least in part, mediated by pulmonary oxidative stress.

The potential involvement of inhaled iron (Fe) in the neurotoxic effects of ultrafine particulate matter air pollution exposure on brain development in mice

BackgroundAir pollution has been associated with neurodevelopmental disorders in epidemiological studies. In our studies in mice, developmental exposures to ambient ultrafine particulate (UFP) matter either postnatally or gestationally results in neurotoxic consequences that include brain metal dyshomeostasis, including significant increases in brain Fe. Since Fe is redox active and neurotoxic to brain in excess, this study examined the extent to which postnatal Fe inhalation exposure, might contribute to the observed neurotoxicity of UFPs. Mice were exposed to 1 µg/m3 Fe oxide nanoparticles alone, or in conjunction with sulfur dioxide (Fe (1 µg/m3) + SO2 (SO2 at 1.31 mg/m3, 500 ppb) from postnatal days 4–7 and 10–13 for 4 h/day.ResultsOverarching results included the observations that Fe + SO2 produced greater neurotoxicity than did Fe alone, that females appeared to show greater vulnerability to these exposures than did males, and that profiles of effects differed by sex. Consistent with metal dyshomeostasis, both Fe only and Fe + SO2 exposures altered correlations of Fe and of sulfur (S) with other metals in a sex and tissue-specific manner. Specifically, altered metal levels in lung, but particularly in frontal cortex were found, with reductions produced by Fe in females, but increases produced by Fe + SO2 in males. At PND14, marked changes in brain frontal cortex and striatal neurotransmitter systems were observed, particularly in response to combined Fe + SO2 as compared to Fe only, in glutamatergic and dopaminergic functions that were of opposite directions by sex. Changes in markers of trans-sulfuration in frontal cortex likewise differed in females as compared to males. Residual neurotransmitter changes were limited at PND60. Increases in serum glutathione and Il-1a were female-specific effects of combined Fe + SO2.ConclusionsCollectively, these findings suggest a role for the Fe contamination in air pollution in the observed neurotoxicity of ambient UFPs and that such involvement may be different by chemical mixture. Translation of such results to humans requires verification, and, if found, would suggest a need for regulation of Fe in air for public health protection.

Particulate matter air pollution exposure disrupts the Nrf2 pathway in sinonasal epithelium via epigenetic alterations in a murine model.

Particulate matter air pollution exposure disrupts the Nrf2 pathway in sinonasal epithelium via epigenetic alterations in a murine model.

Ultrafine particles, particle components and lung function at age 16years: The PIAMA birth cohort study.

Particulate matter (PM) air pollution exposure has been linked to lung function in adolescents, but little is known about the relevance of specific PM components and ultrafine particles (UFP). To investigate the associations of long-term exposure to PM elemental composition and UFP with lung function at age 16years. For 706 participants of a prospective Dutch birth cohort, we assessed associations of forced expiratory volume in 1s (FEV1) and forced vital capacity (FVC) at age 16 with average exposure to eight elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc) in PM2.5 and PM10, as well as UFP during the preceding years (age 13-16years) estimated by land-use regression models. After assessing associations for each pollutant individually using linear regression models with adjustment for potential confounders, independence of associations with different pollutants was assessed in two-pollutant models with PM mass and NO2, for which associations with lung function have been reported previously. We observed that for most PM elemental components higher exposure was associated with lower FEV1, especially PM10 sulfur [e.g. adjusted difference -2.23% (95% confidence interval (CI) -3.70 to -0.74%) per interquartile range (IQR) increase in PM10 sulfur]. The association with PM10 sulfur remained after adjusting for PM10 mass. Negative associations of exposure to UFP with both FEV1 and FVC were observed [-1.06% (95% CI: -2.08 to -0.03%) and -0.65% (95% CI: -1.53 to 0.23%), respectively per IQR increase in UFP], but did not persist in two-pollutant models with NO2 or PM2.5. Long-term exposure to sulfur in PM10 may result in lower FEV1 at age 16. There is no evidence for an independent effect of UFP exposure.

