Displaying publications 1 - 20 of 105 in total

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  1. Chean KY, Abdulrahman S, Chan MW, Tan KC
    Int J Occup Environ Med, 2019 10;10(4):203-215.
    PMID: 31586385 DOI: 10.15171/ijoem.2019.1657
    BACKGROUND: Despite its excellent psychometric properties, St George's Respiratory Questionnaire (SGRQ) has not been previously used in measuring respiratory quality of life (RQoL) among traffic police and firefighters who are at risk of poor respiratory health by virtue of their occupations.

    OBJECTIVE: To assess and compare the RQoL of the occupationally exposed (firefighters and traffic police) and the occupationally unexposed populations in Penang, Malaysia.

    METHODS: We recruited male traffic police and firefighters from 5 districts of Penang by convenient sampling during June to September 2018. Participants completed the SGRQ. Scores (symptoms, activity, impacts, total) were derived using a scoring calculator. Higher scores indicate poorer RQoL. Univariate and multivariate linear regression models were fitted to explore the relationship of the independent predictive factors with participants' RQoL.

    RESULTS: We recruited 706 participants---211 firefighters, 198 traffic police, and 297 from general population. Smokers had significantly higher scores than non-smokers in all SGRQ domains. Regardless of smoking status, the "occupationally exposed group" had higher symptoms score than the "occupationally unexposed group," who had higher activity and impact scores. Smoking status, comorbidity status and monthly income were significant independent predictors of SGRQ total score.

    CONCLUSION: In comparison with the general population, firefighters and traffic police reported poorer RQoL; smoking further deteriorated their respiratory health. There is a need to strengthen preventive health measures against occupational disease and smoking cessation among firefighters and traffic police.

    Matched MeSH terms: Smoking/adverse effects
  2. Muhammad Aidil ZA, Hayati K, Rosliza AM
    Med J Malaysia, 2019 02;74(1):62-66.
    PMID: 30846665
    INTRODUCTION: For the last 30 years, tobacco smoking has continued to be the leading cause of premature deaths in Malaysia. Majority of the smokers in Malaysia are at the precontemplation and contemplation stages. Therefore, for the purpose of increasing smoking cessation among this group, the strategies that motivate them to quit smoking have to be reviewed.

    OBJECTIVE: This study aims to evaluate the effectiveness of carbon monoxide measurement feedback and the standard brief motivation adopted to encourage the smoker to quit.

    METHODS: A single-blind, cluster randomised controlled trial was conducted at ten tertiary colleges in Selangor. The study recruited young adult smokers at the precontemplation and contemplation stages. The subjects in the control group received a standard brief motivational strategy. On the other hand, the intervention group received additional carbon monoxide measurement and a motivational feedback module. A follow up was conducted at the first, third and sixth month to measure changes in smoking cessation stage. Subsequently, the secondary outcomes of a mean number of cigarette consumption and quit smoking attempt were analysed. A total of 160 subjects were required to detect the expected difference of 17% in primary outcomes between the groups. This study utilised Generalised Estimating Equations (GEE) to handle the clustering effects.

    CONCLUSION: Biomedical risk assessment feedback mechanism by using carbon monoxide is a promising aid to motivate the smoker to quit. This mechanism is a relatively easy, quick and non-invasive technique. Thus, it can be utilised as a reinforcement relating to the harmful effect of smoking. Besides, it can also increase the smokers' selfefficacy and decisional balance to adopt behavioural changes.

