Abstract  Acute inhalation toxicity was evaluated in groups of 5 male and 5 female Wistar Albino rats exposed to naphthalene at an actual concentration of 77.7 (+/- 1.79) ppm for 4 hours. Mortality was not observed in any animal; the LC50 value was reported to be and gt; 77.7 ppm. Clinical observations included keeping eyes closed, lacrimation and mouth breathing. Gross necropsy revealed no significant lesions.

Abstract  Naphthalene, a derivative of coal tar, is widely used in industry, with little toxic effects. Its ingestion by children, however, may result in a dramatic and occasionally fatal poisioning.

Abstract  Naphthalene moth balls are potent hemolytic agents, capable of producing an acute, severe and perhaps fatal anemia. Moth ball poisoning should be suspected in children manifesting evidence of sudden hemolytic anemia, and an attempt should be made to demonstrate naphthalene or its derivatives in the urine. Care should be taken to prevent moth balls from being reached by infants and children. α- and β-naphthol and α- and β-naphthoquinone were found in the urine of a child suffering from severe hemolytic anemia due to ingestion of naphthalene moth balls. The hemolytic properties of naphthalene, of the naphthols and naphthoquinones were examined in vitro and in vivo (rabbits). Naphthalene itself was found to be nonhemolytic in vitro or in vivo. The hemolytic power of the naphthalene metabolites in vitro decreased in the following order: α-naphthol, β-naphthol, α-naphthoquinone, β-naphthoquinone. Hemolysis due to α-naphthol was observed in vivo (rabbits). However, its hemolytic action was significantly weaker than in vitro. β-naphthol and the naphthoquinones showed no hemolytic activity in vivo (rabbits). Plasma, cholesterol and lecithin did not inhibit the hemolytic activity of the naphthalene metabolites in vitro. Formation of methemoglobin was not observed.

Abstract  INTRODUCTION An increased risk of lung cancer among asphalt workers has been suggested in epidemiological studies largely based on routine statistics and record linkages [Partanen and Boffetta, 1994]. Given the importance of bitumen and its fume as occupational and environmental exposures, it is important to clarify whether (i) asphalt workers are at increased risk of cancer of the lung, and possibly other organs, and (ii) whether any excess risk can be attributed to exposure to bitumen fume or other agents, such as coal tar. The International Agency for Research on Cancer (IARC) and its collaborators assembled a retrospective cohort of asphalt workers from the asphalt industry (road paving, asphalt mixing, and roofing) in seven European countries (Denmark, Finland, France, Germany, the Netherlands, Norway, and Sweden) and Israel. The primary goal of the study was to assess whether an increased risk of lung cancer is associated with bitumen fume exposure. Details on the study design and the detailed results of the mortality analysis have been reported [Boffetta et al., 2001]. In a companion paper, we report the results of the analysis of mortality based on employment in specific job groups [Boffetta et al., 2003]. In this article, we report results based on assessment of exposure to bitumen and other agents.

Abstract  Individuals may be exposed to solvent mixtures and fuel either at work or home, through air, water and food contamination. Few studies have addressed the genotoxic effects of mixed, low-level exposure to fuel and solvent. This was an optimally designed study where each subject was sampled prior to exposure and after 15 and 30 weeks while exposed, in a repeated measures design with each subject serving as his own control. Fifty men aged between 18 and 50, working on aircraft equipment operation and maintenance at a military installation were included. Eight unexposed men were concurrently sampled. Sister-chromatid exchanges (SCE) and micronuclei (MN) frequency were measured in conjunction with air sampling and expired breath analysis for jet fuel (JP-4), 1,1,1-trichloroethane, methyl ethyl ketone, xylenes, toluene and methylene chloride. Exposure levels measured by industrial hygiene were very low (all means <6 p.p.m.), <10% of the OSHA standard. Expired breath levels were also low, <25 p.p.b. A small but statistically significant increase in the frequency of SCE occurred after 30 weeks of exposure for sheet metal workers (P = 0.003) and for painters (P = 0.05). The MN frequency in the sheet metal workers initially showed a statistically significant increase, but by 30 weeks had decreased. Cigarette smoking, alcohol and caffeine use were not associated with changes from baseline for either MN or SCE. Smokers, however, had significantly higher values of SCEs at baseline than did nonsmokers. In summary, these findings suggest that small increases in SCEs in particular, may serve as a sensitive biologic indicator of low level hydrocarbon exposure in as much as statistically significant changes occurred in the highest exposed groups but not in the low or no exposure groups. Chance occurrence or exposures to other occupational or non-occupational agents cannot be eliminated as a cause of the study findings.

