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.
METHODS: A cross-sectional study was conducted among male farmers from 3 different communities in Sabah, Malaysia. A total of 152 farmers participated in this study of whom 62 farmers had been exposed to either paraquat or malathion or both to varying extents. Questionnaires were designed to record a history of pesticides exposure and other potential risk factors among farmers. All semen samples were collected, processed and analyzed by qualified personnel based on WHO guidelines. Volume, pH, sperm concentration, motility, morphology and WBC count were examined and recorded. The association between pesticide exposure and semen parameters was highly significant.
RESULTS: The mean values of volume, pH, sperm concentration, motility, and WBC count were significantly less in the exposed group than in compared with the non-exposed group, with p<0.005. Those who were exposed to pesticides had greater risk of having abnormal semen parameters than those in with the non exposed group, with p values of less than 0.05. The comparison between semen qualities such as lower sperm count, motility and higher percentage of sperm abnormality of those exposed to different types of pesticides (paraquat and malathion) showed no significant differences.
CONCLUSION: The results showed a significant decline in semen quality with a decline in sperm count, motility and higher percent of teratospermia among subjects with pesticide exposure, and those who were exposed to pesticides had significantly 3 to 9 times greater risk of having abnormal semen parameters.
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.
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.