Effects Of Particulate Air Pollution Research Articles

Particulate matter and bioactive lipid mediators: Insights into the mechanisms of the cardiovascular effects of particulate air pollution

Particulate matter and bioactive lipid mediators: Insights into the mechanisms of the cardiovascular effects of particulate air pollution

Assessing long-term effects of gaseous air pollution exposure on mortality in the United States using a variant of difference-in-differences analysis

Long-term mortality effects of particulate air pollution have been investigated in a causal analytic frame, while causal evidence for associations with gaseous air pollutants remains extensively lacking, especially for carbon monoxide (CO) and sulfur dioxide (SO2). In this study, we estimated the causal relationship of long-term exposure to nitrogen dioxide (NO2), CO, SO2, and ozone (O3) with mortality. Utilizing the data from National Morbidity, Mortality, and Air Pollution Study, we applied a variant of difference-in-differences (DID) method with conditional Poisson regression and generalized weighted quantile sum regression (gWQS) to investigate the independent and joint effects. Independent exposures to NO2, CO, and SO2 were causally associated with increased risks of total, nonaccidental, and cardiovascular mortality, while no evident associations with O3 were identified in the entire population. In gWQS analyses, an interquartile range-equivalent increase in mixture exposure was associated with a relative risk of 1.067 (95% confidence interval: 1.010–1.126) for total mortality, 1.067 (1.009–1.128) for nonaccidental mortality, and 1.125 (1.060–1.193) for cardiovascular mortality, where NO2 was identified as the most significant contributor to the overall effect. This nationwide DID analysis provided causal evidence for independent and combined effects of NO2, CO, SO2, and O3 on increased mortality risks among the US general population.

Comparison of Air Pollution-Mortality Associations Using Observed Particulate Matter Concentrations and Reanalysis Data in 33 Spanish Cities.

Air pollution poses a health hazard in all countries. However, complete data on ambient particulate matter (PM) concentrations are not available in all world regions. Reanalysis data is already a valuable source of exposure data in epidemiological studies examining the relationship between temperature and health. Nevertheless, the performance of reanalysis data in assessing the short-term health effects of particulate air pollution remains unclear. We assessed the performance of CAMS reanalysis (EAC4) data from the European Centre for Medium-Range Weather Forecasts, compared with daily PM concentrations from field monitoring stations, to estimate short-term exposure to PM with an aerodynamic diameter less than 10 μm (PM10) on daily mortality in 33 Spanish provincial capital cities using a two-stage time series regression design. The shape of the PM10 distribution varied substantially between PM observations and CAMS global reanalysis of atmospheric composition (EAC4) reanalysis data, with correlation ranging from 0.21 to 0.58. The pooled mortality risk for a 10 μg/m3 increase in PM10 showed similar estimates using PM concentrations {relative risks (RR) = 1.007, 95% confidence intervals (95% CI) = [1.002, 1.011]} and EAC4 reanalysis data (RR = 1.011, 95% CI = [1.006, 1.015]). However, the city-specific PM10 beta coefficients estimated using PM concentrations and EAC4 reanalysis data showed a low correlation (r = 0.22). The use of reanalysis data should be approached with caution when assessing the association between particulate matter air pollution and health outcomes, particularly in cities with small populations.

Association between Ambient Particulate Air Pollution and Soluble Biomarkers of Endothelial Function: A Meta-Analysis.

