Research progress on effects and mechanisms of short-term exposure to ambient fine particulate matter and its components on blood pressure / 环境与职业医学

Elevated blood pressure is one of the major contributors to cardiovascular disease and premature death. The exposure to ambient fine particulate matter (PM2.5) is closely associated with changes in blood pressure, and even short-term exposure to PM2.5 can lead to an increase in blood pressure. PM2.5 is a complex mixture that exerts different toxicities and triggers increased blood pressure through various mechanisms. Therefore, in this article, we provided a comprehensive review of published studies on the effects of short-term exposure to PM2.5 and its components on blood pressure, and elaborated potential mechanisms from four aspects, including oxidative stress and inflammatory response, endothelial dysfunction, autonomic nervous system disorders and hypothalamus-pituitary-adrenal axis activation, and epigenome alteration. Given the limitations of existing research, future prospective studies can be conducted on diverse populations, using more precise exposure measurement methods and multi-omics approaches, to further elucidate the mechanisms underlying the effects of PM2.5 and its various components on blood pressure. The findings would provide a theoretical foundation for effective protection of public health, particularly vulnerable groups.

Meta-analysis on correlations between short-term exposures to 6 common air pollutants and incidence of ischemic stroke / 环境与职业医学

Background Previous studies using meta-analysis to explore the relationship between air pollution exposure and ischemic stroke (IS) mostly focus on particulate matter-related themes, few include gaseous pollutants in the study, and subgroup analyses of factors such as different lag days, seasons, and genders are rarely been reported. Objective To quantitatively evaluate the relationships between short-term exposures to 6 common air pollutants, including fine particulate matter (PM2.5), inhalable particulate matter (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3), and the incidence of IS. Methods A systematic search was conducted to collect literature studying the 6 common air pollutants and IS published up to May 1, 2022 in 6 databases (China Journal Full-text Database, China Biology Medicine Disc, PubMed, Cochrane Library, Web of Science, and Embase). Literature quality evaluation was performed using the Newcastle-Ottawa Scale. Stata 16.0 software was used to conduct meta-analysis including heterogeneity test, combined effect size, meta-regression, subgroup analysis, sensitivity analysis, and publication bias test. Results A total of 33 articles were qualified for inclusion. The total number of samples included in the literature was 7195631. The meta-analysis results showed that short-term exposures to PM2.5 (OR=1.0082, 95%CI: 1.0049−1.0116), PM10 (OR=1.0017, 95%CI: 1.0008−1.0026), CO (OR=1.0328, 95%CI: 1.0231−1.0426), NO2 (OR=1.0150, 95%CI: 1.0079−1.0222), SO2 (OR=1.0158, 95%CI: 1.0078-1.0238), and O3 (OR=1.0017, 95%CI: 1.0003−1.0032) were associated with an increased risk of IS. PM10 and O3 increased the risk of IS in both lag0 and lag1, while PM2.5, CO, NO2, and SO2 all showed an associated increased risk of IS only in lag0. The results of sensitivity analysis showed stable results for all pollutants studied, and there was no publication bias in the literature on the association of the remaining five pollutants with IS incidence except for the PM2.5-related literature. Conclusion Short-term exposures to PM2.5, PM10, CO, NO2, SO2, and O3 may increase the incidence of IS, with this risk showing the most significant level on the day of IS onset.

Cardiovascular and Cerebrovascular Diseases Induced by Air Pollution / 中国医学科学院学报

Air pollution has severe detrimental effects on public health.A substantial number of studies have demonstrated that air pollution exposure is a risk factor for the occurrence of cardiovascular and cerebrovascular diseases and a cause of non-communicable diseases.Both long-term and short-term exposure to air pollution are associated with respiratory diseases,stroke,coronary artery disease,and diabetes.Aiming to better understand the association,we reviewed the latest studies about the association of air pollution with cardiovascular and cerebrovascular diseases,especially stroke,coronary heart disease,arrhythmia,hypertension,and heart failure,and summarized the underlying mechanisms of the health damage caused by long-term and short-term exposure to air pollution.

Meta-analysis of relationship between short-term ozone exposure and population mortality in China / 环境与职业医学

Background In recent years, our country's atmospheric particulate matter pollution has improved significantly, while ozone (O3) pollution has become increasingly serious. As a secondary pollutant, O3 is closely related to human health. Objective To study the effect of short-term exposure to ozone in ambient air on population mortality in China. Methods A computer search with key words of "ozone or O3", "death", and "time series" in Chinese or "ozone", "mortality", and "China" in English was performed in Web of Science, PubMed, China National Knowledge Infrastructure, Wanfang, and VIP databases to find literature on effects of short-term ozone exposure on population mortality covering a time period from January 1, 1990 to December 31, 2021. According to a set of inclusion and exclusion criteria developed for this study, literaturescreening, quality evaluation, andrelevant data extraction were carried out. Finally, R 4.1.2 software was used to perform meta-analysis to estimate target effect sizes. Results A total of 978 articles were retrieved. According to the inclusion and exclusion criteria, 18 articles were finally included, including 39 effect size estimates. The results showed that every 10 μɡ·m−3 increase in ambient ozone concentration was associated with an increase of 0.45% (95%CI: 0.39%-0.51%), 0.50% (95%CI: 0.33%-0.68%), and 0.60% (95%CI: 0.48%-0.72%) in total, respiratory, and cardiovascular disease mortalities , respectively. The results of subgroup analysis by age, sex, and season showed that when ozone concentration increased 10 μɡ·m−3, an increase of 0.34% (95%CI: 0.17%-0.51%) in mortality was observed in the ≥ 65-year-old population, higher than 0.09% (95%CI: −0.21%-0.39%) increase in the <65-year-old population; the mortality increase in females [0.44% (95%CI: 0.30%-0.58%)] was greater than that in males [0.35% (95%CI: 0.22%-0.48%)]; compared with the warm season [0.29% (95%CI: 0.16%-0.42%)], mortality increase was higher in the cold season [1.03% (95%CI: 0.71%-1.35%)]. Conclusion Ambient ozone is an important factor affecting population mortality. The elderly and women ≥ 65 years old in China are more sensitive to ozone, and the impact of ozone exposure on population mortality is greater in cold season.

