Personal PM2 Research Articles

Organic Components of Personal PM2.5 Exposure Associated with Inflammation: Evidence from an Untargeted Exposomic Approach.

Fine particulate matter (PM2.5) can promote chronic diseases through the fundamental mechanism of inflammation; however, systemic information is lacking on the inflammatory PM2.5 components. To decipher organic components from personal PM2.5 exposure that were associated with respiratory and circulatory inflammatory responses in older adults, we developed an exposomic approach using trace amounts of particles and applied it on 424 personal PM2.5 samples collected in a panel study in Beijing. Applying an integrated multivariate and univariate untargeted strategy, a total of 267 organic compounds were filtered and then chemically identified according to their association with exhaled nitric oxide (eNO)/interleukin (IL)-6 or serum IL-1β/IL-6, with monocyclic and polycyclic aromatic compounds (i.e., MACs and PACs) as the representatives. Indoor-derived species with medium volatility including MACs were mainly associated with systemic inflammation, while low-volatile ambient components that originate from combustion sources, such as PACs, were mostly associated with airway inflammation. Following ambient component exposure, we found an inverted U-shaped relationship on change of eNO with insulin resistance, suggesting a higher risk of cardiopulmonary dysfunction for individuals with homeostatic model assessment for insulin resistance (HOMA-IR) levels > 2.3. Overall, this study provided a practical untargeted strategy for the systemic investigation of PM2.5 components and proposed source-specific inflammatory effects.

Exposure to Air Pollution in Rural Malawi: Impact of Cooking Methods on Blood Pressure and Peak Expiratory Flow.

We made static and personal PM2.5 measurements with a miniature monitor (RTI MicroPEM) to characterise the exposure of women cooking with wood and charcoal in indoor and outdoor locations in rural Malawi, together with measurements of blood pressure and peak expiratory flow rate (PEFR). Mean PM2.5 concentrations of 1338 and 31 µg/m3 were observed 1 m from cookstove locations during cooking with wood and charcoal, respectively. Similarly, mean personal PM2.5 exposures of 706 and 94 µg/m3 were observed during cooking with wood and charcoal, respectively. Personal exposures to PM2.5 in indoor locations were 3.3 and 1.7 times greater than exposures observed in equivalent outdoor locations for wood and charcoal, respectively. Prior to the measured exposure, six out of eight participants had PEFR observations below 80% of their expected (age and height) standardised PEFR. We observed reductions in PEFR for participants cooking with wood in indoor locations. Five out of eight participants reported breathing difficulties, coughing, and eye irritation when cooking with wood but reported that symptoms were less severe when cooking with charcoal. In conclusion, we observed that exposure to PM2.5 was substantially reduced by cooking outdoor with charcoal. As both wood and charcoal fuels are associated with negative environmental and health impacts, the adoption of high-efficiency cookstoves and less polluting sources of energy will be highly beneficial. Cooking outside whenever possible, and minimising the time spent in close proximity to stoves, may be simple interventions that could reduce the risks of exacerbation and progression of respiratory and cardiovascular diseases in Malawi.

Evaluating carbon content in airway macrophages as a biomarker of personal exposure to fine particulate matter and its acute respiratory effects

