Dataset Information

A review of health effects associated with exposure to jet engine emissions in and around airports.

ABSTRACT:

Background

Airport personnel are at risk of occupational exposure to jet engine emissions, which similarly to diesel exhaust emissions include volatile organic compounds and particulate matter consisting of an inorganic carbon core with associated polycyclic aromatic hydrocarbons, and metals. Diesel exhaust is classified as carcinogenic and the particulate fraction has in itself been linked to several adverse health effects including cancer.

Method

In this review, we summarize the available scientific literature covering human health effects of exposure to airport emissions, both in occupational settings and for residents living close to airports. We also report the findings from the limited scientific mechanistic studies of jet engine emissions in animal and cell models.

Results

Jet engine emissions contain large amounts of nano-sized particles, which are particularly prone to reach the lower airways upon inhalation. Size of particles and emission levels depend on type of aircraft, engine conditions, and fuel type, as well as on operation modes. Exposure to jet engine emissions is reported to be associated with biomarkers of exposure as well as biomarkers of effect among airport personnel, especially in ground-support functions. Proximity to running jet engines or to the airport as such for residential areas is associated with increased exposure and with increased risk of disease, increased hospital admissions and self-reported lung symptoms.

Conclusion

We conclude that though the literature is scarce and with low consistency in methods and measured biomarkers, there is evidence that jet engine emissions have physicochemical properties similar to diesel exhaust particles, and that exposure to jet engine emissions is associated with similar adverse health effects as exposure to diesel exhaust particles and other traffic emissions.

SUBMITTER: Bendtsen KM

PROVIDER: S-EPMC7866671 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundCigarette smoking, secondhand cigarette smoke (SHS) exposure, and e-cigarette use ("vaping") are each associated with increased rates of depressive symptoms and other internalizing mental health disorders. The prevalence of vaping has increased greatly, yet the mental health correlates of secondhand exposure to e-cigarette emissions are as yet to be investigated. This study examined the potential adverse mental health outcomes associated with different tobacco exposures (direct and passive), with a particular focus on the mental health correlates of secondhand exposure to e-cigarette emissions.MethodsThe Population Assessment of Tobacco and Health Study data collected from a sample of 16,173 Wave 4 adults were used to test the hypothesis that secondhand e-cigarette emissions exposure is associated with increased odds of internalizing mental health disorders. Individuals were categorized as exclusive cigarette smokers, exclusive e-cigarette users, cigarette and e-cigarette dual users, exclusive noncombustible tobacco users, secondhand smoke exposed non-users, secondhand e-cigarette emissions exposed non-users, and non-users with no current SHS/secondhand e-cigarette aerosol exposure. Adjusted weighted logistic regression analysis was used to investigate the association between exposure type and internalizing problems as assessed by scores on the Global Appraisal of Individual Needs-Short Screener (GAIN-SS), a widely used instrument for assessing mental health problems.ResultsCigarette smokers (AOR = 2.53, 95% CI: 2.19-2.92), e-cigarette users (AOR = 3.14, 2.41-4.09), dual users (AOR = 3.37, 2.85-4.00), noncombustible tobacco users (AOR = 1.48, 1.01-2.17), SHS exposed non-users (AOR = 1.63, 1.37-1.94), and secondhand e-cigarette emissions exposed non-users (AOR = 1.43, 1.03-1.99) were each associated with increased odds of moderate to severe internalizing mental health problems as compared to unexposed non-users. Odds of internalizing problems among SHS and secondhand e-cigarette emissions exposed non-users did not differ (p = 0.46).ConclusionsThis is the first study, to our knowledge, to identify an association between recent secondhand exposure to e-cigarette emissions and mental health problems, and the risk is comparable to that of SHS. Corroboration of this relationship needs further research to explicate directionality and mechanisms underlying this association.

Project description:BackgroundDiesel engine exhaust (DEE) exposure causes lung cancer, but the molecular mechanisms by which this occurs are not well understood.ObjectivesTo assess transcriptomic alterations in nasal epithelium of DEE-exposed factory workers to better understand the cellular and molecular effects of DEE.MethodsNasal epithelial brushings were obtained from 41 diesel engine factory workers exposed to relatively high levels of DEE (17.2-105.4 μg/m3), and 38 unexposed workers from factories without DEE exposure. mRNA was profiled for gene expression using Affymetrix microarrays. Linear modeling was used to identify differentially expressed genes associated with DEE exposure and interaction effects with current smoking status. Pathway enrichment among differentially expressed genes was assessed using EnrichR. Gene Set Enrichment Analysis (GSEA) was used to compare gene expression patterns between datasets.Results225 genes had expression associated with DEE exposure after adjusting for smoking status (FDR q < 0.25) and were enriched for genes in pathways related to oxidative stress response, cell cycle pathways such as MAPK/ERK, protein modification, and transmembrane transport. Genes up-regulated in DEE-exposed individuals were enriched among the genes most up-regulated by cigarette smoking in a previously reported bronchial airway smoking dataset. We also found that the DEE signature was enriched among the genes most altered in two previous studies of the effects of acute DEE on PBMC gene expression. An exposure-response relationship was demonstrated between air levels of elemental carbon and the first principal component of the DEE signature.ConclusionsA gene expression signature was identified for workers occupationally exposed to DEE that was altered in an exposure-dependent manner and had some overlap with the effects of smoking and the effects of acute DEE exposure. This is the first study of gene expression in nasal epithelial cells of workers heavily exposed to DEE and provides new insights into the molecular alterations that occur with DEE exposure.