Associations of maternal and personal smoking with all-cause and cause-specific mortality risk and life expectancy: a prospective cohort study.

OBJECTIVES: The aim of this study was to evaluate the individual and combined effects of maternal smoking during pregnancy (MSDP) and personal smoking on mortality and life expectancy. STUDY DESIGN: A prospective cohort study based on the UK Biobank, with a median follow-up of 12.47 years. METHODS: This study employed multivariate Cox regression to determine the relative risks of mortality from all causes and specific diseases according to maternal and/or personal smoking status and pack-years of smoking (0, 1-20, 21-30, >30). Additionally, this study estimated the additive interaction between the two exposures. Life table analyses were performed using the estimated age-specific mortality rates to forecast life expectancy. RESULTS: Results indicated that MSDP elevated the risk of all-cause mortality (HR = 1.12, 95% CI: 1.09-1.15) and mortality due to neoplasms (HR = 1.10, 95% CI: 1.06-1.12), circulatory (HR = 1.13, 95% CI: 1.06-1.19), respiratory (HR = 1.27, 95% CI: 1.16-1.40) and digestive system diseases (HR = 1.22, 95% CI: 1.08-1.38). Notably, both multiplicative and additive interactions were observed between maternal and personal smoking, with Relative Excess Risk due to Interaction (RERI) values for mortality from all causes, neoplasms, circulatory, and respiratory diseases being 0.21, 0.22, 0.16, and 0.76, respectively. This study also found a trend towards shorter gained life expectancy when maternal smoking and increasing pack-years of personal smoking were combined. CONCLUSIONS: In this cohort study of UK Biobank, MSDP was associated with an increased risk of all-cause mortality and reduced life expectancy, suggesting that quitting smoking during pregnancy might have health and longevity benefits for both generations.

Quantifying the contributions of road and air traffic to ambient ultrafine particles in two urban communities.

Traffic-related activities are widely acknowledged as a primary source of urban ambient ultrafine particles (UFPs). However, a notable gap exists in quantifying the contributions of road and air traffic to size-resolved and total UFPs in urban areas. This study aims to delineate and quantify the traffic's contributions to size-resolved and total UFPs in two urban communities. To achieve this, stationary sampling was conducted at near-road and near-airport communities in Seattle, Washington State, to monitor UFP number concentrations during 2018-2020. Comprehensive correlation analyses among all variables were performed. Furthermore, a fully adjusted generalized additive model, incorporating meteorological factors, was developed to quantify the contributions of road and air traffic to size-resolved and total UFPs. The study found that vehicle emissions accounted for 29% of total UFPs at the near-road site and 13% at the near-airport site. Aircraft emissions contributed 14% of total UFPs at the near-airport site. Notably, aircraft predominantly emitted UFP sizes below 20 nm, while vehicles mainly emitted UFP sizes below 50 nm. These findings reveal the variability in road and air traffic contributions to UFPs in distinct areas. Our study emphasizes the pivotal role of traffic layout in shaping urban UFP exposure.

Impact of Maternal Smoking, Offspring Smoking, and Genetic Susceptibility on Crohn's Disease and Ulcerative Colitis.

BACKGROUND AND AIMS: The long-term impact of maternal smoking during pregnancy (MSDP) on adult offspring's risk of Crohn's disease (CD) and ulcerative colitis (UC) remains uncertain. Our study aims to investigate the individual and combined effects of early life exposure (MSDP), offspring personal behavior (smoking), and genetic risk on the development of CD and UC in adult offspring. METHODS: We conducted a prospective cohort study using UK Biobank data, including 334,083 participants recruited between 2006-2010, with follow-up until December 31, 2021. Multivariable Cox regression models were used to evaluate the associations of genetic factors, maternal and personal smoking, and their combination with CD and UC. RESULTS: Participants exposed to MSDP had an 18% increased risk of CD compared to those without MSDP (hazard ratio (HR) = 1.18, 95% confidence interval (CI) = 1.01-1.39). However, no significant association was found between MSDP and the UC risk (HR = 1.03, 95%CI = 0.92-1.16). Personal smoking increased the risk of CD and UC, and had a numerically amplified effect with MSDP. Participants with high genetic risk and MSDP had a 2.01-fold (95%CI = 1.53-2.65) and a 2.45-fold (95%CI = 2.00-2.99) increased risk of CD and UC, respectively, compared to participants without MSDP and with low genetic risk. CONCLUSIONS: Our prospective cohort study provides evidence that MSDP increases the risk of CD in adult offspring, whereas no evidence supports their causal association. Additionally, smoking and genetic susceptibility had a numerically amplified effect with MSDP on CD and UC, but the interaction lacked statistical significance.

