Effects Of Long-term Exposure Research Articles

Using EEA data to calculate health impacts of air pollution via the AirQ+ model: a practical example

Abstract The AirQ+ software tool for health risk assessment of air pollution, developed by the World Health Organization, helps quantify the effects of exposure to air pollution. Specifically, AirQ+ can estimate the effects of short-term changes in air pollution (based on risk estimates from time-series studies) and the effects of long-term exposures (using life-tables approach and based on risk estimates from cohort studies). AirQ+ is available in English, French, German and Russian. In this presentation, AirQ+ will be loaded with air pollution data from the European Environment Agency datasets for a quick evaluation of health effects from air pollution in an European city.

The effect of outdoor air pollution on Alzheimer’s disease: a systematic review

Abstract Air pollution is one of the largest global environmental risks to public health. Over recent years, neuroimaging techniques have started to uncover the detrimental impact air pollution has had on brain health, including the development of Alzheimer’s Diseases (AD). We systematically reviewed the literature to evaluate the effects of long-term exposure (months to years) to outdoor air pollutants on the development of AD-like neurology. This review was registered on PROSPERO (CRD42023482979) and followed PRISMA guidelines. Four large databases (MEDLINE, Embase, Scopus, and CINAHL) were searched in November 2023 using terms associated with air pollution, neuroimaging, and AD. Only peer-reviewed primary research articles using neuroimaging data to examine AD-like pathology after long-term exposure to air pollutants (Particulate Matter (PM2.5, PM10), SO2, NO2, O3, and/or CO) were included. Titles, abstracts and full-texts were screened, and included articles were quality assessed using the Newcastle Ottawa Scale. A narrative synthesis was conducted to analyse the studies. Our search yielded 397 results, of which eight articles met our inclusion criteria. Articles focused on changes to white matter (n = 5), cortical thickness (n = 6), and grey matter (n = 2). Exposure to PM2.5 was commonly associated with white matter reductions, and PM10 and NO2 exposure was associated with reduced cortical thickness. The effect of exposure to different outdoor pollution on grey matter was inconclusive, with both increases and decreases in grey matter volume observed. This review highlighted how PM2.5, PM10 and NO2 exposure was associated with neurological changes commonly seen in AD. These findings can be used by policymakers and researchers to identify specific pollutants that need greater restrictions and regulations to improve population health. Key messages • PM2.5, PM10 and NO2 exposure are associated with neurological changes commonly seen in AD. • Greater restrictions and regulations are needed on specific pollutants to improve population health.

Age and sex differences in the effects of short- and long-term exposure to air pollution on endothelial dysfunction

Abstract Background Endothelial dysfunction is an integrated index of risk factor burden and a marker of atherosclerotic cardiovascular disease. Air pollution is widely acknowledged as a significant non-traditional risk factor for cardiovascular disease. However, the impact of air pollutants at varying concentrations and exposure durations on endothelial function in different populations remains unclear. Purpose We aimed to use brachial artery flow-mediated dilatation (FMD) to identify demographic differences in the effects of short- and long-term exposure to air pollution on endothelial dysfunction. Methods We measured FMD in 850 participants from October 2016 to January 2020. Location-specific concentrations of fine particulate matter <2.5 μm aerodynamic diameter (PM2.5), inhalable particulate matter <10 μm aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) measured by fixed ambient air monitoring stations were collected for short- and long-term exposure assessment. We used the moving average 7- and 14-day exposures before the date of FMD measurements to estimate the short-term exposure effects and the moving average 12-month exposures before the date of FMD measurements to estimate the long-term exposure effects. Multiple linear regression models and restricted cubic splines were used to assess the associations before and after stratified by age and sex. Results This study eventually included 828 participants [551 (66.5%) younger than 65 years and 553 (66.8%) men]. Each 10 μg/m³ increase in 12-month exposure to PM10 and NO2 was significantly and linearly associated with -0.20% (95% CI: -0.37 to -0.03) and -0.58% (95% CI: -0.99 to -0.18) changes in FMD in all participants. 12-month exposure to gaseous pollutants was also significantly but nonlinearly associated with lower FMD. 7-day exposure to Quartile 4 of SO2 was significantly associated with a 0.70% decrease in FMD compared to Quartile 1 (β = -0.70, 95% CI: -1.40 to -0.008). No relationships were observed between 7- and 14-day exposure to PM2.5, PM10, NO2, CO, and endothelial dysfunction. Although interaction effects were limited to SO2 and sex, significant associations with different air pollutants were only found in men and those younger than 65 years after stratified. Conclusions Long-term exposure to air pollution is strongly associated with decreased endothelial function, and susceptibility to air pollution varies significantly with age and sex. Further identification of different susceptible populations and proactive measures to mitigate air pollution may be beneficial in reducing the burden of cardiovascular disease.

