Ambient PM Exposure Research Articles

Modification of allergic dermatitis on the associations between early-life exposure to size-specific particulate matter and childhood allergic rhinitis

To evaluate the modification of allergic dermatitis on the association between PM exposure and allergic rhinitis in preschool children. This cross-sectional study was based on a questionnaire conducted between June 2019 and June 2020 to caregivers of children aged 3 to 6 years in the kindergartens of 7 Chinese cities to collect information on allergic rhinitis and allergic dermatitis. A mature machine learning-based space-time extremely randomized trees model was applied to estimate early-life, prenatal, and first-year exposure of PM1, PM2.5 and PM10 at 1 km×1 km resolution. A combination of multilevel logistic regression and restricted cubic spline functions was used to quantitatively assess whether allergic dermatitis modifies the associations between size-specific PM exposure and the risk of childhood allergic rhinitis. The results showed that out of 28 408 children, 14 803 (52.1%) were boys and 13 605 (47.9%) were girls; the age of children ranged from 3.1 to 6.8 years, with a mean age of (4.9±0.9) years, of which 3 586 (12.6%) were diagnosed with allergic rhinitis. Among all children, 17 832 (62.8%) were breastfed for more than 6 months and 769 (2.7%) had parental history of atopy. A total of 21 548 children (75.9%) had a mother with an educational level of university or above and 7 338 (29.6%) had passive household cigarette smoke exposure. The adjusted ORs for childhood allergic rhinitis among the children with allergic dermatitis as per interquartile range (IQR) increase in early-life PM1(9.8 μg/m3), PM2.5 (14.9 μg/m3) and PM10 (37.7 μg/m3) were significantly higher than the corresponding ORs among the children without allergic dermatitis [OR: 1.45, 95%CI (1.26, 1.66) vs. 1.33, 95%CI (1.20, 1.47), for PM1; OR: 1.38, 95%CI (1.23, 1.56) vs. 1.32, 95%CI (1.21, 1.45), for PM2.5; OR: 1.56, 95%CI (1.31, 1.86) vs. 1.46, 95%CI (1.28, 1.67), for PM10]. The interactions between allergic dermatitis and size-specific PM exposure on childhood allergic rhinitis were statistically significant (Z value=19.4, all P for interaction<0.001). The similar patterns were observed for both prenatal and first-year size-specific PM exposure and the results of the dose-response relationship were consistent with those of the logistic regression. In conclusion, allergic dermatitis, as an important part of the allergic disease progression, may modify the association between ambient PM exposure and the risk of childhood allergic rhinitis. Children with allergic dermatitis should pay more attention to minimize outdoor air pollutants exposure to prevent the further progression of allergic diseases.

Individual and joint effect of indoor air pollution index and ambient particulate matter on fetal growth: a prospective cohort study.

Limited studies have examined the effect of prenatal exposure to particulate matter with diameter of <2.5 µm (PM2.5) and <1 μm (PM1) on fetal growth using ultrasound measurements with inconsistent results. No study has evaluated the joint effect of the indoor air pollution index and ambient particulate matter on fetal growth. We conducted a prospective birth cohort study in Beijing, China in 2018, including 4319 pregnant women. We estimated prenatal PM2.5 and PM1 exposure using a machine-learning method and calculated the indoor air pollution index based on individual interviews. Gender- and gestational age-adjusted Z-score of the abdominal circumference (AC), head circumference (HC), femur length (FL) and estimated fetal weight (EFW) was calculated and then undergrowth was defined. A generalized estimating equation was used to evaluate the individual and joint effect of indoor air pollution index, PM2.5 and PM1 on fetal Z-score and undergrowth parameters. One unit increase in the indoor air pollution index was associated with -0.044 (95% CI: -0.087, -0.001) and -0.050 (95% CI: -0.094, -0.006) decrease in the AC and HC Z-scores, respectively. PM1 and PM2.5 were associated with decreased AC, HC, FL and EFW Z-scores, and higher risk of undergrowth. Compared with exposure to lower PM1 (≤ median) and no indoor air pollution, those exposed to higher PM1 (> median) and indoor air pollution had decreased EFW Z-scores (β = -0.152, 95% CI: -0.230, -0.073) and higher risk of EFW undergrowth (RR = 1.651, 95% CI: 1.106, 2.464). Indoor air pollution and ambient PM2.5 exposure had a similar joint effect on the Z-scores and undergrowth parameters of fetal growth. This study suggested that indoor air pollution and ambient PM exposure had individual and joint negative effects on fetal growth.