Wearable Sensor-Based Monitoring of Environmental Exposures and the Associated Health Effects: A Review.

Recent advances in sensor technology have facilitated the development and use of personalized sensors in monitoring environmental factors and the associated health effects. No studies have reviewed the research advancement in examining population-based health responses to environmental exposure via portable sensors/instruments. This study aims to review studies that use portable sensors to measure environmental factors and health responses while exploring the environmental effects on health. With a thorough literature review using two major English databases (Web of Science and PubMed), 24 eligible studies were included and analyzed out of 16,751 total records. The 24 studies include 5 on physical factors, 19 on chemical factors, and none on biological factors. The results show that particles were the most considered environmental factor among all of the physical, chemical, and biological factors, followed by total volatile organic compounds and carbon monoxide. Heart rate and heart rate variability were the most considered health indicators among all cardiopulmonary outcomes, followed by respiratory function. The studies mostly had a sample size of fewer than 100 participants and a study period of less than a week due to the challenges in accessing low-cost, small, and light wearable sensors. This review guides future sensor-based environmental health studies on project design and sensor selection.

Characterization of cooking-related ultrafine particles in a US residence and impacts of various intervention strategies.

Interventions that improve air exchange or filter the air have the potential to reduce particle exposures from residential cooking. In this study, we evaluated the effect of using a range hood, opening kitchen windows, and using portable air cleaners (PACs) in various home locations on the concentrations of ultrafine particles (UFPs) at different times and in different rooms during and after cooking. All experiments were conducted using a standardized cooking protocol in a real-world naturally-ventilated apartment located in the northwest United States. Real-time UFP measurements collected from the kitchen, living room, and bedroom locations were used to estimate parameters of a dynamic model, which included time-varying particle emission rates from cooking and particle decay. We found that 1-min mean UFP number concentrations in the kitchen and living room mostly peaked within 0-10 min after cooking ended at levels of 150,000-500,000 particles/cm3. In contrast, the bedroom UFP concentrations were consistently low except for the window-open scenario. While varying considerably with time, the 1-min UFP emission rates were comparable during and within 5-min after cooking, with means (standard deviations) of 0.8 (1.1) × 1012 and 1.1 (1.2) × 1012 particles/min, respectively. Compared with the no-intervention scenario, keeping the kitchen windows open and using a kitchen range hood reduced the mean indoor average UFP concentrations during and 1 h after cooking by ~70% and ~35%, respectively. Along with the range hood on, utilizing a PAC in the kitchen during and after cooking further reduced the mean indoor average UFP levels during and 1 h after cooking by an additional 53%. In contrast, placing the PAC in the living room or bedroom resulted in worse efficacy, with additional 2-13% reductions. These findings provide useful information on how to reduce cooking-related UFP exposure via readily accessible intervention strategies.

The associations of nitrated polycyclic aromatic hydrocarbon exposures with plasma glucose and amino acids.

Nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) have been widely studied for their mutagenic and carcinogenic effects. This study aims to investigate whether exposure to nitro-PAHs is associated with biomarkers of carbohydrate metabolism, an underlying risk factor for metabolic disorder. Early morning urine and blood samples were longitudinally collected two times with a four-week interval from 43 healthy adults. Five urinary amino-PAHs (1-aminonaphthalene, 2-aminonaphthalene, 9-aminophenanthrene, 2-aminofluorene, and 1-aminopyrene) were measured as biomarkers of nitro-PAH exposures. We measured plasma concentrations of glucose and six amino acids that can regulate insulin secretion, including aspartate (Asp), glutamate (Glu), glutamine (Gln), alanine (Ala), Arginine (Arg), and ornithine (Orn). We found that increasing concentrations of 9-aminophenanthrene were significantly associated with increasing glucose levels and with decreasing Asp, Glu, Ala, and Orn levels. We estimated that 26.4 %-43.8 % of the 9-aminophenanthrene-associated increase in glucose level was mediated by Asp, Glu, and Orn. These results suggest that exposure to certain nitro-PAHs affects glucose homeostasis, partly resulting from the depletion of insulin-stimulating amino acids (Asp, Glu, and Orn).

