Risk Factors for Invasive Haemophilus influenzae Disease among Children 2-16 Years of Age in the Vaccine Era, Switzerland 1991-1993

Mūhlemann K (Institute of Medical Microbiology, Friedbūhistrasse 51, University of Berne, CH-3010 Berne, Switzerland), Alexander E R, Weiss N S, Pepe M, Schopfer K and the Swiss H.Influenzae Study Group. Risk factors for invasive Haemophilus influenzae disease among children aged 2-16 years of age in the vaccine era, Switzerland 1991-1993. International Journal of Epidemiology 1996; 25: 1280-1285. Background Continued surveillance, and detailed investigation of direct and indirect effects of conjugated vaccines and risk factors for invasive H. Influenzae serotype b (Hib) disease in the vaccine era are important Methods 143 cases with invasive disease between 1991 and 1993 aged 2-16 years were selected retrospectively from a large incidence trend study. Controls (n = 336) were recruited from local vital registries and matched to cases for age, gender, and residence. Hib vaccination histories among study subjects and their siblings and other sociodemographic variables were obtained by questionnaires completed by the parents of these children. Adjusted odds ratio (OR) estimates were calculated by conditional logistic regression analysis. Results Most vaccinated subjects had received the Polysacchande-Diphtheria Toxoid vaccine and estimated vaccine efficacy was high (95%; 95% confidence interval [Cl] 60-99%). Also, the results suggested that protection afforded by vaccination against Hib extended to the family members of vaccinated children. School attendance was found to be protective against invasive Hib disease (OR : 0.33; Cl : 0.14-0.75). Cases more often than controls reported sufferring from asthma and allergies (OR : 4.8; Cl: 1.2-19 4). Conclusions Post-licensure vaccine efficacy is high among children ≥2 years of age. The observed association between asthma and epiglottis is novel and deserves further investigatio

Cigarette smoking and risk of epithelial ovarian cancer

An increased risk of mucinous ovarian tumors among cigarette smokers has been observed in multiple studies. The association of smoking with other histologic types of ovarian cancer is less clear, but potentially holds greater importance for prevention of disease incidence and mortality. METHODS: In a population-based study of 812 women with ovarian cancer diagnosed in western Washington State from 2002-2005 and 1,313 controls, we assessed the risk associated with cigarette smoking, with a particular focus on tumor subgroups jointly classified according to the degree of invasiveness and histology. Information was collected through in-person interviews, and logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The incidence of both borderline and invasive mucinous ovarian tumors was increased among women with a history of cigarette smoking (ORs and 95% CIs = 1.8, 1.2-2.9, and 1.8, 0.8-4.3, respectively). Increases in risk of these tumor types were most evident among women with greater smoking duration and pack-years of exposure, and among those who had smoked within the prior 15 years. We noted no clear patterns of risk of serous tumors with duration or pack-years of smoking; however, risk of these tumor types was somewhat elevated among women who had smoked within the previous 15 years (for borderline serous tumors, OR and 95% CI = 1.5, 0.9-2.3; for invasive serous tumors, OR and 95% CI = 1.4, 1.1-1.9). The risk of endometrioid, clear cell, and the remaining histologic types of invasive ovarian cancer was not increased among smokers. CONCLUSION: In the aggregate, evidence is insufficient to determine whether smoking is linked with risk of serous or other non-mucinous histologic types of ovarian cancer. Studies that employ additional histopathologic and molecular techniques to more accurately delineate subsets of tumors may improve our understanding of the impact of smoking on ovarian cancer risk

Risk of epithelial ovarian cancer in relation to benign ovarian conditions and ovarian surgery.

OBJECTIVE: Some forms of ovarian neoplasms may be preventable through the removal of precursor lesions. We assessed the risk associated with a prior diagnosis of, and ovarian surgery following, ovarian cysts and endometriosis, with a focus on characterizing risk among tumor subgroups. METHODS: Information was collected during in-person interviews with 812 women with ovarian cancer diagnosed in western Washington State from 2002 to 2005 and 1,313 population-based controls. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: The risk of a borderline mucinous ovarian tumor associated with a history of an ovarian cyst was increased (OR=1.7, 95% CI: 1.0-2.8), but did not vary notably according to receipt of subsequent ovarian surgery. While risk of invasive epithelial ovarian cancer was slightly increased among women with a cyst who had no subsequent ovarian surgery, it was reduced when a cyst diagnosis was followed by surgery (OR = 0.6, 95% CI: 0.4-0.9). This reduction in risk was most evident for serous invasive tumors. Women with a history of endometriosis had a threefold increased risk of endometrioid and clear cell invasive tumors, with a lesser risk increase among women who underwent subsequent ovarian surgery. CONCLUSIONS: Our results suggest differences in the relation of ovarian cysts and endometriosis with risk of specific subtypes of ovarian cancer as well as the possibility that ovarian surgery in women with these conditions may lower the risk of invasive disease