Resveratrol alleviates chronic “real-world” ambient particulate matter-induced lung inflammation and fibrosis by inhibiting NLRP3 inflammasome activation in mice

BackgroundInhalation of fine particulate matter (PM2.5) induces the occurrence of lung inflammation and fibrosis, but its molecular mechanism remains unclear. Resveratrol (RES) is known to have anti-inflammatory properties in many pulmonary diseases. Here, we aimed to investigate the effect of long-term “real-world” ambient PM exposure on lung inflammation and fibrosis and further explore the protective effect and mechanism of RES. Methods and resultsRES (50 and 100 mg/kg.bw) was administered to C57BL/6J mice that were exposed to ambient PM for 5 months. The control group breathed filtered air without RES, and the PM group was exposed to PM without RES. The inflammatory cytokine levels in bronchoalveolar lavage fluid (BALF) and lung fibrosis were evaluated by enzyme-linked immune sorbent assay (ELISA) kits and Masson's trichrome staining. The real-time PCR and Western blot analysis were used to determine the signal pathway. In vivo, PM exposure markedly elevated the levels of inflammatory cytokines and TGF-β1 in BALF, induced lung fibrosis. Meanwhile, PM exposure triggered autophagy process and activated the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome in lung. Also, RES treatment abolished PM-induced lung inflammation and fibrosis, and inhibited autophagic process and NLRP3 inflammasome activation. In vitro, PM2.5-induced cytotoxicity in BEAS-2B cells dose-dependently. Besides, RES alleviated PM2.5-induced cytotoxicity, inhibited autophagic process and NLRP3 inflammasome activity and decreased IL-1β production in BEAS-2B cells. ConclusionLong-term PM exposure induced lung inflammation and fibrosis, and RES intervention alleviated these adverse effects via inhibiting autophagy-related NLRP3 inflammasome activation.

Lung cancer deaths attributable to ambient PM(2.5) exposure in 2016 in China

Objective: To analyze the lung cancer deaths attributable to ambient PM(2.5) exposure in China in 2016. Methods: All data were from the Global Burden of Disease Study 2016 (GBD 2016). Multiple-source data, including satellite observation, ground measurement, chemical migration model simulation, etc., and the data integration model for air quality (DIMAQ) were used to estimate the grid-level exposure to ambient PM(2.5). Data from the vital registry and cancer registry were used to establish statistical model to estimate the lung cancer deaths by province, age and gender. The lung cancer deaths attributable to PM(2.5) were calculated based on the calculation of population attributable fraction (PAF). The GBD world population age structure was adopted to calculate age-standardized rates for comparison among provinces (including 31 provinces, autonomous regions and municipalities directly under the central government, as well as Hong Kong and Macao special administrative regions, excluding Taiwan of China). Results: In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China were 14.56×10(4) (95% uncertainty interval (UI): 9.63×10(4)-19.55×10(4)), accounting for 24.66% (95%UI: 16.38%-33.12%) of total lung cancer deaths. The lung cancer death rate attributable to PM(2.5) increased with age, with the lowest among 25-29 age group (0.25/10(5), 95%UI: 0.17/10(5)-0.34/10(5)), the highest among ≥80 age group (90.70/10(5), 95%UI: 59.85/10(5)-122.20/10(5)). The lung cancer death rate attributable to PM(2.5) among males (14.84/10(5), 95%UI: 9.78/10(5)-19.93/10(5)) was higher than that in females (6.21/10(5), 95%UI: 4.07/10(5)-8.40/10(5)). The age-standardized death rates (ASDR) of lung cancer attributable to PM(2.5) among males and females in China were higher than the global average level. The attributable ASDR of lung cancer varied among provinces, highest in Shandong (13.51/10(5), 95%UI: 9.14/10(5)-18.20/10(5)) and lowest in Tibet (0.85/10(5), 95%UI: 0.44/10(5)-1.51/10(5)). Conclusion: In 2016, the lung cancer deaths attributable to ambient PM(2.5) exposure in China was heavy, and varied in different age groups, genders and provinces.