The burden of cardiovascular diseases caused by ambient particulate air pollution is universal. An increasing number of studies have investigated the potential effects of exposure to particulate air pollution on endothelial function, which is one of the important mechanisms for the onset and development of cardiovascular disease. However, no previous study has conducted a summary analysis of the potential effects of particulate air pollution on endothelial function. To summarize the evidence for the potential effects of short-term exposure to ambient particulate air pollution on endothelial function based on existing studies. A systematic literature search on the relationship between ambient particulate air pollution and biomarkers of endothelial function including endothelin-1 (ET-1), E-selectin, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) was conducted in PubMed, Scopus, EMBASE, and Web of Science up to 20 May 2023. Subsequently, a meta-analysis was conducted using a random effects model. A total of 18 studies were included in this meta-analysis. A 10 μg/m3 increase in short-term exposure to ambient PM2.5 was associated with a 1.55% (95% CI: 0.89%, 2.22%) increase in ICAM-1 and a 1.97% (95% CI: 0.86%, 3.08%) increase in VCAM-1. The associations of ET-1 (0.22%, 95% CI: -4.94%, 5.65%) and E-selectin (3.21%, 95% CI: -0.90% 7.49%) with short-term exposure to ambient PM2.5 were statistically insignificant. Short-term exposure to ambient PM2.5 pollution may significantly increase the levels of typical markers of endothelial function, including ICAM-1 and VCAM-1, suggesting potential endothelial dysfunction following ambient air pollution exposure.

Partiküler Hava Kirliliğinin Bebek Ölümlerine Kısa Dönemdeki Etkisi: 2018-2020 Yılları Ankara İli Örneği

Background: Today, nine out of 10 people on a global scale live in an air pollution environment above the limit values determined. It is predicted that particulate air pollution is a risk factor for 5.3% of deaths under the age of one in Türkiye. In order to examine the causes of infant deaths and take necessary precautions, it is important to investigate air pollution and the possibilities of infant death due to. Aims: This study was carried out to examine the relationship between Particulate Matter (PM) 2.5 and (PM)10 levels observed in Ankara between the years 2018-2020 and infant deaths that occurred at that time. Methods: To examine the relationship poisson regression model, in which the terms formed by the flexible cubic spline function, were mainly used. The effect of each 10 μg/m3 increase in PM2.5 and PM10 on infant mortality, taking into account lags of up to seven days by adjusting for seasonal trends and air temperature effects, was determined by relative risk (RR) and 95% confidence intervals (CI) analyzed by calculation. Results: In the evaluated period, 1295 infant deaths occurred in 754 of 1096 days. The three-year average of the daily average PM2.5 and PM10 levels detected in Ankara is above the limit values. Conclusion: The effect of particulate air pollution on infant mortality in the first week was not detected, this relationship may become detectable when different variables such as possible effect modifiers are included in the models applied. The subject should also be examined under such different conditions.

57 Particles in Outdoor Air: are they all Equal?

Abstract Statement from the Committee on the Medical Effects of Air Pollutants (COMEAP) on the differential toxicity of particulate matter according to source or constituents Particulate matter in outdoor air comes from a wide range of different sources and contains many different chemical components. Understanding which of these sources and components are particularly harmful would help to focus policies and interventions to reduce impacts on health. COMEAP recently (July 2022) published an updated statement on this topic, drawing on recent reviews of the available evidence. It noted that particulate matter, and constituents of particulate matter, associated with combustion and road traffic have received the most research attention. However, there was insufficient coherence in the epidemiological evidence to conclude that these sources of particulate matter play a significantly greater role in the health effects of particulate air pollution than other sources or constituents. A comprehensive review of the evidence reveals that toxicity has been attributed to a wide variety of constituents and sources, possibly acting by a number of different mechanisms. However, the complexity of sources, sizes and chemical composition of particulate matter makes it extremely difficult to identify which characteristics of particles might make them less harmful or more toxic than others. Future research assessing the influence of chemical composition of particulate matter should offer greater insights into toxicity. But, at present, PM2.5 (the mass concentration of fine particulate matter in air) remains the most suitable metric for evaluating health impacts and regulating particulate air pollution.

19 Does Developmental Status and age of the Lung Influence the Hazard Elicited by Exposure to Both Indoor and Outdoor Pollutants?