Abstract 11282: Meta-Analysis of Residential Portable Air Cleaner Use and Circulating Inflammatory Biomarkers

Introduction: Fine particulate matter air pollution (PM 2.5 ) exposure is associated with elevated circulating inflammatory biomarkers implicated in cardiovascular disease (CVD). Portable Air Cleaners (PAC)s reduce PM 2.5 exposure and may lower concentrations of inflammatory biomarkers. Methods: We performed a systematic review and meta-analysis of randomized crossover trials of in-home high efficiency particulate air (HEPA) PACs vs. sham control on changes in CRP, IL-6, and/or TNFα among adults with no smoking exposure using Medline, Embase, and Cochrane Central Register of Controlled Trials with the Ovid Platform, Inspec, Compendix, and Web of Science Core Collection. Two investigators (S.W, D.W.) independently screened and reviewed the studies. We used RevMan 5.3 to perform the meta-analysis. Results: Search results included 459 articles screened, 26 selected for full review, and 14 that met inclusion criteria, representing N=724 participants included in the meta-analysis. Ten studies reported CRP, 9 reported IL-6, and 5 reported TNFα. Based on WHO guidelines, 5 studies were in regions of extreme PM 2.5 exposure (>35 μg/m 3 ), 3 were high (10-35 μg/m 3 ), 3 were low (<10 μg/m 3 ), and 2 lacked baseline PM 2.5 . Median (± S.D.) duration of HEPA/sham use was 9 ± 6.6 days. Reductions in PM 2.5 ranged from 2.6 to 54.9 μg/m 3 (35-82%) and varied by baseline PM 2.5 , although reporting of baseline PM 2.5 was incomplete across trials. Compared to sham PAC use, active PACs were associated with a 7% lower CRP (95% CI -13%, 0%) and 12% lower IL-6 (-22%, -2%), P<0.05 for both (Figure). Subgroup analyses demonstrated consistency of effect of PACs across levels of baseline PM 2.5 . Conclusions: Our data demonstrate that PAC use is associated with significant reductions in circulating CRP and IL-6, with a magnitude of effect similar to clinical trials of statins and IL-1β inhibition. Given the role of inflammation in CVD, PACs may be useful to reduce systemic inflammation and cardiovascular risk.

Interaction between long-term coarse particulate matter exposure and physical activity in relation to overall and respiratory mortality in U.S. women

BACKGROUND AND AIM: Coarse particulate matter (PM2.5-10) air pollution exposure has been linked to respiratory health and increased mortality rates, while higher physical activity has been linked to decreased mortality rates. Increased respiration during physical activity may increase PM exposure, attenuating the benefits of physical activity. We examined the interaction between long-term residential exposure to PM2.5-10 and physical activity on overall and respiratory mortality rates. METHODS: Exposure to PM2.5-10 was assigned to each residential address using a spatio-temporal model and physical activity was reported on biennial questionnaires in the Nurses’ Health Study, a U.S. nationwide prospective cohort. We determined nonaccidental death and cause of death through searching the National Death Index. We followed 106,267 women between 1988 and 2008. We used Cox proportional hazards models to assess associations with each exposure separately and jointly, adjusted for demographics, diet, and individual- and area-level socioeconomic status. RESULTS:We observed 10,928 nonaccidental deaths, of which 918 were attributed to respiratory disease. In adjusted models, 24-month average ambient PM2.5-10 exposure per 10 μg/m3 increase was associated with modest increased risk of overall mortality (HR: 1.06, 95% CI: 1.01-1.11) and respiratory mortality (HR: 1.22, 95% CI: 1.05-1.42). Increasing overall physical activity per 9 metabolic equivalent of task-hours/week increase (based on meeting weekly physical activity recommendations) was associated with decreased risk of overall mortality (HR: 0.94, 95% CI: 0.94-0.95) and decreased risk of respiratory mortality (HR: 0.90, 95% CI: 0.88-0.91). We observed no interactions between PM2.5-10 exposure and physical activity. CONCLUSIONS:Exposure to PM2.5-10 was associated with increased risk of overall and respiratory mortality. Higher physical activity was associated with decreased overall and respiratory mortality; this association remained at all levels of PM2.5-10 experienced in this study, suggesting that the benefits of physical activity outweigh the negative impacts of air pollution exposures. KEYWORDS: air pollution, particulate matter, long-term exposure, respiratory outcomes, mortality