Residential cooking-related PM2.5: Spatial-temporal variations under various intervention scenarios.

Some cooking events can generate high levels of hazardous PM2.5. This study assesses the dispersion of cooking-related PM2.5 throughout a naturally-ventilated apartment in the US, examines the dynamic process of cooking-related emissions, and demonstrates the impact of different indoor PM2.5 mitigating strategies. We conducted experiments with a standardized pan-frying cooking procedure under seven scenarios, involving opening kitchen windows, using a range hood, and utilizing a portable air cleaner (PAC) in various indoor locations. Real-time PM2.5 concentrations were measured in the open kitchen, living room, bedroom (door closed), and outdoor environments. Decay-related parameters were estimated, and time-resolved PM2.5 emission rates for each experiment were determined using a dynamic model. Results show that the 1-min mean PM2.5 concentrations in the kitchen and living room peaked 1-7 min after cooking at levels of 200-1400 µg/m3, which were more than 9 times higher than the peak bedroom levels. Mean (standard deviation) kt for the kitchen, ranging from 0.58 (0.02) to 6.62 (0.34) h-1, was generally comparable to that of the living room (relative difference < 20%), but was 1-5 times larger than that of the bedroom. The range of PM2.5 full-decay time was between 1-10 h for the kitchen and living room, and from 0 to > 6 h for the bedroom. The PM2.5 emission rates during and 5 min after cooking were 2.3 (3.4) and 5.1 (3.9) mg/min, respectively. Intervention strategies, including opening kitchen windows and using PACs either in the kitchen or living room, can substantially reduce indoor PM2.5 levels and the related full-decay time. For scenarios involving a PAC, placing it in the kitchen (closer to the source) resulted in better efficacy.

Health Impact Assessment of the 2020 Washington State Wildfire Smoke Episode: Excess Health Burden Attributable to Increased PM2.5 Exposures and Potential Exposure Reductions.

Major wildfires starting in the summer of 2020 along the west coast of the United States made PM2.5 concentrations in this region rank among the highest in the world. Washington was impacted both by active wildfires in the state and aged wood smoke transported from fires in Oregon and California. This study aims to estimate the magnitude and disproportionate spatial impacts of increased PM2.5 concentrations attributable to these wildfires on population health. Daily PM2.5 concentrations for each county before and during the 2020 Washington wildfire episode (September 7-19) were obtained from regulatory air monitors. Utilizing previously established concentration-response function (CRF) of PM2.5 (CRF of total PM2.5) and odds ratio (OR) of wildfire smoke days (OR of wildfire smoke days) for mortality, we estimated excess mortality attributable to the increased PM2.5 concentrations in Washington. On average, daily PM2.5 concentrations increased 97.1 µg/m3 during the wildfire smoke episode. With CRF of total PM2.5, the 13-day exposure to wildfire smoke was estimated to lead to 92.2 (95% CI: 0.0, 178.7) more all-cause mortality cases; with OR of wildfire smoke days, 38.4 (95% CI: 0.0, 93.3) increased all-cause mortality cases and 15.1 (95% CI: 0.0, 27.9) increased respiratory mortality cases were attributable to the wildfire smoke episode. The potential impact of avoiding elevated PM2.5 exposures during wildfire events significantly reduced the mortality burden. Because wildfire smoke episodes are likely to impact the Pacific Northwest in future years, continued preparedness and mitigations to reduce exposures to wildfire smoke are necessary to avoid excess health burden.

Associations between time-weighted personal air pollution exposure and amino acid metabolism in healthy adults.

