Toxicology and Industrial Health

Lowney, Yvette W ;Ruby, Michael V ;Wester, Ronald C ;Schoof, Rosalind A ;Holm, Stewart E ;Hui, Xiao-Ying ;Barbadillo, Sherry ;Maibach, Howard I

doi: 10.1191/0748233705th205oapmid: 15986571

Current knowledge of percutaneous absorption of arsenic is based on studies of rhesus monkeys using soluble arsenic in aqueous solution, and soluble arsenic mixed with soil (Wester et al., 1993). These studies produced mean dermal absorption rates in the range of 2.0-6.4% of the applied dose. Subsequently, questions arose as to whether these results represent arsenic absorption from environmental media. Factors such as chemical interactions, the presence of other metals, and the effects of weathering on environmental media all can affect the nature of arsenic and its potential for percutaneous absorption. Therefore, research specific to more relevant matrices is important. The focus of this effort is to outline study design considerations, including particle size, application rates, means of ensuring skin contact and appropriate statistical evaluation of the data. Appropriate reference groups are also important. The potential for background exposure to arsenic in the diet possibly obscuring a signal from a dermally applied dose of arsenic will also be addressed. We conclude that there are likely to be many site-or sample-specific factors that will control the absorption of arsenic, and matrix-specific analyses may be required to understand the degree of percutaneous absorption.

Lee, Jin Heon ;Kang, Hee Sook ;Han, Don-Hee

doi: 10.1191/0748233705th210oapmid: 15986572

1,3-Butadiene (BD) is a known rodent and probable human carcinogen (IARC, group 2A) or ‘known to be a human carcinogen’ (Department of Health and Human Services, 2000). Exposure to BD can occur either via petrochemical products or through the general environment. Adducts can be used as biomarkers for biological monitoring of carcinogen exposure. This study investigated the hemoglobin adducts in blood after inhalation exposure to BD in ICR female mice for three weeks (5 h/day-5 days/week). During the inhalation exposure, the body weights of mice were significantly lower from day 9 onward for the 500 ppm BD group and from day 4 onward for the 1000 ppm BD group. On the 1st, 2nd and 3rd weeks after inhalation exposure, the concentrations of HB Val adducts were 1.8, 3.7 and 6.2 pmol/mg globin for the 500 ppm BD group, and 5.7, 7.4 and 16.0 pmol/mg globin for the 1000 ppm BD group. The concentrations of THB Val adducts were 32.0, 42.0 and 55.0 pmol/mg globin for the 500 ppm BD group, and 67.8, 72.7 and 83.5 pmol/mg globin for the 1000 ppm BD group. Their defined ratios were higher at the earlier exposure period and at the lower concentration. They were 17.8, 11.4 and 8.87 for the 500 ppm BD group, and 11.9, 9.8 and 5.2 for the 1000 ppm BD group, on the 1st, 2nd and 3rd weeks after inhalation exposure. THB Val and HB Val adducts appear to be the important hemoglobin adducts for monitoring BD exposure, with the latter being a more predictable biomarker than the former.

