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Air pollution is an environmental factor associated with an increased risk of neurodegenerative diseases, such as Alzheimer's and Parkinson's, characterized by decreased cognitive abilities and memory. The limited models of sporadic Alzheimer's disease fail to replicate all pathological hallmarks of the disease, making it challenging to uncover potential environmental causes. Environmentally driven models of Alzheimer's disease are thus timely and necessary. We used live-cell confocal fluorescent imaging combined with high-resolution stimulated emission depletion (STED) microscopy to follow the response of retinoic acid-differentiated human neuroblastoma SH-SY5Y cells to nanomaterial exposure. Here, we report that exposure of the cells to some particulate matter constituents reproduces a neurodegenerative phenotype, including extracellular amyloid beta-containing plaques and decreased neurite length. Consistent with the existing in vivo research, we observed detrimental effects, specifically a substantial reduction in neurite length and formation of amyloid beta plaques, after exposure to iron oxide and diesel exhaust particles. Conversely, after exposure to engineered cerium oxide nanoparticles, the lengths of neurites were maintained, and almost no extracellular amyloid beta plaques were formed. Although the exact mechanism behind this effect remains to be explained, the retinoic acid differentiated SH-SY5Y cell in vitro model could serve as an alternative, environmentally driven model of neurodegenerative diseases, including Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM2.5) may disrupt women's reproductive hormones, posing potential reproductive risks. However, the exact compositions of PM2.5 responsible for these effects remain unclear. Our investigation explored the long-term impacts of PM2.5 constituents on reproductive hormones, based on a large longitudinal assisted reproductive cohort study in Anhui, China. We included 24,396 reproductive hormone samples from 19,845 women attending assisted reproductive technologies (ART) between 2014 and 2020. Using high-resolution gridded data (1-km resolution), we calculated the residence-specified PM2.5 constituents during the year before the month of hormone testing. Relationships between PM2.5 constituents [organic matter (OM), chloride (Cl-), sulfate (SO42-), ammonium (NH4+), black carbon, and nitrate] and reproductive hormones were investigated using the linear mixed model with subject-specific intercepts. The constituent-proportion model and the constituent-residual model were also constructed. Additionally, cubic spline analysis was used to examine the potential non-linear exposure-response relationship. We found that per interquartile range (IQR) increment in OM was associated with a 5.31 % (3.74 %, 6.89 %) increase in estradiol, and per IQR increment in Cl- and NH4+ were associated with 13.56 % (7.63 %, 19.82 %) and 9.07 % (4.35 %, 14.01 %) increases in luteinizing hormone. Conversely, per IQR increment in OM and Cl- were associated with −7.27 % (-9.34 %, −5.16 %) and −8.52 % (-10.99 %, −5.98 %) decreases in progesterone, and per IQR increment in SO42- was associated with a −9.15 % (-10.31 %, −7.98 %) decrease in testosterone. These associations were held in both proportional and residual models. Moreover, exposure-response curves for estradiol and progesterone with PM2.5 constituents exhibited approximately U-shaped. These results suggested that specific PM2.5 constituents might disrupt reproductive hormone homeostasis in women attending ART, providing new evidence for formulating PM2.5 pollution reduction strategies that could benefit women's reproductive health.

Background: Electrocardiogram (ECG) abnormalities are known to have prognostic value for heart conditions, while evidence on the relationship between long-term exposure to PM2.5 constituents and electrocardiographic (ECG) abnormalities is limited. This study aimed to quantify the association between long-term exposure to PM2.5 constituents and changes in ECG diagnoses. Methods: We designed a longitudinal study among participants with repeated records of ECG examination based on the China National Stroke Screening Survey 2013–2018. Logistic regressions with multiple adjustment, estimated by the generalized estimating equation to incorporate repeated measurements, were used to assess the associations between the occurrence of any physician-diagnosed ECG abnormalities and long-term exposure to PM2.5 constituents. Results: We included 61,094 participants with 132,249 visits. All five constituents (sulfate, nitrate, ammonium, organic matter, and black carbon) were significantly associated with an increased risk of ECG abnormalities. The excess risk of ECG abnormalities per interquartile-range increase in exposure was the highest for sulfate (26%, 95% confidence interval [CI] 23–29%), followed by ammonium (22%, 19–26%), nitrate (21%, 17–24%), black carbon (16%, 13–10%) and organic matter (9%,6%-11%). We also found that atrial fibrillation patients might be susceptible to the adverse effects of PM2.5 constituents on ECG. Conclusion: Differential associations between various constituents of PM2.5 and ECG abnormalities were found. The unequal toxicities for different chemical constituents of ambient particles on cardiovascular electrophysiological endpoints should be taken into consideration when considering the biological pathways linking PM2.5 and cardiovascular conditions.

