Commuters' Personal Exposure Assessment and Evaluation of Inhaled Dose to Different Atmospheric Pollutants.
ABSTRACT: Several studies evaluating exposure to pollutants in microenvironments (MEs) are available in the scientific literature, but studies that evaluate the inhaled doses of pollutants are few in number. Therefore, this study aimed to evaluate the exposure of commuters to different pollutants (i.e., nitrogen dioxide [NO2] and fractionated particulate matter [PM], including ultrafine particles [UFPs]) using miniaturized and portable real-time monitoring instruments in selected MEs; the inhaled doses of these pollutants were estimated for each of these MEs. Measurements were performed along a typical commute, considering different traffic and nontraffic MEs. Experimental data were collected over four working weeks in two different seasons (winter and summer). Different portable and miniaturized instruments were used to evaluate PM and NO2 exposure. Furthermore, physiological parameters were evaluated using a heart rate monitor. The principal results show that higher exposure levels were measured in Underground (for all PM fractions and NO2) and in Car (UFP), while lower levels were measured in Car (PM and NO2) and in Train (UFP). In contrast, higher values of the inhaled cumulative dose were estimated in environments defined as Other, followed by Walking (ht), while lower values were observed in Walking (lt) and in Car.
Project description:Introduction:Particulate matter (PM) and cigarette-related cadmium exposure increases inflammation and smokers' susceptibility to developing lung diseases. The majority of inhaled metals are attached to the surface of ultrafine particles (UFPs). A low inhaled UFP content in exhaled breath condensate (EBC) reflects a high inflammatory status of airways. Methods:EBC was collected from 58 COPD patients and 40 healthy smokers and nonsmokers. Participants underwent spirometry, diffusion capacity, EBC and blood sampling. Environmental pollution data were collected from monitoring stations. UFPs were measured in EBC and serum, and cadmium content was quantified. Results:Subjects with low UFP concentrations in EBC (<0.18×108·mL-1) had been exposed to higher long-term PM2.5 levels versus subjects with high UFP concentrations in EBC (>0.18×108·mL-1) (21.9 µg·m-3 versus 17.4 µg·m-3, p?0.001). Long-term PM2.5 exposure levels correlated negatively with UFP concentrations in EBC and positively with UFP concentrations in serum (r=-0.54, p?0.001 and r=0.23, p=0.04, respectively). Healthy smokers had higher cadmium levels in EBC versus healthy nonsmokers and COPD patients (25.2 ppm versus 23.7 ppm and 23.3 ppm, p=0.02 and p=0.002, respectively). Subjects with low UFP concentrations in EBC also had low cadmium levels in EBC versus subjects with high UFP levels (22.8 ppm versus 24.2 ppm, p=0.004). Conclusions:Low UFP concentration in EBC is an indicator of high-level PM exposure. High cadmium levels in EBC among smokers and the association between cadmium and UFP content in EBC among COPD patients indicate cadmium lung toxicity.
Project description:BACKGROUND:There is growing evidence that exposure to ultrafine particles (UFP; particles smaller than [Formula: see text]) may play an underexplored role in the etiology of several illnesses, including cardiovascular disease (CVD). OBJECTIVES:We aimed o investigate the relationship between long-term exposure to ambient UFP and incident cardiovascular and cerebrovascular disease (CVA). As a secondary objective, we sought to compare effect estimates for UFP with those derived for other air pollutants, including estimates from two-pollutant models. METHODS:Using a prospective cohort of 33,831 Dutch residents, we studied the association between long-term exposure to UFP (predicted via land use regression) and incident disease using Cox proportional hazard models. Hazard ratios (HR) for UFP were compared to HRs for more routinely monitored air pollutants, including particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text]), PM with aerodynamic diameter [Formula: see text] ([Formula: see text]), and [Formula: see text]. RESULTS:Long-term UFP exposure was associated with an increased risk for all incident CVD [[Formula: see text] per [Formula: see text]; 95% confidence interval (CI): 1.03, 1.34], myocardial infarction (MI) ([Formula: see text]; 95% CI: 1.00, 1.79), and heart failure ([Formula: see text]; 95% CI: 1.17, 2.66). Positive associations were also estimated for [Formula: see text] ([Formula: see text]; 95% CI: 1.01, 1.48 per [Formula: see text]) and coarse PM ([Formula: see text]; HR for all [Formula: see text]; 95% CI: 1.01, 1.45 per [Formula: see text]). CVD was not positively associated with [Formula: see text] (HR for all [Formula: see text]; 95% CI: 0.75, 1.28 per [Formula: see text]). HRs for UFP and CVAs were positive, but not significant. In two-pollutant models ([Formula: see text] and [Formula: see text]), positive associations tended to remain for UFP, while HRs for [Formula: see text] and [Formula: see text] generally attenuated towards the null. CONCLUSIONS:These findings strengthen the evidence that UFP exposure plays an important role in cardiovascular health and that risks of ambient air pollution may have been underestimated based on conventional air pollution metrics. https://doi.org/10.1289/EHP3047.
