Quantifying Disparities in Per- and Polyfluoroalkyl Substances (PFAS) Levels in Drinking Water from Overburdened Communities in New Jersey, 2019-2021.

BACKGROUND: Policymakers have become increasingly concerned regarding the widespread exposure and toxicity of per- and polyfluoroalkyl substances (PFAS). While concerns exist about unequal distribution of PFAS contamination in drinking water, research is lacking. OBJECTIVES: We assess the scope of PFAS contamination in drinking water in New Jersey (NJ), the first US state to develop regulatory levels for PFAS in drinking water. We test for inequities in PFAS concentrations by community sociodemographic characteristics. METHODS: We use PFAS testing data for community water systems (CWS) (n=491) from the NJ Department of Environmental Protection (NJDEP) from 2019 to 2021 and demographic data at the block group level from the US Census to estimate the demographics of the NJ population served by CWS. We use difference in means tests to determine whether CWSs serving "overburdened communities" (OBCs) have a statistically significant difference in likelihood of PFAS detections. OBCs are defined by the NJDEP to be census block groups in which: a) at least 35% of the households qualify as low-income, b) at least 40% of the residents identify as people of color, or c) at least 40% of the households have limited English proficiency. We calculate statewide summary statistics to approximate the relative proportions of sociodemographic groups that are served by CWSs with PFAS detections. RESULTS: We find that 63% of all CWSs tested by NJDEP from 2019 to 2021 had PFAS detections in public drinking water, collectively serving 84% of NJ's population receiving water from CWSs. Additionally, CWSs serving OBCs had a statistically significant higher likelihood of PFAS detection and a higher likelihood of exposure above state MCLs. We also find that a larger proportion of people of color lived in CWS service areas with PFAS detections compared to the non-Hispanic white population. DISCUSSION: These findings quantitatively identify disparities in PFAS contamination of drinking water by CWS service area and highlight the extent of PFAS drinking water contamination and the importance of PFAS remediation efforts for protecting environmental health and justice. https://doi.org/10.1289/EHP12787.

Nitrogen dioxide exposure, attentional function, and working memory in children from 4 to 8 years: Periods of susceptibility from pregnancy to childhood.

BACKGROUND: Air pollution exposure during pregnancy and childhood has been linked to executive function impairment in children, however, very few studies have assessed these two exposure periods jointly to identify susceptible periods of exposure. We sought to identify potential periods of susceptibility of nitrogen dioxide (NO2) exposure from conception to childhood on attentional function and working memory in school-aged children. METHODS: Within the Spanish INMA Project, we estimated residential daily NO2 exposures during pregnancy and up to 6 years of childhood using land use regression models (n = 1,703). We assessed attentional function at 4-6 years and 6-8 years, using the Conners Kiddie Continuous Performance Test and the Attention Network Test, respectively, and working memory at 6-8 years, using the N-back task. We used distributed lag non-linear models to assess the periods of susceptibility of each outcome, adjusting for potential confounders and correcting for multiple testing. We also stratified all models by sex. RESULTS: Higher exposure to NO2 between 1.3 and 1.6 years of age was associated with higher hit reaction time standard error (HRT-SE) (0.14 ms (95 % CI 0.05; 0.22) per 10 µg/m3 increase in NO2) and between 1.5 and 2.2 years of age with more omission errors (1.02 (95 % CI 1.01; 1.03) of the attentional function test at 4-6 years. Higher exposure to NO2 between 0.3 and 2.2 years was associated with higher HRT-SE (10.61 ms (95 % CI 3.46; 17.75) at 6-8 years only in boys. We found no associations between exposure to NO2 and working memory at 6-8 years. CONCLUSION: Our findings suggest that NO2 exposure during the first two years of life is associated with poorer attentional function in children from 4 to 8 years of age, especially in boys. These findings highlight the importance of exploring long-term effects of traffic-related air pollution exposure in older age groups.

Household air pollution and attributable burden of disease in rural China: A literature review and a modelling study.

