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January 2017 Abstracts S455

administration as determined by the CES scores. The


P1.01-012 total CES score decreased on average by 4.47, from 45.53
Kava Effects on the Metabolism to 41.06 (p0.053, 95% CI -0.06-9.01). Notably, the
of Tobacco-Specic Carcinogen smoking satisfaction scores decreased by 0.607
4-(Methylnitrosamino)-1-(3-Pyridyl)-1- (p0.024, 95% CI 0.09-1.12).
Butanone (NNK) in Humans Conclusion: This is the rst study investigating the ef-
fect of kava on NNK metabolism in humans and is the
Topic: Tobacco, Radon, Air Pollution, Other Risk rst step to gain a more sophisticated mechanistic un-
Factors derstanding of kavas role in potentially modulating to-
bacco-related lung cancer risk. Short-term kava
Drew Oostra, Naomi Fujioka, Chengguo Xing, administration is safe in healthy adult smokers. Kava
Sreekanth Narayanapillai, Jordan Paladino, holds potential as a possible chemopreventive agent for
Hannah Alves University of Minnesota, Minneapolis/MN/ smokers or tobacco cessation aide.
United States of America
Keywords: Kava, NNK, NNAL, Tobacco smoke
Background: Kava is extracted from the roots of piper
methysticum and is consumed by South Pacic Islanders
as a relaxing beverage. Epidemiologic evidence points to P1.01-013
a protective effect of kava against tobacco-induced lung
Emphysematous Changes and
cancer. NNK is a potent tobacco-specic carcinogen
indisputably linked to lung cancer formation. Kava Pulmonary Function for Asbestos-
reduced NNK-induced lung adenoma formation in the Related Lung Cancer in Japan
A/J mouse model. Data also suggest that enhanced NNAL Topic: Tobacco, Radon, Air Pollution, Other Risk
detoxication may be a potential mechanism by which Factors
kava exerts a chemopreventive effect. In humans, uri-
nary NNAL is a validated biomarker of NNK uptake. We Takumi Kishimoto Asbestos Research Cnter, Okayama
conducted a clinical trial in smokers to assess the effect Rosai Hospital, Okayama/Japan
of kava on NNK metabolism. The primary objective was
to compare urinary total NNAL before and after kava Background: Smoking accelerates the incidence of
administration. Secondary objectives included asbestos-related lung cancer. We evaluated emphyse-
comparing the NNAL-gluc/NNAL-free ratio, determining matous changes by chest CT and pulmonary function for
the safety of kava, and quantifying O6-methylguanine asbestos-related lung cancer in Japan.
adducts. The hypothesis was that kava administration Methods: Two hundred and twenty-two patients of
would result in increased levels of NNAL in the urine asbestos-related lung cancer compensated by Japanese
(and increased NNAL-gluc/NNAL-free ratio), reecting compensation law were evaluated as age, gender,
increased elimination and/or increased detoxication of smoking index, histology, survival, therapy and occupa-
NNK. Additionally, we hypothesized that kava could tional history including rst asbestos exposed age,
reduce O6-methylguanine adducts. asbestos exposing terms and latency from the rst
Methods: We conducted a single-arm, open-label clinical asbestos exposure to lung cancer Radiographic eval-
trial in adult healthy smokers, in which subjects took a uation was done by chest CT using Goddard classica-
commercial kava supplement three times daily for seven tion of emphysema. Pulmonary function test was done
days. Twenty-four hour urine collections were collected by spirometry and ow-volume curve.
at baseline, days 4-5, and days 6-7 of the kava inter- Results: Ages range from 49 to 92 years with a median
vention for NNAL quantication. Blood samples were of 75 years. Male occupied 97.7%. Non-smoker is only
collected at baseline, day 4, and day 7 of the kava 13 patients and other 209 are smokers with Brinkman
intervention for safety monitoring and for DNA adduct Index ranges from 45 to 3000 of a median of 900. For
analysis. Subjects also completed a detailed tobacco histology of lung cancer, 60.4% are adenocarcinoma and
questionnaire, food diary, smoking diary, and cigarette 22.4% of squamous cell carcinoma, 12.6% of small cell
evaluation scale (CES) questionnaire. To date, 17 sub- carcinoma and 1.8 of large cell carcinoma and 2.6% of
jects (goal 18) have completed the study. pleomorphic carcinoma et al. Eighty seven patients were
Results: The results and statistics are being nalized. operated and other 87 patients performed chemo-
Short-term kava administration was safe with no evi- therapy. Best supportive therapy is 34 patients. Median
dence of hepatotoxicity. Subjects experienced less of the survival was 15.8 months. For asbestos histories, median
reinforcing effects of smoking after short-term kava rst exposed age was 23 years, asbestos exposing term
S456 Journal of Thoracic Oncology Vol. 12 No. 1S

