Displaying publications 1 - 20 of 104 in total

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  1. Aminuddin A, Cheong SS, Roos NAC, Ugusman A
    Int J Med Sci, 2023;20(4):482-492.
    PMID: 37057211 DOI: 10.7150/ijms.79889
    Smoking is a risk factor of acute coronary syndrome (ACS) that could increase matrix metalloproteinases (MMPs) levels, leading to unstable coronary artery plaque. The current review aimed to identify the relationship between smoking and MMPs in patients with ACS. Literature search was conducted from inception until March 2022 in three online databases. Risk of bias was assessed using the Newcastle-Ottawa Scale. A meta-analysis was performed, and the odds ratio (OR) together with its 95% confidence interval (CI) were determined. A total of 7,843 articles were identified, and only seven studies were included. Four studies investigated the MMP-3 and MMP-9 related genes and found that smokers with certain MMPs genotypes had high risk of ACS. Smoking also increased the MMPs level in patients with ACS compared with non-smokers. Additionally, a meta-analysis of two studies resulted in an increased odd of ACS in smokers with MMP-3 5A allele versus non-smokers with MMP-3 6A6A allele (OR: 15.94, 95% CI: 10.63-23.92; I2 =55%). In conclusion, the current review highlights the role of MMPs in relation to smoking and ACS. The determination of these roles may help in identifying new ACS markers among smokers and the development of drug-targeted treatment.
    Matched MeSH terms: Smoking/adverse effects
  2. Salari N, Hasheminezhad R, Abdolmaleki A, Kiaei A, Shohaimi S, Akbari H, et al.
    Arch Womens Ment Health, 2022 Dec;25(6):1021-1027.
    PMID: 36445469 DOI: 10.1007/s00737-022-01281-1
    The increased number of female smokers is considered a global health challenge in recent years. One of the detrimental effects of smoking is sexual hormone fluctuation causing female sexual dysfunction (FSD). This systematic review and meta-analysis aimed to investigate the effects of smoking leading to FSD. Electronic databases (PubMed, Scopus, Web of Science, Embase, Science Direct, and Google Scholar) were hired for systematic searching. Until June 2022, whole qualified studies reporting the consequences of smoking on FSD were gathered for data analysis based on the random effects model (CMA software, v.2). Study heterogeneity and publication bias were also assessed using I2 index and Egger test, respectively. Ten eligible studies with a sample size of 15,334 female smokers (18-79 years) were selected. Following data analysis, the odds ratio representing the effects of smoking on FSD was found 1.48 (95%CI: 1.2-1.83), indicating that female smokers were 48% more susceptible to FSD than non-smokers. Also, the publication bias was reported as non-significant (p = 0.178). Since smoking is an increasingly common phenomenon in females and women smokers are 48% more susceptible to the FSD, preparation of necessary health measures by the health policymakers to reduce the number of female smokers and subsequent health services seems necessary.
    Matched MeSH terms: Smoking/adverse effects
  3. GBD 2019 Cancer Risk Factors Collaborators
    Lancet, 2022 Aug 20;400(10352):563-591.
    PMID: 35988567 DOI: 10.1016/S0140-6736(22)01438-6
    BACKGROUND: Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally.

    METHODS: The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented.

    FINDINGS: Globally, in 2019, the risk factors included in this analysis accounted for 4·45 million (95% uncertainty interval 4·01-4·94) deaths and 105 million (95·0-116) DALYs for both sexes combined, representing 44·4% (41·3-48·4) of all cancer deaths and 42·0% (39·1-45·6) of all DALYs. There were 2·88 million (2·60-3·18) risk-attributable cancer deaths in males (50·6% [47·8-54·1] of all male cancer deaths) and 1·58 million (1·36-1·84) risk-attributable cancer deaths in females (36·3% [32·5-41·3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20·4% (12·6-28·4) and DALYs by 16·8% (8·8-25·0), with the greatest percentage increase in metabolic risks (34·7% [27·9-42·8] and 33·3% [25·8-42·0]).

    INTERPRETATION: The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden.

    FUNDING: Bill & Melinda Gates Foundation.

    Matched MeSH terms: Smoking/adverse effects
  4. Smith J, Togawa K, Dresler C, Hawari F, Zain ZM, Stewart B, et al.
    Cancer Epidemiol, 2022 Aug;79:102210.
    PMID: 35785684 DOI: 10.1016/j.canep.2022.102210
    Matched MeSH terms: Smoking/adverse effects
  5. El Tantawi M, Sabbagh HJ, Alkhateeb NA, Quritum M, Abourdan J, Qureshi N, et al.
    PeerJ, 2022;10:e13555.
    PMID: 35860046 DOI: 10.7717/peerj.13555
    BACKGROUND: Oral manifestations and lesions could adversely impact the quality of people's lives. COVID-19 infection may interact with smoking and the impact on oral manifestations is yet to be discovered.