    Matched MeSH terms: Smoking/adverse effects
  3. Hui DS, Ip M, Ling T, Chang SC, Liao CH, Yoo CG, et al.
    Respirology, 2011 Apr;16(3):532-9.
    PMID: 21299688 DOI: 10.1111/j.1440-1843.2011.01943.x
    Antimicrobial resistance is a global problem and the prevalence is high in many Asian countries.
    Matched MeSH terms: Smoking/adverse effects
  4. Haw TJ, Starkey MR, Nair PM, Pavlidis S, Liu G, Nguyen DH, et al.
    Mucosal Immunol, 2016 Jul;9(4):859-72.
    PMID: 26555706 DOI: 10.1038/mi.2015.111
    Chronic obstructive pulmonary disease (COPD) is a life-threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL(+)CD11b(+) monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.
    Matched MeSH terms: Smoking/adverse effects
  5. Razali M, Palmer RM, Coward P, Wilson RF
    Br Dent J, 2005 Apr 23;198(8):495-8; discussion 485.
    PMID: 15849588
    Smoking has been associated with increased risk of periodontitis. The aim of the present study was to compare the periodontal disease severity of adult heavy smokers and never-smokers referred for assessment and treatment of chronic periodontitis.
    Matched MeSH terms: Smoking/adverse effects*
  6. Khajotia R, Somaweera N
    Aust Fam Physician, 2013 Aug;42(8):560-2.
    PMID: 23971064
    Matched MeSH terms: Smoking/adverse effects*
  7. Ngamwong Y, Tangamornsuksan W, Lohitnavy O, Chaiyakunapruk N, Scholfield CN, Reisfeld B, et al.
    PLoS One, 2015;10(8):e0135798.
    PMID: 26274395 DOI: 10.1371/journal.pone.0135798
    Smoking and asbestos exposure are important risks for lung cancer. Several epidemiological studies have linked asbestos exposure and smoking to lung cancer. To reconcile and unify these results, we conducted a systematic review and meta-analysis to provide a quantitative estimate of the increased risk of lung cancer associated with asbestos exposure and cigarette smoking and to classify their interaction. Five electronic databases were searched from inception to May, 2015 for observational studies on lung cancer. All case-control (N = 10) and cohort (N = 7) studies were included in the analysis. We calculated pooled odds ratios (ORs), relative risks (RRs) and 95% confidence intervals (CIs) using a random-effects model for the association of asbestos exposure and smoking with lung cancer. Lung cancer patients who were not exposed to asbestos and non-smoking (A-S-) were compared with; (i) asbestos-exposed and non-smoking (A+S-), (ii) non-exposure to asbestos and smoking (A-S+), and (iii) asbestos-exposed and smoking (A+S+). Our meta-analysis showed a significant difference in risk of developing lung cancer among asbestos exposed and/or smoking workers compared to controls (A-S-), odds ratios for the disease (95% CI) were (i) 1.70 (A+S-, 1.31-2.21), (ii) 5.65; (A-S+, 3.38-9.42), (iii) 8.70 (A+S+, 5.8-13.10). The additive interaction index of synergy was 1.44 (95% CI = 1.26-1.77) and the multiplicative index = 0.91 (95% CI = 0.63-1.30). Corresponding values for cohort studies were 1.11 (95% CI = 1.00-1.28) and 0.51 (95% CI = 0.31-0.85). Our results point to an additive synergism for lung cancer with co-exposure of asbestos and cigarette smoking. Assessments of industrial health risks should take smoking and other airborne health risks when setting occupational asbestos exposure limits.
    Matched MeSH terms: Smoking/adverse effects*
  8. Al-Sadat N, Misau AY, Zarihah Z, Maznah D, Tin Tin Su
    Asia Pac J Public Health, 2010 Jul;22(3 Suppl):175S-180S.
    PMID: 20566551 DOI: 10.1177/1010539510372835
    The use of tobacco by adolescents is a major public health concern worldwide. There are 1.2 billion smokers globally, of which more than 50% are young people. The Southeast Asian countries have about 600 million tobacco smokers within the global burden of tobacco users. Most smokers begin at early stage of life and persist through adulthood. Malaysia alone has about 5 million smokers, 20% of whom are younger than 18 years old. Many factors are implicated in the continuous rising trend of tobacco use among adolescents in Southeast Asia. A triad of family, environmental, and individual factors synergistically acts to motivate adolescents toward smoking. This article discusses the current trends of tobacco use and implications of increasing rise in adolescent smoking in the Southeast Asia region.
    Matched MeSH terms: Smoking/adverse effects
  9. Yarmolinsky J, Relton CL, Lophatananon A, Muir K, Menon U, Gentry-Maharaj A, et al.
    PLoS Med, 2019 Aug;16(8):e1002893.
    PMID: 31390370 DOI: 10.1371/journal.pmed.1002893
    BACKGROUND: Various risk factors have been associated with epithelial ovarian cancer risk in observational epidemiological studies. However, the causal nature of the risk factors reported, and thus their suitability as effective intervention targets, is unclear given the susceptibility of conventional observational designs to residual confounding and reverse causation. Mendelian randomization (MR) uses genetic variants as proxies for risk factors to strengthen causal inference in observational studies. We used MR to evaluate the association of 12 previously reported risk factors (reproductive, anthropometric, clinical, lifestyle, and molecular factors) with risk of invasive epithelial ovarian cancer, invasive epithelial ovarian cancer histotypes, and low malignant potential tumours.