The molecular mechanisms underlying the associations between air pollution exposure and adverse cardiopulmonary effects remain to be better understood. Altered amino acid metabolism may plays an important role in the development of cardiopulmonary diseases and may be perturbed by air pollution exposure. To test this hypothesized molecular mechanism, we conducted an association analysis from an existing intervention study to examine the relations of air pollution exposures with amino acids in 43 Chinese healthy adults. Plasma levels of amino acids were measured using a UPLC-QqQ-MS system. Time-weighted personal exposure to O3, PM2.5, NO2, and SO2 over four time windows, i.e., 12 h, 24 h, 1 week, and 2 weeks, were calculated using the measured indoor and outdoor concentrations coupled with the time-activity data for each participant. Linear mixed-effects models were used to estimate the associations between air pollutants at each exposure window and amino acids by controlling for potential confounders. We observed significant associations between exposures and plasma concentrations of amino acids, with the direction of associations varying by amino acid and air pollutant. While there is little evidence of associations for NO2 and SO2, the associations with amino acids were fairly pronounced for exposure to PM2.5 and O3. In particular, independent O3 (12- and 24-hour) associations were observed with changes in the amino acids that were related to the urea cycle, including aspartate, asparagine, glutamate, arginine, citrulline, and ornithine. Our findings indicated that air pollution may cause acute perturbation of amino acid metabolism, and that O3 and PM2.5 may affect the metabolism of amino acids in different pathways. Main finding: Acute air pollution exposure might affect the perturbation of amino acid metabolism, and in particular, was associated with amino acids in relation to the urea cycle.

Energy consumption of using HEPA-based portable air cleaner in residences: A monitoring study in Seattle, US.

Portable air cleaners (PACs), offering both auto and manual (adjustable) operation modes, are commonly used in residences. Compared with adjustable mode, auto mode's advantage of reducing indoor PM2.5 has been previously demonstrated. This study examines the energy consumption of such PACs in six residences recruited in Seattle, United States, and compares the power consumption between auto and adjustable modes. Each residence went through a one-week-long PAC filtration session under auto and adjustable modes, respectively. PAC power consumption, indoor PM2.5, temperature, and relative humidity (RH) were measured at 10-second intervals in each residence. A linear mixed-effects regression (LMER) model was used to compare the PAC power consumption between the two modes after adjusting for indoor PM2.5, temperature, and RH. Results show that the mean (standard deviation) PAC power consumption under adjustable and auto modes were 7.0 (3.5) and 6.8 (2.6) W, respectively. The average monthly energy consumption of continuous PAC operation was estimated to be ~5 kWh for both modes. Based on the LEMR model, PAC power consumption under auto mode was approximately 3% larger than that under adjustable mode, after adjusting for living-room PM2.5, temperature, and RH levels. The implications for PAC operation mode selection in residential environments were discussed.

Nitrated Polycyclic Aromatic Hydrocarbons and Arachidonic Acid Metabolisms Relevant to Cardiovascular Pathophysiology: Findings from a Panel Study in Healthy Adults.

Concerns on nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) in the environment have mainly arisen from their mutagenic and carcinogenic effects. The objective of this study is to investigate whether nitro-PAH exposures are associated with biomarkers of cardiovascular pathophysiology. In a panel study design, urines and blood samples were collected up to four times with a 2-week interval from 89 healthy adults. We measured 1-naphthylamine, 2-naphthylamine, 9-aminophenanthrene, 2-aminofluorene, and 1-aminopyrene as biomarkers of nitro-PAH exposures. We measured three urinary metabolites of arachidonic acid (AA) including 20-hydroxyeicosatetraenoic acid (20-HETE) from the cytochrome P450 (CYP) pathway, 8-isoprostane from the nonenzymatic pathway, and 11-dehydro-thromboxane B2 (11-dhTXB2) from the cyclooxygenase (COX) pathway. Urinary malondialdehyde, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and 6-sulfatoxymelatonin (aMT6s) were measured to reflect systemic oxidative stress. Plasma concentrations of the soluble P-selectin and von Willebrand factor (vWF) were measured as biomarkers of platelet activation and endothelial dysfunction. We found that increased urinary concentrations of amino-PAHs were significantly associated with increased 20-HETE, 11-dhTXB2, and 8-OHdG and with decreased 8-isoprostane and aMT6s. Increased amino-PAHs were positively associated with P-selectin and vWF, respectively. These results suggest that exposure to nitro-PAHs increases systemic oxidative stress and alters AA metabolism toward CYP and COX pathways, leading to an increased cardiovascular disease risk.

Field measurements of PM2.5 infiltration factor and portable air cleaner effectiveness during wildfire episodes in US residences.

