Chemical characterization of combustion engine exhaust and assessment of helicopter deck operator occupational exposures on an offshore frigate class ship.

Diesel engine exhaust (DE) consists of a complex mixture of gases and aerosols, originating from sources such as engines, turbines, and power generators. It is composed of a wide range of toxic compounds ranging from constituents that are irritating to those that are carcinogenic. The purposes of this work were to characterize DE originating from different engine types on a ship operating offshore and to quantify the potential exposure of workers on the ship's helicopter deck to select DE compounds. Sampling was conducted on a Norwegian Nansen-class frigate that included helicopter operations. Frigate engines and generators were fueled by marine diesel oil, while the helicopter engine was fueled by high flash point kerosene-type aviation fuel. Exhaust samples were collected directly from the stack of the diesel engine and one of the diesel generator exhaust stacks, inside a gas turbine exhaust stack, and at the exhaust outlet of the helicopter. To characterize the different exhaust sources, non-targeted screening of volatile and semi-volatile organic compounds was performed for multiple chemical classes. Some of the compounds detected at the sources are known irritants, such as phthalic anhydride, 2,5-dyphenyl-p-benzoquinone, styrene, cinnoline, and phenyl maleic anhydride. The exhaust from the diesel engine and diesel generator was found to contain the highest amounts of particulate matter and gaseous compounds, while the gas turbine had the lowest emissions. Personal exposure samples were collected outdoors in the breathing zone of a helicopter deck operator over nine working shifts, simultaneously with stationary measurements on the helicopter deck. Elemental carbon, nitrogen dioxide, and several volatile organic compounds are known to be present in DE, such as formaldehyde, acrolein, and phenol were specifically targeted. Measured DE exposures of the crew on the helicopter deck were variable, but less than the current European occupational exposure limits for all compounds, except elemental carbon, in which concentration varied between 0.5 and 37 µg/m3 over nine work shifts. These findings are among the first published for this type of working environment.

Multiwalled Carbon Nanotubes Induce Fibrosis and Telomere Length Alterations.

Telomere shortening can result in cellular senescence and in increased level of genome instability, which are key events in numerous of cancer types. Despite this, few studies have focused on the effect of nanomaterial exposure on telomere length as a possible mechanism involved in nanomaterial-induced carcinogenesis. In this study, effects of exposure to multiwalled carbon nanotubes (MWCNT) on telomere length were investigated in mice exposed by intrapleural injection, as well as in human lung epithelial and mesothelial cell lines. In addition, cell cycle, apoptosis, and regulation of genes involved in DNA damage repair were assessed. Exposure to MWCNT led to severe fibrosis, infiltration of inflammatory cells in pleura, and mesothelial cell hyperplasia. These histological alterations were accompanied by deregulation of genes involved in fibrosis and immune cell recruitment, as well as a significant shortening of telomeres in the pleura and the lung. Assessment of key carcinogenic mechanisms in vitro confirmed that long-term exposure to the long MWCNT led to a prominent telomere shortening in epithelial cells, which coincided with G1-phase arrest and enhanced apoptosis. Altogether, our data show that telomere shortening resulting in cell cycle arrest and apoptosis may be an important mechanism in long MWCNT-induced inflammation and fibrosis.