Effects Of Air Pollution Exposure Research Articles

A comparison of the systematic reviews and meta-analyses conducted to explore the effect of air pollution exposure during pregnancy and the risk of preterm birth

Background and aims There has been a rapid rise in systematic reviews and meta-analyses (SR/MAs) conducted on the association between air pollution exposure during pregnancy and the risk of preterm birth in recent years. Few studies have examined differences in their quality and if they have provided additional insight into the field. This study analysed previous SR/MAs to explore their practices and identify gaps and opportunities for the research field. This work was done to determine if an upcoming SR/MA was needed. Methods A literature search using major English and Chinese databases was performed to find SR/MAs published from 2010 onwards. Information regarding publication date, methods of quality assessment, consideration of population overlap, and primary studies included in their analysis were extracted and compared. Results Seventeen SR/MAs, which included thirteen MAs were conducted from 2010 onwards. A large variety of quality assessment tools were used, but the Newcastle-Ottawa Scale was the most common (n=6). Seven MAs explicitly mentioned that they took population overlap into account. Four SR/MAs were found in 2021 alone, but three did not examine the whole literature and focused on specific study designs or exposure assessment methods. They were thus unable to build on finding of previous work due to exclusion of studies that were included in other SR/MAs. Conclusions A considerable number of SR/MAs provided limited addition to the field as they were conducted without sufficient rigour. This may hinder coming to a consensus on the effect estimate of interest and overlook field-specific biases. Therefore, a new SR/MA with improvements in transparency in reporting, replicability of findings, and quality assessment of studies is required. The protocol of this SR/MA is now registered on PROSPERO and will begin in due course. Keywords Maternal exposure; preterm birth; meta-analysis; birth outcomes, air pollution; pregnancy

OA13.03 Evaluation of Outdoor Air Pollution Exposure (PM2.5) In Female Non-smoking Lung Cancer Patients

More females than males who never smoke have lung cancer. Increasing evidence indicates that air pollution is a major cause of lung cancer in people who have never smoked. In 2013, the International Agency for Research on Cancer classified outdoor air pollution and particulate matter 2.5 micrograms/meter3 (PM2.5) in outdoor air pollution as carcinogenic to humans (Group 1) and causes of lung cancer. The effects of air pollution exposure may take 15 to 20 years to be reflected in the lung adenocarcinoma incidence rate.

The effect of air pollution exposure on risk of outpatient visits for Sjogren's syndrome: A time-series study

BackgroundEmerging evidence showed that air pollutants are associated with development and recurrence of autoimmune disorders, but there is scarce evidence regarding the relationship between air pollutants and Sjogren's syndrome (SS). We sought to investigate whether air pollutants affect the risk of outpatient visits for SS and to quantify the burden of SS visits attributable to air pollution exposure in Hefei, China. MethodsDaily data on outpatient visits for SS, air pollutants and meteorological data in Hefei, China, from January 1, 2015 to December 31, 2020 were obtained. A distributed lag non-linear model in conjunction with a generalized linear model were employed to assess the relationship between air pollution and SS outpatient visits. Stratified analyses were further performed by gender, age and season. Attributable fraction (AF) and attributable number (AN) were used to reflect disease burden. ResultsThere were 4501 records of outpatient visits for SS. Exposure to PM2.5 was associated with increased risk of SS outpatient visits (relative risk (RR) = 1.218, 95% confidence interval (CI): 1.017–1.458, lag 0–14 day). An increase of 24 μg/m3 (interquartile range) in NO2 concentration was associated with 26.3% increase in the risk of SS outpatient visits (RR = 1.263, 95%CI: 1.105–1.445, lag 0–10 day). In contrast, exposure to O3 was associated with decreased risk of SS outpatient visits (RR = 0.692, 95%CI: 0.510–0.939, per 63 μg/m3 in O3 exposure, lag 0–27 day). Stratified analyses showed that females (vs. males) was more vulnerable to SS outpatient visits associated with NO2 and O3 exposure. SS patients aged ≥65 years (vs. aged <65 years) were susceptible to PM2.5 exposure. Exposure to PM2.5 or NO2 in the cold season was associated with higher risk of SS outpatient visits than that in the warm season. In addition, the AN (232, 95%CI: 119, 324) and AF (5.16%, 95%CI: 2.55%, 7.21%) of NO2 exposure were higher than those of PM2.5 exposure. ConclusionPM2.5 and NO2 exposure are associated with increased risk of SS outpatient visits, while O3 exposure appears to be associated with decreased risk of SS outpatient visits. The effect of air pollutants exposure on risk of SS outpatients can be modified by age, gender and season. The burden of SS outpatient visits attributable to NO2 exposure is higher than those attributable to PM2.5 exposure.