The Benefits of Intensive Versus Standard Blood Pressure Treatment According to Fine Particulate Matter Air Pollution Exposure: A Post Hoc Analysis of SPRINT.

Fine particulate matter <2.5 µm (PM2.5) air pollution is implicated in global mortality, especially from cardiovascular causes. A large body of evidence suggests a link between PM2.5 and elevation in blood pressure (BP), with the latter implicated as a potential mediator of cardiovascular events. We sought to determine if the outcomes of intensive BP lowering (systolic BP <120 mm Hg) on cardiovascular events are modified by PM2.5 exposure in the SPRINT (Systolic BP Intervention Trial). We linked annual PM2.5 exposure estimates derived from an integrated model to subjects participating in SPRINT. We evaluated the effect of intensive BP lowering by PM2.5 exposure on the primary outcome in SPRINT using cox-proportional hazard models. A total of 9286 participants were linked to PM2.5 levels (mean age 68±9 years). Intensive BP-lowering decreased risk of the primary outcome more among patients exposed to higher PM2.5 (Pinteraction=0.047). The estimate for lowering of primary outcome was numerically lower in the highest than in the lower quintiles. The benefits of intensive BP-lowering were larger among patients chronically exposed to PM2.5 levels above US National Ambient Air Quality Standards of 12 µg/m3 (hazard ratio, 0.47 [95% CI, 0.29-0.74]) compared with those living in cleaner locations (hazard ratio, 0.81 [95% CI, 0.68-0.97]), Pinteraction=0.037. This exploratory nonprespecified post hoc analysis of SPRINT suggests that the benefits of intensive BP lowering on the primary outcome was greater in patients exposed to higher PM2.5, suggesting that the magnitude of benefit may depend upon the magnitude of antecedent PM2.5 exposure.

Trace element concentrations in ambient air as a function of distance from road

ABSTRACT Traffic-related air pollution is associated with various adverse health effects. In the absence of more complicated exposure assessment techniques, many environmental health studies have used the natural logarithm of distance to road as a proxy for traffic-related exposures. However, research validating this proxy and further explaining the spatial patterns and elemental composition of traffic-related particulate matter air pollution remains limited. In this study, we collected air samples using a mobile particle concentrator that allowed for high sample loading from major roadways in the Greater Boston Area. We found that concentrations of Cl, Ti, V, Cr, Mn, Fe, Co, Cu, Zn, Sr, Zr, Sn, Ba, and Pb were significantly associated with the natural logarithm of distance to road in coarse particulate matter, and total fine particulate mass concentrations of Al, Ca, Ti, Cr, Mn, Fe, Cu, and Zn were significantly associated with natural logarithm of distance to road in fine particulate matter. Road type (A1 or A2 [primary roads or highways] versus A3 [secondary and connecting roads]) was not a significant predictor of any traffic-related elements in particulate matter air pollution. Our results help identify traffic-related elements in particulate matter air pollution and support the use of logarithm of distance to road as a proxy for traffic-related particulate matter air pollution exposure assessment in epidemiological studies.