Abstract Many in vitro studies that focus upon lung toxicology use models that assume, or are specifically based upon adult lung structure, function, and physiology. Yet, the most vulnerable groups of the human population (i.e., young, elderly, and diseased) have an altered lung structure and function. Notably, the developing lung (in utero) and infant lungs exhibit notable differences in term of cell type, number, ratio, organ size and surface area. Recent work has identified the detrimental implications of being exposed to AP while the lung is developing. To elucidate the mechanisms associated with AP exposure to the developing lung, the aim of this study will create and characterise an in vitro model of the foetal human bronchial region composed of cells physiologically appropriate to various stages of development, as well as an older child’s airway, notably the developing alveoli. This will allow us to determine the developmental effects of air pollution particles at an air-liquid interface (ALI) utilising a physiologically relevant aerosol exposure and standardised particulate aiming to mimic indoor and outdoor air pollution. For this work, a global approach will be utilised to determine up and down regulation of various pathways associated with both development and exposure to AP. A further aim will include comparison with an “adult” lung to analysis the potential developmental implications exposure to AP may illicit. This project is funded by the recently initiated RESPIRE project (NE/W002264/1), as part of the SPF Clean Air Programme.

The acute effects of particulate air pollution on lung function in asthmatic children: A multicenter study with intensively repeated measurements

Evidence on the comparative effects of fine particulate matter (PM2.5) and coarse particulate matter (PM10-2.5) on the lung function of asthmatic children remained limited and inconsistent. This study aims to explore the acute effect of PM2.5 and PM10-2.5 on dynamic forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) among asthmatic children. We conducted a multicenter study and obtained intensively repeated measurements of FEV1 and PEF of clinically diagnosed asthmatic children in 89 Chinese cities from January 2017 to May 2021. Linear mixed-effects models combined with a polynomial distributed lag model were employed to evaluate the cumulative lag effect of PM2.5 and PM10-2.5 on daily FEV1 and PEF among asthmatic children. We also evaluated the effect modifications by sex, age, testing time, season, and region. A total of 590 clinically diagnosed asthmatic children with over 0.18 million dynamic lung function records were included in this study. The adverse effect of particulate matter on lung function occurred in a short term and could last for around one week. Specifically, both PM10-2.5 and PM2.5 were associated with decreases in PEF, but only PM10-2.5 could impair the measurements of FEV1. We found that an interquartile range increase in PM10-2.5 and PM2.5 were associated with 5.40 [95% confidence interval (CI): 0.88, 9.92] mL/s and 10.48 (95%CI: 5.14, 15.81) mL/s decrease in PEF, 6.46 (95%CI: 4.53, 8.40) mL and 0.25 (95%CI: −2.03, 2.54) mL decreases in FEV1, respectively. And the estimated effect of PM10-2.5 was stronger than PM2.5 on FEV1. Besides, these changes were larger in the evening and the south region of China. In conclusion, short-term exposure to both PM2.5 and PM10-2.5 could decrease the daily lung function of asthmatic children. The impact of PM10-2.5 was more hazardous than PM2.5.

Particulate Air Pollution and Primary Care Visits in Kosovo: A Time-Series Approach.

This study aimed to investigate the effects of particulate air pollution (PM2.5) on cardiovascular and respiratory diseases in Pristina, Kosovo, in a time-series analysis using daily primary healthcare visits to primary care institutions from 2019 to 2022. For the observation period, 6440 cardiovascular and 15,141 respiratory visits were reported, whereas the daily mean concentrations of PM2.5 ranged between 2.41 and 120.3 µg/m3. Single-lag models indicated a bi-phasic lag structure with increasing effect estimates some days after the air pollution event. In the distributed lag model with seven lags, the effect estimates for the cardiovascular cases indicated the adverse effect of air pollution. The cumulative effect estimate (summed over lag 0 to 6) for an increase of 10 µg/m3 of PM2.5 was a relative risk of 1.010 (95% confidence interval: 1.001-1.019). For respiratory cases, a different lag model (lag 4 through 10) was additionally examined. In this model, significant increases in visits were observed on lags 7 and 8. Overall, no relevant increase in visits occurred during the seven days considered. Visits to general practitioners will often not occur immediately at disease onset because patients will wait, hoping that their health status improves spontaneously. Therefore, we expected some latency in the effects.