Household air pollution prevails in rural residences across China, yet a comprehensive nationwide comprehending of pollution levels and the attributable disease burdens remains lacking. This study conducted a systematic review focusing on elucidating the indoor concentrations of prevalent household air pollutants-specifically, PM2.5, PAHs, CO, SO2, and formaldehyde-in rural Chinese households. Subsequently, the premature deaths and economic losses attributable to household air pollution among the rural population of China were quantified through dose-response relationships and the value of statistical life. The findings reveal that rural indoor air pollution levels frequently exceed China's national standards, exhibiting notable spatial disparities. The estimated annual premature mortality attributable to household air pollution in rural China amounts to 966 thousand (95% CI: 714-1226) deaths between 2000 and 2022, representing approximately 22.2% (95% CI: 16.4%-28.1%) of total mortality among rural Chinese residents. Furthermore, the economic toll associated with these premature deaths is estimated at 486 billion CNY (95% CI: 358-616) per annum, constituting 0.92% (95% CI: 0.68%-1.16%) of China's GDP. The findings quantitatively demonstrate the substantial disease burden attributable to household air pollution in rural China, which highlights the pressing imperative for targeted, region-specific interventions to ameliorate this pressing public health concern.

Dynamic and stationary monitoring of air pollutant exposures and dose during marathons.

Marathon running significantly increases breathing volumes and, consequently, air pollution inhalation doses. This is of special concern for elite athletes who ventilate at very high rates. However, race organizers and sport governing bodies have little guidance to support events scheduling to protect runners. A key limitation is the lack of hyper-local, high temporal resolution air quality data representative of exposure along the racecourse. This work aimed to understand the air pollution exposures and dose inhaled by athletes, by means of a dynamic monitoring methodology designed for road races. Air quality monitors were deployed during three marathons, monitoring nitrogen dioxide (NO2), ozone (O3), particulate matter (PMx), air temperature, and relative humidity. One fixed monitor was installed at the Start/Finish line and one mobile monitor followed the women elite runner pack. The data from the fixed monitors, deployed prior the race, described daily air pollution trends. Mobile monitors in combination with heatmap analysis facilitated the hyper-local characterization of athletes' exposures and helped identify local hotspots (e.g., areas prone to PM resuspension) which should be preferably bypassed. The estimation of inhaled doses disaggregated by gender and ventilation showed that doses inhaled by last finishers may be equal or higher than those inhaled by first finishers for O3 and PMx, due to longer exposures as well as the increase of these pollutants over time (e.g., 58.2 ± 9.6 and 72.1 ± 23.7 µg of PM2.5 for first and last man during Rome marathon). Similarly, men received significantly higher doses than women due to their higher ventilation rate, with differences of 31-114 µg for NO2, 79-232 µg for O3, and 6-41 µg for PMx. Finally, the aggregated data obtained during the 4 week- period prior the marathon can support better race scheduling by the organizers and provide actionable information to mitigate air pollution impacts on athletes' health and performance.

Science-informed Policy Making for Protecting People and the Environment from Radiation.

ABSTRACT: The process to arrive at the radiation protection practices of today to protect workers, patients, and the public, including sensitive populations, has been a long and deliberative one. This paper presents an overview of the US Environmental Protection Agency's (US EPA) responsibility in protecting human health and the environment from unnecessary exposure to radiation. The origins of this responsibility can be traced back to early efforts, a century ago, to protect workers from x rays and radium. The system of radiation protection we employ today is robust and informed by the latest scientific consensus. It has helped reduce or eliminate unnecessary exposures to workers, patients, and the public while enabling the safe and beneficial uses of radiation and radioactive material in diverse areas such as energy, medicine, research, and space exploration. Periodic reviews and analyses of research on health effects of radiation by scientific bodies such as the National Academy of Sciences, National Council on Radiation Protection and Measurements, United Nations Scientific Committee on the Effects of Atomic Radiation, and the International Commission on Radiological Protection continue to inform radiation protection practices while new scientific information is gathered. As a public health agency, US EPA is keenly interested in research findings that can better elucidate the effects of exposure to low doses and low dose rates of radiation as applicable to protection of diverse populations from various sources of exposure. Professional organizations such as the Health Physics Society can provide radiation protection practitioners with continuing education programs on the state of the science and describe the key underpinnings of the system of radiological protection. Such efforts will help equip and prepare radiation protection professionals to more effectively communicate radiation health information with their stakeholders.

Long-term exposure to major constituents of fine particulate matter and neurodegenerative diseases: A population-based survey in the Pearl River Delta Region, China.

