MATERIALS AND METHODS: Pure tone audiometry test was conducted on 263 residents of a rural village who were not exposed to noise. The pack-years of smoking were computed from the subjects' smoking history. The association between pack-years and hearing impairment was assessed. The combined effect of smoking and age on hearing impairment was determined based on prevalence rate ratio.
RESULTS: There was a statistically significant trend in the number of pack-years of smoking and age as risk factors for hearing impairment. The prevalence rates of hearing impairment for nonsmokers aged 40 years and younger, smokers aged 40 years and younger, nonsmokers older than 40 years of age, and smokers older than 40 years of age were 6.9%, 11.9%, 29.7%, and 51.3%, respectively. The prevalence rate ratio for nonsmokers aged 40 years and younger, smokers aged 40 years and younger, nonsmokers older than 40 years of age, and smokers older than 40 years of age (nonsmokers aged 40 years and younger as a reference group) was 1, 1.7, 4.3, and 7.5, respectively. The prevalence rate ratios showed a multiplicative effect of smoking and age on hearing impairment.
CONCLUSION: Age and smoking are risk factors for hearing impairment. It is clear that smoking and age have multiplicative adverse effects on hearing impairment.
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.
METHODS: Logistic regression analysis was used to distinguish associated current smoking characteristics. Five-year predictive risks of CVD, CHD and MI and the impact of simulated interventions were calculated utilizing the Data Collection on Adverse Effects of Anti-HIV Drugs Study (D:A:D) algorithm.
RESULTS: Smoking status data were collected from 4274 participants and 1496 of these had sufficient data for simulated intervention calculations. Current smoking prevalence in these two groups was similar (23.2% vs. 19.9%, respectively). Characteristics associated with current smoking included age > 50 years compared with 30-39 years [odds ratio (OR) 0.65; 95% confidence interval (CI) 0.51-0.83], HIV exposure through injecting drug use compared with heterosexual exposure (OR 3.03; 95% CI 2.25-4.07), and receiving antiretroviral therapy (ART) at study sites in Singapore, South Korea, Malaysia, Japan and Vietnam in comparison to Thailand (all OR > 2). Women were less likely to smoke than men (OR 0.11; 95% CI 0.08-0.14). In simulated interventions, smoking cessation demonstrated the greatest impact in reducing CVD and CHD risk and closely approximated the impact of switching from abacavir to an alternate antiretroviral in the reduction of 5-year MI risk.
CONCLUSIONS: Multiple interventions could reduce CVD, CHD and MI risk in Asian HIV-positive patients, with smoking cessation potentially being the most influential.
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.
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.
MATERIALS AND METHODS: A cross-sectional study was conducted among three secondary schools located in Kudat district, Sabah, Malaysia during the period from June until September 2012. The protocol of this study was approved by ethics committee of Management and Science University, Malaysia. The aims were explained and a consent form was signed by each participant. Respondents were chosen randomly from each school with the help of the headmasters. Self-administrated questionnaires, covering socio-demographic characteristics and general knowledge of lung cancer, were distributed. Once all 150 respondents completed the questionnaire, they passed it to their head master for collecting and recording. All the data were analyzed using Statistical Package for the Social Sciences (SPSS) version 13. ANOVA and t-test were applied for univariate analysis; and multiple linear regression for multivariate analysis.
RESULTS: A total of 150 male secondary school teachers participated in this study. Their mean age was 35.6 ∓ 6.5 (SD); maximum 50 and minimum 23 years old. More than half of the participants were Malay and married (52%, 79%; respectively). Regarding the knowledge about lung cancer, 57.3% of the participants mentioned that only males are affected by lung cancer. Some 70.7% mentioned that lung cancer can be transmitted from one person to another. More than half (56.7%) reported that lung cancer is not the leading cause of death in Malaysian males. As for risk factors, the majority reported that family history of lung cancer is not involved. However, 91.3% were aware that cigarettes are the main risk factor of lung cancer and more than half (52%) believed that second-hand smoking is one of the risk factor of lung cancer. More than half (51.3%) were not aware that asbestos, ionizing radiation and other cancer causing substances are risk factors for lung cancer. Quitting smoking, avoiding second-hand smoking and avoiding unnecessary x-ray image of the chest (53.3%, 96.0%, 87.3%; respectively) are the main preventive measures mentioned by the participants. For the factors that influence the participants knowledge, univariate and multivariate analysis showed that only race was significant.
CONCLUSIONS: Overall, the knowledge of school male teachers about lung cancer was low. However, few items were scored high: cigarettes are the main risk factor; avoiding second-hand smoking; and avoiding x-rays. Interventions to increase lung cancer awareness are needed to improve early detection behavior. Increase the price of pack of cigarettes to RM 20 and banning smoking in public places such as restaurants are highly recommended as primary preventive measures.