Relative Excess Risk Of Interaction Research Articles

Effect of folic acid and DNA methyltransferase 1 on cervical cancer and its precancerous lesion

To explore the effect of folic acid and DNA methyltransferase 1 (DNMT1) on cervical cancer and cervix precancerous lesion. 100 patients with cervix squamous cell carcinoma (SCC), 101 patients with cervical intraepithelial neoplasm (CIN) and 109 patients with cervix inflammation (CI) diagnosed by histology were included in this study. Radioimmunoassay (RIA), polymerase chain reaction (PCR) and Western blot were used to detect the levels of serum folate, HPV16 infection and the expression of DNMT1 protein, respectively. The average levels of serum folate were (2.60 ± 1.61) ng/ml, (3.14 ± 2.08) ng/ml and (3.32 ± 1.74) ng/ml, and the expression of DNMT1 protein were 2.40 ± 0.99, 1.88 ± 0.33 and 0.89 ± 0.29 in the group of SCC, CIN and CI, respectively. The relationship of folate levels and DNMT1 protein expression showed inverse correlation (r = -0.186, P = 0.001). The results in our study indicated that there was an additive interaction between low-level of serum folate and high-expression of DNMT1 protein related to the risk of CIN and SCC, with OR value as 2.50 (95%CI: 1.21 - 9.22) and 6.03 (95%CI: 2.79 - 21.72) respectively. The relative excess risk of interaction (RERI), attributable proportion of interaction (API) and synergy index (S) were 0.92, 0.36 and 2.59 in the CIN group while 2.47, 0.41 and 1.96 in the SCC group. The low level of serum folate and high expression of DNMT1 protein seemed to be associated with high risk of cervical cancer and its precancerous lesion. It suggested that there might be a synergistic action between serum folate and DNMT1 in the progression of cervix carcinogenesis.

Arsenic exposure from drinking water and mortality from cardiovascular disease in Bangladesh: prospective cohort study

Objective To evaluate the association between arsenic exposure and mortality from cardiovascular disease and to assess whether cigarette smoking influences the association.Design Prospective cohort study with arsenic exposure measured in...

The study of the combination detection of HPV-DNA and p16INK4a in cervical lesions

The objective of this study is to detect the infection of human papillomavirus (HPV) and the expression of p16(INK4a) in cervical lesions and to investigate the interaction between hrHPV and p16(INK4a) for cervical lesions and its diagnostic efficiency. hrHPV-DNA was detected by the hybrid capture II (HC-II) system. Immunochemical method was used to detect the expression of p16(INK4a), and histopathologic test was performed to identify cervical lesions. χ(2) test and Spearman's rank correlation were used for statistical analysis. Additive effects model was used to analyze the interaction. The diagnostic sensitivity, specificity, positive predictive values, negative predictive values, accuracy, and the area under the receiver operating characteristic curve were calculated with SPSS 13.0. hrHPV and p16(INK4a) positive rate increased (P < 0.05) with histopathologic diagnosis increasing. The positive rates of hrHPV and p16(INK4a) in negative or chronic inflammation were statistically lower than that in cervical intraepithelial neoplasia (CIN)1, CIN2, CIN3, and squamous-cell carcinoma (SCC) (P < 0.05), respectively. There was a positive interaction between hrHPV and p16(INK4a), relative excess risk of interaction (RERI) was 52.49, attributable proportions of interaction (API) were 72.34%, and the synergy index (S) was 3.75. The specificity and AUC of combining hrHPV with p16(INK4a) were statistically higher than hrHPV or p16(INK4a) alone (P < 0.05). hrHPV and p16(INK4a) are useful markers for the early diagnosis of cervical lesions. A positive interaction between hrHPV and p16(INK4a) is seen. The combination of hrHPV and p16(INK4a) has a higher diagnostic accuracy than hrHPV or p16(INK4a) alone in diagnosis of cervical lesions.

Increased Effect of Obesity on Asthma in Adults with Low Household Income

Background. Both obesity and low income are risk factors of asthma and their joint effect on the disease has not been studied previously. Objective. To examine the influence of obesity and household income and their joint effect on asthma. Methods. The authors conducted an analysis based on data from 115,722 subjects 18+ years of age who participated in a national survey in 2005. Logistic regression analysis was used to adjust for covariates. The joint effect of household income and body mass index (BMI) on asthma was assessed on an additive scale. Results. Obesity associated with an increased risk of asthma was significant in all income categories in women but was only significant in the low-income group in men. A stronger association between obesity and asthma was observed in low- than in high-income families. For men and women combined, the adjusted odds ratio for those with a BMI value of 35 kg/m2 or more versus those with a BMI less than 25 kg/m2 was 2.01 in the low–household income group compared with only 1.47 in the high-income group. The corresponding adjusted relative excess risk of interaction was 1.50 (95% confidence interval [CI]: 0.88, 1.65) for men and women combined and was 2.73 (95% CI: 1.50, 5.39) for women. Conclusion. These data suggested an interactive effect of obesity and low-household income on the prevalence of asthma.