Health Outcomes in Children Associated with Prenatal and Early-Life Exposures to Air Pollution: A Narrative Review.

(1) Background: The developmental origins of health and disease (DOHaD) hypothesis links adverse fetal exposures with developmental mal-adaptations and morbidity later in life. Short- and long-term exposures to air pollutants are known contributors to health outcomes; however, the potential for developmental health effects of air pollution exposures during gestation or early-childhood have yet to be reviewed and synthesized from a DOHaD lens. The objective of this study is to summarize the literature on cardiovascular and metabolic, respiratory, allergic, and neuropsychological health outcomes, from prenatal development through early childhood, associated with early-life exposures to outdoor air pollutants, including traffic-related and wildfire-generated air pollutants. (2) Methods: We conducted a search using PubMed and the references of articles previously known to the authors. We selected papers that investigated health outcomes during fetal or childhood development in association with early-life ambient or source-specific air pollution exposure. (3) Results: The current literature reports that prenatal and early-childhood exposures to ambient and traffic-related air pollutants are associated with a range of adverse outcomes in early life, including cardiovascular and metabolic, respiratory and allergic, and neurodevelopmental outcomes. Very few studies have investigated associations between wildfire-related air pollution exposure and health outcomes during prenatal, postnatal, or childhood development. (4) Conclusion: Evidence from January 2000 to January 2022 supports a role for prenatal and early-childhood air pollution exposures adversely affecting health outcomes during development. Future studies are needed to identify both detrimental air pollutants from the exposure mixture and critical exposure time periods, investigate emerging exposure sources such as wildfire, and develop feasible interventional tools.

The effects of air pollutants exposure on the transmission and severity of invasive infection caused by an opportunistic pathogen Streptococcus pyogenes

Currently, urbanization is associated with an increase in air pollutants that contribute to invasive pathogen infections by altering the host's innate immunity and antimicrobial resistance capability. Streptococcus pyogenes, also known as Group A Streptococcus (GAS), is a gram-positive opportunistic pathogen that causes a wide range of diseases, especially in children and immunosuppressed individuals. Diesel exhaust particle (DEP), a significant constituent of particulate matter (PM), are considered a prominent risk factor for respiratory illness and circulatory diseases worldwide. Several clinical and epidemiological studies have identified a close association between PM and the prevalence of viral and bacterial infections. This study investigated the role of DEP exposure in increasing pulmonary and blood bacterial counts and mortality during GAS M1 strain infection in mice. Thus, we characterized the upregulation of reactive oxygen species production and disruption of tight junctions in the A549 lung epithelial cell line due to DEP exposure, leading to the upregulation of GAS adhesion and invasion. Furthermore, DEP exposure altered the leukocyte components of infiltrated cells in bronchoalveolar lavage fluid, as determined by Diff-Quik staining. The results highlighted the DEP-related macrophage dysfunction, neutrophil impairment, and imbalance in pro-inflammatory cytokine production via the toll-like receptor 4/mitogen-activated protein kinase signaling axis. Notably, the tolerance of the GAS biofilms toward potent antibiotics and bacterial resistance against environmental stresses was also significantly enhanced by DEP. This study aimed to provide a better understanding of the physiological and molecular interactions between exposure to invasive air pollutants and susceptibility to invasive GAS infections.

Effects of air pollution exposure predicting sleep efficiency in children modified by exposure to violence, 4-7 years, in the PROGRESS birth cohort

Effects of air pollution exposure predicting sleep efficiency in children modified by exposure to violence, 4-7 years, in the PROGRESS birth cohort

Invited Perspective: HEPA Filters-An Effective Way to Prevent Adverse Air Pollution Effects on Neurodevelopment?