Ozguner, Fehmi ;Koyu, Ahmet ;Cesur, Gokhan

doi: 10.1191/0748233705th211oapmid: 15986573

Oxidative effects via free radical generation in smokers have been widely investigated. They cause lipid peroxidation, oxidation of proteins and damage to mainly lung and other tissues. In humans, antioxidative capacity of serum is related to antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and melatonin. The effect of cigarette smoking on plasma levels of melatonin and antioxidant enzymes has not been established together yet. Also, it may not be clear if melatonin levels are affected by smoking and melatonin has a protective effect on cigarette smoking-induced free radical damage. The aim of this study is to investigate the relationship between smoking and antioxidant capacity including melatonin, a powerful endogenous antioxidant, and antioxidant enzymes in teenage girls who are active smokers. Additionally, malondialdehyde (MDA) levels were determined in those who have smoked at least one packet a day for three or more years. MDA levels have been used as a convenient index of the lipid peroxidation-related oxidative damage of tissues. Twenty-one young female active smokers who study at the School of Nursing and 21 nonsmoking students (as controls) at the same school were included in the study. The activities of two principal antioxidant enzymes SOD, GSH-Px and plasma levels of MDA were significantly increased but melatonin content of the blood was significantly decreased as compared to nonsmokers. In spite of an increase in antioxidant enzyme activities, MDA levels were slightly increased in smokers. This indicates that antioxidant self-defence mechanisms may not sufficiently protect the respiratory system from smoke-mediated oxidative injury. This result may be related to low melatonin levels in teenage female smokers. It seems that melatonin can reduce free radical damage to the respiratory system induced by cigarette smoke. Further experimental investigations with exogenous melatonin treatments will be needed.

Koyu, Ahmet ;Ozguner, Fehmi ;Cesur, Gokhan ;Gokalp, Osman ;Mollaoglu, Hakan ;Caliskan, Sadettin ;Delibas, Namik

doi: 10.1191/0748233705th212oapmid: 15986574

In this study, the effects of exposure to a 900 MHz and 1800 MHz electromagnetic field (EMF) on serum nocturnal melatonin levels of adult male Sprague-Dawley rats were studied. Thirty rats were used in three independent groups, 10 of which were exposed to 900 MHz, 10 of which were exposed to 1800 MHz and 10 of which were sham-exposed (control). The exposures were performed 30 min/day, for five days/week for four weeks to 900 MHz or 1800 MHz EMF. Control animals were kept under the same environmental conditions as the study groups except with no EMF exposure. The concentration of nocturnal melatonin in the rat serum was measured by using a radioimmunoassay method. There were no statistically significant differences in serum melatonin concentrations between the 900 MHz EMF group and the sham-exposed group (P-0.05). The values at 12:00 pm were 39.119 / 6.5 pg/mL in the sham-exposed group and 34.979 / 5.1 pg/mL in the 900 MHz EMF-exposed group. Also, there were no statistically significant differences in serum melatonin concentrations between the sham-exposed group and the 1800 MHz EMF-exposed group (P-0.05). The values at 12:00 pm were 39.119 / 6.5 pg/mL in the sham-exposed group and 37.969 / 7.4 pg/mL in the exposed group. These results indicate that mobile phones, emitting 900 and 1800 MHz EMF, have no effect on nocturnal serum melatonin levels in rats.

Lemazurier, Emmanuel ;Lecomte, Anthony ;Robidel, Franck ;Bois, Frédéric Y

doi: 10.1191/0748233705th213oapmid: 15986575

Propylene glycol monomethyl ether (PGME) is widely used as a solvent in numerous commercial products. Its chemical synthesis leads to the formation of two isomers: a and b, the latter being usually present in the range of 0.5-1.5%. Isomer α has been shown to be of low toxicity. Isomer β raises concerns as to its reproductive and developmental effects. We evaluated the reproductive and developmental toxicity of two different commercial mixes of PGME (Mix A: 99% isomer α and 0.5% isomer β, Mix B: 98.5% isomer α and 1.5% isomer β) on Sprague-Dawley rats. The use of two mixes allowed us to differentiate between isomer α and isomer β effects. Male and female rats were exposed through drinking water to mixes A or B during a gametogenesis cycle (64 days for males and 15 days for females) to 0, 2, 5, 10 and 15% (v/v) of each mix. These animals (F0) and the three following generations (F1, F2 and F3) were followed. We observed a statistically significant decrease in the number of pups in isomer α-treated animals of generation F1 and a nondose-related variation of the sex ratio in F1 and F2 generations after PGME mix B treatment. The most important effect observed was a decrease in testicular and epididymal sperm counts in relation to PGME isomer β in acute daily exposure, on the first parental generation. The effect evidenced on sex ratio needs further work in order to assay the potential persistent effects of PGME exposure.