Correction to: Personal-Level Protective Actions Against Particulate Matter Air Pollution Exposure

Correction to: Personal-Level Protective Actions Against Particulate Matter Air Pollution Exposure

Selective memory and behavioral alterations after ambient ultrafine particulate matter exposure in aged 3xTgAD Alzheimer\u2019s disease mice

BackgroundA growing body of epidemiological literature indicates that particulate matter (PM) air pollution exposure is associated with elevated Alzheimer’s disease (AD) risk and may exacerbate AD-related cognitive decline. Of concern is exposure to the ultrafine PM (UFP) fraction (≤100 nm), which deposits efficiently throughout the respiratory tract, has higher rates of translocation to secondary organs, like brain, and may induce inflammatory changes. We, therefore, hypothesize that exposure to UFPs will exacerbate cognitive deficits in a mouse model of AD. The present study assessed alterations in learning and memory behaviors in aged (12.5 months) male 3xTgAD and non-transgenic mice following a 2-week exposure (4-h/day, 4 days/week) to concentrated ambient UFPs using the Harvard ultrafine concentrated ambient particle system (HUCAPS) or filtered air. Beginning one month following exposure, locomotor activity, spatial learning and memory, short-term recognition memory, appetitive motivation, and olfactory discrimination were assessed.ResultsNo effects on locomotor activity were found following HUCAPS exposure (number concentration, 1 × 104–4.7 × 105 particles/cm3; mass concentration, 29–132 μg/m3). HUCAPS-exposed mice, independent of AD background, showed a significantly decreased spatial learning, mediated through reference memory deficits, as well as short-term memory deficits in novel object recognition testing. AD mice displayed diminished spatial working memory, potentially a result of olfactory deficits, and short-term memory. AD background modulated HUCAPS-induced changes on appetitive motivation and olfactory discrimination, specifically enhancing olfactory discrimination in NTg mice. Modeling variation in appetitive motivation as a covariate in spatial learning and memory, however, did not support the conclusion that differences in motivation significantly underlie changes in spatial learning and memory.ConclusionsA short-term inhalation exposure of aged mice to ambient UFPs at human-relevant concentrations resulted in protracted (testing spanning 1–6.5 months post-exposure) adverse effects on multiple memory domains (reference and short-term memory) independent of AD background. Impairments in learning and memory were present when accounting for potential covariates like motivational changes and locomotor activity. These results highlight the need for further research into the potential mechanisms underlying the cognitive effects of UFP exposure in adulthood.

High-throughput, semi-automated dithiothreitol (DTT) assays for oxidative potential of fine particulate matter

Fine particulate matter (PM2.5) air pollution exposure is a leading risk factor for adverse health outcomes, including cardiovascular and respiratory morbidity, and premature mortality. Quantification of PM2.5 oxidative potential (i.e., the ability of PM to promote oxidative reactions in solution) is a relatively new paradigm for exploring health risks associated with the various chemical compositions of ambient PM2.5. PM2.5 oxidative potential is commonly measured with the dithiothreitol (DTT) assay, where the DTT loss rate is measured when mixed with a PM2.5 sample extract. However, the DTT assay is time consuming and laborious, with only a few reported automation attempts. We introduce and evaluate a semi-automated DTT assay using a traditional HPLC combined with either UV/vis absorbance or electrochemical detection that has comparable accuracy and sensitivity to manual approaches. Commercial and custom-made electrochemical detectors are also compared before measuring ambient PM2.5 filter samples. The optimized, semi-automated assay can process six samples per hour (an 83% time savings compared to manual analysis). Cost becomes significant for large-scale studies and was also considered; electrochemical detection saved 40% on consumables cost compared to UV/vis detection. The presented liquid-handling automation can be applied to a variety of autosamplers in other laboratories for DTT assay semi-automation.