    METHODS AND FINDINGS: Genetic instruments to proxy 12 risk factors were constructed by identifying single nucleotide polymorphisms (SNPs) that were robustly (P < 5 × 10-8) and independently associated with each respective risk factor in previously reported genome-wide association studies. These risk factors included genetic liability to 3 factors (endometriosis, polycystic ovary syndrome, type 2 diabetes) scaled to reflect a 50% higher odds liability to disease. We obtained summary statistics for the association of these SNPs with risk of overall and histotype-specific invasive epithelial ovarian cancer (22,406 cases; 40,941 controls) and low malignant potential tumours (3,103 cases; 40,941 controls) from the Ovarian Cancer Association Consortium (OCAC). The OCAC dataset comprises 63 genotyping project/case-control sets with participants of European ancestry recruited from 14 countries (US, Australia, Belarus, Germany, Belgium, Denmark, Finland, Norway, Canada, Poland, UK, Spain, Netherlands, and Sweden). SNPs were combined into multi-allelic inverse-variance-weighted fixed or random effects models to generate effect estimates and 95% confidence intervals (CIs). Three complementary sensitivity analyses were performed to examine violations of MR assumptions: MR-Egger regression and weighted median and mode estimators. A Bonferroni-corrected P value threshold was used to establish strong evidence (P < 0.0042) and suggestive evidence (0.0042 < P < 0.05) for associations. In MR analyses, there was strong or suggestive evidence that 2 of the 12 risk factors were associated with invasive epithelial ovarian cancer and 8 of the 12 were associated with 1 or more invasive epithelial ovarian cancer histotypes. There was strong evidence that genetic liability to endometriosis was associated with an increased risk of invasive epithelial ovarian cancer (odds ratio [OR] per 50% higher odds liability: 1.10, 95% CI 1.06-1.15; P = 6.94 × 10-7) and suggestive evidence that lifetime smoking exposure was associated with an increased risk of invasive epithelial ovarian cancer (OR per unit increase in smoking score: 1.36, 95% CI 1.04-1.78; P = 0.02). In analyses examining histotypes and low malignant potential tumours, the strongest associations found were between height and clear cell carcinoma (OR per SD increase: 1.36, 95% CI 1.15-1.61; P = 0.0003); age at natural menopause and endometrioid carcinoma (OR per year later onset: 1.09, 95% CI 1.02-1.16; P = 0.007); and genetic liability to polycystic ovary syndrome and endometrioid carcinoma (OR per 50% higher odds liability: 0.89, 95% CI 0.82-0.96; P = 0.002). There was little evidence for an association of genetic liability to type 2 diabetes, parity, or circulating levels of 25-hydroxyvitamin D and sex hormone binding globulin with ovarian cancer or its subtypes. The primary limitations of this analysis include the modest statistical power for analyses of risk factors in relation to some less common ovarian cancer histotypes (low grade serous, mucinous, and clear cell carcinomas), the inability to directly examine the association of some ovarian cancer risk factors that did not have robust genetic variants available to serve as proxies (e.g., oral contraceptive use, hormone replacement therapy), and the assumption of linear relationships between risk factors and ovarian cancer risk.

    CONCLUSIONS: Our comprehensive examination of possible aetiological drivers of ovarian carcinogenesis using germline genetic variants to proxy risk factors supports a role for few of these factors in invasive epithelial ovarian cancer overall and suggests distinct aetiologies across histotypes. The identification of novel risk factors remains an important priority for the prevention of epithelial ovarian cancer.