Residential greenness and risk of incident dementia: A prospective study of 375,342 participants

IntroductionIncorporation of greenspace may be a novel environmental policy that might result in positive health effects; hence, this study aimed to investigate the association between residential greenness and dementia incidence. The effects of particulate air pollution on mediating dementia were also determined. MethodsA prospective cohort study involving 375,342 UK biobank participants was conducted, in which Cox regression models were used to determine the association of greenspace exposure with the risks of all-cause dementia (ACD), Alzheimer's disease (AD) and vascular dementia (VD). Sociodemographic variables, lifestyle or dietary characteristics and apolipoprotein E4 status were controlled using two levels of adjusted models. Mediation analyses were performed to determine the mediation effects of PMs. ResultsThe results indicated that there were 4929 ACD, 2132 AD, and 1184 VD incidents throughout the 8-year study. In the multi-adjusted model, each interquartile increment in greenspace (buffer 300m) conferred the lower risks of ACD (HR = 0.968, 95% confidence intervals [CI]: 0.938–1.000]) and VD (HR = 0.926, 95% CI: 0.867–0.989). The fourth greenspace quartile conferred also reduced risks of ACD (HR = 0.891, 95% CI: 0.804–0.989) and VD (HR = 0.778, 95% CI: 0.630–0.960) in reference to the first quartile. With regard to 1000m catchment, each interquartile increment conferred a 5.0% (95% CI: 1.8–8.1) lower risk of ACD, and the fourth greenspace quartile conferred a 10.9% (95% CI: 0.9–19.8) lower risk of ACD compared to the first quartile. The protective effect of greenness might be mediated based on the reduction of PM2.5 and PM10 (Pindirect effect<0.05). ConclusionsIncreasing greenness reduces the risk of dementia. This study suggests that greenspace is an environmental strategy that helps prevent dementia.

Size-segregated particle number concentrations and outpatient-department visits for pediatric respiratory diseases in Shanghai, China

BackgroundFew studies have simultaneously explored which size of particles has the greatest impact on the risk for pediatric asthma, bronchitis and upper respiratory tract infections (URTIs). ObjectivesTo investigate the short-term association between size-segregated particle number concentrations (PNCs) and outpatient-department visits (ODVs) for major pediatric respiratory diseases. MethodsDaily counts of pediatric ODVs for asthma, bronchitis and URTIs were obtained from 66 hospitals in Shanghai, China, from 2016 to 2018. Pollutant effects were estimated using Poisson generalized additive models combined with polynomial distributed lag models. We also fitted co-pollutant cumulative effects models included six criteria air pollutants and conducted stratifying analyses by gender, age, season and geographic distances. ResultsWe identified a total of 430,103 patients with asthma, 1,547,013 patients with bronchitis, and 2,155,738 patients with URTIs from the hospitals. Effect estimates increased with decreasing particle size. Ultrafine particle (UFP) and PNCs of 0.10–0.40 µm particles (PNC0.10–0.40) were associated with increased ODVs for asthma, bronchitis and URTIs at cumulative lags up to 3d. Associations tended to appear stable after adjusting for criteria air pollutants. At the cumulative lag 0–2d, each interquartile range increase in UFP was associated with increased ODVs due to asthma (relative risk 1.21, 95% CI: 1.07, 1.38), bronchitis (1.20, 95% CI: 1.07, 1.34) and URTI (1.17, 95% CI: 1.06, 1.30), whereas the associations for PNC0.10–0.40 remained significant but attenuated in magnitude. ConclusionsUFP may be a leading contributor to the adverse respiratory effects of particulate air pollution and the effects increased with decreasing particle size.

Air Pollution in Kosovo: Short Term Effects on Hospital Visits of Children Due to Respiratory Health Diagnoses.