Children’s microvascular traits and air pollution exposure

TPS 671: Cardiometabolic effects of long-term air pollution exposure, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background:Particulate matter air pollution exposure during in utero development may entail adverse health outcomes later in life. The microvasculature undergoes extensive, organ-specific prenatal maturation. There is a growing body of evidence that cardiovascular disease in adulthood is rooted in a dysfunctional fetal and perinatal development, in particular that of the microcirculation. Objectives: We investigate whether prenatal or postnatal exposure to PM2.5 or NO2 air pollution is related to microvascular traits in children at the age of four. Methods: In young children (mean age 4.6 ± 0.4), followed longitudinally within the ENVIRONAGE birth cohort, we measured the retinal microvascular diameters, the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE), and the curvature of the vessel system by means of the tortuosity index (TI). We modelled prenatal and postnatal PM2.5 (particulate matter with a diameter ≤ 2.5 µm) and NO2 exposure levels for each mother’s home address using a high resolution spatiotemporal model. Results: An interquartile range (IQR) increase in prenatal PM2.5 exposure was associated with a 3.64 µm (95% CI: -0.07 to 7.41; p = 0.05), increase in CRVE and a 2.83 µm (95% CI: 0.05 to 5.61; p = 0.05) higher CRAE. Prenatal NO2 exposure was also associated with a widening of both the CRVE and CRAE. In addition, an augmented TI was observed in association with prenatal NO2 exposure. For postnatal exposure, we observe a short-term exposure effect of PM2.5 on the CRAE and a life-time exposure effect of NO2 on the CRAE, CRVE and TI. Conclusions: Our results link both prenatal and postnatal particulate matter air pollution exposure with changes in children’s microvascular traits as a fundamental novel mechanism to explain the developmental origin of cardiovascular disease by ambient air pollution.

Application of the Navigation Guide systematic review methodology and meta-analysis to evaluate the association between prenatal particulate matter air pollution exposure and birth weight

TPS 642: Environmental justice and impacts, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background: Case-control and cohort studies have demonstrated a positive association between prenatal exposure to particulate matter (PM) air pollution and low birth weight (LBW). Previous systematic reviews and meta-analyses report varying effect sizes and significant heterogeneity between studies. The considerable variation in study outcomes reflects methodological differences employed across studies. Objective: The objective of this study was to determine how developmental exposure to ambient particulate air pollution affects birth weight using the Navigation Guide systematic review methodology. Methods: We developed a study protocol and established a criteria to identify the relevant studies. Further, we determined the risk of bias for each study, conducted a quality of evidence and strength of evidence assessment, as well as a meta-analysis across all studies. Results: Forty-three studies met our inclusion criteria. We rated studies generally with low to probably-low risk of bias; however, several studies we judged as high or probably-high risk in the confounding and exposure characterization domains. Based on the meta-analysis, for every 10 µg/m3 increase in particulate matter, a decrease in birth weight was almost always negative. The strength of evidence assessment, for PM2.5, revealed “limited evidence of toxicity” for reducing birth weight when exposure is in the third trimester; for other exposure windows, the evidence is inadequate. For PM10, there is “limited evidence of toxicity” for reducing birth weight when exposure is in the third trimester and during the entire pregnancy; however, the evidence is “inadequate” for other exposure windows. For coarse PM (PM2.5-10), there is “inadequate evidence of toxicity” for reducing birth weight for all exposure windows. Conclusion: While sufficient evidence supports an association between prenatal exposure to ambient particulate matter and low birth weight, the estimated effect depends significantly on study design. Standardizing exposure characterization techniques could help reduce the variation in outcomes.

Effects of short-term exposure to particulate matter air pollution on cognitive performance

This paper assesses the effect of short-term exposure to particulate matter (PM) air pollution on human cognitive performance via a double cross over experimental design. Two distinct experiments were performed, both of which exposed subjects to low and high concentrations of PM. Firstly, subjects completed a series of cognitive tests after being exposed to low ambient indoor PM concentrations and elevated PM concentrations generated via candle burning, which is a well-known source of PM. Secondly, a different cohort underwent cognitive tests after being exposed to low ambient indoor PM concentrations and elevated ambient outdoor PM concentrations via commuting on or next to roads. Three tests were used to assess cognitive performance: Mini-Mental State Examination (MMSE), the Stroop Color and Word test, and Ruff 2 & 7 test. The results from the MMSE test showed a statistically robust decline in cognitive function after exposure to both the candle burning and outdoor commuting compared to ambient indoor conditions. The similarity in the results between the two experiments suggests that PM exposure is the cause of the short-term cognitive decline observed in both. The outdoor commuting experiment also showed a statistically significant short-term cognitive decline in automatic detection speed from the Ruff 2 and 7 selective attention test. The other cognitive tests, for both the candle and commuting experiments, showed no statistically significant difference between the high and low PM exposure conditions. The findings from this study are potentially far reaching; they suggest that elevated PM pollution levels significantly affect short term cognition. This implies average human cognitive ability will vary from city to city and country to country as a function of PM air pollution exposure.

