Little is known about the impacts of specific chemical components on cardiovascular hospitalizations. We examined the relationships of PM2.5 chemical composition and daily hospitalizations for cardiovascular disease in 184 Chinese cities. Acute PM2.5 chemical composition exposures were linked to higher cardiovascular disease hospitalizations on the same day and the percentage change of cardiovascular admission was the highest at 1.76% (95% CI, 1.36-2.16%) per interquartile range increase in BC, followed by 1.07% (0.72-1.43%) for SO42-, 1.04% (0.63-1.46%) for NH4+, 0.99% (0.55-1.43%) for NO3-, 0.83% (0.50-1.17%) for OM, and 0.80% (0.34%-1.26%) for Cl-. Similar findings were observed for all cause-specific major cardiovascular diseases, except for heart rhythm disturbances. Short-term exposures to PM2.5 chemical composition were related to higher admissions and showed diverse impacts on major cardiovascular diseases.

Short-term exposure to ozone has been linked to multiple allergic diseases, but the relationship between ozone exposure and allergic conjunctivitis (AC) remains unclear. This study aimed to investigate the association between short-term exposure to ozone and the risk of AC. We conducted a time-stratified case-crossover study across five Chinese cities from 2014 to 2022. Daily outpatient visit records for AC were identified in five hospitals using either the diagnosis name or ICD-10 code H10.1. Data on air pollution and meteorological conditions were also collected. We first examined the city-specific association between short-term ozone exposure and AC using conditional logistic regression. A random-effects meta-analysis was then conducted to obtain overall estimates. During the study period, 130,093 outpatient visits for AC occurred, with 58.8% (76,482) being male and 41.2% (53,611) female. A one-standard-deviation (SD) increase in ozone was associated with an 8.3% increase (95% CI: 3.8%, 13.0%) in AC outpatient visits. Similar positive associations were observed when adjusting for other pollutants (PM2.5, CO, SO2 and NO2) in two-pollutant and multi-pollutant models. Furthermore, the positive association remained consistent when using mixed-effects regression models or further adjusting for meteorological conditions. In addition, no effect modification of the AC-ozone association by sex, age and season was apparent. This study provides evidence supporting a positive association between short-term ozone exposure and AC risk in China. This highlights the potential value of mitigating ozone pollution to reduce the risk of ocular surface disorders.

Exposure to air pollutants has been associated with DNA damage and increases the risks of respiratory diseases, such as asthma and COPD; however short- and long-term effects of air pollutants on telomere dysfunction remain unclear. We investigated the impact of short- and long-term exposure to fine particulate matter with an aerodynamic diameter below 2.5 μm (PM2.5) on telomere length in human bronchial epithelial BEAS-2B cells, and assessed the potential correlation between PM2.5 exposure and telomere length in the LIGHTS childhood cohort study. We observed that long-term, but not short-term, PM2.5 exposure was significantly associated with telomere shortening, along with the downregulation of human telomerase reverse transcriptase (hTERT) mRNA and protein levels. Moreover, long-term exposure to PM2.5 induced proinflammatory cytokine secretion, notably interleukin 6 (IL-6) and IL-8, triggered subG1 cell cycle arrest, and ultimately caused cell death. Long-term exposure to PM2.5 upregulated the LC3-II/ LC3-I ratio but led to p62 protein accumulation in BEAS-2B cells, suggesting a blockade of autophagic flux. Moreover, consistent with our in vitro findings, our epidemiological study found significant association between annual average exposure to higher PM2.5 and shortening of leukocyte telomere length in children. However, no significant association between 7-day short-term exposure to PM2.5 and leukocyte telomere length was observed in children. By combining in vitro experimental and epidemiological studies, our findings provide supportive evidence linking potential regulatory mechanisms to population level with respect to long-term PM2.5 exposure to telomere shortening in humans.

UNASSIGNED: Ozone pollution is associated with cardiovascular disease mortality, and there is a high correlation between different pollutants. This study aimed to assess the association between ozone and cardiovascular disease deaths and the resulting disease burden in Nanjing, China.
UNASSIGNED: A total of 151,609 deaths from cardiovascular disease were included in Nanjing, China from 2013 to 2021. Daily data on meteorological and air pollution were collected to apply a generalized additional model with multiple pollutants to perform exposure-response analyses, stratification analysis, and evaluation of excess deaths using various standards.
UNASSIGNED: In the multi-pollutant model, an increase of 10 μg/m3 in O3 was significantly associated with a 0.81% (95%CI: 0.49, 1.12%) increase in cardiovascular disease deaths in lag05. The correlation weakened in both the single-pollutant model and two-pollutant models, but remained more pronounced in females, the older group, and during warm seasons. From 2013 to 2021, the number of excess deaths attributed to ozone exposure in cardiovascular disease continued to rise with an increase in ozone concentration in Nanjing. If the ozone concentration were to be reduced to the WHO standard and the minimum level, the number of deaths would decrease by 1,736 and 10,882, respectively.
UNASSIGNED: The risk of death and excess deaths from cardiovascular disease due to ozone exposure increases with higher ozone concentration. Reducing ozone concentration to meet WHO standards or lower can provide greater cardiovascular disease health benefits.