Monitoring of urinary nickel and chromium in metal industries workers in Alborz, Iran

Heavy metal contamination from occupational sources is a cause for concern due to its potential accumulation in the environment and the body of living organisms, which leads to long-term toxic effects. There is limited evidence on the concentration of heavy metals in the body fluids of welding workers. This study aimed to measure the concentration of nickel (Ni) and chromium (Cr) as two main toxic heavy metals in the urine samples of welders and determine the potential relationship of various environmental factors on their concentration levels. This study was conducted in Iran in 2022–2023. Eighty-five urine samples were collected from the studied welding workers. Inductively coupled plasma optical emission spectrometry (ICP-OES) was used to measure the concentration of Ni and Cr. Data related to socio-demographic characteristics (education level, income, work experience, age, and body mass index (BMI)), lifestyle profile (consumption of seafood and canned food, smoking, physical activity), type of ventilation and preventive devices at work, and suffering from underlying diseases (cardiovascular and high blood pressure) were collected using valid questionnaires. Ni and Cr were present in 100% of urine samples with mean concentrations of (1.09 ± 0.294) and (11.45 ± 16.751) µg/g creatinine, respectively. A significant correlation was observed between the mean concentration of Ni and Cr with the level of education, income, work experience, age, consumption of seafood and canned food, smoking, type of ventilation and preventive devices, and underlying diseases (p-value < 0.05). Also, there was no significant difference between Ni concentration and physical activity and Cr concentration with BMI. Lifestyle determinants and not using preventive devices are important predictors of urinary heavy metals in welding workers. Therefore, more research is required to determine the adverse effects of long-term exposure to these heavy metals.

Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes

IntroductionThe general population is chronically exposed to organophosphate pesticides through various routes including ingestion, hand-to-mouth contact, inhalation, and dermal contact. Exposure to organophosphate pesticides during pregnancy impairs fetal development, but the potential long-term effects of gestational organophosphate pesticide exposure are less well understood. MethodsWe investigated associations between gestational organophosphate pesticide exposure and cardiovascular outcomes in 643 children in the Generation R Study, a prospective pregnancy cohort based in Rotterdam, The Netherlands. Urinary organophosphate pesticide metabolites (dimethyl [∑DMAP], diethyl [∑DEAP], and total dialkyl phosphate [∑DAP] metabolites) were quantified in three urine samples collected from pregnant participants, and their children were followed until age 10 years at which time cardiac magnetic resonance imaging, ultrasonography, blood pressure, and serum biomarkers assessed cardiovascular health. Linear regression models estimated associations (β and 95 % confidence interval [CI]) between a one-interquartile range (IQR) increase in averaged gestational exposure biomarker concentrations and z-scored pediatric cardiovascular outcomes. We investigated effect modification of associations by PON1 genotype. ResultsCarotid intima-media thickness z-score was lower (β: -0.14 [95 % CI: −0.25, −0.02]) and HDL cholesterol z-score was higher (β: 0.14 [95 % CI: 0.02, 0.25]) for increases in ∑DEAP concentrations. Carotid intima-media distensibility z-score was lower (β: -0.08 [95 % CI: −0.19, 0.03]) for increases in ∑DMAP concentrations, and systolic blood pressure z-score was higher (β: 0.10 [95 % CI: −0.01, 0.21]) for increases in ∑DMAP and ∑DAP. Among those with PON1-161CC and PON1-L55MTT genotypes, higher organophosphate pesticide concentrations conferred an excess risk of adverse vascular and glycemic outcomes, respectively. ConclusionsWe observed heterogenous associations between gestational organophosphate pesticide exposure and pediatric cardiovascular health: an anti-atherogenic profile was observed for increases in ∑DEAP concentrations, and impairments in multiple aspects of cardiovascular health was observed for increases in ∑DMAP concentrations. PON1-161 and PON1-L55M single nucleotide polymorphisms modified associations for vascular and glycemic outcomes, respectively.