Invited Perspective: HEPA Filters-An Effective Way to Prevent Adverse Air Pollution Effects on Neurodevelopment?

Circulating microRNAs as putative mediators in the association between short-term exposure to ambient air pollution and cardiovascular biomarkers

BackgroundExposure to ambient air pollution is associated with increased cardiovascular morbidity and mortality. Circulating microRNAs (miRNAs) may mediate cardiovascular effects of exposure to air pollution. This study aims to investigate whether circulating miRNAs mediate the associations between short-term human exposure to ambient air pollution and cardiovascular biomarkers. MethodsTwenty-four healthy adults residing in the Research Triangle area of North Carolina, USA were enrolled between December 2016 and July 2019. Circulating miRNAs, protein, and lipid biomarkers were assessed repeatedly for 3 sessions separated by at least 7 days. Linear mixed-effects models were used to assess the associations between air pollutant concentrations obtained from nearby air quality monitoring stations and miRNAs controlling for covariates including omega-3 index, relative humidity, and temperature. miRNAs that were significantly altered were then matched with protein or blood lipid biomarkers using either Ingenuity Pathway Analysis or a literature search. A mediation analysis was performed to test the statistical significance of miRNA’s mediating effects between exposure to air pollution and cardiovascular biomarkers. ResultsShort-term exposure to ambient fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) was associated with changes in 11, 9, and 24 circulating miRNAs, respectively. Pathway analysis showed that several miRNAs including miR-125b-5p, miR-144–5p, miR-26a-5p, and miR-34a-5p may mediate the effects of air pollutant exposure on the changes of downstream protein / lipid biomarkers including serum amyloid A (SAA), C-reactive protein (CRP), soluble vascular adhesive molecules 1 (sICAM1), total cholesterol, and high-density lipoproteins (HDL). Mediation analysis showed that only miR-26a-5p significantly mediated air pollutant (PM2.5 and NO2)-induced effects on blood CRP and total cholesterol levels. For example, 34.1% of PM2.5–associated changes in CRP were significantly mediated by miR-26a-5p at lag4 [indirect effects, 0.06 (0.02, 0.10), P = 0.005]. Similarly, the proportions of indirect effects of miR-26a-5p on the association between NO2 exposure and CRP were 46.8% at lag2 [0.06 (0.02, 0.11), P = 0.003], 61.2% at lag3 [0.05 (0.00, 0.09), P = 0.04], and 30.8% at 5-day moving average [0.06 (0.02, 0.10), P = 0.01]. In addition, omega-3 index may be a significant modifying factor of the mediated effects of miRNAs. ConclusionsThis study demonstrates that short-term exposure to ambient PM2.5, O3, and NO2 was associated with specific circulating miRNAs, and some of which may mediate their effects on the downstream inflammation and blood lipid markers.

Acute effects of ambient air pollution exposure on lung function in the elderly in Hangzhou, China

ABSTRACT Evidence of an association between acute air pollution exposure and lung function in the elderly is limited. This study is cross-sectional. We quantified the effects of air pollution exposure on lung function among 256 elderly by using a linear mixed model. The results revealed that air pollutants had lag effects on lung function after adjusting for confounders. PM2.5 (Lag03, Lag 03 was defined three-day moving average, and so forth), PM10, NO2 (Lag04-Lag05) were significantly associated with reduced FEV1. PM2.5 (Lag01-Lag02), PM10 (Lag0-Lag07), NO2 (Lag0, Lag04), and SO2 (Lag0) were significantly associated with reduced Forced vital capacity (FVC). PM2.5 (Lag04-Lag07) and NO2 (Lag01-Lag07) were significantly associated with reduced FEF25%–75%. The results showed the adverse change was stronger after adjusting for other pollutants in the PM models, and women were more susceptible to air pollutants. Therefore, we should pay attention to the problem of air pollution in the elderly, especially in women.