Paralytic shellfish toxins (PSTs) can pose a serious threat to human health. Among them, saxitoxin (STX) is one of the most potent natural neurotoxins. Here, the copepod Tigriopus japonicus, was exposed to environmentally relevant concentrations (2.5 and 25 μg/L) STX for 48 h. Although no lethal effects were observed at both concentrations, the transcriptome was significantly altered, and displayed a concentration-dependent response. STX exposure decreased the copepod\'s metabolism and compromised immune defense and detoxification. Additionally, STX disturbed signal transduction, which might affect other cellular processes. STX exposure could inhibit the copepod\'s chitin metabolism, disrupting its molting process. Also, the processes related to damage repair and protection were up-regulated to fight against high concentration exposure. Collectively, this study has provided an early warning of PSTs for coastal ecosystem not only because of their potent toxicity effect but also their bioaccumulation that can transfer up the food chain after ingestion by copepods.

Racial/ethnic disparities in the association between short-term (e.g. days, weeks) ambient fine particulate matter (PM2.5) and temperature exposures and stillbirth in the US have been understudied. A time-stratified, case-crossover design using a distributed lag non-linear model (0 to 6-day lag) estimated stillbirth odds due to short-term increases in average daily PM2.5 and temperature exposures among 118,632 Medicaid recipients from 2000-2014. Disparities by maternal race/ethnicity (Black, White, Hispanic, Asian, American Indian) and zip-code level socioeconomic status (SES) were assessed. In the temperature-adjusted model, a 10 μg/m3 increase in PM2.5 concentration was marginally associated with increased stillbirth odds at lag 1 (0.68% 95%CI:[-0.04,1.40]) and lag 2 (0.52% 95%CI:[-0.03,1.06]), but not lag 0-6 (2.80% 95%CI:[-0.81,6.45]). An association between daily PM2.5 concentrations and stillbirth odds was found among Black individuals at the cumulative lag (0-6 days: 9.26% 95%CI:[3.12,15.77]), but not among other races/ethnicities. A stronger association between PM2.5 concentrations and stillbirth odds existed among Black individuals living in zip codes with the lowest median household income (lag0-6:14.13% 95%CI:[4.64,25.79]). Short-term temperature increases were not associated with stillbirth risk among any race/ethnicity. Black Medicaid enrollees, and especially those living in lower SES areas, may be more vulnerable to stillbirth due to short-term increases in PM2.5 exposure.

BACKGROUND: Environmental factors like air pollution and temperature can trigger acute myocardial infarction (AMI). However, the link between large-scale weather patterns (synoptic types) and AMI admissions has not been extensively studied. This research aimed to identify the different synoptic air types in Beijing and investigate their association with AMI occurrences.
METHODS: We analyzed data from Beijing between 2013 and 2019, encompassing 2556 days and 149,632 AMI cases. Using principal component analysis and hierarchical clustering, classification into distinct synoptic types was conducted based on weather and pollution measurements. To assess the impact of each type on AMI risk over 14 days, we employed a distributed lag non-linear model (DLNM), with the reference being the lowest risk type (Type 2).
RESULTS: Four synoptic types were identified: Type 1 with warm, humid weather; Type 2 with warm temperatures, low humidity, and long sunshine duration; Type 3 with cold weather and heavy air pollution; and Type 4 with cold temperatures, dryness, and high wind speed. Type 4 exhibited the greatest cumulative relative risk (CRR) of 1.241 (95%CI: 1.150, 1.339) over 14 days. Significant effects of Types 1, 3, and 4 on AMI events were observed at varying lags: 4-12 days for Type 1, 1-6 days for Type 3, and 1-11 days for Type 4. Females were more susceptible to Types 1 and 3, while individuals younger than 65 years old showed increased vulnerability to Types 3 and 4.
CONCLUSIONS: Among the four synoptic types identified in Beijing from 2013 to 2019, Type 4 (cold, dry, and windy) presented the highest risk for AMI hospitalizations. This risk was particularly pronounced for males and people under 65. Our findings collectively highlight the need for improved methods to identify synoptic types. Additionally, developing a warning system based on these synoptic conditions could be crucial for prevention.

