Most amyotrophic lateral sclerosis (ALS) cases are sporadic (∼90%) and environmental exposures are implicated in their etiology. Large industrial facilities are permitted the airborne release of certain chemicals with hazardous properties and report the amounts to the US Environmental Protection Agency (EPA) as part of its Toxics Release Inventory (TRI) monitoring program. The objective of this project was to identify industrial chemicals released into the air that may be associated with ALS etiology. We geospatially estimated residential exposure to contaminants using a de-identified medical claims database, the SYMPHONY Integrated Dataverse®, with ∼26,000 nationally distributed ALS patients, and non-ALS controls matched for age and gender. We mapped TRI data on industrial releases of 523 airborne contaminants to estimate local residential exposure and used a dynamic categorization algorithm to solve the problem of zero-inflation in the dataset. In an independent validation study, we used residential histories to estimate exposure in each year prior to diagnosis. Air releases with positive associations in both the SYMPHONY analysis and the spatio-temporal validation study included styrene (false discovery rate (FDR) 5.4e-5), chromium (FDR 2.4e-4), nickel (FDR 1.6e-3), and dichloromethane (FDR 4.8e-4). Using a large de-identified healthcare claims dataset, we identified geospatial environmental contaminants associated with ALS. The analytic pipeline used may be applied to other diseases and identify novel targets for exposure mitigation. Our results support the future evaluation of these environmental chemicals as potential etiologic contributors to sporadic ALS risk.

Manganese (Mn) is an essential trace element, but an excess or accumulation can be toxic. Until now, few studies have examined the effects of maternal Mn level on the risk of spontaneous preterm birth (SPB). The aims of this study were to examine the association between maternal Mn level and the risk of SPB at the early stage of pregnancy, and investigate whether this association was modified by single nucleotide polymorphisms (SNPs) in genes of superoxide dismutase (SOD) and catalase (CAT). We conducted a nested case-control study in three maternal and child health care hospitals in Shanxi province, China, from December 2009 to December 2013. From an overall cohort of 4229 women, 528 were included in our study, including 147 cases of SPB and 381 controls. Maternal blood samples were collected during 4–22 gestational weeks. The maternal serum concentrations of Mn was measured using inductively coupled plasma–mass spectrometry. We found the maternal Mn concentration in the case group (median: 1.55 ng/mL) was significantly higher than that in the control group (median: 1.27 ng/mL). Compared to the lowest level, the SPB risk was significantly increased to 1.44 (95%CI: 0.60–3.43), 2.42 (95%CI: 1.06–5.55) and 2.46 (95%CI: 1.08–5.62) respectively for the second, third and fourth quartiles in first trimester, but not significant in second trimester or overall. When exposure to a high Mn level, women who with AA (6.36, 95%CI: 1.57–25.71) and AG (3.04, 95%CI: 1.59–5.80) of rs2758352, with CC (2.34, 95%CI: 1.31–4.18) of rs699473, and with GG (2.26, 95%CI: 1.22–4.16) of rs769214 were more likely to develop a SPB, but not among women with other genotypes. In conclusion, high maternal serum Mn level is associated with the increased SPB risk in first trimester, and the association is modified by maternal SNPs of SOD2, SOD3 and CAT.

The comprehensive sources of particulate matter (PM) require air purification materials to possess both high filtration efficiencies and low air resistances in an effort to provide healthcare. However, the assembly of multiple-layered filters with different functions leads to high pressure drop and high operating cost. Therefore, a multifunctional air filter that can provide excellent air filtration capacity and healthcare is highly desired. Here, a novel bifunctional polyacrylonitrile/attapulgite hierarchical-structured filter with low air resistance and high adsorption capacity was designed and fabricated by embedding attapulgite nanorods during a facile electrospinning process. The hierarchical polyacrylonitrile/attapulgite membranes showed only a ∼64 Pa resistance for 0.1 μm PM. Another benefit of using the attapulgite nanorods is an adsorption effect for hazardous heavy metal ions that accompany airborne ultrafine PMs. Thereby this hierarchical membrane simultaneously exhibits an enhanced filtration performance and hazardous protection ability. Furthermore, due to the electret effect of the attapulgite nanorods, the surface potential of the membrane remains at above 2.2 kV after 600 min of continuous use, which could improve the air filtration efficiency and ensure the long-term service life of the filters. This work may provide a new approach for the design and development of multifunctional air filters for simultaneously capturing ultrafine PMs and any other accompanying hazardous chemicals.