Project description:Fine particulate matter (PM2.5), levels of which are about 6 times the 2014 WHO air quality guidelines for 190 cities in China, has been found to be associated with various adverse health outcomes. In this study, personal PM2.5 exposures were monitored along a fixed routine that included 19 types of non-residential micro-environments (MEs) on 4 hazy days (ambient PM2.5 292 ± 70 ?g m-3) and 2 non-hazy days (55 ± 16 ?g m-3) in Nanjing, China using miniaturized real-time portable particulate sensors that also collect integrated filters of PM2.5 (MicroPEMs, Research Triangle Institute (RTI), NC). Gravimetric correction is necessary for nephelometer devices in calculating real-time PM levels. During both hazy and non-hazy days, personal PM2.5 levels were generally higher in MEs with noticeable PM2.5 sources than MEs serving as receptor sites, higher in open MEs than indoor MEs, and higher in densely populated MEs than MEs with few people. Personal PM2.5 levels measured during hazy and non-hazy days were 242 ± 91 ?g m-3 and 103 ± 147 ?g m-3, respectively. The ratio of personal exposure to ambient PM2.5 levels (rp/a ) was less than 1.0 and less variable on hazy days (0.85 ± 0.31); while it was larger than 1.0 and more variable on non-hazy days (1.71 ± 1.93), confirming the importance of local sources other than ambient during non-hazy days. Air handling methods (e.g., ventilation/filtration) impacted personal exposures in enclosed locations on both types of days. Street food vendors with cooking emissions were MEs with the highest personal PM2.5 levels while subway cars in Nanjing were relatively clean due to good air filtration on both hazy and non-hazy days. In summary, on hazy days, personal exposure was mainly affected by the regional ambient levels, while on non-hazy days, local sources together with ambient levels determined personal exposure levels.
Project description:Exposure to airborne particulate pollutants is intimately linked to vascular oxidative stress and inflammatory responses with clinical relevance to atherosclerosis. Particulate matter (PM) has been reported to induce endothelial dysfunction and atherosclerosis. Here, we tested whether ambient ultrafine particles (UFP, diameter <200 nm) modulate eNOS activity in terms of nitric oxide (NO) production via protein S-glutathionylation. Treatment of human aortic endothelial cells (HAEC) with UFP significantly reduced NO production. UFP-mediated reduction in NO production was restored in the presence of JNK inhibitor (SP600125), NADPH oxidase inhibitor (Apocynin), anti-oxidant (N-acetyl cysteine), and superoxide dismutase mimetics (Tempol and MnTMPyP). UFP exposure increased the GSSG/GSH ratio and eNOS S-glutathionylation, whereas over-expression of Glutaredoxin-1 (to inhibit S-glutathionylation) restored UFP-mediated reduction in NO production by nearly 80%. Thus, our findings suggest that eNOS S-glutathionylation is a potential mechanism underlying ambient UFP-induced reduction of NO production.