BACKGROUND: Model-estimated air pollution exposure products have been widely used in epidemiological studies to assess the health risks of particulate matter with diameters of ≤2.5 µm (PM2.5). However, few studies have assessed the disparities in health effects between model-estimated and station-observed PM2.5 exposures.
METHODS: We collected daily all-cause, respiratory and cardiovascular mortality data in 347 cities across 15 countries and regions worldwide based on the Multi-City Multi-Country collaborative research network. The station-observed PM2.5 data were obtained from official monitoring stations. The model-estimated global PM2.5 product was developed using a machine-learning approach. The associations between daily exposure to PM2.5 and mortality were evaluated using a two-stage analytical approach.
RESULTS: We included 15.8 million all-cause, 1.5 million respiratory and 4.5 million cardiovascular deaths from 2000 to 2018. Short-term exposure to PM2.5 was associated with a relative risk increase (RRI) of mortality from both station-observed and model-estimated exposures. Every 10-μg/m3 increase in the 2-day moving average PM2.5 was associated with overall RRIs of 0.67% (95% CI: 0.49 to 0.85), 0.68% (95% CI: -0.03 to 1.39) and 0.45% (95% CI: 0.08 to 0.82) for all-cause, respiratory, and cardiovascular mortality based on station-observed PM2.5 and RRIs of 0.87% (95% CI: 0.68 to 1.06), 0.81% (95% CI: 0.08 to 1.55) and 0.71% (95% CI: 0.32 to 1.09) based on model-estimated exposure, respectively.
CONCLUSIONS: Mortality risks associated with daily PM2.5 exposure were consistent for both station-observed and model-estimated exposures, suggesting the reliability and potential applicability of the global PM2.5 product in epidemiological studies.

BACKGROUND: PM2.5 and its chemical components increase health risks and are associated with depression and gut microbiota. However, there is still limited evidence on whether gut microbiota and short-chain fatty acids (SCFAs) mediate the association between PM2.5, PM2.5 chemical components, and antenatal depression. The purpose of this study was to investigate the mediating role of maternal gut microbiota in correlations between short-term exposure to PM2.5, short-term exposure to PM2.5 chemical components, and antenatal depression.
METHODS: Demographic information and stool samples were collected from 75 pregnant women in their third trimester. Their exposure to PM2.5 and PM2.5 chemical components was measured. Participants were divided into the non-antenatal depression group or the antenatal depression group according to the cut-off of 10 points on the Edinburgh Postnatal Depression Scale (EPDS). The gut microbiota were analyzed using the 16 S rRNA-V3/V4 gene sequence, and the concentration of PM2.5 and its chemical components was calculated using the Tracking Air Pollution in China (TAP) database. Gas chromatography-mass spectrometry was used to analyze SCFAs in stool samples. In order to assess the mediating effects of gut microbiota and SCFAs, mediation models were utilized.
RESULTS: There were significant differences between gut microbial composition and SCFAs concentrations between the non-antenatal depression group and the antenatal depression group. PM2.5 and its chemical components were positively associated with EPDS scores and negatively associated with genera Enterococcus and Enterobacter. Genera Candidatus_Soleaferrea (β = -7.21, 95%CI -11.00 to -3.43, q = 0.01) and Enterococcus (β = -2.37, 95%CI -3.87 to -0.87, q = 0.02) were negatively associated with EPDS scores, indicating their potential protective effects against antenatal depression. There was no significant association between SCFAs and EPDS scores. The mediating role of Enterococcus between different lagged periods of PM2.5, PM2.5 chemical component exposure, and antenatal depression was revealed. For instance, Enterococcus explained 29.23% (95%CI 2.16-87.13%, p = 0.04) of associations between PM2.5 exposure level at the day of sampling (lag 0) and EPDS scores.
CONCLUSIONS: Our study highlights that Enterococcus may mediate the associations between PM2.5, PM2.5 chemical components, and antenatal depression. The mediating mechanism through which the gut microbiota influences PM2.5-induced depression in pregnant women still needs to be further studied.

UNASSIGNED: Prolonged exposure to sunlight is known to induce photoaging of the skin, leading to various skin changes and disorders, such as dryness, wrinkles, irregular pigmentation, and even cancer. Ultraviolet A (UVA) and ultraviolet B (UVB) radiation are particularly responsible for causing photoaging.
UNASSIGNED: This study aims to identify and compare photoaging rat models exposed to UVA and UVB.
UNASSIGNED: This research method compared macroscopic (scoring degree of wrinkling) and microscopic (histology) signs and symptoms on skin samples of rat exposed to UVA and UVB for 4 weeks at a radiation dose of 840mJ/cm2.
UNASSIGNED: The results of this study indicated that the degree of wrinkling was highest in rat skin exposed to UVB rays by 51% (p<0.05). UVB histological results showed that the epidermis layer (40 µm, p<0.05) was thickened and the dermis layer (283 µm, p<0.05) was thinned in the skin of mice exposed to UVB light. The UVB group, showed the density of collagen in the dermis with a mean value of 55% (p<0.05).
UNASSIGNED: Our results suggest that short-term exposure to UVB radiation (in the acute, subacute or subchronic phase) induces more rapid and pronounced damage to rat skin when compared to UVA radiation exposure.