Wildfires have frequently occurred in the western United States (US) during the summer and fall seasons in recent years. This study measures the PM2.5 infiltration factor in seven residences recruited from five dense communities in Seattle, Washington, during a 2020 wildfire episode and evaluates the impacts of HEPA-based portable air cleaner (PAC) use on reducing indoor PM2.5 levels. All residences with windows closed went through an 18-to-24-h no filtration session, with five of seven following that period with an 18-to-24-h filtration session. Auto-mode PACs, which automatically adjust the fan speed based on the surrounding PM2.5 levels, were used for the filtration session. 10-s resolved indoor PM2.5 levels were measured in each residence's living room, while hourly outdoor levels were collected from the nearest governmental air quality monitoring station to each residence. Additionally, a time-activity diary in minute resolution was collected from each household. With the impacts of indoor sources excluded, indoor PM2.5 mass balance models were developed to estimate the PM2.5 indoor/outdoor (I/O) ratios, PAC effectiveness, and decay-related parameters. Among the seven residences, the mean infiltration factor ranged from 0.33 (standard deviation [SD]: 0.06) to 0.76 (SD: 0.05). The use of auto-mode PAC led to a 48%-78% decrease of indoor PM2.5 levels after adjusting for outdoor PM2.5 levels and indoor sources. The mean (SD) air exchange rates ranged from 0.30 (0.13) h-1 to 1.41 (3.18) h-1 while the PM2.5 deposition rate ranged from 0.10 (0.54) h-1 to 0.49 (0.47) h-1. These findings suggest that staying indoors, a common protective measure during wildfire episodes, is insufficient to prevent people's excess exposure to wildfire smoke, and provides quantitative evidence to support the utilization of auto-mode PACs during wildfire events in the US.

Distinct Ultrafine Particle Profiles Associated with Aircraft and Roadway Traffic.

The Mobile ObserVations of Ultrafine Particles study was a two-year project to analyze potential air quality impacts of ultrafine particles (UFPs) from aircraft traffic for communities near an international airport. The study assessed UFP concentrations within 10 miles of the airport in the directions of aircraft flight. Over the course of four seasons, this study conducted a mobile sampling scheme to collect time-resolved measures of UFP, CO2, and black carbon (BC) concentrations, as well as UFP size distributions. Primary findings were that UFPs were associated with both roadway traffic and aircraft sources, with the highest UFP counts found on the major roadway (I-5). Total concentrations of UFPs alone (10-1000 nm) did not distinguish roadway and aircraft features. However, key differences existed in the particle size distribution and the black carbon concentration for roadway and aircraft features. These differences can help distinguish between the spatial impact of roadway traffic and aircraft UFP emissions using a combination of mobile monitoring and standard statistical methods.

Impacts of implementing Healthy Building guidelines for daily PM2.5 limit on premature deaths and economic losses in urban China: A population-based modeling study.

Given a large fraction of people's exposure to urban PM2.5 occur indoors, reducing indoor PM2.5 levels may offer a more feasible and immediate way to save substantial lives and economic losses attributable to PM2.5 exposure. We aimed to estimate the premature mortality and economic loss reductions associated with achieving the newly established Chinese indoor air guideline and a few hypothetical indoor PM2.5 guideline values. We used outdoor PM2.5 concentrations from 1497 monitoring sites in 339 Chinese cities in 2015, coupled with a steady-state mass balance model, to estimate indoor concentrations of outdoor-infiltrated PM2.5. Using province-specific time-activity patterns for urban residents, we estimated outdoor and indoor exposures to PM2.5 of outdoor origin. We then proceeded to use localized census-based concentration-response models and the value of statistical life estimates to calculate premature deaths and economic losses attributable to PM2.5 exposure across urban China. Finally, we estimated potentially avoidable mortality and corresponding economic losses by meeting the current 24-hour based guideline and various hypothetical indoor limits for PM2.5. In 2015 in urban areas of mainland China, the city-specific annual mean outdoor and indoor PM2.5 concentrations ranged 9-108 µg/m3 and 5-56 µg/m3, respectively. Indoor exposures contributed 62%-91% daily and 68%-83% annually to the total time-weighted exposures. The potential reductions in total deaths and economic losses for the scenario in which daily indoor concentrations met the current guideline of 75 µg/m3, 37.5 µg/m3, and 25 µg/m3 were 16.9 (95% CI: 0.7-62.1) thousand, 87.7 (95% CI: 9.7-197.7) thousand, and 165.5 (95% CI: 30.8-304.0) thousand, respectively. The corresponding reductions in economic losses were 5.7 (95% CI: 0.2-34.8) billion, 29.4 (95% CI: 2.4-109.6) billion, and 55.2 (95% CI: 7.7-168.0) billion US Dollars, respectively. Deaths and economic losses would be reduced exponentially within the range of 0-75 µg/m3 for hypothetical indoor PM2.5 limits. The findings demonstrate the effectiveness of reducing indoor concentrations of outdoor-originated PM2.5 in saving substantial lives and economic losses in China. The analysis provides quantitative evidence to support the implementation of an indoor air quality guideline or standard for PM2.5.

