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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., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

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/m 3 , BC (1.26 (1.03-1.53) per 0.5 × 10 - 5 /m), NO 2 (1.13 (0.93-1.38) per 10 μg/m 3 ) and inverse for O 3 (0.71 (0.54-0.93) per 10 μg/m 3 ). 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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)