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Epidemiology
Published in Samuel C. Morris, Cancer Risk Assessment, 2020
Finally, there are two principal considerations in applying the results: exposure and the character of the population. Because combustion-related air pollution is a common problem which appears in many circumstances, dose-response functions derived from coke-oven workers or gas-retort workers find many applications. In addition to being at much lower concentrations, the air pollution mix in each case is qualitatively different. Sometimes these differences can be of great importance. Samples taken at modern coal gasification plants have had few or none of the 4-and 5-ring polycyclic compounds in the CTPV samples which were believed to be the active agents in the coke-oven case. In diesel exhaust, the nitro-aromatic compounds seem likely to be the more important agents. Both of these situations might well result in poor predictions of cancer risk when estimated directly from coke-oven worker dose-response functions. Even when applied to the “same” situation there can be problems. Because of the pollution controls and other safeguards in place at coke ovens today, the exposure to coke-oven workers is not only lower than before, but undoubtedly different qualitatively. Even in applying the ecological study results of BaP and air pollution, one finds that in the past 20 years BaP levels have decreased considerably although some other components of the organic mix have not (Nisbet et al., 1983). A method of “tailoring” the epidemiologically derived dose-response functions using results of short-term bioassays is described in Chapter 12.
Evaluating Toxic Tort Cases
Published in Julie Dickinson, Anne Meyer, Karen J. Huff, Deborah A. Wipf, Elizabeth K. Zorn, Kathy G. Ferrell, Lisa Mancuso, Marjorie Berg Pugatch, Joanne Walker, Karen Wilkinson, Legal Nurse Consulting Principles and Practices, 2019
William P. Gavin, Mark A. Love, Wendie A. Howland
Diesel exhaust is a complex mixture of particulate matter (soot), inorganic chemicals (e.g., nitrogen dioxide), and organic chemicals. The organic chemicals include many different kinds of polycyclic aromatic hydrocarbons (PAHs). Many of the chemicals found in diesel exhaust, including benzo(a)pyrene, are also found in cigarette smoke and environmental tobacco smoke. Some PAHs are recognized carcinogens. Likewise, some of the inorganic chemicals in diesel exhaust are pulmonary irritants. The PAHs in diesel exhaust are absorbed onto the soot in the exhaust. When inhaled, the smallest soot particles carry the PAHs to the alveoli.
Epidemiology of Head and Neck Carcinoma
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Kristen B. Pytynia, Kristina R. Dahlstrom, Erich M. Sturgis
Other factors have been implicated in the aetiology of laryngeal SCC, particularly among individuals who do not smoke or use alcohol. Laryngeal SCC may be related to laryngopharyngeal reflux disease or gastro--oesophageal reflux disease, although studies conflict and most are retrospective and may suffer from recall bias and misclassification of reflux disease status.66–69 Occupational and environmental exposures in the form of inhalation of potentially toxic fumes have also been implicated. These include exposure to diesel exhaust, wood oven smoke, second-hand smoke and asbestos, but the extent of risk is unclear.70
Global burden of tracheal, bronchus, and lung cancer attributable to occupational carcinogens in 204 countries and territories, from 1990 to 2019: results from the global burden of disease study 2019
Published in Annals of Medicine, 2023
Yan Zhang, Mi Mi, Ning Zhu, Zhijun Yuan, Yuwei Ding, Yingxin Zhao, Yier Lu, Shanshan Weng, Ying Yuan
Occupational exposure to diesel engine exhaust is the third largest contributor to the occupational TBL cancer burden. Our study’s results revealed that the age-standardized SEV rate of occupational exposure to diesel engine exhaust increased for both sexes combined. Diesel engines are widely used in transportation and power supply (mining, construction work, professional driving, agriculture, and other activities that apply diesel-powered vehicles and tools), making occupational exposure to diesel exhaust common [46]. Achieving an acceptable level of exposure to diesel engine exhaust is likely to require significant policy changes and prompt turnover of the existing fleet of old diesel-powered machinery and vehicles [47]. Fortunately, the US and EU have introduced increasingly stringent diesel engine road emissions standards (US 2010 and Euro 6), followed by other countries (e.g. China, India, Brazil) [48]. However, such exposure reductions will take decades to impact the TBL cancer burden.
A controlled chamber study of effects of exposure to diesel exhaust particles and noise on heart rate variability and endothelial function
Published in Inhalation Toxicology, 2022
Leo Stockfelt, Yiyi Xu, Anders Gudmundsson, Jenny Rissler, Christina Isaxon, Jonas Brunskog, Joakim Pagels, Patrik T. Nilsson, Margareta Berglund, Lars Barregard, Mats Bohgard, Maria Albin, Inger Hagerman, Aneta Wierzbicka
Analyses of other outcomes from the same exposure setup as reported here (DINO project) found that diesel exposure did not cause genotoxicity, oxidative stress or inflammation in peripheral blood mononuclear cells (PBMCs), but suggested possible genotoxic effects of noise (Hemmingsen et al. 2015). One publication showed that diesel exhaust induced respiratory symptoms, decreased peak expiratory flow and increased inflammatory markers in blood (Xu et al. 2013). In line with the current study no interactions were found between diesel and noise exposure on these respiratory effects. Theoretically, a decrease in HF HRV could increase the inflammatory response, as it is known that the parasympathetic branch of ANS is involved in the modulation of the anti-inflammatory response (Borovikova et al. 2000; Tracey 2007). There are also some studies reporting correlations between PM-induced systemic inflammation and effects on HRV as well as on vascular function (Sloan et al. 2007; Tamagawa et al. 2008; Luttmann-Gibson et al. 2010). Despite null results for some outcomes, taking into account previously reported outcomes of the DINO project, our overall interpretation of the findings are in line with the evidence of associations between PM exposure and systemic inflammation, indicating that effects on both systemic inflammation and the autonomic nervous system are important intermediate steps for the increased risk of cardiovascular disease.
A systematic review of the health effects associated with the inhalation of particle-filtered and whole diesel exhaust
Published in Inhalation Toxicology, 2020
Chelsea A. Weitekamp, Lukas B. Kerr, Laura Dishaw, Jennifer Nichols, McKayla Lein, Michael J. Stewart
Diesel exhaust is a major contributor to ambient air pollution in urban areas (Yin et al. 2010). The exhaust emissions from diesel engines have been linked to a variety of adverse health effects, including airway inflammation (Ghio et al. 2012), vascular dysfunction (Mills et al. 2005), developmental toxicity (Ema et al. 2013), neuroinflammation (Levesque et al. 2011; Costa et al. 2017), and respiratory mortality (Atkinson et al. 2016), among others. In addition, diesel engine exhaust is categorized as ‘carcinogenic to humans’ by the International Agency for Research on Cancer (IARC 2014). Interestingly, particulate matter (PM) is often considered the primary driver of the adverse health effects associated with diesel exhaust exposure (Sydbom et al. 2001; Lall et al. 2011; Ristovski et al. 2012). Fine particulate matter (PM2.5; <2.5 µm aerodynamic diameter) is well studied and there are strong causal associations between PM2.5 exposure and cardiovascular and pulmonary diseases (US EPA 2009; Brook et al. 2010; Landrigan et al. 2018). Furthermore, there is evidence that ultrafine PM (<100 nm aerodynamic diameter) may have a greater potential for toxicity per-mass than that of PM2.5 given the higher surface area of the particles and greater ability to adsorb organic chemicals and metals (Cassee et al. 2013; Li et al. 2016; Tyler et al. 2016).