Associations of ozone exposure with urinary metabolites of arachidonic acid.

BACKGROUND: Ozone (O3) exposure has been associated with biomarkers of platelet activation and oxidative stress. The metabolism of arachidonic acid (AA) plays an important role in platelet activation and oxidative stress. However, AA metabolic pathways have not been examined in relation to O3 and other air pollutants. METHODS: Early morning urine and fasting blood were longitudinally collected up to four times from 89 healthy adults (22-52 years old, 25 women) in Changsha City, China. We measured three urinary AA metabolites, namely 11-dehydro-Thromboxane B2 (11-dhTXB2) produced from the arachidonic cyclooxygenase pathway, 20-hydroxyeicosatetraenoic acid (20-HETE) from the CYPs pathway, and 8-isoprostane from the non-enzymatic pathway. Urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured as indicators of oxidative damage to lipids and DNA, respectively. We measured soluble P-selectin (sCD62p) concentrations in plasma as an indicator of platelet activation. Indoor and outdoor air pollutants were measured and combined with participants' time-activity pattern to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week periods prior to biospecimen collection, respectively. Linear mixed-effects models were used to examine the relationships of AA metabolites with air pollutant exposures, plasma sCD62p, and urinary MDA & 8-OHdG. RESULTS: We found that a 10% increase in 12 h and 24 h O3 exposure were associated with increases in urinary11-dhTXB2 by 1.4% (95%, 0.1% to 2.6%) and 1.3% (0.05% to 2.5%), respectively. These associations remained robust after adjusting for co-pollutant exposures. No significant associations were observed between 11-dhTXB2 and other pollutants or between O3 exposures and other AA metabolites. All the three AA metabolites were significantly and positively associated with urinary MDA and 8-OHdG, whereas only urinary 11-dhTXB2 was significantly and positively associated with plasma sCD62p. CONCLUSIONS: A metabolite of AA from the cyclooxygenase pathway was positively associated with short-term O3 exposure, and with a plasma marker of platelet activation and two urinary markers of oxidative stress. The results suggest that O3 exposure may contribute to increased platelet activation and oxidative damages via altering the metabolism of AA.

Health Impact Assessment of PM2.5 attributable mortality from the September 2020 Washington State Wildfire Smoke Episode.

Major wildfires that started in the summer of 2020 along the west coast of the U.S. have made PM2.5 concentrations in cities in this region rank among the highest in the world. Regions of Washington were impacted by active wildfires in the state, and by aged wood smoke transported from fires in Oregon and California. This study aims to assess the population health impact of increased PM2.5 concentrations attributable to the wildfire. Average daily PM2.5 concentrations for each county before and during the 2020 Washington wildfire episode were obtained from the Washington Department of Ecology. Utilizing previously established associations of short-term mortality for PM2.5, we estimated excess mortality for Washington attributable to the increased PM2.5 levels. On average, PM2.5 concentrations increased 91.7 µg/m3 during the wildfire episode. Each week of wildfire smoke exposures was estimated to result in 87.6 (95% CI: 70.9, 103.1) cases of increased all-cause mortality, 19.1 (95% CI: 10.0, 28.2) increased cardiovascular disease deaths, and 9.4 (95% CI: 5.1, 13.5) increased respiratory disease deaths. Because wildfire smoke episodes are likely to continue impacting the Pacific Northwest in future years, continued preparedness and mitigations to reduce exposures to wildfire smoke are necessary to avoid this excess health burden.

Impacts of the COVID-19 responses on traffic-related air pollution in a Northwestern US city.

