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Male and female F-344 rats and B6C3F1 mice (10/sex/group) were exposed to N,N-dimethylformamide (DMF) by whole body inhalation exposure at 0, 50, 100, 200, 400, or 800 ppm, 6 h/day, 5 days/week, for 13 weeks. A concentration-dependent depression in body weight occurred in rats of both sexes at 400 (6-11%) and 800 ppm (20-22%). In contrast, all weight changes in both sexes of mice were within 10% of controls. No rats died, while 5 mice died from nonexposure-related causes. Relative liver weights were significantly increased at all DMF concentrations in both sexes and both species. Activities of serum sorbitol dehydrogenase (SDH) were statistically increased in male and female rats (200 to 800 ppm) on study days 4, 24, and 91 (13 weeks). Activities of alanine aminotransferase (ALT) and isocitrate dehydrogenase (ICD) were statistically increased in both sexes of rats exposed to 800 ppm DMF at all time points. Cholesterol (CHOL) levels were statistically increased in male and female rats (50-800 ppm) at all sampling time points. Levels of total bile acids (TBA) were statistically increased in both sexes of rats (400-800 ppm) on days 24 and 91. Centrilobular hepatocellular necrosis (minimal to moderate) was seen in rats of both sexes exposed at 400 and 800 ppm, with the lesions more severe in females. Centrilobular hepatocellular hypertrophy (minimal to mild) was found in all groups of DMF-exposed male mice, and in female mice exposed at 100-800 ppm. For male and female rats the no-observed-adverse-effect concentration (NOAEC) for microscopic liver injury was 200 ppm. The NOAEC was 50 ppm for female mice, but an NOAEC based upon the absence of microscopic liver injury was not determined in male mice.

To evaluate the potential health hazards of diesel engine emissions in underground coal mines, inhalation studies were performed using three species of animals. A wide range of toxicological responses was measured. Exhaust was provided by a 425 in.3 displacement four-cycle, water-cooled, naturally aspirated diesel engine (Caterpillar Model 3304) equipped with a water scrubber. Exposures were 7 h/day, 5 dayslweek, for periods up to 24 months. Micronized coal dust was generated using a Wright dust feeder. Four exposures were evaluated: (1) filtered ambient air, (2) 2 mg/m3 diesel particulate, (3) 2 mg/m3 respirable coal dust, and (4) 1 mg/m3 each of 2 and 3. Gaseous and vapor concentrations were similar in both exposures employing diesel exhaust. Male cynomolgus monkeys, Fischer-344 male and female rats, and female CD-1 mice were the experimental subjects. Monkeys were sacrificed at 24 months, rats at 3, 6, 12, and 24 months, and mice at 1, 3, and 6 months.Gross morphology and histopathology demonstrated that both diesel and coal dust particles are deposited in the lungs and retained in alveolar tissue. Alveolar type I1 cell hyperplasia and pulmonary lipidosis occurred in rats, being most evident in rats exposed to diesel exhaust alone. There was, however, no evidence of emphysema or chronic bronchitis, and only minimal fibrosis was seen in association with the retained particulate. Both particulates affected the defense mechanisms of the lung. Exposure to coal dust activated responses associated with phagocytosis, whereas exposure to diesel exhaust depressed them. Severity of influenza challenge increased concomitantly with decreased interferon production in diesel-exposed mice. Exposure to diesel emissions did not result in genotoxic effects as measured by increases in sister chromatid exchange, A summary of animal studies conducted by the Downloaded from LEWIS ET AL chromosomal aberrations, micronucleus testing, and urine genotoxic assays. Pulmonary function studies in monkeys showed mild obstructive airway disease in coal dust, diesel exhaust, and the combined exposed animals. This effect was most pronounced in monkeys exposed to diesel exhaust. Evidence of restrictive lung disease was not seen in any group. Clearance of F304 particles appeared to be stimulated by exposure to diesel exhaust in the first 3 months, but long-term clearance of diesel particulate appeared to be inhibited. No evidence was found for increases in tumorogenicity (rats) or induction of xenobiotic metabolizing enzymes in the lung or liver (rats). Humoral and cellular immunities were not significantly affected by exposure (rats). No adverse seminal effects were observed in monkeys exposed for 2 years. There was no frank evidence of chronic toxicity as demonstrated by changes in mortality, body weight gains, organ-body weight ratios, or clinical parameters in rats or monkeys. Synergistic effects between diesel exhaust and coal dust were not demonstrated. 346 at RMIT UNIVERSITY on July 13, 2015 ijt.sagepub.com Downloaded from DIESEL EMISSION...

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The initial goal of occupational reproductive health research is to effectively study the many toxicants, physical agents, and biomechanical and psychosocial stressors that may constitute reproductive hazards in the workplace. Although the main objective of occupational reproductive researchers and clinicians is to prevent recognized adverse reproductive outcomes, research has expanded to include a broader spectrum of chronic health outcomes potentially affected by reproductive toxicants. To aid in achieving these goals, the National Institute for Occupational Safety and Health, along with its university, federal, industry, and labor colleagues, formed the National Occupational Research Agenda (NORA) in 1996. NORA resulted in 21 research teams, including the Reproductive Health Research Team (RHRT). In this report, we describe progress made in the last decade by the RHRT and by others in this field, including prioritizing reproductive toxicants for further study; facilitating collaboration among epidemiologists, biologists, and toxicologists; promoting quality exposure assessment in field studies and surveillance; and encouraging the design and conduct of priority occupational reproductive studies. We also describe new tools for screening reproductive toxicants and for analyzing mode of action. We recommend considering outcomes such as menopause and latent adverse effects for further study, as well as including exposures such as shift work and nanomaterials. We describe a broad domain of scholarship activities where a cohesive system of organized and aligned work activities integrates 10 years of team efforts and provides guidance for future research.

An experimental study was conducted to evaluate changes in pulmonary reactivity resulting from repeated vanadium pentoxide (V2O5) dust inhalation. The study assessed pulmonary reactivity to V2O5 through the use of provocation challenges, and compared V2O5 reactivity before and after subchronic V2O5 exposure. A total of 24 adult, male cynomolgus monkeys (Macaca fascicularis) were exposed by inhalation for 6 h per day, 5 days per week, for 26 weeks. Two V2O5-exposed groups (n = 8 each) received equal weekly V2O5 exposures (concentration x time) with different exposure profiles. One V2O5-exposed group received 0.1 mg V2O5 m-3 on Mondays, Wednesday and Fridays, with a twice-weekly peak exposure of 1.1 mg V2O5 m-3 on Tuesdays and Thursdays, and was included to investigate the influence of an exposure regimen with peaks on the development of pulmonary hyper-reactivity. The other V2O5-exposed group received a constant daily concentration of 0.5 mg V2O5 m-3. A control group (n = 8) received filtered, conditioned air. Pre-exposure challenges with V2O5 produced a concentration-dependent impairment in pulmonary function, characterized by airway obstructive changes (increased resistance and decreased flow). Analysis of respiratory cells recovered from the lung by bronchoalveolar lavage demonstrated that airway obstruction was accompanied by a significant influx of inflammatory cells into the lung. Subchronic V2O5 inhalation did not produce an increase in V2O5 reactivity in comparison to the control group, and cytological, immunological and skin test results indicate the absence of allergic sensitization. Instead, a trend toward decreased pulmonary reactivity was found following subchronic V2O5 inhalation.(ABSTRACT TRUNCATED AT 250 WORDS)