Periodontitis, the progressive loss of the alveolar bone around the teeth and the major cause of tooth loss in adults, is due to oral microorganisms, including Porphyromonas gingivalis. Periodontitis is associated with a local overly aggressive immune response and a spectrum of systemic effects, but the role of this condition in orodigestive cancers is unclear. We prospectively examined clinically ascertained periodontitis (N = 12,605) and serum IgG immune response to P.gingivalis (N = 7852) in relation to orodigestive cancer mortality among men and women in the National Health and Nutrition Examination Survey III. A detailed oral health exam was conducted from 1988 to 1994 in survey Phases I and II, whereas serum IgG for P.gingivalis was measured from 1991 to 1994 in Phase II only. One hundred and five orodigestive cancer deaths were ascertained through 31 December 2006. Periodontitis (moderate or severe) was associated with increased orodigestive cancer mortality [relative risks (RR) = 2.28, 95% confidence interval (CI) = 1.17-4.45]; mortality risks also increased with increasing severity of periodontal disease (P trend = 0.01). Periodontitis-associated mortality was in excess for colorectal (RR = 3.58; 95% CI = 1.15-11.16) and possibly for pancreatic cancer (RR = 4.56; 95% CI = 0.93-22.29). Greater serum P.gingivalis IgG tended to be associated overall with increased orodigestive cancer mortality (P trend = 0.06); P.gingivalis-associated excess orodigestive mortality was also found for healthy subjects not exhibiting overt periodontal disease (RR = 2.25; 95% CI = 1.23-4.14). Orodigestive cancer mortality is related to periodontitis and to the periodontal pathogen, P.gingivalis, independent of periodontal disease. Porphyromonas gingivalis is a biomarker for microbe-associated risk of death due to orodigestive cancer.

Objective Persistent colonization by Helicobacter pylori, and especially by cagA-positive strains, has been related to several health outcomes with effects in opposite directions. Thus, it is important to evaluate its influence on both total and category-specific mortality. Design We conducted prospective cohort analyses in a nationally representative sample of 9895 participants enrolled in the National Health and Nutrition Examination Survey III (NHANES III) to assess the association of H. pylori status with all-cause and cause-specific mortality. Analyses for the association of H. pylori cagA positivity with mortality were conducted in 7,384 subjects with data on H. pylori cagA status. Results In older individuals (> 40.6 years of age), H. pylori was not associated with all-cause mortality (hazard ratio [HR], 1.00; 95% confidence interval [CI], 0.84–1.18). There was an inverse association of H. pylori status with stroke mortality (HR, 0.67; 95% CI, 0.44–1.08), and the inverse association was stronger for H. pylori cagA positivity, with the HR of 0.45 (95% CI, 0.27–0.75). H. pylori also was strongly positively related to gastric cancer mortality. After we adjusted p-values using the Benjamini–Hochberg false discovery rate (FDR) method to account for multiple comparisons, these associations remained, and H. pylori status was not related to other outcomes.. Conclusion Our findings suggest that H. pylori has a mixed role in human health, but is not a major risk factor for all-cause mortality.

The authors conducted a cross-sectional study to assess the relation between arsenic exposure from drinking water and plasma levels of markers of systemic inflammation and endothelial dysfunction (matrix metalloproteinase-9, myeloperoxidase, plasminogen activator inhibitor-1, soluble E-selectin, soluble intercellular adhesion molecule-1 (ICAM-1), and soluble vascular adhesion molecule-1 (VCAM-1)) using baseline data from 668 participants (age, >30 years) in the Health Effects of Arsenic Longitudinal Study in Bangladesh (2007-2008). Both well water arsenic and urinary arsenic were positively associated with plasma levels of soluble VCAM-1. For every 1-unit increase in log-transformed well water arsenic (ln μg/L) and urinary arsenic (ln μg/g creatinine), plasma soluble VCAM-1 was 1.02 (95% confidence interval: 1.01, 1.03) and 1.04 (95% confidence interval: 1.01, 1.07) times greater, respectively. There was a significant interaction between arsenic exposure and higher body mass index, such that the increased levels of plasminogen activator inhibitor-1 and soluble VCAM-1 associated with arsenic exposure were stronger among people with higher body mass index. The findings indicate an effect of chronic arsenic exposure from drinking water on vascular inflammation and endothelial dysfunction that could be modified by body mass index and also suggest a potential mechanism underlying the association between arsenic exposure and cardiovascular disease.