BACKGROUND: Exposure to PM2.5 has been linked to neurodegenerative diseases, with limited understanding of constituent-specific contributions. OBJECTIVES: To explore the associations between long-term exposure to PM2.5 constituents and neurodegenerative diseases. METHODS: We recruited 148,274 individuals aged ≥ 60 from four cities in the Pearl River Delta region, China (2020 to 2021). We calculated twenty-year average air pollutant concentrations (PM2.5 mass, black carbon (BC), organic matter (OM), ammonium (NH4+), nitrate (NO3-) and sulfate (SO42-)) at the individuals' home addresses. Neurodegenerative diseases were determined by self-reported doctor-diagnosed Alzheimer's disease (AD) and Parkinson's disease (PD). Generalized linear mixed models were employed to explore associations between pollutants and neurodegenerative disease prevalence. RESULTS: PM2.5 and all five constituents were significantly associated with a higher prevalence of AD and PD. The observed associations generally exhibited a non-linear pattern. For example, compared with the lowest quartile, higher quartiles of BC were associated with greater odds for AD prevalence (i.e., the adjusted odds ratios were 1.81; 95% CI, 1.45-2.27; 1.78; 95% CI, 1.37-2.32; and 1.99; 95% CI, 1.54-2.57 for the second, third, and fourth quartiles, respectively). CONCLUSIONS: Long-term exposure to PM2.5 and its constituents, particularly combustion-related BC, OM, and SO42-, was significantly associated with higher prevalence of AD and PD in Chinese individuals. ENVIRONMENTAL IMPLICATION: PM2.5 is a routinely regulated mixture of multiple hazardous constituents that can lead to diverse adverse health outcomes. However, current evidence on the specific contributions of PM2.5 constituents to health effects is scarce. This study firstly investigated the association between PM2.5 constituents and neurodegenerative diseases in the moderately to highly polluted Pearl River Delta region in China, and identified hazardous constituents within PM2.5 that have significant impacts. This study provides important implications for the development of targeted PM2.5 prevention and control policies to reduce specific hazardous PM2.5 constituents.

Ongoing exposure to endocrine disrupting phthalates and alternative plasticizers in neonatal intensive care unit patients.

Due to endocrine disrupting effects, di-(2-ethylhexyl) phthalate (DEHP), a plasticizer used to soften plastic medical devices, was restricted in the EU Medical Devices Regulation (EU MDR 2017/745) and gradually replaced by alternative plasticizers. Neonates hospitalized in the neonatal intensive care unit (NICU) are vulnerable to toxic effects of plasticizers. From June 2020 to August 2022, urine samples (n = 1070) were repeatedly collected from premature neonates (n = 132, 4-10 samples per patient) born at <31 weeks gestational age and/or <1500 g birth weight in the Antwerp University Hospital, Belgium. Term control neonates (n = 21, 1 sample per patient) were included from the maternity ward. Phthalate and alternative plasticizers' metabolites were analyzed using liquid-chromatography coupled to tandem mass spectrometry. Phthalate metabolites were detected in almost all urine samples. Metabolites of alternative plasticizers, di-(2-ethylhexyl)-adipate (DEHA), di-(2-ethylhexyl)-terephthalate (DEHT) and cyclohexane-1,2-dicarboxylic-di-isononyl-ester (DINCH), had detection frequencies ranging 30-95 %. Urinary phthalate metabolite concentrations were significantly higher in premature compared to control neonates (p = 0.023). NICU exposure to respiratory support devices and blood products showed increased phthalate metabolite concentrations (p < 0.001). Phthalate exposure increased from birth until four weeks postnatally. The estimated phthalate intake exceeded animal-derived no-effect-levels (DNEL) in 10 % of samples, with maximum values reaching 24 times the DNEL. 29 % of premature neonates had at least once an estimated phthalate intake above the DNEL. Preterm neonates are still exposed to phthalates during NICU stay, despite the EU Medical Devices Regulation. NICU exposure to alternative plasticizers is increasing, though currently not regulated, with insufficient knowledge on their hazard profile.

Global quantification of emerging and legacy per- and polyfluoroalkyl substances in indoor dust: Levels, profiles and human exposure.