The Republic of Kosovo is a small country in the Balkans. The capital city of Pristina hosts most of its population and is situated in a mountain basin with poor air exchange, especially during winter. Domestic heating, road transport, industry and coal-fired power plants contribute to high levels of air pollution. We performed a time-series analysis on effects of particulate air pollution (PM2.5) on respiratory health of children and adolescents, using hospital admission and ambulatory visit numbers from the pediatric university clinic. From 2018 until 2020, daily mean concentrations of PM2.5 ranged between 2.41 and 161.03 µg/m³. On average, there were 6.7 ambulatory visits per day with lower numbers on weekends and during the first COVID-19 wave in 2020. An increase in PM2.5 led to an immediate increase in visit numbers that lasted over several days. Averaged over a full week, this amounted to about a 1% increase per 10 µg/m³. There were, on average, 1.7 hospital admissions per day. Two and three days after a rise in air pollution, there was also a rise in admission numbers, followed by a decline during the consecutive days. This might indicate that the wards were overstressed because of high admission numbers and restricted additional admissions.

Spatial Interpolation of Toxic air Pollutants in Jeddah City, Saudi Arabia

This work aimed to study hazardous air pollutants in Jeddah city, between 2010 - 2018. The study of the spatial distribution of (NOX, SO2, PM10) was done by the application of the geostatistical method IDW. Daily observation Data were collected from three field observation stations (Bani Malik, Stadium, Industrial activity), and treated in ArcGIS environment. According to the obtained results, in the year 2010, NOX varies between (25 – 62.99 ppb), with very important concentrations in the south of the study area, surrounding the industrial activities. While in the year 2018, the highest concentrations were between (25 – 30.99 ppb) in the north of the study area. the spatial distribution of SO2 was very important in the south of the study area, compared to the highest concentrations in the north in 2018. 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Fine particulate matter and vasoactive 20-hydroxyeicosatetraenoic acid: Insights into the mechanisms of the prohypertensive effects of particulate air pollution

BackgroundEmerging evidence suggests that biological intermediates play an important role in initiating fine particulate matter (PM2.5)-associated prohypertensive pathways, but sensitive biomarkers for this pathway are lacking. AimTo explore whether short-term exposure to PM2.5 is associated with the concentration of 20-hydroxyeicosatetraenoic acid (20-HETE), a potent vasoactive lipid relevant to the pathophysiology of hypertension. MethodsIn this longitudinal panel study, we repeatedly (up to seven times) measured the blood concentrations of 20-HETE in 120 adults living in Beijing, China. Ambient exposure metrics included the concentrations of hourly PM2.5 mass and daily PM2.5 constituents, including three carbonaceous components, eight water-soluble ions, and 16 trace elements. Linear mixed-effects models were used to examine the associations between the change in the 20-HETE concentration and short-term exposure to ambient PM2.5 metrics after adjustment for age, sex, body mass index, behavioral exposure, socioeconomic characteristics, and meteorological factors. ResultsThe interquartile range (IQR) increase in the 7–15-hour-lag exposure to PM2.5 (80 μg/m3) was associated significantly with a 5.3% (95% confidence interval [CI], 0.1–10.7%) to 6.5% (95% CI, 1.7–11.6%) increase in the blood concentration of 20-HETE. The magnitude of the association differed by age, sex, prediabetic status, obesity, and hypertensive status, with a significantly greater increase in 20-HETE observed among those with fasting plasma glucose concentrations ≥ 6.1 mmol/L. In addition to the PM2.5 mass, the 20-HETE concentration was associated consistently with IQR increases in the 1-day lag exposure to organic carbon (5.7%), black carbon (9.5%), nitrate (3.9%), chloride (2.9%), copper (5.5%), zinc (4.7%), barium (4.1%), and lead (6.2%). The organic carbon estimate was robust in the two-pollutant models. Furthermore, increased 20-HETE correlated with elevated blood pressure (BP), although no mediation of 20-HETE on PM2.5-associated BP change was found. ConclusionsThe 20-HETE blood concentration increased significantly in response to short-term exposure to ambient PM2.5, which may be partly responsible for the prohypertensive effects of PM2.5.