It remains unclear whether carbon content in airway macrophages (AM) can predict personal short-term exposure to fine particulate matter (PM2.5) air pollution and its respiratory health effects. We aimed to evaluate the pathway from personal PM2.5 exposure to adverse respiratory outcomes through AM carbon content. We designed a longitudinal panel study with 3 scheduled follow-ups among 113 non-smoking patients of chronic obstructive pulmonary disease in Shanghai, China, from April 2017 to January 2019. We quantified AM carbon content from induced sputum by image analysis, tested lung function and measured sputum levels of 4 pro-inflammatory cytokines and 2 anti-inflammatory cytokines. We applied the “meet in the middle” approach incorporating linear mixed-effect models to evaluate the associations from external PM2.5 exposure to respiratory outcomes through AM carbon content. Our results indicated that personal exposure to PM2.5 within 24 h was significantly associated with decreased forced expiratory volume in 1s and anti-inflammatory cytokines, as well as increased macrophages and pro-inflammatory cytokines. These changes were accompanied by increased areas of AM carbon and higher percentage of AM area occupied by carbon, both of which were associated with increased levels of pro-inflammatory cytokines and decreased levels of anti-inflammatory cytokines. Exposure to ambient black carbon and organic carbon in PM2.5 within 2 days was significantly associated with increased AM carbon area and percentage of AM area occupied by carbon. Our findings reinforced the causality in respiratory health effects of PM2.5 in which increased AM carbon content might serve as a valid exposure biomarker.

Declines in heart rate variability associated with short-term PM2.5 exposure were modified by blood pressure control and treatment: A multi-city panel study in China

Exposure to fine particulate matter (PM2.5) was associated with altered heart rate variability (HRV). However, whether blood pressure (BP) control and angiotensin II receptor blocker (ARB) treatment modifies the associations was seldom addressed. Therefore, we conducted a 3-phase panel study among 282 hypertensive subjects aged 35–74 years in four cities of China to address this issue. Real-time personal PM2.5 sampling and 24-h ambulatory electrocardiogram monitoring were performed repeatedly in 3 different seasons. Linear mixed-effects models were fitted overall and by control status of BP and ARB treatment to assess the associations between short-term PM2.5 exposure and HRV. The average hourly PM2.5 concentrations (Mean ± SD) ranged from 19.3 ± 18.2 μg/m3 to 99.4 ± 76.9 μg/m3 across study phases and cities. Generally, PM2.5 exposure was associated with decreased hourly and 24-h HRV. However, these adverse impacts were attenuated among patients with controlled BP (<140/90 mmHg). For each 10 μg/m3 increment in moving average of previous 2 days' (MA2d) PM2.5 exposure, 24-h SDNN (standard deviation of NN intervals) and rMSSD (root mean square of successive RR interval differences) decreased by 0.89% (95% CI: 0.19%–1.59%) and 2.98% (95% CI: 1.04%–4.89%) among patients with uncontrolled BP (≥140/90 mmHg), whereas no obvious declines were observed among those with controlled BP (Pdifference = 0.007 and 0.022, respectively). Furthermore, ARB treatment alleviated or eliminated PM2.5-associated declines in hourly and 24-h HRV among those with uncontrolled BP. For instance, 24-h SDNN decreased by 1.31% (95% CI: 0.54%–2.07%) with a 10 μg/m3 increment in lag 2 days’ PM2.5 exposure in ARB nonusers, whereas no obvious changes were observed in ARB users (Pdifference = 0.021). In conclusion, although PM2.5 exposure would decrease HRV, better BP control and ARB treatment could attenuate these adverse impacts, which provides supporting evidence for alleviating autonomic dysfunction of hypertension patients living in areas with high-level PM2.5.

Association of personal fine particulate matter and its respiratory tract depositions with blood pressure in children: From two panel studies

Evidence is limited regarding the acute effects of personal fine particulate matter (PM2.5) exposure and its respiratory tract depositions on the alteration of children's blood pressure (BP). We conducted 2 longitudinal panel studies in 2 cities to evaluate the relations of 72-h real-time personal PM2.5 exposure and its depositions in 3 respiratory tract regions over different lag times with BP and the risk of prehypertension and hypertension among 286 children aged 4–12 years. We found the strongest effects of PM2.5 exposure on increased BP and risk of prehypertension and hypertension at lag 2 day, in dose-response manner, even when PM2.5 below Chinese Ambient Air Quality Standard (CAAQS) Grade II. Moreover, compared to PM2.5, tracheobronchial and alveolar depositions displayed more evident effects on BP outcomes. Interestingly, all above relationships were stronger among children in Guangzhou with lower PM2.5 and its deposited doses than those in Weinan. Additionally, boys and those with daily extra-school activity ≥ 1 h were more susceptible to PM2.5-induced BP effects with significant interactions. Our results highlighted that short-term PM2.5 exposure and its respiratory tract depositions were dose-responsive related to higher BP, prevalence of prehypertension and hypertension among children, even when PM2.5 below CAAQS II.

