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Association of urinary arsenic concentration with incident diabetes was examined in American Indians from Arizona who have a high prevalence of type 2 diabetes and were screened for diabetes between 1982 and 2007. The population resides where drinking water contains arsenic at concentrations above federally recommended limits. A total of 150 nondiabetic subjects aged ≥25 years who subsequently developed type 2 diabetes were matched by year of examination and sex to 150 controls who remained nondiabetic for ≥10 years. Total urinary arsenic concentration, adjusted for urinary creatinine level, ranged from 6.6 µg/L to 123.1 µg/L, and inorganic arsenic concentration ranged from 0.1 µg/L to 36.0 µg/L. In logistic regression models adjusted for age, sex, body mass index, and urinary creatinine level, the odds ratios for incident diabetes were 1.11 (95% confidence interval (CI): 0.79, 1.57) and 1.16 (95% CI: 0.89, 1.53) for a 2-fold increase in total arsenic and inorganic arsenic, respectively. Categorical analyses suggested a positive relationship between quartiles of inorganic arsenic and incident diabetes (P = 0.056); post-hoc comparison of quartiles 2–4 with quartile 1 revealed 2-fold higher odds of diabetes in the upper quartiles (OR = 2.14, 95% CI: 1.19, 3.85). Modestly elevated exposure to inorganic arsenic may predict type 2 diabetes in American Indians. Larger studies that include measures of speciated arsenic are required for confirmation. [ABSTRACT FROM PUBLISHER]

Hyperpigmentation, hyperkeratoses, and Bowen's disease are hallmarks of chronic arsenic exposure. The association between arsenic-induced skin lesions and subsequent internal cancers is examined by using a community-based prospective study. The cohort was enrolled from an arseniasis-endemic area in southwestern Taiwan, where 2,447 residents participated in skin examinations during the late 1980s. The number of participants diagnosed with hyperpigmentation was 673; with hyperkeratosis, 243; and with skin cancer (Bowen's disease or non–melanoma skin cancer), 378. Newly diagnosed internal cancers were ascertained through linkage with National Cancer Registry profiles. Cox regression was performed to estimate hazard ratios with 95% confidence intervals for potential risk predictors. Compared with participants without skin lesions, patients affected with skin cancers had a significantly increased risk of lung cancer (hazard ratio = 4.64, 95% confidence interval: 2.92, 7.38) and urothelial carcinoma (hazard ratio = 2.02, 95% confidence interval: 1.23, 3.30) after adjustment for potential confounders and cumulative arsenic exposure. Hyperkeratosis is significantly associated with an increased lung cancer risk (hazard ratio = 2.76, 95% confidence interval: 1.35, 5.67). A significant interactive effect on lung cancer risk between hyperkeratosis and cigarette smoking was identified, which suggests that patients with hyperkeratosis who have been exposed to arsenic should cease smoking. [ABSTRACT FROM PUBLISHER]

An epidemiologic systems analysis of diarrhea in children in Pakistan is presented. Application of additive Bayesian network modeling to 2005–2006 data from the Pakistan Social and Living Standards Measurement Survey reveals the complexity of child diarrhea as a disease system. The key distinction between standard analytical approaches, such as multivariable regression, and Bayesian network analyses is that the latter attempt to not only identify statistically associated variables but also, additionally and empirically, separate these into those directly and indirectly dependent upon the outcome variable. Such discrimination is vastly more ambitious but has the potential to reveal far more about key features of complex disease systems. Additive Bayesian network analyses across 41 variables from the Pakistan Social and Living Standards Measurement Survey identified 182 direct dependencies but with only 3 variables: 1) access to a dry pit latrine (protective; odds ratio = 0.67); 2) access to an atypical water source (protective; odds ratio = 0.49); and 3) no formal garbage collection (unprotective; odds ratio = 1.32), supported as directly dependent with the presence of diarrhea. All but 2 of the remaining variables were also, in turn, directly or indirectly dependent upon these 3 key variables. These results are contrasted with the use of a standard approach (multivariable regression). [ABSTRACT FROM PUBLISHER]

