Asbestos, Pleural Plaques, and Lung Cancer: Untangling the Relationships

Harber, Philip

doi:10.1164/rccm.201908-1676ed

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…Although studies have found that asbestos exposure and smoking increase the risk of cancer, the presence of pleural plaques does not necessarily implicate added risk [17 ▪▪ ,18].…”

Section: Pleural Plaquesmentioning

confidence: 99%

Asbestos-associated pulmonary disease

Caceres

Venkata

2023

Current Opinion in Pulmonary Medicine

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Purpose of reviewExposure to asbestos can cause both benign and malignant, pulmonary and pleural diseases. In the current era of low asbestos exposure, it is critical to be aware of complications from asbestos exposure; as they often arise after decades of exposure, asbestos-related pulmonary complications include asbestosis, pleural plaques, diffuse pleural thickening, benign asbestos-related pleural effusions and malignant pleural mesothelioma.Recent findingsMultiple recent studies are featured in this review, including a study evaluating imaging characteristics of asbestos with other fibrotic lung diseases, a study that quantified pleural plaques on computed tomography imaging and its impact on pulmonary function, a study that examined the risk of lung cancer with pleural plaques among two large cohorts and a review of nonasbestos causes of malignant mesothelioma.SummaryAsbestos-related pulmonary and pleural diseases continue to cause significant morbidity and mortality. This review summarizes the current advances in this field and highlights areas that need additional research.

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“…Although studies have found that asbestos exposure and smoking increase the risk of cancer, the presence of pleural plaques does not necessarily implicate added risk [17 ▪▪ ,18].…”

Section: Pleural Plaquesmentioning

confidence: 99%

Asbestos-associated pulmonary disease

Caceres

Venkata

2023

Current Opinion in Pulmonary Medicine

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“…To date, most tumors can be attributed to one or more environmental irritants or unhealthy lifestyle factors, which are also associated with a wide spectrum of chronic inflammatory diseases ( Table 1 ). For instance, alcohol abuse is implicated in chronic hepatitis and hepatocarcinoma [ 12 ], H. pylori infection can cause chronic gastritis and gastric cancer [ 13 ], asbestos-dependent silicosis contributes to lung cancer, patients with gingivitis and periodontitis have a higher risk of oral cancer [ 14 ], and long-term UV exposure can lead to dermatitis and skin cancer. In addition, smoking-related bronchitis is associated with lung cancer [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species Bridge the Gap between Chronic Inflammation and Tumor Development

Long

et al. 2022

Oxidative Medicine and Cellular Longevity

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According to numerous animal studies, adverse environmental stimuli, including physical, chemical, and biological factors, can cause low-grade chronic inflammation and subsequent tumor development. Human epidemiological evidence has confirmed the close relationship between chronic inflammation and tumorigenesis. However, the mechanisms driving the development of persistent inflammation toward tumorigenesis remain unclear. In this study, we assess the potential role of reactive oxygen species (ROS) and associated mechanisms in modulating inflammation-induced tumorigenesis. Recent reports have emphasized the cross-talk between oxidative stress and inflammation in many pathological processes. Exposure to carcinogenic environmental hazards may lead to oxidative damage, which further stimulates the infiltration of various types of inflammatory cells. In turn, increased cytokine and chemokine release from inflammatory cells promotes ROS production in chronic lesions, even in the absence of hazardous stimuli. Moreover, ROS not only cause DNA damage but also participate in cell proliferation, differentiation, and apoptosis by modulating several transcription factors and signaling pathways. We summarize how changes in the redox state can trigger the development of chronic inflammatory lesions into tumors. Generally, cancer cells require an appropriate inflammatory microenvironment to support their growth, spread, and metastasis, and ROS may provide the necessary catalyst for inflammation-driven cancer. In conclusion, ROS bridge the gap between chronic inflammation and tumor development; therefore, targeting ROS and inflammation represents a new avenue for the prevention and treatment of cancer.

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