    Matched MeSH terms: Smoking/adverse effects
  10. Zain RB, Razak IA
    Community Dent Oral Epidemiol, 1989 Jun;17(3):148-9.
    PMID: 2786793
    The association between cigarette smoking and the prevalence of oral mucosal lesions was examined in 495 Malaysian army personnel. No associations between cigarette smoking and recurrent aphthous ulcerations, pre-leukoplakia and frictional keratosis could be obtained in this study. Positive associations were found between cigarette smoking and leukoedema as well as denture stomatitis. There was a negative association between cigarette smoking and the presence of coated tongue.
    Matched MeSH terms: Smoking/adverse effects
  11. Wickramatilake CM, Mohideen MR, Pathirana C
    Ann Endocrinol (Paris), 2015 Jul;76(3):260-3.
    PMID: 26142486 DOI: 10.1016/j.ando.2015.04.008
    OBJECTIVE: There is limited data on the assessment of relationship between sex hormones, metabolic syndrome (MS) and inflammation. Therefore, our objective was to examine the relationship between metabolic syndrome, testosterone and inflammation.
    PATIENTS AND METHODS: It was a cross-sectional study which included 309 subjects in the age range of 30-70years. Blood was analyzed for plasma glucose, serum lipids, total testosterone (TT) and high-sensitivity C-reactive protein (hs-CRP).
    RESULTS: There were 153 patients with metabolic syndrome and 156 without MS according to modified NCEP guidelines. Age, BMI, obesity, dyslipidaemia, smoking (OR=2.35, CI=1.35-4.09), LDL-Ch, low TT (OR=0.76, CI=0.38-1.52) and elevated hs-CRP (OR=1.56, CI=0.87-2.80) were significant independent predictors of MS (all P<0.05).
    CONCLUSIONS: The low testosterone and high hs-CRP levels are independent predictors of metabolic syndrome.
    KEYWORDS: Hommes; Inflammation; Men; Metabolic syndrome; Syndrome métabolique; Testosterone; Testostérone
    Matched MeSH terms: Smoking/adverse effects
  12. Chean KY, Goh LG, Liew KW, Tan CC, Choi XL, Tan KC, et al.
    BMJ Open, 2019 07 09;9(7):e025491.
    PMID: 31289057 DOI: 10.1136/bmjopen-2018-025491
    OBJECTIVES: This qualitative study aims to construct a model of the barriers to smoking cessation in the primary care setting.

    DESIGN: Individual in-depth, semistructured interviews were audio-taped, then verbatim transcribed and translated when necessary. The data were first independently coded and then collectively discussed for emergent themes using the Straussian grounded theory method.

    PARTICIPANTS AND SETTING: Fifty-seven current smokers were recruited from a previous smoking related study carried out in a primary care setting in Malaysia. Current smokers with at least one failed quit attempts were included.

    RESULTS: A five-theme model emerged from this grounded theory method. (1) Personal and lifestyle factors: participants were unable to resist the temptation to smoke; (2) Nicotine addiction: withdrawal symptoms could not be overcome; (3) Social cultural norms: participants identified accepting cigarettes from friends as a token of friendship to be problematic; (4) Misconception: perception among smokers that ability to quit was solely based on one's ability to achieve mind control, and perception that stopping smoking will harm the body and (5) Failed assisted smoking cessation: smoking cessation services were not felt to be user-friendly and were poorly understood. The themes were organised into five concentric circles based on time frame: those actionable in the short term (themes 1 and 2) and the long term (themes 3, 4, 5).

    CONCLUSIONS: Five themes of specific beliefs and practices prevented smokers from quitting. Clinicians need to work on these barriers, which can be guided by the recommended time frames to help patients to succeed in smoking cessation.