    OBJECTIVES: The aim of this study was to assess the self-reported presence of oral lesions by COVID-19-infected young adults and the differences in the association between oral lesions and COVID-19 infection in smokers and non-smokers.

    METHODS: This cross-sectional multi-country study recruited 18-to-23-year-old adults. A validated questionnaire was used to collect data on COVID-19-infection status, smoking and the presence of oral lesions (dry mouth, change in taste, and others) using an online platform. Multi-level logistic regression was used to assess the associations between the oral lesions and COVID-19 infection; the modifying effect of smoking on the associations.

    RESULTS: Data was available from 5,342 respondents from 43 countries. Of these, 8.1% reported COVID-19-infection, 42.7% had oral manifestations and 12.3% were smokers. A significantly greater percentage of participants with COVID-19-infection reported dry mouth and change in taste than non-infected participants. Dry mouth (AOR=, 9=xxx) and changed taste (AOR=, 9=xxx) were associated with COVID-19- infection. The association between COVID-19-infection and dry mouth was stronger among smokers than non-smokers (AOR = 1.26 and 1.03, p = 0.09) while the association with change in taste was stronger among non-smokers (AOR = 1.22 and 1.13, p = 0.86).

    CONCLUSION: Dry mouth and changed taste may be used as an indicator for COVID-19 infection in low COVID-19-testing environments. Smoking may modify the association between some oral lesions and COVID-19-infection.