Inequity in consumption of goods and services adds to racial–ethnic disparities in air pollution exposure

Fine particulate matter (PM2.5) air pollution exposure is the largest environmental health risk factor in the United States. Here, we link PM2.5 exposure to the human activities responsible for PM2.5 pollution. We use these results to explore "pollution inequity": the difference between the environmental health damage caused by a racial-ethnic group and the damage that group experiences. We show that, in the United States, PM2.5 exposure is disproportionately caused by consumption of goods and services mainly by the non-Hispanic white majority, but disproportionately inhaled by black and Hispanic minorities. On average, non-Hispanic whites experience a "pollution advantage": They experience ∼17% less air pollution exposure than is caused by their consumption. Blacks and Hispanics on average bear a "pollution burden" of 56% and 63% excess exposure, respectively, relative to the exposure caused by their consumption. The total disparity is caused as much by how much people consume as by how much pollution they breathe. Differences in the types of goods and services consumed by each group are less important. PM2.5 exposures declined ∼50% during 2002-2015 for all three racial-ethnic groups, but pollution inequity has remained high.

AMBIENT AIR POLLUTION ASSOCIATES WITH ARTERIAL INFLAMMATION: POSSIBLE MEDIATION OF CARDIOVASCULAR DISEASE RISK

Particulate matter (PM) air pollution exposure associates with MACE. We hypothesized that: 1) PM associates with higher arterial wall inflammation (ArtI) and 2) higher ArtI mediates the association between PM and MACE. Individuals (N=477, median age (IQR): 55 (44-66) years, 42% male) without

Pervasive Developmental Disorder and Particulate Matter Air Pollution before, during and after Pregnancy: A Case-Cohort Study within the National Infant Medical Check-Up Cohort

Background: There is increasing interest in the effect of air pollution in children&amp;#8217;s neurodevelopment but the evidence remains inconclusive. This study investigated the association of particulate matter air pollution exposure and pervasive developmental disorder(PDD) throughout the first 6 years of life.Methods: We conducted a case-cohort study of participants born in Korea in the year of 2008 who underwent at least the first medical check-up provided by The National Health Insurance Database until December 31, 2013. The study assessed all 761 subjects who were diagnosed with PDD till the age of six along with a subcohort of six times of that size, 5,178 subjects, selected as a 2.5% random sample of the full target cohort. Diagnosis of PDD was based on the payment and treatment data at the clinic. Daily averages of PM with diameters &amp;#8804; 2.5 &amp;#956;m (PM2.5) and &amp;#8804; 10 &amp;#956;m (PM10) were predicted from a spatiotemporal model for South Korea and linked to residential addresses. A weighted Cox proportional hazards model was used to estimate adjusted hazard ratio (aHR) with 95% confidence intervals (CI) for PDD in infants exposed to particulate matter air pollution.Results: A significant association was found between 10 &amp;#956;g/m3 increment in the PM2.5 concentration and PDD with adjusted RR of 1.12 (95% CI 1.04-1.20) among the participants with the same address before and after pregnancy. Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and when all periods were included, whereas the association with the 9 months of pregnancy remained. The association between PDD and PM2.5 was stronger for exposure during the third trimester (OR &amp;#61; 1.32 per IQR increase in PM2.5; 95% CI: 1.16, 1.49) than during the first two. There was little association between PM10 and PDD.Conclusions: The results suggest higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with the risk of developing PDD.