Traffic-related air pollution associated with chronic kidney disease among elderly residents in Taipei City

Chen, Szu-Ying; Chu, Dachen; Lee, Jui-Huan; Yang, Yaru; Chan, Chang-Chuan

doi:10.1016/j.envpol.2017.11.084

Cited by 99 publications

(82 citation statements)

References 37 publications

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“…Exposure to PM 2.5 could lead to chronic systematic inflammation [3], [14], [15], [16], [17]. It has been wildly demonstrated that PM 2.5 is associated with inflammatory cytokines whereby it stimulates the over-expression of various transcription factor genes and inflammation-related cytokine genes, contributing to inflammatory injury [33], [34], [35].…”

Section: Discussionmentioning

confidence: 99%

“…A new longitudinal study supplies early evidence that PM 2.5 exposure is associated with reduced kidney function, and an elevated rate of kidney function decline over time [2], [3]. Kidney injury molecule-1 (KIM-1), a recently discovered transmembrane protein, is undetectable in normal kidneys, but it is significantly induced in renal injury including acute kidney injury (AKI) and chronic kidney disease (CKD) [4], [5], [6].…”

Section: Introductionmentioning

confidence: 99%

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iRhom2 loss alleviates renal injury in long-term PM2.5-exposed mice by suppression of inflammation and oxidative stress

Qin

et al. 2018

Redox Biology

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Particulate matter (PM2.5) is a risk factor for organ injury and disease progression, such as lung, brain and liver. However, its effects on renal injury and the underlying molecular mechanism have not been understood. The inactive rhomboid protein 2 (iRhom2), also known as rhomboid family member 2 (Rhbdf2), is a necessary modulator for shedding of tumor necrosis factor-α (TNF-α) in immune cells, and has been explored in the pathogenesis of chronic renal diseases. In the present study, we found that compared to the wild type (iRhom2+/+) mice, iRhom2 knockout (iRhom2-/-) protected PM2.5-exposed mice from developing severe renal injury, accompanied with improved renal pathological changes and functions. iRhom2-/- mice exhibited reduced inflammatory response, as evidenced by the reduction of interleukin 1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α) and IL-18 in kidney samples, which might be, at least partly, through inactivating TNF-α converting enzyme/TNF-α receptors (TACE/TNFRs) and inhibitor of α/nuclear factor κ B (IκBα/NF-κB) signaling pathways. In addition, oxidative stress was also restrained by iRhom2-/- in kidney of PM2.5-exposed mice by enhancing heme oxygenase/nuclear factor erythroid 2-related factor 2 (HO-1/Nrf-2) expressions, and reducing phosphorylated c-Jun N-terminal kinase (JNK). In vitro, blockage of HO-1 or Nrf-2 rescued the inflammatory response and oxidative stress that were reduced by iRhom2 knockdown in PM2.5-incubated RAW264.7 cells. Similar results were observed in JNK activator-treated cells. Taken together, our findings indicated that iRhom2 played an essential role in regulating PM2.5-induced chronic renal damage, thus revealing a potential target for preventing chronic kidney diseases development.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

iRhom2 loss alleviates renal injury in long-term PM2.5-exposed mice by suppression of inflammation and oxidative stress

Qin

et al. 2018

Redox Biology

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“…The nanoscale particles, often containing large amounts of toxic compounds such as metals and hydrocarbons, can also exert direct or indirect toxicity toward extrapulmonary organs such as the kidneys [3,4]. Recently, some epidemiological studies have reported a strong and consistent association between PM 2.5 exposure and reduced kidney function as well as an increased rate of renal function decline [5][6][7]. Studies have also shown that mid-/long-term exposure to high levels of PM 2.5 can induce kidney damage in rodents [8,9].…”

Section: Introductionmentioning

confidence: 99%

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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Background: Exposure to airborne fine particulate matter (PM 2.5 ) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM 2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM 2.5 exposure in human proximal tubule epithelial cells (HK-2 cells).Results: PM 2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and timedependent manner. PM 2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM 2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM 2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2. Conclusions:Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM 2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM 2.5 induced through repression of oxidative stress and apoptosis.

