Emergency and Continuous Exposure Guidance Levels for Selected Submarine Contaminants Volume 2 (2008) / Chapter Skim
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Pages 129-150
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From page 129... ...
Although it has been reported that workers exposed to mist oils have an increased risk of cancer, contamination of the mineral oils with polycyclic aromatic hydrocarbons (PAH, some known to be carcinogenic) confounds interpretation of the observed results.
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From page 130... ...
However, there are a few occupational standards for mineral oil mist, and they are listed in Table 8-4. TABLE 8-4 Inhalation Exposure Levels for Mineral Oil Mist Organization Type of Level Exposure Level Reference Occupational 0.2 mg/m3, inhalable particulate mass (draft)
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No current or proposed values were provided for aft section of submarine. Abbreviations: CEGL, continuous exposure guidance level; EEGL, emergency exposure guidance level.
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From page 132... ...
However, a combined analysis of workers exposed to straight cutting oil or a mixture of straight cutting oil and soluble cutting oil did exhibit an increased prevalence in cough or phlegm. Respiratory function and pulmonary function were also impaired in straight-cutting-oil-exposed workers who smoked.
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2003. Respiratory toxicology of mineral oils in laboratory animals.
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1997. Exposure to mineral oil mist and respiratory symptoms in marine engineers.
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The committee's recommendations for ozone exposure guidance levels are provided at the conclusion of the chapter with a discussion of the adequacy of the data for defining them and the research needed to fill remaining data gaps. PHYSICAL AND CHEMICAL PROPERTIES Ozone is a highly reactive atmospheric gas whose molecule consists of three atoms of oxygen.
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. In 1999, an estimated 90 million residents of the United States lived in areas where ambient ozone concentrations exceeded the NAAQS.
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Several well-designed studies have been conducted to investigate the pulmonary responses of healthy, nonsmoking human subjects acutely exposed to near ambient concentrations of ozone in environmentally controlled inhalation chambers. Those acute ozone exposures have resulted in pulmonary-function alterations, such as a decrease in inspiratory capacity; mild bronchoconstriction; rapid, shallow breathing during exercise; and symptoms of cough or pain on inspiration.
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Adams 1986 Decrease in FVC and FEV1 at 0.18 ppm 0.12 6.6 h, IE 10 men, 18-33 years old Folinsbee et al. 1988 Mean FEV1 decrements of 13% after 6.6 h and FVC of 8.3%; cough and discomfort increased with exposure; airway responsiveness to methacholine doubled after ozone exposure 0.08, 0.10 6.6 h, IE 38 men, mean age 25 years McDonnell et al.
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Prepublication Copy 139
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From page 140... ...
Similar studies have also demonstrated significant decrements in pulmonary function with ozone exposures as low as 0.12 ppm (Kulle et al.
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(1997) found that acute ozone exposureresponse models of changes in lung function in humans should be consistent with the following observations: (1)
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, some of which are near ambient concentrations commonly in urban atmospheres with photochemical smog (≤ 0.5 ppm) , have been reported to cause airway epithelial injury particularly in the nasal passages and the distal conducting airways, especially in the centriacinar regions of the lung where terminal conducting airways have interfaces with the most proximal gas-exhange regions of the lung (the alveolar parenchyma)
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From page 143... ...
The rat strain least sensitive to acute ozone injury was the F344 rat. Several studies have indicated that as ozone exposures continue for 3-7 days, the increases in BAL fluid PMNs and protein peak in the first few days and then attenuate, returning to near preexposure numbers.
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. After 90 days of exposure, there was ciliated cell necrosis, degenerated ciliated cells with few or attenuated cilia, and mucous-cell hyperplasia in the surface epithelium lining the proximal nasal airways.
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The monkeys that received ozone exposures only during alternate months had for the most part pulmonary alterations equivalent to those in the group receiving ozone exposures throughout the entire 18-month period and in some cases greater alterations, such as greater collagen deposition. In the rat study, there were no significant differences between the two exposure groups; both groups had more bronchiole-alveolar duct junctions as determined by morphometric analyses.
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. Ozone exposures at high ambient concentrations (0.08-0.22 ppm)
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Several experimental studies in animals and humans have shown that the reduction in pulmonary function with acute ozone exposure is mediated through the parasympathetic system. Ozone stimulates vagal afferents, including C fibers and rapidly adapting receptors, and this results in vagal reflexes that cause increases in airway resistance and frequency of respiration, symptoms of respiratory irritation, and a decrease in tidal volume (Beckett et al.
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Navy values are provided for comparison. TABLE 9-4 Emergency and Continuous Exposure Guidance Levels for Ozone U.S.
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. In those studies, ozone exposures caused dose-dependent symptoms of cough and chest discomfort, increases in airway responsiveness to methacholine challenge, and consistent but transient decrements in pulmonary function, such as FEV1 and FVC.
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1991. Modulation of human alveolar macrophage properties by ozone exposure in vitro.
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