Progress in research of relationship between ambient air PM(2.5) and lung diseases

Fine Particulate Matter (PM(2.5)-particles with an aerodynamic diameter ≤2.5 μm) can penetrate deeply into the lung, deposit in the alveoli, and consequently impair lung function. Both short term and long term exposures to PM(2.5) are associated with the incidence of respiratory diseases (e.g. asthma, chronic obstructive pulmonary disease, lung cancer). This paper summarizes the effects of ambient air PM(2.5) exposure on human respiratory system revealed by epidemiological studies.

Residential infiltration of fine and ultrafine particles in Edmonton

Airborne indoor particles arise from both indoor sources and ambient particles that have infiltrated indoors. The intra-urban variability of infiltration factors (Finf) is a source of measurement error in epidemiological studies estimating exposure from a central site measurement, hence information on the within and between-home variability of Finf is useful to better characterize ambient PM exposure. The objective of this paper was to estimate magnitudes and predictors of daily residential infiltration factors (Finf) and ambient/non-ambient components of indoor ultrafine particle (UFP) and fine particle (FP) concentrations. FPs and UFPs were measured continuously for 7 consecutive days in 74 Edmonton homes in winter and summer 2010 (50 homes in each season). Simultaneous measurements of outdoor (near-home) FP and ambient (at a central site) UFP concentrations were also measured. Daily infiltration factors were estimated for each home; considerable variability was seen within and between homes. For FPs, seasonal-averaged Finf (the average of the 7 daily Finf estimates) ranged from 0.10 to 0.92 in winter (median = 0.30, n = 49) and 0.31 to 0.99 in summer (median = 0.68, n = 48). For UFPs, the seasonal-averaged Finf ranged from 0.08 to 0.47 across homes in winter (median = 0.21, n = 33 houses) and from 0.16 to 0.94 in summer (median = 0.57, n = 48). The higher median Finf in summer was attributed to a high frequency of open windows. Daily infiltration factors were also estimated based on the indoor/outdoor PM1 sulfur ratio. These estimates were poorly correlated with DustTrak-based FP infiltration factor estimates; the difference may be due to losses of volatile components on the PM1 filter samples. Generalized linear mixed models were used to identify variables significantly associated with Finf and the non-ambient component of indoor FP and UFP concentrations. Wind speed was consistently associated with Finf across all seasons for both FPs and UFPs. The use of an air cleaner was associated with reduced UFP infiltration factors in summer, suggesting a potential method of reducing infiltrated UFPs. Various cooking activities and smoking were associated with the non-ambient component of indoor FP and UFP concentrations. On average, the majority of indoor FPs were of ambient origin while the majority of UFPs were of indoor origin. In summer, more of the indoor FP and UFP concentrations were from ambient origin, compared to winter, due to the higher infiltration factors. The variability in FP and UFP Finf within and between homes may cause substantial exposure misclassification in epidemiological studies using only ambient measurements.

Influence of human activity patterns, particle composition, and residential air exchange rates on modeled distributions of PM2.5 exposure compared with central-site monitoring data