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“…This in turn may increase the risk of incident acute respiratory failure. Furthermore, some studies found that one-year PM 2.5 exposure was associated with lower renal function in the general population (22,23). Although no human studies have ever investigated whether short-term PM2.5 exposure is linked to the incidence of acute kidney injury, some animal experiments have demonstrated that short-term exposure to fine particulates , urban particulates, or diesel exhaust particulates, could induce inflammation and oxidative stress in peri-renal adipose tissue (24), increase cytokine expression in the kidney (25), and aggravate experimental acute renal failure (26) in rats, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Consistent with the increasing trend of major ANCI, patients with higher PM 2.5 exposure were more likely to receive invasive hemodynamic monitoring, such as arterial line (aOR=1. 22 Median LOS in ICCU and hospital were 1.1 days (IQR, 0.8-2.6 days) and 6.3 days (IQR, 3.8-10.9 days), respectively. The overall rate of primary endpoint was 7.6% during hospitalization of study patients, with 6.5% occurring in ICCU.…”

mentioning

confidence: 92%

Association of Fine Particulate Matter Exposure with Acute Noncardiovascular Critical Illnesses and In-hospital Outcomes in Patients Receiving Intensive Cardiac Care

Chen

Liu

Huang

et al. 2020

Preprint

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Background The effect of short-term exposure to fine particulate matter (PM2.5) on the incidence of acute noncardiovascular critical illnesses (ANCIs) and clinical outcomes is unknown in patients with acute cardiovascular diseases.Methods We conducted a retrospective study in 2,337 admissions to an intensive cardiac care unit (ICCU) from June 2016 to May 2017. We used the 2-day average PM2.5 concentration before ICCU admission to estimate the individual exposure level, and patients were divided into 3 groups according to the concentration tertiles. Major ANCI was defined as the composite of acute respiratory failure, acute kidney injury, gastrointestinal hemorrhage, or sepsis. The primary endpoint was allcause death or discharge against medical advice in extremely critical condition.Results During the 12-month study period, the annual median concentration of PM2.5 in Chengdu, China was 48 µg/m3 (IQR, 33-77 µg/m3). More than 20 percent of admissions were complicated by major ANCI, and the primary endpoints occurred in 7.6% of patients during their hospitalization. The association of short-term PM2.5 exposure levels with the incidence of acute respiratory failure (adjusted OR [odds ratio] =1.31, 95%CI [confidence interval]1.12-1.54) and acute kidney injury (adjusted OR=1.20, 95%CI 1.02-1.41) showed a significant trend. Additionally, there were numerically more cases of sepsis (adjusted OR=1.21, 95%CI 0.92-1.60) and gastrointestinal hemorrhage (adjusted OR=1.29, 95%CI 0.94-1.77) in patients with higher exposure levels. After further multivariable adjustment, short-term PM2.5 exposure levels were still significantly associated with incident major ANCI (adjusted OR=1.32, 95%CI 1.12-1.56), as well as a higher incidence of the primary endpoint (adjusted OR=1.52, 95%CI 1.09-2.12).Conclusion Short-term PM2.5 exposure before ICCU admission was associated with an increased risk of incident major ANCI and worse in-hospital outcomes in patients receiving intensive cardiac care.

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Traffic-related air pollution associated with chronic kidney disease among elderly residents in Taipei City

Cited by 99 publications

References 37 publications

iRhom2 loss alleviates renal injury in long-term PM2.5-exposed mice by suppression of inflammation and oxidative stress

iRhom2 loss alleviates renal injury in long-term PM2.5-exposed mice by suppression of inflammation and oxidative stress

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

Association of Fine Particulate Matter Exposure with Acute Noncardiovascular Critical Illnesses and In-hospital Outcomes in Patients Receiving Intensive Cardiac Care

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