Long-term effect of exposure to ambient air pollution on the risk of active tuberculosis.

PMID: 

Int J Infect Dis. 2019 Oct ;87:177-184. Epub 2019 Jul 30. PMID: 31374344

Abstract Title: 

Long-term effect of exposure to ambient air pollution on the risk of active tuberculosis.

Abstract: 

OBJECTIVES: To explore the long-term effect of exposure to ambient air pollution on the risk of active tuberculosis (TB).METHODS: We constructed a distributed-lag nonlinear model (DLNM) to evaluate the relatively long-term influence of outdoor PM, PM, SOand NOexposure on active TB risk in the city of Lianyungang in Jiangsu Province, China.RESULTS: There were 7,282 TB cases reported in the study area during 2014-2017, with annual median (interquartile range) concentrations of PM, PM, SOand NOat 45.86 (34.57-64.14)μg/m, 85.43 (62.86-116.14)μg/m, 22.00 (15.71-30.86)μg/mand 30.00 (23.29-38.57)μg/m, respectively. The single-pollutant model showed that for each 10 μg/mincrease in concentration, the cumulative relative risk of TB was 1.12 (lag 0-24 weeks, 95% CI: 1.03-1.22) for PMwith reference to 35 μg/m; 1.11 (lag 0-21 weeks, 95% CI: 1.06-1.17) for PMwith reference to 70 μg/m; 1.37 (lag 0-20 weeks, 95% CI: 1.16-1.62) for SOwith reference to 60 μg/m; and 1.29 (lag 0-22 weeks, 95% CI: 1.11-1.49) for NOwith reference to 40 μg/m. In the multipollutant model considering both PMand NO, the association remained significant.CONCLUSIONS: Our results revealed a potential association between outdoor exposure to PM, PM, SO, and NOand active TB. Considering that people from developing countries continue to be exposed to both severe outdoor air pollution and high rates of latent TB infection, the association between worsening air pollution and active TB deserves further attention.

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Short-term air pollution exposure is associated with hospital length of stay and hospitalization costs among inpatients with type 2 diabetes.

PMID: 

J Toxicol Environ Health A. 2018 ;81(17):819-829. Epub 2018 Jul 17. PMID: 30015599

Abstract Title: 

Short-term air pollution exposure is associated with hospital length of stay and hospitalization costs among inpatients with type 2 diabetes: a hospital-based study.

Abstract: 

Air pollution is a risk factor for type 2 diabetes (T2D), exerting heavy economic burden on both individuals and societies. However, there is no apparent report regarding the influence of air pollutants such as particulate matter (PMand PM), sulfur dioxide (SO), carbon monoxide (CO), nitrogen dioxide (NO), and ozone (O) on financial burden to individuals and societies suffering from T2D. This study aimed to determine whether short-term (no more than 16 d) air pollution exposure was associated with T2D-related length of stay (LOS) and hospitalization expenses incurred by patients. This investigation examined 2840 T2D patients hospitalized from December 17, 2013 to May 31, 2016 in China. Multiple linear regression analysis was applied to determinethe association between short-term (no more than 16 d) ambient air pollution, LOS, and hospitalization expenses, controlling for age, gender, ethnicity, marital status, and weather conditions. Sulfur dioxide (SO) and carbon monoxide (CO) were significantly positively while nitrogen dioxide (NO) was negatively associated with presence of T2D, LOS, and expenses. A 10-μg/mrise in 16-d (lag 0-15) average concentrations of SOand CO prior to hospitalization was correlated with a significant elevation in LOS and elevation in expenses in T2D patients. However, a 10-μg/mrise in 16-d average NOwas associated with marked negative alterations in LOS and hospital costs in T2D patients. Taken together, data demonstrate that exposure to air pollutants impacts differently on LOS and hospitalization costs for T2D patients. This is the first apparent report regarding the correlation between air pollution exposure and clinical costs of T2D in China. It is of interest that air pollutants affected T2D patients differently as evidenced by LOS and clinical expenses where SOand CO exhibited a positive adverse relationship in contrast to NO.

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Short-term effects of ambient air pollution on hospitalization for respiratory disease in Taiyuan, China.