Short-term effects of air pollutant exposure on small airway dysfunction, spirometry, health-related quality of life, and inflammatory biomarkers in wildland firefighters: a pilot study

ABSTRACT We aim to assess small airway dysfunction, spirometry, health-related quality of life (HR-QoL), and inflammatory biomarkers between the wildland firefighters and healthy controls. Lung function including impulse oscillometry (IOS) and spirometry, HR-QoL measured by the 36-Item Short Form Survey (SF-36) and St. George’s Respiratory Questionnaire (SGRQ), high sensitivity C-Reactive Protein (hsCRP), and D-dimer were collected twice in the non-pollution period and pollution period. Gaussian regression was used for comparison all parameters between two groups. The results showed that the changes in area under reactance curve between 5 Hz and resonant frequency (AX) between the non-pollution and pollution periods in wildland firefighters was significantly higher compared to healthy controls (adjusted mean difference = 0.15 kPa/L, 95%CI;0.01, 0.28, p = 0.032). Our pilot study concluded that there was short-term effect on small airway function in wildland firefighter air pollutant exposure. However, there was no effect on spirometry, HRQoL, and inflammatory biomarkers in young wildland firefighters. Clinical Trials Registry: Study ID: TCTR20200828005

Effects of air pollution exposure on inflammatory and endurance performance in recreationally trained cyclists adapted to traffic-related air pollution.

The aim of the present study was to analyze the effects of traffic-related air pollution (TRAP) on markers of inflammatory, neuroplasticity, and endurance performance-related parameters in recreationally trained cyclists who were adapted to TRAP during a 50-km cycling time trial (50-km cycling TT). Ten male cyclists performed a 50-km cycling TT inside an environmental chamber located in downtown Sao Paulo (Brazil), under TRAP or filtered air conditions. Blood samples were obtained before and after the 50-km cycling TT to measure markers of inflammatory [interleukin-6 (IL-6), C-reactive protein (CRP), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1)] and neuroplasticity [brain-derived neurotrophic factor (BDNF)]. Rating of perceived exertion (RPE), heart rate (HR), and power output (PO) were measured throughout the 50-km cycling TT. There were no significant differences between experimental conditions for responses of IL-6, CRP, and IL-10 (P > 0.05). When compared with exercise-induced changes in filtered air condition, TRAP provoked greater exercise-induced increase in BDNF levels (TRAP = 3.3 ± 2.4-fold change; Filtered = 1.3 ± 0.5-fold change; P = 0.04) and lower exercise-induced increase in ICAM-1 (Filtered = 1.1 ± 0.1-fold change; TRAP = 1.0 ± 0.1-fold change; P = 0.01). The endurance performance-related parameters (RPE, HR, PO, and time to complete the 50-km cycling TT) were not different between TRAP and filtered air conditions (P > 0.05). These findings suggest that the potential negative impacts of exposure to pollution on inflammatory, neuroplasticity, and performance-related parameters do not occur in recreationally trained cyclists who are adapted to TRAP.

Maternal air pollution exposure during the first trimester of pregnancy and markers of inflammation and endothelial dysfunction

BackgroundMaternal exposure to air pollutants has been associated with pregnancy complications and adverse birth outcomes. Endothelial dysfunction, an imbalance in vascular function, during pregnancy is considered a key element in the development of pre-eclampsia. Environmental exposure to particulate matter (PM) during the first trimester of pregnancy might increase maternal inflammatory status thus affecting fetal growth, possibly leading to preterm delivery. ObjectivesThe purpose of the study was to evaluate possible effects of PM10 and PM2.5 exposure on fetal growth in healthy pregnant women at the end of the first trimester of pregnancy by investigating the relationship between circulating biomarkers of inflammation (IL-6), early systemic prothrombotic effects (CRP, plasma fibrinogen, PAI-1) and endothelial dysfunction (sICAM-1 and sVCAM-1). Methods295 pregnant women were recruited. Individual PM exposure was assigned to each subject by calculating the mean of PM10 and PM2.5 daily values observed during the 30, 60, and 90 days preceding enrolment (long-term) and single lag days back to fourteen days (short-term), and circulating plasma biomarkers were determined. ResultsFor long-term exposure, we observed an increase in sVCAM-1 and a decrease of PAI-1 levels for each 10 μg/m3 increase in PM10 concentration. Decreases in IL-6 and CRP levels were associated with each 10 μg/m3 PM2.5 increase. For short-term exposure, the levels of sVCAM-1 and PAI-1 were found to be associated with PM10 exposure, whereas fibrinogen levels were associated with PM2.5 exposure. Maternal plasmatic fibrinogen levels were negatively associated with the crown-rump length (p-value = 0.008). DiscussionThe present study showed that both long- and short-term exposures to PM are associated with changes in circulating levels of biomarkers in pregnant women reflecting systemic inflammation and endothelial dysfunction/activation. Our findings support the hypothesis that inflammation and endothelial dysfunction might have a central role in modulating the detrimental effects of air pollution exposure during pregnancy.

