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pstcwpwVru2oOtin summer. On the other hand, in nonSS type room, eight volunteersall showed some symptoms. As the result, we insist that it is possibleto create healthy school.

doi:10.1016/j.toxlet.2009.06.615

Abstracts / Toxicology L

44tudies of pre- or post-supplementation of Mentha piperitaeaves extract on arsenic induced hepatic injuries in mice

mbika Sharma ∗, Mukesh Kumar Sharma, Madhu Kumar

Zoology Department, University of Rajasthan, Jaipur, India

ethods: Health hazards caused by the one of the most toxic metalarsenic” in drinking water have become a great concern to theillions of people. Exposure to arsenic occurs mostly in the work-

lace, near hazardous waste sites and in areas with unusually highatural levels of arsenic in rocks. Liver toxicity and hepatocellulararcinoma are major health concerns in area of arsenic poison-ng. Our earlier studies showed that Mentha piperita is a promising

etalloprotective antioxidant that ameliorates the arsenic inducedepatotoxicity. In the present investigation we have evaluated Men-ha (1 g/kg b.wt. DDW, orally) pre (up to 10 days before arsenic) andost (up to 30 days after arsenic) efficacies in preventing the oxida-ive damages induced by arsenic (4 mg/kg b.wt. in 0.9% NaCl; i.p. atnce only) in Swiss albino mice.

Results: Pre-treatment Mentha showed protection on earlyutopsy intervals in terms of increase in body weight, liver weight,epatic LDH and serum alkaline phosphatase activities along-withecreased hepatic LPO, ACP, ALP, SGOT and SGPT activities. Liveristopathology also showed earlier sign of reparation with nor-al hepatocytes as compared to hepatocytoplasmic vacuolization,

egranulation and various nuclear changes in arsenic intoxicatednimals. Post-supplementation of Mentha showed protection onate autopsy intervals both in terms of biochemical and histopathol-ical alterations.

Conclusion: These studies strongly support that Mentha piperitaombating arsenic induced hepatotoxicity.

oi:10.1016/j.toxlet.2009.06.613

45olycyclic aromatic hydrocarbons in consumer products—etabolism and toxicity in human skin

ristin Stolpmann 1,∗, Frank Henkler 1, Christoph Hutzler 1,himant Desai 2, Shantu Amin 2, Andreas Luch 1

Federal Institute for Risk Assessment (BfR), Department of Productafety, Berlin, Germany, 2 Penn State Milton S. Hershey Medicalenter, Department of Pharmacology, Hershey, United States

olycyclic aromatic hydrocarbons (PAHs) require enzymatic con-ersion into electrophilic metabolites to exert genotoxic effects.AHs are present in coal tar and industrial exhaust fumes. Humanxposure to these ubiquitous environmental carcinogens occursainly by dietary uptake or via inhalation. However, PAHs con-

titute also a serious health hazard as contaminants in certainonsumer products, e.g. hammer grips. Although little is knownbout metabolism and toxicity of PAHs in human skin, the der-al route requires consideration in the overall risk assessment of

hese compounds. Such data are crucial for proficient risk evalu-tion, in particular for those PAHs (e.g. benzo[a]pyrene, BaP) thatave proven strong genotoxicity in certain bioassays.

One aim of this study was to determine cytochrome P450

nzyme (CYP) induction and the pattern of metabolic productsormed from BaP in human keratinocytes. Since recent publica-ions suggest that PAHs can affect inflammation responses, welso addressed PAH-mediated regulation of apoptotic and proin-

189S (2009) S57–S273 S203

ammatory pathways. Primary human keratinocytes and cell linesere exposed to BaP and the major metabolites were identified

nd quantified by means of LC-MS. Western blot analyses anduantitative real-time PCR confirmed BaP-triggered upregulationf CYP1A1 and 1B1, both of which are central in catalyzing BaPctivation. We further identified various BaP intermediates andharacterized alternate routes of metabolism likely to be affectedy inflammatory stimuli. Enhanced expression of proapoptotic andnflammatory receptors such as Fas, tumor necrosis factor receptorTNFR)-1 and TNFR-2 was also found in keratinocytes upon expo-ure to BaP. The molecular pattern and functional implications ofhe induction of these pathways by PAHs warrants further clarifi-ation.

oi:10.1016/j.toxlet.2009.06.614

46suggestion of “Healthy School” with low volatile organic com-ounds (VOCs)

asamich Hanazato 1,∗, Emiko Todaka 1, Hiroko Nakaoka 1,iroshi Seto 1,2, Chisato Mori 1,3

Chiba University, Chiba, Kashiwa, Japan, 2 Tokyo Kenbikyoinoundation, Tachikawa, Japan, 3 Chiba University, Department ofioenvironmental Medicine, Chiba, Japan

t has been a critical issue to improve indoor air quality of schoolnvironment for children’s health. In Japan, Sick School SyndromeSS), which school students become sick because of volatile organicompounds (VOCs) indoor air of school building, has been a bigroblem. It is urgently necessary to create healthy school buildingo that students do not diagnose SS.

The cause of SS is VOCs from interior materials such as wallaper, ceiling materials, adhesive and furniture. We built a two-tory reinforced concrete (RC) building with selected materials sohat the VOCs indoor air becomes as low as possible. The room’seiling, wall paper and floor are all polyvinyl chloride (PVC) sheetshich are produced with special care to avoid contamination in therocess of manufacture. Twenty tables and 60 chairs in the roomere manufactured with the special care not to emit VOCs. 116OCs indoor air has been analyzed and calculated five times fromight after the completion of the construction in November 2007ntil October 2008. The total VOCs were 73 �g/m3 in November007, 46 �g/m3 in January 2008 notwithstanding the introductionf furniture, 60 �g/m3 in May, 259 �g/m3 in July and 94 �g/m3 inctober. Seven healthy volunteers evaluated the room and five of

hem showed no symptoms, two of them showed some symptoms