PMID: 

Int J Environ Res Public Health. 2018 10 1 ;15(10). Epub 2018 Oct 1. PMID: 30275384

Abstract Title: 

Short-Term Effects of Ambient Air Pollution on Hospitalization for Respiratory Disease in Taiyuan, China: A Time-Series Analysis.

Abstract: 

In this study, we estimated the short-term effects of ambient air pollution on respiratory disease hospitalization in Taiyuan, China. Daily data of respiratory disease hospitalization, daily concentration of ambient air pollutants and meteorological factors from 1 October 2014 to 30 September 2017 in Taiyuan were included in our study. We conducted a time-series study design and applied a generalized additive model to evaluate the association between every 10-μg/m³ increment of air pollutants and percent increase of respiratory disease hospitalization. A total of 127,565 respiratory disease hospitalization cases were included in this study during the present period. In single-pollutant models, the effect values in multi-day lags were greater than thosein single-day lags. PMat lag02 days, SO₂ at lag03 days, PMand NO₂ at lag05 days were observed to be strongly and significantly associated with respiratory disease hospitalization. No significant association was found between O₃ and respiratory disease hospitalization. SO₂ and NO₂ were still significantly associated with hospitalization after adjusting for PMor PMinto two-pollutant models. Females and younger population for respiratory disease were more vulnerable to air pollution than males and older groups. Therefore, some effective measures should be taken to strengthen the management of the ambient air pollutants, especially SO₂ and NO₂, and to enhance the protection of the high-risk population from air pollutants, thereby reducing the burden of respiratory disease caused by ambient air pollution.

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Ambient air pollution exposures and risk of drug-resistant tuberculosis.

PMID: 

Environ Int. 2019 03 ;124:161-169. Epub 2019 Jan 12. PMID: 30641260

Abstract Title: 

Ambient air pollution exposures and risk of drug-resistant tuberculosis.

Abstract: 

BACKGROUND: Few epidemiological studies have explored the effects of air pollution on the risk of drug-resistant tuberculosis (DR-TB).OBJECTIVE: To investigate the short and long term residential concentrations of ambient air pollutants (particulate matter

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Acute effects of air pollution on influenza-like illness in Nanjing, China: A population-based study.

PMID: 

Chemosphere. 2016 Mar ;147:180-7. Epub 2016 Jan 7. PMID: 26766354

Abstract Title: 

Acute effects of air pollution on influenza-like illness in Nanjing, China: A population-based study.

Abstract: 

Influenza-like illness causes substantial morbidity and mortality. Air pollution has already been linked to many health issues, and increasing evidence in recent years supports an association between air pollution and respiratory infections. It is a pioneer study in China to quantify the effects of air pollution on influenza-like illness. This study used wavelet coherence analysis and generalized additive models to explore the potential association between air pollution (including particulate matter with aerodynamic diameter≦2.5 μm (PM2.5), particulate matter with aerodynamic diameter ≦10 μm (PM10) and nitrogen dioxide (NO2)) and influenza-like illness (a total of 59860 cases) in Nanjing, China from January 1, 2013 to December 31, 2013. The average concentrations of PM2.5, PM10 and NO2 were 77.37 μg/m(3), 135.20μg/m(3) and 55.80 μg/m(3). An interquartile range increase in PM2.5 concentration was associated with a 2.99% (95% confidence interval (CI): 1.64%, 4.36%) increase in daily influenza-like cases on the same day, while the corresponding increase in NO2 was associated with a 3.77% (95% CI: 2.01%, 5.56%) increase in daily cases. People aged 0-4 were proved to be significantly susceptible to PM10 and NO2; 5-14 ages were significantly susceptible to PM2.5 and PM10; and 15-24 ages were significantly susceptible to all the analyzed air pollutants. Air pollution effects tended to be null or negativefor patients aged over 25, which might be due to the small number of influenza-like cases in this age group. This study can be useful for understanding the adverse health effects of air pollution and the cause of influenza-like illness.

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The role of pro-/anti-inflammation imbalance in Aβ42 accumulation of rat brain co-exposed to fine particle matter and sulfur dioxide.