Mediating effects of gut microbiota in the associations of air pollutants exposure with adverse pregnancy outcomes

BackgroundThe aim of this study was to investigate alterations in gut microbiota after exposure to air pollutants during pregnancy and its mediation effect in inducing adverse pregnancy outcomes (APOs). MethodsParticipants (n = 916) were enrolled between 2017 and 2018 from a prospective cohort study of pregnant women in Guangzhou, China. The relative abundance of fecal microbiota was profiled using 16SrRNA V4 region sequencing. Exposure to air pollutants in each trimester of pregnancy was assessed using measurements from the nearest monitoring station. APOs including pre-term birth (PTB), post-term birth (POTB), low birth weight (LBW), macrosomia fetus (MF), birth defects (BDs), pathological cesarean section (PCS) and postpartum hemorrhage (PPH)) were determined by referring to reliable clinical records and diagnostic criteria. Univariate analysis, multivariate analysis and mediation analysis were performed to estimate the association among air pollutants, gut microbiota and APOs. ResultsAir pollutants exposure during pregnancy was significantly correlated with the alterations in the gut microbiota, and increased risks of various APOs by 1.07–1.36-fold (P < 0.05). The mediation analyses indicated that alterations in Eggerthella, Phascolarctobacterium and Clostridium partially mediated the effects of air pollutants exposure (PM2.5, PM10, O3, NO2 and SO2) on APOs. The relative abundance of f_Micrococcaceae explained 11.39%, 64.90% and 54.80% of the correlation between SO2, PM2.5, PM10 and POTB, respectively; whereas g_Rothia explained 11.97%, 67.80% and 54.50%, respectively. g_Parabacteroides explained 53.0% of the correlation between PM2.5 and PTB. ConclusionsIncreased air pollutants exposure during pregnancy may induce adverse pregnancy outcomes via alteration of the gut microbiota.

Association between Particulate Matter Pollution Concentration and Hospital Admissions for Hypertension in Ganzhou, China.

Fine particulate matter (PM2.5) and respirable particulate matter (PM10) are two major air pollutants with toxic effects on the cardiovascular system. Hypertension, as a chronic noncommunicable cardiovascular disease, is also a risk factor for several diseases. We applied generalized linear models with a quasi-Poisson link to assess the effect of air pollution exposure on the number of daily admissions for patients with hypertension. In addition, we established a two-pollutant model to evaluate PM2.5 and PM10 hazard effect stability by adjusting the other gaseous pollutants. Results showed that during the study period, 24 h mean concentrations of ambient PM2.5 and PM10 at 38.17 and 59.84 μg/m3, respectively, and a total of 2,611 hypertension hospital admissions were recorded. Air pollution concentrations significantly affected the number of hospitalizations for hypertension approximately 2 months after exposure. For each 10 μg/m3 increase in PM2.5 and PM10 in single-pollutant models, the number of hospitalizations for hypertension increased by 7.92% (95% CI: 5.48% to 10.42%) and 4.46% (95% CI: 2.86% to 5.65%), respectively, at the lag day with the strongest effect. NO2, O3, CO, and SO2 had different significant effects on the number of hospitalizations over the same time period, and PM2.5 and PM10 still showed robust significant effects after adjustment of gas pollutants through a two-pollutant model. These findings may contribute to a better understanding of the health effects of ambient particulate matter.