Interaction between exposure to environmental smoke and the family history of chronic bronchitis (CB) on the risk of CB in rural females in Liuyang city, Hunan province

To explore the relationships and interaction among the exposure to environmental smoke, family history of chronic bronchitis (CB) and CB, in rural women. A population-based case-control study chi(2) was used to analyze the relationship between environmental smoke exposure, CB family history and CB. Additive effects model was used to analyze the interaction. In the first stage, 157 CB patients were screened from 24 268 women residents (prevalence rate is 6.47 per thousand), then 92 patients (case group) and 114 healthy women (control group) were investigated in the second stage. Results showed that: coal/firewood for heating (OR = 36.21) and CB family history (OR = 6.41) might serve as the risk factors of CB in rural women (P < 0.05). Factors as frequent cooking and using coal/firewood for heating had a positive interaction with family history of CB in rural women, CB with S as 5.39 and 9.02, attributable proportions of interaction (API) as 72% and 88%, relative excess risk of interaction (RERI) as 6.50 and 225.99, respectively. Using coal/firewood for heating and CB family history might be the risk factors of CB for rural women. A positive interaction between cooking frequently, heating model and CB family history was also seen.

Total Tissue Factor Pathway Inhibitor and Incident Venous Thrombosis: The Longitudinal Investigation of Thromboembolism Etiology

Introduction: Tissue Factor Pathway Inhibitor (TFPI) inhibits tissue factor, a potent coagulation initiator. Limited evidence suggests that low TFPI levels are associated with increased risk of venous thromboembolism (VT).Methods: VT was ascertained in the Longitudinal Investigation of Thromboembolism Etiology, which combines data from the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study. Total TFPI was measured in a nested case-control sample. With 12 years of follow-up, 534 cases of new VTE were age-, sex-, and race-frequency matched with 1091 controls. The odds ratio for VT was determined for quartiles of TFPI, and for the bottom 5% versus the top 95% in logistic regression models adjusting for demographics (age, race, gender, study), coagulation factors (Factors VII, VIII, IX, XI, D-dimer), and other VT risk factors. To evaluate for greater than additive interactions we calculated the percent relative excess risk of interaction between TFPI and other VT risk factors.Results: Mean TFPI in ng/mL (standard deviation) in cases and controls was 36.4 (12.8) and 35.0 (11.1), respectively. Increasing quartiles of TFPI were associated with male gender and increasing age, body mass index, factors VII, VIII, IX, XI, and D-dimer (all p<0.05). TFPI quartiles were not related to ethnicity, factor V Leiden, or the prothrombin gene polymorphism. Compared with those in the upper 95%, those in the bottom 5% of TFPI (32 cases, 56 controls) had an age-, sex-, race-, and cohort-adjusted odds ratio of 1.35 (0.86, 2.12) for VT. Adjusting for factors VII, VIII, IX, XI, and D-dimer increased the odds ratio to 1.93 (1.05, 3.53). Further addition of BMI to the coagulation factor adjusted model slightly attenuated the odds ratio to 1.70 (0.98, 2.93). There were no associations of TFPI in quartiles or as a continuous variable with VT. TFPI in the bottom fifth percentile did not demonstrate greater than additive interaction with factor V Leiden or with higher BMI.Conclusions: Associations of high TFPI levels with VT were masked by concurrent higher procoagulant levels. After adjusting for procoagulant factors and D-dimer, TFPI ≤ 5% was associated with a 1.9-fold increased odds of VT. These data suggest high total TFPI may be a response to procoagulant states.

Modification of Risk of Arsenic-Induced Skin Lesions by Sunlight Exposure, Smoking, and Occupational Exposures in Bangladesh

The risk of skin lesions associated with arsenic exposure from drinking water in Bangladesh is considerably greater in men than in women. Using baseline data from 11,062 cohort members in the Health Effects of Arsenic Longitudinal Study in Araihazar, Bangladesh, we performed a cross-sectional analysis to evaluate whether the association between arsenic exposure from drinking water and the risk of skin lesions is modified by tobacco smoking, excessive sunlight, the use of fertilizer, and the use of pesticides. A time-weighted well arsenic concentration was estimated for each participant by incorporating history of well use. Relative excess risk for interaction (RERI) and its 95% confidence intervals (CIs) were estimated using adjusted prevalence odds ratios. We observed a synergistic effect between the highest level of arsenic exposure (> 113 microg/L) and tobacco smoking on risk of skin lesions in men (RERI = 1.5 [95% CI = 0.3 to 2.7] overall and 1.7 [0.2 to 3.4] for the subpopulation with longer-term arsenic exposure). We also observed suggestive synergistic effects between higher levels (28.1-113.0 microg/L and 113.1-864.0 microg/L) of arsenic exposure and fertilizer use in men (RERI = 1.0 [-0.2 to 2.2] and 1.3 [-0.2 to 2.9] respectively). Furthermore, the risk of skin lesions associated with any given level of arsenic exposure was greater in men with excessive sun exposure. The patterns of effect estimates in women indicate similar-but-weaker interaction effects of arsenic exposure with tobacco smoking and fertilizer use. These findings help explain why the risk of arsenic-related skin lesions was much greater in men than in women in Bangladesh. Because most arsenic-induced skin cancers arise from these skin lesions, treatment and remediation plans should take into consideration these etiologic cofactors.