    Matched MeSH terms: Smoking/adverse effects
  6. Huan NC, Sidhu C, Thomas R
    Clin Chest Med, 2021 12;42(4):711-727.
    PMID: 34774177 DOI: 10.1016/j.ccm.2021.08.007
    Pneumothorax is a common problem worldwide. Pneumothorax develops secondary to diverse aetiologies; in many cases, there may be no recognizable lung abnormality. The pathogenetic mechanism(s) causing spontaneous pneumothorax may be related to an interplay between lung-related abnormalities and environmental factors such as smoking. Tobacco smoking is a major risk factor for primary spontaneous pneumothorax; chronic obstructive pulmonary disease is most frequently associated with secondary spontaneous pneumothorax. This review article provides an overview of the historical perspective, epidemiology, classification, and aetiology of pneumothorax. It also aims to highlight current knowledge and understanding of underlying risks and pathophysiological mechanisms in pneumothorax development.
    Matched MeSH terms: Smoking/adverse effects
  7. Feeny E, Dain K, Varghese C, Atiim GA, Rekve D, Gouda HN
    BMJ, 2021 07 19;374:n1516.
    PMID: 34281828 DOI: 10.1136/bmj.n1516
    Matched MeSH terms: Smoking/adverse effects
  8. Mocci E, Kundu P, Wheeler W, Arslan AA, Beane-Freeman LE, Bracci PM, et al.
    Cancer Res, 2021 Jun 01;81(11):3134-3143.
    PMID: 33574088 DOI: 10.1158/0008-5472.CAN-20-3267
    Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 × 10-8 was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, P interaction = 3.08 × 10-9). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r 2 = 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings. SIGNIFICANCE: This large genome-wide interaction study identifies a susceptibility locus on 2q21.3 that significantly modified PDAC risk by smoking status, providing insight into smoking-associated PDAC, with implications for prevention.
    Matched MeSH terms: Smoking/adverse effects*
  9. Liau CS, Mogan P, Thomas W
    J Steroid Biochem Mol Biol, 2021 04;208:105786.
    PMID: 33189851 DOI: 10.1016/j.jsbmb.2020.105786
    Lung cancer is increasing in incidence particularly among women, associated with a global change in smoking habits. Steroid hormones, particularly oestrogen exert an influence on tumour progression in tissues where their target receptor is expressed. Oestrogen receptor, particularly ERβ is highly expressed in the lung and becomes more highly expressed in lung carcinogenesis. Genes involved in the process of lung carcinoma progression and signalling cascades linked to invasion and angiogenesis are modulated by oestrogen receptors. This review intends to collate recently published evidence identifying a role for oestrogen in the initiation and progression of lung carcinoma and how these two processes are differentially affected by circulating oestrogens both in women and in men. Circulating oestrogens may be a significant risk factor in women's susceptibility to lung carcinoma and also provide an additional approach for more targeted therapy.
    Matched MeSH terms: Smoking/adverse effects
  10. Jochems SHJ, Reulen RC, van Osch FHM, Witlox WJA, Goossens ME, Brinkman M, et al.
    Int J Cancer, 2020 Oct 15;147(8):2091-2100.
    PMID: 32285440 DOI: 10.1002/ijc.33008
    While the association between fruit consumption and bladder cancer risk has been extensively reported, studies have had inadequate statistical power to investigate associations between types of fruit and bladder cancer risk satisfactorily. Fruit consumption in relation to bladder cancer risk was investigated by pooling individual data from 13 cohort studies. Cox regression models with attained age as time scale were used to estimate hazard ratios (HRs) for intakes of total fruit and citrus fruits, soft fruits, stone fruits, tropical fruits, pome fruits and fruit products. Analyses were stratified by sex, smoking status and bladder cancer subtype. During on average 11.2 years of follow-up, 2836 individuals developed incident bladder cancer. Increasing fruit consumption (by 100 g/day) was inversely associated with the risk of bladder cancer in women (HR = 0.92; 95% CI 0.85-0.99). Although in women the association with fruit consumption was most evident for higher-risk nonmuscle invasive bladder cancer (NMIBC; HR = 0.72; 95% CI 0.56-0.92), the test for heterogeneity by bladder cancer subtype was nonsignificant (P-heterogeneity = .14). Increasing fruit consumption (by 100 g/day) was not associated with bladder cancer risk in men (HR = 0.99; 95% CI 0.94-1.03), never smokers (HR = 0.96; 95% CI 0.88-1.05), former smokers (HR = 0.98; 95% CI 0.92-1.05) or current smokers (HR = 0.95; 95% CI 0.89-1.01). The consumption of any type of fruit was not found to be associated with bladder cancer risk (P values > .05). Our study supports no evidence that the consumption of specific types of fruit reduces the risk of bladder cancer. However, increasing total fruit consumption may reduce bladder cancer risk in women.
    Matched MeSH terms: Smoking/adverse effects
  11. Sirol Aflah Syazatul S, Piciucchi S, Tomassetti S, Ravaglia C, Dubini A, Poletti V
    Sci Rep, 2020 07 02;10(1):10906.
    PMID: 32616807 DOI: 10.1038/s41598-020-67938-y
    Bronchiolitis manifests as a variety of histological features that explain the complex clinical profiles and imaging aspects. In the period between January 2011 and June 2015, patients with a cryobiopsy diagnosis of bronchiolitis were retrospectively retrieved from the database of our institution. Clinical profiles, imaging features and histologic diagnoses were analysed to identify the role of cryobiopsy in the diagnostic process. Twenty-three patients with a multidisciplinary diagnosis of small airway disease were retrieved (14 females, 9 males; age range 31-74 years old; mean age 54.2 years old). The final MDT diagnoses were post-infectious bronchiolitis (n = 5), constrictive bronchiolitis (n = 3), DIPNECH (n = 1), idiopathic follicular bronchiolitis (n = 3), Sjogren's disease (n = 1), GLILD (n = 1), smoking-related interstitial lung disease (n = 6), sarcoid with granulomatous bronchiolar disorder (n = 1), and subacute hypersensitivity pneumonitis (n = 2). Complications reported after the cryobiopsy procedure consisted of two cases of pneumothorax soon after the biopsy (8.7%), which were successfully managed with the insertion of a chest tube. Transbronchial cryobiopsy represents a robust and mini-invasive method in the characterization of small airway diseases, allowing a low percentage of complications and good diagnostic confidence.
    Matched MeSH terms: Smoking/adverse effects
  12. Khan AH, Sulaiman SAS, Hassali MA, Khan KU, Ming LC, Mateen O, et al.
    BMC Public Health, 2020 Jun 04;20(1):854.
    PMID: 32498682 DOI: 10.1186/s12889-020-08856-6
    BACKGROUND: Smoking plays a key role in the development of tuberculosis (TB) infection and is also a predictor of poor TB treatment prognosis and outcomes. The current study was conducted to determine the prevalence of smoking and to assess the effects of smoking on treatment outcomes among TB patients.

    METHODS: A multi-center retrospective study design was used to collect data from TB patients in four different states of Malaysia, namely Penang, Sabah, Sarawak, and Selangor. The study included medical records of TB patients admitted to the selected hospitals in the period from January 2006 to March 2009. Medical records with incomplete data were not included. Patient demographics and clinical data were collected using a validated data collection form.

    RESULTS: Of all patients with TB (9337), the prevalence of smokers was 4313 (46.2%). Among smokers, 3584 (83.1%) were associated with pulmonary TB, while 729 (16.9%) were associated with extrapulmonary TB. Male gender (OR = 1.43, 95% CI 1.30-1.58), Chinese ethnicity (OR = 1.23, 95% CI 1.02-1.49), Sarawak indigenous ethnicity (OR = 0.74, 95% CI 0.58-0.95), urban residents (OR = 1.46, 95% CI 1.33-1.61), employed individuals (OR = 1.21, 95% CI 1.09-1.34), alcoholics (OR = 4.91, 95% CI 4.04-5.96), drug abusers (OR = 7.43, 95% CI 5.70-9.60) and presence of co-morbid condition (OR = 1.27, 95% CI 1.16-1.40) all showed significant association with smoking habits. This study found that 3236 (75.0%) patients were successfully treated in the smokers' group, while 4004 (79.7%) patients were non-smokers. The proportion of deaths (6.6%, n = 283), defaulters (6.6%, n = 284) and treatment interruptions (4.7%, n = 204) was higher in the smokers' group.