Increasing risk of gestational diabetes and preeclampsia associated with long-term exposure effects of air pollution

Increasing risk of gestational diabetes and preeclampsia associated with long-term exposure effects of air pollution

Air Pollutants and Asthma Hospitalization in the Medicaid Population.

Rationale: Risk of asthma hospitalization and its disparities associated with air pollutant exposures are less clear within socioeconomically disadvantaged populations, particularly at low degrees of exposure. Objectives: To assess effects of short-term exposures to fine particulate matter (particulate matter with an aerodynamic diameter of ⩽2.5 μm [PM2.5]), warm-season ozone (O3), and nitrogen dioxide (NO2) on risk of asthma hospitalization among national Medicaid beneficiaries, the most disadvantaged population in the United States, and to test whether any subpopulations were at higher risk. Methods: We constructed a time-stratified case-crossover dataset among 1,627,002 hospitalizations during 2000-2012 and estimated risk of asthma hospitalization associated with short-term PM2.5, O3, and NO2 exposures. We then restricted the analysis to hospitalizations with degrees of exposure below increasingly stringent thresholds. Furthermore, we tested effect modifications by individual- and community-level characteristics. Measurements and Main Results: Each 1-μg/m3 increase in PM2.5, 1-ppb increase in O3, and 1-ppb increase in NO2 was associated with 0.31% (95% confidence interval [CI], 0.24-0.37%), 0.10% (95% CI, 0.05 - 0.15%), and 0.28% (95% CI, 0.24 - 0.32%) increase in risk of asthma hospitalization, respectively. Low-level PM2.5 and NO2 exposures were associated with higher risk. Furthermore, beneficiaries with only one asthma hospitalization during the study period or in communities with lower population density, higher average body mass index, longer distance to the nearest hospital, or greater neighborhood deprivation experienced higher risk. Conclusions: Short-term air pollutant exposures increased risk of asthma hospitalization among Medicaid beneficiaries, even at concentrations well below national standards. The subgroup differences suggested individual and contextual factors contributed to asthma disparities under effects of air pollutant exposures.

Associations of air pollutants with pneumonia hospital admissions in Qingdao, China: a prospective cohort study.

Studies about the pneumonia morbidity effects of various air pollution exposure are still limited in China. We aimed to explore the short-term effect of air pollutants exposure on pneumonia admission and identify the vulnerable groups in Qingdao, China. From January 2015 to October 2017, a prospective cohort involving 433,032 participants across 3 counties in Qingdao were enrolled in the study. Distributed lag nonlinear model (DLNM) was applied to assess the associations between air pollutants and pneumonia hospitalizations. There were 636 cases of pneumonia, with an annual incidence density of 54.33 per 100,000 person-years (95% CI: 50.11, 58.56). A 10μg/m3 increment of sulfur dioxide (SO2) distributed at a 4-week lag in Qingdao was associated with increased pneumonia hospitalizations, with a risk ratio of 2.10 (95% CI: 1.06, 4.13). Subgroup analyses indicate that PM ≤ 2.5μm in aerodynamic diameter and SO2 showed stronger effects on pneumonia in females than males, whereas people in urban regions were more vulnerable to nitrogen dioxide and ozone (O3) than the others. We also observed distinct acute effects and harvesting effects of SO2 and O3 on pneumonia in urban areas. Strategies should be taken to further reduce levels of ambient PM2.5, SO2, and O3.

Effects of air pollutant exposure on lung function in exercisers: a systematic review and meta-analysis.

The aim of this study is to systematically evaluate the effect of air pollutant exposure on lung function in exercisers. Computer search Web of Science, PubMed, EBSCO and Cochrane Library, MINORS scale for literature quality evaluation, and Stata 12.0 software for statistical analysis. According to the literature inclusion and exclusion criteria, a total of 14 pieces of literature were screened and included in the Meta-analysis, and the literature quality was relatively high. Meta-analysis shows that air pollutant exposure has no significant effect on FVC, FEV1 and PEF of exercisers (p>0.05); but it can significantly increase the FeNO level of exercisers [Z=2.26, p = 0.024, SMD=-0.228, 95% CI= (-0.426, -0.031)]. Egger linear regression analysis shows that FVC [β=-4.64, p = 0.004, 95% CI= (-7.32,-1.95)] has the possibility of publication bias; FEV1, PEF and FeNO p>0.05 and 95% CI contains 0, there is no publication bias in the included literature. There is no sensitivity problem in the included literature, and the combined result is robust and reliable. Exposure to air pollutants may cause allergic airway inflammation by increasing FeNO levels in exercised populations, and adversely affecting human health.