Long-Term Neurotoxic Effects and Alzheimer's Disease Risk of Early EHDPP Exposure in Zebrafish: Insights from Molecular Mechanisms to Adult Pathology.

2-Ethylhexyl diphenyl phosphate (EHDPP), ubiquitously monitored in environmental media, is highly bioaccumulative and may pose long-term risks, even after short-term exposure. In this investigation, larval zebrafish were exposed to 0.05, 0.5, and 5.0 μg/L EHDPP from 4 to 120 h postfertilization (hpf) to examine the long-term neurotoxicity effects of early exposure. Exposure to 5.0 μg/L EHDPP yielded hyperactive locomotor behavior, which was characterized by increased swimming speed, larger turning angles, and heightened sensitivity to light-dark stimulation. The predicted targets of EHDPP (top 100 potential macromolecules) were primarily associated with brain diseases like Alzheimer's disease (AD). Comparisons of differentially expressed genes (DEGs) from AD patients (GSE48350) and RNA-seq data from EHDPP-exposed zebrafish confirmed consistently abnormal regulatory pathways. EHDPP's interaction with M1 and M5 muscarinic acetylcholine receptors likely disrupted calcium homeostasis, leading to mitochondrial dysfunction and neurotransmitter imbalance as well as abnormal locomotor behavior. Especially, 5.0 μg/L EHDPP exposure during early development (4-120 hpf) triggered early- and midstage AD-like symptoms in adulthood (180 dpf), characterized by cognitive confusion, aggression, blood-brain barrier disruption, and mitochondrial damage in brains. These findings provide deep insights into the long-term neurotoxicity effects and Alzheimer's disease risks of early EHDPP exposure at extremely low dosages.

Childhood Air Pollution Exposure Associated with Self-reported Bronchitic Symptoms in Adulthood.

Rationale: Few studies have examined the effects of long-term childhood air pollution exposure on adult respiratory health, including whether childhood respiratory effects underlie this relation. Objectives: To evaluate associations between childhood air pollution exposure and self-reported adult bronchitic symptoms while considering child respiratory health in the Southern California Children's Health Study. Methods: Exposures to nitrogen dioxide (NO2), ozone, and particulate matter <2.5 μm and <10 μm in diameter (PM10) assessed using inverse-distance-squared spatial interpolation based on childhood (birth to age 17 yr) residential histories. Bronchitic symptoms (bronchitis, cough, or phlegm in the past 12 mo) were ascertained via a questionnaire in adulthood. Associations between mean air pollution exposure across childhood and self-reported adult bronchitic symptoms were estimated using logistic regression. We further adjusted for childhood bronchitic symptoms and asthma to understand whether associations operated beyond childhood respiratory health impacts. Effect modification was assessed for family history of asthma, childhood asthma, and adult allergies. Measurements and Main Results: A total of 1,308 participants were included (mostly non-Hispanic White [56%] or Hispanic [32%]). At adult assessment (mean age, 32.0 yr; standard deviation [SD], 4.7), 25% reported bronchitic symptoms. Adult bronchitic symptoms were associated with NO2 and PM10 childhood exposures. Odds ratios per 1-SD increase were 1.69 (95% confidence interval, 1.14-2.49) for NO2 (SD, 11.1 ppb) and 1.51 (95% confidence interval, 1.00-2.27) for PM10 (SD, 14.2 μg/m3). Adjusting for childhood bronchitic symptoms or asthma produced similar results. NO2 and PM10 associations were modified by childhood asthma, with greater associations among asthmatic individuals. Conclusions: Childhood NO2 and PM10 exposures were associated with adult bronchitic symptoms. Associations were not explained by childhood respiratory health impacts; however, participants with childhood asthma had stronger associations.

Effects of 4G Long-Term Evolution Electromagnetic Fields on Thyroid Hormone Dysfunction and Behavioral Changes in Adolescent Male Mice.