Statin use and risk of community acquired pneumonia in older people: population based case-control study

Objective To test the hypothesis that hydroxymethyl glutaryl coenzyme A reductase inhibitors (statins) may decrease the risk of community acquired pneumonia

Toxicology and Epidemiology: Improving the Science with a Framework for Combining Toxicological and Epidemiological Evidence to Establish Causal Inference

Historically, toxicology has played a significant role in verifying conclusions drawn on the basis of epidemiological findings. Agents that were suggested to have a role in human diseases have been tested in animals to firmly establish a causative link. Bacterial pathogens are perhaps the oldest examples, and tobacco smoke and lung cancer and asbestos and mesothelioma provide two more recent examples. With the advent of toxicity testing guidelines and protocols, toxicology took on a role that was intended to anticipate or predict potential adverse effects in humans, and epidemiology, in many cases, served a role in verifying or negating these toxicological predictions. The coupled role of epidemiology and toxicology in discerning human health effects by environmental agents is obvious, but there is currently no systematic and transparent way to bring the data and analysis of the two disciplines together in a way that provides a unified view on an adverse causal relationship between an agent and a disease. In working to advance the interaction between the fields of toxicology and epidemiology, we propose here a five-step "Epid-Tox” process that would focus on: (1) collection of all relevant studies, (2) assessment of their quality, (3) evaluation of the weight of evidence, (4) assignment of a scalable conclusion, and (5) placement on a causal relationship grid. The causal relationship grid provides a clear view of how epidemiological and toxicological data intersect, permits straightforward conclusions with regard to a causal relationship between agent and effect, and can show how additional data can influence conclusions of causalit

Genetic polymorphisms in the catechol estrogen metabolism pathway and breast cancer risk

Background: This study investigated whether single nucleotide polymorphisms (SNPs) in genes within the catechol estrogen metabolism pathway altered the risk of breast cancer alone or in combination, as well as whether menopausal hormone therapy (HT) modified the effect of these SNPs on breast cancer risk. Methods: In a population-based case-control study of breast cancer, 891 cases and 878 controls were genotyped for six functional SNPs in the COMT, CYP1B1, GSTM1, GSTP1, and GSTT1 genes. Results: Women homozygous with the T allele in CYP1B1*2 (Ser119; rs1056827) were at 1.69 (95% confidence interval [CI]: 1.17-2.46) times the risk of women homozygous with the G allele; women homozygous with the G allele in GSTP1 (Val105; rs1695) were at 0.73 (95% CI: 0.54-0.99) times the risk of breast cancer compared to women homozygous with the A allele. No other SNPs tested were associated with breast cancer to any appreciable degree. Potential gene-gene and gene-HT interactions were investigated. Conclusion: With the exception of GSTP1 and possibly CYP1B1*2, our findings do not provide support for the role of genetic variation in the catechol estrogen metabolism pathway and breast cancer risk in post-menopausal women

Absence of an association of human polyomavirus and papillomavirus infection with lung cancer in China: a nested case–control study

Abstract Background Studies of human polyomavirus (HPyV) infection and lung cancer are limited and those regarding the association of human papillomavirus (HPV) infection and lung cancer have produced inconsistent results. Methods We conducted a nested case–control study to assess the association between incident lung cancer of various histologies and evidence of prior infection with HPyVs and HPVs. We selected serum from 183 cases and 217 frequency matched controls from the Yunnan Tin Miner’s Cohort study, which was designed to identify biomarkers for early detection of lung cancer. Using multiplex liquid bead microarray (LBMA) antibody assays, we tested for antibodies to the VP1 structural protein and small T antigen (ST-Ag) of Merkel cell, KI, and WU HPyVs. We also tested for antibodies against HPV L1 structural proteins (high-risk types 16, 18, 31, 33, 52, and 58 and low-risk types 6 and 11) and E6 and E7 oncoproteins (high risk types 16 and 18). Measures of antibody reactivity were log transformed and analyzed using logistic regression. Results We found no association between KIV, WUV, and MCV antibody levels and incident lung cancer (P-corrected for multiple comparisons >0.10 for all trend tests). We also found no association with HPV-16, 18, 31, 33, 52, and 58 seropositivity (P-corrected for multiple comparisons >0.05 for all). Conclusions Future studies of infectious etiologies of lung cancer should look beyond HPyVs and HPVs as candidate infectious agents