This study investigated the occurrence and distribution of per- and polyfluoroalkyl substances (PFASs) in house dust samples from six regions across four continents. PFASs were detected in all indoor dust samples, with total median concentrations ranging from 17.3 to 197 ng/g. Among the thirty-one PFAS analytes, eight compounds, including emerging PFASs, exhibited high detection frequencies in house dust from all six locations. The levels of PFASs varied by region, with higher concentrations found in Adelaide (Australia), Tianjin (China), and Carbondale (United States, U.S.). Moreover, PFAS composition profiles also differed among regions. Dust from Australia and the U.S. contained high levels of 6:2 fluorotelomer phosphate ester (6:2 diPAP), while perfluorooctanoic acid (PFOA) and perfluorooctane sulfonic acid (PFOS) were predominant in other regions. Furthermore, our results indicate that socioeconomic factors impact PFAS levels. The assessment of human exposure through dust ingestion and dermal contact indicates that toddlers may experience higher exposure levels than adults. However, the hazard quotients of PFASs for both toddlers and adults were below one, indicating significant health risks are unlikely. Our study highlights the widespread occurrence of PFASs in global indoor dust and the need for continued monitoring and regulation of these chemicals.

Novel indices reveal that pollinator exposure to pesticides varies across biological compartments and crop surroundings.

Declines in insect pollinators have been linked to a range of causative factors such as disease, loss of habitats, the quality and availability of food, and exposure to pesticides. Here, we analysed an extensive dataset generated from pesticide screening of foraging insects, pollen-nectar stores/beebread, pollen and ingested nectar across three species of bees collected at 128 European sites set in two types of crop. In this paper, we aimed to (i) derive a new index to summarise key aspects of complex pesticide exposure data and (ii) understand the links between pesticide exposures depicted by the different matrices, bee species and apple orchards versus oilseed rape crops. We found that summary indices were highly correlated with the number of pesticides detected in the related matrix but not with which pesticides were present. Matrices collected from apple orchards generally contained a higher number of pesticides (7.6 pesticides per site) than matrices from sites collected from oilseed rape crops (3.5 pesticides), with fungicides being highly represented in apple crops. A greater number of pesticides were found in pollen-nectar stores/beebread and pollen matrices compared with nectar and bee body matrices. Our results show that for a complete assessment of pollinator pesticide exposure, it is necessary to consider several different exposure routes and multiple species of bees across different agricultural systems.

A review of air pollution as a driver of cardiovascular disease risk across the diabetes spectrum.

The prevalence of diabetes is estimated to reach almost 630 million cases worldwide by the year 2045; of current and projected cases, over 90% are type 2 diabetes. Air pollution exposure has been implicated in the onset and progression of diabetes. Increased exposure to fine particulate matter air pollution (PM2.5) is associated with increases in blood glucose and glycated hemoglobin (HbA1c) across the glycemic spectrum, including normoglycemia, prediabetes, and all forms of diabetes. Air pollution exposure is a driver of cardiovascular disease onset and exacerbation and can increase cardiovascular risk among those with diabetes. In this review, we summarize the literature describing the relationships between air pollution exposure, diabetes and cardiovascular disease, highlighting how airborne pollutants can disrupt glucose homeostasis. We discuss how air pollution and diabetes, via shared mechanisms leading to endothelial dysfunction, drive increased cardiovascular disease risk. We identify portable air cleaners as potentially useful tools to prevent adverse cardiovascular outcomes due to air pollution exposure across the diabetes spectrum, while emphasizing the need for further study in this particular population. Given the enormity of the health and financial impacts of air pollution exposure on patients with diabetes, a greater understanding of the interventions to reduce cardiovascular risk in this population is needed.

Seasonal extreme temperatures and short-term fine particulate matter increases pediatric respiratory healthcare encounters in a sparsely populated region of the intermountain western United States.

BACKGROUND: Western Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important. METHODS: We explored short-term exposure to air pollution on children's respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0-17 from 2017-2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season. RESULTS: For asthma, increases of 1 µg/m3 in PM2.5 exposure 7-13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6-12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4-10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods. CONCLUSIONS: Delayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.

Confounder-dependent Bayesian mixture model: Characterizing heterogeneity of causal effects in air pollution epidemiology.

Several epidemiological studies have provided evidence that long-term exposure to fine particulate matter (pm2.5) increases mortality rate. Furthermore, some population characteristics (e.g., age, race, and socioeconomic status) might play a crucial role in understanding vulnerability to air pollution. To inform policy, it is necessary to identify groups of the population that are more or less vulnerable to air pollution. In causal inference literature, the group average treatment effect (GATE) is a distinctive facet of the conditional average treatment effect. This widely employed metric serves to characterize the heterogeneity of a treatment effect based on some population characteristics. In this paper, we introduce a novel Confounder-Dependent Bayesian Mixture Model (CDBMM) to characterize causal effect heterogeneity. More specifically, our method leverages the flexibility of the dependent Dirichlet process to model the distribution of the potential outcomes conditionally to the covariates and the treatment levels, thus enabling us to: (i) identify heterogeneous and mutually exclusive population groups defined by similar GATEs in a data-driven way, and (ii) estimate and characterize the causal effects within each of the identified groups. Through simulations, we demonstrate the effectiveness of our method in uncovering key insights about treatment effects heterogeneity. We apply our method to claims data from Medicare enrollees in Texas. We found six mutually exclusive groups where the causal effects of pm2.5 on mortality rate are heterogeneous.

