Genotoxicity of inhaled nanosized TiO(2) in mice.

In vitro studies have suggested that nanosized titanium dioxide (TiO(2)) is genotoxic. The significance of these findings with respect to in vivo effects is unclear, as few in vivo studies on TiO(2) genotoxicity exist. Recently, nanosized TiO(2) administered in drinking water was reported to increase, e.g., micronuclei (MN) in peripheral blood polychromatic erythrocytes (PCEs) and DNA damage in leukocytes. Induction of micronuclei in mouse PCEs was earlier also described for pigment-grade TiO(2) administered intraperitoneally. The apparent systemic genotoxic effects have been suggested to reflect secondary genotoxicity of TiO(2) due to inflammation. However, a recent study suggested that induction of DNA damage in mouse bronchoalveolar lavage (BAL) cells after intratracheal instillation of nanosized or fine TiO(2) is independent of inflammation. We examined here, if inhalation of freshly generated nanosized TiO(2) (74% anatase, 26% brookite; 5 days, 4 h/day) at 0.8, 7.2, and (the highest concentration allowing stable aerosol production) 28.5 mg/m(3) could induce genotoxic effects in C57BL/6J mice locally in the lungs or systematically in peripheral PCEs. DNA damage was assessed by the comet assay in lung epithelial alveolar type II and Clara cells sampled immediately following the exposure. MN were analyzed by acridine orange staining in blood PCEs collected 48 h after the last exposure. A dose-dependent deposition of Ti in lung tissue was seen. Although the highest exposure level produced a clear increase in neutrophils in BAL fluid, indicating an inflammatory effect, no significant effect on the level of DNA damage in lung epithelial cells or micronuclei in PCEs was observed, suggesting no genotoxic effects by the 5-day inhalation exposure to nanosized TiO(2) anatase. Our inhalation exposure resulted in much lower systemic TiO(2) doses than the previous oral and intraperitoneal treatments, and lung epithelial cells probably received considerably less TiO(2) than BAL cells in the earlier intratracheal study.

Urinary hydroxy-metabolites of naphthalene, phenanthrene and pyrene as markers of exposure to diesel exhaust.

OBJECTIVE: The objective of this study was to assess the exposure of bus-garage and waste-collection workers to polycyclic aromatic hydrocarbons (PAHs) derived from diesel exhaust by the measurement of levels of seven urinary PAH metabolites: 2-naphthol, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, 1+9-hydroxyphenanthrene, 4-hydroxyphenanthrene and 1-hydroxypyrene. SUBJECTS AND METHODS: One urine sample from each of 46 control persons, and one pre-shift and two post-shift spot urine samples from 32 exposed workers were obtained in winter and in summer. The metabolites were analysed after enzymatic hydrolysis by high performance liquid chromatography (HPLC) with fluorescence detection. RESULTS: The sum of seven PAH metabolites (mean 3.94 +/- 3.40 and 5.60 +/- 6.37 micromol/mol creatinine in winter and summer, respectively) was higher [P=0.01, degrees of freedom (df) =61.2 and P=0.01, df=67.6 in winter and summer, respectively] in the exposed group than in the control group (mean 3.18 +/- 3.99 and 3.03 +/- 2.01 micromol/mol creatinine in winter and summer, respectively). The mean concentrations of 2-naphthol among exposed and controls ranged between 3.34 and 4.85 micromol/mol creatinine and 2.51 and 2.58 micromol/mol creatinine, respectively (P<0.01 in winter, P<0.03 in summer). The mean level of the hydroxyphenanthrenes in the samples of exposed workers was between 0.40 and 0.70 micromol/mol creatinine and in the control samples 0.40-0.60 micromol/mol creatinine. The concentration of 1-hydroxypyrene was higher among exposed workers in both pre-shift and post-shift samples (mean 0.10-0.15 micromol/mol creatinine) than in control group (mean 0.05-0.06 micromol/mol creatinine) in winter (P=0.002, df=78) and in summer (P<0.001, df=68). CONCLUSIONS: The urinary hydroxy-metabolites of naphthalene, phenanthrene and pyrene showed low exposure to diesel-derived PAHs; however, it was higher in exposed workers than in control group. Urinary PAH monohydroxy-metabolites measured in this study did not correlate with the PAHs in the air samples, reported earlier, in 2002 and 2003.

Exposure of garbage truck drivers and maintenance personnel at a waste handling centre to polycyclic aromatic hydrocarbons derived from diesel exhaust.

Exposure to diesel exhaust was evaluated in summer and winter by measuring vapour and particle phase polycyclic aromatic hydrocarbons (PAHs). Fifteen PAHs were simultaneously determined from the air samples obtained from truck drivers collecting household waste and maintenance personnel at a waste handling centre. The major compounds analysed from the personal air samples of exposed workers were naphthalene, phenanthrene and fluorene. The total PAH exposure (sum of 15 PAHs) of garbage truck drivers ranged from 71 to 2,660 ng m(-3) and from 68 to 900 ng m-3 in the maintenance work. The exposure of garbage truck drivers to benzo[a]pyrene (B[a]P) ranged from the mean of 0.03 to 0.3 ng m(-3) whereas no B[a]P in control samples or in those collected from maintenance workers was detected. A statistically significant difference in diesel-derived PAH exposure between the garbage truck drivers and the control group in both seasons (in summer p = 0.0022, degrees of freedom (df) 70.5; and in winter p < 0.0001, df = 80.4) was observed. Also, a significant difference in PAH exposure between the garbage truck drivers and the maintenance workers (in summer p < 0.0001, df = 50.1; and in winter p < 0.0001, df = 44.2) was obtained.