Central-site monitors do not account for factors such as outdoor-to-indoor transport and human activity patterns that influence personal exposures to ambient fine-particulate matter (PM(2.5)). We describe and compare different ambient PM(2.5) exposure estimation approaches that incorporate human activity patterns and time-resolved location-specific particle penetration and persistence indoors. Four approaches were used to estimate exposures to ambient PM(2.5) for application to the New Jersey Triggering of Myocardial Infarction Study. These include: Tier 1, central-site PM(2.5) mass; Tier 2A, the Stochastic Human Exposure and Dose Simulation (SHEDS) model using literature-based air exchange rates (AERs); Tier 2B, the Lawrence Berkeley National Laboratory (LBNL) Aerosol Penetration and Persistence (APP) and Infiltration models; and Tier 3, the SHEDS model where AERs were estimated using the LBNL Infiltration model. Mean exposure estimates from Tier 2A, 2B, and 3 exposure modeling approaches were lower than Tier 1 central-site PM(2.5) mass. Tier 2A estimates differed by season but not across the seven monitoring areas. Tier 2B and 3 geographical patterns appeared to be driven by AERs, while seasonal patterns appeared to be due to variations in PM composition and time activity patterns. These model results demonstrate heterogeneity in exposures that are not captured by the central-site monitor.

Effects of particulate air pollution on blood pressure in a highly exposed population in Beijing, China: a repeated-measure study

BackgroundParticulate Matter (PM) exposure is critical in Beijing due to high population density and rapid increase in vehicular traffic. PM effects on blood pressure (BP) have been investigated as a mechanism mediating cardiovascular risks, but results are still inconsistent. The purpose of our study is to determine the effects of ambient and personal PM exposure on BP.MethodsBefore the 2008 Olympic Games (June 15-July 27), we examined 60 truck drivers and 60 office workers on two days, 1-2 weeks apart (n = 240). We obtained standardized measures of post-work BP. Exposure assessment included personal PM2.5 and Elemental Carbon (EC, a tracer of traffic particles) measured using portable monitors during work hours; and ambient PM10 averaged over 1-8 days pre-examination. We examined associations of exposures (exposure group, personal PM2.5/EC, ambient PM10) with BP controlling for multiple covariates.ResultsMean personal PM2.5 was 94.6 μg/m3 (SD = 64.9) in office workers and 126.8 (SD = 68.8) in truck drivers (p-value < 0.001). In all participants combined, a 10 μg/m3 increase in 8-day ambient PM10 was associated with BP increments of 0.98 (95%CI 0.34; 1.61; p-value = 0.003), 0.71 (95%CI 0.18; 1.24; p-value = 0.01), and 0.81 (95%CI 0.31; 1.30; p-value = 0.002) mmHg for systolic, diastolic, and mean BP, respectively. BP was not significantly different between the two groups (p-value > 0.14). Personal PM2.5 and EC during work hours were not associated with increased BP.ConclusionsOur results indicate delayed effects of ambient PM10 on BP. Lack of associations with exposure groups and personal PM2.5/EC indicates that PM effects are related to background levels of pollution in Beijing, and not specifically to work-related exposure.

The Response of Children with Asthma to Ambient Particulate Is Modified by Tobacco Smoke Exposure

Ambient particulate matter concentrations have been positively associated with urinary leukotriene E(4) (LTE(4)) levels and albuterol usage in children with asthma but interactions with environmental tobacco smoke (ETS) exposure have not been demonstrated despite obvious exposure to both pollutants in an urban setting. To assess the health effects of concurrent ETS and ambient particulate matter exposure in children with asthma. Albuterol usage and LTE(4) levels were monitored in 82 urban schoolchildren with asthma over three consecutive fall to spring school periods. Concentrations of morning maximum ambient particulate matter <2.5 μm in aerodynamic diameter (mmPM(2.5)) and urine cotinine levels were also measured daily. Albuterol usage and LTE(4) were related to mmPM(2.5) concentrations on days when urine cotinine levels were low (<10 ng/ml/mg creatinine); on these days, mean albuterol usage and LTE(4) increased up to 5 or 6% per 10 μg/m(3) increase in mmPM(2.5). In contrast, no significant relationship was observed when cotinine was high, although mean albuterol usage and LTE(4) levels were greater in this case. Model fits for LTE(4) levels as a function of mmPM(2.5) concentrations were improved when mmPM(2.5) concentrations were logged, suggesting a nonlinear dose-response relationship between particulate matter exposure concentrations and airway mediators of asthma, for which the relationship tends to flatten at higher concentrations. This study suggests that ETS modifies the acute effects of low-level ambient PM(2.5) exposure on childhood asthma. This negative interaction, the smaller effect of particulate matter exposure in children exposed to higher ETS, may be related to a nonlinear dose-response relationship between asthma mediators and particulate exposures.

