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Increased systemic oxidative stress, implicated in adverse pregnancy outcomes for both mothers and fetuses, has been associated with gestational exposure to air pollutants such as polycyclic aromatic hydrocarbons (PAHs), fine particulate matter (PM 2.5), and nitrogen dioxide (NO 2). However, it is unclear whether exposure to pollutants at levels below the current air quality standards can increase oxidative stress in pregnant women. In a cohort of 305 pregnant persons residing in western New York, we examined the association between exposure to PM 2.5 , NO 2 , and PAHs (measured as urinary 1-hydroxypyrene) and urinary biomarkers of oxidative stress (malondialdehyde [MDA] and 8-hydroxy-2′-deoxyguanosine [8-OHdG]) measured in each trimester. After controlling for gestational stage, maternal age, lifestyles, and socioeconomic factors, each interquartile range (IQR) increase in 1-hydroxypyrene concentration (65.8 pg/ml) was associated with a 7.73% (95%CI: 3.18%,12.3%) higher in MDA levels throughout the pregnancy and in the first and second trimester. An IQR increase in PM 2.5 concentration (3.20 μg/m3) was associated with increased MDA levels in the first trimester (8.19%, 95%CI: 0.28%,16.1%), but not the 2nd (−7.99%, 95% CI: 13.8%, −2.23%) or 3rd trimester (−2.81%, 95% CI: 10.0%, 4.38%). The average cumulative PM 2.5 exposures in the 3–7 days before urine collection were associated with increased 8-OHdG levels during the second trimester, with the largest difference (22.6%; 95% CI: 3.46%, 41.7%) observed in relation to a one IQR increase in PM 2.5 concentration in the previous 7 days. In contrast, neither oxidative stress biomarker was associated with NO 2 exposure. Observed in pregnant women exposed to low-level air pollution, these findings expanded previously reported associations between systemic oxidative stress and high-level PM 2.5 and PAH concentrations. Further, the first and second trimesters may be a susceptible window during pregnancy for oxidative stress responses to air pollution exposure. [Display omitted] • Gestational PM 2.5 and NO 2 exposure are below national standards. • Short-term exposure to PM 2.5 was associated with urinary oxidative biomarkers. • Urinary 1-hydroxypyrene was associated with lipid peroxidation biomarker. • Stronger associations were observed in early- and mid-pregnancy. [ABSTRACT FROM AUTHOR]

Background: There is a discourse on whether air pollution mixture or air pollutant components are causally linked to increased mortality. In particular, there is uncertainty on whether the association of NO2 with mortality is independent of fine particulate matter (PM2.5). Furthermore, effect modification by temperature on air pollution-related mortality also needs more evidence.Methods: We used the Chinese Longitudinal Healthy Longevity Study (CLHLS), a prospective cohort with geographical and socio-economic diversity in China. The participants were enrolled in 2008 or 2009 and followed up in 2011-2012, 2014, and 2017-2018. We used remote sensing and ground monitors to measure nitrogen dioxide (NO2), fine particulate matter (PM2.5) , and temperature. We used the Cox-proportional hazards model to examine the association between component and composite air pollution and all-cause mortality, adjusted for demographic characteristics, lifestyle, geographical attributes, and temperature. We used the restricted cubic spline to visualize the concentration-response curve.Results: Our study included 11 835 individuals with an average age of 86.9 (SD: 11.4) at baseline. Over 55 606 person-years of follow-up, we observed 8 216 mortality events. The average NO2 exposure was 19.1 μg/m3 (SD: 14.1); the average PM2.5 exposure was 52.8 μg/m3 (SD: 15.9). In the single pollutant models, the mortality HRs (95% CI) for 10 μg/m3 increase in annual average NO2 or PM2.5 was 1.114 (1.085, 1.143) and 1.244 (1.221, 1.268), respectively. In the multi-pollutant model co-adjusting for NO2 and PM2.5, the HR for NO2 turned insignificant: 0.978 (0.950, 1.008), but HR for PM2.5 was not altered: 1.252 (1.227, 1.279). PM2.5 and higher mortality association was robust, regardless of NO2. When acccounting for particulate matter, NO2 exposure appeared to be harmful in places of colder climates and higher seasonal temperature variation.Conclusions: We see a robust relationship of PM2.5 exposure and premature mortality in advance aged individuals, however, NO2 exposure and mortality was only harmful in places of colder climate such as northeast China, indicating evidence of effect modification by temperature. Analysis of NO2 without accounting for its collinearity with PM2.5, may lead to overestimation. [ABSTRACT FROM AUTHOR]