Radiofrequency electromagnetic fields (RF-EMFs) can penetrate tissues and potentially influence endocrine and brain development. Despite increased mobile phone use among children and adolescents, the long-term effects of RF-EMF exposure on brain and endocrine development remain unclear. This study investigated the effects of long-term evolution band (LTE) EMF exposure on thyroid hormone levels, crucial for metabolism, growth, and development. Four-week-old male mice (C57BL/6) were exposed to LTE EMF (whole-body average specific absorption rate [SAR] 4 W/kg) or a positive control (lead; Pb, 300 ppm in drinking water) for 4 weeks. Subsequently, the mice underwent behavioral tests including open field, marble burying, and nest building. Blood pituitary and thyroid hormone levels, and thyroid hormone-regulating genes within the hypothalamus-pituitary-thyroid (HPT) axis were analyzed. LTE exposure increased T3 levels, while Pb exposure elevated T3 and T4 and decreased ACTH levels. The LTE EMF group showed no gene expression alterations in the thyroid and pituitary glands, but hypothalamic Dio2 and Dio3 expressions were significantly reduced compared to that in the sham-exposed group. Pb exposure altered the hypothalamic mRNA levels of Oatp1c1 and Trh, pituitary mRNA of Trhr, and Tpo and Tg expression in the thyroid. In conclusion, LTE EMF exposure altered hypothalamic Dio2 and Dio3 expression, potentially impacting the HPT axis function. Further research is needed to explore RF-EMF's impacts on the endocrine system.

Early life air pollution exposures and thyroid function in children: A prospective cohort study

Studies on early life ambient air pollution exposures and childhood thyroid function are scarce. This study aimed to evaluate the relationships between early life fine particulate matter (≤2.5 μm; PM2.5) and nitrogen dioxide (NO2) exposures and thyroid function in children. We measured the levels of thyrotropin, triiodothyronine, and free thyroxine in children (n = 684) residing in a rural Korean area at age 2, 4, 6, or 8 years from 2012 to 2020 in the Environment and Development of Children cohort. The relationship between residential average exposure levels of PM2.5 and NO2 during pregnancy and 1-year average levels before visit and thyroid function during childhood were analyzed. Inverse association between increases of 10 μg/m3 in PM2.5 during the first trimester and thyrotropin levels at aged 4 (β, −0.12; 95% CI: −0.22, −0.02) and 6 years (β, −0.16; 95% CI: −0.26, −0.06) were observed. No association was found between PM2.5 exposure during the second and third trimester and childhood TSH levels. Childhood PM2.5 exposure was positively associated with thyrotropin rise at aged 4 (β, 0.2; 95% CI: 0.06, 0.35) and 6 years (β, 0.16; 95% CI: 0.02, 0.29) and inversely related with free thyroxine levels at aged 8 years (β, −0.04; 95% CI: −0.07, −0.01). No relationship between NO2 exposure and thyroid function was found. In conclusion, association between PM2.5 exposure and childhood thyrotropin levels varied depending on exposure timing. Early gestational exposure showed an inverse relationship, whereas childhood exposure were positively associated with childhood thyrotropin levels. The long-term effects of early life air pollution exposure and underlying mechanisms should be investigated in future studies.

Exposure to PFOA, PFOS, and PFHxS induces Alzheimer's disease-like neuropathology in cerebral organoids

Per- and polyfluoroalkyl substances (PFASs), a class of ubiquitous synthetic organic chemicals, are widely utilized across various industrial applications. However, the long-term neurological health effects of PFAS mixture exposure in humans remain poorly understood. To address this gap, we have designed a comprehensive study to predict and validate cell-type-specific neurotoxicity of PFASs using single-cell RNA sequencing (scRNA-seq) and cerebral organoids. Cerebral organoids were exposed to a PFAS mixture at concentrations of 1 × (10 ng/ml PFOS and PFOA, and 1 ng/ml PFHxS), 30 × , and 900 × over 35 days, with a follow-up analysis at day 70. Pathological alterations and lipidomic profiles were analyzed to identify disrupted molecular pathways and mechanisms. The scRNA-seq data revealed a significant impact of PFASs on neurons, suggesting a potential role in Alzheimer's Disease (AD) pathology, as well as intellectual and cognitive impairments. PFAS-treated cerebral organoids exhibited Aβ accumulation and tau phosphorylation. Lipidomic analyses further revealed lipid disturbances in response to PFAS mixture exposure, linking PFAS-induced AD-like neuropathology to sphingolipid metabolism disruption. Collectively, our findings provide novel insights into the PFAS-induced neurotoxicity, highlighting the significance of sphingolipid metabolism in the development of AD-like neuropathology. The use of cerebral organoids and scRNA-seq offers a powerful methodology for evaluating the health risks associated with environmental contaminants, particularly those with neurotoxic potential.