In-vitro oxidative potential and inflammatory response of ambient PM2.5 in a rural region of Northwest China: Association with chemical compositions and source contribution

Overproduction of reactive oxygen species (ROS) induced by atmospheric particles and subsequent inflammatory responses are considered as one of the most important pathological mechanisms with regard to the adverse effects of air pollution exposure. In this study, fine particulate matter (PM2.5) samples were collected at a rural site in Guanzhong Basin, Northwest China, in both summer (August 3–23, 2016) and winter (January 5–February 1, 2017). Then, human bronchial epithelial BEAS-2B cells were exposed to the PM2.5, cultured for 24 h, and then assayed for particle-induced ROS and three inflammatory factors (tumor necrosis-α (TNF-α), interleukin-6 (IL-6), and interferon-γ (IFN-γ)) in vitro. The oxidative potential (OP) induced by winter PM2.5 samples was higher than that induced by summertime samples, whereas inflammatory values showed contrasting seasonal variations. Both OP and inflammatory factors were significantly correlated with most chemical compounds in winter, but not in summer, which was thought to be related mainly to the higher contribution from secondary aerosols formed during the warm season. Source apportionment results showed secondary aerosols formation have significant contribution to OP of PM2.5 in both seasons, but the dominant oxidation processes is different. Secondary nitrates-related process was the major contributors regulating the OP in winter; however, secondary sulfates formation were mainly responsible for the ROS responses in summer. For primary emission, biomass burning, rather than coal emission or vehicle exhaust, was the significant source for OP of PM2.5 in winter. In most cases, the source contribution of each inflammatory factor was similar to that of the ROS. Our results highlighted the significant health risk of atmospheric aerosols from biomass burning in the rural regions of Guanzhong Basin, Northwest China.

Prenatal exposure to air pollution and the risk of macrosomia: Identifying windows of susceptibility

This study explores the effects of prenatal exposure to air pollution on the risk of macrosomia and its window of susceptibility.We conducted a retrospective cohort study utilizing records of birth certificates for all full-term live newborns born in Xi'an city, China from January 1, 2015, to December 31, 2018.Weekly- and trimester-specific exposures of PM2.5, PM10, NO2, and O3 during pregnancy were calculated by inverse distance weighting (IDW) based on their residences. Cox proportional hazard model and distributed lag models (DLMs) were performed to estimate the effects of air pollution exposure during pregnancy on macrosomia risk and its window of susceptibility.In total, 318,323 full-term newborns were identified, including 24,996 (7.8%) cases of macrosomia. An IQR increase in PM2.5 exposure (45.46 μg/m3) from the 33rd until the 37th weeks of gestation was positively associated with an elevated risk of macrosomia, with the strongest effect in the 37th weeks (HR = 1.007, 95%CI: 1.002–1.013). The window of susceptibility for NO2 exposure on macrosomia risk was in the 29th–35th gestational weeks, with the strongest effect in the 34th weeks (IQR = 21.96 μg/m3, HR = 1.006, 95%CI:1.000–1.013). For prenatal exposure to O3, 5th–24th weeks of gestation was identified as susceptible windows for elevated risk of macrosomia, with the strongest associations observed in the 15th weeks (IQR = 80.53 μg/m3, HR = 1.022, 95%CI: 1.011–1.033). However, we did not observe any associations between weekly exposure of PM10 and macrosomia.Our findings imply that the windows of susceptibility to PM2.5 and NO2 exposure on macrosomia are mainly in late pregnancy, whereas the windows of susceptibility to O3 exposure are in early and middle pregnancy.