PMID: 

Toxicol Mech Methods. 2017 Oct ;27(8):568-574. Epub 2017 Jun 20. PMID: 28565962

Abstract Title: 

The role of pro-/anti-inflammation imbalance in Aβ42 accumulation of rat brain co-exposed to fine particle matter and sulfur dioxide.

Abstract: 

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SOand fine particulate matter (PM). Rats were exposed alternately to PMwith different dosages (1.5, 6.0 and 24.0 mg/kg body weight) and SOat the level of 5.6 mg/m. The results showed that the combined exposure to PMand SOenhanced the mRNA expression and protein level of TNF-α and IL-6 in rat cortex and hippocampus relative to the control, SOand PMalone. Instead, TGF-β1 mRNA and protein level were down-regulated in the brain. Additionally, PMat medium and/or high dose caused marked increase in Aβ42 level and PM + SOinduced further increase of Aβ42 level in the cortex and hippocampus. It suggests that SOand PMcan synergistically exert inflammation responses and induce Aβ42 accumulation in the brain. Also, it is notable that the Aβ42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PMand SOcan induce the imbalance of pro-/anti-inflammatory cytokine, resulting in Aβ42 accumulation of rat brain cortex and hippocampus.

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Early kidney damage induced by subchronic exposure to Particulate matter.

PMID: 

Part Fibre Toxicol. 2016 12 12 ;13(1):68. Epub 2016 Dec 12. PMID: 27955691

Abstract Title: 

Early kidney damage induced by subchronic exposure to PMin rats.

Abstract: 

BACKGROUND: Particulate matter exposure is associated with respiratory and cardiovascular system dysfunction. Recently, we demonstrated that fine particles, also named PM, modify the expression of some components of the angiotensin and bradykinin systems, which are involved in lung, cardiac and renal regulation. The endocrine kidney function is associated with the regulation of angiotensin and bradykinin, and it can suffer damage even as a consequence of minor alterations of these systems. We hypothesized that exposure to PMcan contribute to early kidney damage as a consequence of an angiotensin/bradykinin system imbalance, oxidative stress and/or inflammation.RESULTS: After acute and subchronic exposure to PM, lung damage was confirmed by increased bronchoalveolar lavage fluid (BALF) differential cell counts and a decrease of surfactant protein-A levels. We observed a statistically significant increment in median blood pressure, urine volume and water consumption after PMexposure. Moreover, increases in the levels of early kidney damage markers were observed after subchronic PMexposure: the most sensitive markers,β-2-microglobulin and cystatin-C, increased during the first, second, sixth and eighth weeks of exposure. In addition, a reduction in the levels of specific cytokines (IL-1β, IL-6, TNF-α, IL-4, IL-10, INF-γ, IL-17a, MIP-2 and RANTES), and up-regulated angiotensin and bradykinin system markers and indicators of a depleted antioxidant response, were also observed. All of these effects are in concurrence with the presence of renal histological lesions and an early pro-fibrotic state.CONCLUSION: Subchronic exposure to PMinduced an early kidney damage response that involved the angiotensin/bradykinin systems as well as antioxidant and immune imbalance. Our study demonstrates that PMcan induce a systemic imbalance that not only affects the cardiovascular system, but also affects the kidney, which may also overall contribute to PM-related diseases.

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In vitro short-term exposure to air pollution PM2.5-0.3 induced cell cycle alterations and genetic instability in a human lung cell coculture model.

PMID: 

Environ Res. 2016 May ;147:146-58. Epub 2016 Feb 11. PMID: 26874047

Abstract Title: 

In vitro short-term exposure to air pollution PM2.5-0.3 induced cell cycle alterations and genetic instability in a human lung cell coculture model.