Urinary metabolites of polycyclic aromatic hydrocarbons after short-term fine particulate matter exposure: A randomized crossover trial of air filtration

Research on the relationship between short-term exposure to fine particulate matter (PM2.5) and urinary metabolites of polycyclic aromatic hydrocarbons (PAHs) is sparse in the nonoccupationally exposed populations. A quasi-experimental observation of haze events nested within a randomized crossover trial of alternative 1-week real or sham indoor air filtration was conducted to evaluate the associations of urinary monohydroxy-PAHs (OH-PAHs) with short-term exposure to PM2.5 and PM2.5-bound PAHs. The study was conducted among 57 healthy college students in Beijing, China. PM2.5-bound PAHs and urinary OH-PAHs were quantified using gas chromatography coupled with a triple-quadrupole tandem mass spectrometer. Linear mixed-effect models were applied to evaluate the association of urinary OH-PAHs with time-weighted personal PM2.5 and PM2.5-bound PAHs, controlling for potentially confounding variables. The results demonstrated that air filtration could markedly reduce external exposure to PM2.5 and PM2.5-bound parent, nitrated, and oxygenated PAHs. In the intervention trial, the urinary concentrations of 2-hydroxyfluorene (2-OH-FLU) and 9-hydroxyphenanthrene (9-OH-PHE) were elevated significantly by 16.5% (95% CI, 2.1%, 33.1%) and 37.9% (95% CI, 8.4%, 75.4%), respectively, in association with a doubling increase in personal PM2.5 exposure. Urinary 9-OH-PHE was also significantly positively associated with the increase in the sum of PM2.5-bound parent PAHs. Furthermore, the levels of urinary OH-PAHs such as 2-OH-FLU and 9-OH-PHE in the haze events were elevated by 31.1% (95% CI, 8.7%, 53.4%) and 73.5% (95% CI, 16.0%, 131.0%), respectively, in association with a doubling increase in personal PM2.5 exposure. The findings indicated that urinary 2-OH-FLU and 9-OH-PHE could serve as potential internal exposure biomarkers for assessing short-term PM2.5 exposure in nonoccupational populations.

Personal exposure to fine particulate matter and blood pressure: Variations by particulate sources

Fine particulate matter (PM2.5) is a complex mixture of components which has been associated with various cardiovascular effects, such as elevated blood pressure (BP). However, evidences on specific sources behind these effects remain uncertain. Based on 140 72-h personal measurements among a panel of 36 health college students in Shanghai, China, we assessed associations between source-apportioned PM2.5 exposure and BP changes. Based on personal filter samples, PM2.5 source apportionment was conducted using Positive Matrix Factorization (PMF) model. Linear mixed-effects models were applied to evaluate associations of source-specific PM2.5 exposure with BP changes. Seven sources were identified in PMF analysis. Among them, secondary sulfate (41%) and nitrate (24%) sources contributed most to personal PM2.5, followed by industrial emissions (15%), traffic-related source (10%), coal combustion (6.2%), dust (2.4%) and aged sea salt (1.1%). We found nitrate, traffic-related source and coal combustion were significantly associated with increased BP. For example, an interquartile range increase in PM2.5 from traffic-related source was significantly associated with increase in systolic BP [1.5 (95% CI: 0.26, 2.7) mmHg], diastolic BP [1.2 (95% CI: 0.10, 2.2) mmHg] and mean arterial pressure [1.2 (95% CI: 0.15, 2.2) mmHg]. This is the first investigation linking personal PM2.5 source profile and BP changes. This study provides evidence that several anthropogenic emissions (especially traffic-related emission) may be particularly responsible for BP increases, and highlights that the importance of development of health-oriented PM2.5 source control strategies.