Risk of death from hematological malignancies in the South Urals Population Exposed to Radiation cohort

The results of studies of long-term effects of population exposure in the South Urals in the 1950s were based for a long time on studies of the effects of exposure in the Techa River cohort and later in the East Urals Radioactive Trace cohort. After the creation of the South Urals Population Exposed to Radiation cohort, combining all persons exposed in the South Urals in the period from January 1, 1950, to December 31, 1960 the size of the cohort doubled, follow-up period reached 71 years, and the number of person-years at risk increased to 1,964,333. The average dose to red bone marrow for all cohort members was 231mGy. Regression analysis using a simple parametric excess relative risk model was performed using the EPICURE statistical package. The analysis resulted in confirmation of a statistically significant (p &lt;0.001) linear doseresponse relationship of mortality for all hemoblastoses, and leukemia. The excess relative risk and 95% confidence intervals of death at 2-year latency period from all hemoblastoses were 0.71/Gy (0.28;1.31); from all leukemias - 1.28/Gy (0.55-2.39) and from leukemias excluding chronic lymphocytic leukemia -1.52/Gy (0.64-2.94). The quadratic model also significantly described the dose dependence; (the differences between the models were not significant). Increasing the follow-up period to 71 years resulted in a slight decrease in risk estimates. The width of the confidence intervals of the risk estimates decreased by more than a factor of 3 compared to earlier studies in the Techa River cohort, which indicates a decrease in uncertainties of risk estimates. Increasing the size of the cohort made it possible to obtain significant risk values for individual population groups (by sex, age, etc.). Analysis of risk values modification did not reveal significant differences in dose dependence on the studied factors, including attained age and age at exposure. The study will be continued to investigate in more detail the influence of time-dependent factors on dose dependence, as well as to assess the risk of death from different cellular forms of leukemia.

Plastic debris exposure and effects in rivers: Boundaries for efficient ecological risk assessment.

Until recently, plastic pollution research was focused on the marine environments, and attention was given to terrestrial and freshwater environments latter. This discussion paper aims to put forward crucial questions on issues that limit our ability to conduct reliable plastic ecological risk assessments in rivers. Previous studies highlighted the widespread presence of plastics in rivers, but the sources and levels of exposure remained matters of debate. Field measurements have been carried out on the concentration and composition of plastics in rivers, but greater homogeneity in the choice of plastic sizes, particularly for microplastics by following the recent ISO international standard nomenclature, is needed for better comparison between studies. The development of additional relevant sampling strategies that are suited to the specific characteristics of riverine environments is also needed. Similarly, we encourage the systematic real-time monitoring of environmental conditions (e.g., topology of the sampling section of the river, hydrology, volumetric flux and velocity, suspended matters concentration) to better understand the origin of variability in plastic concentrations in rivers. Furthermore, ingestion of microplastics by freshwater organisms has been demonstrated under laboratory conditions, but the long-term effects of continuous microplastic exposure in organisms are less well understood. This discussion paper encourages an integrative view of the issues involved in assessing plastic exposure and its effects on biota, in order to improve our ability to carry out relevant ecological risk assessments in river environments.

Lysosomal disruption, mitochondrial impairment, histopathological and oxidative stress in rat's nervous system after exposure to a neonicotinoid (imidacloprid).