Reflections on the scope and the future of Particle and Fibre Toxicology

Within 5 years of its first publication in December 2004, Particle and Fibre Toxicology has become a well recognized open access, peer-reviewed, online journal with an (unofficial) impact factor of 5.5. This major achievement is due to the dedication of former Editors-in-Chief Professors Ken Donaldson and Paul Borm, and, of course also due to the high quality of manuscripts that have been submitted by authors from all over the world. Recent years have shown a significant increase in papers dealing with nanomaterials and nanotoxicology, whilst the small margin between ambient PM exposure and current standards continues to provide a constant flow of manuscripts on this topic. This however, does not imply that we can relax now.

Kupffer cell activation by ambient air particulate matter exposure may exacerbate non-alcoholic fatty liver disease

Owing to increased obesity, non-alcoholic fatty liver disease (NAFLD) is now the most prevalent liver disease in the United States. NAFLD is considered a component of metabolic syndrome, a cluster of disorders that also includes diabetes mellitus, dyslipidemia, arteriosclerosis, and hypertension. Exposure to ambient air particulate matter with aerodynamic diameters < 2.5 microm (PM(2.5)) is a risk factor for arteriosclerosis and lung disease, but its effect on NAFLD is unknown. PM(2.5) induces pulmonary dysfunction via Toll-like receptor (TLR) activation on alveolar macrophages. TLR activation of Kupffer cells, resident hepatic macrophages, and subsequent pro-inflammatory cytokine production have been shown to play a key role in NAFLD progression. We hypothesized that PM(2.5) exposure is a significant risk factor for the progression of NAFLD. Thus, following exposure of male C57BL/6 mice fed high fat chow (HFC) to concentrated air particulate matter (CAPs) or filtered air for 6 weeks, progression of NAFLD was evaluated by standardized histological assessment of hepatic inflammation and fibrosis. In mice fed HFC, the hepatic inflammatory grade (3.00 +/- 0.00 vs. 1.50 +/- 0.71, P < 0.001) and fibrosis stage (1.00 +/- 0.00 vs. 0.60 +/- 0.52, P = 0.023) were both significantly higher in mice exposed to CAPs versus filtered air, respectively. Increased numbers of Kupffer cells contained PM in CAPs-exposed mice scores of (2.00 +/- 0.94 vs. 0.20 +/- 0.42, respectively, P < 0.001). PM exposure increased IL-6 secretion up to seven-fold in a dose-dependent manner by isolated wild-type but not TLR4(-/-) Kupffer cells (P < 0.050). In conclusion, ambient PM(2.5) exposure may be a significant risk factor for NAFLD progression.

The benefits of whole-house in-duct air cleaning in reducing exposures to fine particulate matter of outdoor origin: A modeling analysis

Health risks of fine particle air pollution (PM(2.5)) are an important public health concern that has the potential to be mitigated in part by interventions such as air cleaning devices that reduce personal exposure to ambient PM(2.5). To characterize exposure to ambient PM(2.5) indoors as a function of residential air cleaners, a multi-zone indoor air quality model was used to integrate spatially resolved data on housing, meteorology, and ambient PM(2.5), with performance testing of residential air cleaners to estimate short-term and annual average PM(2.5) of outdoor origin inside residences of three metropolitan areas. The associated public health impacts of reduced ambient PM(2.5) exposure were estimated using a standard health impact assessment methodology. Estimated indoor levels of ambient PM(2.5) varied substantially among ventilation and air cleaning configurations. The median 24-h average indoor-outdoor ratio of ambient PM(2.5) was 0.57 for homes with natural ventilation, 0.35 for homes with central air conditioning (AC) with conventional filtration, and 0.1 for homes with central AC with high efficiency in-duct air cleaner. Median modeled 24-h average indoor concentrations of PM(2.5) of outdoor origin for those three configurations were 8.4, 5.3, and 1.5 microg/m(3), respectively. The potential public health benefits of reduced exposure to ambient PM(2.5) afforded by air cleaning systems were substantial. If the entire population of single-family homes with central AC in the modeling domain converted from conventional filtration to high-efficiency in-duct air cleaning, the change in ambient PM(2.5) exposure is estimated to result in an annual reduction of 700 premature deaths, 940 hospital and emergency room visits, and 130,000 asthma attacks in these metropolitan areas. In addition to controlling emissions from sources, high-efficiency whole-house air cleaner are expected to reduce exposure to particles of outdoor origin and are projected to be an effective means of managing public health impacts of ambient particle pollution.