Adverse effects of short-term personal exposure to fine particulate matter on the lung function of patients with chronic obstructive pulmonary disease and asthma: a longitudinal panel study in Beijing, China.

Fine particulate matter (PM2.5) is an important environmental factor affecting human health. However, most studies on PM2.5 and health have used data from fixed monitoring sites to assess PM2.5 exposure, which may have introduced misleading information on the exposure-response relationship. We aimed to assess the effect of short-term personal PM2.5 exposure on lung function in patients with chronic obstructive pulmonary disease (COPD) and asthma. To achieve this, we conducted a longitudinal panel study among 37 COPD patients and 45 asthma patients from Beijing, China. The COPD group and the asthma group completed 148 and 180 lung function tests, respectively. We found that in COPD patients, for every 10-μg/m3 increase in PM2.5 exposure at lag2, the FEV1, FVC and DLco decreased by -0.014 L (95% CI -0.025, -0.003), -0.025 L (95% CI -0.050, -0.003) and -0.089 mmol/min/kPa (95% CI -0.156, -0.023), respectively. There was also a decrease of -0.023 L/s (95% CI -0.042, -0.003) and -0.017 L/s (95% CI -0.032, -0.002) in MMEF at lag3 and lag03, respectively. In the asthma group, every 10-μg/m3 increase in PM2.5 exposure led to a reduction of -0.012 L (95% CI -0.023, -0.001), -0.042 L (95% CI -0.081, -0.003) and -0.061 L/s (95% CI -0.116, -0.004) in the FEV1, FVC and PEF at lag3, respectively. Our findings suggest that PM2.5 exposure may primarily affect both airway function and lung diffusion function in COPD patients, and airway function in asthma patients.

Association between long-term exposure to fine particulate matter and diabetic retinopathy among diabetic patients: A national cross-sectional study in China

BackgroundWhile the relationship between ambient air pollution and diabetes mellitus has recently been reported, data on the association between fine particulate matter (PM2.5) and diabetic complications are limited, especially in microvascular diseases such as diabetic retinopathy. ObjectivesTo investigate the associations between long-term exposure to PM2.5 and the prevalence of diabetic retinopathy in adult diabetic patients in rural China. MethodsThe study population was based on the Rural Epidemiology for Glaucoma in China (REG-China), a national cross-sectional survey conducted in rural China. This analysis selected diabetic patients with or without diabetic retinopathy. A satellite-based spatiotemporal model was used to estimate personal PM2.5 exposure. Logistic regression models were used to investigate the effect of long-term PM2.5 exposure on diabetic retinopathy. ResultsThe analysis included 3111 diabetic participants, 329 of whom were diagnosed with diabetic retinopathy. The median level of exposure to PM2.5 from 2000 to2016 was 59.9 μg/m3. For each 10 μg/m3 increase in PM2.5, the adjusted odds ratio (95% confidence interval) for diabetic retinopathy was 1.41 (1.27, 1.57). In subgroup analyses, the effect of PM2.5 on diabetic retinopathy was significantly stronger in participants who self-reported alcohol consumption. ConclusionThese findings suggest that long-term exposure to high PM2.5 was associated with the risk of diabetic retinopathy among diabetic patients in rural China.