Abstract: 

Although its adverse health effects of air pollution particulate matter (PM2.5) are well-documented and often related to oxidative stress and pro-inflammatory response, recent evidence support the role of the remodeling of the airway epithelium involving the regulation of cell death processes. Hence, the overarching goals of the present study were to use an in vitro coculture model, based on human AM and L132 cells to study the possible alteration of TP53-RB gene signaling pathways (i.e. cell cycle phases, gene expression of TP53, BCL2, BAX, P21, CCND1, and RB, and protein concentrations of their active forms), and genetic instability (i.e. LOH and/or MSI) in the PM2.5-0.3-exposed coculture model. PM2.5-0.3 exposure of human AM from the coculture model induced marked cell cycle alterations after 24h, as shown by increased numbers of L132 cells in subG1 and S+G2 cell cycle phases, indicating apoptosis and proliferation. Accordingly, activation of the TP53-RB gene signaling pathways after the coculture model exposure to PM2.5-0.3 was reported in the L132 cells. Exposure of human AM from the coculture model to PM2.5-0.3 resulted in MS alterations in 3p chromosome multiple critical regions in L132 cell population. Hence, in vitro short-term exposure of the coculture model to PM2.5-0.3 induced cell cycle alterations relying on the sequential occurrence of molecular abnormalities from TP53-RB gene signaling pathway activation and genetic instability.

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Ambient fine particulate matter inhibits innate airway antimicrobial activity in preschool children in e-waste areas.

PMID: 

Environ Int. 2019 02 ;123:535-542. Epub 2019 Jan 5. PMID: 30622078

Abstract Title: 

Ambient fine particulate matter inhibits innate airway antimicrobial activity in preschool children in e-waste areas.

Abstract: 

Ambient fine particulate matter (PM) is a risk factor for respiratory diseases. Previous studies suggest that PMexposure may down-regulate airway antimicrobial proteins and peptides (AMPs), thereby accelerating airway pathogen infection. However, epidemiological research is scarce. Hence, we estimated the associations between individual PMchronic daily intake (CDI) and the levels of the airway AMP salivary agglutinin (SAG), as well as peripheral leukocyte counts and pro-inflammatory cytokines, of preschool children in Guiyu (an e-waste area) and Haojiang (a reference area located 31.6 km to the east of Guiyu). We recruited 581 preschool children from Guiyu and Haojiang, of which 222 were included in this study for a matching design (Guiyu: n = 110 vs. Haojiang: n = 112). Air PMpollution data was collected to calculate individual PMCDI. The mean concentration of PMin Guiyu was higher than in Haojiang, resulting in a higher individual PMCDI. Concomitantly, saliva SAG levels were lower in Guiyu children (5.05 ng/mL) than in Haojiang children (8.68 ng/mL), and were negatively correlated with CDI. Additionally, peripheral counts of white blood cells, and the concentrations of interleukin-8 and tumor necrosis factor-alpha, in Guiyu children were greater than in Haojiang children, and were positively associated with CDI. Similar results were found for neutrophils and monocytes. To our knowledge, this is the first study on the relationship between PMexposure and innate airway antimicrobial activity in children, in an e-waste area, showing that PMpollution may weaken airway antimicrobial activity by down-regulation of saliva SAG levels, which might accelerate airway pathogen infection in children.

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Short-interval exposure to ambient fine particulate matter (PM2.5) exacerbates the susceptibility of pulmonary damage.

PMID: 

Biomed Pharmacother. 2019 May ;113:108737. Epub 2019 Mar 7. PMID: 30852418

Abstract Title: 

Short-interval exposure to ambient fine particulate matter (PM2.5) exacerbates the susceptibility of pulmonary damage in setting of lung ischemia-reperfusion injury in rodent: Pharmacomodulation of melatonin.

Abstract: 

This study tested the hypothesis that exposure to ambient fine particulate matter (PM) pollution increased susceptibility of rat lung to damage from acute ischemia-reperfusion (IR) injury that was reversed by melatonin (Mel) treatment. Male-adult SD rats (n = 30) were categorized into group 1 (normal control), group 2 (PMonly), group 3 (IR only at day 8 after PMexposure), group 4 (PM+ IR) and group 5 (PM+ IR + Mel), and all animals were sacrificed by day 10 after PMexposure. Oxygen saturation (%) was significantly higher in group 1 than in other groups and significantly lower in group 4 than in groups 2, 3 and 5 but it did not differ among the latter three groups (p 

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