Perfluorooctanoic acid (PFOA) is persistent in the human body; the general population has serum levels of approximately 4 ng/mL. It causes tumors of the liver, pancreas, and testicles in rodents. The authors studied the mortality of 5,791 workers exposed to PFOA at a DuPont chemical plant in West Virginia, using a newly developed job exposure matrix based on serum data for 1,308 workers from 1979–2004. The estimated average serum PFOA level was 350 ng/mL. The authors used 2 referent groups: other DuPont workers in the region and the US population. In comparison with other DuPont workers, cause-specific mortality was elevated for mesothelioma (standardized mortality ratio (SMR) = 2.85, 95% confidence interval (CI): 1.05, 6.20), diabetes mellitus (SMR = 1.90, 95% CI: 1.35, 2.61), and chronic renal disease (SMR = 3.11, 95% CI: 1.66, 5.32). Significant positive exposure-response trends occurred for both malignant and nonmalignant renal disease (12 and 13 deaths, respectively). PFOA is concentrated in the kidneys of rodents, and there are prior findings of elevated kidney cancer in this cohort. Multiple-cause mortality analyses tended to support the results of underlying-cause analyses. No exposure-response trend was seen for diabetes or heart disease mortality. In conclusion, the authors found evidence of positive exposure-response trends for malignant and nonmalignant renal disease. These results were limited by small numbers and restriction to mortality data, which are of limited relevance for several nonfatal outcomes of a priori interest. [ABSTRACT FROM PUBLISHER]

Inorganic arsenic is metabolized to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). Limited evidence suggests that the ability to fully metabolize arsenic into DMA influences susceptibility to disease. To determine whether percentage of MMA was predictive of disease, the authors used data from a case-control study conducted in Bangladesh (2001–2003). Persons who were diagnosed with keratosis, melanosis, Bowen's disease, or squamous cell carcinoma were matched on age, sex, and village to persons without these conditions. This analysis was restricted to persons who had no missing data on covariates (859 cases, 868 controls). A path analysis was used to evaluate simultaneously the association between the percentage of all urinary arsenic metabolites and the odds of skin lesions using PROC CALIS in SAS, version 9.1 (SAS Institute, Inc., Cary, North Carolina) and Mplus, version 6.1 (Muthén & Muthén, Los Angeles, California). The odds of skin lesions were significantly associated with log10 percentage of MMA (adjusted odds ratio (ORadj) = 1.56, 95% confidence interval (CI): 1.15, 2.12) but not log10 percentage of inorganic arsenic (ORadj = 1.06, 95% CI: 0.75, 1.50) or log10 percentage of DMA (ORadj = 1.07, 95% CI: 0.33, 3.46). This novel analysis confirmed that persons who excrete a higher proportion of MMA have a greater risk of skin lesions after data are adequately controlled for urinary arsenic metabolites, current arsenic exposure, and other risk factors. [ABSTRACT FROM PUBLISHER]

Arsenic in drinking water causes increased mortality from several cancers, ischemic heart disease, bronchiectasis, and other diseases. This paper presents the first evidence relating arsenic exposure to pulmonary tuberculosis, by estimating mortality rate ratios for Region II of Chile compared with Region V for the years 1958–2000. The authors compared mortality rate ratios with time patterns of arsenic exposure, which increased abruptly in 1958 in Region II and then declined starting in 1971. Tuberculosis mortality rate ratios in men started increasing in 1968, 10 years after high arsenic exposure commenced. The peak male 5-year mortality rate ratio occurred during 1982–1986 (rate ratio = 2.1, 95% confidence interval: 1.7, 2.6; P < 0.001) and subsequently declined. Mortality rates in women were also elevated but with fewer excess pulmonary tuberculosis deaths (359 among men and 95 among women). The clear rise and fall of tuberculosis mortality rate ratios in men following high arsenic exposure are consistent with a causal relation. The findings are biologically plausible in view of evidence that arsenic is an immunosuppressant and also a cause of chronic lung disease. Finding weaker associations in women is unsurprising, because this is true of most arsenic-caused health effects. Confirmatory evidence is needed from other arsenic-exposed populations. [ABSTRACT FROM PUBLISHER]