Cardiovascular Effects of Particulate Air Pollution.

Inhalation of fine particulate matter (PM2.5), produced by the combustion of fossil fuels, is an important risk factor for cardiovascular disease. Exposure to PM2.5 has been linked to increases in blood pressure, thrombosis, and insulin resistance. It also induces vascular injury and accelerates atherogenesis. Results from animal models corroborate epidemiological evidence and suggest that the cardiovascular effects of PM2.5 may be attributable, in part, to oxidative stress, inflammation, and the activation of the autonomic nervous system. Although the underlying mechanisms remain unclear, there is robust evidence that long-term exposure to PM2.5 is associated with premature mortality due to heart failure, stoke, and ischemic heart disease.

Proinflammatory lipid signals trigger the health effects of air pollution in individuals with prediabetes

Individuals with metabolic disorders exhibit enhanced susceptibility to the cardiovascular health effects of particulate air pollution, but the underlying mechanisms are not yet understood. We aim to assess whether changes in proinflammatory lipid signals are associated with fine particulate matter (PM2.5) exposure in individuals with and without prediabetes. A longitudinal panel study was conducted in Beijing, China, and included 120 participants followed up over 589 clinical visits from August 2013 to February 2015. We measured 12 lipids derived from arachidonic acid pathways in blood samples of the participants via targeted lipidomic analyses. Ambient PM2.5 concentrations were continuously monitored at a station for associations with the lipids. Among the 120 participants, 110 (mean [SD] age at recruitment, 56.5 [4.2] years; 31 prediabetics) who visited the clinic at least twice over the follow-up period were assigned exposure values of the outdoor residential PM2.5 concentrations during the 1–14 days preceding each clinical visit. With an interquartile range increase in the 1-day-lag PM2.5 exposure (64.0 μg/m3), the prediabetic group had consistently greater increases in the concentration of arachidonate metabolites derived from the cytochrome P450 (CYP450) pathway (5,6-DHET, 15.8% [95% CI, 3.5–29.7%]; 8,9-DHET, 9.7% [95% CI, 0.6–19.6%]; 11,12-DHET, 8.3% [95% CI, 1.9–15.1%]; 14,15-DHET, 7.4% [95% CI, 0.9–14.4%]; and 20-HETE, 8.9% [95% CI, 1.0–17.5%]), compared with the healthy group. Among CYP450-derived lipids, 14,15-DHET and 20-HETE significantly mediated 8% and 8% of the PM2.5-associated increase in white blood cells, 10% and 13% of that in neutrophils, and 20% and 23% of that in monocytes, respectively, in the prediabetic group. In conclusion, proinflammatory lipid signals from CYP450 pathways triggered the health effects of particulate air pollution in individuals with prediabetes, suggesting that targeting lipid metabolism has therapeutic potential to attenuate or prevent the cardiovascular effects of air pollution in susceptible populations.

The Association Between Particulate Air Pollution and Respiratory Mortality in Beijing Before, During, and After the 2008 Olympic and Paralympic Games