Sex differences and dietary patterns in the association of air pollutants and hypertension.

BACKGROUND: Hypertension is one of the major public health problems in China. Limited evidence exists regarding sex differences in the association between hypertension and air pollutants, as well as the impact of dietary factors on the relationship between air pollutants and hypertension. The aim of this study was to investigate the sex-specific effects of dietary patterns on the association between fine particulate matter (PM2.5), ozone(O3) and hypertension in adults residing in Jiangsu Province of China. METHODS: A total of 3189 adults from the 2015 China Adult Chronic Disease and Nutrition Surveillance in Jiangsu Province were included in this study. PM2.5 and O3 concentrations were estimated using satellite space-time models and assigned to each participant. Dietary patterns were determined by reduced rank regression (RRR), and multivariate logistic regression was used to assess the associations of the obtained dietary patterns with air pollutants and hypertension risk. RESULTS: After adjusting for confounding variables, we found that males were more sensitive to long-term exposure to PM2.5 (Odds ratio (OR) = 1.42 95%CI:1.08,1.87), and females were more sensitive to long-term exposure to O3 (OR = 1.61 95%CI:1.15,2.23). Traditional southern pattern identified through RRR exhibited a protective effect against hypertension in males (OR = 0.73 95%CI: 0.56,1.00). The results of the interaction between dietary pattern score and PM2.5 revealed that adherence to traditional southern pattern was significantly associated with a decreased risk of hypertension in males (P < 0.05), while no significant association was observed among females. CONCLUSIONS: Our findings suggested that sex differences existed in the association between dietary patterns, air pollutants and hypertension. Furthermore, we found that adherence to traditional southern pattern may mitigate the risk of long-term PM2.5 exposure-induced hypertension in males.

Explore the effect of apparent temperature and air pollutants on the admission rate of acute myocardial infarction in Chongqing, China: a time-series study.

OBJECTIVE: Limited research has been conducted on the correlation between apparent temperature and acute myocardial infarction (AMI), as well as the potential impact of air pollutants in modifying this relationship. The objective of this study is to investigate the lagged effect of apparent temperature on AMI and assess the effect modification of environmental pollutants on this association. DESIGN: A time-series study. SETTING AND PARTICIPANTS: The data for this study were obtained from the Academy of Medical Data Science at Chongqing Medical University, covering daily hospitalisations for AMI between 1 January 2015 and 31 December 2016. Meteorological and air pollutant data were provided by China's National Meteorological Information Centre. OUTCOME MEASURES: We used a combined approach of quasi-Poisson generalised linear model and distributed lag non-linear model to thoroughly analyse the relationships. Additionally, we employed a generalised additive model to investigate the interaction between air pollutants and apparent temperature on the effect of AMI. RESULT: A total of 872 patients admitted to hospital with AMI were studied based on the median apparent temperature (20.43°C) in Chongqing. Low apparent temperature (10th, 7.19℃) has obvious lagged effect on acute myocardial infarction, first appearing on the 8th day (risk ratio (RR) 1.081, 95% CI 1.010 to 1.158) and the greatest risk on the 11th day (RR 1.094, 95% CI 1.037 to 1.153). No lagged effect was observed at high apparent temperature. In subgroup analysis, women and individuals aged 75 and above were at high risk. The interaction analysis indicates that there exist significant interactions between PM2.5 and high apparent temperature, as well as nitrogen dioxide (NO2) and low apparent temperature. CONCLUSION: The occurrence of decreased apparent temperature levels was discovered to be linked with a heightened relative risk of hospitalisations for AMI. PM2.5 and NO2 have an effect modification on the association between apparent temperature and admission rate of AMI.

Exposure to Concurrent Heatwaves and Ozone Pollution and Associations with Mortality Risk: A Nationwide Study in China.