Benzene is widely employed in the field of production, and its toxicity on biological systems has received increasing attention. Cell proliferation is a major life characteristic of living organisms. KLF15 and NOTCH1 are mature and classical genes in cell proliferation studies, particularly in the area of tumor investigation. The aim of this study was to investigate the effect and mechanism of VNN3 on cell proliferation induced by 1,4-benzoquinone (1,4-BQ), an important metabolite of benzene, and obtain a sensitive biomarker for the hazard screening and health care of benzene exposure. Normally growing AHH-1 cells were cultured in vitro and were incubated with different concentrations of 1,4-BQ (0, 10, 20, and 40 μM) for 24 h. A CCK-8 assay was used to assess the cell viability, whereas EdU was used to detect the cell proliferation of AHH-1 cells. The expression of VNN3, KLF15 and NOTCH1 was detected by real-time PCR. Moreover, a lentiviral model was constructed in AHH-1 cells to interfere with VNN3 expression. The results showed that 1,4-BQ clearly increased the expression of VNN3. Moreover, 1,4-BQ dose-dependently inhibited cell proliferation and caused increased KLF15 expression; in contrast, the NOTCH1 expression decreased in AHH-1 cells. Furthermore, following interference with the VNN3 expression, the cell proliferation inhibition and the expression of KLF15 and NOTCH1 were rescued. To further investigate the action of VNN3 in benzene hematotoxicity, we assessed it in benzene-exposed workers. The results showed that there was a remarkable correlation between the VNN3 expression and hemogram, which included RBC, NEUT and HGB. In addition, analysis of the KLF15 and NOTCH1 expression showed that the VNN3 expression was related to cell proliferation, which was consistent with the in vitro results. In conclusion, VNN3 influences cell proliferation induced by 1,4-BQ by regulating the expression of KLF15 and NOTCH1. VNN3 may represent a potential biomarker of benzene toxicity.

Data on fine particulate matter (PM2.5) in China were first announced in 2013. The primary objective of this study was to evaluate the acute effects of PM2.5 on asthma morbidity in Beijing, China. A total of 978,658 asthma hospital visits consisting of 928,607 outpatient visits, 40,063 emergency room visits and 9988 hospital admissions from January 1, 2010, to June 30, 2012, were identified from the Beijing Medical Claim Data for Employees. A generalized additive Poisson model was applied to explore the association between PM2.5 and health service use. The mean daily PM2.5 concentration was 99.5 μg/m3 with a range from 7.2 μg/m3 to 492.8 μg/m3. Ambient PM2.5 concentration was significantly associated with increased use of asthma-related health services. Every 10 μg/m3 increase in PM2.5 concentration on the same day was significantly associated with a 0.67% (95% CI, 0.53%–0.81%), 0.65% (95% CI, 0.51%–0.80%), and 0.49% (95% CI, 0.35%–0.64%) increase in total hospital visits, outpatient visits and emergency room visits, respectively. The exposure–response association between PM2.5 concentration and hospital visits for asthma exacerbations was approximately linear. In conclusion, this study found that short-term elevations in PM2.5 concentration may increase the risk of asthma exacerbations. Our findings contribute to the limited scientific literature concerning the acute effects of PM2.5 on asthma morbidity outcomes in developing countries.

Landfills, as well as other waste management facilities are well-known bioaerosols sources. These places may foment antibiotic-resistance in bacterial bioaerosol (A.R.B.) due to inadequate pharmaceutical waste disposal. This issue may foster the necessity of using last-generation antibiotics with extra costs in the health care system, and deaths. The aim of this study was to reveal the multi-antibiotic resistant bacterial bioaerosol emitted by a sanitary landfill and the surrounding area. We evaluated the influence of environmental conditions in the occurrence of A.R.B. and biological risk assessment. Antibiotic resistance found in the bacteria aerosols was compared with the AWaRE consumption classification. We used the BIOGAVAL method to assess the workers' occupational exposure to antibiotic-resistant bacterial bioaerosols in the landfill. This study confirmed the multi-antibiotic resistant in bacterial bioaerosol in a landfill and in the surrounding area. Obtained mean concentrations of bacterial bioaerosols, as well as antibiotic-resistant in bacterial bioaerosol (A.R.B.), were high, especially for fine particles that may be a threat for human health. Results suggest the possible risk of antibiotic-resistance interchange between pathogenic and non-pathogenic species in the landfill facilities, thus promoting antibiotic multi-resistance genes spreading into the environment.