Portable air cleaners are increasingly used in polluted areas in an attempt to reduce human exposure; however, there has been limited work characterizing their effectiveness at reducing exposure. With this in mind, we recruited forty‐three children with asthma from suburban Shanghai and deployed air cleaners (with HEPA and activated carbon filters) in their bedrooms. During both 2‐week filtration and non‐filtration periods, low‐cost PM2.5 and O3 air monitors were used to measure pollutants indoors, outdoors, and for personal exposure. Indoor PM2.5 concentrations were reduced substantially with the use of air cleaners, from 34 ± 17 to 10 ± 8 µg/m3, with roughly 80% of indoor PM2.5 estimated to come from outdoor sources. Personal exposure to PM2.5 was reduced from 40 ± 17 to 25 ± 14 µg/m3. The more modest reductions in personal exposure and high contribution of outdoor PM2.5 to indoor concentrations highlight the need to reduce outdoor PM2.5 and/or to clean indoor air in multiple locations. Indoor O3 concentrations were generally low (mean = 8±4 ppb), and no significant difference was seen by filtration status. The concentrations of pollutants and the air cleaner effectiveness were highly variable over time and across homes, highlighting the usefulness of real‐time air monitors for understanding individual exposure reduction strategies. [ABSTRACT FROM AUTHOR]

The Relationship of Indoor, Outdoor and Personal Air (RIOPA) Study was undertaken to evaluate the contribution of outdoor sources of air toxics, as defined in the 1990 Clean Air Act Amendments, to indoor concentrations and personal exposures. The concentrations of 18 volatile organic compounds (VOCs), 17 carbonyl compounds, and fine particulate matter mass (PM2.5) were measured using 48-h outdoor, indoor and personal air samples collected simultaneously. PM2.5 mass, as well as several component species (elemental carbon, organic carbon, polyaromatic hydrocarbons and elemental analysis) were also measured; only PM2.5 mass is reported here. Questionnaires were administered to characterize homes, neighborhoods and personal activities that might affect exposures. The air exchange rate was also measured in each home. Homes in close proximity (<0.5?km) to sources of air toxics were preferentially (2:1) selected for sampling. Approximately 100 non-smoking households in each of Elizabeth, NJ, Houston, TX, and Los Angeles, CA were sampled (100, 105, and 105 respectively) with second visits performed at 84, 93, and 81 homes in each city, respectively. VOC samples were collected at all homes, carbonyls at 90%and PM2.5 at 60%of the homes. Personal samples were collected from nonsmoking adults and a portion of children living in the target homes. This manuscript provides the RIOPA study design and quality control and assurance data. The results from the RIOPA study can potentially provide information on the influence of ambient sources on indoor air concentrations and exposure for many air toxics and will furnish an opportunity to evaluate exposure models for these compounds.Journal of Exposure Analysis and Environmental Epidemiology (2005) 15, 123-137. doi:10.1038/sj.jea.7500379 Published online 23 June 2004 [ABSTRACT FROM AUTHOR]