Fine particulate matter (PM 2.5) may disrupt women's reproductive hormones, posing potential reproductive risks. However, the exact compositions of PM 2.5 responsible for these effects remain unclear. Our investigation explored the long-term impacts of PM 2.5 constituents on reproductive hormones, based on a large longitudinal assisted reproductive cohort study in Anhui, China. We included 24,396 reproductive hormone samples from 19,845 women attending assisted reproductive technologies (ART) between 2014 and 2020. Using high-resolution gridded data (1-km resolution), we calculated the residence-specified PM 2.5 constituents during the year before the month of hormone testing. Relationships between PM 2.5 constituents [organic matter (OM), chloride (Cl-), sulfate (SO 4 2-), ammonium (NH 4 +), black carbon, and nitrate] and reproductive hormones were investigated using the linear mixed model with subject-specific intercepts. The constituent-proportion model and the constituent-residual model were also constructed. Additionally, cubic spline analysis was used to examine the potential non-linear exposure-response relationship. We found that per interquartile range (IQR) increment in OM was associated with a 5.31 % (3.74 %, 6.89 %) increase in estradiol, and per IQR increment in Cl- and NH 4 + were associated with 13.56 % (7.63 %, 19.82 %) and 9.07 % (4.35 %, 14.01 %) increases in luteinizing hormone. Conversely, per IQR increment in OM and Cl- were associated with −7.27 % (-9.34 %, −5.16 %) and −8.52 % (-10.99 %, −5.98 %) decreases in progesterone, and per IQR increment in SO 4 2- was associated with a −9.15 % (-10.31 %, −7.98 %) decrease in testosterone. These associations were held in both proportional and residual models. Moreover, exposure-response curves for estradiol and progesterone with PM 2.5 constituents exhibited approximately U-shaped. These results suggested that specific PM 2.5 constituents might disrupt reproductive hormone homeostasis in women attending ART, providing new evidence for formulating PM 2.5 pollution reduction strategies that could benefit women's reproductive health. [Display omitted] • Long-term exposure to PM 2.5 constituents on reproductive hormones. • Elevated estradiol levels were associated with organic matter. • Decreased progesterone levels were associated with organic matter and chloride. • Decreased testosterone levels were associated with sulfate. • Elevated luteinizing hormone levels were associated with chloride and ammonium. [ABSTRACT FROM AUTHOR]

Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort. Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18–N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO 2), black carbon (BC), ozone (O 3), particulate matter ≤2.5 μm (PM 2.5) and several elemental constituents of PM 2.5. Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income. Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM 2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03–1.66) per 5 μg/m3, BC (1.26 (1.03–1.53) per 0.5 × 10− 5/m), NO 2 (1.13 (0.93–1.38) per 10 μg/m3) and inverse for O 3 (0.71 (0.54–0.93) per 10 μg/m3). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality. • Large population-based European cohort and fine-scale exposure resolution. • PM2.5 is positively associated with chronic kidney disease (CKD) mortality. • PM2.5 elemental constituents from different sources are related to CKD mortality. • The observed associations manifest below current European PM2.5 limit values. [ABSTRACT FROM AUTHOR]

• Annual PM 2.5 constituent exposure was associated with abnormal ECG outcomes. • Per IQR increase of sulfate related to a 26% increased risk of ECG abnormalities. • Differential toxicity of PM 2.5 constituents on ECG may inform policy making. Electrocardiogram (ECG) abnormalities are known to have prognostic value for heart conditions, while evidence on the relationship between long-term exposure to PM 2.5 constituents and electrocardiographic (ECG) abnormalities is limited. This study aimed to quantify the association between long-term exposure to PM 2.5 constituents and changes in ECG diagnoses. We designed a longitudinal study among participants with repeated records of ECG examination based on the China National Stroke Screening Survey 2013–2018. Logistic regressions with multiple adjustment, estimated by the generalized estimating equation to incorporate repeated measurements, were used to assess the associations between the occurrence of any physician-diagnosed ECG abnormalities and long-term exposure to PM 2.5 constituents. We included 61,094 participants with 132,249 visits. All five constituents (sulfate, nitrate, ammonium, organic matter, and black carbon) were significantly associated with an increased risk of ECG abnormalities. The excess risk of ECG abnormalities per interquartile-range increase in exposure was the highest for sulfate (26%, 95% confidence interval [CI] 23–29%), followed by ammonium (22%, 19–26%), nitrate (21%, 17–24%), black carbon (16%, 13–10%) and organic matter (9%,6%-11%). We also found that atrial fibrillation patients might be susceptible to the adverse effects of PM 2.5 constituents on ECG. Differential associations between various constituents of PM 2.5 and ECG abnormalities were found. The unequal toxicities for different chemical constituents of ambient particles on cardiovascular electrophysiological endpoints should be taken into consideration when considering the biological pathways linking PM 2.5 and cardiovascular conditions. [ABSTRACT FROM AUTHOR]