Imidacloprid (IMI), a neonicotinoid pesticide, has been widely used due to its high efficiency against insect pests. However, its prolonged exposure may pose significant risks to non-target organisms, including mammals. Recent studies have raised concerns about its potential neurotoxicity, yet the underlying mechanisms remain poorly understood. This study aimed to assess the neurotoxic effects of chronic Imidacloprid exposure in Wistar rats, focusing on oxidative stress, mitochondrial dysfunction, and lysosomal disruption. Wistar rats were orally administered two doses of Imidacloprid (5mg/kg and 50mg/kg body weight) for three months. Neurotoxic effects were assessed by measuring key biochemical markers such as the enzymatic activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione S-transferase (GST). Non-enzymatic markers, including glutathione (GSH) levels and malondialdehyde (MDA) index, were also evaluated. Mitochondrial function was assessed by analyzing oxygen consumption, swelling, and membrane permeability and histopathological changes. Lysosomal stability was examined using the Neutral Red Retention Time (NRRT) assay. Neutral red is a dye that accumulates in the acidic environment of lysosomes. Healthy lysosomes retain the dye, while compromised lysosomes lose it, indicating destabilization. By measuring the amount of neutral red retained in lysosomes, the NRRT assay assesses lysosomal integrity. Lysosomal pH variations were also monitored to evaluate functional changes. Microscopic analysis provided insight into structural changes in lysosomes and other cell components. Lysosomal destabilization was further confirmed by morphological alterations observed through light microscopy, revealing a progressive, time-dependent degeneration of lysosomal structures, including lysosomal expansion, neutral red dye leakage, and cell rounding. These changes reflected a temporal evolution of lysosomal damage, progressing from minor structural disruptions to more severe alterations as exposure continued, observable at the microscopic level. During the study, clinical observations of intoxicated rats included symptoms such as lethargy, reduced activity levels, and impaired motor coordination. High-dose Imidacloprid exposure led to noticeable behavioral changes, including decreased exploratory behavior and altered grooming patterns. Additionally, signs of neurotoxic effects, such as tremors or ataxia, were observed in the rats exposed to the higher dose, reflecting the systemic impact of chronic pesticide exposure. The results revealed a significant decrease in the enzymatic activities of CAT, GPx, and SOD, accompanied by an increase in GST activity. A notable reduction in glutathione levels and a rise in MDA index were observed, indicating enhanced oxidative stress in the brain. Mitochondrial impairment was evidenced by disturbances in oxygen consumption, increased swelling, and altered membrane permeability. Lysosomal destabilization was confirmed by reduced retention of neutral red dye, structural changes in lysosomes, and a significant rise in lysosomal pH in the IMI-exposed groups. In addition, the histopathological features indicate that imidacloprid at the given dose and exposure duration may have caused notable neurotoxic effects in Wistar rat brain tissue. Chronic exposure to Imidacloprid induces oxidative stress, mitochondrial dysfunction, lysosomal disruption and histopathological alterations in the central nervous system of Wistar rats. These findings provide valuable insights into the neurotoxic mechanisms of neonicotinoid pesticides, highlighting the need for further research to understand the long-term effects of Imidacloprid exposure on mammalian health.

Detrimental effect of prenatal progesterone exposure on anxiety and depressive-like responses in adult male and female rat offspring: role of plasma, hippocampal corticosterone and hippocampal progesterone receptors

In clinical practice, the use of exogenous progesterone (Pro) is often required in assisted reproduction programs due to reduced levels of the hormone and the risk of miscarriage. Exposure to the hormone reduces anxiety in rodents, but the long-term effects of prenatal exposure in adult offspring are unknown. Therefore, the present study was designed to investigate the effect of prenatal Pro treatment on anxiety- and depression-like behavior and the effect on plasma, hippocampal corticosterone (CORT) and hippocampal progesterone receptor (PR) in young adult male and female rat offspring. The behavioral responses of offspring of both sexes were tested in the open field, and the elevated plus maze tests, and for depressive-like behavior in the sucrose preference test, the forced swimming test and the splash test. CORT levels and PR expression were measured by ELISA. The results indicate that prenatal Pro exposure at low and high doses (10 and 50 mg/kg, s.c. during G0-G10) induces anxiogenic and depressive-like effects compared to vehicle-treated controls, which are associated with high plasma and hippocampal CORT levels and upregulated hippocampal PR in male and female adult offspring. Our results demonstrate that prenatal Pro exposure has detrimental effects on the emotional status of male and female adult offspring, which may be associated with long-term changes in hormonal homeostasis.

Blowin’ in the wind: Long-term downwind exposure to air pollution from power plants and adult mortality

We estimate the causal effects of long-term exposure to air pollution emitted from fossil fuel power plants on adult mortality. We leverage quasi-experimental variation in daily wind patterns, which is further instrumented by the county orientation from the nearest power plant. We find that the county’s fraction of days spent downwind of plants within 20 miles in the last 10 years is associated with increased mortality from COVID-19 through the third peak in mortality in January 2021. This effect is more pronounced in fenceline communities with high poverty rates, low health insurance coverage, and low educational attainment.