Project description:In the previous studies regarding the effects of exposure to ambient air pollution on biological markers and/or behavior of animals, the gaseous pollutants are not separated from the particulate matter (PM). Hence the synergetic effect of gaseous pollutants and PM was not considered. In this regard, current study was aimed to devolve a new method for separation of PM from gaseous pollutants. Also, the effect of exposure to fine particulate matter (PM2.5) on the Alzheimer and depressive cognitive-like behaviors in rats after 3 and 6 months were investigated. Three chambers were designed including exposure group 1 (PM2.5 plus gaseous pollutants alone), exposure group 2 (gaseous pollutants alone) and control group (clean air). Exposure time was 5 h per day (9.00 a.m.-2.00 p.m.) for 4 days per week. The concentration of PM2.5 and gaseous pollutants (O3, NO2, and SO2) were monitored in the exposure hours, continuously. Concentration of PM2.5 by beta attenuation method and concentration of O3, NO2, and SO2 by UV fluorescence was monitored. Also, the concentration of metals including Al, Cr, Mn, Pb, Cd, Ni, Fe, and Cu and 16-polycyclic aromatic hydrocarbons (PAHs) bound PM2.5 by inductively coupled plasma mass spectrometry (ICP-MS) and gas chromatography-mass spectrometry (GC-MS) were analyzed, respectively. Cognitive-like behavior related to Alzheimer and depressive behaviors were determined by Y maze and Force swimming. The concentration of PM2.5 in the 3 and 6 months exposure was higher than WHO guideline, significantly (p-value <0.05). The concentration of O3, NO2 and SO2 in the 3 and 6 months exposure was lower than WHO guideline, significantly (p-value <0.05). The order of metals in the PM2.5 according to mean concentration Al > Ca > Cu > Cd > Na > Fe > Cr > Ni > Mn > Pb. Also, the sum concentration of 16-PAHs in the PM2.5 in the 3 and 6 months exposure was 45.7 ± 37.15 ng/m3 and 30.04 ± 25.27 ng/m3, respectively. Exposure to PM2.5 cannot significantly increase Alzheimer and depressive cognitive-like behaviors in the rats. Also, a significant difference between male and female in Alzheimer and depressive cognitive-like behaviors not observed. •A new method for separation of PM2.5 from other PM in the ambient air by ECO-PM sampler was presented.•A new method for separation of PM2.5 from gaseous pollutants in the ambient air by HEPA filter and active carbon was presented.•Tow exposure groups including exposure 1: PM2.5 plus gaseous pollutants and exposure 2: gaseous pollutants only were designed for increased accuracy of the in-vivo study.•Exposure to PM2.5 cannot cause significant increased Alzheimer and depressive cognitive-like behaviors in the rats.
Project description:Previous studies have reported increased risks of myocardial infarction in association with elevated ambient particulate matter (PM) in the previous hour(s). However, whether PM can trigger mechanisms that act on this time scale is still unclear. We hypothesized that increases in PM are associated with rapid changes in measures of heart rate variability and repolarization. We used data from panel studies in Augsburg, Germany, and Rochester, New York, USA, and two controlled human exposure studies in Rochester. Data included ECG recordings from all four studies, controlled exposures to (concentrated) ultrafine particles (UFP; particles with an aerodynamic diameter <100 nm) and ambient concentrations of UFP and fine PM (PM2.5, aerodynamic diameter <2.5 μm). Factor analysis identified three representative ECG parameters: standard deviation of NN-intervals (SDNN), root mean square of successive differences (RMSSD), and T-wave complexity. Associations between air pollutants and ECG parameters in the concurrent and previous six hours were estimated using additive mixed models adjusting for long- and short-term time trends, meteorology, and study visit number. We found decreases in SDNN in relation to increased exposures to UFP in the previous five hours in both of the panel studies (e.g. Augsburg study, lag 3 hours: -2.26%, 95% confidence interval [CI]: -3.98% to -0.53%; Rochester panel study, lag 1 hour: -2.69%; 95% CI: -5.13% to -0.26%) and one of the two controlled human exposure studies (1-hour lag: -13.22%; 95% CI: -24.11% to -2.33%). Similarly, we observed consistent decreases in SDNN and RMSSD in association with elevated PM2.5 concentrations in the preceding six hours in both panel studies. We did not find consistent associations between particle metrics and T-wave complexity. This study provided consistent evidence that recent exposures to UFP and PM2.5 can induce acute pathophysiological responses.
Project description:Fetal heart rate (FHR) monitoring is essential for fetal management during pregnancy and delivery but results in many false-positive diagnoses. Air pollution affects the uterine environment; thus, air pollution may change FHR reactivity. This study assessed the association between exposure to air pollution during pregnancy and FHR monitoring abnormalities using 2005-2010 data from the Japan Perinatal Registry Network database. Participants were 23,782 singleton pregnant women with FHR monitoring, without acidemia or fetal asphyxia. We assessed exposure to air pollutants, including particulate matter (PM), ozone, nitrogen dioxide (NO2), and sulfur dioxide (SO2). In a multi-trimester model, first-trimester PM exposure was associated with false positives in FHR monitoring (odds ratio [OR] per interquartile range (10.7 ?g/m3) increase?=?1.20; 95% CI: 1.05-1.37), but not second-trimester exposure (OR?=?1.05; 95% CI: 0.91-1.21) and third-trimester exposure (OR?=?1.06; 95% CI: 0.96-1.17). The association with first-trimester PM exposure persisted after adjustment for exposure to ozone, NO2, and SO2; however, ozone, NO2, and SO2 exposure was not associated with false positives in FHR monitoring. First-trimester PM exposure may alter fetal cardiac response and lead to false positives in FHR monitoring.