Influence of COVID-19 lockdown overlapping Chinese Spring Festival on household PM2.5 in rural Chinese homes

During the 2019 novel coronavirus (COVID-19) pandemic, many countries took strong lockdown policy to reduce disease spreading, resulting in mitigating the ambient air pollution due to less traffic and industrial emissions. However, limited studies focused on the household air pollution especially in rural area, the potential risk induced by indoor air pollution exposure was unknown during this period. This field study continuously measured real-time PM2.5 levels in kitchen, living room, and outdoor in the normal days (Period-1) and the days of COVID-19 lockdown overlapping the Chinese Spring Festival (Period-2) in rural homes in China. The average daily PM2.5 concentrations increased by 17.4 and 5.1 μg/m3 in kitchen and living room during Period-2, respectively, which may be due to more fuel consumption for cooking and heating caused by larger family sizes than those during the normal days. The ambient PM2.5 concentration in rural areas in Period-2 decreased by 6.7 μg/m3 compared to the Period-1, less than the drop in urban areas (26.8 μg/m3). An increase of mass fraction of very fine particles in ambient air was observed during lockdown overlapping annual festival days, which could be explained by the residential solid fuel burning. Due to higher indoor air pollution level and longer time spent in indoor environments, daily personal exposure to PM2.5 was 134 ± 40 μg/m3 in Period-2, which was significantly higher than that during in Period-1 (126 ± 27 μg/m3, p < 0.05). The increase of personal PM2.5 exposure during Period-2 could potentially have negative impact on human health, indicating further investigations should be performed to estimate the health impact of global COVID-19 lockdown on community, especially in rural homes using solid fuels as the routine fuels.

Identification of High Personal PM2.5 Exposure during Real Time Commuting in the Taipei Metropolitan Area

There has been an increase in the network of mass rapid transit (MRT) and the number of automobiles over the past decades in the Taipei metropolitan area, Taiwan. The effects of these changes on PM2.5 exposure for the residents using different modes of transportation are unclear. Volunteers measured PM2.5 concentrations while commuting in different modes of transportation using a portable PM2.5 detector. Exposure to PM2.5 (median (range)) was higher when walking along the streets (40 (10–275) µg/m3) compared to riding the buses (35 (13–65) µg/m3) and the cars (15 (8–80) µg/m3). PM2.5 concentrations were higher in underground MRT stations (80 (30–210) µg/m3) and inside MRT cars running in underground sections (80 (55–185) µg/m3) than those in elevated MRT stations (33 (15–35) µg/m3) and inside MRT cars running in elevated sections (28 (13–68) µg/m3) (p &lt; 0.0001). Riding motorcycle also was associated with high PM2.5 exposure (75 (60–105 µg/m3), p &lt; 0.0001 vs. walking). High PM2.5 concentrations were noted near the temples (588 ± 271 µg/m3) and in the underground food court of a night market (405 ± 238 µg/m3) where the eatery stalls stir-fried and grilled food (p &lt; 0.0001 vs. walking). We conclude that residents in the Taipei metropolitan area may still be exposed to high PM2.5 during some forms of commuting, including riding underground MRT.

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

Association of fine particulate matter with glucose and lipid metabolism: a longitudinal study in young adults

ObjectivesThis study aimed to evaluate whether PM2.5 exposure in a highly polluted area (>100 µg/m3) affects glucose and lipid metabolism in healthy adults.MethodsWe recruited 110 healthy adults in Baoding city,...

Characterizing outdoor infiltration and indoor contribution of PM2.5 with citizen-based low-cost monitoring data

Epidemiological research on the adverse health outcomes due to PM2.5 exposure frequently relies on measurements from regulatory air quality monitors to provide ambient exposure estimates, whereas personal PM2.5 exposure may deviate from ambient concentrations due to outdoor infiltration and contributions from indoor sources. Research in quantifying infiltration factors (Finf), the fraction of outdoor PM2.5 that infiltrates indoors, has been historically limited in space and time due to the high costs of monitor deployment and maintenance. Recently, the growth of openly accessible, citizen-based PM2.5 measurements provides an unprecedented opportunity to characterize Finf at large spatiotemporal scales. In this analysis, 91 consumer-grade PurpleAir indoor/outdoor monitor pairs were identified in California (41 residential houses and 50 public/commercial buildings) during a 20-month period with around 650000h of paired PM2.5 measurements. An empirical method was developed based on local polynomial regression to estimate site-specific Finf. The estimated site-specific Finf had a mean of 0.26 (25th, 75th percentiles: [0.15, 0.34]) with a mean bootstrap standard deviation of 0.04. The Finf estimates were toward the lower end of those reported previously. A threshold of ambient PM2.5 concentration, approximately 30μg/m3, below which indoor sources contributed substantially to personal exposures, was also identified. The quantified relationship between indoor source contributions and ambient PM2.5 concentrations could serve as a metric of exposure errors when using outdoor monitors as an exposure proxy (without considering indoor-generated PM2.5), which may be of interest to epidemiological research. The proposed method can be generalized to larger geographical areas to better quantify PM2.5 outdoor infiltration and personal exposure.