    CONCLUSIONS: Smoking has a strong influence on TB and is a major barrier towards treatment success (OR = 0.76, 95% CI 0.69-0.84, p 

    Matched MeSH terms: Smoking/adverse effects*
  13. Rampal L
    Med J Malaysia, 2020 05;75(3):95-97.
    PMID: 32467531
    No abstract provided.
    Matched MeSH terms: Smoking/adverse effects
  14. 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
  15. 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
  16. 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*
  17. Murphy N, Ward HA, Jenab M, Rothwell JA, Boutron-Ruault MC, Carbonnel F, et al.
    Clin Gastroenterol Hepatol, 2019 Jun;17(7):1323-1331.e6.
    PMID: 30056182 DOI: 10.1016/j.cgh.2018.07.030
    BACKGROUND & AIMS: Colorectal cancer located at different anatomical subsites may have distinct etiologies and risk factors. Previous studies that have examined this hypothesis have yielded inconsistent results, possibly because most studies have been of insufficient size to identify heterogeneous associations with precision.

    METHODS: In the European Prospective Investigation into Cancer and Nutrition study, we used multivariable joint Cox proportional hazards models, which accounted for tumors at different anatomical sites (proximal colon, distal colon, and rectum) as competing risks, to examine the relationships between 14 established/suspected lifestyle, anthropometric, and reproductive/menstrual risk factors with colorectal cancer risk. Heterogeneity across sites was tested using Wald tests.

    RESULTS: After a median of 14.9 years of follow-up of 521,330 men and women, 6291 colorectal cancer cases occurred. Physical activity was related inversely to proximal colon and distal colon cancer, but not to rectal cancer (P heterogeneity = .03). Height was associated positively with proximal and distal colon cancer only, but not rectal cancer (P heterogeneity = .0001). For men, but not women, heterogeneous relationships were observed for body mass index (P heterogeneity = .008) and waist circumference (P heterogeneity = .03), with weaker positive associations found for rectal cancer, compared with proximal and distal colon cancer. Current smoking was associated with a greater risk of rectal and proximal colon cancer, but not distal colon cancer (P heterogeneity = .05). No heterogeneity by anatomical site was found for alcohol consumption, diabetes, nonsteroidal anti-inflammatory drug use, and reproductive/menstrual factors.

    CONCLUSIONS: The relationships between physical activity, anthropometry, and smoking with colorectal cancer risk differed by subsite, supporting the hypothesis that tumors in different anatomical regions may have distinct etiologies.

    Matched MeSH terms: Smoking/adverse effects*
  18. Hartono RK, Hamid SA, Hafizurrachman M
    Asian Pac J Cancer Prev, 2019 May 25;20(5):1403-1408.
    PMID: 31127899
    Background: The incident of malignant cancer due to smoking habit becomes a public health problem especially
    in the developing countries. Active smokers neglect to stop smoking even though various studies proved that smoking
    increases the risk of cancer. While, previous studies have assessed the incident risk of cancer but have not performed the
    validity of the measurement. The aim of this study is to know the number of cigarettes that contribute to the incidence
    of malignant cancer. Methods: A study with retrospective cohort design has been conducted by using a set of public
    data of Indonesia Family Life Survey (IFLS) in 2007 and 2014. All active smokers (n= 748) who were in good health
    condition in 2007, were traced in 2014 and then being diagnosed with cancer with considering age, gender, healthy
    eating habit, and regular physical activity. Data has been analysed by using logistic regression by performing Adjusted
    Risk Ratio (ARR) and the result of validity measurement. Results: The incident of malignant cancer in 2014 were skin,
    liver, stomach and oral cavity. Smoking 21-30 per day in 2007 were significantly increased risk of having malignant
    cancer in 2014 at ARR: 6.88; SE:6.13 with the accuracy were 93.8%. The risk and accuracy were higher if smoke >30
    cigarettes per day (ARR:7.523; SE:7.019; accuracy 95.5%). This study also found that the risk of cancer was significantly
    increase with age (99% CI; ARR: 1.065; SE: 0.026). Conclusions: Cigarette smoking behaviour increased the risk any
    types incident of cancer. Total number >20 cigarettes smoked per day contributes to the incidence of malignant cancer.
    Matched MeSH terms: Smoking/adverse effects*
  19. 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
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