Project description:BACKGROUND:Health effects of air pollution on anaemia have been scarcely studied worldwide. We aimed to explore the associations of long-term exposure to ambient air pollutants with anaemia prevalence and haemoglobin levels in Chinese older adults. METHODS:We used two-level linear regression models and modified Poisson regression with robust error variance to examine the associations of particulate matter (PM) and nitrogen dioxide (NO2) on haemoglobin concentrations and the prevalence of anaemia, respectively, among 10,611 older Chinese adults enrolled in World Health Organization (WHO) Study on global AGEing and adult health (SAGE) China. The average community exposure to ambient air pollutants (PM with an aerodynamic diameter of 10 ?m or less (PM10), 2.5 ?m or less (PM2.5), 1 ?m or less (PM1) and nitrogen dioxide (NO2)) for each participant was estimated using a satellite-based spatial statistical model. Haemoglobin levels were measured for participants from dried blood spots. The models were controlled for confounders. RESULTS:All the studied pollutants were significantly associated with increased anaemia prevalence in single pollutant model (e.g., the prevalence ratios associated with an increase in inter quartile range in three years moving average PM10 (1.05; 95% CI: 1.02-1.09), PM2.5 (1.11; 95% CI: 1.06-1.16), PM1 (1.13; 95% CI: 1.06-1.20) and NO2 (1.42; 95% CI: 1.34-1.49), respectively. These air pollutants were also associated with lower concentrations of haemoglobin: PM10 (-0.53; 95% CI: -0.67, -0.38); PM2.5 (-0.52; 95% CI: -0.71, -0.33); PM1 (-0.55; 95% CI: -0.69, -0.41); NO2 (-1.71; 95% CI: -1.85, -1.57) respectively. CONCLUSIONS:Air pollution exposure was significantly associated with increased prevalence of anaemia and decreased haemoglobin levels in a cohort of older Chinese adults.
Project description:For traffic-related pollutants like ultrafine particles (UFP, Dp < 100 nm), a significant fraction of overall exposure occurs within or close to the transit microenvironment. Therefore, understanding exposure to these pollutants in such microenvironments is crucial to accurately assessing overall UFP exposure. The aim of this study was to develop models for predicting in-cabin UFP concentrations if roadway concentrations are known, taking into account vehicle characteristics, ventilation settings, driving conditions and air exchange rates (AER). Particle concentrations and AER were measured in 43 and 73 vehicles, respectively, under various ventilation settings and driving speeds. Multiple linear regression (MLR) and generalized estimating equation (GEE) regression models were used to identify and quantify the factors that determine inside-to-outside (I/O) UFP ratios and AERs across a full range of vehicle types and ages. AER was the most significant determinant of UFP I/O ratios, and was strongly influenced by ventilation setting (recirculation or outside air intake). Inclusion of ventilation fan speed, vehicle age or mileage, and driving speed explained greater than 79% of the variability in measured UFP I/O ratios.
Project description:Ambient air pollution has been implicated in the development of hypertensive disorders of pregnancy (HDP). However, evidence of the association between air pollution and HDP is still limited, and the effects of gaseous air pollutants on HDP and their time windows of exposure have not been well studied.We used the Florida birth registry data to investigate the associations between air pollutants (NO2, SO2, PM(2.5), O3 and CO) and the risks of HDP in 22,041 pregnant women in Jacksonville, Florida, USA from 2004 to 2005. Further, we examined whether air pollution exposure during different time windows defined by trimesters and the entire pregnancy had different effects on HDP.The single-pollutant logistic regression model showed that exposure to four pollutants during the full pregnancy period was significantly associated with prevalence of HDP after adjusting for covariates: NO2 (OR=1.21, 95% CI 1.09 to 1.35), PM2.5 (OR=1.24, 95% CI 1.08 to 1.43), SO2 (OR=1.13, 95% CI 1.01 to 1.25) and CO (OR=1.12, 95% CI 1.03 to 1.22) per IQR increase. Similar effects were observed when first trimester exposure to NO2, SO2 and CO, and second trimester exposures to PM2.5 were examined. Consistent results were confirmed in multiple-pollutant models.This study suggests that exposure to high levels of air pollution during early pregnancy and the full gestational period was associated with increased prevalence of HDP in Florida, USA.