A community-based study on associations between PM2.5 and PM1 exposure and heart rate variability using wearable low-cost sensing devices.

Few studies have investigated the effect of personal PM2.5 and PM1 exposures on heart rate variability (HRV) for a community-based population, especially in Asia. This study evaluates the effects of personal PM2.5 and PM1 exposure on HRV during two seasons for 35 healthy adults living in an urban community in Taiwan. The low-cost sensing (LCS) devices were used to monitor the PM levels and HRV, respectively, for two consecutive days. The mean PM2.5 and PM1 concentrations were 13.7±11.4 and 12.7±10.5μg/m3 (mean±standard deviation), respectively. Incense burning was the source that contributed most to the PM2.5 and PM1 concentrations, around 9.2μg/m3, while environmental tobacco smoke exposure had the greatest impacts on HRV indices, being associated with the highest decrease of 20.2% for high-frequency power (HF). The results indicate that an increase in PM2.5 concentrations of one interquartile range (8.7μg/m3) was associated with a change of-1.92% in HF and 1.60% in ratio of LF to HF power (LF/HF). Impacts on HRV for PM1 were similar to those for PM2.5. An increase in PM1 concentrations of one interquartile range (8.7μg/m3) was associated with a change of-0.645% in SDNN,-1.82% in HF and 1.54% in LF/HF. Stronger immediate and lag effects of PM2.5 exposure on HRV were observed in overweight/obese subjects (body mass index (BMI) ≥24kg/m2) compared to the normal-weight group (BMI <24kg/m2). These results indicate that even low-level PM concentrations can still cause changes in HRV, especially for the overweight/obese population.

Impacts of Chinese spring festival on household PM2.5 pollution and blood pressure of rural residents.

Household air pollution (HAP) from residential combustion considerably affects human health in rural China. Large-scale population migration and rural lifestyle changes during the Spring Festival are supposed to change the household air pollution and health risks; however, limited field study has determined its impacts on HAP and short-term health outcomes. A field study was conducted in rural areas of Southern China before and during the Spring Festival to explore the associations between HAP and blood pressure considering different factors such as cooking fuel, heating fuel, and smoking. Stationary real-time PM2.5 monitors were used to measure PM2.5 concentrations of the kitchen, living room, and yard of 156 randomly selected households. Personal exposure to PM2.5 was calculated based on the results of stationary samplers and corresponding time local residents spent in different microenvironments, and one adult resident was recruited of each family for the blood pressure measurement. Both personal exposure to PM2.5 and blood pressures of local residents increased during Spring Festival compared to the days before the holiday. Based on generalized linear model coupled with dominance analysis approach, it was found that personal PM2.5 exposure was positively associated with the factors of population size and the types of cooking and heating fuels with the relative contributions of approximately 82%, and systolic blood pressure (SBP, 100-120mmHg as normal range for adults) was positively and significantly associated with personal PM2.5 exposures with the relative contribution of 11%. The findings in this study demonstrated that Spring Festival can give rise to increase of HAP and hypertension risks, also related to tremendous solid fuel use, suggesting further policy making on promoting cleaner energy in rural areas and more attention on large population migration during national holidays.