BACKGROUND: Concurrent extreme events are projected to occur more frequently under a changing climate. Understanding the mortality risk and burden of the concurrent heatwaves and ozone (O3) pollution may support the formulation of adaptation strategies and early warning systems for concurrent events in the context of climate change. OBJECTIVES: We aimed to estimate the mortality risk and excess deaths of concurrent heatwaves and O3 pollution across 250 counties in China. METHODS: We collected daily mortality, meteorological, and air pollution data for the summer (1 June to 30 September) during 2013-2018. We defined heatwaves and high O3 pollution days, then we divided the identified days into three categories: a) days with only heatwaves (heatwave-only event), b) days with only high O3 pollution (high O3 pollution-only event), and c) days with concurrent heatwaves and high O3 pollution (concurrent event). A generalized linear model with a quasi-Poisson regression was used to estimate the risk of mortality associated with extreme events for each county. Then we conducted a random-effects meta-analysis to pool the county-specific estimates to derive the overall effect estimates. We used mixed-effects meta-regression to identify the drivers of the heterogeneity. Finally, we estimated the excess death attributable to extreme events (heatwave-only, high O3 pollution-only, and concurrent events) from 2013 to 2020. RESULTS: A higher all-cause mortality risk was associated with exposure to the concurrent heatwaves and high O3 pollution than exposure to a heatwave-only or a high O3 pollution-only event. The effects of a concurrent event on circulatory and respiratory mortality were higher than all-cause and nonaccidental mortality. Sex and age significantly impacted the association of concurrent events and heatwave-only events with all-cause mortality. We estimated that annual average excess deaths attributed to the concurrent events were 6,249 in China from 2017 to 2020, 5.7 times higher than the annual average excess deaths attributed to the concurrent events from 2013 to 2016. The annual average proportion of excess deaths attributed to the concurrent events in the total excess deaths caused by three types of events (heatwave-only events, high O3 pollution-only events, and concurrent events) increased significantly in 2017-2020 (31.50%; 95% CI: 26.73%, 35.53%) compared with 2013-2016 (9.65%; 95% CI: 5.67%, 10.81%). Relative excess risk due to interaction revealed positive additive interaction considering the concurrent effect of heatwaves and high O3 pollution. DISCUSSION: Our findings may provide scientific basis for establishing a concurrent event early warning system to reduce the adverse health impact of the concurrent heatwaves and high O3 pollution. https://doi.org/10.1289/EHP13790.

Effects of environmental exposure to iron powder on healthy and elastase-exposed mice.

Prolonged exposure to iron powder and other mineral dusts can threaten the health of individuals, especially those with COPD. The goal of this study was to determine how environmental exposure to metal dust from two different mining centers in Brazil affects lung mechanics, inflammation, remodeling and oxidative stress responses in healthy and elastase-exposed mice. This study divided 72 male C57Bl/6 mice into two groups, the summer group and the winter group. These groups were further divided into six groups: control, nonexposed (SAL); nonexposed, given elastase (ELA); exposed to metal powder at a mining company (SAL-L1 and ELA-L1); and exposed to a location three miles away from the mining company (SAL-L2 and ELA-L2) for four weeks. On the 29th day of the protocol, the researchers assessed lung mechanics, bronchoalveolar lavage fluid (BALF), inflammation, remodeling, oxidative stress, macrophage iron and alveolar wall alterations (mean linear intercept-Lm). The Lm was increased in the ELA, ELA-L1 and ELA-L2 groups compared to the SAL group (p < 0.05). There was an increase in the total number of cells and macrophages in the ELA-L1 and ELA-L2 groups compared to the other groups (p < 0.05). Compared to the ELA and SAL groups, the exposed groups (ELA-L1, ELA-L2, SAL-L1, and SAL-L2) exhibited increased expression of IL-1ß, IL-6, IL-10, IL-17, TNF-α, neutrophil elastase, TIMP-1, MMP-9, MMP-12, TGF-ß, collagen fibers, MUC5AC, iNOS, Gp91phox, NFkB and iron positive macrophages (p < 0.05). Although we did not find differences in lung mechanics across all groups, there were low to moderate correlations between inflammation remodeling, oxidative stress and NFkB with elastance, resistance of lung tissue and iron positive macrophages (p < 0.05). Environmental exposure to iron, confirmed by evaluation of iron in alveolar macrophages and in air, exacerbated inflammation, initiated remodeling, and induced oxidative stress responses in exposed mice with and without emphysema. Activation of the iNOS, Gp91phox and NFkB pathways play a role in these changes.