GIS-based models for ambient PM exposure and health impact assessment for the UK

GIS-based models have been developed to map ambient PM10 and PM25 mass concentrations across the UK. The resulting maps are used for the assessments of air quality required by the EU ambient air quality directives, health impact assessment and the development of UK air quality policy. Maps are presented for 2006 along with projections to 2020. The largest single contribution to the UK population-weighted mean annual mean background concentrations of PM10 in 2006 is estimated to be from secondary PM (43%), followed by the contribution from primary PM (24%). Concentrations are predicted to decline by 15% for PM10 and 13% for PM25 over the period from 2006 to 2020. The extent of exceedence of the 24-hour limit value is predicted to decline from 1.9% to 0.1% of urban major roads over the same period. The potential health benefits of reductions in ambient PM are large. A reduction in concentration of 0.93 μg m-3 as a result of a possible package of measures has been estimated within the UK Air Quality Strategy to result in a reduction in life years lost of approximately 2 - 4 million over a period of 100 years.

Exposure to diesel exhaust induces changes in EEG in human volunteers

BackgroundAmbient particulate matter and nanoparticles have been shown to translocate to the brain, and potentially influence the central nervous system. No data are available whether this may lead to functional changes in the brain.MethodsWe exposed 10 human volunteers to dilute diesel exhaust (DE, 300 μg/m3) as a model for ambient PM exposure and filtered air for one hour using a double blind randomized crossover design. Brain activity was monitored during and for one hour following each exposure using quantitative electroencephalography (QEEG) at 8 different sites on the scalp. The frequency spectrum of the EEG signals was used to calculate the median power frequency (MPF) and specific frequency bands of the QEEG.ResultsOur data demonstrate a significant increase in MPF in response to DE in the frontal cortex within 30 min into exposure. The increase in MPF is primarily caused by an increase in fast wave activity (β2) and continues to rise during the 1 hour post-exposure interval.ConclusionThis study is the first to show a functional effect of DE exposure in the human brain, indicating a general cortical stress response. Further studies are required to determine whether this effect is mediated by the nanoparticles in DE and to define the precise pathways involved.

Estimating effects of ambient PM2.5 exposure on health using PM2.5 component measurements and regression calibration

Most air pollution and health studies conducted in recent years have examined how a health outcome is related to pollution concentrations from a fixed outdoor monitor. The pollutant effect estimate in the health model used indicates how ambient pollution concentrations are associated with the health outcome, but not how actual exposure to ambient pollution is related to health. In this article, we propose a method of estimating personal exposures to ambient PM(2.5) (particulate matter less than 2.5 microm in diameter) using sulfate, a component of PM(2.5) that is derived primarily from ambient sources. We demonstrate how to use regression calibration in conjunction with these derived values to estimate the effects of personal ambient PM(2.5) exposure on a continuous health outcome, forced expiratory volume in 1 s (FEV(1)), using repeated measures data. Through simulation, we show that a confidence interval (CI) for the calibrated estimator based on large sample theory methods has an appropriate coverage rate. In an application using data from our health study involving children with moderate to severe asthma, we found that a 10 microg/m3 increase in PM(2.5) was associated with a 2.2% decrease in FEV(1) at a 1-day lag of the pollutant (95% CI: 0.0-4.3% decrease). Regressing FEV(1) directly on ambient PM(2.5) concentrations from a fixed monitor yielded a much weaker estimate of 1.0% (95% CI: 0.0-2.0% decrease). Relatively small amounts of personal monitor data were needed to calibrate the estimate based on fixed outdoor concentrations.