Background: Exposure to ambient fine particulate matter (PM2.5) has been linked with premature mortality, but sources of PM2.5 have been less studied.Methods: We evaluated associations between source-specific PM2.5 exposures and cause-specific short-term mortality in eight California locations from 2002 to 2011. Speciated PM2.5 measurements were source-apportioned using Positive Matrix Factorization into eight sources and combined with death certificate data. We used time-stratified case-crossover analysis with conditional logistic regression by location and meta-analysis to calculate pooled estimates.Results: Biomass burning was associated with all-cause mortality lagged 2 days after exposure (lag2) (% changelag2 in odds per interquartile range width increase in biomass burning PM2.5 = 0.8, 95% confidence interval [CI] = 0.2, 1.4), cardiovascular (% changelag2 = 1.3, 95% CI = 0.3, 2.4), and ischemic heart disease (% changelag2 = 2.0, 95% CI = 0.6, 3.5). Vehicular emissions were associated with increases in cardiovascular mortality (% changelag0 = 1.4, 95% CI = 0.0, 2.9). Several other sources exhibited positive associations as well. Many findings persisted during the cool season. Warm season biomass burning was associated with respiratory/thoracic cancer mortality (% changelag1 = 5.9, 95% CI = 0.7, 11.3), and warm season traffic was associated with all-cause (% changelag0 = 1.9, 95% CI = 0.1, 3.6) and cardiovascular (% changelag0 = 2.9, 95% CI = 0.1, 5.7) mortality.Conclusions: Our results suggest that acute exposures to biomass burning and vehicular emissions are linked with cardiovascular mortality, with additional sources (i.e., soil, secondary nitrate, secondary sulfate, aged sea salt, and chlorine sources) showing associations with other specific mortality types. [ABSTRACT FROM AUTHOR]

Background The link between PM 2.5 exposure and adverse health outcomes is well documented from studies across the world. However, the reported effect estimates vary across studies, locations and constituents. We aimed to conduct a meta-analysis on associations between short-term exposure to PM 2.5 constituents and mortality using city-specific estimates, and explore factors that may explain some of the observed heterogeneity. Methods We systematically reviewed epidemiological studies on particle constituents and mortality using PubMed and Web of Science databases up to July 2015.We included studies that examined the association between short-term exposure to PM 2.5 constituents and all-cause, cardiovascular, and respiratory mortality, in the general adult population. Each study was summarized based on pre-specified study key parameters (e.g., location, time period, population, diagnostic classification standard), and we evaluated the risk of bias using the Office of Health Assessment and Translation (OHAT) Method for each included study. We extracted city-specific mortality risk estimates for each constituent and cause of mortality. For multi-city studies, we requested the city-specific risk estimates from the authors unless reported in the article. We performed random effects meta-analyses using city-specific estimates, and examined whether the effects vary across regions and city characteristics (PM 2.5 concentration levels, air temperature, elevation, vegetation, size of elderly population, population density, and baseline mortality). Results We found a 0.89% (95% CI: 0.68, 1.10%) increase in all-cause, a 0.80% (95% CI: 0.41, 1.20%) increase in cardiovascular, and a 1.10% (95% CI: 0.59, 1.62%) increase in respiratory mortality per 10 μg/m 3 increase in PM 2.5 . Accounting for the downward bias induced by studies of single days, the all-cause mortality estimate increased to 1.01% (95% CI: 0.81, 1.20%). We found significant associations between mortality and several PM 2.5 constituents. The most consistent and stronger associations were observed for elemental carbon (EC) and potassium (K). For most of the constituents, we observed high variability of effect estimates across cities. Conclusions Our meta-analysis suggests that (a) combustion elements such as EC and K have a stronger association with mortality, (b) single lag studies underestimate effects, and (c) estimates of PM 2.5 and constituents differ across regions. Accounting for PM mass in constituent's health models may lead to more stable and comparable effect estimates across different studies. Systematic review registration PROSPERO: CRD42017055765. [ABSTRACT FROM AUTHOR]