Association of short-term exposure to source-specific PM2.5 with the cardiovascular response during pregnancy in the Shanghai MCPC study

Fine particulate matter (PM2.5) has been reported to be associated with the risk of cardiovascular diseases in pregnancy, but few studies have investigated its association with physiological changes in the cardiovascular system; furthermore, the possible effects of source-specific PM2.5 have not been explored. 176 pregnant women were enrolled from the Shanghai Maternal-Child Pairs Cohort (MCPC) in this study to assess the associations between source-specific PM2.5 and changes in the cardiovascular system. Personal PM2.5 exposure measurements and echocardiography examinations were carried out during two follow-up visits (second trimester: 17.3 ± 1.6 weeks and third trimester: 32.3 ± 2.2 weeks) from February 2017 to September 2018. Various chemical components in PM2.5 samples were then determined, including elements, ions, and organic/elemental carbon. Positive matrix factorization (PMF) was used for source apportionment of PM2.5, and linear mixed-effects models were developed to estimate associations between source-specific PM2.5 and the cardiovascular response. Nine pollution factors were identified, namely, secondary sulfate/nitrate, secondary organic carbon (SOC), coal combustion, motor vehicle emissions, residual oil combustion, cosmetics, sea salt, dust and industry emissions. An interquartile range (IQR) increase in residual oil combustion was associated with decreases in cardiac output [−5.25% (95% confidence interval (CI): −9.60, −0.69)] and cardiac index [−5.13% (95% CI: −9.38, −0.70)]. An IQR increase in dust was associated with decreased left ventricular ejection fraction [−0.65% (95% CI: −1.17, −0.11)] and left ventricular fractional shortening [−0.97% (95% CI: −1.69, −0.21)]. In addition, the total PM2.5 mass, cosmetics, and secondary pollution factors (secondary sulfate/nitrate and SOC) were also associated with changes in cardiac structure. The results indicated that short-term exposure to PM2.5 from residual oil combustion and dust appeared to be potential risk factors for decreased left ventricular systolic function in pregnant women. Further research is needed to confirm these preliminary findings.

Acute effects of personal exposure to fine particulate matter on salivary and urinary biomarkers of inflammation and oxidative stress in healthy adults

Non-invasive bio-samples, such as saliva and urine, are promising tools for assessment of inflammation and oxidative stress biomarkers. Few studies have investigated potential responses of those biomarkers towards short-term PM2.5 exposure. We conducted a longitudinal study with 4 repeated examinations among 40 healthy, nonsmoking adults in Shanghai, China. Personal samplings were performed for PM2.5 exposure assessment. Then, five biomarkers, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), alpha-1 antitrypsin (A1AT) in saliva and 8-Iso-Prostaglanding F2α (8-iso-PGF2α), total antioxidant capacity (TAC) in urine, were measured. We fitted linear mixed-effect models to evaluate short-term effect of personal PM2.5 exposure on salivary and urinary biomarkers, adjusting for potential confounders of meteorology, sociodemographic characteristics and biomarker detection. We also explored sensitive time windows of exposure for different biomarkers. We found robust associations of salivary CRP, TNF-α, and urinary 8-iso-PGF2α with PM2.5 exposure, and responses of salivary inflammatory markers occurred more acutely than urinary oxidative stress markers. For instance, a 10 μg/m3 increase in PM2.5 was associated with an elevation of 5.49% (95% CI: 1.17%, 9.99%) in CRP and 7.05% (95% CI: 1.29%, 13.13%) in TNF-α both at lag 12 h, and 6.97% (95% CI: 1.33%, 12.92%) in 8-iso-PGF2α at lag 01 d. Based on non-invasive samples, this study provided evidence on effect of PM2.5 exposure on responses of systematic inflammation and oxidative stress. Sub-daily (6–12 h) and daily (≥24 h) period after PM2.5 exposure might be sensitive time window to detect the responses of salivary (i.e. CRP, TNF) and urinary biomarkers (i.e. 8-iso-PGF2α), respectively.

