Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets

Lan, Qing; Vermeulen, Roel; Dai, Yufei; Ren, Dianzhi; Hu, Wei; Duan, Huawei; Niu, Yong; Xu, Jianing; Fu, Wei; Meliefste, Kees; Zhou, Baosen; Yang, Jincai; Meng, Yahan; Jia, Xiaowei; Meng, Tao; Peng, Bin; Kim, Christopher; Bassig, Bryan A.; Hosgood, H. Dean; Silverman, Debra T.; Zheng, Yuxin; Rothman, Nathaniel

doi:10.1136/oemed-2014-102556

Cited by 23 publications

(50 citation statements)

References 13 publications

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“…To evaluate dose‐response trends, linear regression was used to compare cytokine levels across tertiles of PM 2.5 and EC exposure relative to control workers, as well as for exposed workers only. As we previously reported [Lan et al, ], a very high correlation was observed between EC and OC (Spearman r = 0.86, P < 0.0001) and between EC and soot (Spearman r = 0.91, P < 0.0001). Therefore, separate analyses were not conducted for OC and soot.…”

Section: Methodssupporting

confidence: 83%

“…IL‐8, MIP‐1β, and MCP‐1 belong to the chemokine family that are expressed and released by a wide range of normal cells such as monocytes, neutrophils, macrophages, keratinocytes, fibroblasts, and endotheliocytes. Our previous studies showed a decrease in neutrophils (4146 ± 1164 cells/μL) and monocytes (310 ± 110 cells/μL) in DEE exposed workers compared with controls (4633 ± 1530 cells/μL and 330 ± 150 cells/μL, respectively), although the differences were not statistically significant ( P = 0.07 and 0.08, respectively) [Lan et al, ; Dai et al, ]. An in vitro study showed that DEE exposure suppresses the release of cytokines from human and murine alveolar macrophages [Amakawa et al, ].…”

Section: Discussionmentioning

confidence: 96%

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Occupational exposure to diesel engine exhaust and serum cytokine levels

Dai

Ren

Bassig

et al. 2017

Environ and Mol Mutagen

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The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross-sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)-1, IL-6, IL-8, tumor necrosis factor (TNF)-α, macrophage inflammatory protein (MIP)-1β, and monocyte chemotactic protein (MCP)-1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP-1β were significantly reduced by ∼37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM concentrations in all subjects (P < 0.001) as well as in exposed subjects only (P = 0.001). Levels of IL-8 and MIP-1β were significantly lower in workers in the highest exposure tertile of PM (>397 µg/m ) compared to unexposed controls. Further, significant inverse exposure-response relationships for IL-8 and MCP-1 were also found in relation to increasing PM levels among the DEE exposed workers. Given that IL-8, MIP-1β, and MCP-1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144-150, 2018. © 2017 Wiley Periodicals, Inc.

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Section: Methodssupporting

confidence: 83%

Section: Discussionmentioning

confidence: 96%

Occupational exposure to diesel engine exhaust and serum cytokine levels

Dai

Ren

Bassig

et al. 2017

Environ and Mol Mutagen

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“…52,99 CD8 + T cells, similar to other subsets, have the capacity to undergo transcriptional reprogramming and release pro-allergic cytokines. 100 Many environmental triggers selectively lead to the accumulation of CD8 + T cells in the lung including viruses, changes in air quality (ozone and diesel exhaust), and cigarette smoke [5][6][7][8][9][10] (Table 1).…”

Section: Pathogenic Role Of Cd8 + T Cells In Asthmamentioning

confidence: 99%

“…Corticosteroids may also have a limited role in preventing asthma exacerbations, further suggesting that the triggers of exacerbation may involve cells and pathways that are less responsive to corticosteroids. Different triggers of asthma exacerbation result in diverse immune‐inflammatory outcomes, including accumulation of different inflammatory cells and pathways that exhibit differential steroid responsiveness (Table ).…”

Section: Introductionmentioning

confidence: 99%

Spectrum of T‐lymphocyte activities regulating allergic lung inflammation

Gelfand

Joetham

Wang

et al. 2017

Immunological Reviews

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Despite advances in the treatment of asthma, optimization of symptom control remains an unmet need in many patients. These patients, labeled severe asthma, are responsible for a substantial fraction of the disease burden. In these patients research is needed to define the cellular and molecular pathways contributing to disease which in large part are refractory to corticosteroid treatment. The causes of steroid-resistant asthma are multifactorial and result from complex interactions of genetics, environmental factors, and innate and adaptive immunity. Adaptive immunity, addressed here, integrates the activities of distinct T cell subsets and by definition is dynamic and responsive to an ever-changing environment and the influences of epigenetic modifications. These T-cell subsets exhibit different susceptibilities to the actions of corticosteroids and, in some, corticosteroids enhance their functional activation. Moreover, these subsets are not fixed in lineage differentiation but can undergo transcriptional reprogramming in a bidirectional manner between protective and pathogenic effector states. Together, these factors contribute to asthma heterogeneity between patients but also in the same patient at different stages of their disease. Only by carefully defining mechanistic pathways, delineating their sensitivity to corticosteroids, and determining the balance between regulatory and effector pathways, will precision medicine become a reality with selective and effective application of targeted therapies.

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“…An example of an assignment variable measured with random error is CD4 count, which is used to determine ART eligibility among HIV-positive patients [ 15 , 16 ]. In addition to random measurement error, CD4 counts are affected by exogenous factors, such as exercise [ 17 ], exposure to diesel exhaust [ 18 ], and smoking [ 19 ]. These factors result in substantial variability in CD4 count measurement.…”

Section: The Regression Discontinuity Designmentioning

confidence: 99%

Regression Discontinuity for Causal Effect Estimation in Epidemiology

2016

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Regression discontinuity analyses can generate estimates of the causal effects of an exposure when a continuously measured variable is used to assign the exposure to individuals based on a threshold rule. Individuals just above the threshold are expected to be similar in their distribution of measured and unmeasured baseline covariates to individuals just below the threshold, resulting in exchangeability. At the threshold exchangeability is guaranteed if there is random variation in the continuous assignment variable, e.g., due to random measurement error. Under exchangeability, causal effects can be identified at the threshold. The regression discontinuity intention-to-treat (RD-ITT) effect on an outcome can be estimated as the difference in the outcome between individuals just above (or below) versus just below (or above) the threshold. This effect is analogous to the ITT effect in a randomized controlled trial. Instrumental variable methods can be used to estimate the effect of exposure itself utilizing the threshold as the instrument. We review the recent epidemiologic literature reporting regression discontinuity studies and find that while regression discontinuity designs are beginning to be utilized in a variety of applications in epidemiology, they are still relatively rare, and analytic and reporting practices vary. Regression discontinuity has the potential to greatly contribute to the evidence base in epidemiology, in particular on the real-life and long-term effects and side-effects of medical treatments that are provided based on threshold rules – such as treatments for low birth weight, hypertension or diabetes.

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Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets

Abstract: This study provides new insights into the underlying mechanism of DEE carcinogenicity.

Cited by 23 publications

References 13 publications

Occupational exposure to diesel engine exhaust and serum cytokine levels

Occupational exposure to diesel engine exhaust and serum cytokine levels

Spectrum of T‐lymphocyte activities regulating allergic lung inflammation

Regression Discontinuity for Causal Effect Estimation in Epidemiology

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