    Matched MeSH terms: Smoking/adverse effects*
  13. Hermizi H, Faizah O, Ima-Nirwana S, Ahmad Nazrun S, Norazlina M
    Calcif. Tissue Int., 2009 Jan;84(1):65-74.
    PMID: 19020790 DOI: 10.1007/s00223-008-9190-x
    This study was conducted to determine the effectiveness of three forms of vitamin E supplements following nicotine treatment on bone histomorphometric parameters in an adult male rat model. Rats were divided into seven groups: baseline (B, killed without treatment), control (C, normal saline for 4 months), nicotine (N, nicotine for 2 months), nicotine cessation (NC), tocotrienol-enhanced fraction (TEF), gamma-tocotrienol (GTT), and alpha-tocopherol (ATF). Treatments for the NC, TEF, GTT, and ATF groups were performed in two phases. For the first 2 months they were given nicotine (7 mg/kg), and for the following 2 months nicotine administration was stopped and treatments with respective vitamin E preparations (60 mg/kg) were commenced except for the NC group, which was allowed to recover without treatment. Rats in the N and NC groups had lower trabecular bone volume, mineral appositional rate (MAR), and bone formation rate (BFR/BS) and higher single labeled surface and osteoclast surface compared to the C group. Vitamin E treatment reversed these nicotine effects. Both the TEF and GTT groups, but not the ATF group, had a significantly higher trabecular thickness but lower eroded surface (ES/BS) than the C group. The tocotrienol-treated groups had lower ES/BS than the ATF group. The GTT group showed a significantly higher MAR and BFR/BS than the TEF and ATF groups. In conclusion, nicotine induced significant bone loss, while vitamin E supplements not only reversed the effects but also stimulated bone formation significantly above baseline values. Tocotrienol was shown to be slightly superior compared to tocopherol. Thus, vitamin E, especially GTT, may have therapeutic potential to repair bone damage caused by chronic smoking.
    Matched MeSH terms: Smoking/adverse effects
  14. Neo KS, Goh KT, Sam CT
    PMID: 11127329
    A survey was conducted between 1995 and 1997 to assess the impact of introduction of unleaded petrol and other public health measures on the blood lead level of the population. The geometric mean blood lead level of 269 government employees as determined by graphite furnace atomic absorption spectroscopy, was 66.0 microg/l, much lower than that recorded before introduction of lead-free petrol. Using multiple regression analysis, factors significantly associated with blood lead levels were: exposure to traffic, age (>50 years) and active smoking. Passive smoking, exposure to recent paint work, consumption of alcohol and traditional medicine were found not to be significantly associated with the blood lead level.
    Matched MeSH terms: Smoking/adverse effects*
  15. Rampal L
    Med J Malaysia, 2020 05;75(3):95-97.
    PMID: 32467531
    No abstract provided.
    Matched MeSH terms: Smoking/adverse effects
  16. Hughes K, Yeo PP, Lun KC, Thai AC, Sothy SP, Wang KW, et al.
    J Epidemiol Community Health, 1990 Mar;44(1):29-35.
    PMID: 2348145 DOI: 10.1136/jech.44.1.29
    STUDY OBJECTIVE: The aim of the study was to examine cardiovascular risk factors to see how these might explain differences in cardiovascular disease mortality among Chinese, Malays, and Indians in the Republic of Singapore.
    DESIGN: The study was a population based cross sectional survey. Stratified systematic sampling of census districts, reticulated units, and houses was used. The proportions of Malay and Indian households were increased to improve statistical efficiency, since about 75% of the population is Chinese.
    SETTING: Subjects were recruited from all parts of the Republic of Singapore.
    SUBJECTS: 2143 subjects aged 18 to 69 years were recruited (representing 60.3% of persons approached). There were no differences in response rate between the sexes and ethnic groups.
    MEASUREMENTS AND MAIN RESULTS: Data on cardiovascular risk factors were collected by questionnaire. Measurements were made of blood pressure, serum cholesterol, low and high density lipoprotein cholesterol, fasting triglycerides and plasma glucose. In males the age adjusted cigarette smoking rate was higher in Malays (53.3%) than in Chinese (37.4%) or Indians (44.5%). In both sexes, Malays had higher age adjusted mean systolic blood pressure: males 124.6 mm Hg v 121.2 mm Hg (Chinese) and 121.2 mm Hg (Indians); females 122.8 mm Hg v 117.3 mm Hg (Chinese) and 118.4 mm Hg (Indians). Serum cholesterol, low density lipoprotein cholesterol and triglyceride showed no ethnic differences. Mean high density lipoprotein cholesterol in males (age adjusted) was lower in Indians (0.69 mmol/litre) than in Chinese (0.87 mmol/litre) and Malays (0.82 mmol/litre); in females the mean value of 0.95 mmol/litre in Indians was lower than in Chinese (1.05 mmol/litre) and Malays (1.03 mmol/litre). Rank prevalence of diabetes for males was Indians (highest), Malays and then Chinese; for females it was Malays, Indians, Chinese.
    CONCLUSIONS: The higher mortality from ischaemic heart disease found in Indians in Singapore cannot be explained by the major risk factors of cigarette smoking, blood pressure and serum cholesterol; lower high density lipoprotein cholesterol and higher rates of diabetes may be part of the explanation. The higher systolic blood pressures in Malays may explain their higher hypertensive disease mortality.
    Matched MeSH terms: Smoking/adverse effects