The Relationship of Indoor, Outdoor and Personal Air (RIOPA) study was designed to investigate residential indoor, outdoor and personal exposures to several classes of air pollutants, including volatile organic compounds, carbonyls and fine particles (PM2.5). Samples were collected from summer, 1999 to spring, 2001 in Houston (TX), Los Angeles (CA) and Elizabeth (NJ). Indoor, outdoor and personal PM2.5 samples were collected at 212 nonsmoking residences, 162 of which were sampled twice. Some homes were chosen due to close proximity to ambient sources of one or more target analytes, while others were farther from sources. Median indoor, outdoor and personal PM2.5 mass concentrations for these three sites were 14.4, 15.5 and 31.4?µg/m3, respectively. The contributions of ambient (outdoor) and nonambient sources to indoor and personal concentrations were quantified using a single compartment box model with measured air exchange rate and a random component superposition (RCS) statistical model. The median contribution of ambient sources to indoor PM2.5 concentrations using the mass balance approach was estimated to be 56%for all study homes (63%, 52%and 33%for California, New Jersey and Texas study homes, respectively). Reasonable variations in model assumptions alter median ambient contributions by less than 20%. The mean of the distribution of ambient contributions across study homes agreed well for the mass balance and RCS models, but the distribution was somewhat broader when calculated using the mass balance model with measured air exchange rates.Journal of Exposure Analysis and Environmental Epidemiology (2005) 15, 17-28. doi:10.1038/sj.jea.7500378 Published online 12 May 2004 [ABSTRACT FROM AUTHOR]

Abstract: Recent studies suggest that DNA oxidative damage be related to the chemical constituents of ambient particles. The purpose of this study was to examine whether particulate polycyclic aromatic hydrocarbons (PAHs) and quinone-structure chemicals increase body burden of oxidative stress in human exposed to heavy traffic volume. We recruited two nonsmoking security guards who worked at a university campus gate near a heavily trafficked road. Each subject wore a personal air sampler for 24h per day to estimate exposures to 24 PAHs and anthraquinone (AnQ) in PM2.5. Daily pre- and post-work shift spot urines were collected for 29d from each subject. Urine samples were analyzed for 8-hydroxy-2′-deoxyguanosine (8-OHdG). Additionally, using 19 organic tracers other than 24 PAHs and AnQ, a receptor source apportionment model of chemical mass balance was applied to determine the contributions of sources on the PM: gasoline vehicle, diesel vehicle, coal burning, vegetable debris, cooking, natural gas and biomass burning. The relationship among urinary 8-OHdG, individual PAH, and AnQ was demonstrated as follows: the average urinary concentration of 8-OHdG was increased more than three times after 8-h work-shift than those before the work shift. All the 24 PAH and AnQ levels were positively and significantly associated with the post-work urinary 8-OHdG. The results from source apportionment suggest vehicular emission to be the dominant source of personal exposure to PM2.5. Our finding indicates that personal air exposures to 24 individual PAHs and AnQ originating from traffic emissions are important in increasing oxidative burdens in human body. [Copyright &y& Elsevier]

The exposome overhauls conventional environmental health impact research paradigms and provides a novel methodological framework that comprehensively addresses the complex, highly dynamic interplays of exogenous exposures, endogenous exposures, and modifiable factors in humans. Holistic assessments of the adverse health effects and systematic elucidation of the mechanisms underlying environmental exposures are major scientific challenges with widespread societal implications. However, to date, few studies have comprehensively and simultaneously measured airborne pollutant exposures and explored the associated biomarkers in susceptible healthy elderly subjects, potentially resulting in the suboptimal assessment and management of health risks. To demonstrate the exposome paradigm, we describe the rationale and design of a comprehensive biomarker and biomonitoring panel study to systematically explore the association between individual airborne exposure and adverse health outcomes. We used a combination of personal monitoring for airborne pollutants, extensive human biomonitoring, advanced omics analysis, confounding information, and statistical methods. We established an exploratory panel study of Biomarkers of Air Pollutant Exposure in Chinese people aged 60–69 years (China BAPE), which included 76 healthy residents from a representative community in Jinan City, Shandong Province. During the period between September 2018 and January 2019, we conducted prospective longitudinal monitoring with a 3-day assessment every month. This project: (1) leveraged advanced tools for personal airborne exposure monitoring (external exposures); (2) comprehensively characterized biological samples for exogenous and endogenous compounds (e.g., targeted and untargeted monitoring) and multi-omics scale measurements to explore potential biomarkers and putative toxicity pathways; and (3) systematically evaluated the relationships between personal exposure to air pollutants, and novel biomarkers of exposures and effects using exposome-wide association study approaches. These findings will contribute to our understanding of the mechanisms underlying the adverse health impacts of air pollution exposures and identify potential adverse clinical outcomes that can facilitate the development of effective prevention and targeted intervention techniques. [ABSTRACT FROM AUTHOR]