Verification on the Developmental Toxicity of Short-term Exposure to Phenol in Rats / 生物医学与环境科学（英文）

Objective@#To verify the health advisory for short-term exposure to phenol.@*Methods@#The method of this validation experiment was the same as the US Environmental Protection Agency (EPA) methodology for toxicology experiments used to determine phenol drinking water equivalent level (DWEL). Pregnant female Sprague-Dawley rats were administered phenol in distilled water by gavage at daily doses of 15, 30, 60, 120, and 240 mg/kg body weight (b.w.) from implantation (the 6th day post-mating) to the day prior to the scheduled caesarean section (the 20th day of pregnancy). The following information was recorded: general behavior; body weight; number of corpus luteum, live birth, fetus, stillbirth, and implantation; fetal gender; body weight; body length; tail length; and abnormalities and pathomorphological changes in the dams.@*Results@#In the 60 mg/kg b.w. dose group, the mortality of pregnant rats increased with increasing doses, suggesting maternal toxicity. Fetal and placental weights decreased as phenol dose increased from 30 mg/kg b.w., and were significantly different compared those in the vehicle control group, which suggested developmental toxicity in the fetuses. However, the phenol-exposed groups showed no significant change in other parameters compared with the vehicle control group ( > 0.05).@*Conclusion@#Despite using the same method as the US EPA, a different NOEAL of 15 mg/(kg·d) was obtained in this study.

Occupational exposure limits of methyl t-butyl ether in workplace air / 中国职业医学

OBJECTIVE: To establish the occupational exposure limits for methyl t-butyl ether(MTBE) in the air of workplace in China. METHODS: According to the GBZ/T 210.1-2008 Guide for Establishing Occupational Health Standards--Part 1: Occupational Exposure Limits for Airborne Chemicals in the Workplace, we collected and analyzed data on physical and chemical properties, toxicology, occupational epidemiology and foreign occupational exposure limits related to MTBE by literature search. A total of 180 occupational workers exposed to MTBE were selected as exposure group, and 155 workers and administrative logistics personnel without exposure to MTBE were selected as the control group. Occupational hygiene investigation and occupational physical examination were carried out. We deduced the occupational exposure limits for MTBE in workplace air in China by combining literature data. RESULTS: The time-weighted average(TWA) of MTBE in the workplace air developed by the United States of America and Britain is 180.00 mg/m~3. The short-term exposure limit(STEL) of MTBE in the workplace air developed by Australia and New Zealand is 270.00 mg/m~3. The concentration of TWA(C_(TWA)) of MTBE in the exposure group was less than 0.08-4.90 mg/m~3. The concentration of short term exposure was less than 0.10-14.28 mg/m~3, and the C_(TWA) was less than 0.02-83.66 mg/m~3, in parts of workplaces. There was no statistically significant difference on the self-conscious discomfort and the abnormality in physical examination between these two groups(P>0.05). CONCLUSION: It's recommended that the permissible concentration-TWA of MTBE should be set at 180.00 mg/m~3, and the permissible concentration-STEL should be set at 270.00 mg/m~3 in China.

Effects of Beryllium on Human Serum Immunoglobulin and Lymphocyte Subpopulation

To investigate the effects of short-term exposure of beryllium on the human immune system, the proportion of T-lymphocytes such as CD3+, CD4+, CD8+, CD95, and NK cells, andthe proportion of B cells and TNFalpha level in peripheral blood and immunoglobulins in the serum of 43 exposed workers and 34 healthy control subjects were studied. External exposure to beryllium was measured by atomic absorption spectrometer as recommended by the NIOSH analytical method 7300. T lymphocyte subpopulation analysis was carried out with flow cytometer. The working duration of exposed workers was less than 3 months and the mean ambient beryllium level was 3.4 microg/m3, 112.3 microg/m3, and 2.3 microg/m3 in molding (furnace), deforming (grinding), and sorting processes, respectively (cited from Kim et al., 2008). However, ambient beryllium level after process change was non-detectable (< 0.1 microg/m3). The number of T lymphocytes and the amount of immunoglobulins in the beryllium-exposed workers and control subjects were not significantly different, except for the total number of lymphocytes and CD95 (APO1/FAS). The total number of lymphocytes was higher in the beryllium-exposed individuals than in the healthy control subjects. Multiple logistic regression analysis showed lymphocytes to be affected by beryllium exposure (odd ratio = 7.293; p < 0.001). These results show that short-term exposure to beryllium does not induce immune dysfunction but is probably associated with lymphocytes proliferation.