was 32 years and the latency of lung cancer was 50 quantied, while with the Condence intervals (CI),
years. For Goddard score of emphysematous changes, the statistical signicance for the error level less 0,05
28% showed 0 point and 33% of 1w4 points and more (p) was deend.
than 21 points occupied only 4%, which means very low Results: According to the investigation results, malig-
percentages of emphysematous changes for these nant disease of two members in one family was found
asbestos-related lung cancer, nonetheless of high per- in 13,5% of the IG, 9,4% of the CG, respectively. Cur-
centages of heavy smokers. For pulmonary function test, rent smokers (CS) with present hereditary factor had
FEV1.0% is 70.5%11.3% and % FEV1.0 is 85.622.2%. almost 4 times (OR3,95; 95% CI, 1,78-8,77), greater
More than half patients are normal pulmonary function risk to become ill compared to the never smokers (NS)
except more than 1,000 of Brinkman index or more than without hereditary factor. The risk was greater when
15 points of Goddard score. From the classication of the same would be compared to the NS with present
GOLD criteria, 54.1% are normal, stage 1 is 20.7%, stage hereditary factor (OR8,76; 95%CI, 1,80-42,68). In the
2 is 22.5 % stage 3 is 1.8% and stage 4 is only 0.9%. diseased, the professional exposition was present in
Conclusion: Almost all of asbestos-related lung cancer 68,6% from IG, versus 67% in the CG. The highest risk
in Japan are heavy smoker, but 61% showed none or low for LC was found in transport workers (OR2,50;95%
grade of emphysematous changes by chest CT and only CI, 1,01-6,15) and automehanics (OR2,31;95%CI,
2.7% had severe pulmonary dysfunction. 0,76-7,07). CS represented 67% of diseased in-
Keywords: Asbestos, smoking, emphysema lung cancer dividuals versus 40,5% of the CG. The risk for them to
develop LC was 5,54 (95%CI, 3,0-10,23), times
signicantly greater compared to the NS. The risk for
the disease was signicantly greater in individuals
P1.01-014
who were smoking >20years (y), >20cigarettes/day
The Role of Hereditary Factor, (c/day), compared to those, who, in the same time
Profession and the Habit of Cigarette period, smoked <20c/day (OR3,78; 95% CI, 2,04-
Smoking in Developing Lung Cancer 7,01). The risk to develop LC in former smokers (FS),
who >20y smoked >20c/day was 2,40 (95% CI,
Topic: Tobacco, Radon, Air Pollution, Other Risk
0,94-6,14), times greater compared to those, who
Factors
smoked >20y, <20c/day.
Irina Pavlovska,1 Nikola Orovcanec,2 Conclusion: This disease developed twice more
Biljana Tausanova,2 Beti Zarova2 1Department of commonly in the examined individuals, exposed to pro-
Epidemiology, Institute of Epidemiology and Biostatistics, fessional carcinogens. The LC is multifactor disease for
Skopje/Macedonia, 2Department of Epidemiology, which development, besides smoking, as a main deter-
Institute of Epidemiology and Biostatistics, Medical minant, in mutual interaction are the genetic and other
Faculty, Skopje/Macedonia factors of the surrounding and the way of living.
Keywords: lung cancer, hereditary factor, cigarette
Background: Lung cancer (LC) is the most common and smoking, occupation
deadliest cancer in the world. In the Republic of
Macedonia, within the period 2002-2012, the LC took the
rst place according to the frequency of appearing in
men, while it was on the fourth place in women. The P1.01-015
number of the risk factors is great being connected with Polyphenols-Rich Fruit Extracts Prevent
the occurrence of LC. The aim of this study was to
Tobacco Specic Nitrosamine-Induced
analyze the role of genetic factor, professional exposure
and the habit of cigarette smoking in occurrence of lung DNA Damage in Lung Epithelial Cells
cancer. Topic: Protective Factors, Risk Reduction,
Methods: The research was conducted as a case-con- Smoking Cessation
trol study. It included 185 patients diseased of LC
(investigated group-IG) and the same number of per- D.I.M. Amararathna,1 D.W. Hoskin,2 M. Johnston,3
sons without malignant disease (control group-CG). In H.P.V. Rupasinghe1 1Environmental Sciences, Dalhousie
the study were included only interviewees with University, Truro/NS/Canada, 2Pathology, Microbiology
pathohistologically conrmed LC. Through calculating and Immunology, and Surgery, Dalhousie University,
the risks of the Odds ratio (OR), the risk-factors, Halifax/NS/Canada, 3Beatrice Hunter Cancer Research
which had a role in occurrence of the disease, were Institute, Halifax/NS/Canada

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