Although recent studies have suggested that tooth loss is positively related to the risk of gastric non-cardia cancer, the underlying oral health conditions potentially responsible for the association remain unknown. We investigated whether clinical and behavioral measures of oral health are associated with the risk of gastric precancerous lesions. We conducted a cross-sectional study of 131 patients undergoing upper gastrointestinal endoscopy. Cases were defined as those with gastric precancerous lesions including intestinal metaplasia or chronic atrophic gastritis on the basis of standard biopsy review. A validated structured questionnaire was administered to obtain information on oral health behaviors. A comprehensive clinical oral health examination was performed on a subset of 91 patients to evaluate for periodontal disease and dental caries experience. A total of 41 (31%) cases of gastric precancerous lesions were identified. Compared with non-cases, cases were significantly more likely to not floss their teeth [odds ratio (OR) = 2.89, 95% confidence interval (CI): 1.09-7.64], adjusting for age, sex, race, body mass index, smoking status, educational attainment and Helicobacter pylori status in serum. Among participants who completed the oral examination, cases (n = 28) were more likely to have a higher percentage of sites with gingival bleeding than non-cases [OR = 2.63, 95% CI: 1.37-5.05 for a standard deviation increase in bleeding sites (equivalent to 19.7%)], independent of potential confounders. Our findings demonstrate that specific oral health conditions and behaviors such as gingival bleeding and tooth flossing are associated with gastric precancerous lesions.

Rationale: Exposure to arsenic through drinking water has been linked to respiratory symptoms, obstructive lung diseases, and mortality from respiratory diseases. Limited evidence for the deleterious effects on lung function exists among individuals exposed to a high dose of arsenic. Objectives: To determine the deleterious effects on lung function that exist among individuals exposed to a high dose of arsenic. Methods: In 950 individuals who presented with any respiratory symptom among a population-based cohort of 20,033 adults, we evaluated the association between arsenic exposure, measured by well water and urinary arsenic concentrations measured at baseline, and post-bronchodilator-administered pulmonary function assessed during follow-up. Measurements and Main Results: For every one SD increase in baseline water arsenic exposure, we observed a lower level of FEV 1 (246.5 ml; P , 0.0005) and FVC (253.1 ml; P , 0.01) in regression models adjusted for age, sex, body mass index, smoking, socioeconomic status, betel nut use, and arsenical skin lesions status. Similar inverse relationships were observed between baseline urinary arsenic and FEV 1 (248.3 ml; P , 0.005) and FVC (255.2 ml; P , 0.01) in adjusted models. Our analyses also demonstrated a dose-related decrease in lung function with increasing levels of baseline water and urinary arsenic. This association remained significant in never-smokers and individuals without skin lesions, and was stronger in male smokers. Among male smokers and individuals with skin lesions, every one SD increase in water arsenic was related to a significant reduction of FEV 1 (274.4 ml, P , 0.01; and 2116.1 ml, P , 0.05) and FVC (272.8 ml, P ¼ 0.02; and 2146.9 ml, P ¼ 0.004), respectively. Conclusions: This large population-based study confirms that arsenic exposure is associated with impaired lung function and the deleterious effect is evident at low-to moderate-dose range.Keywords: arsenic exposure; lung function; Bangladesh Arsenic from drinking water has been linked with cancers, dermatologic, cardiovascular, reproductive, and neurotoxic outcomes among adults and children (1-8). Chronic exposure to arsenic has also been linked to nonmalignant respiratory effects including respiratory symptoms, chronic obstructive pulmonary disease, and respiratory disease mortality (9-12). However, the evidence of the effect of arsenic exposure on lung function is limited, especially at the low-to moderate-dose ranges. Several studies from arsenic-endemic areas of South Asia reported lower FEV 1 and FVC among individuals with arsenical skin lesions or drinking water with very high levels of arsenic (.250 mg/L) (13-15). Interestingly, a recent retrospective study from Chile identified that those exposed to arsenic either in utero or early life had a lower FEV 1 (11.5%; P ¼ 0.04) and FVC (12.2%; P ¼ 0.04) in adulthood compared with those unexposed (16).The published studies measuring pulmonary function involved small sample sizes and most lacked individual-level exposure data or measured arseni...