To improve ambient air quality during the 2008 Summer Olympic and Paralympic Games, the Chinese Government and Beijing’s municipal government implemented comprehensive emission control policies in Beijing and its neighboring regions before and during this period. The goal of this study was to investigate the association between particulate air pollution and cause-specific respiratory mortality before, during and after the period of the Olympic Games. Further, we wanted to assess whether changes in pollutant concentrations were linked to changes in respiratory mortality. We obtained daily data on mortality due to respiratory diseases (coded as J00-J99 according to the International Classification of Diseases and Related Health Problems 10th revision [ICD10]) and pneumonia (ICD10: J12–18), meteorology, particulate matter less than 10 µm or 2.5 μm in diameter (PM10, PM2.5) and particle number size distribution from official monitoring networks and sites located on the Peking University campus between May 20 and December 1, 2008. We assessed the effects of particulate air pollution on daily respiratory mortality using confounder-adjusted Quasi-Poisson regression models. Furthermore, we estimated air pollution effects for three periods—before (May 20 to July 20, 2008), during (August 1 to September 20, 2008) and after (October 1 to December 1, 2008)—by including interaction terms in the models. We found associations between different particle metrics and respiratory and pneumonia mortality, with more pronounced effects in smaller particle size ranges. For example, an interquartile range increase of 7,958 particles/cm3 in ultrafine particles (particles &amp;lt;100 nm in diameter) led to a 16.3% (95% confidence interval 4.3%; 26.5%) increase in respiratory mortality with a delay of seven days. When investigating the sub-periods, results indicate that a reduction in air pollution during the Olympics resulted in reduced (cause-specific) respiratory mortality. This reduction was especially pronounced for pneumonia mortality. The findings suggest that even a short-term reduction in pollution concentrations may lead to health benefits and that smaller particles in the ultrafine size range may be particularly important for respiratory health.

Effect of short-term exposure to particulate air pollution on heart rate variability in normal-weight and obese adults

BackgroundThe adverse effects of particulate air pollution on heart rate variability (HRV) have been reported. However, it remains unclear whether they differ by the weight status as well as between wake and sleep.MethodsA repeated-measure study was conducted in 97 young adults in Beijing, China, and they were classified by body mass index (BMI) as normal-weight (BMI, 18.5–24.0 kg/m2) and obese (BMI ≥ 28.0 kg/m2) groups. Personal exposures to fine particulate matter (PM2.5) and black carbon (BC) were measured with portable exposure monitors, and the ambient PM2.5/BC concentrations were obtained from the fixed monitoring sites near the subjects’ residences. HRV and heart rate (HR) were monitored by 24-h Holter electrocardiography. The study period was divided into waking and sleeping hours according to time-activity diaries. Linear mixed-effects models were used to investigate the effects of PM2.5/BC on HRV and HR in both groups during wake and sleep.ResultsThe effects of short-term exposure to PM2.5/BC on HRV were more pronounced among obese participants. In the normal-weight group, the positive association between personal PM2.5/BC exposure and high-frequency power (HF) as well as the ratio of low-frequency power to high-frequency power (LF/HF) was observed during wakefulness. In the obese group, personal PM2.5/BC exposure was negatively associated with HF but positively associated with LF/HF during wakefulness, whereas it was negatively correlated to total power and standard deviation of all NN intervals (SDNN) during sleep. An interquartile range (IQR) increase in BC at 2-h moving average was associated with 37.64% (95% confidence interval [CI]: 25.03, 51.51%) increases in LF/HF during wakefulness and associated with 6.28% (95% CI: − 17.26, 6.15%) decreases in SDNN during sleep in obese individuals, and the interaction terms between BC and obesity in LF/HF and SDNN were both statistically significant (p < 0.05). The results also suggested that the effects of PM2.5/BC exposure on several HRV indices and HR differed in magnitude or direction between wake and sleep.ConclusionsShort-term exposure to PM2.5/BC is associated with HRV and HR, especially in obese individuals. The circadian rhythm of HRV should be considered in future studies when HRV is applied.Graphical abstract

Estimation of excess mortality due to long-term exposure to PM2.5 in continental United States using a high-spatiotemporal resolution model