Abstract  The TLV-TWA 10 ppm (52 mg/m3) and TLV-STEL of 15 ppm (79 mg/m3) are recommended for occupational exposure to naphthalene. These values are intended to minimize the potential for eye and respiratory tract irritation and ocular toxicity that can include cataract formation, optical neuritis, lens opacities, and retinal degeneration. Other adverse effects may include headache, loss of appetite, nausea, and blood dyscrasia, such as hemolytic anemia and hemoglobinuria. Systemic poisoning following dermal contact and absorption of naphthalene warrants a Skin notation. Based on the very limited evidence of carcinogenicity in rodents, pulmonary adenomas in female mice but not in the male mice or in rats of either sex, exposed by inhalation for 2 years, an A4, Not Classifiable as a Human Carcinogen, notation is assigned. Sufficient data were not available to recommend a SEN notation.

Abstract  This article present the results of the extension of the follow-up of a cohort of workers employed in an Italian oil refinery. 1,583 workers employed in 1949-1982 in a northern Italy oil refinery plant were followed-up for mortality as of May 31, 1991. Environmental measurements documented potential exposure to benzene. Standardized mortality ratios (SMR) and their 95% confidence intervals (95% CI) were calculated using as references national (1949-1968) and regional mortality rates (1969-1991). Elevated mortality from lymphoma (seven deaths, SMR 190, 95% CI 76-391) and leukemia (eight deaths, SMR 225, 95% CI 97-443) was observed. No consistent trends by length of employment or time since first exposure were apparent. Nonetheless, the excess risk was particularly and significantly increased among workers with 15 or more years of employment, and 30 or more years since first employment. The findings of elevated mortality from leukemia and lymphoma are in agreement with those of other oil refinery studies. Chance, confounding, or other biases might have played a marginal, if any, role in determining the results. Exposure to benzene is a biologically plausible explanation.

Abstract  Quinones represent a class of toxicological intermediates which can create a variety of hazardous effects in vivo, including acute cytotoxicity, immunotoxicity, and carcinogenesis. The mechanisms by which quinones cause these effects can be quite complex. Quinones are Michael acceptors, and cellular damage can occur through alkylation of crucial cellular proteins and/or DNA. Alternatively, quinones are highly redox active molecules which can redox cycle with their semiquinone radicals, leading to formation of reactive oxygen species (ROS), including superoxide, hydrogen peroxide, and ultimately the hydroxyl radical. Production of ROS can cause severe oxidative stress within cells through the formation of oxidized cellular macromolecules, including lipids, proteins, and DNA. Formation of oxidatively damaged bases such as 8-oxodeoxyguanosine has been associated with aging and carcinogenesis. Furthermore, ROS can activate a number of signaling pathways, including protein kinase C and RAS. This review explores the varied cytotoxic effects of quinones using specific examples, including quinones produced from benzene, polycyclic aromatic hydrocarbons, estrogens, and catecholamines. The evidence strongly suggests that the numerous mechanisms of quinone toxicity (i.e., alkylation vs oxidative stress) can be correlated with the known pathology of the parent compound(s).

Abstract  Jet fuel is a common occupational exposure among commercial and military maintenance workers. JP-8 jet fuel, a military formulation, has shown immunotoxic effects in mice, but little data exist for humans. The aim of this cross-sectional study was to determine whether immune cell counts in the peripheral blood were altered among tank entry workers at three Air Force bases. After adjusting for covariates, fuel system maintenance personnel (n = 45) were found to have significantly higher counts of white blood cells (P = 0.01), neutrophils (P = 0.05), and monocytes (P = 0.02) when compared with a low-exposure group (n = 78), but no differences were noted in the numbers of total lymphocytes, T-cells, T-helper cells, T-suppressor cells, natural killer cells, and B-cells. Investigations are needed to evaluate the functional ability of these cells to produce lymphokines and cytokines and modulate the immune system.

Abstract  Final rept. 1 Jan 1989-31 Dec 2003. To measure the association between occupational jet fuel exposure and invasive cancer occurrence in the U.S. Air Force (USAF). Cancer data from January 1, 1989 to December 31, 2003 were extracted from a U.S. military cancer registry and linked to information from the Air Force Personnel Center. Based on job descriptions, et fuel exposure was categorized as high, moderate or low. Conditional logistic regressions were used to calculate odds ratios for fuel exposure with cancer occurrence as the primary outcome of interest. The odds ratios for cancer occurrence in the moderate and high exposure groups were 0.84 (95% Cl 0.65-1.09) and 0.73 (95% Cl 0.32-1.64), respectively, when compared to the low exposure group. A null association was observed between occupational jet fuel exposure and invasive cancer in the USAF.