Toxicological effects of personal exposure to fine particles in adult residents of Hong Kong.

Toxicological studies have demonstrated the associations between fine particle (PM2.5) components and various cytotoxic endpoints. However, few studies have investigated the toxicological effects of source-specific PM2.5 at the individual level. To investigate the potential impact of source-specific PM2.5 on cytotoxic effects, we performed repeated personal PM2.5 monitoring of 48 adult participants in Hong Kong during the winter and summer of 2014-2015. Quartz filters were analyzed for carbonaceous aerosols and water-soluble ions in PM2.5. Teflon filters were collected to determine personal PM2.5 mass and metal concentrations. The toxicological effects of personal PM2.5 exposure-including cytotoxicity, inflammatory response, and reactive oxygen species (ROS) production-were measured using A549cells invitro. Personal PM2.5 samples collected in winter were more effective than those collected in summer at inducing cytotoxicity and the expression of proinflammation cytokine IL-6. By contrast, summer personal PM2.5 samples induced high ROS production. We performed a series of statistical analyses, Spearman correlation and a source apportionment approach with a multiple linear regression (MLR) model, to explore the sources contributing most significantly to personal PM2.5 bioreactivity. Secondary inorganic species and transition metals were discovered to be weak-to-moderately associated with cytotoxicity (rs: 0.26-0.55; p<0.01) and inflammatory response (rs: 0.26-0.44; p<0.05), respectively. Carbonaceous aerosols (i.e., organic and elemental carbon; rs: 0.23-0.27; p<0.05) and crustal material (Mg and Ca) was positively associated with ROS generation. The PMF-MLR models revealed that tailpipe exhaust and secondary sulfate contributed to ROS generation, whereas secondary nitrate was the major contributor to PM2.5 cytotoxicity and inflammation. These results improve and variate the arguments for practical policies designed to mitigate the risks posed by air pollution sources and to protect public health.

Personal exposure monitoring of PM2.5 among US diplomats in Kathmandu during the COVID-19 lockdown, March to June 2020

The 2019 Novel Coronavirus SARS-CoV 2 (COVID-1911COVID-19: 2019 Novel Coronavirus SARS-CoV 2, PM2.5: particulate matter with diameter smaller than 2.5 mg; BAM: Beta attenuation monitor, RAC: room air cleaner.) pandemic has severely impacted global health, safety, economic development and diplomacy. The government of Nepal issued a lockdown order in the Kathmandu Valley for 80 days from 24 March to 11 June 2020. This paper reports associated changes in ambient PM2.5 measured at fixed-site monitors and changes in personal exposure to PM2.5 monitored by APT Minima by four American diplomats who completed monitoring before and during lockdown (24 h for each period per person, 192 person-hours in total). Time activities and use of home air pollution mitigation measures (use of room air cleaners (RACs), sealing of homes) were recorded by standardized diary. We compared PM2.5 exposure level by microenvironment (home (cooking), home (other activities), at work, commuting, other outdoor environment) in terms of averaged PM2.5 concentration and the contribution to cumulative personal exposure (the product of PM2.5 concentration and time spent in each microenvironment). Ambient PM2.5 measured at fixed-sites in the US Embassy and in Phora Durbar were 38.2% and 46.7% lower than during the corresponding period in 2017–2019. The mean concentration of PM2.5 to which US diplomats were exposed was very much lower than the concentrations of ambient levels measured at fixed site monitors in the city both before and during lockdown. Within-person comparisons suggest personal PM2.5 exposure was 50.0% to 76.7% lower during lockdown than before it. Time spent outdoors and cooking at home were large contributors to cumulative personal exposure. Low indoor levels of PM2.5 were achieved at work and home through use of RACs and measures to seal homes against the ingress of polluted air from outside. Our observations indicate the potential reduction in exposure to PM2.5 with large-scale changes to mainly fossil-fuel related emissions sources and through control of indoor environments and activity patterns.