Stroke and fine particulate matter (PM₂.₅) are two important public health concerns worldwide. Although numerous studies have reported the associations between PM₂.₅ and stroke, scientific evidence in China is incomplete, particularly the effect of PM₂.₅ on the acute incidence and national acute health burdens of stroke attributed to PM₂.₅ pollution. This study identified about 131,947 registered patients and 23,018 deaths due to stroke in 10 counties located in various regions from 2013 to 2017. Using a time-stratified case-crossover design, this study evaluated the associations between short-term exposure to PM₂.₅ and the risks of acute incidence and mortality for different types of stroke on the same spatiotemporal scale. With a 10 μg/m³ increase in the PM₂.₅ concentration, the acute incidence risk increased by 0.37% (0.15%, 0.60%) for stroke, 0.46% (0.21%, 0.72%) for ischemic stroke, and −0.13% (−0.73%, 0.48%) for hemorrhagic stroke. The corresponding values for the mortality risk were 0.71% (0.08%, 1.33%), 1.09% (0.05%, 2.14%), and 0.43% (−0.44%, 1.31%) for stroke, ischemic stroke and hemorrhagic stroke, respectively. Compared with the other groups, females and patients aged over 64 years presented higher incidence and mortality risks, while the group aged >75 years may exhibit a greater risk of mortality. Based on the estimated effects, we evaluated 43,300 excess deaths and 48,800 acute incidences attributed to short-term PM₂.₅ exposure across China in 2015. This study provided robust estimates of PM₂.₅-induced stroke incidence and mortality risks, and susceptible populations were identified. Excess mortality and morbidity attributed to short-term PM₂.₅ exposure indicate the necessity to implement health care and prevention strategies, as well as medical resource allocation for noncommunicable diseases in regions with high levels of air pollution.

Triclocarban (TCC), a broad-spectrum lipophilic antibacterial agent, is the main ingredient of personal and health care products. Nonetheless, its ubiquitous presence in the environment has been established to negatively affect the reproduction in humans and animals. In this work, we studied the possible toxic effects of TCC on mouse oocytes maturation in vitro. Our findings revealed that TCC-treated immature mouse oocytes had a significantly reduced rate of polar body extrusion (PBE) compared to that of control. Further study demonstrated that the cell cycle progression and cytoskeletal dynamics were disrupted after TCC exposure, which resulted in the continuous activation of spindle assembly checkpoint (SAC). Moreover, TCC-treated oocytes had mitochondrial damage, reduced ATP content, and decreased mitochondrial membrane potential (MMP). Furthermore, TCC exposure induced oxidative stress and subsequently triggered early apoptosis in mouse oocytes. Besides, the levels of histone methylation were also affected, as indicated by increased H3K27me2 and H3K27me3 levels. In summary, our results revealed that TCC exposure disrupted mouse oocytes maturation through affecting cell cycle progression, cytoskeletal dynamics, oxidative stress, early apoptosis, mitochondria function, and histone modifications in vitro.

Evidence of health effects following early life exposure to short-to-medium duration of high pollution levels is extremely limited.We aimed to evaluate the associations between: 1. intrauterine exposure to fine particulate matter (PM2.5) from coal mine fire emissions and the frequencies of general practitioner attendances and dispensations of prescribed asthma inhalers, steroid skin creams, and antibiotics during the first year of life; 2. infant exposure and those outcomes during the year following the fire.All participants were recruited from the Latrobe Valley of Victoria, Australia. Participants’ 24-h average and hourly peak mine fire-specific PM2.5 exposures from 09/02/2014 to 31/03/2014 were estimated using chemical transport modelling. Outcome data were obtained from the Australian Medicare Benefits Schedule and Pharmaceutical Benefits Scheme from each child’s birth to 31/12/2016. We used negative binomial and logistic regression models to independently assess risks of the outcomes associated with every 10 and 100 μg m−3 increase in average or peak PM2.5 exposure, respectively, while adjusting for potential confounders.We included 286 of 311 children whose parents consented to be linked, comprising 77 with no exposure, 88 with intrauterine exposure and 121 with exposure in infancy. 10- and 100- μg m−3 increases in average and peak PM2.5 exposure during infancy were associated with greater incidence of antibiotics being dispensed during the year following the fire: the adjusted incidence rate ratios were 1.24 (95% CI 1.02, 1.50, p = 0.036) and 1.14 (1.00, 1.31, p = 0.048) respectively. No other significant associations were observed.Exposure to coal mine fire emissions during infancy was associated with increased dispensing of antibiotics. This could reflect increased childhood infections or increased prescriptions of antibiotics in the year following the fire.