This study evaluates the COVID-19 impacts on traffic-related air pollution, including ultrafine particles (UFPs), PM2.5, black carbon (BC), NO, NO2, NOx, and CO in a Northwestern US city. Hourly traffic, air pollutants, and meteorological data on/near a major freeway in the downtown of Seattle, Washington, were collected for five weeks before and ten weeks after the Washington Stay Home Order (SHO) was enacted, respectively (February 17-May 31, 2020). The pollutants between pre- and post-SHO periods were compared, and their differences were statistically tested. Besides, first-order multivariate autoregressive (MAR(1)) models were developed to reveal the impacts specific to the change of traffic due to the COVID-19 responses while controlling for meteorological conditions. Results indicate that compared with those in the post-SHO period, the median traffic volume and road occupancy decreased by 37% and 52%, respectively. As for pollutants, the median BC and PM2.5 levels significantly decreased by 25% and 33%, relatively, while NO, NO2, NOx, and CO decreased by 33%, 29%, 30%, and 17%, respectively. In contrast, neither size-resolved UFPs nor total UFPs showed significant changes between the two periods, although larger particles (≥115.5 nm) decreased by 4-29%. Additionally, significant differences were found in meteorological conditions between the two periods. Based on the MAR(1) models, controlling for meteorological conditions, the COVID-19 responses were associated with significant decreases in median levels of traffic-related pollutants including 11.5-154.0 nm particles (ranging from -3% [95% confidence interval (CI): -1%, -4%] to -12% [95% CI: -10%, -14%]), total UFPs (-7% [95% CI: -5%, -8%]), BC (-6% [95% CI: -5%, -7%]), PM2.5 (-2% [95% CI: -1%, -3%]), NO, NO2, NOx (ranging from -3% [95% CI: -2%, -4%] to -10% [95% CI: -18%, -12%]), and CO (-4% [95% CI, -3%, -5%]). These findings illustrate that the conclusion of the COVID-19 impacts on urban traffic-related air pollutant levels could be completely different in scenarios whether meteorology was adjusted for or not. Fully adjusting for meteorology, this study shows that the COVID-19 responses were associated with much more reductions in traffic-related UFPs than PM2.5 in the Seattle region, in contrast to the reverse trend from the direct empirical data comparison.

Endogenous melatonin mediation of systemic inflammatory responses to ozone exposure in healthy adults.

BACKGROUND/AIM: Melatonin is a free radical scavenger and an anti-inflammatory biomolecule. Air pollution exposure has been associated with increased inflammatory responses. We hypothesize that endogenous melatonin plays a role in inflammatory responses to air pollution exposure. METHODS: We tested this hypothesis in a cohort of 53 healthy adults (22-52 years old, 16 women), none of whom were on melatonin supplementation. Early morning urine and fasting blood were collected from each participant longitudinally up to three times. We analyzed urinary 6-sulfatoxymelatonin (aMT6s), as a surrogate of circulating melatonin, and pro- and anti-inflammatory cytokines in the plasma samples. Indoor and outdoor air pollutants were measured and combined with participants' time-activity patterns to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week periods prior to biospecimen collection, respectively. Linear mixed-effects models were used to examine the relationships among urinary aMT6s, personal pollutant exposure, and plasma cytokines. A mediation analysis was conducted to examine the role of aMT6s in the relationships between pollutant exposures and inflammatory cytokines. RESULTS: One interquartile range (4.2 ppb) increase in 2-week O3 exposure was associated with a -26.2% (95% CI: -43.9% to -2.8%) decrease in aMT6s. Within the range of endogenous aMT6s concentrations (0.5-53.0 ng/ng creatinine) across the participants, increased aMT6s was associated with decreased pro-inflammatory cytokines including IL-1ß, IL-8, IL-17A, IFN-γ, and TNF-α. These cytokines were significantly and positively associated with 2-week average O3 exposure. Furthermore, 7.4% to 17.4% of the O3-cytokine associations were mediated by aMT6s. We did not find similar effects for the other pollutants. CONCLUSIONS: Pro-inflammatory responses to O3 exposure in the preceding 2 weeks partly resulted from the depletion of endogenous melatonin by O3.

Inflammatory and oxidative stress responses of healthy adults to changes in personal air pollutant exposure.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22-52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O3, PM2.5, NO2, and SO2 exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O3 exposures and significantly but positively associated with 2-week O3 exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO2 exposures, respectively. However, we did not find clear associations of PM2.5 and SO2 exposure with proinflammatory cytokines and with MDA. The removal of an O3-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1ß, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O3 for different time durations may affect systemic inflammatory responses in different ways.