PubMed · 5575680
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W F Van Ganse, B G Ferris, J E Cotes. 1971. Cigarette smoking and pulmonary diffusing capacity.. https://doi.org/10.1378/chest.59.5_supplement.33s
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Soft-tissue sarcoma has been proposed to be a candidate for a dioxin-induced cancer. However, previous epidemiologic studies have suffered from poor exposure data and mixed exposures. We studied the association between sarcoma risk and individually estimated dioxin exposure in a general population exposed to relatively low levels of dioxin via food. A multicenter prospective case-control study was conducted in 4 university hospitals and 12 other hospitals in southern Finland. Participants included 110 patients with soft-tissue sarcoma (cases) and 227 area- and age-matched controls. Controls were patients operated for appendicitis. Individual dioxin concentrations were analyzed from subcutaneous fat samples by gas chromatography-mass spectrometry. The average (range) dioxin concentration was 33.4 (4.4-145.5) ng/kg (toxic equivalencies in fat according to WHO). No increased risk associated with increased dioxin concentration was observed. In contrast, the highest risk of sarcoma was found at low levels of dioxin. Odds ratios for different quintiles as compared with the lowest quintile of dioxins (median, 11.5 ng/kg) varied from 0.43 (95% CI = 0.18-1.05) to 0.65 (95% CI = 0.22-1.95). The result was little affected by studied confounders and the findings were similar for different sarcoma subtypes, age groups and study areas. The results imply that dioxin does not increase the risk of soft-tissue sarcoma at the present population levels.
There are few well-established patient risk factors associated with human papillomavirus (HPV) infection in cancers of the oral cavity and oropharynx. The purpose of this study was to determine if there were significant different risk factors and tumor characteristics between HPV-positive and HPV-negative cancer cases. HPV was evaluated in cancer tissue and exfoliated oral cells of 193 oral cavity/oropharynx cancer patients using PCR and direct DNA sequencing. A patient questionnaire collected information about risk factors, sexual practices and medical history. The prevalence of HPV high-risk (HR) types was 20% in cancer cases. Three types were identified: HPV-16 (87%), HPV-18 (3%) and HPV-33 (11%). Risk factors for HPV-HR included younger age (< or = 55 years vs. > 55 years; adjusted OR = 3.4; 95% CI = 1.6-7.3) and younger-age cases who had more lifetime sex partners (adjusted OR = 3.8; 95% CI = 1.4-10.1), practiced oral-genital sex (adjusted OR = 4.3; 95% CI = 1.8-10.4) or oral-anal sex (adjusted OR = 19.5; 95% CI = 3.4-113). Compared to HPV-negative cancers, HPV-HR cancers were more likely to have a positive HPV-HR exfoliated oral cytology test (adjusted OR = 7.8; 95% CI = 3.4-18.4), later stage (adjusted OR = 3.0), nodal involvement (adjusted OR = 4.1) and advanced grade (adjusted OR = 3.0). This study shows new evidence that the prevalence of oncogenic mucosal HPV is higher in younger-age oral cavity/oropharynx cancer cases whose sexual practices are typically associated with sexual transmission of the virus. HPV detection also appears to be an indicator of advanced disease characteristics that may require different clinical treatment for this subset of patients. An exfoliated oral cytology test for HPV was a significant predictor of HR types in the cancers, suggesting that an oral rinse may provide an early biomarker of infected tumors.
OBJECTIVE: To determine the relative contribution of various risk factors to the development of Parkinson's disease (PD). METHODS: Ten variables that were independently associated with PD in a health system population-based case-control study of epidemiological risk factors for the disease were jointly assessed. Stepwise logistic regression, adjusted for sex, race and age was used to develop a multiple variate model that best predicted the presence of PD. The population attributable risk was estimated for each variable in the final model, as well as for all factors together. RESULTS: The 10 initial variables included >20 years occupational exposure to manganese or to copper, individually; >20 years joint occupational exposure to either lead and copper, copper and iron, or lead and iron; a positive family history of PD in first- or second-degree relatives; occupational exposure to insecticides or herbicides; occupational exposure to farming; and smoking. Logistic regression resulted in a final model that included >20 years joint occupational exposure to lead and copper (p=0.009; population attributable risk [PAR]=3.9%), occupational exposure to insecticides (p=0.002; PAR=8.1%), a positive family history of PD in first- and second-degree relatives (p=0.001; PAR=12.4%), and smoking </=30 pack-years or not smoking (p=0.005; PAR=41.4%). All four variables combined had a PAR=54.1%. CONCLUSIONS: Our final model of PD risk suggests that occupational, environmental lifestyle and, likely, genetic factors, individually and collectively, play a significant role in the etiology of the disease. Clearly, additional risk factors remain to be determined through future research.