  17. Quek DK, Lim LY, Ong SB
    Med J Malaysia, 1989 Sep;44(3):210-23.
    PMID: 2626136
    In a prospective case-control study over a two-year period involving 1006 women, 264 women with acute myocardial infarction (AMI), 305 with non-infarct acute coronary syndromes (CAD) were compared with 437 women with no coronary heart disease (Controls), to determine the relationship between cigarette smoking and other risks factors with coronary heart disease. A history of current cigarette smoking was strongly associated with the risk of coronary events for both AMI And CAD (p less than 0.001). 23.9% of patients with acute coronary syndromes were current smokers, compared with only 12.8% among controls. Overall, women smokers had about a two-fold increase in risk for all coronary events. Younger women smokers (less than 40 years) and those between 61-70 years had particularly higher risks (10.3 and 2.7 times respectively (p less than 0.01, p less than 0.02). A dose-response pattern of increased AMI risks (from 2.0 to 2.9 times) among women smokers was also found, corresponding to the number of cigarettes smoked per day (p less than 0.05). Other significant coronary risk factors established were: postmenopausal status (OR 6.5), diabetes mellitus (OR 5.1), hypertension (OR 1.6), family history of premature coronary heart disease less than 50 years (OR 1.3) and use of oral contraceptive pills (OR 1.4). Our results thus emphasize that cigarette smoking is an important determinant of acute coronary events even among Malaysian women.
    Matched MeSH terms: Smoking/adverse effects*
  18. van Roekel EH, Trijsburg L, Assi N, Carayol M, Achaintre D, Murphy N, et al.
    Nutrients, 2018 May 22;10(5).
    PMID: 29789452 DOI: 10.3390/nu10050654
    Identifying the metabolites associated with alcohol consumption may provide insights into the metabolic pathways through which alcohol may affect human health. We studied associations of alcohol consumption with circulating concentrations of 123 metabolites among 2974 healthy participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Alcohol consumption at recruitment was self-reported through dietary questionnaires. Metabolite concentrations were measured by tandem mass spectrometry (BIOCRATES AbsoluteIDQTM p180 kit). Data were randomly divided into discovery (2/3) and replication (1/3) sets. Multivariable linear regression models were used to evaluate confounder-adjusted associations of alcohol consumption with metabolite concentrations. Metabolites significantly related to alcohol intake in the discovery set (FDR q-value < 0.05) were further tested in the replication set (Bonferroni-corrected p-value < 0.05). Of the 72 metabolites significantly related to alcohol intake in the discovery set, 34 were also significant in the replication analysis, including three acylcarnitines, the amino acid citrulline, four lysophosphatidylcholines, 13 diacylphosphatidylcholines, seven acyl-alkylphosphatidylcholines, and six sphingomyelins. Our results confirmed earlier findings that alcohol consumption was associated with several lipid metabolites, and possibly also with specific acylcarnitines and amino acids. This provides further leads for future research studies aiming at elucidating the mechanisms underlying the effects of alcohol in relation to morbid conditions.
    Matched MeSH terms: Smoking/adverse effects
  19. Karen-Ng LP, Marhazlinda J, Rahman ZA, Yang YH, Jalil N, Cheong SC, et al.
    Asian Pac J Cancer Prev, 2011;12(5):1161-6.
    PMID: 21875259
    Dietary isothiocyanates (ITCs) found in cruciferous vegetables (Brassica spp.) has been reported to reduce cancer risk by inducing phase II conjugating enzymes, in particular glutathione S-transferases (GSTs). This case-control study was aimed at determining associations between dietary ITCs, GSTs polymorphisms and risk habits (cigarette smoking, alcohol drinking and betel-quid chewing) with oral cancer in 115 cases and 116 controls. Information on dietary ITC intake from cruciferous vegetables was collected via a semi-quantitative food frequency questionnaire (FFQ). Peripheral blood lymphocytes were obtained for genotyping of GSTM1, GSTT1 and GSTP1 using PCR multiplex and PCR-RFLP. Chi-square and logistic regression were performed to determine the association of ITC and GSTs polymorphism and risk of oral cancer. When dietary ITC was categorized into high (greater than/equal to median) and low (less than median) intake, there was no significant difference between cases and control group. Logistic regression yielding odd ratios resulted in no significant association between dietary ITC intake, GSTM1, GSTT1 or GSTP1 genotypes with oral cancer risk overall. However, GSTP1 wild-type genotype was associated with later disease onset in women above 55 years of age (p= 0.017). Among the men above 45 years of age, there was clinical significant difference of 17 years in the age of onset of oral cancer between GSTP1 wild-type + low ITC intake and GSTP1 polymorphism + high ITC intake (p= 0.001). Similar conditions were also seen among men above 45 years of age with risk habits like drinking and chewing as the earlier disease onset associated with GSTP1 polymorphism and high ITC intake (p< 0.001). This study suggests that combination effects between dietary ITCs, GSTP1 polymorphism and risk habits may be associated with the risk of oral cancer and modulate the age of disease onset.
    Matched MeSH terms: Smoking/adverse effects
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