Temperature dependent sensitivity of the harpacticoid copepod Nitokra spinipes to marine algal toxins

Harmful algal blooms (HABs) – proliferated algae densities, often producing toxins – have increasingly been found in ocean and coastal areas. Recent studies show that rising temperatures contribute to HAB occurrence, but the broader influence of climate change on these outbreaks is less quantified. Of particular concern is the limited research on HAB toxin effects under varying temperatures, especially regarding primary consumers such as copepods, a crucial component of aquatic ecosystems. Therefore, we examined the impact of marine toxins on the harpacticoid copepod Nitokra spinipes, a model organism for marine ecotoxicology, in the context of climate change. We evaluated the toxicity of four purified, commonly occurring algal toxins, at three different temperatures in the laboratory. First, adult females were exposed to a concentration series of toxins at 15, 20, and 25 °C for 48 hours. EC50 values of domoic acid ranged from 8.79 ± 1.93 μg L-1 to 25.97 ± 11.96 μg L-1. Nauplii, aged 48 to 72 hours, were exposed at 18, 20 and 22 °C for the same duration. Less sensitive compared to adults, the EC50 of domoic acid in this case varied from 57.26 ± 6.82 μg L-1 to 97.24 ± 6.45 μg L-1. Both results indicated a temperature-dependent EC50. For the chronic toxicity tests, larval development ratio (LDR), brood size and inter-brood time of domoic acid (DA), yessotoxin (YTX), saxitoxin (STX), and microcystin-LR (MC-LR) were examined at 18, 20 and 22 °C. We observed that with increasing temperatures, LDR increased, whereas brood size significantly decreased as DA, YTX or STX concentrations rose. No interaction between temperature and algal toxins was found but a temperature dependent sensitivity of copepods towards DA, YTX and STX was revealed. Our research provides insights into the effects of long-term exposure to algal toxins on marine copepods and the potential impacts of climate warming.

Effects of long-term exposure to high-altitude on episodic memory: The moderating role of daytime dysfunction

Chronic exposure to high-altitude hypoxic environments may influence short-term memory and working memory. However, its impact on long-term memory, specifically episodic memory, remains understudied. In this study, we systematically investigated the effects of long-term exposure to high altitude (3650 m) on episodic memory, including item memory and source memory. Moreover, we examined the moderating role of daytime dysfunction on the relationship between altitude and episodic memory. In total, 97 participants were enrolled in the study: 49 were from the high-altitude (HA) group, comprising those born and raised in low altitude (LA) areas (< 500 m) and had migrated to HA for 2∼3 years after turning 18; and 48 were from the LA group, who had never lived at high altitudes. Episodic memory was evaluated using a what-when-where task, whereas daytime dysfunction was measured by the Pittsburgh Sleep Quality Index. For item memory, hit rate and correct rejection rate were significantly lower in the HA group relative to the LA group. For source binding memory, the performance in what-where binding and what-when-where binding were decreased in the HA group, but the what-when binding did not differ between the two groups. Furthermore, the effects of altitude on hit rate, what-where binding, and what-when-where binding were significantly pronounced in individuals with higher levels of daytime dysfunction. These findings suggest that long-term exposure to high-altitude hypoxic environments influences episodic memory performance, including item recognition and source-binding memory. Specifically, spatial source memory is affected by high-altitude exposure, whereas temporal source memory remains unaffected. Moreover, these results highlight the importance of considering sleep quality, especially good daytime function, in maintaining optimal episodic memory function following chronic exposure to high altitudes.

The Effect of Long-Term Particulate Matter Exposure on Respiratory Mortality: Cohort Study in China.

Particulate matter (PM), which affects respiratory health, has been well documented; however, substantial evidence from large cohorts is still limited, particularly in highly polluted countries and for PM1. Our objective was to examine the potential causal links between long-term exposure to PMs (PM2.5, PM10, and more importantly, PM1) and respiratory mortality. A total of 580,757 participants from the Guangzhou area, China, were recruited from 2009 to 2015 and followed up through 2020. The annual average concentrations of PMs at a 1-km spatial resolution around the residential addresses were estimated using validated spatiotemporal models. The marginal structural Cox model was used to estimate the associations of PM exposure with respiratory mortality, accounting for time-varying PM exposure. Results were stratified by demographics and lifestyle behaviors factors. Among the participants, the mean age was 48.33 (SD 17.55) years, and 275,676 (47.47%) of them were men. During the follow-up period, 7260 deaths occurred due to respiratory diseases. The annual average concentrations of PM1, PM2.5, and PM10 showed a declining trend during the follow-up period. After adjusting for confounders, a 6.6% (95% CI 5.6%-7.6%), 4.2% (95% CI 3.6%-4.7%), and 4.0% (95% CI 3.6%-4.5%) increase in the risk of respiratory mortality was observed following each 1-μg/m3 increase in concentrations of PM1, PM2.5, and PM10, respectively. In addition, older participants, nonsmokers, participants with higher exercise frequency, and those exposed to a lower normalized difference vegetation index tended to be more susceptible to the effects of PMs. Furthermore, participants in the low-exposure group tended to be at a 7.6% and 2.7% greater risk of respiratory mortality following PM1 and PM10 exposure, respectively, compared to the entire cohort. This cohort study provides causal clues of the respiratory impact of long-term ambient PM exposure, indicating that PM reduction efforts may continuously benefit the population's respiratory health.