BackgroundExposure to fine particulate matter (<2.5 mm in aerodynamic diameter, PM2.5) pollution, even at low concentrations is associated with increased mortality. Estimates of the magnitude of the effect of particulate air pollution on mortality are generally done on a coarse spatial scale, such as 0.5°, and may fail to capture small spatial differences in exposure and baseline rates, which can bias results and impede the ability to consider environmental justice. We estimated the burden of mortality attributable to long-term exposure to ambient PM2.5 among adults in the Continental United States on a 1 km scale, in order to provide information for decision makers setting health priorities. MethodsWe conducted a health impact assessment for 2015 using a model predicting U.S. PM2.5 concentrations at a spatial resolution of 1 km cells. We applied a concentration-response curve from a recently published meta-analysis of long-term PM2.5 mortality association which incorporates new findings at high and low PM2.5 concentrations. We computed the change in deaths in each grid cell, based on its grid cell population, Zip code level baseline mortality rates, and exposure under two scenarios; a decrease of PM2.5 exposure levels by 40% and a decrease of PM2.5 exposure levels to the county minimum PM2.5 concentrations. ResultsWe estimated the deaths would fall by 104,786 (95% CI 57,016–135,726) and 112,040 (95% CI 63,261-159,116) attributable to 40% reduction and reduction to the county minimum PM2.5 concentrations, respectively. The greatest mortality impact due to 40% reduction in PM2.5 was observed in California with; 11,621 (95% CI; 7156-15,989) and Texas with; 9616 (95% CI; 5798–13,352) excess deaths attributable to annual mean PM2.5 concentrations of 9.54 and 9.12 μg m−3, respectively. Within city analyses showed substantial heterogeneity in risk. The estimated Attributable fraction (AF %) in locations with high PM2.5 levels was 8.6% (95% CI 5.4–11.7) compared to the overall AF% of 4.9% (95% CI; 2.9–6.8). In comparison, results using county average PM2.5 were smaller than the estimates from the 1 km PM2.5 datasets. Similarly, estimates using county-level mortality rates were smaller than estimates based on Zip-code level mortality rates. ConclusionsOur study provides evidence of major health benefits expected from reducing PM2.5 exposure, even in regions with relatively low PM2.5 concentrations. Spatial characteristics of exposure and baseline mortality (e.g., accuracy, scales, and variations) in disease burden studies can significantly impact the results.

Residential greenness and birth outcomes: Evaluating the mediation and interaction effects of particulate air pollution

BackgroundThe few studies that examined the association between residential greenness and birth outcomes have produced inconsistent results, and the underlying mechanisms of these associations remain unclear. ObjectivesWe examined the mediation and interaction effects of particulate matter (PM) air pollution on the relationship between greenness exposure during the first and third trimesters of pregnancy and birth outcomes, including preterm birth (PTB), term low birth weight (TLBW), small for gestational age (SGA), birth weight (BW), and head circumference (HC). MethodsWe conducted a retrospective cohort study on 16,184 singleton live births between 2010 and 2012 in Taiwan. Residential greenness was estimated based on the normalized difference vegetation index (NDVI), and the PM information during the first and third trimesters was estimated through hybrid kriging land use regression and ordinary kriging interpolation methods. Multiple regression analyses were performed to evaluate the associations between greenness exposure and birth outcomes. We estimated the mediating effects of PM associated with greenness exposure on birth outcomes through causal mediation analyses. We also examined the potential multiplicative and additive interactions between greenness exposure and PM and their effects on birth outcomes. ResultsThe first trimester NDVI exposure was associated with reduced risks for PTB, TLBW, and SGA, which had an adjusted OR (aOR) of 0.93 (95% CI: 0.89–0.97), 0.91 (95% CI: 0.83–0.99), and 0.95 (95% CI: 0.91–1.00), respectively, per 0.1 unit increase in multi-pollutant models. The causal mediation analysis showed that PM mediated approximately 5–19% of the association between first and third trimester greenness and PTB and mediated approximately 15–37% of the association between greenness and SGA. We identified multiplicative interactions in log scale between first trimester PM10 and NDVI exposure for SGA (aORinteraction = 0.92, p = 0.03) and HC (estimateinteraction = 1.47, p = 0.04). ConclusionsThis study revealed beneficial associations between residential greenness and birth outcomes, including PTB, TLBW, and SGA. The associations were partly mediated by a reduction in exposure to PM air pollution. SummaryThe beneficial effects of greenness on PTB and SGA are partly mediated by a reduction in exposure to PM air pollution.