Interactive effects of long-term exposure to air pollutants on SARS-CoV-2 infection and severity: a northern Italian population-based cohort study.

We examined interactions, to our knowledge not yet explored, between long-term exposures to particulate matter (PM 10 ) with nitrogen dioxide (NO 2 ) and ozone (O 3 ) on SARS-CoV-2 infectivity and severity. We followed 709,864 adult residents of Varese Province from 1 February 2020 until the first positive test, COVID-19 hospitalization, or death, up to 31 December 2020. We estimated residential annual means of PM 10 , NO 2 and O 3 in 2019 from chemical-transport and random-forest models. We estimated interactive effects of pollutants with urbanicity on SARS-CoV-2 infectivity, hospitalization, and mortality endpoints using Cox regression models adjusted for socio-demographic factors and comorbidities, and additional cases due to interactions using Poisson models. 41,065 individuals were infected, 5,203 were hospitalized and 1,543 died from COVID-19 during follow-up. Mean PM 10 was 1.6 times higher and NO 2 2.6 times higher than WHO limits, with wide gradients between urban and non-urban areas. PM 10 and NO 2 were positively associated with SARS-CoV-2 infectivity and mortality, and PM 10 with hospitalizations in urban areas. Interaction analyses estimated that the effect of PM 10 (per 3.5 µg/m 3 ) on infectivity was strongest in urban areas (HR=1.12, 95%CI:1.09-1.16), corresponding to 854 additional cases per 100,000 person-years, and in areas at high NO 2 co-exposure (HR=1.15, 1.08-1.22). At higher levels of PM 10 co-exposure the protective association of ozone reversed (HR=1.32, 1.17-1.49), yielding to 278 additional cases per µg/m 3 increase in O 3 . We estimated similar interactive effects for severity endpoints. We estimate that interactive effects between pollutants exacerbated the burden of SARS-CoV-2 pandemic in urban areas.

Long-term exposure to wildland fire smoke PM2.5 and mortality in the contiguous United States

Despite the substantial evidence on the health effects of short-term exposure to ambient fine particles (PM2.5), including increasing studies focusing on those from wildland fire smoke, the impacts of long-term wildland fire smoke PM2.5 exposure remain unclear. We investigated the association between long-term exposure to wildland fire smoke PM2.5 and nonaccidental mortality and mortality from a wide range of specific causes in all 3,108 counties in the contiguous United States, 2007 to 2020. Controlling for nonsmoke PM2.5, air temperature, and unmeasured spatial and temporal confounders, we found a nonlinear association between 12-mo moving average concentration of smoke PM2.5 and monthly nonaccidental mortality rate. Relative to a month with the long-term smoke PM2.5 exposure below 0.1 μg/m3, nonaccidental mortality increased by 0.16 to 0.63 and 2.11 deaths per 100,000 people per month when the 12-mo moving average of PM2.5 concentration was of 0.1 to 5 and 5+ μg/m3, respectively. Cardiovascular, ischemic heart disease, digestive, endocrine, diabetes, mental, and chronic kidney disease mortality were all found to be associated with long-term wildland fire smoke PM2.5 exposure. Smoke PM2.5 contributed to approximately 11,415 nonaccidental deaths/y (95% CI: 6,754, 16,075) in the contiguous United States. Higher smoke PM2.5-related increases in mortality rates were found for people aged 65 and above. Positive interaction effects with extreme heat were also observed. Our study identified the detrimental effects of long-term exposure to wildland fire smoke PM2.5 on a wide range of mortality outcomes, underscoring the need for public health actions and communications that span the health risks of both short- and long-term exposure.